. 2010 Mar 23;16(Suppl 1):14–170.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):14–15.
Background and Purpose:
The most serious consequence of cerebral aneurysms is their rupture - causing intracranial bleeding into subarachnoid space and a high mortality rate. However currently there is no certain quantitative method to estimate the process of growth and rupture in cerebral aneurysms. In this research, energy loss (EL) has been proposed to approximate the hemodynamic lesion inside of aneurysms. 40 IC-PC (Internal Carotid - Posterior Communicating) aneurysms were selected from patients with sizes smaller than 10 [mm]; four ruptured-aneurysms, and 36 unruptured-aneurysms were analysed.
Materials and Methods:
A computational tool; computational fluid dynamics (CFD) has been introduced as the main calculation tool. Another efficient transfer system based on angiography visualization software; RealINTAGE®, was also developed to convert the DICOM format clinical image data into available vessel geometries. The systems are able to efficiently convert the clinical image data (MRI, CT and DSA angiography) (DICOM) into computational available vessel shape geometries (STL format) in 10 to 20 minutes. The whole estimation process including data transfer and simulation is targeted to supply available feedback for clinical diagnosis in half to one hour.
Clinical data source
The original clinical angiographies are selected from the clinical database in the Jikei University School of Medicine (JUSM). In this study, 40 patients with the same location (IC-PC) of cerebral aneurysms and similar geometries were selected from our database. The angiographies of pre-rupture-aneurysms were measured, on average, 5 months before the aneurysm ruptured at the patient's last examination. The four patients (age: 62-71, mean: 66.7, and size: 4.3-5.2 [mm], mean: 5 [mm]) were finally bled and dilation consequence which were named pre-rupture-aneurysms in this study. Other 36 patients of unruptured aneurysms were chosen from a stable group; age 40-78, mean: 60.1, and size: 5.3-10.5 [mm], mean: 6.7 [mm]. The angiographies of unruptured-aneurysms in this study were selected from their first examination, and the observation period of unruptured history was an average of 12 month which was longer than the period of the pre-rupture-aneurysm group. All patients were female. The geometries of aneurysms with flow stream lines were shown in Figure 1.
Figure 1.
Aneurysm rupture estimation by using
Aneurysm risks evaluation method: Energy loss
The energy loss of flows were due to its loss of power, such as when passed through complicated units. Generally, the main reasons as to flow energy loss were flow separation, turbulence and flow attachment. From observations of the flows within aneurysms, the flow pattern appeared very complex, with the occurrence of jet flows, swirling and separation and flow attachment. The interior flows of the aneurysm were highly dependent on the location and geometry of the parent artery. It is considered that a part of the lost power was transferred into other types of energy, such as heat and power to wear away aneurysm surfaces. This hemodynamic energy loss is assumed to be one of the major factors in the development, growth and final rupture of aneurysms. In order to calculate the difference of energy loss when flows pass through the aneurysms, the aneurysms were removed on-screen (named as non-aneurysms) by using visualization software. The simulations of non-aneurysms were carried at the same flow conditions as all cases of with-aneurysms. The energy loss (energy difference) was calculated using the equation 1.
| (1) |
Where, E [W] is energy calculated from the artery domain inlet and outlet.
| (2) |
Where, P [Pa] is pressure, v [m/s] is velocity, Q [m3/s] is flow rate, i and o indicate inlet and outlet.
In order to estimate various sizes of aneurysms using a standard method, the energy loss is proposed to be divided by its volume. The volume energy loss ELv was calculated as equation 3.
| (3) |
Results:
The EL, calculated at the rupture-aneurysms, was on average, over five times higher than the stable unruptured-aneurysms (figure 1). Through observation of the blood flow patterns, the flow inside therupture-aneurysms appeared more complex, and they crashed strongly into aneurysm surfaces (figure 2). On the contrary, the flow inside of the unruptured-aneurysms passed smoothly through the aneurysms. The average WSSs on aneurysms at heart peak systolic condition is shown on figure 3. On the other hand, however, there was no significant difference in magnitude and gradient in WSSs between the two groups of aneurysms.
Figure 2.
Velocity vectors and stream lines
Figure 3.
The average WSS; did not have a statistically significant difference (P=0.8>0.1)
Conclusion:
The research found that flows appeared more complex – with higher disturbances in the pre-rupture-aneurysm. The EL created by flow through the aneurysms indicates a clear differentiation between pre-rupture and unruptured aneurysms. The results indicate that the EL may be an important parameter to estimate aneurysm growth and rupture.
References
- 1.Qian Y, Harada T, Fukui K, Umezu M, Takao H, Maruyama Y. Hemodynamic analysis of cerebral aneurysm and stenosed carotid bifurcation using computational fluid dynamics technique, Life system modeling and simulation. International conference LSMS. 2007;LNBI 4689:292–9. [Google Scholar]
- 2.Qian Y, Fukui K, Umezu M, Takao H, Ishibash T, Murayama Y. Cerebral aneurysm rupture and unrupture risk factor analysis using computational fluid dynamics technique. Interventional Neuroradiology. 2007;13(Suppl 2):387. [Google Scholar]
interv neuroradiol. 2010 Mar 23;16(Suppl 1):16–21.
Purpose
The introduction of microcatheter delivered devices designed to achieve reconstruction of the parent arteries harbouring aneurysms has provided an alternative therapy for wide neck large and giant aneurysms and also for fusiform aneurysms.
These devices consist of mesh tubes with very fine holes that enable flow to be diverted from the aneurysm sac and yet preserve the patency of jailed side branches.
The aim of this project is to survey all users of these devices in Australia and New Zealand since their introduction here and provide a summary of their experience.
Materials and Methods
All neurointerventionists in Australia and New Zealand were contacted by phone and email to participate in this study on a deidentified basis and to provide data to be entered into a pooled database which form the basis of this report.
The same data template was sent to all participants to provide data on patient demographics, antiplatelet therapy, aneurysm size and location, immediate clinical complications and technical difficulties in stent deployment and longest follow-up data. Two devices were used: The Silk stent (Balt Extrusion, Montmorency, France) and the Pipeline Embolization Device [PED] (ev3, USA).
Detailed data as per template was available for 57 patients with 60 aneurysms. 23 of these aneurysms were treated with Silk stents and 37 were treated with PED. Only a summary of data was available for another 22 patients treated with PED. However, this summary contained adequate details of complications enabling a comprehensive review this.
Hence for data handling, the study was divided into 3 groups: Silk, Pipeline I (group with detailed results) and Pipeline II (group with summarised results).
In total, there is data for 79 patients with 84 aneurysms. We estimated that this account for about 85% to 90% of aneurysms treated by these devices in Australia and New Zealand to date.
Results
Silk Stents
Demographics
There were 23 patients with 23 aneurysms:
4 males (17 %) and 19 females (83 %). Age ranged from 32 - 77 with a mean of 57.2 years.
Internal carotid aneurysms (ICA - cavernous and supraclinoid) : 18
ICA - base of skull : 2
Posterior communicating aneurysm : 1
Basilar aneurysm : 1
Cervical ICA aneurysm : 1
Aneurysm size ranged from 6 to 30 mm, with one fusiform aneurysm.
A total of 26 stents were used in 23 aneurysms with and average of 1.1 stent per patient.
20 aneurysms were treated with 1 stent (maximum aneurysm size: 30mm, maximum neck size: 17 mm)
3 aneurysms required 2 stents: One fusiform and one 27X19 mm base of skull aneurysm.
The first stent of the third aneurysm failed to deploy and was removed and replaced with another Silk. All patients were elective.
Antiplatelet medication
Data for antiplatelet medication were available for 19 patients
17 (94%) were on dual antiplatelets (aspirin and clopidogrel). 2 patients were allergic to aspirin and one developed allergy to clopidogrel after 2 to 3 weeks, with cessation of the medication in these 3 patients.
Technical Complications
Stent stenosis.
3 of 23 patients required angioplasty for:
stenosis due to compression by aneurysm
failure of stent to open proximally
stent not fully opened initially
Difficulty & Failure to deploy
3 of 26 stents failed to deploy properly and all 3 stents had to be removed. One stent was replaced with a second Silk stent at the same session, in the second patient, the aneurysm was coiled, and in the third patient, the aneurysm was subsequently treated with a Pipeline stent.
3 patients needed angioplasties either for existing stenosis of the parent artery or to open the proximal portion of stent during deployment.
Vasospasm
During the process of placing the stents, 2 of 23 patients developed vasospasm and needed glyceryl trinitrate
(GTN) to successfully treat the vasospasm.
Others
One (1/23) patient had a small dissection distal to stent which healed without clinical problems.
One (1/23) patient had a dissection in the high cervical carotid, presumably due to the guide catheter manipulation, and required angioplasty to successfully reopen channel. There were no clinical sequelae including stroke.
Stent Thrombosis
There was no immediate or delayed stent thrombosis.
Clinical complications
Acute
No patients suffered acute haemorrhage, infarction or transient ischaemic attack (TIA) during the procedure or in the immediate post procedural period. There was no death.
Delayed
Follow up period of 1 to 12 months on 20 patients were available. This excluded the 2 patient who had their Silk stents removed and not replaced by another Silk. One other patient had no follow up imaging yet.
1. TIA: There was one (1/20) TIA, amaurosis, despite still on clopidogrel and aspirin. This was the patient with the 26 mm (17 mm neck) cavernous carotid aneurysm in which the first stent failed to open and had to be replaced with a second silk. The aneurysm grew by 4 mm before finally completely thrombosed.
2. Stroke & Death None
3. Aneurysm enlargement:
There was one (1/20) basilar aneurysm which grew in size since treatment, and at the 6 month follow up, it was less than 25% occluded.
4. Aneurysm rupture:
One (1/20) developed a carotid cavernous fistula at 4 months and was treated by carotid sacrifice. This was a 21 mm (10 mm neck) paraopthalmic carotid aneurysm originally treated with a single Silk stent.
Follow-up
Period: 1 to 12 months
Follow up period of 1 to 12 months on 20 patients (21 aneurysms) were available. This excluded the 2 patient who had their Silk stents removed and not replaced by another Silk.
Aneurysm Occlusion
100 % occlusion - 8/20 (40%)
75-100% occlusion - 7/20 (35%)
50-75% occlusion - 2/20 (10%)
25-50% occlusion - 1/20 (5%)
0-25% occlusion - 2/20 (10%)
All stents were patent.
Jailed Branches
There were 10 carotid jailed branches, ophthalmic and posterior communicating arteries. 9 remained patent in a follow up period of 2 to 12 months. One ophthalmic was occluded by 12 months.
The basilar aneurysm stent patient did not have an infarct by 6 months indicating that the perforators remained patent.
Pipeline Stents
Pipeline Patient Group 1
Demographics
There were 34 patients with 37 aneurysms
4 males (12 %) and 30 females (88 %). Age ranged from 32 - 83 with a mean of 55.1 years.
Internal carotid aneurysms (ICA - cavernous and supraclinoid) : 26
ICA - base of skull : 260
Posterior communicating aneurysm : 268
Basilar aneurysm : 262
Cervical ICA aneurysm : 260
Vertebral : 261
Aneurysm size (available for 36 aneurysms) ranged from 4 to 32 mm (saccular) and 8.0 - 35 mm (fusiform).
A total of 56 stents were used in 37 aneurysms in 34 patients with an average of 1.6 stent per patient, and 1.5 stents per aneurysm.
17 aneurysms were treated with 1 stent: (maximum aneurysm size: 32 mm, maximum neck size: 10 mm)
15 aneurysms required 2 stents: (maximum aneurysm size: 28 mm, maximum neck size: 14 mm)
2 aneurysms required 3 stents: (35 mm fusiform aneurysm & a greater than 25mm diameter carotid aneurysm) There were 3 acute patients and 28 elective patients.
Antiplatelet medication
Data for antiplatelet medication were available for 32 patients
31 (97%) were on dual antiplatelets (aspirin and clopidogrel). 1 patient (3%) was on clopidogrel only.
Technical Complications
Stent stenosis.
No stenosis was reported
Stent Thrombosis
There was one stent thrombosis less than 12 hours post deployment.
Difficulty & Failure to deploy
1. One stent shortened excessively and deployment of second stent resulted in stent looping and kinking in the neck of aneurysm with resultant ongoing amaurosis despite aspirin and clopidogrel therapy.
Vasospasm
This was not reported
Clinical complications
Acute
No patients suffered acute haemorrhage or infarction
-
2 elective patients had TIA:
a. One patient had ongoing amaurosis despite aspirin and clopidogrel therapy after difficulty with deployment of 2 stents in the same aneurysm
b. One patient with a 12 mm cavernous carotid aneurysm (neck of 10 mm) treated with 2 stents suffered stent thrombosis (despite being premedicated with aspirin and clopidogrel) and hemiplegia requiring intraarterial thrombolysis with abciximab and heparin with complete recovery
Death: A 37 year old female with an acute 35 mm fusiform carotid aneurysm treated with 3 stents died following aneurysm rupture on deployment of the third stent.
Delayed
Follow up period of 2 days to 5 months on 23 patients were available.
The remainder of the patients had their procedures performed only recently, and have not had their follow up yet
-
TIA: 1 patient had TIA.
a. A 57 year old male with a 14 mm left carotid paraopthalmic aneurysm (neck size: 5 mm) treated electively with 1 stent developed TIA at 3 months after stopping clopidogrel.
-
Stroke and death: 1 patient died
a. A 56 year old female with a 12 mm basilar tip aneurysm treated electively with 1 stent had a pontine infarction at 1 month despite being on aspirin and clopidogrel therapy resulting in death.
Aneurysm enlargement: None reported
Aneurysm rupture: None reported
Follow-up
Period: 2 days to 5 months
Follow up period of 2 days to 5 months on 23 patients were available.
The remainder of the patients had their procedures performed only recently, and have not had their follow up yet
Aneurysm Occlusion
100 % occlusion - 14/23 (58%)
75-100% occlusion - 4/23 (17%)
50-75% occlusion - 0/23 (0%)
25-50% occlusion - 0/23 (0%)
0-25% occlusion - 1/23 (24%)
All stents were patent.
Jailed Branches
There were 21 jailed carotid branches in 16 patients, (ophthalmic, anterior choroidal, anterior inferior cerebellar [AICA] and posterior communicating arteries). All 21 remained patent in a follow up period of 2 days to 5 months.
The patient with a basilar aneurysm initially treated within an Enterprise stent with subsequent deployment of a PED within the Enterprise did not have an infarct by 1 week indicating that the perforators remained patent.
Another patient with 12 mm basilar tip aneurysm treated electively with 1 stent had a pontine infarction at 1 month indicating perforators occlusion.
Pipeline Patient Group II
There were 22 patients with 24 aneurysms
Acute Cases
These consisted of 5 acute subarachnoid haemorrhage patients, 3 were treated within 48 hours and 2 treated within 2 to 3 weeks.
Complications
1. Stent Deployment problem, Rerupture and Death:
There was one death. Initial treatment of this patient consisted of 2 stents with antiplatelet agents. The stents did not open properly and had to be angioplastied with Hyperglide balloon.
Despite an angiogram showing that the aneurysm appearing virtually occluded on day 2, it reruptured 5 days post stenting in the setting of vasospasm. The angiogram suggested redirection of blood into the aneurysm. A third stent was deployed with angioplasty of vasospasm. The patient died.
Elective Cases
There were 17 elective patients, 3 of whom had previous stents.
2 presented with mass effect: One with decreased visual acuity in the eye (no change after treatment), and one with quadriparesis from a vertebro-basilar aneurysm (improvement of symptoms after 53 days).
11 patients had 1 stent
6 patients had 2 stents
5 patients had 3 stents
There was an average of 2.2 stents per patient.
Antiplatelet medication
All were on aspirin and clopidogrel
Complications
There was no acute or delayed complication including stroke or TIA in this elective group.
Follow-up
All 17 patients had CTA at 1 month.
Aneurysm Occlusion
1100 % occlusion - 16/17 (94%)
Partial occlusion - 1/17 (6%)
Discussions
This is not a matched control study between the 2 types of flow diverters.
The Silk group (up to 12 months) has longer follow up period than the Pipeline group (up to 5 months)., and a significant proportion of the Pipeline group has only been treated recently and therefore has no follow up data yet.
We have detailed data for 57 patients (60 aneurysms: 23 Silk and 37 Pipeline patients) and only a summary of data for the third group of 22 Pipeline patients. The total for all groups is 79 patients.
Of the 57 patients, 14 % were male and 86 % female. The aneurysms were mostly large or giant with the average diameter in the Silk group of 14.1 mm and the pipeline group of 12.6 mm.
Of the 57 patients, the average stent used per aneurysm is 1.1 in the Silk group and 1.5 in the Pipeline group. This may be due to longer lengths available for the Silk stents and despite the somewhat larger aneurysms.
The vast majority of patients had dual antiplatelets regime as recommended by the manufacturers.
Technical Complications
As a group, the stents have a small incidence of deployment difficulties including excessive shortening, kinking and failure to open fully requiring balloon angioplasty.
Other complications during deployment include dissection of the parent arteries during manipulation of the guide catheters and the stents in these often torturous parent arteries.
Vasospasm of parent arteries requiring vasodilator infusion happened infrequently.
Clinical complications
2 patients (2/79: 2.5 %), both electives, developed TIA after difficult stent deployment. This may be due to trauma to the parent vessel. A third patient (1/79: (1.3%) developed TIA after stopping clopidogrel at 3 months.
Only 4 vertebro basilar aneurysms were treated in the group of 57 patients. One patient (25%) 56 year old female died of a pontine infarction 1 month later following treatment despite dual antiplatelet therapy. This is obviously of concern as the stents are meant to allow side branches to remain patent. Are the perforators too small in some patients? Do their antiplatelet activity need to be monitored closely? Note that this group does not include the vertebro basilar aneurysm patient of the third Pipeline II group.
The basilar aneurysm of one of these 4 patients enlarged after treatment and was less than 25 % occluded at 6 months. Given the above complication, retreatment with a further stent within the first one would raise concern.
Also of concern is the one patient (1/79: 1.2%) with acute stent thrombosis requiring urgent thrombolysis, despite this patient being premedicated with dual antiplatelet regime. Is this due to patient resistance to antiplatelet medication? Should patients have their antiplatelet activity checked prior to stenting?
There were 3 aneurysm rupture (3/79: 3.8%). 2 were associated with treatment of acute aneurysms. One ruptured following deployment of the third stent, and the other ruptured 5 days later in association with vasospasm. The other was a delayed rupture at 4 months resulting in a carotid cavernous fistula (CCF).
In the second case, the aneurysm appeared nearly occluded 2 days after placing of 2 Pipeline stents. It appeared that the vasospasm redirected blood back into the aneurysm causing it to rupture.
In the case of the development of CCF, the rupture so soon after placement of the stent suggest that the stent itself may have change the hemodynamics to predispose to rupture.
These cases should instigate a search for possible aetiology of aneurysm rupture following stent deployment. It appears that despite substantial angiographic occlusion, a persistent or recurrent jet of blood into the aneurysm may predispose it to rupture. Part of the follow up may be to look for a jet whether by digital subtraction angiography or by other imaging means.
In addition, should there be adjunctive coils embolisation as well in some of these aneurysms, particularly in the acute group, to prevent rupture post stenting, especially as antiplatelet agents are required as well.
Stent and Vessel patency
More encouraging is that every stent remained patent in a follow up period from 2 days to 12 months.
Excluding the posterior circulation perforators, all except one of 31 jailed side branches remained patent on follow up (97%). However, it would appear that 25% (1/4) of patients with jailed basilar perforators occluded.
Aneurysm occlusion
In the group of 57 patients with detailed data, a significant proportion (slightly more than 50%) are completely occluded at follow up to 12 months. However, from the above results it would appear that the partially occluded ones continue to have a small risk of rupture.
Conclusion
The data would suggest that there is a role for using flow diverter stents for treatment of large and fusiform aneurysm for which there is no other satisfactory endovascular or surgical treatment.
The occlusion rate is promising in this small series and short period of follow up.
The complication rates, both technical and clinical, are low. Nevertheless, they are serious including major stroke and death and aneurysm rupture post treatment.
Further studies are required to determine the cause of rupture after stent placement. The aetiology and the risk factors and need to be determined to allow better patient selection and possible remedy. In particular, can the stent change the hemodynamics of the jet into the aneurysm for the worse? Does a residual jet predispose to rupture? Is vasospasm a risk factor? What is the best imaging technique to show the "jet"?
It would appear that jailed major carotid side branches including the anterior choroidal arteries have a very low risk of occlusion, but the basilar perforators maybe different and of a higher risk of occlusion. Are the middle, anterior and posterior perforators also subject to higher risks? How should we manage these patients? Obviously adequate antiplatelet regime is essential and this raises the question of activity testing of these drugs.
The flow diverters hold significant promise for treating "untreatable" aneurysms hitherto, but there is a small but significant risk that needs to be further elucidated and managed.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):22.
Cerebral arterial aneurysms (AAs) are currently treated mostly by endovascular methods, this latter therapy being considered as preferable to surgical clipping. Both managements however remain gross mechanical methods applied to a disease that is recognized more and more as being a vascular wall disorder of biological origin and not as a simple vascular herniation, the AA being thus a morphological symptom (a phenotypic expression?) of a biological disease.
AA are lesions acquired during life because of exposure to risk factors, and not exclusively to congenital defects or malformations. They represent thus the answer of the vessel wall to these risk factors that can be considered as triggers for the creation of AA. Signs of protease activities, cell death, chronic inflammation have indeed been described in the wall of the AA, in which they seem to be associated to wall degeneration, and secondarily to rupture. The factors that create and maintain protease activity, cell death and inflammation remain currently unprecised. Due to histopathologic similarities with early atherosclerotic lesions and aortic aneurysms, one could hypothesize that the same factors inducing inflammation and degeneration in these latter pathologies, could also work in the AA wall.
Recently contribution of bone-marrow-derived myo-intimal cells to fibrotic lesion formation after mechanical or immunological vascular injury has been described. These cells might be used as local or systemic transplants that repopulate and strengthen the decellularized and degenerated AA wall. Experimental works on percutaneous transplantation of genetically-modified aulogous fibroblasts have also been performed in order to use these cells as a cellular platform for locoregional secretion of therapeutic proteins to treat specific diseases.
The mechanisms leading to degeneration and inflammation need to be clearly elucidated to understand why, how, and when AA rupture. Experimental models reproducing precisely the pathobiology of the AA wall must be developed in order to escape from the erroneous rigid mechanical concepts of the disease, and in order to test novel therapeutic concepts or bioactive embolization devices. These new ways of exploration may represent future important new potentials for management of vascular pathologies.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):23.
Introduction
From the early point of non-randomized clinical trial of detachable coil, GDC, which started in 1991, it became obvious that coils placed in the aneurysm may be compressed or migrated, reopening initially occluded lumen of aneurysms. In-vitro studies illustrated maximum volume of metal in the completely packed aneurysm is less than 30%. Due to hemodynamic stress and tendency of coils to reform to preformed shape, a mesh of coils changes and becomes compacted. Reported rates of overall recanalization range from 15 to 35%. It is certain that location and size of aneurysm dictate possibility of recurrence.
To minimize a chance of recurrence, so called bioactive coils have been introduced since 2002. The first such newer generation coils, Matrix, was intended to promote inflammatory reaction in the initial thrombus making more permanent organized connective tissue. The second one was Hydrocoil. Platinum coils are inserted into the expandable hydrogel. The gel material increases its volume in contact with blood. Animal study showed that once it is inserted in aneurysm lumen, expanded gel occupies more space and promotes fibrosis in gap between hydrogel loops. The third one available in clinical practice is coils with polyglycolic acid material in the middle of platinum string. Number of trials and publications of case series have been carried out to show durability and clinical effectiveness for each of such coils.
Review of Clinical Trials
-
MAPS; Matrix And Platinum Science
The MAPS trial examines Target Aneurysm Recurrence Rates: clinically relevant recurrence rates resulting in target aneurysm reintervention, rupture/re-rupture and/or neuro logic death for Matrix 2® and GDC® Coils used for the treatment of intracranial saccular aneurysms. The trial will compare TAR rates to recurrences measured by angiographic analysis and assess the utility of angiographic analysis for predicting clinically relevant recurrences.
-
HELPS; Hydrocoil Endovascular aneurysm occlusion and Packing Study
Four hundred ninety-nine patients were recruited, 250 for bare platinum coils and 249 for hydrocoils. Mean aneurysm size was 6.5 mm (26% were ≥ 10 mm), 53% were recently ruptured aneurysms, and an assist device was used in 46%. The initial coiling results showed complete and near complet occlusion rate was 78.5% in hydorcoils and 85.55 in bare platinum coils. Seventy procedural adverse events were reported in hydrogel coils and 86 in control arms. No difference was found between arms in the operator assessment of angiographic occlusions (P = .3). It is planned to collect 3-6 months and 15-18 months followup angiographic results.
-
HCAT; Hydrocoil Cerecyte Aneurysm Treatment
The primary outcome of this trial is to compare clinical and angiographic outcomes in patients receiving HES or Cerecyte Coils. Clinical status will be evaluated immediately post treatment, then at 5-7 months and angiographic follow up at 12-18 months.
-
PRET; Patients prone to Recurrence after Endovascular Treatment
A multicenter randomized, single-blind controlled trial comparing hydrogel-coated coils to standard platinum coils in two types of patients: All patients with a large intracranial aneurysm ≥10mm (PRET-1) or with a major recurrence after previous coiling (PRET-2), eligible for endovascular treatment.
Conclusion
Up to present, most of trials and publications regarding use of bioactive coils are either non-randomized registry or case series. Even reports of randomized control trial are only short term results, not sufficient to demonstrate long-term durability. Premarketing as well as post-approval clinical series of each device failed to show these bioactive coils reduce rates of recanalization significantly.
References
- 1.White PM, Lewis SC, Nahser H, et al. HydroCoil Endovascular Aneurysm Occlusion and Packing Study (HELPS trial): procedural safety and operator-assessed efficacy results. AJNR Am J Neuroradiol. 2008;29:217–23. doi: 10.3174/ajnr.A0936. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 2.Murayama Y, Vinuela F, Ishi A, et al. Initial clinical experience with Matrix detachable coils for the treatment of intracranial aneurysms. J Neurosurg. 2006;105:192–99. doi: 10.3171/jns.2006.105.2.192. [DOI] [PubMed] [Google Scholar]
- 3.Linfante I, Deleo MJ, Gounis MJ, et al. Cerocyte versus Platinium coils in the treatment of intracranial aneurysms: packing attenuation and clinical midterm results. AJNR Am J Neuroradiol. 2009;30:1456–1501. doi: 10.3174/ajnr.A1617. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 4.Henkes H, Fischer S, Weber W, et al. Endovascular coil occlusion of 1811 intracranial aneurysms: early angiographic and clinical results. Neurosurgery. 2004;54:268–80. doi: 10.1227/01.neu.0000103221.16671.f0. [DOI] [PubMed] [Google Scholar]
- 5.Raymond J, Guilbert F, Weill A, et al. Long-term angiographic recurrences after selective endovascular treatment of aneurysms with detachable coils. Stroke. 2003;34:1398–403. doi: 10.1161/01.STR.0000073841.88563.E9. [DOI] [PubMed] [Google Scholar]
- 6.White PM, Raymond J. Endovascular coiling of cerebral aneurysms using "bioactive" or coated-coil technologies: A systemic review of the Literature. AJNR Am J Neuroradiol. 2009;30:219–226. doi: 10.3174/ajnr.A1324. [DOI] [PMC free article] [PubMed] [Google Scholar]
interv neuroradiol. 2010 Mar 23;16(Suppl 1):24.
Arterial dissection has two pathological features; one is aneurysm formation and the other is dissecting occlusion. As the clinical manifestation, the former ruptures, and the latter causes cerebral ischemia. Aneurysm type includes so-called dissection aneurysms with fusiform or pearl and string shape as well as blister-like aneurysm at dorsal ICA, bleb and beads-like aneurysm at perforators, et al. While, stenotic type includes the PICA-involved vertebral artery dissection causing Wallenberg syndrome, traumatic or iatrogenic dissection on the catheter intervention and acute occlusion of main trunk of intracranial vessels in young patients.
Occurrence of dissection is initiated with the degenerative background like as cystic medionecrosis and is promoted with external and internal factors like as trauma, infection, aging, arteritis, acute medium necrosis, hemodynamic stress, intimal injury and atherosclerosis. Dissection is introduced with the tearing or fragmentation of internal elastic lamina particularly induced in the patients with connective tissue disorders, and is finally expressed by the local laceration of intima and subsequent influx of blood into the dissecting lumen. Most intracranial dissection shows one entry type, however, dissection on the peripheral artery or iatrogenic dissection due to balloon angioplasty tends to develop entry-reentry type. Although most entry-reentry type leads to stenosis, some of the one entry type forms aneurysm. Such difference of clinical manifestation may be due to the depth of dissecting layer.
Mechanical dissection is usually caused by the traction stress against the vessel or by strong external impact with the bump of bone edge and due to piercing and tearing off the intima on the catheter intervention. Most traumatic dissection is associated with thrombo-embolic stroke due to the early migration of thrombus formed at the dissecting site. Dissecting lumen occasionally enlarges and develops aneurysm. According to our experimental research such various clinical and morphologic feature depends on the entry size and inflow volume. As for the time course stenotic change will be regressed within a few months, however, the persistent occlusion will not recover. While dissecting aneurysm will enlarge in the subacute stage, however, the morphologically stable aneurysm will not change or rather regress, and occasionally result in spontaneous thrombosis.
Arterial dissection may be more common and more frequent incidents than those we have recognized. Some of acute cerebral ischemic syndrome and hemorrhagic events may be explained by the similar mechanism and pathogenesis of dissection.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):25–28.
The optimal management of patients with asymptomatic unruptured saccular intracranial aneurysms (UIA) remains controversial. The most significant complication is rupture and subarachnoid hemorrhage (SAH), with its attendant morbidity and mortality. Hence the goal of therapy is to identify those patients in whom the risks posed by the aneurysm itself outweigh those of the possible treatment options, and where treatment is indicated, to identify the optimal strategy among the choices available.
Unruptured intracranial aneurysms are not rare. Estimates of their prevalence based on autopsy and angiographic series have ranged greatly - from less than 1% to more than 10%, depending on patient population and study methodology. As expected, retrospective autopsy series have yielded the lowest apparent prevalence, while prospective angiographic series the highest. On the basis of a large systematic review of available series, their prevalence in the general population has been estimated at around 2%.i Aneurysms are more common in women, patients with polycystic kidney disease, older patients and those with a first degree relative with aneurysm or SAH. Other risk factors consistently associated with aneurysm formation are cigarette smoking, hypertension and excessive alcohol useii.
When considering whether to treat an UIA, a crucial piece of information is natural history, specifically likelihood of rupture. The ISUIA investigators have published the largest restospective (ISUIA-1iii, 1449 patients, >12,000 patient years follow up) and prospective (ISUIA-2iv, 1692 patients, >6500 patient years follow up) studies on the natural history of UIA. In ISUIA-1, based on a mean follow up of 8.3 years, the annual rate of rupture was 0.3% ; 1% and 0.05% respectively for aneurysms greater or less than 1 cm. Posterior circulation and posterior communicating aneurysms were associated with higher risk. In the group of patients who received conservative treatment in the prospective ISUIA-2 study, the mean rate of SAH per patient-year was 0.8% over a mean follow up of 4.1y. The cumulative five year risk of bleeding for anterior circulation aneurysms was 0% for aneurysms less than 7 mm in size(1.5% in those with previous fully treated aneurismal SAH), 2.6% for aneurysms 7-12 mm in size and 14.5-40% for larger aneurysms. For posterior circulation and posterior communicating aneurysms, 5 year rupture rates ranged from 2.5% for <7 mm aneurysms to 50% for giant aneurysms. These data have supported a more conservative approach to small anterior circulation aneurysms in recent years, with the caveat that a 0% rate of rupture of <7mm aneurysms in ISUIA-2 is implausibly low given that in clinical series of ruptured aneurysms, these make up 35-50%v, pointing to possible selection bias.Wermer et alvi have published a meta-analysis of 19 studies (including the ISUIA data) published between 1966 and 2005 with a total of 6556 UIAs in 4705 patients with a mean follow up of 5.6 years. The overall risk of rupture per patient-year at risk was 1.2% for studies with mean follow up less than 5y, 0.6% for mean follow up between 5 and 10y and 1.3% for studies with greater than 10y follow up. Size greater than 5mm, symptomatic aneurysm , posterior circulation location, female gender, age greater than 60 and Japanese or Finnish descent were associated with greater risk, as was smoking, although the later was not statistically significant.
Undoubtedly, there are other factors which influence the rate of rupture. Likely candidates include patient specific factors such as background vasculopathy, hypertension, alcohol use and family history and aneurysm specific factors such as morphology (lobulation, daughter sac, aspect ratiovii), hemodynamics, aneurysm growth rate and multiplicity. The presence of mural thrombus and calcification also likely influence rupture risk. Although the data supporting these variables remains inconclusive, they must be kept in mind in the clinical decision making processviii.
Next we must consider the treatment risks and benefits. A systematic review by Lanterna et alix of the literature concerning coil embolization of UIAs published between 1990 and 2002 (1379 patients in 29 studies), indicated an overall procedure related permanent morbidity and mortality rate of 7% and 0.6% respectively with a reduction in reported morbidity rates to 4.5% in later studies. A large retrospective single-institution case series by Standhardt et al x of all 173 UIA patients treated by endovascular means over a 12 year period from 1992-2004 indicated a procedure related mortality rate of 0.5% and permanent morbidity rate of 2.5% (1% severe deficit). In a consecutive series of 146 unruptured aneurysms treated by GDC coiling, Holmin et al report a mortality of 0% and permanent morbidity in 3.4%xi. While these figures compare favorably to surgical series, no randomized clinical trial has directly compared the morbidity and mortality of endovascular versus surgical management in UIAs. In the ISAT trialxii, in 2143 patents with ruptured aneurysms in which surgical and endovascular treatment were judged to be in clinical equipoise, the rate of death or dependence at 1 year was significantly less in the endovascular group (24 vs. 31%) with a lower cumulative mortality over 7 years.
In ISUIA-2 (iv), the morbidity of surgical and endovascular therapy were prospectively compared in a nonrandomized group of patients, 1917 of whom received surgery and 451 who received endovascular repair. The risk of death or disability at 1 year was significantly less in the endovascular cohort than in the surgical group (12.6 and 9.8% respectively; 10.1 and 7.1% in the group with previously treated aneurysmal SAH). Overall, the patients in the endovascular group were older, with larger aneurysms and a greater proportion of basilar and 26 cavernous aneurysms. These results suggest that when both treatments are feasible, up-front risk from endovascular procedures is lower than that of surgery.
But what about efficacy? Consideration of treatment efficacy is limited by relatively small numbers of patients, length of follow up, and mixing of ruptured and unruptured aneurysm data. It has been accepted that satisfactorily clipped aneurysms are effectively cured, and surgical series have indeed demonstrated a very low re- rupture rate in follow up of clipped aneurysms that have been completely excluded based on angiography. In one series of clipped ruptured aneurysms followed for a mean of 10 years, annual rates of 0.14% recurrent SAH and 0.09% asymptomatic regrowth were seenxiii. There has been concern regarding the long term durability of endovascular treatment. Published rates of residual/remnant aneurysm following endovascular treatment have been in the range of 5-20%, recanalization rates between 15-35%, and retreatment rates up to 13%. Lower degree of aneurysm occlusion and recanalization are thought to be risk factors for rerupture, although the data have been conflictingxiv, xv.
Despite this, the rates of rebleeding have been low. In a retrospective analysisxvi of 173 coiled unruptured aneurysm patients treated at a single institution between 1992 and 2004 for a mean of 3.7 years, 3 patients ruptured (0.5% annual rupture rate), and all of these were giant posterior circulation aneurysms. In the series by Holmin et al (xi), retreatment rate was 12% and rebleeding occurred in only one patient (0.68% of coiled UIAs) at median follow up of nearly 5 years. The CARAT xvii(Cerebral Aneurysm Rerupture after Treatment) investigators identified all aneurismal SAH patients treated at their institutions between 1996-98 and reviewed the results in 1010 patients treated by either surgery (711) or coiling (299) followed for a mean of 4.4 years. Annual rates of retreatment were 13.3% for coiling and 2.6% for clipping in the first year, 4.5 and 0% in the second year and 1.1 and 0% respectively thereafter. While late retreatment was more common in the coiling group, no late retreatment lead to death or disability. Rates of rehemorrhage were low for both groups but were slightly lower in the surgical cohort (annual rates of rerupture for coiling and surgery 4.9 and 2% respectively in the first year and 0.11% and 0% in subsequent years). Combining their data with the rerupture rates in ISAT, the early benefit of coiling would only be reversed after 70 years of follow up. Projecting their data onto the disability/death data from ISUIA, the impact of retreatment would not outweigh the early befit of coiling even after 100 y of follow up. In summary, the rate of aneurysm rupture after treatment and need for repeat treatment is somewhat greater for endovascular therapy, but the difference appears to be small in comparison to the lower rates of procedure related morbidity.
From a health care system perspective, another question is whether the treatment of unruptured aneurysms is cost effective in terms of its ability to prevent costs of hospitalization and long term care. An analysis using Dutch data showed that for 50 year old patients, treatment using both surgical and endovascular techniques was cost effective for a wide range of rupture rate scenarios above 0.3% per year, slightly more so in womenxviii.
Finally, in applying this disparate information to specific clinical scenarios, it is important to consider the data from the literature in the context of patient-specific, aneurysm-specific, and treatment-specific factors, in order to provide individualized recommendations regarding treatment.
Patient-specific factors relating to life expectancy are crucial parameters in determining the appropriateness of UIA treatment. In patients of advanced age or with significant comorbidities the reduced life expectancy of the patient may result in the up-front risk of treatment exceeding the potential beneficial reduction in risk of SAH. Nonmodifiable risk factors for rupture such as female gender, etiologic factors, and modifiable risk factors which may increase the risk of rupture, such as smoking, alcohol use and hypertension should also be taken into account. Idiosyncratic factors such as excessive or debilitating anxiety pertaining to a small unruptured aneurysm may result in the need for treatment to be considered for aneurysms that might otherwise be followed. Patient factors can also influence the choice of therapy. Excessive tortuosity of the extracranial vessels can render endovascular treatment difficult or impossible, favoring surgery in some cases. Some patients may reject the idea of follow up and the possibility of recurrence that goes with endovascular treatment. On the other hand, significant comorbidity may render a patient unable to tolerate the stresses of conventional surgery rendering endovascular treatment more attractive.
Next, aneurysm specific factors must be integrated. As discussed above, size plays an important but by no means exclusive role. In addition to influencing predictions about risk of rupture, aneurysm size can influence the choice of therapy. Coiling of very small aneurysms (<2-3 mm) has been associated with increased risk of rupture while coiling of giant aneurysms has been associated with coil compaction and recanalization. Morphologic factors can influence whether coiling is possible and whether assistive techniques such as balloon remodeling or stent-assisted techniques are required. Important parameters which can predict immediate post coiling occlusion rates include absolute size of the neck, dome to neck ratio, aneurysm shape, and incorporation of branch vesselsxix.
Aneurysm location is of course another important factor. General rules of thumb are that basilar termination aneurysms, which present a difficult surgical access, are often more suitable for endovascular treatment. MCA bifurcation aneurysms often have unfavorable branch vessel geometry and are surgically accessible, hence often (but not always) better suited to clipping. For aneurysms in other locations, both treatments are often possible. For example, for distal/peripheral aneurysms, both clipping and endovascular vessel sacrifice are possibilities. For anterior and posterior communicating aneurysms, both treatments can often be considered. In many cases, clinical, morphological and local endovascular/surgical experience are the deciding factors. In other words. patient and aneurysm factors need to be considered in the context of the technology available and institutional expertise (Therapy factors). With the advent of new technologies, the repertoire of both surgical and endovascular therapies will continue to expand. Examples of this include recent advances in flow diverting stents and cerebrovascular bypass procedures.
Coming back to the clinical vignette, a presumably healthy 40 year old female patient with >30 years life expectancy, and an anterior circulation aneurysm 7 mm in diameter, we would expect the cumulative risk of rupture to exceed 15-30%, much greater than the risk posed by endovascular or surgical treatment. In this location, both surgery and coiling are feasible, but we would want to offer the most effective treatment with the lowest risk. For aneurysms where both options are equally feasible, we would advocate coiling given the lower up front risks as discussed above. However, in this case, based on the image provided, incorporation of the A2s into the neck may increase the risks of coiling both in terms of thromboembolic complication and residual aneurysm, while this aneurysm is also quite suitable for surgery. Therefore, this case ultimately highlights how important it is that decisions regarding choice of treatment be made in a systematic manner, based on careful analysis of the patient, the aneurysm, and all of the available therapeutic options.
Figure 1.
Factors to be considered in providing patients with an individualized treatment recommendation.
References
- 1.Rinkel GJ, Djibuti M, Algra A, Gijn J. Prevalence and risk of rupture of intracranial aneurysms: a systematic review. Stroke. 1998 Jan;29(1):251–6. doi: 10.1161/01.str.29.1.251. [DOI] [PubMed] [Google Scholar]
- 2.Feigin VL, Rinkel GJ, Lawes CM, Algra A, Bennett DA, van Gijn J, Anderson CS. Risk factors for subarachnoid hemorrhage: an updated systematic review of epidemiological studies. Stroke. 2005 Dec;36(12):2773–80. doi: 10.1161/01.STR.0000190838.02954.e8. Epub 2005 Nov 10. [DOI] [PubMed] [Google Scholar]
- 3.International Study of Unruptured Intracranial Aneurysms Investigatore. Unruptured intracranial aneurysms--risk of rupture and risks of surgical intervention. N Engl J Med. 1998 Dec 10 Dec 12;339(24):1725–33. doi: 10.1056/NEJM199812103392401. [DOI] [PubMed] [Google Scholar]
- 4.Wiebers DO, Whisnant JP, Huston J 3rd, Meissner I, Brown RD Jr, Piepgras DG, Forbes GS, Thielen K, Nichols D, O'Fallon WM, et al. International Study of Unruptured Intracranial Aneurysms Investigators Unruptured intracranial aneurysms: natural history, clinical outcome, and risks of surgical and endovascular treatment. Lancet. 2003 Jul 12;362(9378):103–10. doi: 10.1016/s0140-6736(03)13860-3. [DOI] [PubMed] [Google Scholar]
- 5.Weir B. r Patients with small, asymptomatic, unruptured intracranial aneurysms and no history of subarachnoid hemorrhage should be treated conservatively: against. Stroke. 2005 Feb;36(2):410–1. doi: 10.1161/01.STR.0000152272.34969.80. [DOI] [PubMed] [Google Scholar]
- 6.Wermer MJ, van der Schaaf IC, Algra A. Rinkel GJ. Risk of rupture of unruptured intracranial aneurysms in relation to patient and aneurysm characteristics: an updated meta-analysis. Stroke. 2007 Apr;38(4):1404–10. doi: 10.1161/01.STR.0000260955.51401.cd. Epub 2007 Mar 1. [DOI] [PubMed] [Google Scholar]
- 7.Ujiie H, Tamano Y, Sasaki K, Hori T. Is the aspect ratio a reliable index for predicting the rupture of a saccular aneurysm? Neurosurgery. 2001 Mar;48(3):495–502. doi: 10.1097/00006123-200103000-00007. discussion 502-3. [DOI] [PubMed] [Google Scholar]
- 8.Lall RR, Eddleman CS, Bendok BR, Batjer HH. Unruptured intracranial aneurysms and the assessment of rupture risk based on anatomical and morphological factors: sifting through the sands of data. Neurosurg Focus. 2009 May;26(5):E2. doi: 10.3171/2009.2.FOCUS0921. [DOI] [PubMed] [Google Scholar]
- 9.Lanterna LA, Tredici G, Dimitrov BD, Biroli F. Treatment of unruptured cerebral aneurysms by embolization with guglielmi detachable coils: case-fatality, morbidity, and effectiveness in preventing bleeding--a systematic review of the literature. Neurosurgery. 2004 Oct;55(4):767–75. doi: 10.1227/01.neu.0000137653.93173.1c. discussion 775-8. [DOI] [PubMed] [Google Scholar]
- 10.Standhardt H, Boecher-Schwarz H, Gruber A, Benesch T, Knosp E, Bavinzski G. Endovascular treatment of unruptured intracranial aneurysms with Guglielmi detachable coils: short- and long-term results of a single- centre series. Stroke. 2008 Mar;39(3):899–904. doi: 10.1161/STROKEAHA.107.496372. Epub 2008 Feb 7. [DOI] [PubMed] [Google Scholar]
- 11.Holmin S, Krings T, Ozanne A, Alt JP, Claes A, Zhao W, Alvarez H, Rodesch G, Lasjaunias P. Intradural saccular aneurysms treated by Guglielmi detachable bare coils at a single institution between 1993 and 2005: clinical long-term follow-up for a total of 1810 patient-years in relation to morphological treatment results. Stroke. 2008 Aug;39(8):2288–97. doi: 10.1161/STROKEAHA.107.508234. Epub 2008 Jun 26. [DOI] [PubMed] [Google Scholar]
- 12.Molyneux A, Kerr R, Stratton I, Sandercock P, Clarke M, Holman R International Subarachnoid Aneurysm Trial (ISAT) Collaborative Group International Subarachnoid Aneurysm Trial (ISAT) of neurosurgical clipping versus endovascular coiling in 2143 patients with ruptured intracranial aneurysms: a randomised trial. Lancet. 2002 Oct 26;360(9342):1267–74. doi: 10.1016/s0140-6736(02)11314-6. [DOI] [PubMed] [Google Scholar]
- 13.Tsutsumi K, Ueki K, Usui M, et al. Risk of recurrent SAH after complete obliteration of intracranial aneurysms. Stroke. 1998;29:2511. doi: 10.1161/01.str.29.12.2511. [DOI] [PubMed] [Google Scholar]
- 14.Johnston SC, Dowd CF, Higashida RT, Lawton MT, Duckwiler GR, Gress DR CARAT Investigators. Predictors of rehemorrhage after treatment of ruptured intracranial aneurysms: the Cerebral Aneurysm Rerupture After Treatment (CARAT) study. Stroke. 2008 Jan;39(1):120–5. doi: 10.1161/STROKEAHA.107.495747. Epub 2007 Nov 29. [DOI] [PubMed] [Google Scholar]
- 15.Willinsky RA, Peltz J, da Costa L, R Agid, RI Farb, KG terBrugge. Clinical and angiographic follow-up of ruptured intracranial aneurysms treated with endovascular embolization. AJNR Am J Neuroradiol. 2009 May;30(5):1035–40. doi: 10.3174/ajnr.A1488. Epub 2009 Mar 19. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 16.Standhardt H, Boecher-Schwarz H, Gruber A, Benesch T, Knosp E, Bavinzski G. Endovascular treatment of unruptured intracranial aneurysms with Guglielmi detachable coils: short- and long-term results of a single- centre series. Stroke. 2008 Mar;3(3):899–904. doi: 10.1161/STROKEAHA.107.496372. Epub 2008 Feb 7. [DOI] [PubMed] [Google Scholar]
- 17.CARAT Investigators. Rates of delayed rebleeding from intracranial aneurysms are low after surgical and endovascular treatment. Stroke. 2006 Jun;37(6):1437–42. doi: 10.1161/01.STR.0000221331.01830.ce. [DOI] [PubMed] [Google Scholar]
- 18.Greving JP, Rinkel GJ, Buskens E, Algra A. Cost-effectiveness of preventive treatment of intracranial aneurysms. New data and uncertainties. Neurology. 2009 Mar 18; doi: 10.1212/01.wnl.0b013e3181a2a4ea. [DOI] [PubMed] [Google Scholar]
- 19.Kiyosue H, Tanoue S, Okahara M, Hori Y, Nakamura T, Nagatomi H, Mori H. Anatomic features predictive of complete aneurysm occlusion can be determined with three-dimensional digital subtraction angiography. AJNR Am J Neuroradiol. 2002 Aug;23(7):1206–13. [PMC free article] [PubMed] [Google Scholar]
interv neuroradiol. 2010 Mar 23;16(Suppl 1):29.
Large and giant intracranial aneurysms often pose technical challenges in their endovascular treatment. The use of traditional deconstructive techniques, including parent artery occlusion and aneurysm trapping, is currently limited to those patients who are not eligible for reconstructive techniques due to advanced age, severe vessel tortuosity or extremely complex aneurysm shape. Reconstructive techniques attempt to isolate the aneurysm sac while preserving the parent artery, using different embolic materials including coils, balloons, liquid materials and stents, etc. Between September 1998 to November 2009, 128 patients with large or giant intracranial aneurysms of anterior circulation were treated via endovascular approach at our institution. Our experience demonstrates that endovascular treatment of large or giant intracranial aneurysms remains technically challenging; However, with the development of new embolic materials and techniques, especially after the advent of flexible cover stent and flow diverter device, endovascular reconstructive treatment of large or giant intracranial aneurysms looks the most promising.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):30.
The morphology and structure of artery tree in posterior circulation is different from the internal carotid system. The category of the aneurysms harbored in the vertebrobasilar axis is variable. Very large aneurysms with wide neck in this region are great challenges to both of surgical and endovascular treatments, because of their poor natural history and high therapeutic M&M rate. According to the locations, they can involve the BA tip, upper segment (between SCA and AICA), middle segment (involved AICA), inferior segment (between AICA and VA bifurcation) and vertebral intracranial segment. The aneurysms can be divided into two subgroups: ruptured and unruptured, or "true" and dissected aneurysms. Although endovascular technique bring hope to these ugly lesions, there is still no satisfied resolution.
There are two main reasons:
The basilar trunk is a channel communicating the anterior circulation from the Pcoms, communicating the contralateral flow from the other vertebral artery. Occluding the parent artery cannot prevent the rupture of aneurysm effectively.
Vital branches or perforators can be involved by the aneurysms or even arise from the wall of aneurysms. The occlusion will bring the patient severe risks.
From our limited experience, we found:
To the ruptured or unruptured "true" aneurysms, we have to isolate the aneurysmal wall from the circulation any remanent will be related to the second bleeding. The methods including stent assisted coil embolization and trapping with coil embolization.
To the unruptured dissected aneurysms, occluding the parent artery or flow diverting with stent can reduce the thrombogenic risks and mass effects.
In many cases, staged or combined treatment could be safer.
In this talk, we will discuss several typical cases supporting the above ideas.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):31.
Cerebral Vasospasm (CV) contributes to poor outcome in approximately 15% to 20% of patients after subarachnoid haemorrhage (SAH) and continues to be a major cause of morbidity. Angiographic CV is seen in 30% to 70% of patients, with a typical onset 3 to 5 days after the haemorrhage, maximal narrowing at 5 to 14 days and a gradual resolution over 2 to 4 weeks. Approximately 50% will develop symptomatic CV, referred to as delayed ischaemic neurological deficit (DIND), which may resolve or progress to cerebral infarction. Approximately 50% of patients with symptomatic CV will develop infarctions, and 15-20% will develop a disabling stroke or die.
After aneurysmal SAH, a multifaceted cascade of events is initiated, ultimately leading to vasospasm. Breakdown products of blood in the subarachnoid space probably are the triggering factor. Ca-dependent and -independent vasoconstriction, spasmogens including oxyhaemoglobin, lipid peroxides, an imbalance between endothelium- derived vasoconstrictor (endothelin) and vasodilator (NO) substances, NO toxicity, arachidonic acid metabolites, inflammatory cascades, neurogenic factors, endothelial proliferation, and apoptosis, are among those factors that, acting through interconnected pathways, result in the development of CV
Early management of the ruptured aneurysm allows more aggressive and early management of CV.
The American Heart Association and Stroke Council have established guidelines for the management of CV, including triple-H therapy, nimodipine and the use of cerebral angioplasty and/or selective vasodilator therapy.
Guidelines for the Management of Aneurysmal SAH (AHA/ASA Guidelines):
Management of cerebral vasospasm after SAH (Bederson JB et al, Stroke, 2009;40:994-1025.)
Oral nimodipine is indicated to reduce poor outcome related to aneurysmal SAH (Class 1, Level of Evidence A). The value of other calcium antagonists, whether administered orally or intravenously, remains uncertain.
Treatment of cerebral vasospasm begins with the early management of the ruptured aneurysm, and in most cases, maintaining normal circulating blood volume and avoiding hypovolaemia are probably indicated (Class 11a, Level of Evidence B).
One reasonable approach to symptomatic cerebral vasospasm is volume expansion, induction of hypertension, and haemodilution (triple-H therapy) (Class 11a, Level of Evidence B).
Alternatively, cerebral angioplasty and/or selective intraarterial vasodilator therapy may be reasonable after, together with, or in the place of triple-H therapy, depending on the clinical scenario (Class 11b, Level of Evidence B).
A variety of other therapies for the prevention and treatment of CV have been investigated with varying success. Clot removal, HA1077, magnesium, anti-inflammatory agents, statins, endothelin-1 antagonists, free-radical scavengers and nitric oxide donors have been investigated. Currently, Clazosentan, an endothelin receptor antagonist, is under study in the CONSCIOUS trial. Statins and magnesium are also under current investigation. Further randomized, blinded, placebo-controlled trials are required.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):32.
Cerebral vasospasm was defined as reversible narrowing of cerebral vessels. It commonly occurs in 4 to 14 days after subarachnoid hemorrhage (SAH) and usually involves the proximal arteries composing the circle of Willis. Vasospasm remains the leading cause of stroke, morbidity and mortality after aneurysm ruptures. Because vasospasm is first and foremost a hemodynamic problem, current treatment objective is to prevent cerebral ischemia and infarction by restoring adequate blood flow and toward optimizing cerebral perfusion and minimizing secondary brain ischemic change.
Endovascular therapies frequently play a role in the aggressive treatment of vasospasm. These include intra- arterial infusion of vasodilators (also known as chemical angioplasty) and transluminal balloon angioplasty (TBA). Both methods have their unique associated risks and benefits and are usually undertaken after refractory to maximal medial therapy.
In contrast to the regimens of conventional intravenous treatment of vasospasm, the chemical angioplasty have some advantages including direct action, higher local concentration, and lower systemic dosages and adverse effects. This has led to growing use of intra-arterial vasodilators (eg, nimodipine, nicardipine, papaverine.etc). Previous studies reported variable clinical success and showed about 57-90% immediate angiographic relief from vasospasm. A study with quantified blood vessel responsiveness showed an average increase in vessel diameter of 26.5% in patients undergoing treatments. The major disadvantage of chemical angioplasty is the temporal effect of vasodilators. Therefore, repeated the procedure is needed in some selected patients.
TBA is very effective at reversing angiographic spasm of large proximal vessels. It produces a sustained reversal of arterial narrowing by disruption of connective tissue in the medial of cerebral arteries. Although clinical improvement is inconsistent, some retrospective data suggest that early TBA (within 2 hours from onset of symptoms) is associated with sustained clinical improvement. In addition to traditional TBA, prophylactic TBA had been reported with promising clinical results. However, TBA is usually limited to proximal vessel segments; and it demands an experienced endovascular surgeon and is associated with significant risks. Despite the excellent results of TBA as demonstrated on angiographic studies, varying degrees of success in reversal of neurological deficits caused by cerebral vasospasm have been reported, ranging from 31 to 93% of patients with improvement after treatment. Major complications of TBA are encountered in about 5% of procedures and include vessel rupture, occlusion, dissection and hemorrhage from unsecured aneurysms. Thus, when comparing procedural complications with the poor natural history of vasospasm, TBA has emerged as an important therapeutic intervention in selected patients.
Both TBA and chemical angioplasty have been used as primary interventional therapy to reverse cerebral vasospasm in patients of medically refractory treatment. The selection of interventional procedure is largely depended on the experiences of operators. However, TBA is selected when the vasospasm involves in the proximal segmental arteries. On the contrary, chemical angioplasty was commonly applied in those patients suffered from diffused vasospasm. On rare occasion, combination of both methods may have larger and longer effect to reverse the vasospasm. Future studies on newer intra-arterially administered agents with longer effects and less adverse reaction may further increase the use of chemical angioplasty. The results of the continuing trial on the prophylactic as well as the continued refinements in balloon and catheter technology should further define and advance the role of TBA in the treatment of SAH vasospasm.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):33.
Introduction
Endovascular treatment of intracranial arterial aneurysm has been proven to be effective. However, there are aneurysms that can be only partially treated and those with recurrence or recanalisation. In this presentation, management of residual/ recurrent aneurysms is discussed.
Methods, Results
Six hundred and sixteen patients were treated for symptomatic and asymptomatic aneurysms during the period of 2002-2009 in our institution by either endovascular means or direct surgery. Surgery was considered as the first choice of treatment whenever the surgeon feels that the aneurysm is clippable and can be tolerated considering the patient's clinical status. Endovascular treatment was the choice when complete (or near complete) occlusion is considered possible and if there is any downside for direct surgery. Surgery was the chosen as initial treatment in 62% of the patients.
Retreatment was performed in 20 cases(8 in surgery group and 12 in endovascular group) for incomplete treatment or reappearance of the aneurysms. In three cases, staged treatment strategy was planned since initial treatment. In the group of retreatment after initial surgery 3 cases were managed by additional clipping, 4 cases by endovascular treatment and one case with both treatment. In the group of retreatment after endovascular surgery, 6 cases were clipped, 6 cases underwent second endovascular treatment.
There were cases that were observed without further treatment. There was no complication caused by the second treatment except one ischemic complication in a case of an MCA aneurysm clipped after previous coiling.
Conclusions
Additional treatment for these group of patients is shown to be a safe procedure. Management strategy of residual/recurrent aneurysms will be presented and discussed.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):34.
Because the natural courses and management strategies are quite different according to their clinical presentation, dissecting aneurysms should be subdivided into ruptured and unruptured ones. As for the unruptured dissecting aneurysms, their management is quite controversial, and seems beyond the scope of this brief discussion with case review.
On the contrary, ruptured dissecting or ICA-blister aneurysms cause high rate of early rebleeding to result in a grave outcome, and it is widely accepted that aggressive management is mandatory. Endovascular internal trapping of the involved segment of the parent artery is generally used, and is one of the most reliable techniques to prevent rebleeding. However, this procedure is not suitable for the cases that involve the basilar artery, ICA or dominant VA with poor collaterals, or the arterial segment bearing the origin of the anterior choroidal artery or the dominant PICA. Although post-treatment recurrence or rebleeding has been reported, reconstructive treatment such as stent-assisted coiling or stent-only therapy can be an alternative treatment option in such cases.
To prevent recurrence or rebleeding after reconstructive endovascular treatment, we have treated ruptured dissecting or ICA-blister aneurysms using multiple overlapping stents with or without coiling. We used these techniques to more than forty cases of ruptured dissecting or ICA-blister aneurysms, and obtained very promising clinical and angiographic follow-up results. In this brief review with case examples, we present our experiences of using such techniques as an alternative treatment option for ruptured dissecting or ICA-blister aneurysms not suitable for internal trapping.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):35–37.
Despite major advances in diagnostic and therapeutic resources, management decisions in the treatment of brain AVMs may still be a challenge. Improved diagnostic modalities, such as magnetic resonance imaging, contribute to an increasing number of incidentally diagnosed AVMs26,27, and better and new therapeutic strategies allow for treatment of previously untreatable lesions, but unfortunately with potential morbidity16-21,28. The main goal of the treatment of brain AVMs is to preserve neurological function mainly by preventing intracranial hemorrhage and its consequences. Therefore, understanding the natural history of brain AVMs, especially related to risk of future hemorrhage, is crucial. Ondra et al7 published the results of almost 24 years of follow-up in a cohort of bAVM patients in Finland, and established an annual risk of bAVM hemorrhage of 4% per year, regardless bAVM characteristics and clinical presentation. Graf5, Crawford3 and Fults4 showed that bAVMs may have different behavior during follow up, with an increased risk of bleeding in the first year after diagnosis. In a more recent series, Mast et al23 demonstrated that the risk of hemorrhage in follow-up can be widely variable, from 2.2% to 17.8% per year, depending on presentation, AVM venous drainage and sex. It is becoming increasingly evident that bAVMs represent a heterogeneous group of lesions, with different clinical presentations and most likely different outcomes. With more therapeutic options available, determination of the future risk of bleeding is crucial to provide adequate management, either guiding towards an aggressive treatment plan aiming complete occlusion for bAVMs with risk factors for hemorrhage or supporting a more conservative approach for those without it.
Multiple factors are mentioned as being related to increased risk of hemorrhage: presentation with hemorrhage, presence of deep venous drainage, associated aneurysms, AVM location, size, male sex, venous outlet restriction, mean pressure and type of feeding arteries, sex and age8-11,13,15,23,25,29-34. Some agreement is present concerning the role of presentation with hemorrhage and the presence of deep venous drainage as risk factors for intracranial hemorrhage, but the literature provides divergent information regarding other factors. A common confounder in most series is the inclusion of the presenting hemorrhage in the number of bleeding events, making hard to determine accurately the risk of follow-up hemorrhage. Mast et al23 reported that the most important risk factor for future hemorrhage from a brain AVM after diagnosis is presentation with hemorrhage. In a later report with data from the same group, Stapf et al12 showed that the risk of hemorrhage can vary widely depending on the presence and number of risk factors that included age, hemorrhagic presentation, deep location and deep venous drainage. The risk was evaluated from the time of diagnosis to the beginning of treatment, with a relatively short follow up time, and excluding partially treated bAVMs. Instead of reflecting pure natural history, we chose not to remove from analysis lesions partially treated once the risk of hemorrhage is present until complete AVM obliteration35,36, and the management of brain AVMs often requires multiple interventions and different modalities of treatment, sometimes taking years before the lesion is completely obliterated. We believe that the inclusion of partially treated bAVMs provides useful information since they are a relatively common occurrence in any center for cerebrovascular disease, and also allowed us to analyse the impact of partial embolization.The prospective risk of hemorrhage in our series was 4.61% per year, in accordance with other major papers on natural history2-5,7. This risk was higher in the first year after diagnosis (4.80%), decreasing after the second year. The distribution of outcomes following the 89 hemorrhage events is depicted in Figure 01. Six percent (5/89) patients died as a result of the hemorrhage, while 35% had significant functional impairment (GOS 2 or 3).
There were no significant predictors of poor outcome (GOS 3 or less) identified in univariate or multivariate analysis. Multivariate analysis showed that presentation with hemorrhage (HR: 2.208, p>0.01) was an important independent predictor of risk of future hemorrhage. Deep venous drainage (HR: 1.59, p=0.07) and the presence of associated aneurysms (HR: 1.59, p= 0.07) were associated with a trend towards increased risk for future AVM hemorrhage. Our results support others that showed an increased risk of hemorrhage in the first year after diagnosis. The practical implication is that intervention, if warranted, should commence sooner rather than later after diagnosis, especially for brain AVMs that presented with hemorrhage or harbour the mentioned angioarchitectural risk factors. The reported rate of aneurysms associated with bAVMs vary widely (2.7% to 58%) in the literature, depending on the definition of what would represent an associated aneurysm, the type of angiography utilized (selective versus super-selective) and referral patterns25,37-39. Regarding the cause of the hemorrhage, in an earlier review of our series, Redekop25 reported that the cause of hemorrhage was almost equally distributed between aneurysms and AVMs. In our cohort, brain AVMs with associated aneurysms represented 17.9% of the patients, and had an increased risk of bleeding in follow-up.
Furthermore, this risk remained elevated even after 5 years of follow up (6%/year), and partial treatment, most of the times target endovascular occlusion of the aneurysm, did not alter the risk significantly. This may suggest that the risk of hemorrhage in these complex lesions is not just the simple summation of the risk of each separated lesion, but that each angioarchitectural characteristic is actually a marker of a more severe intracranial vasculopathy, therefore more prone to hemorrhage. Endovascular therapy is frequently used in the management of bAVMs but it is still unclear whether or not partial treatment changes the risk of hemorrhage40,41. Despite low efficacy in achieving total AVM occlusion, embolization is used successfully in order to occlude deep feeders before surgical resection, decrease nidus size to allow for radiosurgery or to eliminate perceived weak points such as intranidal aneurysms. Our data showed that partial embolization had no effect on the future risk of bleeding and may actually increase it in selected subgroups. These results should be interpreted with care. Those were groups with relatively small numbers and unique characteristics that may reflect a different hemorrhage risk and a bias in the selection of lesions for treatment may be present. Associated aneurysms, especially intranidal lesions, may herald a more severe vasculopathy where the risk of hemorrhage is higher and therefore comparison may not be appropriate, and perhaps more aggressive interventions justified. We still evaluate the treatment options for patients with bAVMs and associated aneurysms, including target embolization, in special for intranidal aneurysms, in a case-by-case basis.Nevertheless, considering the whole cohort, there is no evidence that partial embolization has any beneficial effect in the risk of future hemorrhage from a brain AVM. These results should not alter the fundamental role of endovascular therapy in the management of bAVMs, especially as surgical and radio-surgical adjuvant, but partial treatment of lesions not amenable to cure probable should not be recommended with the aim of decrease the risk of hemorrhage.
Conclusion
Presentation with hemorrhage, the presence of associated aneurysms and of deep venous drainage are independent risk factors for future hemorrhage from brain AVMs. Lesions that present with hemorrhage and/or have associated aneurysms have a risk of (re)-bleeding twice as high as brain AVMs without these characteristics, and the risk is highest in the first years after diagnosis. Brain AVMs with associated aneurysms have a higher risk of hemorrhage even after five years of diagnosis. Partial embolization of bAVMs does not decrease the risk of future hemorrhage. This information should be taken into consideration when deciding among therapeutic options for bAVMs, and more effective means in the short term (surgery or total embolization) might be advantageous for patients harbouring high-risk lesions. On the other hand, therapeutic approaches that entail longer obliteration times might be targeted to patients having a lower risk natural history for hemorrhage.
References
- 1.Arteriovenous malformations of the brain in adults. N Engl J Med. 1999;340(23):1812–8. doi: 10.1056/NEJM199906103402307. [DOI] [PubMed] [Google Scholar]
- 2.Brown RD, Jr, Wiebers DO, Forbes G, et al. The natural history of unruptured intracranial arteriovenous malformations. J Neurosurg. 1988;68(3):352–7. doi: 10.3171/jns.1988.68.3.0352. [DOI] [PubMed] [Google Scholar]
- 3.Crawford PM, West CR, Chadwick DW, Shaw MD. Arteriovenous malformations of the brain: natural history in unoperated patients. J Neurol Neurosurg Psychiatry. 1986;49(1):1–10. doi: 10.1136/jnnp.49.1.1. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 4.Fults D, Kelly DL., Jr Natural history of arteriovenous malformations of the brain: a clinical study. Neurosurgery. 1984;15(5):658–62. doi: 10.1227/00006123-198411000-00003. [DOI] [PubMed] [Google Scholar]
- 5.Graf CJ, Perret GE, Torner JC. Bleeding from cerebral arteriovenous malformations as part of their natural history. J Neurosurg. 1983;58(3):331–7. doi: 10.3171/jns.1983.58.3.0331. [DOI] [PubMed] [Google Scholar]
- 6.Ogilvy CS, Stieg PE, Awad I, et al. Recommendations for the management of intracranial arteriovenous malformations: a statement for healthcare professionals from a special writing group of the Stroke Council, American Stroke Association. Circulation. 2001;103(21):2644–57. doi: 10.1161/01.cir.103.21.2644. [DOI] [PubMed] [Google Scholar]
- 7.Ondra SL, Troupp H, George ED, Schwab K. The natural history of symptomatic arteriovenous malformations of the brain: a 24-year follow-up assessment. J Neurosurg. 1990;73(3):387–91. doi: 10.3171/jns.1990.73.3.0387. [DOI] [PubMed] [Google Scholar]
- 8.Kader A, Young WL, Pile-Spellman J, et al. The influence of hemodynamic and anatomic factors onhemorrhage from cerebral arteriovenous malformations. Neurosurgery. 1994;34(5):801–7. doi: 10.1227/00006123-199405000-00003. discussion 807-8. [DOI] [PubMed] [Google Scholar]
- 9.Mansmann U, Meisel J, Brock M, Rodesch G, Alvarez H, Lasjaunias P. Factors associated with intracranial hemorrhage in cases of cerebral arteriovenous malformation. Neurosurgery. 2000;46(2):272–9. doi: 10.1097/00006123-200002000-00004. discussion 279-81. [DOI] [PubMed] [Google Scholar]
- 10.Marks MP, Lane B, Steinberg GK, >Chang PJ. Hemorrhage in intracerebral arteriovenous malformations: angiographic determinants. Radiology. 1990;176(3):807–13. doi: 10.1148/radiology.176.3.2389040. [DOI] [PubMed] [Google Scholar]
- 11.Pollock BE, Flickinger JC, Lunsford LD, Bissonette DJ, Kondziolka D. Factors that predict the bleeding risk of cerebral arteriovenous malformations. Stroke. 1996;27(1):1–6. doi: 10.1161/01.str.27.1.1. [DOI] [PubMed] [Google Scholar]
- 12.Stapf C, Mast H, Sciacca RR, et al. Predictors of hemorrhage in patients with untreated brain arteriovenous malformation. Neurology. 2006;66(9):1350–5. doi: 10.1212/01.wnl.0000210524.68507.87. [DOI] [PubMed] [Google Scholar]
- 13.Stefani MA, Porter PJ, terBrugge KG, Montanera W, Willinsky RA, Wallace MC. Angioarchitectural factors present in brain arteriovenous malformations associated with hemorrhagic presentation. Stroke. 2002;33(4):920–4. doi: 10.1161/01.str.0000014582.03429.f7. [DOI] [PubMed] [Google Scholar]
- 14.Turjman F, Massoud TF, Vinuela F, Sayre JW, Guglielmi G, Duckwiler G. Correlation of the angioarchitectural features of cerebral arteriovenous malformations with clinical presentation of hemorrhage. Neurosurgery. 1995;37(5):856–60. doi: 10.1227/00006123-199511000-00002. discussion 860-2. [DOI] [PubMed] [Google Scholar]
- 15.Willinsky R, Lasjaunias P, Terbrugge K, Pruvost P. Brain arteriovenous malformations: analysis of the angio- architecture in relationship to hemorrhage (based on 152 patients explored and/or treated at the hopital de Bicetre between 1981 and 1986) J Neuroradiol. 1988;15(3):225–37. [PubMed] [Google Scholar]
- 16.Andrade-Souza YM, Zadeh G, Scora D, Tsao MN, Schwartz ML. Radiosurgery for basal ganglia, internal capsule, and thalamus arteriovenous malformation: clinical outcome. Neurosurgery. 2005;56(1):56–63. doi: 10.1227/01.neu.0000145797.35968.ed. discussion 63-4. [DOI] [PubMed] [Google Scholar]
- 17.Castel JP, Kantor G. [Postoperative morbidity and mortality after microsurgical exclusion of cerebral arteriovenous malformations. Current data and analysis of recent literature] Neurochirurgie. 2001;47(2-3 Pt 2):369–83. [PubMed] [Google Scholar]
- 18.Coffey RJ, Nichols DA, Shaw EG. Stereotactic radiosurgical treatment of cerebral arteriovenous malformations. Gamma Unit Radiosurgery Study Group. Mayo Clin Proc. 1995;70(3):214–22. doi: 10.4065/70.3.214. [DOI] [PubMed] [Google Scholar]
- 19.Haw CS, terBrugge K, Willinsky R, Tomlinson G. Complications of embolization of arteriovenous malformations of the brain. J Neurosurg. 2006;104(2):226–32. doi: 10.3171/jns.2006.104.2.226. [DOI] [PubMed] [Google Scholar]
- 20.Heros RC, Morcos J, Korosue K. Arteriovenous malformations of the brain. Surgical management. Clin Neurosurg. 1993;40:139–73. [PubMed] [Google Scholar]
- 21.Morgan MK, Rochford AM, Tsahtsarlis A, Little N, Faulder KC. Surgical risks associated with the management of Grade I and II brain arteriovenous malformations. Neurosurgery. 2004;54(4):832–7. doi: 10.1227/01.neu.0000114264.78966.be. discussion 837-9. [DOI] [PubMed] [Google Scholar]
- 22.Fleetwood IG, Marcellus ML, Levy RP, Marks MP, Steinberg GK. Deep arteriovenous malformations of the basal ganglia and thalamus: natural history. J Neurosurg. 2003;98(4):747–50. doi: 10.3171/jns.2003.98.4.0747. [DOI] [PubMed] [Google Scholar]
- 23.Mast H, Young WL, Koennecke HC, et al. Risk of spontaneous haemorrhage after diagnosis of cerebral arteriovenous malformation. Lancet. 1997;350(9084):1065–8. doi: 10.1016/s0140-6736(97)05390-7. [DOI] [PubMed] [Google Scholar]
- 24.Spetzler RF, Martin NA. A proposed grading system for arteriovenous malformations. J Neurosurg. 1986;65(4):476–83. doi: 10.3171/jns.1986.65.4.0476. [DOI] [PubMed] [Google Scholar]
- 25.Redekop G, TerBrugge K, Montanera W, Willinsky R. Arterial aneurysms associated with cerebral arteriovenous malformations: classification, incidence, and risk of hemorrhage. J Neurosurg. 1998;89(4):539–46. doi: 10.3171/jns.1998.89.4.0539. [DOI] [PubMed] [Google Scholar]
- 26.Brown RD Jr, Wiebers DO, Torner JC, O'Fallon WM. Incidence and prevalence of intracranial vascular malformations in Olmsted County, Minnesota, 1965 to 1992. Neurology. 1996;46(4):949–52. doi: 10.1212/wnl.46.4.949. [DOI] [PubMed] [Google Scholar]
- 27.Stapf C, Mohr JP, Choi JH, Hartmann A, Mast H. Invasive treatment of unruptured brain arteriovenous malformations is experimental therapy. Curr Opin Neurol. 2006;19(1):63–8. doi: 10.1097/01.wco.0000200546.14668.78. [DOI] [PubMed] [Google Scholar]
- 28.Hartmann A, Pile-Spellman J, Stapf C, et al. Risk of endovascular treatment of brain arteriovenous malformations. Stroke. 2002;33(7):1816–20. doi: 10.1161/01.str.0000020123.80940.b2. [DOI] [PubMed] [Google Scholar]
- 29.Duong DH, Young WL, Vang MC, et al. Feeding artery pressure and venous drainage pattern are primary determinants of hemorrhage from cerebral arteriovenous malformations. Stroke. 1998;29(6):1167–76. doi: 10.1161/01.str.29.6.1167. [DOI] [PubMed] [Google Scholar]
- 30.Khaw AV, Mohr JP, Sciacca RR, et al. Association of infratentorial brain arteriovenous malformations with hemorrhage at initial presentation. Stroke. 2004;35(3):660–3. doi: 10.1161/01.STR.0000117093.59726.F9. [DOI] [PubMed] [Google Scholar]
- 31.Kubalek R, Moghtaderi A, Klisch J, Berlis A, Quiske A, Schumacher M. Cerebral arteriovenous malformations: influence of angioarchitecture on bleeding risk. Acta Neurochir (Wien) 2003;145(12):1045–52 discussion 1052.. doi: 10.1007/s00701-003-0143-x. [DOI] [PubMed] [Google Scholar]
- 32.Meisel HJ, Mansmann U, Alvarez H, Rodesch G, Brock M, Lasjaunias P. Cerebral arteriovenous malformations and associated aneurysms: analysis of 305 cases from a series of 662 patients. Neurosurgery. 2000;46(4):793–800. doi: 10.1097/00006123-200004000-00004. discussion 800-2. [DOI] [PubMed] [Google Scholar]
- 33.Stapf C, Khaw AV, Sciacca RR, et al. Effect of age on clinical and morphological characteristics in patients with brain arteriovenous malformation. Stroke. 2003;34(11):2664–9. doi: 10.1161/01.STR.0000094824.03372.9B. [DOI] [PubMed] [Google Scholar]
- 34.Stefani MA, Porter PJ, terBrugge KG, Montanera W, Willinsky RA, Wallace MC. Large and deep brain arteriovenous malformations are associated with risk of future hemorrhage. Stroke. 2002;33(5):1220–4. doi: 10.1161/01.str.0000013738.53113.33. [DOI] [PubMed] [Google Scholar]
- 35.Miyamoto S, Hashimoto N, Nagata I, et al. Posttreatment sequelae of palliatively treated cerebral arteriovenous malformations. Neurosurgery. 2000;46(3):589–94. doi: 10.1097/00006123-200003000-00013. discussion 594-5. [DOI] [PubMed] [Google Scholar]
- 36.Steinberg GK, Fabrikant JI, Marks MP, et al. Stereotactic helium ion Bragg peak radiosurgery for intracranial arteriovenous malformations. Detailed clinical and neuroradiologic outcome Stereotact Funct. Neurosurg. 1991;57(1-2):36–49. doi: 10.1159/000099554. [DOI] [PubMed] [Google Scholar]
- 37.Lasjaunias P, Piske R, Terbrugge K, Willinsky R. Cerebral arteriovenous malformations (C. AVM) and associated arterial aneurysms (AA). Analysis of 101 C. AVM cases, with 37 AA in 23 patients. Acta Neurochir (Wien) 1988;91(1-2):29–36. doi: 10.1007/BF01400524. [DOI] [PubMed] [Google Scholar]
- 38.Stapf C, Mohr JP, Pile-Spellman J, et al. Concurrent arterial aneurysms in brain arteriovenous malformations with haemorrhagic presentation. J Neurol Neurosurg Psychiatry. 2002;73(3):294–8. doi: 10.1136/jnnp.73.3.294. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 39.Turjman F, Massoud TF, Vinuela F, Sayre JW, Guglielmi G, Duckwiler G. Aneurysms related to cerebral arteriovenous malformations: superselective angiographic assessment in 58 patients. AJNR Am J Neuroradiol. 1994;15(9):1601–5. [PMC free article] [PubMed] [Google Scholar]
- 40.Meisel HJ, Mansmann U, Alvarez H, Rodesch G, Brock M, Lasjaunias P. Effect of partial targeted N-butyl- cyano-acrylate embolization in brain AVM. Acta Neurochir (Wien) 2002;144(9):879–87. doi: 10.1007/s00701-002-0978-6. discussion 888. [DOI] [PubMed] [Google Scholar]
- 41.Wikholm G, Lundqvist C, Svendsen P. The Goteborg cohort of embolized cerebral arteriovenous malformations: a 6-year follow-up. Neurosurgery. 2001;49(4):799–805.. doi: 10.1097/00006123-200110000-00004. discussion 805-6. [DOI] [PubMed] [Google Scholar]
- 42.da Costa L, Wallace MC, Ter Brugge KG, O'Kelly C, Willinsky RA, Tymianski M. The natural history and predictive features of hemorrhage from brain arteriovenous malformations. Stroke. 2009 Jan;40(1):100–5. doi: 10.1161/STROKEAHA.108.524678. Epub 2008 Nov 13. [DOI] [PubMed] [Google Scholar]
interv neuroradiol. 2010 Mar 23;16(Suppl 1):38.
Purpose
The purpose of this report is to review our experience for treatment of direct and very high flow intracranial AV fistulas by disconnecting at the AV junction.
Materials and Methods
From 2006 to 2009 among the 150 cerebral AVMs there are three cases with direct and very high flow intracranial AV fistulas. One boy 15 years-old and two girls: one is 18 years-old and one is 14 years-old. The main symptoms of these patients were seizures and fainting. The direct AV shunt was located in posterior cerebral artery in 2 cases the other one in anterior cerebral artery. The draining vein was connected to the vein of Galen in one and draining to the superficial cerebral vein in two of the cases. The first case was treated in 2006 by injection pure glue but failed to stop the AV shunt because of enlargement of the feeder artery and very high flow AV shunt. Then the AV junction was approached with 2 microcatheters and deployed two coils to work together against coil migration to the huge venous pouch. When the second deployed coil was stable ;the proximal coil was detached afterwards ,then the distal coil was kept for supporting the following coils deployment by using the proximal microcatheter. If coiling alone cannot control the AV shunt; the non-detachable balloon was used for more supportive technique ,or else the diluted glue was the alternate material to fix the coils mass which finally the first distal coil was detached.
Results
Three cases of direct and very high flow intracranial AV fistulas were treated successfully by using the double coils technique without any related procedure complication. Clinical symptoms after the procedure had improved and now at least more than one year follow up these patients have no symptoms and follow up angiograms reveal the AV fistulas were cured and draining venous pouches shrunk themselves.
Conclusions
In our experience, double catheters technique can be performed safely to disconnect the very high flow intracranial AV fistulas. The benefit of this technique is to reduce the amount of coils and eliminate the risks after filling the venous pouch(es) without completely closure of the fistulas.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):39.
Background and Purpose
The successfull rate of endovascular treatment of brain arteriovenous malformations (AVMs) with N-butyl cyanoacrylate (Histoacryl) according to the reporters were very differents. This study aims to correlate the angioarchitecture of AVMs with their complete obliteration of such treatment in a Vietnam's population.
Methods
A total of 161 patients with 162 AVMs were studied between May 2000 and May 2009. The angiographic features of each brain AVM were analyzed on angiography associated with CT or/and MRI, include: location of AMVs (cortical, deep feeders and both of them); maximum size of nidus (<3cm, 3-6cm and >=6cm); location and number (1; 2; and >2) of feeders; and location and numbers (1; 2; and >2) of draining veins; classification according to Spetzler-Martin from I to V grade. Univariate and multivariate analyses were conducted in order to test the associations between morphological features and complete obliteration of AVMs.
Results
Complete embolization was achieved in 46 cases (28.4%). Embolization resulted in mortalily rate of 4.35% and a morbidity rate of 1.24%. AVMs had total embolization with with single feeder in 92.86% (OR, 43.66; 95% CI, 8.64 to 220.70) and with AVMs <3cm in 47.31% (OR, 17.20; 95% CI, 5.50 to 84.46). Complete embolization was negatively associated with AVMs location, site of feeders, site and number of venous drainage.
Conclusion
This study suggest that the overall cure rate of AVMs with histoacryl embolization was 28.4%. AVMs with single feeder and small nidus (<3cm) were significant asociated features for complete embolization.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):40.
In our institute, the treatment of a dural arteriovenous fistula (DAVF) depends on the severity of the symptoms and the angiographic findings especially the venous drainage pattern of the lesion. Low-risk DAVFs that have minimal symptoms or antegrade sinus drainage can be treated conservatively. We apply definite or palliative treatment to the patient does not tolerate the symptoms. All high-risk DAVFs (Cognard grade IIa or higher), or patients with severe clinical symptoms (vision deterioration, ophthalmoplegia, cerebral ischemia or hemorrhage, seizures, focal neurologic deficit, or progressive dementia) should receive definite treatment. The treatment of choice in our institute is endovascular embolization. The treatment was planned according to the grading of DAVF. Transvenous embolization (TVE) was the method of choice for treating DAVF, if the normal cerebral veins not drain into the lesion sinus and the lesion sinus was accessible. We used all available imaging data including CTAs, DSAs, MRAs for treatment planning. We applied the imaging data to analyze the best route to approach the point of the fistula. We usually designed 2 routes for the transvenous approach for each case. Sometimes, we even apply the parallel treatment or angioplasty to preserve the dural sinus. In patients with occluded sinus, we always try to cross the occluded access site. If the transvenous approach failed or preservation of normal cortical venous drainage was technically difficult, we changed the treatment to transarterial embolization (TAE) such as occluded the feeders and fistulas with liquid embolic material or coiling the fistula after accessing to the fistula from the arterial route. With the combination of modern materials and techniques, the procedure can yield a high rate of cure with minimal complications.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):41.
Dural arteriovenous fistula (DAVF) respresents a protean group of arteriovenous shunts, both in anatomical and clinical manifestations. Historically, although endovascular therapy has been the mainstay of treatment for the past 20 years, results with "conventional" embolic agents administered transarterially have been mixed and often disappointing, requiring retreatment or "salvage" transvenous occlusion or even radiotherapy or open surgery for definitive cure. Cyanoacrylate adhesives have proved efficacious in transarterial treatment, but their use requires considerable experience and expertise, and is limited by the chemical adhesive nature of the agents. Ethyl vinyl alcohol copolymer (Onyx), since it has become widely available, has made transarterial embolisation of DAVF with a view to definitive cure not only feasible, but relatively simple, in that the operator does not necessarily require the same difficult-to-acquire skills needed for safe and effective use of cyanoacrylates.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):42.
The treatment of dural arteriovenous fistulas (DAVF) requires a multidisciplinary approach. It has been recognized that fistulae involving the anterior cranial fossa and tentorium are at the greatest risk for haemorrhage owing to the propensity for leptomeningeal venous drainage (LMVD). When considering the treatment strategies for DAVF, it is important to clarify angiographically the exact location of the fistulae and venous drainage route from both the DAVF and normal brain tissue.
Although endovascular therapy has become the predominant therapy for intracranial DAVF, there continues to be a group of fistulae that require surgical management to decrease the risk of intracerebral haemorrhage. Surgery is often required for fistulas drained solely by LMVD such as those located in the anterior cranial fossa, tentorial DAVF, DAVF with an isolated sinus, where endovascular therapy has an unacceptable stroke risk, and DAVF that remain patent despite endovascular treatment.
The aim of surgery is fistulae interruption rather than arterial disconnection. This includes local packing, complete excision of the fistulae, isolation of the fistulae, or disconnection of arterialized LMVD from the site of the DAVF. Although seemingly complex angiographically, DAVF that drain purely through LMVD can be safely obliterated by surgical clipping the arterialized draining vein as it exits the dura. Preoperative embolization of the feeding artery may be required to reduce intraoperative blood loss and stereotactic localization of the DAVF is often useful.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):43.
Radiosurgery is an effective and safe treatment alternative for brain AVM with less invasiveness. With similar rationale, radiosurgery has been reasonably applied to DAVF with same targeting technique and resulted in good clinical outcome for decades. Compared to BAVM, DAVF react prompter to radiosurgery. Different from other treatment strategies, the abnormal arteriovenous communications involved in DAVF are the only target for radiation in DAVF radiosurgery. The complexity, numbers of territory and feeding arteries are relatively less crucial in radiosurgery. This unique therapeutic rationale makes the patient-selection and clinical decision-making of radiosurgery be different from interventional or surgical treatments. Nevertheless, the latent period for radiation effect evolution and the long waiting time for cure remain a major drawback in DAVF radiosurgery.
Based on 450 intracranial DAVF cases (211 DAVF of cavernous sinus and 139 DAVF at other locations) treated from 1993 to 2009 at a single institute, typical DAVF cases for radiosurgery, overall treatment results, and complications are presented. Moreover, the weakness of radiosurgery for DAVF, the possibility of combining multidisciplinary treatments and the cases that radiosurgery serves as a complementary to other treatments will be discussed.
References
- 1.Guo WY, Pan DH, Wu HM, et al. Radiosurgery as a treatment alternative for dural arteriovenous fistulas of the cavernous sinus. AJNR. 1998;19:1081–1087. [PMC free article] [PubMed] [Google Scholar]
- 2.Pan DH, Chung WY, Guo WY, et al. Stereotactic radiosurgery for the treatment of dural arteriovenous fistulas involving the transverse-sigmoid sinus. J Neurosurg. 2002;96:823–829. doi: 10.3171/jns.2002.96.5.0823. [DOI] [PubMed] [Google Scholar]
- 3.Wu HM, Pan DH, Chung WY, et al. Gamma Knife surgery for the management of intracranial dural arteriovenous fistulas. J Neurosurg. 2006;(suppl 105):43–51. doi: 10.3171/sup.2006.105.7.43. [DOI] [PubMed] [Google Scholar]
interv neuroradiol. 2010 Mar 23;16(Suppl 1):44.
Aim
To analyze results of endovascular treatment of dural AVF.
Introduction
Dural AVF is usually a sequel to thrombosis of dural venous sinuses. The dural AVF is usually seen within a year or two of the diagnosis of venous sinus thrombosis. Clinical diagnosis is extremely difficult. It is often missed on MRI, MRA and CTA. Several classifications testify to the difficulties in diagnosis and treatment. Treatment and cure is also extremely difficult. Various methods of endovascular treatment have been tried - these include embolization using particulate matter, liquid embolic materials using glue, occlusion of affected sinuses using platinum coils sometimes in combination with glue, stenting of occluded venous sinuses. The best results have been with the use of Onyx, a new liquid embolic agent.
Materials
Records of 50 cases of dural AVF have been treated over the last 13 years by various endovascular methods were analyzed. All patients have CT scans, MRI and MRA for pre-op workup. DSA with bilateral ICA, Bil ECA, Bil VA and subclavian arteriogram is done. The exact site of AVF is identified. All different feeders are visualized. Competition between venous outflow of brain and AVF is analyzed. Venous anomalies including sinus occlusions are identified.
Results
There were no deaths and no neurological complications. Complete anatomical cure with excellent clinical outcome was obtained in all patients with onyx and platinum coils with or without glue. Partial or near complete cure was obtained using glue alone. One patient, who had been treated for right transverse sinus dural AVF presented with new dural AVF in the parietal superior sagittal sinus which was treated by surgical excursion of the falx and division of parasagittal dura parallel to the sinus.
Conclusions
Embolization with Onyx is method of choice for treatment of dural AVF.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):45.
Reality
The name of "flow diverter stent" is born with the new generation of breaded stent. The concept of diverting the flow, in order to treat intracranial aneurysms, was first understood and then intentionally used, for about four years, when performing Y stenting with regular laser cut stents. In fact the analysis of the long term results in patients who got an aneurysm treatment, even after simple stenting were clearly demonstrating that part of the "healing" process due to stenting was related to diversion of the flow. Our personal statistics, over 1268 aneurysms during the last five years, regarding long term results shows: For all sizes of aneurysms and according to a simple binary scale (angiographic modification yes or no, comparing immediate post treatment angiogram and long term control angiogram), we have 14,3% change in the stented group and 33,3% in the non stented group (chi square P=0,0001). If we consider only the aneurysm ≤ 10mm then we have 3,1% modification in the stented group and 28.6 % in the non stented group which does represent a very significant difference (chi square P <0,0001).
Expectation
From the beginning Flow diverter stents were presented as being able to cure aneurysms alone (more frequently with multiple telescopic stents) without additional coils in the sac. Most of the first treatments with FD were dedicated to giant aneurysms and dissecting aneurysms. There is no question about the fact that ii is true. FD do open a new opportunity for treating those very difficult or impossible to treat aneurysms and the current results confirm that. The recent expectation is that FD could be also very useful for treatment of regular berry aneurysms of the circle of Willis and for the time being it seems that it is true. Are we expecting that FD will progressively replace regular coiling and stenting for regular aneurysm the answer is no.
Unsolved problems
Should we use a single FD or multiple FD in telescopic manner? Why do some aneurysms bleed after FD delivery? What is the rational for not putting coils in the sac when using FD, knowing that some aneurysms bleed before getting completely thrombosed? What is the modification of the flow and of the intra saccular pressure induced by the FD? What is the impact of the FD on the wall of the parent artery proximal and distal to the aneurysm neck? How should we make FD evolved?
All those questions will be discussed and argued.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):46.
Background and Purpose
Cerebrovascular diseases are associated with high morbidity and mortality and therefore present a significant therapeutic challenge. As platelets have a critical role in the pathophysiology of stroke, there is a clear need for better understanding of the role of platelets during interventions. Today, antiplatelet agents constitute a valid therapeutic approach in the prevention and treatment of arterial thromboembolic events.
Recent studies suggest that the use of dual antiplatelet therapy provide more potent platelet inhibition, and may lead to more favorable clinical outcomes in patients with history of cerebrovascular events. On the basis of this evidence, for patients who undergo an intracranial stenting procedure, dual antiplatelet therapy is emerging as the new standard of care.
As more intensive P2Y12 inhibition is translated into less ischemic/thromboembolic events, the fear of the neurointerventionalist remains the increased rate of bleeding. In some cases, tailoring the treatment may improve safety of the P2Y12 inhibitors. Some patients may also have enough platelet inhibition, with lower dosage. Venue of point of care instruments might help to better adjust their treatment.
Traditional antithrombotic therapies are susceptible to significant fluctuations in antithrombotic effect due to myriad drug-drug (e.g. PPI and clopidogrel), drug-food interactions and patient factors (e.g. allergy, hypersensibility, low response). The efficacy and safety of the currently available agents may sometimes be affected by these individual factors.
Methods
A computerized search of the National Library of medicine database of literature (PubMed), Medscape and Cochrane Library, was conducted with 3 goals. (1) To identify published cerebrovascular interventional data on the use of antithrombotic agents when performing intracranial stenting. (2) To identify data that can be used as the basis for monitoring the use of antiplatelet agents during neuroendovascular procedures. (3)To identify data that could potentially be extrapolated from the cardiovascular literature/clinical experience to be translated into the neurointerventional practice.
Data Sources
PubMed, Medscape, the Cochrane Library
Discussion
This presentation will update clinicians with the latest data relating to the prevention and treatment of arterial thromboembolism and what's new on the horizon for improving outcomes in patients at risk for thrombosis during intracranial stenting procedures.
The audience will also hear some insights on recently completed clinical trials on novel antiplatelet drugs such as ticagrelor, cangrelor, elinogrel, etc...The landscape of antiplatelet therapy is rapidly changing, with new therapies entering the world marketplace and landmark trials providing critical efficacy and safety information on new drugs.
Conclusion
Scientific evidence regarding coagulation and aggregation management in neurovascular interventions still limited. Promising results from clinical trials of novel agents could overcome limitations of existing therapies. We still need additional data to tailor treatment to individual patient.
Competing interests
This presentation is not sponsored or endorsed by Boston Scientific Corporation .This presentation does not refer to or promote specific devices manufactured by Boston Scientific Corporation. The speaker has no financial relationship with any pharmaceutical company.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):47–48.
Idiopathic intracranial hypertension (IIH) is a disease found predominately in middle aged obese females. There is an elevation in CSF pressure but no evidence of an abnormality of CSF composition. Intracranial pressure (ICP) is dependent on a balance between the production and reabsorption of CSF. Davson et al1 modelled the relationship between ICP and the formation and reabsorption of CSF showing that,
where Rout is the resistance of CSF outflow, FRCSF is the formation rate of CSF, and PSS is the sagittal sinus pressure. Rearranging Davson's equation, we find that the CSF-SSS pressure gradient is equal to the product of the CSF rate of production and the resistance to flow across the arachnoid granulations, ie,
In a report by King et al2 in which they studied 21 patients with IIH, a mean CSF pressure of 27 mm Hg and sagittal sinus pressure of 22 mm Hg gave a CSF-superior sagittal sinus (SSS) gradient of 5 mm Hg, which is in the normal range (2-6 mm Hg). Malm et al3 used a technique of constant flow to measure FRCSF and showed it to be normal in this condition. If the CSF-SSS gradient (left half of the equation) is normal and the rate of formation (half the right side of the equation) are normal, then the Rout (the remaining part) must also be normal in IIH. Therefore, the elevated venous pressure is the sole variable effecting the elevation in CSF pressure in IIH. A view also noted by Karahalios et al4.
If the above is true then why is this disease still classified as idiopathic? There have been two areas of ongoing controversy. 1) The elevated CSF pressure causes the elevated venous pressure and not the other way around and 2) 15-20% of patients do not have an apparent cause for an elevated venous pressure.
Controversy 1). In the first instance most patients with IIH have been found to have stenoses in the dominant outflow transverse sinus5. Many of these stenoses reduce the outflow by more than 70% in area and would be deemed significant if found on the arterial side of the vascular tree. Direct manometry has shown the pressure gradients across these stenoses to average 24 mm Hg,2 which would also suggest that these stenoses were significant by the usual criteria. Finally, I have measured the arterial inflow and venous outflow in 21 patients with IIH and stenoses and found, on average, a 13% reduction in the sagittal sinus outflow as a percentage of the inflow in IIH.6 This indicates that 140 mL/min bypasses the dominant outflow stenosis via the collateral vessels,6 again suggesting significance. However, when King et al removed CSF and simultaneously measured the venous pressure in IIH they noted that the venous pressure dropped to normal2. This indicated that the elevated venous pressure was due to an overly compliant venous outflow collapsing under the CSF pressure. This caused controversy because it was suggested that by this mechanism the original cause of the elevated CSF pressure could not be explained. This is not necessarily correct because if a positive feed back loop were operating, then an elevated CSF pressure could collapse the transverse sinus and the elevated venous pressure that developed would feed back to increase CSF pressure because venous pressure sets the CSF pressure. The underlying problem then would be the overly compliant vein and the elevated CSF and venous pressures would occur secondary to this. It follows that this condition could be treated by attacking either side of the feedback loop (ie, reducing the CSF pressure with placement of a shunt tube or by placing a stent into the overly compliant transverse sinus will break the loop).
Controversy 2). In patients who have IIH but no evidence of an outflow stenosis Karahalios et al indicated that the IIH was due to an elevation in right atrial pressure elevating sagittal sinus pressure and therefore CSF pressure4. They measured the CVP in five patients with morbid obesity in the supine position and found a mean pressure of 11.8 mmHg. In the supine position the sagittal sinus is only marginally above the level of the right atrium and because an atrial pressure of 11.8 mmHg can support a column of blood 16 cm high, it is not surprising that the atrial pressure appeared to feed all the way back to the cerebral sinuses and limit CSF reabsorption. However we cannot explain IIH on the basis of right heart failure alone, humans spend approximately two thirds of their lives awake with their heads and thoraces vertical not horizontal. Normally, in the non-obese person under these circumstances, the jugular veins are collapsed and the venous pressure in the neck is at atmospheric pressure. The sagittal sinus pressure is normally subatmospheric in the erect position and therefore atrial pressure will does not affect CSF absorption. In the case of an obese patient with an atrial pressure of 11.8 mmHg, the superior vena cava and jugular veins will be distended for a distance of 16 cm above the atrium (to about the level of the lower neck) but will be collapsed above this level. Thus, in the erect position a moderately elevated CVP will still not influence the sinus pressure and not directly affect CSF absorption. With the neck veins collapsed, the sagittal sinus pressure will only depend on the intracranial venous outflow resistance and the amount of blood flowing through these veins (Ohm's law). I measured the cerebral blood flow in patients with IIH but no evidence of stenosis and found an increase in flow approximating 50% above normal7. Therefore, in IIH without stenoses the elevated CSF pressure occurs secondary to elevated venous pressure but the pressure is not due to an increase in venous resistance. As Ohm's law predicts an elevation in venous pressure can occur purely as a consequence of an increase in blood flow.
References
- 1.Davson H, Welch K, Segal MB eds. Physiology and pathophysiology of the cerebrospinal fluid. New York: Churchill Livingstone; 1987. pp. 485–21. [Google Scholar]
- 2.King JO, Mitchell PJ, Thomson KR, et al. Manometry combined with cervical puncture in idiopathic intracranial hypertension. Neurology. 2002;58:26–30. doi: 10.1212/wnl.58.1.26. [DOI] [PubMed] [Google Scholar]
- 3.Malm J, Kristensen B, Markgren P, et al. CSF hydrodynamics in idiopathic intracranial hypertension: A long- term study. Neurology. 1992;42:851–58. doi: 10.1212/wnl.42.4.851. [DOI] [PubMed] [Google Scholar]
- 4.Karahalios DG, Rekate HL, Khayata MH, Apostolides PJ. Elevated intracranial venous pressure as a universal mechanism in pseudotumor cerebri of varying etiologies. Neurology. 1996;46:198–202. doi: 10.1212/wnl.46.1.198. [DOI] [PubMed] [Google Scholar]
- 5.Higgins JN, Gillard JH, Owler BK, et al. MR venography in idiopathic intracranial hypertension: unappreciated and misunderstood. J Neurol Neurosurg Psychiatry. 2004;72:621–25. doi: 10.1136/jnnp.2003.021006. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 6.Bateman GA. Arterial inflow and venous outflow in idiopathic intracranial hypertension associated with venous outflow stenoses. J Clin Neurosci. 2008;15:402–408. doi: 10.1016/j.jocn.2007.03.018. [DOI] [PubMed] [Google Scholar]
- 7.Bateman GA. Association between arterial inflow and venous outflow in idiopathic and secondary intracranial hypertension. J Clin Neurosci. 2006;13:550–556. doi: 10.1016/j.jocn.2005.06.005. [DOI] [PubMed] [Google Scholar]
interv neuroradiol. 2010 Mar 23;16(Suppl 1):49.
Idiopathic Intracranial Hypertension (also known as Benign Intracranial Hypertension, or Pseudotumour Cerebri) is a condition which in many cases is neither "idiopathic" nor "benign".
This disorder is responsible for chronic headache and disability, progressive visual loss, CSF leaks and in severe cases, intracranial pressure crises and even death.
Imaging findings will be discussed with a focus on ATECO MR Venography, Direct Retrograde Cerebral Venography and Manometry (DRCVM) and CSF Pressure Monitoring.
Controversies in management of this condition and our approach to interventional management with venous stenting, and outcomes in our series of 48 patients will be outlined, together with pitfalls in interventional management.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):50–51.
Patients with deep vein and cerebral dural sinus thrombosis (CVST) often have a variable clinical course and unpredictable neurological outcome. Ever since Ribes in 1825 described the condition at autopsy, numerous publications, largely in the form of case reports and small clinical series, have been added to the literature, a consensus regarding the appropriate treatment remains elusive.
With new endovascular techniques and devices, direct thrombolysis and thrombectomy without a craniotomy is becoming increasingly common. Endovascular treatment of CVST has the potential advantages of acute dissolution of clot, allowing normalization of blood flow, decreased ICP, and rapid improvement of severe symptoms. Conversely, these invasive procedures are also associated with risks such as hemorrhage, vessel dissection, and pulmonary embolism.
Systemic Anticoagulation
Systemic heparin is still the gold standard of care in cerebral venous thrombosis after the first successful use in 1941 by Lyons. Cochrane Collaboration conducted a meta-analysis in 2002 on two randomized, placebo-controlled trials using unfractionated and low molecular weight Heparins. It was concluded that anticoagulation was safe and associated with a non-significant, yet potentially important, improvement in outcome with additional benefit of DVT and pulmonary embolism prevention. More recently, the International Study of Cerebral vein and Dural Sinus Thrombosis (ISCVT), found a trend toward improved outcomes in the anticoagulation group(12.7% dead or dependent in the anticoagulation group vs 18.3.% in the control group), the difference was not significant. Several reviews and European Federation of Neurological Societies (EFNS) guidelines continue to support the efficacy and safety of anticoagulation in CVST(Class IIa,Level B).
Interventional Therapies
Intra-sinus chemical thrombolysis is believed to be better restoring venous blood flow than heparin. Thrombolysis is also used when the patient's condition worsens despite heparin and symptomatic treatment. The most frequently described cause of worsening is inadequate anticoagulation. Clinical deterioration due to thrombosis progression in properly anticoagulated patients is rarely observed. When it is observed, thrombolytic treatment should be considered as a valid option. The application of Urokinase, Streptokinase or Tissue Plasminogen Activator tPA via transfemoral catheterization to the thrombus has been reported in many case series. Some results were very encouraging but some trials demonstrated increase risk of ICH especially when haemorrhage was already present. Canhao et al. reviewed 72 studies and Cochrane Collaboration also conducted a review of chemical trhombolysis. Overall, there is reasonable evidence to suggest that in some patients the local infusion of fibrinolytics agents can afford significant recovery, although other therapeutic options with a superior safety profile may exist (Class IIb, Level B).
In general, hemorrhagic risk is higher in thrombolysis compared to heparin, especially when a pretreatment hemorrhage is already present. Thus, this fear that hemorrhagic stroke can deteriorate due to thrombolysis treatment leads to the development of improved mechanical techniques that lower the risk of bleeding.
Mechanical thrombolysis
One of these devices is rheolytic thrombectomy, which utilizes the Venturi effect which creates a negative pressure fragmenting and aspirating the cerebral venous thrombus. These devices can be utilized in combination with thrombolysis. The AngioJet Rheolytic Thrombectomy System (Possis Medical, Minneapolis, MN) consists of a single-use catheter, single-use pump set, and multi-use drive unit. The same drive unit and pump set are compatible with various catheters with different design features. Thrombectomy is accomplished with the introduction of a pressurized saline jet stream through the directed orifices in the catheter distal tip. The jets generate a localized low pressure zone via the Bernoulli effect, which entrains and macerates thrombus. The saline and clot particles are then sucked back into the exhaust lumen of the catheter and out of the body for disposal. Treatment with the device takes about one minute. The system however,has a more rigid catheter delivery system which makes distal clot difficult to reach by transvenous femoral route.
Other aspirating system such as the Penumbra (Penumbra Inc. USA) coupled with Neuron carrying catheter has been used. The system uses a unique microcatheter and separator based thrombus debulking approach. The clot is fragmented by the separator and aspirated by special continue low suction pump.
Balloon angioplasty and thrombectomy are inexpensive methods. The use of transvenous Fogarty balloon catheter in conjunction with systemic anticoagulation has demonstrated clinical improvement. Other types of guidewire mounted balloon e.g. Stealth, Hyperglide or Hyperform can travel even further to distal SSS for clot retrieval. However, dislodgement of large clot during retrieval of balloon into the jugular vein can cause significant pulmonary embolism.
The adoption of transarterial clot retrieval devices e.g. Merci I and Merci II for CVST have been proposed. While some investigators are adopting retrievable stent e.g. Solitare (eV3, USA), Catcher(Balt) for clot maceration and removal with promising potential. The use of self-expanding stent e.g. Wall stent (Boston Scientific) to compress the clot to the sigmoid and transverse sinuses wall with recreation of a channel for venous return has been used for short segment of thrombosis.
Conclusion
Cerebral venous thrombosis remains a therapeutic challenge. Based on available evidence, systemic anticoagulation as initial step is safe even in the setting of pre-existing ICH. Combination with intra-sinus chemical thrombolysis and mechanical thrombectomy has to be judged by each individual case. It has to be based on the site, degree and progression of thrombosis. In patient with ICH, the safety of fibrinolysis is uncertain, mechanical thrombectomy in conjunction with systemic anticoagulation is probably preferred. Apart from multi- factorial causes, thrombosis of cerebral veins can present in many forms. In one end of the spectrum, it presents as acute venous stroke when alternative venous route is lacking in the cerebral circulation. The other end of the spectrum, thrombosis occurs silently and progresses to form dural arterial fistula and CCF. On the contrary, such forms of venous condition have to be treated idiosyncratically by augmentation of thrombosis by coil or glue rather than by thrombolysis.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):52.
Spinal cord vascular shunts (SCAVSs) can be classified according to their type, their localization, their number, their gross appearance, their angioarchitecture.and their links to eventual associated metameric disorders.
If one considers the dura as a barrier, 4 different types of SCAVSs can be recognized:
-paraspinal AV shunts (AVSs) are located outside the spine and may have neurological consequences due to compression of the cord by venous ectasias, congestion of the cord because of venous reflux into spinal cord veins, or intradural haemorrhage
-epidural AVSs develop in the epidural space between the external surface of the dura and the internal surface of the vertebra, in the spinal canal. Neurological symptoms may occur in these lesions if the venous drainage is redirected towards spinal cord veins.
-dural AVSs are abnormal arteriovenous communications inside the dura, mostly situated near the nerve root exit at the level of the inter-vertebral foramen. The venous drainage is either segmental following a radicular vein, or intersegmental through an emissary vein that pierces the dura between two spinal nerves. Neurological symptoms are created by the congestion of the spinal cord veins responsible for a venous ischemic myelopathy.
-intradural AVSs can affect the nerve root(s), the filum terminale or the cord itself. The symptoms created can either be related to chronic venous ischemia or to acute haemorrhages. Two types of shunt can be distinguished
-arterio-venous fistulas (AVFs) represent direct communications between arteries and veins without any interposition of any pathological segment. They are always superficial and can be divided into micro AVFs (small size lesions fed by one or multiple arteries of different calibres and draining into moderately enlarged veins), and macro AVFs (large high-flow shunts fed by large arteries and draining directly into a giant venous ectasia, characteristic of the lesion with secondary congestion of the cord veins)
-arteriovenous malformations (AVMS) are nidus type lesions with a vascular network that is interposed between arteries and veins. They can be either superficial in the subpial space, or can invade the cord parenchyma and be intramedullary.
Intradural AVSs can be further distinguished in 3 groups:
-the first group encompasses single shunts attributable to a genetic hereditary disorder. The main syndrome in which genetic links can be recognized is HHT. In our experience, HHT related lesions have always been MAVFs, particularly in the pediatric population. Multiple lesions were not related to HHT in our population of patients.
-the second group involves multiple SCAVSs of any type. These lesions are not hereditary. Three types of multiple non hereditary lesions can be described:
-shunts with a metameric link. These multiple lesions are located on the same metamere, or on the cord and the nerve root. The association is metameric if the myelomere involved in with the SCAVS corresponds to that of the involved nerve. Cobb syndrome (spinal cord arterio-venous metameric syndrome, or SAMS) can obviously be regrouped in that category.
-multi-myelomeric shunts are well circumscribed lesions located on several myelomeres of the cord. The multiplicity is assessed if the various shunts are separated by normal cord parenchyma.
-syndromic SCAVSs are associated to vascular limb malformations, as those encountered in Parkes-Weber or Klippel Trenaunay syndromes.
-the third group contains single lesions. They can be either nidus-type or micro fistulous-type AVSs (MAVFs belonging to the genetic hereditary type of lesions). Single lesions can affect any of the nervous structures in the intradural space (nerve root, filum, cord)
This classification of intradural SCAVSs tries to replace the lesions in a broader context regarding their diagnosis and history. It uses physiological and genetic data, and emphasize that SCAVSs are expressions of more complex disorders that extend far beyond the rough description of radiological pictures. It helps to understand the relationships between various diseases and allows to build up anatomical and diagnostic correspondences between shunts that may be located in different anatomical areas at first sight. Therefore these lesions cannot be considered only as morphological targets, and reasonable and new therapeutic goals, strategies and end points need to be established.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):53.
Spinal cord arteriovenous shunts (SCAVSs) are considered to have a poor natural history with bad neurological outcome, their progressive evolution being made of progressive impairments rythmed by acute episodes of deficits mainly related to haemorrhages.
The rarity of the disease makes the understanding of these lesions somewhere difficult, as only few papers in the literature have detailed the clinical evolution of SCAVSs.
It has been considered by Aminoff and Logue in 1974 that severe locomotor disability developed in 19 % of patients with SCAVSs within 6 months of the onset of any functional impairment in the legs, and in 50% of cases within 3 years, while only 9% of patients were capable of unrestricted walking. However, their paper was published before the recognition by Kendall in 1977 of spinal dural arteriovenous shunts (SDAVFs ) as a distinct pathological entity: the two different diseases (SCAVSs and SDAVSs) may have been mixed, so that precise understanding of the natural history of each of these lesions remained confused. Hurth in 1978 reported a series of 150 cases among which 130 could be recognized as "true" SCAVSs. Hurth emphasized that 24% of patients suffered bleeding at one stage or another during progression of the disease, with 89% of haemorrhages as first manifestation. Apart from haemorrhage, the neurological manifestations of spinal cord arterio-venous shunts were rather unspecific. Sixty-nine percent of patients presented with stepwise progression, the final results being almost always a major impairment in spinal function. Hurth also pointed in his series that two factors undoubtedly affected the progression of the symptoms: the position of the lesion that he called "intramedullary" or "extramedullary", and the localisation of the lesion (shunts located in the cervical region having a higher tendency to haemorrhage). He concluded that the so-called "extramedullary arteriovenous malformations" (in fact superficial AVFs) progressed steadily with major clinical impairment occurring within 4-6 years, and that the rapidity of deterioration in "intramedullary arteriovenous malformations" varied according to the localization of the lesion: 80% of untreated patients with cervical shunts were independent within 5 years after diagnosis, while 60% of untreated patients with thoraco-lumbar shunts were self-sufficient during the same period of 5 years.
Thanks to a meta-analysis of the papers published on that topic, it seems acceptable to conclude that after diagnosis of a SCAVS, a large number of patients (40-69% according to the series) will undergo neurological deterioration in a stepwise fashion, with episodes of relapse occurring in about 80% of patients, but with acute episodes of haemorrhagic accidents, a significant percentage or the latter leading to death. This progression of symptoms brings to a dependant clinical status with severe neurological dysfunctions in a time frame of maximum 6 years after the onset of symptoms.
The review of our series in 2004 also allowed to distinguish several groups of populations and malformations. Most of the children in our series (70%) presented with haemorrhage (either hematomyelias or subarachnoid haemorrhages ([SAH]), cervical AVSs being more prone to bleed than other localisations. Recurrent haemorrhages rarely occurred before treatment, and spontaneous recovery was the rule in most of the cases (>70%) after few weeks or months. In adults, progressive neurological symptoms as initial clinical manifestation were seen in 49% of patients, while 45% of adults with SCAVSs presented with haemorrhage (predominantly SAH). Bleeds were more prone to occur in cervical SCAVSs. Spontaneous recovery was observed in 72% of adult patients who had bled. Only 3.6% of adult patients in our series rebled during the first year after the diagnosis.
Although SCAVSs are located in highly eloquent tissues and can have severe consequences if they bleed, their short term prognosis after haemorrhage seems less serious than thought initially. The improvement noted in most of the cases indicates that emergent treatment, either surgical or endovascular, has no place in the primary management of these lesions, as furthermore early rebleeds are rarely seen. No proof of the impact of early treatment on the quality of recovery has been found at this stage, and the rate of spontaneous recovery seen in our series compares favourably with the post surgical course.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):54.
Three different modalities are currently used to evaluate Spinal Vasculature. These are
1) Digital Subtraction Angiography (DSA)
2) Magnetic Resonance Angiography (MRA)
3) Computed Tomography Angiography (CTA).
DSA is the current gold standard in the evaluation of Spinal vessels with an excellent spatial resolution of 0.2mm and a temporal resolution of less than 10secs. However DSA in addition to being invasive, with significant morbidity, is a time consuming procedure which may not always be completed in one session, with consequent increase in total radiation dose and patient discomfort.
MRA and CTA have been used as alternatives to Spinal DSA and their advantages and disadvantages will be explored in the lecture.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):55.
Spinal dural arteriovenous fistula (SDAVF) can be located anywhere from the craniocervical junction to the sacrum. It can require up to 40 selective injections into intercostal, lumbar, sacral, cervical and intracranial arteries to localise with catheter angiography (CA)1. A non invasive test that can accurately predict the fistula level can expedite the subsequent angiography and embolization procedure by directing the interventionist to the levels specified by the non invasive test initially. MR spinal angiography (MRSA) can correctly predict the level (+/- one level) in 73% of patients2. However, because of limited field of view of 1.5T magnets, 2 or 3 separate MRSA examinations were required to localize the fistula in 50% of patients in one study3. Multi detector CT angiography (MDCTA) has the advantage of very short time scan time and high spatial resolution compared with MRSA, and the scan length can cover the entire spine in one examination.
Recent studies4,5 have demonstrated that MDCTA has useful clinical applications in the diagnosis and management of spinal vascular diseases. Our own study6 has shown that MDCTA is 100 % sensitive in localising the SDAVF to at least 1 level in all patients. The positive predictive value (PPV) for each level localised is 75%.
However, Multiple SDAVF could present a problem. Multiple SDAVF is rare. In a study of 49 patients, 1 patient (2%) had 2 fistulas (T5 & T9) with the second lesion diagnosed on a subsequent occasion after failure to improve after curative treatment of the initial fistula7. Some SDAVF have bimetameric arterial supply by intersegmental anastomosis from 2 adjacent levels.
During angiography and endovascular treatment, providing that the adjacent levels have been checked for intersegmental anastomosis, it is reasonable to stop searching for other possible levels once the level(s) specified by MDCTA are confirmed by CA and proceed to embolize the confirmed levels. If after treatment and the patient’s symptoms do not improve and there is persistent MR abnormalities despite adequate surgery or embolization, a repeat MDCTA can be performed to search for a subsequent level.
Spinal cord arteriovenous malformation is much rarer than SDAVF, but MDCTA has been shown to be useful in this type of malformation as well4.
Thus by accurately localising the arterial feeders with MDCTA, endovascular treatment can be greatly expedited.
References
- 1.Willinsky RA, Lasjaunias P, TerBrugge KG. Angiography in the investigation of spinal dural arteriovenous fistula: a protocol with application of the venous phase. Neuroradiology. 1990;32:114–116. doi: 10.1007/BF00588560. [DOI] [PubMed] [Google Scholar]
- 2.Saraf-Lavi Efrat, Bowen Brian C, Quencer Robert M, Sklar Evelyn ML, Holz Alan, Falcone Steve, Latchaw Richard E, Duncan Robert, Wakhloo Ajay. Detection of Spinal Dural Arteriovenous Fistulae with MR Imaging and Contrast-Enhanced MR Angiography: Sensitivity, Specificity, and Prediction of Vertebral Level. AJNR Am J Neuroradiol. 2002 May;23:858–867. [PMC free article] [PubMed] [Google Scholar]
- 3.Farb RI, Kim JK, Willinsky RA, Montanera WJ, TerBrugge K. Spinal dural arteriovenous fistula localization with a technique of first-pass gadolinium-enhanced MR angiography: initial experience. Radiology. 2002;222:843–850. doi: 10.1148/radiol.2223010826. [DOI] [PubMed] [Google Scholar]
- 4.Si-jia G, Meng-wei Z, Xi-ping L, Yu-shen Z, Jing-hong L, Zhong-hui W, Pei-zhuo Z, Qiang S, Qiang W, Chuan-sheng L, et al. The clinical application studies of CT spinal angiography with 64-detector row spiral CT in diagnosing spinal vascular malformations. Eur J Radiol. 2009;71(1):22–8. doi: 10.1016/j.ejrad.2008.04.005. [DOI] [PubMed] [Google Scholar]
- 5.Yamaguchi S, Nagayama T, Eguchi K, Takeda M, Arita K, Kurisu K. Accuracy and pitfalls of multidetector- row computed tomography in detecting spinal dural arteriovenous fistulas. J Neurosurg Spine. 2010;12(3):243–8. doi: 10.3171/2009.9.SPINE0971. [DOI] [PubMed] [Google Scholar]
- 6.Chong W, Holt M, Phan T. Localisation of Spinal Dural Arteriovenous Fistula by Multi Detector CT Angiography to Expedite Endovascular Treatment. Interventional Neuroradiology. 2007;13(2):130–131. [Google Scholar]
- 7.van Dijk JM, terbrugge KG, Willinsky RA. Multiplicity of dural arteriovenous fistulas. Neurosurg. 2002;96:76–78. doi: 10.3171/jns.2002.96.1.0076. [DOI] [PubMed] [Google Scholar]
interv neuroradiol. 2010 Mar 23;16(Suppl 1):56.
Spinal cord arteriovenous malformation and fistula are the major parts of spinal vascular malformations, of which the lesions located in the cord or on the surface of the cord, including spinal cord arteriovenous malformations, perimedullary arteriovenous fistula and Cobb's syndrome, not including spinal dural arteriovenous fistula. Spinal cord vascular malformations are not easy to be cured with microsurgical or endovascular technique only. But endovascular embolisation plays the important roles in the therapeutic strategy.
Since 1986, we have accumulated rich experience on either embolisation or surgery of spinal vascular malformations. Each case was discussed on its MRI and angiography before the treatment, to decide how to achieve anatomical cure safely. Some cases were treated only with embolisation, or only with surgery, or with combination of the both techniques.
The targets of embolisation were anterior parts (via anterior spinal artery) and high flow lesions (via anterior and/or posterior spinal artery) of the malformations. The main material of embolisation was NBCA or Glubran with different concentration. In some AVFs or special AVMs, embolisation can obliterate the lesion completely. In some cases, Embolisation in the particular part of spinal cord vascular malformation gives the great help to surgical remove the lesion safely. It plays the functions as minimizing surgical trauma (especially to the anterior column), landmarks to identify the vascular architecture and decreasing the vessel tension.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):57.
Spinal vascular diseases are considered rare. The relative incidence of SAVM to BAVM are less than 1:10. However; nowadays spinal vascular lesions could be precisely diagnosed especially with good quality MRI/ MRA and chances of updated endovascular management make these rare and difficult disease possible be treated with good and stable clinical outcome.
As the vascular anatomy of spine are more organized related to metameric origin so classifications of spinal vascular diseases should follow these anatomy and types of angioarchitectures
Classification of spinal vascular lesions following the locations are:
Parachordal arteriovenous fistulae
Spinal extradural and paraspinal arteriovenous fistulas
Isolated (VVF and other locations)
May associated with systematized dysplasia, e.g. von Recklinghausen's disease
Spinal dural arteriovenous fistulas
Isolated
Multiple
Spinal cord vascular malformation : perimedullary/superficial/ deep location
Isolated (arteriovenous malformation, arteriovenous fistula)
Multiple
Metameric (Cobbs and other syndromes-SAMS* and associations)
Nonmetameric (Rendu-Osler-Weber and Klippel-Trenaunay syndromes and others)
Spinal cord telangiectasias
Cavernous vascular malformations (cavernomas)
(SAMS : spinal arteriovenous metameric syndrome (1-31))
Dural arteriovenous shunts or fistulas (DAVSs or DAVFs) are a broad group of diseases that share involvement of the epidural space and adjacent dura mater and bony structures.
The cranio spinal epidural spaces were categorized into three different compartments - ventral, dorsal and lateral. Each compartment has its specific drainage role in relation to the embryologic development of the venous system of the central nervous system (CNS) and surrounding bony structures. The ventral epidural space drains structures derived from the notochord and adjacent sclerotomes. The dorsal epidural group is related to the drainage of the spinous processes at the spinal level and to the vault and calvarium cranially. The lateral epidural group collects the emissary bridging veins of the pial venous system of the spinal cord and brain.
The dural arteriovenous shunts (DAVS) developing in these spaces predictably drain either in the sub arachnoid veins or in the epidural-paraspinal collectors according to the epidural compartment involved. Additional co- morbidity like epidural veins thrombosis or high flow characteristics of the DAVS will be responsible for changes in the draining pattern of otherwise anticipated spinofugal or craniofugal drainage. This embryologically based classification establishes homologies between spinal and cranial epidural spaces, thus allowing epidemiological and clinical comparison including spinal and cranial DAVSs.
Lateral epidural shunts
The most typical ones correspond to the space where spinal DAVFs are located. Intracranial locations include DAVS draining into emissary-bridging veins of the brainstem and their homologues draining deep cerebral structures, such as the condyloid vein at the foramen magnum, the superior petrosal vein, the basal vein, the vein of Galen, the veins of the anterior cranial fossa (lamina cribriformis/ethmoid) and the orbit. The drainage is always directed to the cortical or perimedullary veins, therefore the DAVS developing there are always considered to be aggressive11-13. In this group the following DAVS locations are encountered: lateral "spinal dural AV shunts", marginal sinus (lateral portion, with the emissary-bridging vein to the condyloid vein, falco-tentorial (vein of Galen), petrosal and basi-tentorial , Breschet sinus, para cavernous region (embryonic tentorial sinus remnants), intra orbital shunts and lamina cribriformis.
SDAVshunts (fistula or malformation) are the acquired AV shunt located within or adjacent to dura(mainly at intervertebral foramen level) along the spinal canal. They usually presented after 4th -5th decade of life and 85% are male predominant or M:F = 5:1 (opposite to dural AV shunt at skull base which F>>M). The location could be from sacral level to the Foramen Magnum level but are mainly located at T-L regions. The venous drainage can be extensive and could reach dural sinus even shunt located at sacral level.
Pathology - Clinical presentation
The arterial supply is mostly arise from a dural (radicular) branch of the dorsospinal artery at intervertebral foramen level. They could be "Bimetameric" supply. They are usually small AV shunt (mostly fistula or small nidus) .The venous drainage is usually tortuous single draining vein pierces dura (distance from accompanying nerve root) to reach perimedullary venous system and they could produce venous hypertension of the medullary vein (cord)
SDAVS : pathophysiology
The patient. with more symptoms are the one who have anterior and posterior drainage(more than posterior alone) as well as with downward or Caudal drainage (more than upward or cephalad). Typical cord changes in long standing lesion are "neocapillaries" within the cord which should be differentiated from nidus. The primarily parenchymal changes are from congested intrinsic venous network of the spinal cord; secondary from chronic extensive hypoxia from long standing venous congestion.
SDAVS : The treatment indications are for all patients (either by endovascular or surgery)
The treatment aim are for cure if possible which mean the occlusion of the proximal draining vein and the micro AV shunt. Contraindication for endovascular treatment are usually if the ASA originates from the same pedicle as the SDAVS which superselective catheterization cannot be safely done or the extra spinal longitudinal anastomosis cannot be clearified; to prevent accidentally embolization of the ASA
SDAVS : Endovascular Treatment:
As the afferent arteries size are between 40-60 micron so Liquid embolic material is the embolic material of choice to reach the shunt and the proximal vein and particle will not be effective. The average results are up to 80% of the patient showed clinical improvement from endovascular treatment Clinical improvement depended on shorter time between onset of symptoms and treatment. Additional anti-coagulation treatment ,ay be considered if the clinical improvement is stopped as well as in the patient with descending venous drainage and absence of radicular vein opacified at T level for AVS at L-S
SDAVS : Surgical Treatment
The aim is to interrupt the drainage vein by coagulation and excision of the dura at the site using bipolar coagulation. The cluster of abnormal vessels at inner aspect of the dura are usually seen at surgery.Another surgical option is Duroplasty at the level of the lesion. There are average same result as endovascular treatment if exact site of the fistula was found.
Series of SDAV shunts and results of treatment will be presented.
References
- 1.Lasjaunias P, Berenstein A, terBrugge K. Surgical Neuroangiography 1 Clinical Vascular Anatomy and Variations. Springer. (2 ed) 2001 [Google Scholar]
- 2.Cullen S DF, Ozanne A, Alvarez H, Mercier PH, Brassier G, Lasjaunias J. The anastomotic venous circle of the base of the brain. Interventional Neuroradiology. 2005;11:325–32. doi: 10.1177/159101990501100404. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 3.Krings T, Mull M, Bostroem A, Otto J, Hans FJ, Thron A. Spinal epidural arteriovenous fistula with perimedullary drainage. Case report and pathomechanical considerations. J Neurosurg Spine. 2006;5:353–8. doi: 10.3171/spi.2006.5.4.353. [DOI] [PubMed] [Google Scholar]
- 4.Lasjaunias P, Geibprasert S, Pereira V, Krings T, Jiarakongmun P, Aurboonyawat T, Pongpech S. Classification of Dural arteriovenous shunts (DAVS) based on the Craniospinal Epi dural Venous drainage of the central nervous system and adjacent bony structures. Japanese Journal of Neurosurgery. 2008;17(5):356–361. [Google Scholar]
- 5.Geiboprsert S, Pereira V, Krings T, Tougoat F, Pongpech S, Lasjaunias P. Stroke. 2008 Oct;39(10):2783–94. doi: 10.1161/STROKEAHA.108.516757. [DOI] [PubMed] [Google Scholar]
interv neuroradiol. 2010 Mar 23;16(Suppl 1):59–60.
Indications of percutaneous vertebroplasty include vertebral fractures of different causes, including osteoporosis, benign or malignant tumor. The main reason of vertebroplasty is for pain relief. Vertebroplasty can fill the osteolytic space of tumor, fracture line, cleft and cavity inside avascular necrosis, and trabecular space, thus prevent further collapse of vertebral body, and provide stability. Vertebroplasty may prevent development of cardiopulmonary and gastrointestinal symptoms because of small capacity of the thoracic and abdominal cavity as result of multiple thoracic and lumbar vertebral fractures. In recent years, there are much advancement in the medical treatment of osteoporosis, thus, the necessity of vertebroplasty to treat osteoporotic vertebral fracture may be less. In patients with osteoporotic vertebral fracture, active medical treatment of osteoporosis is very important to prevent new fractures.
Not all vertebral fracture needs vertebroplasty. Old fracture does not need vertebroplasty. MRI can detect new, or unhealed fractures that may benefit from vertebroplasty by showing edema, a cavity or cleft inside (avascular necrosis), or enhancement (if contrast MRI was performed). Whole body bone scan may show increased uptake at the level with new or unhealed fracture. These new or unhealed fractures usually may have deep seated midline back pain clinically. The pain usually is most severe on lying down to bed, or rising from bed. On physical examination, tenderness or knocking pain may be elicited at the corresponding spinous process.
Patients with transverse fracture involving the anterior and posterior elements of the spine may be extremely instable, thus, a contraindication of vertebroplasty. In vertebral fractures with retropulsion, vertebroplasty cannot relieve the spinal cord compression or spinal stenosis. MRI can also show associated spinal problems whose symptoms will not relieve after vertebroplasty.
There were countless reports in the past to appreciate the effect of percutaneous vertebroplasty in the treatment of osteoporotic vertebroplasty, including pain reduction, wedge deformity correction, and prevention of further collapse in the cemented vertebral body.
In recent 1-2 years, there are big debates regarding to treatment of vertebral fracture from osteoporosis. There are two reports of multicenter, randomized, double-blind, placebo-controlled trials of treatment of painful osteoporotic vertebral fractures. Buchbinder R et al found that there was no beneficial effect of vertebroplasty as compared with a sham procedure in patients with painful osteoporotic vertebral fractures, at 1 week or at 1, 3, or 6 months after treatment. Kallmes DF concluded improvements in pain and pain-related disability associated with osteoporotic compression fractures in patients treated with vertebroplasty were similar to the improvements in a control group.
However, selection bias cannot be entirely ruled out, since 30% of potentially eligible participants declined to participate in Buchbinder's study. And there was higher crossover rate in the group received sham operation at the Kallmes' report. Possibly more patients in the control group had unsatisfactory pain outcomes but we were unable to detect this difference with measurement of pain intensity in his study.
From these report, we learn:
Vertebroplasty may not necessary for pain control in most patients with osteoporotic vertebral fracture.
Sham operation may be enough to cure most patients' pain with unknown reasons.
-
Vertebroplasty or kyphoplasty may still beneficial in the following conditions or effects of osteoporotic vertebral fractures:
(1) Patients with avascular necrosis in their vertebral bodies, because avascular necrosis in vertebral body was not evaluated in these two studies.
(2) Prevention of further collapse of the vertebral body, kyphosis, and further retropulsion to result in spinal cord compression, because morphological change after vertebroplasty was not evaluated in these two studies.
(3) Prevention of pulmonary function impairment and gastrointestinal disturbances as a result of reduction of thoracic and abdominal spaces from vertebral fractures.
Vertebroplasty have immediate and persistent effect of pain relief, vertebral height recovery, and wedge deformity correction. New adjacent fracture in short term is one possible problem in patients with severe osteoporosis. From our previous study, 48% of 60 patients had new fractures during a follow-up period of more than one year (14 ± 3 months). 63% of these fractures were adjacent to a cemented vertebral body. Therefore, we have to do preventive vertebroplasty on adjacent vertebral body, especially when bone cement has reached the endplate or disc space. We can achieve prevention of kyphosis only if vertebroplasty with preventive vertebroplasty on adjacent levels were performed immediately, or vertebroplasty at level of new fractures was done immediately before permanent vertebral deformity occurs, and good anti-osteoporosis medical treatment starts early to prevent new vertebral fracture.
References
- 1.Teng MMH. Selection of patients and levels for percutaneous vertebroplasty based on clinical and basic research. Interventional Neuroradiology. 2007;13(S2):69–70. [Google Scholar]
- 2.Rachelle Buchbinder, et al. A Randomized Trial of Vertebroplasty for Painful Osteoporotic Vertebral Fractures. New England J of Medicine. August 6 2009;361:557–568. doi: 10.1056/NEJMoa0900429. [DOI] [PubMed] [Google Scholar]
- 3.David F, Kallmes , et al. A Randomized Trial of Vertebroplasty for Osteoporotic Spinal Fractures. New England J of Medicine. 2009;361:569–579. doi: 10.1056/NEJMoa0900563. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 4.Chang CY, Teng MMH, et al. Percutaneous vertebroplasty for patients with osteoporosis: a one year follow- up. Acta Radiologica. 2006;47:568–573. doi: 10.1080/02841850600690405. [DOI] [PubMed] [Google Scholar]
- 4.Teng MMH, et al. Follow Up on Percutaneous Vertebroplasty using PMMA in Osteoporotic Patients. Rivista Di Neuroradiologia (The Neuroradiology Journal) 2006;19:551–55. doi: 10.1177/197140090601900412. [DOI] [PubMed] [Google Scholar]
interv neuroradiol. 2010 Mar 23;16(Suppl 1):61.
Minimal invasive percutaneous techniques for disc lesions offer good results with good patient compliance and low cost. They reduce the occurrence of post surgical complications like infections or hypertrophic scar tisues. The aim of all Percutaneous treatment is to reduce the intra-discal pressure in different ways creating the space required for retropulsion, digestion of the disc.
Nowadays among all available techniques IDET and chemodiscolysis with O2 O3 mixture with periganglionic infiltration are preferred. The therapeutic efficacy of Ozonucleolysis ranges between 70% to 90%. No early or late neurological or infectious complications have been reported following O2 O3 injections.
In my presentation I will share my experience of 3000 treated cases during the period of 5 years at Lahore General Hospital, Post Graduate Medical Institute (PGMI) and National Hospital Defence Lahore, Pakistan..
All these treated by intra discal, with periganglionic or peravertabral oxygen ozone injections. Patient's age between 20 to 70 years underwent percutaneous ozonalnucleolysis under angiofluro with asceptic technique and short hospital stay.
No side effects were reported at short and long term follow-up clinical results, hence evaluated with the modified Manab method sharing 85% success rate. In our experience ozone gas therapy in treatment of herniated disc has revolutionized the Percutaneous approach to nerve root disease making it safer cheaper and easier to repeat than treatments currently in use.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):62.
For the majority of neurosurgeons there are generally accepted guidelines that form an established framework for management of disc lesions. The management of paradigms for treatment of "crush" fractures are far less certain.
I will discuss when and why a neurosurgeon will recommend surgical intervention for these pathologies. I will also provide my opinion on the role radiologists and other practitioners play in treatment of conditions associated with degenerative change and ageing to the vertebral column.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):63–65.
Cerebral Arteriovenous Fistula (CAVF) is the name we assign to an intracranial direct communication from artery to vein, without intervening "nidus" and located in the subpial meningeal space. As the AV shunt is located in the subpial space, its drainage pattern may impact the regional brain parenchymal areas as it will eventually suffer from the hemodynamic impact of the fistula. If the vein draining the lesion is subpial for a long segment, as it may be in certain CAVMs, its chances of interfering with regional brain parenchyma circulation and creating damage are maximal till it joins a significant outlet that takes it across the subarachnoid space to the dural sinuses away from the regional brain vasculature. However, during its subpial portion, the venous channel is in direct connection with the venules participating both in arterial drainage and water homeostasis. Conversely, if the drainage of a lesion is immediately subarachnoid when the subarachnoid transit distance is short, as it tends to be in CAVFs, the subpial venous congestion will be reduced including the chance for regional atrophic changes and melting-brain syndrome. Some high-flow lesions encountered in infants may lead to macrocrania but not to cortical atrophy (as long as the dural sinuses are patent). This is easy to understand if the hyperpressure resulting from the AV shunt is exerted at the dural sinus level, compromising its function to absorb CSF. The brain remains protected in the absence of active resistance at the veno-dural junction, where the draining vein opens as long as the sinus remains patent. Evolution of the macrocrania and the subsequent jugular vein occlusion in an initially subarachnoid draining lesion, regardless of its size, may create not only a severe water disorder, but also rapid venous ischemia, infarction and hemorrhage in any area of the brain. In addition to venous dural failure, subarachnoid and rapid subpial congestion occurs. The focal neurological symptoms at that time have no relationship to the topography of the AV shunt itself and can potentially be bilateral and multifocal.
Vein of Galen Malformations (Subarachnoid AVSs)
The vein of Galen arteriovenous malformation (VGAM) is a choroidal arteriovenous disease where the actual shunt lies in the sub-arachnoid space. Raybaud et al were the first to recognize that the ectatic vein in VGAM is, in fact, the median vein of prosencephalon, the embryonic precursor of the vein of Galen itself. Additionally, there is persistence of alternative routes for deep venous drainage and most often the choroidal vein and the thalamostriate vein do not drain into the vein of Galen. The clinical presentation of VGAM and its natural history vary significantly from C-AVMs. The management options, timing of intervention and potential complication make it imperative that this condition be recognized precisely and accurately and managed at an experienced center at the optimal moment in time in order to achieve a normally developing child.
There is no evidence to suggest arterial ischemia to occur with vein of Galen Malformations (arterial steal does no exist) and venous ischemia is a late phenomenon only occurring when venous reflux developed after jugular bulb occlusion and without venous capture of the cerebral cortical venous system by the cavernous sinus plexus.
It is unclear why in some patients apoptotic phenomena occur in utero or shortly after birth that preclude good outcome despite adequate management of the AVS. To anticipate such outcome will be needed in order to avoid aggressive but unnecessary therapy strategies.
Dural Sinus Malformations (Dural AVSs)
Dural arteriovenous shunts (DAVS's) represent abnormal shunts within the dura. Theoretically, they can occur at any site within the dura, but most frequently they develop near the venous sinuses. Venous drainage may occur into the dural sinuses, into osteodural veins, retrogradely via leptomeningeal veins towards the cortical cerebral, cerebellar or perimedullary veins, or any combination thereof. Arterial supply is usually from adjacent branches of the dural arteries, less frequently from osseous branches while pial supply is rare.
The term malformation was used in the past for all types of DAVS's, pediatric and adults, but we have found this to be inappropriate, as it implies a developmental origin in all of them. DAVS's have been demonstrated in utero and may clinically present at neonatal age. Their association with a malformation of the dural sinuses attests to their developmental origin. On the other hand there is good evidence that these shunts in adults are acquired.
Similar to VGMs we do not belief that arterial ischemia can occur as the result of so called arterial steal in patients with DAVSs. The arterial supply towards the DAVS is exclusively from dural vasculature which is distinct from cerebral supply. Ischemia with DAVS does occur but is of venous origin as venous hyperpressure and cortical venous reflux will result in venous infarction globally or regionally. Similar to VGMs this process can start in utero and be irreversible leading to a melting brain syndrome. While most neonates presenting under those circumstances tend to have high flow AVSs the more common presentation of neonatal DAVSs is the type with slow flow shunts associated to malformation of the dural sinuses and their outcome is related to preservation of flow within the grossly enlarged dural pouches which also drain the brain venous system and thrombosis will necessarily cause cerebral venous infarction.
Pediatric Aneurysms
Paediatric aneurysms differ in many of their features when compared to adult aneurysms in their gender prevalence, aetiology, anatomical distribution, configuration, size and multiplicity.
Incidence
Intracranial aneurysms in the pediatric age-group represent less than 5% of the total number of intracranial aneurysms in the general population.
The higher incidence of intracranial aneurysms in women among the adult population is reversed in the pediatric
population, in which the male to female ratio varies from 2:1 in infants up to 8 years of age to a nearly equal ratio of 1.2:1 in the 10- to 20-year age-group.
Presentation
When assessing the entire pediatric age group, patients with intracranial aneurysms present with subarachnoid hemorrhage about 70% of the time.The incidence of hemorrhage, however, is reported to be as high as 82% if only infants and children below 5 years of age were considered. The incidence appears to progressively decrease and to be as low as 45% if only children over 5 years of age are considered. Symptoms related to mass effect occur in about 20% of all children as the initial presenting symptom of an intracranial aneurysm.
Etiology
In children, as in adults, the etiology of aneurysms is mostly unknown. A clear underlying cause for a childhood aneurysm is found in less then 50% of cases. Although still often regarded as congenital as far as being present at birth, neither adult nor pediatric aneurysms are truly congenital in nature. The incidence of each type of aneurysm must be adjusted to the patient's age at presentation. While dissections are dominant during the first 5 years of life, saccular aneurysms are more common in children older than 6 years.
Traumatic aneurysms account for about 5%-15% of pediatric aneurysms. Of these, about 40% involve the distal anterior cerebral artery complex (adjacent to the falx), 35% involve the major vessels along the skull base and 25% are cortical in location. A mortality rate of 31% has been reported in children with traumatic intracranial aneurysms that were not treated.
Infectious Aneurysms
Infectious aneurysms account for 5%-15% of pediatric aneurysms. While they can be caused by fungal infections, they are most often of bacterial origin and often complicate bacterial endocarditis in infants with congenital or rheumatic heart disease.
Dissecting aneurysms (non-traumatic)
The frequency of dissecting aneurysms in the pediatric age group is four times that of in adults. This type of aneurysm tend to be located at the posterior circulation especially P1 and P2 segments of the posterior cerebral artery (PCA), supraclinoid internal carotid artery (ICA) and at the middle cerebral artery (MCA).
Giant aneurysms
Giant aneurysms are known to be of increased incidence in children - about four times more common than in adults. Their reported incidence in this age group is between 20 and 45%. Giant aneurysms should not only be distinguished because of their size, but also as a group within the dissection category.
Location of childhood aneurysms
The bifurcation of the internal carotid artery is the commonest single site for aneurysms in children. In fact, children have a fivefold increased incidence of carotid artery termination aneurysms with an incidence of 24%-54% for this location.
Multiplicity of aneurysms in children
The incidence of multiple aneurysms in the same patient in children has been reported to be considerably lower than that in adults and only 2% of children with saccular aneurysms showed multiplicity.
Management
Open surgery and endovascular approach both offer reconstructive and deconstructive options meaning excluding the aneurysm from the blood stream while preserving the parent vessel versus occlusion of the aneurysm and the parent vessel. Thus, both open surgery and endovascular treatment are appropriate for saccular, fusiform and giant aneurysms. Over the last years there has been a gradual shift from traditional surgical approaches towards endovascular treatment of paediatric aneurysms. This trend towards favouring endovascular treatment is noted in our group since 1997. Excluding the conservatively treated aneurysms 87.5% of aneurysms were treated by endovascular means and only 15% by surgery since 1997, while prior to that year 40% were treated by endovascular approach and 60% by surgery.
Patients treated by endovascular means had better clinical outcome surgically treated group. In the surgical group 44.4% of the patients made a good recovery, 44.4% had significant residual neurological deficit and 11.1% died. In the endovascular treatment group 77% of patients made a good recovery and 23% were left with significant neurological deficit. None of the patients treated by endovascular means died.
Conclusion
Whenever possible, endovascular treatment for paediatric aneurysms is the recommended approach, since it offers both constructive and deconstructive techniques and a better clinical outcome.
References
- 1.Lasjaunias P. Chapter 5: aneurysms in children. Berlin Heidelberg: Springer-Verlag; 1997. Vascular diseases in neonates, infants and children. [Google Scholar]
- 2.Laughlin S, Terbrugge KG, Willinsky RA, Armstrong DC, Montanera WJ, Humphreys RP. Endovascular management of pediatric intracranial aneurysms. Interventional Neuroradiology. 1997;3:205–214. doi: 10.1177/159101999700300303. [DOI] [PubMed] [Google Scholar]
- 3.Lasjaunias PL, Campi A, Rodesch G, Alvarez H, Kanaan I, Taylor W. Aneurysmal disease in children. Review of 20 cases with intracranial arterial localisations. Interventional Neuroradiology. 1997;3:215–229. doi: 10.1177/159101999700300304. [DOI] [PubMed] [Google Scholar]
- 4.Agid R, Souza MP, Reintamm G, Armstrong D, Dirks P, TerBrugge KG. The role of endovascular treatment for pediatric aneurysms. Childs Nerv Syst. 2005;21(12):1030–6. doi: 10.1007/s00381-005-1152-2. [DOI] [PubMed] [Google Scholar]
- 5.Lasjaunias P, Wuppalapati S, Rodesch G, Ozanne A. Intracranial aneurysms in children aged under 15 years: review of 59 consecutive children with 75 aneurysms. Childs Nerv Syst. 2005 Jun;21(6):437–50. doi: 10.1007/s00381-004-1125-x. [DOI] [PubMed] [Google Scholar]
- 6.Sanai N, Quinones-Hinojosa A, Gupta NM, Perry V, Sun PP, Wilson CB, Lawton MT, et al. Pediatric intracranial aneurysms: durability of treatment following microsurgical and endovascular management. J Neurosurg. 2006;104(2):82–89. doi: 10.3171/ped.2006.104.2.3. [DOI] [PubMed] [Google Scholar]
- 7.Lasjaunias P, Berenstein A, ter Brugge K. Surgical Neuroangiography. Vol. 3. Berlin, Germany: Springer-Verlag; 2004. [Google Scholar]
interv neuroradiol. 2010 Mar 23;16(Suppl 1):66–68.
Classification
We separate spinal cord arteriovenous shunts in children into two distinct groups:
1: niduses, an abnormal network is interposed between arteries and veins (SCAVMs)
2: fistulas, a direct communication is seen between an artery and a vein (SCAVFs)
Although both types of lesions are found in the subpial space, niduses may be buried partially or totally in the spinal cord itself. Conversely, large arterio venous fistulas (AVF) always remain superficial to the cord, as in the rest of the central nervous system and can probably even be located in the sub arachnoid space. The ventrally located ones however are deeper in the sulcus mimicking intra medullary ones. The venous drainage is likely to interfere with the intrinsic venous network in both nidus and ventral AVFs; however the dorsal AVFs will rapidly create congestion of the entire sub arachnoid venous system and eventually produce similar effects yet often remote from the AVF site.
Most of spinal cord AVS in all age-groups are single; however, 28% can be associated with some type of dysplasia: cutaneous vascular malformation, vertebral body vascular lesion, Cobb syndrome (skin, vertebrae, cord involvement at the same segment) described to day as SAMS. In 9% of cases, a Heriditary Hemorrhagic Telengiectasia (HHT)(Rendu-Osler-Weber) disease and a high-flow type were noted, and in 5% a Klippel- Trenaunay syndrome (part of the SAMS group). Reciprocally, it certainly justifies the use of magnetic resonance imaging (MRI) as a screening modality in the situations in which a peripheral vascular anomaly is found. Associated SCAVM and cavernomas have not been reported.
Multifocal SCAVM are rare. The association of a SCAVM and a cerebral AVM is exceptional and does not justify the systematic search for this association when confronted with either diagnosis.
Natural History and Clinical Aspects
SCAVM in the pediatric population represents a therapeutic challenge, as the effects of the disease may produce serious functional disorders and residual handicap. The natural history of SCAVM is usually poor, with progressive worsening of the neurological symptoms and an increase in the mortality rate after a second hemorrhage.
Rodesch reviewed spinalAVS 64% SCAVM, 30% dural AVS, 4% PSAVS and 2% radicular AVM. PSAVS were mostly found in patients under 15 years of age. No dural shunts were encountered in the pediatric population with only one exception in a HHT child operated upon for a perimedullary SCAVF that subsequently developed a Dural AVF at a different level.
Neonatal and infants
Neonatal SCAVMs are particularly rare. The transdural venous narrowed segment makes the possibility of congestive cardiac failure from a thoracic or lumbar SCAVM exceptional. If we consider this diagnosis among the possible AVS causes of cardiac failure in neonates, then the SCAVMs represent 1%-2% of them in our experience and they correspond to the large epidural AVFs.
The association of HHT with SCAVF in children is well documented. There is little in the literature, however addressing the presentation of this disease in neonates and infants. The AVF type of SCAVM is highly suggestive of HHT as seen in CAVFs were it has been suggested that it become one of the criteria to make the HHT diagnosis. The diagnosis does not require multifocality or cutaneo-mucous telangiectasias, which are rare at that age.
The neonatal and infant age groups represent a yet more specific cohort within the pediatric population. For example, in contrast to an earlier report (Rodesch 2004) that found that 70% of pediatric patients with spinal arteriovenous shunts of all age groups presented with hemorrhage (versus 45% of adults), in the present case series which pertained children below 2 years of age, hemorrhagic presentation was rare (23%). In addition, while in the total pediatric population the nidal-type AVMs predominates (67%), in the series below 2 years of age the majority of patients had fistulae. Perhaps the most striking finding in this cohort was the association with a genetic abnormality, whether hereditary such as in HHT or a non-hereditary somatic mutation as in SAMS.
Children after 2 years
The diagnosis of SCAVM is now made more rapidly at all ages, in contrast to the previous series in the literature with the advances in diagnostic imaging possibilities for this disease in this particular age-group, the time elapsing between the initial symptom and the diagnosis now only being a few days or weeks. Some patients may have a longer time delay before their lesion is recognized. The initial symptoms rapidly subside and the possibility of a SCAVM is not entertained until a second event occurs later. Sometimes a moderate deficit is noted early, but the child is not brought for consultation and diagnosis until a few years later. In all series about one third of the SCAVMs are located at the cervical level and the remaining at the thoraco-lumbar level However the mean age of onset varies according to the level (11.2 years at the cervical cord, 7.9 years at the thoraco-lumbar level).
Most of the symptoms in the pediatric population have a sudden onset. This is understandable with hemorrhage but one would expect neurological symptoms to develop more slowly when the venous drainage of the lesion creates a progressive congestion of the perimedullary pial network or because of the compression from venous ectasias. Such progressive onset of symptoms occurred in 9% of children.
In Rodesch series (2004) 30 patients (20 AVMs; 10 AVFs) were seen before 15years of age, most had their first symptoms at that age. No filum terminale lesion was detected in children. In this group 70% of lesions revealed with hemorrhage. Spontaneous total or subtotal recovery of neurological co-morbidity occurred in 72% of cases that had bled. Early hemorrhage reoccurred in 9 % of the cases, prior to time of referral. The incidence of hemorrhagic onset varied according to the localization of the SCAVSs : 82% of the cervical SCAVSs presented with bleeding; 69% of the thoracic and one third of the lumbo-sacral ones.
Within the group that bled, hematomyelia occured in 52% as proven by CT or MR . It was responsible for severe acute neurological central deficits, associating motor, sensitive and sphincter disorders in 2/3 of the cases. 48% children presented with subarachnoid hemorrhage (SAH), with also sudden onset of acute neurological symptoms. They were less severe than those encountered in those with hematomyelia. Four patients complained of SAH without neurological deficits. The diagnosis in all the SAH cases was made because of clinical signs, bloody CSF at lumbar puncture, and negative MRI that failed to show any clot in the cord. No patient died because of their hemorrhage.
Recovery of the symptoms depended on the intensity of the bleed, leaving the patients with permanent sequellae or minimal complaints at follow-up. From the 21 patients that presented with hemorrhage, 72% had after a few weeks or months a Karnovski score equal or above 80. Recurrent hemorrhage occurred in 9% of patients prior to consultation.
Within the Rodesch group of 30 lesions, 10/30 could be divided into 4 microAVFs (40%) and 6 MacroAVFs (60%).
5/6 of these MacroAVFs (83%) were associated with HHT and no child with a microAVF was suspected of HHT.
In the group of microAVFs, all manifested with acute post hemorrhagic neurological symptoms, hematomyelia (3/4) and subarachnoid hemorrhage (1/4).
All MacroAVFs were located in the thoracic or lumbar region. 4/ 6 (67%) MacroAVFs revealed by hemorrhage (3/4 SAH and 1/4 HM). By comparison with the group of lesions diagnosed before 2 years the risks of hemorrhage is even higher in children.
Haemorrhage is the most frequent symptom at presentation.
Neurological deficits associated with to hematomyelia vary according to the site of the clot. In general, hematomyelia gives rise to more severe neurological symptoms and longer and less complete recoveries than SAH alone.
Neurological deficits (without hemorrhage) revealed the SCAVM in 31%-37%.
Neurological deficits that arise suddenly are likely due to local hemodynamic disturbances following venous outlets thromboses rather than arterial steal. The positive impact of the use of anti-coagulantion in these situations, and the angiographically demonstrated venous occlusions in some rare cases, tend to support this pathophysiological mechanism. Finally, patients with single-hole arteriovenous fistulas (AVF), which should be the ones to provoke "steal" manifestations, usually present with hemorrhage (after 2 years) and not with acute non-hemorrhagic onset. In rare situations, acute or "post-traumatic" low back pain without hemorrhage may lead to the discovery of an SCAVM. In other situations, pain that is localised or radiating along a nerve root may be associated with the other deficits without being the revealing symptom. Isolated radicular symptoms are rare.
The lesion can be an "incidental finding" discovered during screening of a cutaneo-thoracic vascular dysplasia in 6% of neurologically asymptomatic children.
Diagnosis
Diagnosis of SCAVM is now rapidly established with the use of MRI, which represents the diagnostic modality of choice to be used if a spinal cord dysfunction is suspected. In fact, nearly all SCAVM are seen on MRI with the exception of some ventrally located microAVFs being MR occult. The diagnosis is confirmed by spinal cord angiography, which remains the gold standard for precise analysis of the vascular anatomy.
Angioarchitecture
Arterial stenosis and arterial aneurysms are seldom demonstrated.
Cases reports of spinal cord artery aneurysms are rare and, if diagnosed during hematomyelia, regardless of age may correspond to a thrombosed AVF; those seen in the pediatric population are unruptured and always associated with thoracic SCAVMs Pouches developed on the cord it self should be read differently: one should remember that the anterior spinal artery aneurysms are in the subpial space. False aneurysms are thus present when hemorrhagic manifestations have occurred and they will indicate the site of the rupture of the SCAVM (on the arterial or the venous side). They represent the weakest and the most dangerous part of the SCAVM. They often result from an upstream rupture due to a downstream thrombosis. Their persistence is an indication to perform a targetted embolisation if a complete exclusion cannot be offered. We percieve that arterial rupture is more frequent in SCAVMs than with intra cranial AVMs , where more venous hemorrhages take place.
The most remarkable architectural features noted also in SCAVMs, still remain on the venous side of the lesions, indicating the key role played by the veins in the clinical eloquence of SCAVM. Venous ectasias and venous stenoses are frequently seen. These pouches can be very large, give rise to few symptoms and yet may enlarge the spinal canal and erode the bony margins. The pouches and ectasias are associated with the highest-flow lesions. Pial perimedullary venous reflux and congestion (absence of immediate drainage into a radicular vein and into extradural lakes are almost constant. Some rare congestion of the radicular veins, particularly at the thoraco- cervical junction, mimic an associated AVM, covering like a sleeve the emergence of the nerve up to the epidural space, where it drains.
The aspect of the nidus is sometimes misleading with either venular congestion from a microAVF which will be cured with a simple embolisation, to a congested intrinsic network with capillary ectasia and limited venous drainage without evidence of outlets restrictions.
Treatment
Therapeutic management is proposed after analysis of the lesional and regional angioarchitecture is completed in an attempt to understand the past history of the lesion and its clinical expression and to anticipate its natural history. Our therapeutic goal is primarily to completely exclude the AVS in order to protect the child from future rebleeding or deficit. Total exclusion is rarely obtained in SCAVMs, whatever treatment is applied yet it is nearly always obtained in SCAVFs. Our therapeutic objectives depend upon the predictable embolisation risks. If they seem too high according to the clinical status of the child, partial occlusion constitutes an acceptable therapeutic choice if embolisation is targetted at the weak points of the architecture and performed with a permanent agent. In general, the challenges involved in the management of SCAVM are different in niduses and fistulas.
Embolization
In our experience embolization is always chosen as the first treatment modality. Embolization of SCAVM usually entails distal injection of a permanent embolic agent into the AVM itself and not a proximal occlusion. the following 20 years, endovascular occlusion has been done with N-butyl cyanoacrylate (Histoacryl). The use of coils is limited to some SCAVFs. In the ruptured SCAVM group, with hematomyelia and deficit, clinical recovery and/or resorbtion of the hematoma is expected. The first therapeutic procedure usually takes place 6-8 weeks after the initial accident. Early rebleeding is not known to occur in this disease yet differences may exist in babies.
Results
Following embolisation, total occlusion is obtained in less than 20% of patients. This rate is higher in AVFs whether micro or macro and in babies. Half of the cases have 75% of their SCAVM excluded. No lesions have been embolised with less than 50% obliteration. All the patients improved after embolisation, and 2/3 of them are actually neurologically normal on follow up. Follow-up in this group ranges from 1.5 to 13 years.
Although this disease is rare, particularly in this population and despite the eloquence of the surrounding tissues, which require a specific anatomic and technical experience, SCAVM management in the pediatric population does not represent a significantly different challenge from that in other AVS of the central nervous system in this age- group. The role of surgery in spinal cord vascular diseases in children is limited, provided that endovascular alternatives can lead to significant, safe and stable results. However, in some cases when embolisation was performed with non-permanent agents, surgery has been proposed as a therapeutic adjunct.
References
- Berenstein A, Jr, Lasjaunias P, 3rd, ter Brugge K, et al. Ch 15 Spinal cord arteriovenous malformations . Neuroangiography. Springer Verlag. [Google Scholar]
interv neuroradiol. 2010 Mar 23;16(Suppl 1):69.
Spinal cord arteriovenous shunts associated to Hereditary Haemorrhagic Telengiectasia (HHT)(or Rendu-Osler- Weber disease: ROW) are of macrofistulous type (MAVFs), and can be regrouped in the category of genetic hereditary SCAVSs. HHT in SCAVSs is not linked to multiplicity of lesions. These SCAVSs are characterized by a large venous ectasia, easily recognizable on MRI, that drains primarily the high flow AV shunt, before congestioning secondarily the spinal cord veins. They are always superficial to the cord and vascularized by one or multiple enlarged arteries. Most of these MAVFs in ROW disease are found in the pediatric population. The neurological symptoms can be either acute (related to haemorrhages or to partial thrombosis of the venous ectasia), or progressive, by direct compression of the cord by the ectasia, or by venous congestion and myelopathy. The diagnosis of HHT is confirmed by application of the Curaçao criteria or by genetic testing.
Treatment of these lesions is mostly endovascular: angiography should depict the precise shunting point by analyzing the regional and lesional angioarchitecture and the fistula is then disconnected by injection of high concentrated glue. All patients in our series harbouring MAVFs have been successfully cured and have seen their lesion disconnected in totality. The diagnosis of HHT in these patients should lead to further examination for HHT related lesions, as pulmonary fistulas.
Cobb syndrome is a spinal cord arteriovenous metameric disease belonging to the group of multiple shunts with a metameric link. The lesions extend over the same metamere and affect the skin, the muscles and soft tissues, the bone and the cord. Neurological symptoms can be related either to the SCAVS itself or to the spinal / paraspinal lesion if the latter one drains towards the cord, or compresses the cord itself. Analysis of the semiology , in correlation with the MRI and angio pictures, depicts the origin of the symptoms and helps to orient the treatment. Eùbolization is the preferred therapy in this lesions and should be directed towards the symptomatic disease, allowing thus improvement or stabilization of the symptoms in most of the cases.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):70.
The past several years has seen much new developments in acute ischaemic stroke therapy and secondary stroke prevention therapy. The ECASS3 trial showed that intravenous tissue plasminogen activator (tPA) can be effective even when used up to 4.5 hours. In parallel with the growing acceptance of tPA for acute stroke therapy, much stride has been made in the area of telemedicine to provide this therapy to peripheral hospitals.
There are now several large studies supporting the idea that an organized approach to TIA management and urgent commencement of appropriate therapies can reduce recurrent stroke. Further, new trial show that anti- thrombin inhibitor is a valid alternative to Warfarin for the prevention stroke in patients with atrial fibrillation. The publication of recent trials such as ICSS shows that carotid endarterectomy continues to be procedure of choice in patients with symptomatic carotid artery disease. This trial and the upcoming release of the CREST trial results show that randomised control trials continue to be the best way to determine patient management.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):70.
In this section, I'll illustrate atypical presentations of arterial stroke, venous stroke, and amyloid haemorrhage.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):71–72.
A prospectively collected data from 1985 to 1993, in France found the incidence to be 8/100 000. The age distribution of stroke reveals a fairly equal incidence from age 2 onwards and a significantly increased incidence during the neonatal and infancy period.
Presentation
Neonates with strokes tend to present with convulsions and rarely, if ever, with an appreciable focal neurological deficit in the acute phase. Infants tend to present with pathologically early hand preference as a sign of previous stroke. In children Ppresentation of stroke in later childhood is typically an acute neurological deficit.
Etiology:
The etiologies of arterial ischemic stroke in childhood are often multifactorial and in the majority of children (80%), a specific etiologic cause for the stroke can be found:
emboli from cardiac origin (15%), dissections (15%), intra cranial acute arteriopathy (30%), moyamoya (15%).
Acute regressive cerebral arteriopathy is characterised by a transient attack of cerebral arterial wall and accounts for 26% of childhood strokes in Sebire's series (1996). This arteriopathy could be due to an acute angiitis, possibly triggered by infectious agents such as varicella zoster virus.
Dissection affect the ICA intracranially just after the cavernous sinus and often bilaterally non symmetrically and more rarely at the cervical level. Conversely the VA is often involved at the level of C1 or C2 spaces where it presents as a focal narrowing with intra luminal clotting and distal emboli.
Moyamoya disease is a primary vascular disease characterized by progressive stenosis and eventual occlusion of the supra-clinoid portion of the internal carotid artery and the adjacent segments of the middle and anterior cerebral arteries. In response, an abnormal vascular network of small collateral vessels develops to bypass the area of occlusion.
Sickle cell anemia (SCA) is the most common hemoglobinopathy associated with cerebrovascular disease it is the cause of 6% of hemiplegia in North American children. About 25% of patients with SCA develop cerebrovascular complications (1/3 are clinically apparent), and 80% of these are under 15 years of age. The annual risk of stroke is 0,7% per year.
Certain inherited abnormalities of the clotting system may predispose patients to thrombosis and stroke, which can be arterial or venous. Protein C, protein S, antithrombin III and dysfibrinogenaemia should all be considered in cases of unexplained stroke in the pediatric population. The presence of certain anti-phospholipid antibodies among, including the lupus anti-coagulant, may result in abnormal coagulation and cerebral infarcts in children. Homocystinuria due to cystathione b-synthase deficiency is one of the metabolic disorders known to predispose patients to arterial and venous thrombosis with cerebral infarcts.
Imaging of arterial stroke in children
CT is still considered to be the modality of choice to detect the presence of hemorrhage acutely after the onset of symptoms but MRI is best able to demonstrate evidence of early infarction even in the first few hours after the onset of symptoms. Cerebral angiography is still considered to be the best method to visualize the extra- and intracranial vasculature, but continued improvements and refinements in time of flight MR angiography (MRA) or MRI with contrast enhancement have made this modality a realistic non-invasive alternative, particularly in the pediatric population.
Treatment and Management
Treatment after acute cerebral infarction should follow guidelines for standard medical care of the ill child. The role of systemic or intra-arterial thrombolytic therapy currently actively pursued in adults has so far been rarely explored in children with acute onset of arterial ischemic stroke.
Outcome and Prognosis
Prognosis for children after stroke has generally thought to be better than for adults. Neonates with arterial ischemia had fewer poor outcomes then the older infants and children (deVeber et al 2001). In the same cohort it was shown that while 31% of neonates had a poor outcome this was increased to 46% in infants and children presenting with arterial stroke.
The risk of recurrent stroke in children is reported to be low, although the duration of follow-up in most reports is less than 5 years.
References
- 1.Chabrier S, Rodesch G, Lasjaunias P, et al. Transient cerebral arteriopathy: a disorder recognized by serial angiograms in children with stroke. J Child Neurol. 1998;13(1):27–32. doi: 10.1177/088307389801300105. [DOI] [PubMed] [Google Scholar]
- 2.deVeber G, MacGregor D, Curtis R, et al. Neurologic outcome in survivors of childhood arterial ischemic stroke and sinovenous thrombosis. J Child Neurol. 2000;15:316–24. doi: 10.1177/088307380001500508. [DOI] [PubMed] [Google Scholar]
- 3.Kirton A, deVeber G. Therapeutic approaches and advances in pediatric stroke. NeuroRx. 2006;3:133–142. doi: 10.1016/j.nurx.2006.01.003. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 4.Husson B, Lasjaunias P. Radiological approach to disorders of arterial brain vessels associated with childhood arterial stroke - a comparison between MRA and contrast agiograpy. Pediatr Radiol. 2004;34:10–15. doi: 10.1007/s00247-003-1109-0. [DOI] [PubMed] [Google Scholar]
- 5.Rafay MF, Armstrong D, Deveber G, et al. Craniocervical arterial dissrction in children: clinical and radiographic presentation and outcome. J Child Neurol. 2006;21(1):8–16. doi: 10.1177/08830738060210010101. [DOI] [PubMed] [Google Scholar]
- 6.Bhattacharya JJ, Luo CB, Alvarez H, et al. PHACES syndrome: a review of eight previously unreported cases with late arterial occlusions. Neuroradiology. 2004 Mar;46(3):227–33. doi: 10.1007/s00234-002-0902-z. [DOI] [PubMed] [Google Scholar]
- 7.Husson B, Lasjaunias P. Radiological approach to disorders of arterial brain vessels associated with childhood arterial stroke - a comparison between MRA and contrast agiograpy. Pediatr Radiol. 2004;34:10–15. doi: 10.1007/s00247-003-1109-0. [DOI] [PubMed] [Google Scholar]
interv neuroradiol. 2010 Mar 23;16(Suppl 1):73.
Plain CT remains the basis of the imaging management in stroke. The accessibility, speed of image acquisition, sensitivity to hemorrhage and relatively inexpensive technology are the main reasons for this. In profound territorial hyper-acute ischemia however, it is well known that plain CT commonly does not reveal the true extent and degree of the parenchymal insult. The early medical intervention trials did consider the CT head as a decision making tool but this is extremely limiting when trying to triage patients appropriately, particularly when there can be significant risks to interventions.
CT angiography is a non-invasive technique that can provide information about the status of the bulk flow of blood in the neurovascular axis. The level of occlusive disease has practical implications for the treating clinician. Equally the status of the micro-circulation could be assessed, providing dynamic information on the degree of hypoperfusion and physiological compensation.
CT perfusion is a non-invasive technique that provides perfusion parametric information through out regions of the brain. Maps of cerebral blood flow (CBF), cerebral blood volume (CBV) and mean transit time (MTT) can be calculated and quantitative values of each obtained. The CBF and MTT maps describe the extent of the hypoperfusion lesion, whereas the most profoundly affected regions can be shown as a decrease in CBV. The latter equates with the restricted diffusion lesion on MRI and representative of the ischaemic core. A comparison between parametric maps can reveal areas that are hypoperfused but still viable - termed the ischaemic penumbra. This zone is under threat, may have lost electrical function and is maintained in the acute situation by collateral blood flow. If the proximal vascular obstruction is not relieved, the core may grow into the penumbra and the infarct is seen to extend. The characteristics of the penumbra will be discussed.
CT does expose some patients to significant amounts of ionizing radiation. Inappropriate doses of radiation have been described particularly with CTP. This has been topical of late in the global media and radiation safety authorities are currently investigating. Institutions must be cognizant of radiation dose and adhere to the ALARA principle.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):74–75.
Introduction
The incidence of acute arterial ischemia is estimated to be 2400 annually in a population of 1 million inhabitants.
25% of these will be recurrent strokes. Each year among this population 700 patients will die and 600 will be dependent survivors and 1100 will be independent survivors. The average length of hospital stay in North America is 42 days and the total healthcare cost associated with patients sustaining an acute stroke is 20 billion dollars per year in North America.
Neuroimaging of Acute Stroke
Imaging of acute stroke is carried out to rule out lesions that may mimic acute stroke. Imaging will need to differentiate hemorrhage vs. ischemia and it will need to include blood vessel imaging in order to demonstrate underlying vessel wall disorders vs. luminal occlusion by an embolus.
Cerebral "stroke" is a heterogenous disorder with cerebral ischemia representing 80% of the causes of the stroke and cerebral hemorrhage representing 20%. Among the causes of cerebral ischemia about 20% are cardiac related and 20% are large vessel arterial sclerotic disease related and 20% are small vessel occlusions.
The pathology of ischemic stroke is related to the insufficient amount of cerebral blood flow. This neuronal dysfunction occurs when there is less than 30ml per 100 grams per minute of blood flow and cell death will occur if there is less than 12ml per 100 grams per minute of blood flow. The outcome of the ischemia depends on the degree and distribution of the ischemia, the duration of the ischemia, collateral arterial supply and sensitivity of the individual CNS cell types.
Imaging findings on CT in patient with acute stroke are loss of gray white differentiation and sulcal effacement on the plain CT examination and diminished mean transit time, blood flow and blood volume on the CTA examination. MRI examination is more sensitive to early changes in ischemic stroke. In particular diffusion weighted imaging is used to assess the amount of irreversible ischemia vs. perfusion weighted changes which are believed to indicate the amount of brain tissue at risk for infarction if no intervention is carried out. The perfusion-diffusion weighted imaging mismatch represents our main guideline for active intervention.
Blood vessel imaging is also necessary to determine whether the luminal occlusion is caused by a blood clot or whether it is caused by a vessel wall abnormalities such as in dissection. It is also of help in distinguishing acute ischemia from arterial causes vs. those created by venous pathology.
Management
Randomized trials have been performed and proven that the use of intravenous thrombolytic therapy within 3 hours after onset of acute cerebral ischemia does improve clinical outcome. Intra-arterial thrombolytic therapy has also proven to be beneficial for outcome when carried within a six-hour window following the onset of acute cerebral ischemia. Currently, multiple trials are underway to investigate the role of combined intravenous and intra-arterial therapy at various time intervals. The therapeutic window for intra-arterial therapy can probably be extended to 12 hours when the ischemia involves the vertebral basilar circulation. The role of intra-arterial thorombolytic therapy beyond the accepted therapeutic window is associated with significant increased incidence of hemorrhagic conversion and poor outcome.
While thrombolytic therapy has proven to result in improved clinical outcome when applied according to now accepted guidelines it is often frustrating to notice that recanalization and reperfusion does not occur despite properly administered intra-venous or intra-arterial thrombolytic therapy. Under these circumstances, mechanical devices have been proposed as an alternative solution and their role is currently still being explored. Mechanical clot removal would have the theoretical advantage of being faster and more efficient.
Vessel wall imaging remains critical prior to the institution of thrombolytic therapy or even mechanical clot retraction in order to avoid the wrong type of intervention. For instance in patients with arterial dissection associated with acute cerebral ischemia the role of anti-coagulation with or without thrombolytic therapy needs to be considered as part of the treatment regimen.
Conclusion
There is a definite role for endovascular treatment in the management of acute stroke using intra-arterial thrombolytic therapy as it extends the treatment window beyond that of intravenous therapy.
References
- 1.Wardlaw JM, Murray V, Berge E, Del Zoppo GJ. Thrombolysis for acute ischaemic stroke. Cochrane Database Syst Rev. 2009 Oct 7;4:CD000213. doi: 10.1002/14651858.CD000213.pub2. [DOI] [PubMed] [Google Scholar]
- 2.Mattle HP, Arnold M, Georgiadis D, Baumann C, Nedeltchev K, Benninger D, Remonda L, von Büdingen C, Diana A, Pangalu A, et al. Comparison of intraarterial and intravenous thrombolysis for ischemic stroke with hyperdense middle cerebral artery sign. Stroke. 2008 Feb;39(2):379–83. doi: 10.1161/STROKEAHA.107.492348. [DOI] [PubMed] [Google Scholar]
- 3.Mazighi M, Serfaty JM, Labreuche J, Laissy JP, Meseguer E, Lavallée PC, Cabrejo L, Slaoui T, Guidoux C, Lapergue B, et al. Comparison of intravenous alteplase with a combined intravenous-endovascular approach in patients with stroke and confirmed arterial occlusion (RECANALISE study): a prospective cohort study. Lancet Neurol. 2009 Sep;8(9):802–9. doi: 10.1016/S1474-4422(09)70182-6. Epub 2009 Jul 31. [DOI] [PubMed] [Google Scholar]
- 4.Schonewille WJ, Wijman CA, Michel P, Rueckert CM, Weimar C, Mattle HP, Engelter ST, Tanne D, Muir KW, Molina CA, et al. Treatment and outcomes of acute basilar artery occlusion in the Basilar Artery International Cooperation Study (BASICS): a prospective registry study. Lancet Neurol. 2009 Aug;8(8):724–30. doi: 10.1016/S1474-4422(09)70173-5. [DOI] [PubMed] [Google Scholar]
- 5.Furlan A, Higashida R, Wechsler L, Gent M, Rowley H, Kase C, Pessin M, Ahuja A, Callahan F, Clark WM, et al. Intra-arterial prourokinase for acute ischemic stroke. The PROACT II study: a randomized controlled trial. Prolyse in Acute Cerebral Thromboembolism. JAMA. 1999 Dec 1;282(21):2003–11. doi: 10.1001/jama.282.21.2003. [DOI] [PubMed] [Google Scholar]
- 6.The National Institute of Neurological Disorders and Stroke rt-PA Stroke Study Group. Tissue plasminogen activator for acute ischemic stroke. N Engl J Med. 1995 Dec 14;333(24):1581–7. doi: 10.1056/NEJM199512143332401. [DOI] [PubMed] [Google Scholar]
- 7.Jahan R, Vinuela F. Treatment of acute ischemic stroke: intravenous and endovascular therapies. Expert Rev Cardiovasc Ther. 2009 Apr;7(4):75–87. doi: 10.1586/erc.09.13. [DOI] [PubMed] [Google Scholar]
- Ecker , et al. Local intra-arterial fibrolysis in acute hemispheric stroke. Cerebral Vascular Diseases. 2003;Volume 15:25–63. [Google Scholar]
- 8.Berg-Bammer , et al. Long term outcome after local intra-arterial fibrolysis of basilar artery thrombosis. Cerebral Vascular Diseases. 2000;Volume 10:183–188. doi: 10.1159/000016054. [DOI] [PubMed] [Google Scholar]
interv neuroradiol. 2010 Mar 23;16(Suppl 1):76.
A recent systemic review of the outcome after stenting for intracranial stenosis, revealed a wide variation of adverse event rate and concluded that wide spread application of intracranial stenting outside the setting of randomized trials does not seem to be justified. It described that Suh et al.'s event rate, i.e. minor and major stroke and death from all causes, within six months was 10% which actually represent an overall event rate in the stable (4.1% event rate) and unstable (25.1% event rate) patient groups. Suh et al.'s concept conveyed an important message that the outcome of intracranial stenting depends on the patient's presenting condition. In this study, the stable patient group included those patients who had resolved, improving or stationary symptoms before the stent placement procedure. The unstable patient group included patients who had progressive or fluctuating neurologic symptoms (NIHSS ≥4) corresponding to intracranial stenosis presenting within two days before the stent placement procedure. Therefore, the application of intracranial stenting would be used for acute (≤6 hours) stroke patients associated with mechnical thrombolysis, unstable (≤48 hours), stable (≥ 48 hours), and asymptomatic patients (≥ 6 months).
Although the increased event rate in the unstable patient group may be related to many undetermined factors, Suh et al. partially attributed the high rate of major adverse events in the unstable patient group compared with the stable patient group to subacute thrombosis or hyperperfusion which might be regarded as two major complications leading to major adverse events within the 30-day post-procedural period.
Such a trend in the event rate difference was also clearly demonstrated when the patients indicated were divided according the presenting symptom pattern, as we listed the event rate based on the references which included more than 50 patients. For the stable patients, the event rate ranged from 4.1 to 9.3% regardless of stent type. Therefore, we assumed that a 5% event rate would be expected after intracranial stenting with a bare metal stent in stable patients and that a higher event rate might be related to the physician's inexperience as there was a higher event rate in the first 50% patients even in stable patients. Furthermore, most other studies with a smaller number of patients revealed more than a 13% adverse event rate, thus indicating the possible association of the patient's condition and the physician's inexperience.
Therefore, the therapeutic time window (stable vs. unstable patients) should be considered before deciding on performing intracranial stenting as well as when evaluation of the outcome as one of the most important factors affecting the adverse event rate after intracranial stenting is the presenting symptom pattern. Furthermore, it is also emphasized that stabilizing unstable patients by controlling the risk factors with medication, including antiplatelet agents, can improve the outcome of intracranial stenting.
References
- 1.Suh DC, Kim EH. The Therapeutic Time Window Related to the Presenting Symptom Pattern, That Is, Stable Versus Unstable Patients, Can Affect the Adverse Event Rate of Intracranial Stenting. Stroke. 2009 Oct;4(10):e588–9 PubMed PMID: 1974;51-84. doi: 10.1161/STROKEAHA.109.558817. [DOI] [PubMed] [Google Scholar]
- 2.Suh DC, Kim JK, Choi JW, Choi BS, Pyun HW, Choi YJ, Kim M-H, Yang HR, Ha HI, Kim SJ, et al. Intracranial stenting of severe symptomatic intracranial stenosis: results of 100 consecutive patients. AJNR. 2008;29:781–785. doi: 10.3174/ajnr.A0922. [DOI] [PMC free article] [PubMed] [Google Scholar]
interv neuroradiol. 2010 Mar 23;16(Suppl 1):77.
Endovascular stent assisted angioplasty management of carotid atherosclerosis remains controversial. The publication of major prospective trials has provided valuable information, and has been associated with significant change in practice, before other ongoing trials have been concluded. These trials will be analysed, local practice patterns discussed, and recommendations presented for discussion. The question of whether carotid stent assisted angioplasty should be performed in patients otherwise eligible for carotid endarterectomy has seemingly been answered in the negative by the evidence from these recent major trials. What that current role is and whether the (soon to be published) CREST trial will change this remain topics for discussion.
References
- 1.Brown MM, et al. Safety results of the international carotid stenting study (ICSS), early outcome of patients randomized between carotid stenting and endarterectomy for symptomatic carotid stenosis. Cerebrovasc Dis. 2009;27:10. [Google Scholar]
- 2.Mas J-L, et al. Endarterectomy vs angioplasty in patients with symptomatic severe carotid stenosis (EVA-3S) trial: results up to 4 years from a randomized multicentre trial. Lancet Neurol. 2008;7(10):885. doi: 10.1016/S1474-4422(08)70195-9. [DOI] [PubMed] [Google Scholar]
- 3.Eckstein HH, et al. Results of the stent protected angioplasty vs carotid endarterectomy (SPACE) study to treat symptomatic stenoses at 2 years: a multinational prospective randomized trial. Lancet Neurol. 2008;7(10):893. doi: 10.1016/S1474-4422(08)70196-0. [DOI] [PubMed] [Google Scholar]
interv neuroradiol. 2010 Mar 23;16(Suppl 1):78.
Two locations of carotid bulb stenosis in high-risk patients can be determined the relationship of each location to atherosclerotic risk factors and clinical features. Atherosclerotic carotid plaques of apical versus body lesions, defined according to the area and extent of plaque involvement, may be differently related to atherosclerotic risk factors, mode of symptom presentation, infarct pattern, procedure-related factors, and clinical outcomes. Apical lesions, more common than body lesion, were associated with pseudoocclusion, whereas body lesions were associated with hyperlipidemia, a wedge-shaped cortical infarct pattern, older age, alcohol intake, and hyperperfusion syndrome. Atherosclerotic carotid bulb stenosis in two distinctive locations, body and apical revealed that hyperlipidemia and cortical wedge-shaped infarcts were more frequently associated with body than with apical stenosis at the time of presentation.
The safety and efficacy of Simultaneous Bilateral Carotid Stenting (SBCAS) have not been evaluated in detail. Our data revealed no significant differences in the stroke risk factors between the SBCAS and the control group. HPS occurred more commonly in SBCAS (ie, 16.7%, 4/24) compared with 2.9% (5/175) in the control group (P = .014). However, there was no statistical significance between 2 groups in the event rate of stroke (minor and/or major stroke), death, or restenosis at 6 months.
Management of symptomatic carotid pseudo-occlusion (CPO) is controversial, especially when high-risk patients with CPO present with variable symptom patterns. A good outcome (mRS ≤ 2) was achieved in 44 patients (92%) at six months. There were five events (10%) within six months, i.e. three minor strokes, one major stroke caused by hemorrhage, and one death excluding two deaths not related to stroke. Hyperperfusion (n = 4) was the most common cause of events leading to two minor strokes and a major stroke. Although initial NIHSS (P = .012) was related to poor outcome (mRS >2) compared to the control group, there was no statistical significance between two groups in the event rate of stroke, death or restenosis. Therefore, outcome of carotid stenting in high-risk patients with symptomatic CPO did not reveal any difference compared with controls. Poor outcome was related to the initial NIHSS (> 4). Hyperperfusion tended to be more commonly related to an event occurring after stenting.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):79.
Japan Carotid Atherosclerosis Study (JCAS) is the multicenter prospective registry of patients with carotid stenosis (>50%) which has been conducted since 2003 in Japan. 1013 patients (men: 86%, mean age of 69.8 years) were enrolled in this study, including 510 symptomatic and 503 asymptomatic patients. 443 patients were treated with carotid endarterectomy (CEA), 317 with carotid artery stenting (CAS) with Guardwire (distal protection balloon), and 253 with medical therapy. Thirty-day morbi-mortality rate in CEA and CAS was 3.2% and 3.5%, respectively. In the mean follow-up period of 847days, ipsilateral stroke occurred 6.09% of patients in medical, 0.54% in CEA, and 0.39% in CAS group(p<0.0005). Restenosis was found in 10.7% in patients treated with CEA, and 5.4% with CAS (p=0.016).
The carotid stenting was first approved in Japan with the use of Precise stent & Angioguard filter in October 2007. Indications include more than 50% stenosis for symptomatic and more than 80% stenosis for asymptomatic stenosis in CEA-high risk patient. Since then, the number of patients treated with CAS has been dramatically increasing. About 5300 patients were treated with CAS and 3100 with CEA in 2008 in Japan. 841 patients in 68 hospitals were enrolled in the post marketing surveillance (PMS) since the approval. Most of them were treated in the department of neurosurgery. 87% were men and 58% had a previous stroke or TIA. In 656 patients, both Precise and Angioguard were used properly. Major adverse effect (MAE) was recorded in 45 patients (6.9%) of the 656 patients, including 0.3% of death, 0.2% of acute myocardial infarction, and 6.6% of acute stroke. MAE was 8.4% and 4.7% in 381 symptomatic and 275 asymptomatic patients, respectively. MAE was recorded in 13.5%, 17.5%, and 4.9% of patients with no flow, slow flow, and normal flow during the procedure. In 102 patients, precise and distal and/or proximal balloon was used instead of the filter because of a large plaque and/or extremely high grade stenosis. In this group, major adverse effect was recorded in 12 patients (11.8%). The rate of MAE at high volume hospitals treating 30 cases or more was 3.8%, whereas, it was 6.9% at other. The flow stagnation will be a strong risk factor of MAE of CAS and the learning curve will exist. More effort should be made to get better results.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):80.
Experience with mechanical thrombectomy for acute stroke intervention from one of the busiest stroke intervention programs in the US will be shared.The Southeast Regional Stroke Center based at Erlanger Health System in Chattanooga,Tennessee has over 1200 stroke admissions/year and performs approximately 100 stroke interventions annually.The interventional team has been involved in the research and development of current thrombectomy devices.Current techniques and recommendations for utilization of these devices will be discussed.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):81.
Conditions that can present as stroke mimics include migraine, focal SAH, seizure, eclampsia/posterior reversible leucoencephalopathy, mitochondrial diseases and brain tumour. I shall illustrate cases where recognition of these mimics can help patient management.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):82.
Intracranial artery stenosis is a major cause of stroke, it carries a risk of stroke of 8%-22% per annum1-4 and may have varying degrees of risk based on the location and severity of stenoses, this rate is more higher in Asian than other district. The treatment for these disease remains controversial.
Although articles about the angiplasty with or without stent reported the effectiveness and good clinical outcomes for this diseases, we also pay attention to the high risk of this techniques, Despite of the results of the prospective Warfarin-Aspirin Symptomatic Intracranial Disease (WASID) study highlight the significant morbidity and mortality of the patients with high grade stenosis who accepted best medical treatment. but some of the patients with good collateral circulations who accepted medical therapy have good clinical outcomes.so, the indications for angioplasty must be redefined according to the collateral circulations.and Randomized controlled clinical trial of symptomatic intracranial artery stenosis is urgently needed.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):83–84.
Patients with deep vein and cerebral dural sinus thrombosis (CVST) often have a variable clinical course and unpredictable neurological outcome. Ever since Ribes in 1825 described the condition at autopsy, numerous publications, largely in the form of case reports and small clinical series, have been added to the literature, a consensus regarding the appropriate treatment remains elusive.
With new endovascular techniques and devices, direct thrombolysis and thrombectomy without a craniotomy is becoming increasingly common. Endovascular treatment of CVST has the potential advantages of acute dissolution of clot, allowing normalization of blood flow, decreased ICP, and rapid improvement of severe symptoms. Conversely, these invasive procedures are also associated with risks such as hemorrhage, vessel dissection, and pulmonary embolism.
Systemic Anticoagulation
Systemic heparin is still the gold standard of care in cerebral venous thrombosis after the first successful use in 1941 by Lyons. Cochrane Collaboration conducted a meta-analysis in 2002 on two randomized, placebo-controlled trials using unfractionated and low molecular weight Heparins. It was concluded that anticoagulation was safe and associated with a non-significant, yet potentially important, improvement in outcome with additional benefit of DVT and pulmonary embolism prevention. More recently, the International Study of Cerebral vein and Dural Sinus Thrombosis (ISCVT), found a trend toward improved outcomes in the anticoagulation group(12.7% dead or dependent in the anticoagulation group vs 18.3.% in the control group), the difference was not significant. Several reviews and European Federation of Neurological Societies (EFNS) guidelines continue to support the efficacy and safety of anticoagulation in CVST(Class IIa,Level B).
Interventional Therapies
Intra-sinus chemical thrombolysis is believed to be better restoring venous blood flow than heparin. Thrombolysis is also used when the patient's condition worsens despite heparin and symptomatic treatment. The most frequently described cause of worsening is inadequate anticoagulation. Clinical deterioration due to thrombosis progression in properly anticoagulated patients is rarely observed. When it is observed, thrombolytic treatment should be considered as a valid option. The application of Urokinase, Streptokinase or Tissue Plasminogen Activator tPA via transfemoral catheterization to the thrombus has been reported in many case series. Some results were very encouraging but some trials demonstrated increase risk of ICH especially when haemorrhage was already present. Canhao et al. reviewed 72 studies and Cochrane Collaboration also conducted a review of chemical trhombolysis. Overall, there is reasonable evidence to suggest that in some patients the local infusion of fibrinolytics agents can afford significant recovery, although other therapeutic options with a superior safety profile may exist (Class IIb, Level B).
In general, hemorrhagic risk is higher in thrombolysis compared to heparin, especially when a pretreatment hemorrhage is already present. Thus, this fear that hemorrhagic stroke can deteriorate due to thrombolysis treatment leads to the development of improved mechanical techniques that lower the risk of bleeding.
Mechanical thrombolysis
One of these devices is rheolytic thrombectomy, which utilizes the Venturi effect which creates a negative pressure fragmenting and aspirating the cerebral venous thrombus. These devices can be utilized in combination with thrombolysis. The AngioJet Rheolytic Thrombectomy System (Possis Medical, Minneapolis, MN) consists of a single-use catheter, single-use pump set, and multi-use drive unit. The same drive unit and pump set are compatible with various catheters with different design features. Thrombectomy is accomplished with the introduction of a pressurized saline jet stream through the directed orifices in the catheter distal tip. The jets generate a localized low pressure zone via the Bernoulli effect, which entrains and macerates thrombus. The saline and clot particles are then sucked back into the exhaust lumen of the catheter and out of the body for disposal. Treatment with the device takes about one minute. The system however,has a more rigid catheter delivery system which makes distal clot difficult to reach by transvenous femoral route.
Other aspirating system such as the Penumbra (Penumbra Inc. USA) coupled with Neuron carrying catheter has been used. The system uses a unique microcatheter and separator based thrombus debulking approach. The clot is fragmented by the separator and aspirated by special continue low suction pump.
Balloon angioplasty and thrombectomy are inexpensive methods. The use of transvenous Fogarty balloon catheter in conjunction with systemic anticoagulation has demonstrated clinical improvement. Other types of guidewire mounted balloon e.g. Stealth, Hyperglide or Hyperform can travel even further to distal SSS for clot retrieval. However, dislodgement of large clot during retrieval of balloon into the jugular vein can cause significant pulmonary embolism.
The adoption of transarterial clot retrieval devices e.g. Merci I and Merci II for CVST have been proposed. While some investigators are adopting retrievable stent e.g. Solitare (eV3, USA), Catcher(Balt) for clot maceration and removal with promising potential. The use of self-expanding stent e.g. Wall stent (Boston Scientific) to compress the clot to the sigmoid and transverse sinuses wall with recreation of a channel for venous return has been used for short segment of thrombosis.
Conclusion
Cerebral venous thrombosis remains a therapeutic challenge. Based on available evidence, systemic anticoagulation as initial step is safe even in the setting of pre-existing ICH. Combination with intra-sinus chemical thrombolysis and mechanical thrombectomy has to be judged by each individual case. It has to be based on the site, degree and progression of thrombosis. In patient with ICH, the safety of fibrinolysis is uncertain, mechanical thrombectomy in conjunction with systemic anticoagulation is probably preferred. Apart from multi- factorial causes, thrombosis of cerebral veins can present in many forms. In one end of the spectrum, it presents as acute venous stroke when alternative venous route is lacking in the cerebral circulation. The other end of the spectrum, thrombosis occurs silently and progresses to form dural arterial fistula and CCF. On the contrary, such forms of venous condition have to be treated idiosyncratically by augmentation of thrombosis by coil or glue rather than by thrombolysis.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):85.
One third of patients with new onset epilepsy have seizures that will prove to be medically intractable. Surgery aimed at complete treatment or reduction of seizures may be appropriate for some of these patients. The presence of a readily identifiable lesion for epilepsy is associated with a much better outcome following surgery.
In approximately 20 to 30% of patients refractory to antiepileptic drugs however, no lesion can be identified. A diagnostic imaging algorithm will be provided for further investigation of those patients that present with MR negative epilepsy studies.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):86.
The role of neuroimaging in epilepsy is to detect, localise and characterise lesions causing seizures as well as to localise normal structures and functions. MRI is generally the imaging technique of choice for identifying the structural basis of the epilepsies. fMRI, PET and SPECT assess cerebral function and functional impairment.
Surgery is considered in those patients with severe refractory epilepsy threatening development, specific infantile epileptic syndromes, developmental tumours and constant epileptogenic focus on EEG (+/- lesion on MRI).
Pediatric imaging centres have specific requirements including dedicated anaesthetists, educational play therapists, mock MRI scanner and distraction techniques in order to ensure a child friendly environment for maximal co-operation.
Underlying structural pathologies can be found in most children with refractory epilepsy. These include congenital malformations of development, focal cortical dysplasias, tuberous sclerosis, developmental tumours, sequelae of perinatal birth injuries and hippocampal sclerosis.
Multimodal integration of EEG with high resolution multiplanar MRI co-registered with interictal and ictal SPECT and PET increase the ability to identify the location of the epileptogenic zone. fMRI can be used in older children and adults for language lateralization and motor/ sensory mapping in order to minimise postoperative morbidity to eloquent cortex. Advanced MRI techniques such as DTI, MTI, EEG- fMRI or MRS may enable identification of some abnormalities not isolated on conventional MRI. Tractography derived from DTI is a method to demonstrate structural connectivity. Neurochemical methods using alpha11-C-methyl-L-tryptophan uptake may be used to isolate epileptogenic tubers.
Clinical neuroimaging continues to develop and improve the quality of care for patients with severe epilepsy. This will be illustrated by case studies from the Combined Epilepsy Clinic of the Royal Childrens Hospital and the Brain Research Institute, Melbourne.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):87.
In the clinical setting of epilepsy, imaging is used to identify epileptogenic substrates. When a responsible lesion is discovered and the seizure syndrome cannot be controlled medically, surgical treatment is often considered. Functional imaging can be used in the planning of such patients with the intent of minimizing surgical morbidity.
Diffusion imaging utilizes the directional impedance of water molecules to map out macro and microscopic structure. Diffusion Tensor Imaging (DTI) allows a more accurate characterization of this microscopic directional water movement. Diffusion parameters include mean diffusivity, which provides information of the magnitude of diffusion and fractional anisotropy, which represents the degree of structure present in the imaging voxel. Alterations in these parameters can be seen in and around foci of brain injury, neoplasia and congenital malformations. This may need to be considered in the surgical planning. Varying degrees of anisotropy disturbance, both localized and remote, can be demonstrated in patients with temporal lobe epilepsy. Utilizing the directional component of the tensor information, white matter trajectories can be mapped out in a process called tractography. Eloquent white matter tracts can be more readily displayed and therefore considered in the surgical work-up of these patients. The identification of Meyer's Loop of the visual pathway is an example of this.
The alteration in oxygen extraction and more importantly local cerebral blood volume is a response to an increase in localized neuronal activity. This blood oxygen level dependant (BOLD) contrast in response to a specific task can lateralize specific language functions and identify the locality of cortical loci involved in specific motor tasks. There is a good correlation with electro-cortical stimulation at surgery and the intracarotid sodium amytal test.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):88.
Epilepsy surgery for medically refractory epilepsy has increased significantly in recent years. Although, as a last resort, vagal nerve stimulators can be offered to patients, the real challenge to surgeons is the identification of the epileptogenic focus/foci, the relationship to eloquent cortex, and fiber tracts.
Improvements in foci localization have occurred firstly through the increased number of MRI sequences now available, and secondly through cortical mapping and high frequency oscillations, which has detected areas of seizure onset "earlier" than previously, and when combined with inter-ictal activity has extended the area for resection of the focus/foci. However, in doing so, imaging, both anatomical and functional, has become more important in aiding the surgeon to achieve maximum resection with minimal morbidity.
In this presentation new technology, the application of imaging and the dilemmas faced by the surgeon will be discussed.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):89.
The brachial plexus is an anatomically challenging region. In this short presentation, basic anatomy will be reviewed. The MRI imaging protocol used at Peter MacCallum Cancer Centre will be described, followed by discussion of normal MRI appearance.
Brachial plexus assessment in the setting of malignancy can be difficult, in particular, distinction between malignant infiltration and radiation plexopathy. This will be illustrated using selected cases.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):90.
Peripheral neuropathies can be focal, multifocal or generalised. The most common focal neuropathy (carpal tunnel syndrome) can be reliably diagnosed electrophysiologically with a high sensitivity and specificity in routine clinical practice and imaging studies for this condition have a limited role. Imaging does have some advantages over electrodiagnostics in that it can identify unusual causes of compression in the carpal tunnel such as a ganglion cysts or infiltration associated with amyloid or myxoedematous infiltration. The electrophysiology of recurrent carpal tunnel syndrome is more complex and in this situation additional evidence of nerve compression in the form of imaging studies may be helpful prior to subjecting the patient to further surgery. However at this stage it is not clear how well imaging distinguishes recurrent compression of the median nerve following surgery. Imaging may have a greater role for ulnar neuropathies at the elbow or peroneal neuropathies at the knee where the sensitivity of electrodiagnostic tests to detect and localise the site pathology is less. Imaging is essential for localising less common focal neuropathies which might be due to compression by tumour or following an ischaemic or stretching event such as sciatic neuropathy following hip replacement. It has a complimentary role with EMG to distinguish between cervical nerve root avulsion versus a traumatic brachial plexus lesion or to rule out tumour in lumbosacral plexopathies.
The majority of multifocal and generalised neuropathies are axonal in nature. In this situation imaging is probably of limited benefit. Imaging is most valuable when it can be used to indicate an inflammatory, demyelinating process by showing thickening of nerves or nerve trunks and contrast enhancement.
There has been interest lately in using techniques such as ultrasound to detect fibrillations in denervated muscle and MRI to identify denervated muscle or muscle inflammation. The sensitivity and specificity of these techniques and their ability to distinguish neuropathic from myopathic disorders needs further investigation.
Improvement in imaging techniques which allow a diagnosis without having to resort to nerve or muscle biopsy in conditions such as CIDP, leprosy, amyloid angiopathy, vasculitis and some hereditary neuropathies would be extremely useful.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):91.
Patients with peripheral nerve symptoms commonly present with a fairly well defined problem such as Carpal or Cubital Tunnel Syndrome and apart from confirming the diagnosis with clinical examination and marking the severity of the condition with Nerve Conduction Tests, surgeons can proceed to treatment without need for imaging.
Alternatively, imaging of the peripheral nerve forms an integral part of the assessment of patients presenting with a mass lesion either of the peripheral nerve or producing extrinsic compression of the nerve.
Between these two groups there is a significant group of patients with peripheral nerve pathology where imaging may play a role. These patients, such as the patient recovering from a closed nerve injury, the patient with recurrent symptoms of compression following surgery or the patient presenting with a vague or atypical history where a compression neuropathy is being considered. It is these patients where the progression in imaging techniques and analysis may be of significant help to the surgeon.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):92.
Learning Objectives
To present the MRI features of selected cases of common peripheral neuropathies
Background
Traditionally neurophysiology of peripheral nerves has been the mainstay of identification, characterisation and localisation of the specific level of many acquired peripheral neuropathies, as well as the underlying pathological causes.
Imaging Findings
MRI appearances of selected peripheral nerves in mononeuropathies and peripheral neuropathies and underlying pathological causes are presented, including radial, ulnar, median, common peroneal and posterior tibial nerves.
Primary features of entrapment syndromes are: 1.Abnormal high signal in the neuropathic nerve on T2-weighted or 'water weighted' images images. 2. Abnormal calibre of the entrapped nerve which includes thickening (the most common appearance) or thinning, kinking or 'bowstringing'. 3. The underlying pathology such as tumour, fibrous bands, synovial cysts for example, causing the entrapment.
Secondary features such as muscle denervation changes are subcategorised into acute and chronic changes, both of which may be visible on MRI simultaneously depending on the time course of the neuropathy.
Conclusion
MRI of the peripheral nerves should be considered as an important adjunct in the diagnosis and management of many common acquired peripheral neuropathies.
MRI can characterise the neuropathic nerve, localise exact site of entrapment, as well as the underlying pathological cause.
It is particularly useful in characterisation of ulnar neuropathy where electrophysiology is inconclusive and fails to localise the site of the neuropathy, and in fact in this situation MRI is the most sensitive test.
MRI often demonstrates secondary changes of denervation in muscle which may be either acute or chronic. Both the primary and secondary MRI features of peripheral mononeuropathies can significantly impact treatment and management of peripheral neuropathies, particularly entrapment neuropathies.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):93.
Learning Objectives
To present the MRI appearances of Pirifomis Syndrome.
Background
Piriformis Syndrome is a controversial entity defined as neuropathy or neuritis secondary to compression or irritation of the proximal sciatic nerve, characterized by buttock or gluteal muscle pain with radiation to the lower leg with mixed pattern of L5 and S1 nerve root manifestations.There are varying degrees of lower limb musculature weakness and varying degrees of denervation on MRI.
Traditionally Piriformis syndrome is diagnosed by a combination of history, clinical examination and neurophysiological /electrophysiological studies, the latter of which are usually performed by a subset of neurologists.
The exact cause is often not found and the neurophysiological studies often do not localize the level of the lesion.
MRI of the lumbar spine is often negative.
Imaging Findings
MRI imaging include includes primary abnormalities of the sciatic nerve including signal and configuration changes as well as anatomic variations of piriformis muscle including fibrous bands arising from piriformis muscle.
Secondary changes affecting the lower limb musculature include acute and chronic patterns of muscle denervation.
Conclusion
MRI of the proximal sciatic nerve is useful adjunct in the identification and localization of causes of Piriformis syndrome.
Anatomic variations of Piriformis muscle and sciatic nerve predisposing to piriformis syndrome are relatively common.
Triggers include trauma to gluteal region, prolonged sitting, athletic overuse, repetitive stretching.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):94.
Head and Neck imaging is evolving fast and new applications emerge. One of the new applications with the highest impact is "Cone Beam CT". This CT system uses a flat panel detector and patients can often be examined in a sitting position. The major advantage is that the irradiation dose used is 50 to 85% lower than low dose conventional CT. Applications are sinus imaging, dentascan, 3D-maxillofacial imaging, TMJ, trauma etc.
Other new applications that will be illustrated in this lecture are high resolution CT of the temporal bone (0.23 × 0.23 × 0.1 mm), MR software used to calculate the volume of vestibulocochlear schwannomas and high resolution imaging of the temporal bone at 3 Tesla. In these three topics the progress made in temporal bone imaging is discussed and very small structures, only visible at 3 Tesla will be shown.
High resolution imaging of the cranial nerves also improved at 3 Tesla and the use of balanced-FFE and 3D- DRIVE images now allow visualisation of very small nerve branches inside the CSF spaces and basal foramina.
The value of intrathecal gadolinium in the detection CSF leaks has repetitively been confirmed. Unfortunately contrast-companies remain un-interested to validate their products for intrathecal injection and hence this technique can still not routinely be used.
Finally, the use of diffusion MR in the head and neck will be discussed. It allows characterization of tumors and lymph nodes (benign vs malignant) and also helps to predict treatment outcome. All the above new applications will be demonstrated and discussed in this lecture.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):95.
Today high resolution CT imaging is still the imaging technique of choice to look for fractures running through the facial nerve canal or to look for a congenital abnormal course of the facial nerve at the level of the middle ear. Facial nerve canal involvement in case of cholesteatoma or invasion by another head and neck tumor can also be evaluated by CT. Prior to surgery, exact localisation of the course of the facial nerve canal is also best seen on CT images.
However, in case of Bell's palsy, the diagnosis is best confirmed and other pathology is best excluded on gadolinium-enhanced T1-weighted MR images through the internal auditory canal (IAC). Submillimetric heavily T2-weighted images are needed to further distinguish whether the enhancement on the T1 images is caused by neuritis (fusiform enlargement) or by a schwannoma (nodular). Magnetic Resonance also replaced CT for several other indications: detection of central causes of facial palsy, congenital abnormal course of the facial nerve in the cerebellopontine angle or IAC, perineural tumour spread (parotid tumors or head and neck squamous cell carcinoma) along the facial nerve, lesions affecting the side branches (greater superficial petrosal nerve, chorda tympani...) of the facial nerve etc. Even in case of trauma, the oedema of the labyrinthine segment of the facial nerve which can cause severe ischemia of the nerve, can only be depicted on MR. Finally, hemifacial spasm is also best studied on MR.
The most frequent lesions of the facial nerve will be illustrated and discussed in this lecture and the value of CT and/or MR in the detection of these lesions will be addressed.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):96.
Benign inflammatory sinonasal disease and resultant symptomatology is common in the general population. Routine unenhanced low-dose paranasal sinus CT is commonly performed in an outpatient setting as an initial and final investigation.
A minority of these examinations may reveal complex and atypical patterns of sinonasal opacification, or the presence of a discrete sinonasal mass lesion.
Imaging approach
A multimodality approach with both CT and MR is requisite for optimal characterization of sinonasal mass lesions. Utilizing both modalities will help distinguish non-neoplastic from neoplastic pathologies, and benign from malignant neoplasms. In some cases, consideration of imaging features in conjunction with clinical data can suggest certain diagnoses.
CT is optimal for defining sinonasal anatomy, patterns of osseous remodelling, expansion or destruction, and characterizing focal calcifications or matrix mineralization of osseous or cartilaginous lesions.
MR imaging is excellent for distinguishing tumour from benign mucosal thickening, obstructive or inspissated secretions. Perineural disease and locoregional spread beyond the sinonasal cavity to orbit, skull base or intracranial compartment is optimally documented with MR and is mandatory for accurate staging of sinonasal malignant disease.
Pathology
Non-neoplastic mass-like lesions include infective/ inflammatory conditions such as retention cysts, sinonasal polyposis, allergic fungal sinusitis, focal mycetoma and mucocoeles. Other conditions which can present as a sinonasal mass include encephalocoeles and odontogenic lesions. Benign neoplasms can mimic more aggressive disease and include entities such as fibro-osseous disease, osteomata, juvenile angiofibroma, haemangioma, inverting papilloma.
Malignant lesions of the sinonasal cavity are rare, comprising approximately 3% of head and neck cancer. Numerous histologic types are reported, typical imaging findings of the more common lesions will be reviewed. Most sinonasal malignancies involve the maxillary sinus, nasal cavity and ethmoid sinuses. Lesions arising from the frontal or sphenoid sinuses are rare. The clinical presentation of sinonasal malignancy is often nonspecific, patients complain of chronic nasal obstruction and epistaxis. Pain may suggest perineural tumour infiltration.
Epithelial malignancy predominates, and squamous cell carcinoma is overall the most prevalent malignant lesion, accounting for up to 80%, occurring most often in the maxillary sinus.
Glandular epithelial malignancies include adenocarcinoma and minor salivary gland lesions such as adenoid cystic carcinoma. Other lesions include esthesioneuroblastoma, sinonasal Non-Hodgkin Lymphoma (NHL) and melanoma.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):97.
Today the anatomy and pathology of the peripheral vestibular system, the vestibular nerves, the vestibular nuclei, vestibular afferents and efferents, vestibule-spinal and vestibule-ocular system are best examined using MRI. CT is only helpful in case of trauma and otodystrophy involving the osseous labyrinth. Therefore MRI became the method of choice to study patients with balance disorders and vertigo.
The vestibular signs (deviations, vestibulo-ocular nystagmus) are used to distinguish involvement of the peripheral vestibular system from an involvement of the central vestibular system. Hence the radiologist must dispose of all available clinical information in order to be able to perform a tailored radiological examination.
Screening of patients with tinnitus should be non-invasive. Most of the pathology causing tinnitus (VIIIth nerve schwannomas, dural fistulas, glomus tumors, meningiomas etc.) can only be detected in a reliable way on MR. However, MR only has an acceptable yield when the tinnitus is unilateral, pulsatile or objective. Today, conventional angiography is restriced to those patients who benefit from an intravascular treatment.
In this presentation, the coils and sequences to be used in patients presenting with central/peripheral vertigo and tinnitus will be discussed in detail.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):98.
Detection of nerve involvement by a head and neck tumor causes a dramatical increase in tumor staging (T4). Adenoid cystic carcinoma arising from salivary glands, squamous cell carcinoma, basal cell carcinoma, melanoma, lymphoma and sarcoma are frequently assoiated with perineural tumor spread (PNS). This PNS can occur in the absence of clinical signs, hence the radiologist routinely has to exclude nerve involvement in all patients with head and neck cancer. Tumor spread is most frequent along the maxillary (V2) or mandibular (V3) branches of the trigeminal nerve although tumor can less frequently also follow the ophthalmic branch (V1). The mastoid segment of the facial nerve is another typical extension route and tumors will also follow the connections between the facial and trigeminal nerve. Tumor spread along the hypoglossal nerve is less frequent. Involved nerves enhance, are thickened and cause enlargement of the foramina, fissures and canals they pass through and eventually the tumor will extend intracranially and become more difficult to treat or intreatable. PNS can be detected on axial and coronal high resolution gadolinium-enhanced T1-weighted images although more and more isotropic sub- millimetric gadolinium-enhanced fat suppressed 3D-FFE or VIBE images are used. In this refresher course the typical routes of PNS will be illustrated and the signs of PNS will be covered. Special attention will be payed to the imaging techniques which should be used to detect tumor spread. An overview of the anatomical sites were it is easiest to pick up PNS and which should therefore always be checked will also be given.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):99.
Sensorineural hearing loss (SNHL) results from pathology involving either the cochlea ("sensory") or central auditory pathway ("neural").
Embryology and Anatomy
The otic placode develops as a neuroectodermal thickening in the third gestational week. Invagination into the underlying mesenchyme results in formation of the otic pit and subsequent otocyst. The otic capsule forms between the 4th and 8th weeks around the developing otocyst (membranous labyrinth).
The sensory bipolar neuronal cell bodies are contained within the cochlear modiolus, receiving sensory information from the organ of Corti, and transmitting this data to the brainstem cochlear nuclei via axons which constitute the cochlear nerve.
Ipsilateral and contralateral ascending fibres arising from the cochlear nuclear complex, some of which synapse in the superior olivary nucleus, comprise the lateral lemniscus. Central connections via the inferior colliculus and medial geniculate body result in bilateral cortical representation at primary auditory cortex in the superior temporal gyrus.
Imaging SNHL
Temporal bone CT and MRI are complementary for the assessment of SNHL. Temporal bone CT is an appropriate initial investigation for paediatric SNHL, accurately depicting congenital and acquired anomalies of the inner ear. In adults, MR is the higher yield modality, accurately characterizing lesions within the cerebellopontine angle (CPA) and internal auditory canal (IAC), whilst permitting assessment of the central auditory pathway.
Pathology
Paediatric causes of SNHL include congenital (genetic or environmental) or acquired inner ear anomalies and less commonly, lesions of the CP angle or IAC. In the majority of cases of SNHL due to a congenital inner ear anomaly, an anatomic lesion is not detectable by current neuroimaging techniques.
SNHL in adults is most often due to 'presbycusis' or age-related hearing loss, and is occult on imaging. Vestibular schwannoma is the commonest cause of SNHL detectable by imaging. Other aetiologies include trauma and neoplastic, vascular and inflammatory lesions of the CP angle, IAC or labyrinth. Lesions of the central auditory pathway which can cause SNHL are a heterogenous group and include demyelinating, ischemic and neoplastic pathologies.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):100.
Today CT and MR are used to study skull base lesions. CT is helpful to depict bone destruction and to detect calcifications inside or at the edges of the lesion. However, MR can depict bone destruction as well and is also able to demonstrate soft tissue involvement and therefore became the method of choice.
Often skull base lesions cannot be characterised immediately and first one has to distinguish tumors from pseudo- tumors. Signal characteristics on MR are very helpful (e.g. chondrosarcoma, giant-cell granuloma) but one should also always look at the adjacent arteries: tumors encase arteries, infections cause obliteration of the arteries. Some tumors can be recognized by their location in the skull base (e.g. intra-osseous pituitary adenomas) or by the way they do not respect fissures (e.g. plasmocytoma-multiple myeloma).
Nevertheless, even with all the possible imaging experience we can acquire, a correct diagnosis is frequently only possible after microscopic examination. The material can be collected surgically but in many cases this is at the cost of important morbidity. The lesion and histological material can often be reached in a less destructive way by using CT-guided needle biopsy. The two most popular approaches are: 1) between the coronoid process and the collum of the mandible 2) between the lateral wall of the sinus and ascending ramus of the mandible.
Finally, MR-diffusion can also be used to distinguish cholesteatoma from inflammation/granulation tissue/cholesterol granuloma etc. This diagnostic technique is now able to avoid un-necessary surgery in patients suspected to have an acquired cholesteatoma and will also eliminate the need for second-look surgery. The financial consequences of this MR application are obvious.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):101.
The decision to perform imaging is usually based on clinical evaluation (otoscopy). Until now, the imaging technique of choice to confirm or detect a cholesteatoma was CT Scan.
If the clinical diagnosis was clear, CT was used to provide a surgical road map and to detect indirect signs, warning for potential imminent complications, such as labyrinthine fistulas, tegmen defects and facial nerve involvement. However, CT cannot distinguish cholesteatoma from other soft tissues, which is especially problematic in a completely opacified middle ear.
The advent of new MRI protocols, such as late enhanced T1 weighted images and non-EPI diffusion, allow for specific characterization of the cholesteatoma. On MR, it can be unambiguously distinguished form other soft tissue such as scar tissue, cholesterol granuloma, granulation tissue and fluid. Moreover, MR avoids the irradiation of the patient.
Our results indicate that the non-EPI diffusion weighted sequence (non-EPI DWI) outperforms the late Gadolinium enhanced T1 weighted sequence. The advantages of non-EPI DWI are: 1/ more reliable characterization of the lesion due to a better contrast resolution; 2/ no need for contrast (Gadolinium is expensive, and carries a risk for renal fibrosis); 3/ a much shorter examination time, allowing for a higher patient throughput, which is very important for the logistic organization of the medical imaging department.
We will present a practical flowchart for decision making in the work-up of primary cholesteatoma cases, and for the detection of residual or recurrent disease.
In conclusion, in our departments we only use CT scan as a strictly pre-operative examination to provide the surgeon with a surgical roadmap and to detect potential complication signs. MR provides all other needed information for the pathognomonic diagnosis, the extent of the lesion and the follow-up of operated cases.
CT and especially "high resolution" 0,23 × 0,23 mm CT is used in almost all other indications. This high resolution is needed to detect subtle changes in case of otosclerosis and even subtle footplate changes can now be detected. The same goes for subtle congenital malformations of the ossicles (especially the stapes), the oval and round window and the facial nerve canal. It is obvious that also small fractures or dislocations of the ossicles can also better be depicted. On top of this better detecters today allow to acquire images with both a very high spatial resolution and high contrast resolution. The result is that the ossicles, some plicae/ligaments/tendons and calcifications (tympanosclerosis) can also be seen even when only little or no air is remaining in the middle ear cavity. Hence, the advent of new high resolution multi-detector CT has made middle ear imaging much more accurate but has not prevented MR to become the image modality of choice in case of cholesteatoma.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):102.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):102.
Purpose
To analyze the safety and efficacy of the remodelling technique compared to the standard coiling technique in two large multicenter series concerning the endovascular treatment of ruptured (CLARITY) and unruptured intracranial aneurysms (ATENA).
Materials and Methods
Both series were large, multicenter, prospective series conducted in France (20 centers in CLARITY, 27 in ATENA). In CLARITY, 768 patients (361 females and 247 males; age: 19-80 years, mean: 51.0 ± 11.1 years) having a total of 768 ruptured aneurysms were treated by coiling alone in 608 patients (79.2%) and by the remodelling technique in 160 patients (19.8%). In ATENA, 547 patients (383 females and 164 males; age: 22-83 years, mean: 51.0 ± 11.1 years) having a total of 572 aneurysms were treated by coiling alone in 325 patients, and by the remodelling technique in 222 patients in ATENA.
Results
The overall rate of adverse events related to the treatment - regardless of whether they lead to clinical consequences or not - was 17.4% (106/608) for coiling and 16.9% (27/160) for remodelling in ruptured aneurysms, and 10.8% (35/325) for coiling and 11.7% (26/222) for remodelling in unruptured aneurysms. In ruptured and unruptured aneurysms, the rate of thromboembolic events and intraoperative rupture was similar in coiling and remodelling group.
The morbimortality related to the treatment was lower (but not significantly) in remodelling group (3.8%) compared to coiling group (5.1%) in ruptured aneurysms. In unruptured aneurysms, morbimortality was not different in both groups (3.1% in coiling group and 3.7% in remodelling group).
The rate of adequate occlusion was significantly higher in remodelling group (94.9%) compared to coiling group (88.5%) in ruptured aneurysms, but was similar in both groups in unruptured aneurysms.
Conclusion
In two large series dealing with ruptured and unruptured aneurysms, the safety of the remodelling technique is similar in coiling and remodelling groups. In ruptured aneurysms, the remodelling technique is more efficacious than coiling technique regarding the immediate postoperative anatomical results. According to these results, the remodelling technique can be widely used in both ruptured and unruptured aneurysms.
References
- 1.Pierrot L, Spelle L, Leclerc X, Cognard C, Bonafé A, Moret J. Endovascular treatment of Unruptured Intracranial Aneurysms : Comparison of Safety of remodeling technique and standard treatment with coils. Radiology. 2009;251:846–855. doi: 10.1148/radiol.2513081056. [DOI] [PubMed] [Google Scholar]
interv neuroradiol. 2010 Mar 23;16(Suppl 1):103.
Background
Internal carotid artery (ICA) bifurcation aneurysms are uncommon. Treatment by surgical clipping is fraught with potential complications of which the most concerning is perforator artery injury. Studies have demonstrated using Guglielmi detachable coils (GDC) to embolise these aneurysms. This is the first documented case describing the use of a stent to induce aneurysm thrombosis and concurrently mechanically dilate the vasospastic internal and middle carotid arteries (MCA).
Methods
A 35-year-old ethnic Chinese woman with good past health collapsed at home with a consequent Glasgow Coma Score (GCS) of 14/15 upon admission. There was no focal neurological deficit. A computed tomography brain scan showed diffuse subarachnoid hemorrhage and digital subtraction angiography (DSA) showed a 2mm wide neck saccular aneurysm of the right ICA bifurcation. The patient remained neurologically stable and a repeat DSA on day 10 of admission revealed a markedly spastic terminal ICA therefore the initially planned coil embolisation was abandoned. Nimodipine and hypervolemic- hypertensive- hemodilutional (triple 'H') therapy was continued. On day 16, a third DSA showed a persistently spastic terminal ICA and proximal MCA (M1 segment). A Neuroform© stent (Boston Scientific, Natick, MA, USA) was deployed across the aforementioned spastic portion covering the aneurysm neck.
Results
The immediate post-stenting angiogram showed improved right MCA region circulation and decreased blood flow within the aneurysm sac. The patient regained full consciousness with no focal neurological deficit and transcranial Doppler ultrasonography confirmed resolved vasospasm. A 4- month follow-up DSA showed complete obliteration of the aneurysm with neither significant ICA nor MCA stenosis.
Conclusion
Stenting the ICA bifurcation to treat aneurysms of this region in addition to treating its vasospastic segment is a viable option in an endovascular neurosurgeons' armamentarium.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):104.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):108.
Purpose
Restenosis is a major concern following stent-angioplasty of intracranial atherosclerotic stenosis. Drug eluting stents (DES) have been demonstrated to reduce the restenosis rate in coronary stent-angioplasty, however application of DES to cerebral arteries has been limited. We report our results of intracranial stent-angioplasty using DES.
Methods and Materials
From December 2003 to December 2007, stent-angioplasty with coronary DES were tried in 62 intracranial atherosclerotic lesions (59 patients, 39 male and 20 female, aged 40-77 years, median: 61.6 year). There were 3 technical failures in placing stents over lesions. Stenting was performed in 59 lesions (success rate 95%). Locations of lesion were 21 ICA (11 cavernous, 5 petrous, 5 intracranial segment), 20 MCA, 12 VA, 5 BA, 1 PCA. Three different types of DES were used (38 Medtronics, 13 Boston Scientific, 8 Cordis). Stent diameters were 2.25mm in 10 lesions, 2.5mm in 10, 2.75mm in 11, 3.0mm in 13, 3.5mm in 12, 4mm in 3 lesions. Stent lengths were between 8mm and 24 mm. In 2 cases, DES was used for treatment of restenosis following PTAS with bare metal stent.
Results
There were 3 procedure related complications: 2 thromboembolism and 1 perforation. Radiological follow up was performed in 34 of 59 lesions lesions (57%: 29 DSA, 4 CTA, 1 MRA) between 2 weeks and 12 months after treatment (mean 6.8 months). There were 3 occlusions detected (at 2 weeks, 6 months and 10 months) and 1 restenosis at 9 months. Total rate of occlusion and restenosis was 12% (4/34). Clinical evaluation by modified Rankin Score was available in 50 patients. There was improvement in 32 patients, no change in 16, worsening in 2.
Conclusion
Cerebral angioplasty with DES can be an effective method for the treatment of cerebral arterial stenosis, particularly with low restenosis rates. However, further study in a large cohort and longer follow up is necessary to evaluate the usefulness of DES in cerebral stent-angioplasty.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):109.
Summary
A 13-year-old boy with clinical and radiological findings consisting with AGS, stable after the first year of life, presented with an acute skin leucocytoclastic vasculitis, followed by cerebral haemorrhage with evidence of multiple cerebral aneurysms. To our knowledge this is the first report of multiple cerebral aneurysms and intracranial haemorrhage being a complication of AGS.
Introduction
AGS is a rare autosomal recessive encephalopathy, the clinical and radiological features of which mimic the sequelae of acquired in-utero viral infections. The neuroimaging findings are: leukoencephalopathy, cortical atrophy, acquired microcephaly, and intracranial bilateral calcifications variably involving the deep grey matter, periventricular white matter and cerebellum. After the acute phase, usually in the first year of life, clinical features and neuroradiological findings typically stabilise. The main extra-neurological symptoms are chilblain-like skin lesions, usually on the fingers, toes and ears. Cerebrospinal fluid (CSF) shows chronic lymphocytosis and elevated interferon-alpha (INF-alpha) levels. At least five genes, if mutated, can give rise to AGS, a genetically heterogeneous disorder. The different genetic mutations have a common pathogenetic mechanism, affecting the process of eliminating the nucleic acids physiologically released by normal cell death. In AGS patients, the intracellular accumulation of damaged DNA induces INF-alpha production from glial cells, resulting in significant brain injury.
Case Report
A 2-month-old full term infant, after an uneventful pregnancy with an unremarkable neonatal history, presented with hypotonia, dystonic posture, generalized seizures, gastro-oesophageal reflux and refusal to eat. Initial MRI showed ventricular enlargement and a symmetrical leukoencephalopathy, which involved the frontal and parietal more than the temporal and occipital lobes.. A few months later, head CT revealed punctate bilateral calcifications involving the basal ganglia and periventricular WM. Clinical and neuroradiological findings remained almost stable after the first year of life, consistent with AGS. At the age of 13 years, the patient presented with an acute leucocytoclastic vasculitis of the skin. Cranial MRI showed a mild progression of brain atrophy, without significant changeof the WM signal abnormalities, sparing the corpus callosum, internal capsule and cerebellum and including right temporal pole subcortical cysts. Three months later the boy presented with stiffness, headache, and severe hypertonus in the left hemisoma. CT revealed a deep right temporal/parietal intracerebral haematoma with blood penetration into the ventricular system. DSA showed diffuse vasospasm, and three aneurysms.
Discussion
The AGS genetic mutation produces permanence of damaged endogenous DNA-RNA, resulting in an inappropriate immune systemic response, with increased secretion of INF-alpha. In the initial (active) stage of the disease, the high CSF level of INF-alpha is probably responsible for a cascade of events leading to an autoimmune inflammatory reaction, including calcifying vasculitis of brain and systemic vessels. In our patient, the appearance of new lymphocytic vasculitis of the skin could be associated with a new phase of intracranial microangiopathy, with a possible role in the pathogenesis of aneurysm growth and rupture.
In conclusion, we have highlighted the fact that new skin symptoms in patients with AGS, particularly if associated with elevated INF-alpha CSF levels,, increase the need for prompt MRI follow-up, including cerebral MRA, in order to rule out asymptomatic cerebral aneurysms.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):110.
Background
Infantile neuroaxonal dystrophy (INAD) is a rare neurodegenerative disorder, involving axons of both the central and the peripheral nervous system, with presence of axonal swelling and spheroids bodies (SB) as pathological hallmark. The disorder is characterised by infantile onset, with arrest and rapid regression of motor and cognitive developmental milestones, hypotonia evolving to spastic tetraplegia, and visual impairment. Eighty percent of patients with INAD have mutations in the PLA2G6 gene. More recently two different syndromes with allelic disorders of the same gene have been identified causing atypical neuroaxonal dystrophies with brain iron accumulation (NBIA).. In the early stage of the disease the diagnosis of INAD may be difficult, based only on clinical and neurophysiological findings. Traditionally the definitive diagnosis of INAD required the demonstration of axonal SB by biopsy. The evidence that large proportions of INAD have a mutation in the PLA2G6 gene allows molecular diagnosis and often negates the need for biopsy. The most frequent MRI sign of INAD is diffuse and progressive cerebellar atrophy. High T2 signal of the cerebellar cortex, likely resulting from gliosis, was initially considered a "pathognomonic" sign of the disease, but it is not always present and it may appear only in an later phase of the disease.
Purpose
Our purpose was to review the clinical reports, the longitudinal MRI studies, and the available neuropathological features of a group of patients with clinical and radiological INAD phenotype in order to identify the earliest and most important MRI signs of the disease and their evolution, and to correlate the clinical/radiological phenotype with the genetic mutations when results of molecular study were available.
Materials and Methods
Detailed reviews of the clinical and MRI features of nine patients (4M: 5F) with clinical and MRI onset and evolution strongly supportive of INAD diagnosis, were analysed in order to identify the earliest and most important features suggesting diagnosis. All the patients had clinical onset within the first two years of life. The mean age at onset was ten months. We evaluated the MRI findings of the first study as well as any follow up studies, and correlated these findings with the clinical features present at the time of the exam and with the patient's age. IFive patients had Proton MR Spectroscopy (H+MRS), diffusion MRI (DWI), and diffusion tensor (DTI) analysis in additional to conventional MRI.
Results and Conclusions
Progressive cerebellar atrophy was the only MRI finding reported in all patients. The high signal cerebellar cortex was not a constant finding; it was also noted in two cases without definitive genetic or pathological evidence of INAD. We did not observe decreased T2 signal intensity in the GP or substantia nigra, reported in NBIA due to PANK2 gene mutations or to rare atypical NBIA with mutation in the PLA2G6. The value of other cerebral and optic nerve MRI abnormalities and the role of advanced MR techniques, such as proton MRS, DWI and DTI, was evaluated. Most of the children in our group were tested negative for inborn errors of metabolism. The recognition of clinical and MRI features consisting with INAD reduces the need for extensive metabolic testing and steers the molecular analysis, avoiding the need for biopsy to confirm diagnosis. On the other hand, some patients with typical clinical and pathological features of INAD are negative for PLA2G6 mutations; therefore, the absence of either PLA2G6 mutations or pathological evidence may not exclude the diagnosis of INAD when strongly suggested by clinical and MRI diagnostic criteria, allowing the possibility of genetic heterogeneity for the INAD phenotype.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):111.
Introduction
Audit of clinical activity is a critical process to the delivery of good clinical outcomes. Accurate knowledge of outcomes enables patients to be appropriately informed about treatment options and allows clinicians to identify areas for improvement.
Method, Result and Discussion
Typically audit is an additional task for medical staff to complete after urgent clinical duties are attended to. Isolating audit from clinical activity can result in delayed, inaccurate or incomplete entry.
We present a combined clinical management system and audit tool which extracts data from standard forms such as outpatient clinical assessment forms and operation reports. Designed by a neurosurgeon with radiologist input the key design principle of the system is avoiding double entry of data. Rather than adding to the residents work the system improves efficiency in areas such as clinical handover and discharge summaries. As a result it has been enthusiastically received by medical staff.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):112.
Purpose
Intracranial vertebral artery dissecting aneurysms often present with severe subarachnoid hemorrhage and neurological injury. The purpose of this study is to evaluate treatment efficacy and outcome of endovascular treatment of intracranial vertebral artery dissecting aneurysms.
Brief Statement of Methods
Retrospective review of endovascular treatment of dissecting vertebral artery aneurysms was performed in 6 patients. Five men and 1 woman (age range 40-65 years; mean age 49.5 years) were treated over an 3-year period. Three patients presented with subarachnoid hemorrhage and one with headache. Two patients had an incidentally discovered aneurysm. Treatment included coil occlusion of the artery at the aneurysm in 4 patients (deconstructive method), balloon-in-stent coil placement in one, and stent-assisted coil placement in one (reconstructive method).
Summary of Results
Technical success was achieved in all patients, with no post- procedural neurological deficit. Parent artery sacrifice including aneurysm was successful in all cases, whereas both patients treated with reconstructive method suffered coil compaction and recurrence.
Conclusions
Intracranial vertebral dissecting aneurysm can be treated safely with deconstructive and reconstructive endovascular methods. Endovascular treatment has the benefit of being minimally invasive and is associated with a very low rate of complications and a high rate of technical success.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):113.
Objectives
To review the natural history of residual venous pouches post embolization of traumatic carotid cavernous fistula, and to correlate residual venous pouches and ophthalmoplegic symptoms.
Material & Method
We retrospectively reviewed all traumatic carotid cavernous fistula (TCCF) cases from January 1995 to September 2009. Patients with residual venous pouches post fistula embolization and at least 2 imaging follow ups were included in the study.
Results
21 patients (16 males, 5 females) were identified (mean age 27.5 years). The overall size of venous pouches ranged from 3 to 30 mm, with interval follow up from 15 to 647 days. 6/21 patients had complete closure of the fistula by transarterial balloon placement. 4/6 patient were fully clinical recovered during follow up, with asymptomatic venous pouches ranging from 3 to 10 mm. 1/6 patient was fully clinical recovered during early follow up but developed new mild ophthalmoplegia on day 80 (slightly limited abduction of about 10%). His angiogram showed an 18mm venous pouch. No further treatment was undertaken and on follow up he had stable mild ophthalmoplegia. 1/6 patient was partially clinical improved during follow up and had a 20mm venous pouch with stable mild ophthalmoplegia. No further treatment was done. In 15/21 patients the fistula was partly closed at initial follow up followed by complete closure later. 2/15 patients were fully clinical recovered during follow up, with asymptomatic venous pouches of 10 and 16mm. 11/15 patients were partially clinical improved during follow up, with venous pouches ranging from 3 to 13mm. Residual symptoms were simple ophthalmoplegia without chemosis or proptosis. 1/15 patient had stable symptoms with a 10-mm venous pouch, which was not treated. 1 patient developed progressive opthalmoplegia. Of the 4 treated cases 2 patients had persistent ophthalmoplegia, with one increasing the size of the pouch from 28 to 36 mm and one stable at 10mm. After pouch embolization the symptoms are still stable. 1 patient had no residual symptoms but had co-existing pseudoaneurysm in the sphenoid sinus. 1 patient developed progressive ophthalmoplegia on 53days post treatment, with a new 15mm venous pouch on angiogram. Follow up status after further treatment indicated clinical improvement. Patients who had complete clinical recovery after fistulous treatment (7/21) had varying sizes of venous pouches (range; 3 to 18mm). No new symptoms occurred during follow up. Of these, one pouch increased in size from 16 to 34mm over 36 days, without developing new symptoms. Spontaneous thrombosis was demonstrated in two venous pouches (3mm and 6mm) on follow up at day96 and day 365 respectively. Complete clinical recovery was noted in these patients. Rupture of a 6mm venous pouch was shown in one patient leading to recurrent carotid cavernous fistula at day 193.
Conclusion
Venous pouches may occur during follow up of TCCF, despite complete closure of the fistula on the post treatment angiogram, possibly due to early deflation or migration of balloon. rarely a few pouches may thrombose spontaneously leading to cure, or rupture leading to recurrent fistula. Some pouches are asymptomatic even though large in size. Venous pouches should be treated therefore only in patients with persistent, progressive or newly developing ophthalmoplegia.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):114.
Purpose of Study
The authors present their experience with mechanical embolectomy as a treatment modality for patients with acute cerebral ischemia.
Methods
From July 2006 to September 2009 mechanical embolectomy by means of the Merci Retriever was performed in a group of 40 patients who presented with symptoms of acute brain artery occlusion(27 men, 13 women; ages 28-78, average age 57). After CT examination including CT perfusion an embolectomy by means of the Merci Retriever was urgently performed. Anterior brain circulation was occluded in twenty eight patients, posterior brain circulation in twelve patients.
Results
Successful reperfusion was achieved in thirty four patients (85%). In six patients (15%) reperfusion was unsuccessful. In seven cases the procedure was complicated with ICH within 24 hours. Intra-arterial administration of alteplase (3 mg) was necessary in eleven patients. PTA was performed in seven cases and stent implantation in eight cases. The resulting modified Rankin Score 30 days following treatment was 1 or 2 in 19 cases (47.5%), modified Rankin Score was 6 in 9 cases (22.5%). No patient died within 30 days post unsuccessful mechanical embolectomy by means of the Merci Retriever. Thirteen patients (32.5%) had died at one-year follow- up.
Conclusions
Mechanical embolectomy is a proven treatment modality for selected patients with acute cerebral ischemia, as it is very effectively able to revascularise occluded arteries within an eight-hour therapeutic window.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):115.
Purpose of Study
During carotid artery stenting (CAS) under local anesthesia, hemodynamic instability (hypotension, bradycardia etc.) has been reported to occur. Hemodynamic instability during CAS under local anesthesia may be a risk factor for complications, especially in elderly patients. We evaluated hemodynamic stability during CAS under general anesthesia in elderly patients with high grade carotid artery stenosis.
Methods
CAS procedures were performed in 15 patients under general anesthesia, using sevoflurane and nitrous oxide in oxygen, in patients aged 65 years or older between November 2007 and February 2009. All CAS procedures were performed for high grade stenoses (>70% in NASCET criteria). Nine procedures were performed for symptomatic stenoses. Degree of systolic blood pressure change, hypotension, and bradycardia during CAS were assessed.
Results
The mean age of patients was 69 ± 3.2 years old. The mean degree of stenosis before and after CAS was 75.8±7.5% and 25.9±9.8%, respectively. No hypotension (SBP < 80 mmHg) occurred during procedures. Transient bradycardia (HR < 50/min) occurred in 1 patient during procedure (0.6%). The mean systolic blood pressure change was 35±11.9mmHg. No procedure was complicated with stroke during and after CAS.
Conclusion
General anesthesia using sevoflurane and nitrous oxide in oxygen depressed baroreceptor reflex sensitivity, induced hemodynamic stability during CAS, and may decrease the rate of occurrence of complications in elderly patients with a high-grade carotid artery stenosis.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):116.
Purpose
To develop a canine model of acute cerebral artery embolic occlusion using radio-opaque clots and to evaluate the feasibility and effectiveness of the self-expanding stent for the treatment of an acute embolic occlusion.
Materials and Methods
Five male mongrel dogs were used for this study. Various mixtures of whole blood, thrombin and barium sulfate were tested in vitro using a transparent silicone tube to develop a radio-opaque clot for an embolic occlusion model.. A radio-opaque clot comprising 10mL whole blood, 50 IU thrombin and 1g barium sulfate, was used for establishing the embolic occlusion model. An injection of the radio-opaque clot through a guiding catheter occluded each vertebral artery, and a Neuroform stent was then placed across the radio-opaque clot. The technical success rate for placement of the stent to the targeted vessel was evaluated (defining success as the safe placement of the stent at the site of the occluded vessel, with full coverage of the lesion without fragmentation and distal embolization of the clot). The recanalisation rate, as measured by the Arterial Occlusive Lesion score (AOL), and degree of residual stenosis was also evaluated. In two dogs we tried to get a specimen of the stented vertebral arteries, to evaluate how the clot and the stent might contribute to vascular injuries that may happen during the endovascular procedure.
Results
One dog died of an unknown cause during the induction of anesthesia. In two dogs, only one vertebral artery was used, whereas both vertebral arteries were used in the rest. Six vertebral arteries were successfully occluded. Fragmentation and distal migration of the clot occurred in one case during microcatheter passage, and one stent could not cover the whole length of the radio-opaque clot. The technical success rate for stent placement without complication was 66.7%. The AOL score after stent placement was 2 in all cases, and the recanalisation rate was 100%. Residual stenosis was 35.6±18.6%. On microscopic examination the stent was placed at the center of the clot, and the clot was captured between the stent mesh and arterial wall.
Conclusion
Using an endovascular method, it is feasible to create an acute cerebral artery embolic occlusion canine model with radio-opaque clot. Self-expanding stents were effective in revascularizing cerebrovascular embolic occlusion. Fragmentation with distal embolization of the clot may occur during microcatheter passage. The self-expanding stent appeared to achieve recanalisation by pushing the clot to the arterial wall, capturing the clot between the stent mesh and the wall of the artery.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):117.
Purpose
Stents and coils placed for endovascular treatment of intracranial aneurysm produce a susceptibility artifact that may make it difficult to evaluate the patency of the parent artery and completeness of endovascular treatment. We studied the clinical usefulness of time-resolved 3D contrast-enhanced MRA (4D MRA) after stent-assisted coil embolization for intracranial aneurysm by comparing with 3D TOF.
Materials and Methods
TOF and 4D MRA were obtained using 3T MRI (Signa HDx; GE Medical Systems, Milwaukee, WI) in 18 patients (19 aneurysms) treated with stent-assisted coil embolisation (Enterprise = 4, Neuroform = 15). One neuroradiologist evaluated MIP images and source images of 4D MRA and TOF for quality of the stented segment of intracranial arteries and completeness of coil embolization. The image quality of the stented intracranial arteries according to each MRA method (4D MRA VS. 3D TOF) and each self-expanding stent (Enterprise v Neuroform) was rated from grade 0 to grade 4, and was compared using the Chi-squared test and Spearman's Rho correlation test. We also classified completeness of endovascular treatment into three categories (complete occlusion, residual neck, and residual aneurysm), and compared concordance rate of each MRA method for evaluating completeness of stent-assisted coil embolization using DSA as a standard of reference in seven patients.
Results
The quality of the 4D MRA was significantly superior to that of TOF (p = 0.018). In 3D TOF the quality of arteries stented with Enterprise stent was superior to that of the arteries stented with Neuroform (p = 0.000). In 4D MRA, the quality of arteries stented with Enterprise stent seemed to be superior to that of the arteries stented with Neuroform (p = 0.063). Concordance rate of MIP images of 3D TOF and 4D MRA for evaluating completeness of stent-assisted coil embolization was 28.6% and 71.4%, respectively. Concordance rate of source images for evaluating completeness of stent-assisted coil embolization was 71.4%. There were 3 patients whose results of source images and MIP images of 3D TOF were discrepant. However, there was no discrepancy in 4D MRA images.
Conclusion
MIP images from 4D MRA seem to be superior to MIP images of TOF for evaluating completeness of stent- assisted coiling of intracranial aneurysm. 4D MRA showed higher image quality of the parent arteries compared with TOF. Enterprise stents seemed to have higher susceptibility artifacts that might cause non-visualization of the parent arteries. 4D MRA might become a valuable noninvasive, follow-up imaging modality after stent- assisted coiling embolization.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):118.
Purpose
To evaluate the outcome for patients with acute stroke in the territory of the middle cerebral artery (MCA) who had undergone stent implantation in the proximal segment of internal carotid artery (ICA) in addition to intra- arterial thrombolysis (IAT).
Materials and Methods
Stent implantation and retrospective analysis of clinical and radiological data were approved by the Institutional ethical committee. 22 patients (16 men, 6 women; mean age, 66 years) with acute stroke in the territory of the MCA occurring after occlusion in the ipsilateral ICA were treated with recanalisation of the ICA using stents and IAT of the MCA thrombus. Recanalisation rates, post-thrombolysis hemorrhage, and clinical outcome (baseline and discharge National Institute of Health Stroke Scale [NIHSS], mortality, three-month modified Rankin scale [mRS]) were evaluated.
Results
ICA recanalisation after stent deployment was successful in 20 patients (90.9%). Good recanalisation of the MCA after urokinase (UK) infusion was achieved in 16 of 20 patients (80%). The mean UK dose was 200,000 IU (range 50,000 - 400,000). No patients developed symptomatic haemorrhage. Mortality rate was 9.1% (n = 2). The median baseline NIHSS scores showed improvement from 13.6 to 5.6, at presentation and discharge respectively. At three months good outcome was noted in 14 of 22 patients (63.6%; mRS, 0-2).
Conclusions
Stent implantation in the proximal segment of the ICA, and IAT of MCA occlusions seems to improve the clinical outcome for patients with acute stroke. -
interv neuroradiol. 2010 Mar 23;16(Suppl 1):119.
Purpose
To present 2 cases of unusual spontaneous intralesional hemorrhage in venous malformations of the head and neck. Both were treated successfully with percutaneous intralesional sclerosing therapy.
Material and Method
From 2000-2009, a total of 60 patients who had venous malformations of the head and neck were treated at Siriraj Hospital, Bangkok, Thailand by percutaneous sclerosing therapy:absolute alcohol was the used prior to 2006, and bleomycin after 2006. Of the 60 patients two patients (3.3%) presented with rapidly severe progressive enlargement of the vascular malformation and are reviewed here .
Patient No.1
A 37-year-old female, who had an anomaly of left ear since birth, presented with rapid progressive swelling of neck and face after minor trauma to the shoulder 3 days earlier. CT scan revealed a huge hematoma at left side of neck and upper chest wall with compression of left subclavian and jugular vein. A small pocket of vascular enhancement was noted at the supraclavicular region. Percutaneous puncture was performed and after free flow of blood from the cannula, a test contrast medium injection confirmed the vascular space. 40 ml of absolute alcohol was injected. Further swelling of the lesion and face were observed in the following 2 days. This was thought due to the effect of alcohol. Some resolution was noticed at 2 weeks.
Patient No 2
A 62-year-old female was known to have a stable venous malformation on her right cheek for more than 30 years. Surgery had been performed 9 years prior to presentation. She presented with spontaneous rapid expansion of the lesion with ecchymosis developing over a 2 day period. CT scan showed a large loculated hematoma with some enhancing vessels. Percutaneous puncture was successful and demonstrated abnormal venous channels. Intralesional bleomycin injection of 15 ml was performed The bleeding stopped. and the hematoma gradually resolved over time and at ^ months was clinically insignificant..
Conclusion
Spontaneous intralesional hemorrhage is an unusual presentation of venous malformation. An urgent percutaneous sclerosing therapy is recommended as the initial treatment of choice. The sclerosing agents such as absolute alcohol or bleomycin, are the same as those recommended for venous malformation,. CT or other imaging modalities are helpful to localize the extent of the lesion and to provide guidance for optimal puncture of the abnormal vascular channels.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):120.
Background and Purpose
The pathophysiology of IIH remains unknown. TS stenoses have been observed in a high proportion of these patients. Stent placement to remove this potential obstruction to venous outflow has been proposed as a treatment option for patients with IIH refractory to medical treatment.
Materials and Methods
Retrospective review of the clinical presentation, treatment, and outcome of patients with refractory IIH evaluated for venous sinus stent placement at a tertiary care center.
Results
Thirteen female patients with IIH were evaluated for sinovenous stent placement. Moderate sinus stenoses with normal intrasinus pressures were found in 3 patients and therefore stent placement was not performed. Ten patients had elevated intrasinus pressures (pressure gradient across stenosis, 11-50 mmHg), which decreased following unilateral TS stent placement. Headaches improved or resolved in all stented patients. Papilledema resolved completely or almost completely in 8 patients and significantly improved in 2 patients. One patient developed optic atrophy. There were no major periprocedural complications.
Conclusions
In this small case series, restoring the patency of stenotic venous sinuses with a stent in patients with refractory IIH resulted in symptomatic improvement in all treated patients. The safety and efficacy of this procedure should be evaluated in a randomized controlled study to determine its role within the armamentarium of therapeutic options for patients with IIH.
Abbreviations
BMI- body mass index; IIH - idiopathic intracranial hypertension; TS - transverse sinus; TVOs- transient visual obscurations
interv neuroradiol. 2010 Mar 23;16(Suppl 1):121.
Purpose of Study
To study the safety of endovascular treatment of intracranial aneurysms
Methods
Total of 214 intracranial aneurysms were treated by endovascular route from January 2003 till December 2009 in department of Neuroradiology at All India Institute of Medical Sciences (AIIMS), India. There were 110 males and 104 females, age ranged from 14 to 75 years (mean-55 years, SD-8.48years). 40 aneurysms were giant (>25mm/complex). Most aneurysms presented with SAH (>80%, small-moderate size, only 15/40 giant aneurysms), mass effect or nonspecific headache in 25 cases. 34 aneurysms were un-ruptured, five had stroke at the onset. Pseudoaneurysm (n=2) presented with epistaxis. 140 aneurysms were located in the anterior circulation and 74 in the posterior circulation. 60 aneurysms had a broad (>4mm) neck, rest had a narrow neck. 178 aneurysms were sacular, 20 dissecting, 10 serpiginous and 4 were flow-related.
Results
Indication for endovascular treatment was: 1. Patient's preference, 2 Difficult surgery, 3. Failed surgery (n=20), 4. AVMs associated with aneurysms, 5. Multiple aneurysms (n=50). Narrow neck aneurysms were treated with detachable coils, 9 by balloon occlusion, 3 by parent vessel occlusion with coils, 2 by balloon-aneurysm neck occlusion, 30 by stent-assisted coiling, 20 by balloon-assisted coiling, and in one case, aneurysm had thrombosed by itself. Complete aneurysm occlusion was achieved in all with narrow neck, while only 12/40 (34%) cases) with broad neck had total occlusion. Complete or near-total occlusion was achieved in (80.3%) cases.
Complications
Procedure-related morbidity was encountered in 12 cases, with thromboembolism in 4, parent vessel occlusion in one case with infarcts. Six patients died (mortality-3%) due to aneurysm perforation. Groin hematoma occurred in 4 patients, balloon deflation in one case and arterial dissection in one case but, none gave rise to clinical complications.
Conclusions
Intracranial including giant/complex aneurysms can be safely treated by endovascular route with good occlusion rate of over 80%, with acceptable clinical complication (6%) and mortality rates (3%).
interv neuroradiol. 2010 Mar 23;16(Suppl 1):122.
Objective
The purpose of this retrospective study was to report the experience of the endovascular treatment for vertebral artery aneurysms and to discuss treatment strategy.
Methods
During a 3-year period, 15 patients with 15 vertebral artery (VA) aneurysms were treated by endovascular surgery; they included 11 VA dissecting aneurysm and 4 VA-posterior inferior cerebellar artery (PICA) bifurcation saccular aneurysms. Overall, 9 (60%) of patients presented with hemorrhage, and two with ischemic symptoms. Other four were unruptured aneurysms and one of them caused cerebellar ataxia due to the compression of inferior cerebellar peduncle.
Results
Endovascular internal trapping was performed 9 of VA dissecting aneurysms as the PICA was originated from the distal VA in all 9 cases, one proximal VA occlusion was selected for the PICA-involved type of VA dissecting aneurysm. Endosaccular coil embolization was performed for all VA-PICA saccular aneurysms. One large VA- PICA aneurysm was treated by endosaccular coil embolization following OA-PICA bypass because the PICA was originated directly from the dome. Two patients had re-treatments for recanalization; one was surgical proximal VA clipping following three endovascular trapping, one was additional coil embolization following endosaccular embolization.
Conclusions
Endovascular therapy is a primary and effective alternative for aneurysms involving vertebral artery. Collaborative, multidisciplinary team approach must be necessary for treating complicated vertebral artery aneurysms.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):123.
Purpose
To review the anatomy and MRI appearances of normal, dilated and giant Virchow Robin (VR) spaces and to illustrate their differential diagnoses, associations and involvement in specific disease processes.
VR spaces are normal, anatomical spaces that surround penetrating vessels as they course through the brain parenchyma. They are pial lined, interstitial, fluid-filled structures that are seen with increasing frequency with higher spatial resolution MRI studies. In most cases, VR spaces are of no clinical significance however they are important as they may be misdiagnosed for other conditions. Dilated VR spaces are commonly mistaken for lacunar infarcts however VR spaces can be differentiated by their specific signal characteristics, morphology and distribution. Widespread dilatation of VR spaces is associated with microangiopathy. It has also been suggested that they may be associated with mild traumatic brain injury and early primary demyelination. VR spaces may be directly involved in disease processes such as Cryptococcus infection.
Atypical VR spaces may be markedly enlarged, bizarre in shape and may exert mass effect. They may resemble cystic neoplasms and are occasionally associated with adjacent T2-hyperintensity. The purported mechanisms of their development and their differential diagnoses are also discussed.
Conclusion
A knowledge of the characteristic imaging features of typical and atypical VR spaces may avoid misdiagnosis of these usually incidental findings. Specific disease processes may be may directly involve VR spaces.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):124.
Dural arteriovenous fistulas (DAVFs) are arteriovenous shunts from a dural arterial supply to a dural venous drainage channel. These fistulas involve the cavernous sinus, transverse-sigmoid sinus, superior sagittal sinus, inferior and superior petrosal sinus, sphenoparietal sinus, anterior cranial base, tentorium, craniocervical junction, and anterior condylar confluence.
Anterior condylar arteriovenous fistula (AVF) is rare and very important subgroup of posterior fossa AVF. The purpose of this paper is to report a rare case of a 55 year old male with progressive and worsening pulsatile tinnitus who is diagnosed to have an anterior condylar arteriovenous fistula and also, the success of endovascular treatment of transvenous embolization with coils of the hypoglossal canal.
Transvenous coil embolization in anterior condylar confluence arteriovenous fistula has long been recognized as the most effective measure for treating an intracranial DAVF and proved to be curative in most cases presented in various series.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):125.
Abstract
To avoid postoperative hyperperfusion state, strict management of blood pressure after the procedure is highly recommended. As another treatment option, we performed staged carotid stenting in carefully selected patients who presented severely impaired CBF.
Method
From 2005 to 2009, we performed 154 carotid stenting in 122 patients. Judging from the preoperative clinical symptoms and examinations including: angiography, SPECT, MRI, and ultrasound, we carefully selected 14 high- risk patients. Patients with soft unstable plaque were excluded from this study. Of these two were acute near occlusion cases. The 14 high-risk patients were initially treated by balloon angioplasty with or without a protection device. We usually used a PTA balloon with diameter of 2.5-3.0mm for initial angioplasty. After one or two months, we observed CBF and CVR with an acetazolamide using SPECT. Carotid stenting was performed within one month of the initial angioplasty. All patients were carefully monitored in intensive care unit after the operation for one or two days. Postoperative blood pressure was strictly controlled below baseline of the preoperative level. A postoperative diffusion-weighted MRI was performed within 5 days of the procedure to monitor distal embolism. The CBF and CVR were repeated one or two months after the carotid baseline preoperative measure. The postoperative diffusion-weighted MRI was performed within 5 days of the procedure to monitor distal embolism. The CBF and CVR were observed one or two months after the carotid stenting.
Results
None of the patients with 2-staged procedure presented postoperative hyperperfusion as indicated clinically by lack of hemorrhage, convulsion or other neurological deficits. Most cases demonstrated improved CBF and CVR on SPECT examination after the staged stenting. Asymptomatic distal embolism was detected on diffusion weighted MRI postoperatively in two patients.
Conclusions
Staged carotid stenting for severely impaired CBF patients resulted in good outcome. This method of staged carotid stenting seems very safe and feasible. A patient with unstable plaque should be excluded from this staged procedure so that acute obstruction or massive distal embolism is prevented.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):126.
Purpose
To report a rare case of arteriovenous shunt or malformation related to a malignant pineal region tumor that presented to Ramathibodi Hospital Medical School.
Materials and Methods
Retrospectively case review. The clinical onset and therapeutic response, imaging, including CT scan, MRI, MRA and MR spectroscopy cerebral angiogram in a patient with malignant pineal region tumor with co-existing arteriovenous shunt or AVMs was identified Clinical follow up between October 2009 to December 2009 was reviewed.
Results
Our case is of a 7 years old boy who presented with progressive headache for 4 months, decreased hearing, diplopia , unilateral decreased VA left eye, and ataxia on physical examination. CT scan of the brain showed an enhancing mass at midbrain and pineal region, with encasement of the cerebral aqueduct, causing a moderate degree of obstructive hydrocephalus. There was also a markedly enhancing vascular structure above the mass. The patient underwent VP shunt placement with clinical improvement before he was referred to our institute. MRI and MRA of the brain was done and showed marked enlargement of the mass and also progressive enlargement of the vascular lesion, indicating of progressive arteriovenous shunt. Additionally MR spectroscopy of the mass shows high Ch/Cr ratio and decreased NAA peak, indicating malignant stigmata of the tumor. Differential diagnosis included of PNET, malignant germ cell tumor or less common malignant lymphoma. Cerebral angiogram showed evidence of arteriovenous shunting or AVMs, supplied by multiple perforating branches and posterior choroidal branches, with rapid draining to an enlarged draining vein through dilated vein of Galen. There was no significant staining or hypervascularity of the mass in the midbrain. Therapeutic whole ventricular radiation therapy of the mass was performed, with a total dose 4,960 Gy, and improvement of neurological symptoms.. F/U CT scan and MRI of the brain 6 weeks show marked decrease in size of the midbrain mass. However, the size of the arteriovenous shunt had not significantly changed.
Conclusion
Arteriovenous shunts related to intracranial or spinal cord tumors are rare, and the most frequent masses with AV shunt are hemangioblastomas, which typically shows a cystic mass with an intense enhancing mural nodule, and surrounding or adjacent enlarged vessels, from intratumoral AV shunts. Typical cerebral and spinal angiogram of hemangioblastomas in our experience show hypervascular supply of the masses with intense staining of the mass before draining into the veins, which are slightly earlier than the surrounding brain or spinal cord parenchyma. In this case, the cerebral angiogram did not show significant tumor staining, but immediate draining to the enlarged choroidal veins which is not typical for intratumoral AV shunt, but rather typical for the co-existing choroidal AVMs. Brain parenchymal changes related to AVMs are more commonly the result of resolving hematoma, venous or arterial infarction or post radiation necrosis response from radiation therapy for the brain AVMs. However, in summary our case most likely represents s a co-incidental symptomatic malignant midbrain tumor with a non ruptured choroidal AVM.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):127.
Purpose
Sigmoid sinus diverticulum is a rare dural sinus anomaly regarded as one of the very rare causes of pulsatile tinnitus. There are only a few international reports about their surgical or endovascular management. We report another case which was treated interventionally with a review of a few related literatures.
Methods and Results
A 31-year-old female presented with a pulsatile tinnitus on her right ear for 3 years. Her tinnitus was decreased by compressing on her ipsilateral (right) jugular area, and increased by compressing on her contralateral (left) jugular area. Otoscopic and neurologic examination showed no abnormality. On the CT scan , a 7x6mm sized sigmoid sinus diverticulum with relatively narrow neck (4.5mm) was found on the lateral aspect of the right proximal sigmoid sinus. We embolized the diverticulum with 2 detachable platinum coils without stent-assistance via a transfemoral venous approach under local anesthesia and the tinnitus instantly disappeared. There was no recurrence of symptom after 11 months.
Conclusions
We report another case of sigmoid sinus diverticulum which had caused pulsatile tinnitus and was cured interventionally with only 2 detachable coils under local anesthesia.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):128.
Purpose
Middle cerebral artery (MCA) aneurysms often have features that may be unfavorable to coil embolization. However, endovascular treatment of MCA aneurysms is a growing trend due to improvements of the devices and new technique. The aim of this study was to report our experience of coil embolization of MCA aneurysms.
Materials and Methods
From April 2007 to May 2009, 164 consecutive patients underwent endovascular treatment at our institute; 17 (10.4%) of them had MCA aneurysms (14 unruptured, 3 ruptured; mean age, 65.5 years). We retrospectively reviewed of these patients to determine the angiographic feature, technical result and clinical outcome.
Results
Among 17 patients with MCA aneurysms, embolization was successful in 15 patients (technical success rate: 88.2%). In 2 patients, the procedures failed due to its complex angiographic geometry. Adjunctive endovascular techniques were used in 5 patients to protect branch vessels at the neck. There were no procedure related complications and complete or near complete occlusion was achieved in all 15 patients.
Conclusions
Coil embolization of MCA aneurysms can be carried out with high rates of technical success with acceptable morbidity.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):129.
Introduction
Carotid stenting occasionally results in hyperperfusion syndrome, and rarely causes fatal intracerebral hemorrhage (ICH). The purpose of this study was to determine efficacy and safety of staged carotid balloon angioplasty and stent placement.
Patients & Technique
Since May 2005, we performed balloon angioplasty and stent placement in separate sessions in cases of impaired cerebral perfusion due to extremely severe stenosis of the carotid artery. One to two weeks after angioplasty with a 3-mm or 4-mm diameter balloon catheter, stent placement was performed with distal protection. A consecutive 23 cases were reviewed in terms of clinical and radiologic outcome and procedure-related complications.
Results
21 male and 2 female patients underwent the staged procedures. Median age of the patients was 71 years (range, 50 to 83). Median interval between balloon angioplasty and stent placement was 7 days (range, 7 to 18). Balloon angioplasty was performed with 3-mm balloon catheter in 20 cases, 3.5-mm in 1 and 4-mm in 2. No patient experienced procedure-related hyperperfusion syndrome or ICH. There was no thromboembolic event during the period between balloon angioplasty and stent placement. Excellent clinical outcome could be achieved in all the cases except one who suffered from delayed stent thrombosis.
Conclusion
Staged balloon angioplasty and stent placement seems to be a safe and effective procedure in cases of impaired cerebral perfusion that are at risk of procedure-related hyperperfusion syndrome or ICH.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):130.
Purpose
To determine the associated factors with the long term clinical outcome of the patients with cranial dural arteriovenous shunts (dAVF)
Methods
Retrospective review of 180 patients who had cranial dAVFs at Siriraj Hospital, Bangkok, Thailand, between 1992-2009 were performed. Demographics, clinical presentations, imaging, locations, multiplicity, angiographic patterns, endovascular procedures, complications and clinical follow up datas were analysed.
Results
Total 180 patients, 65% was female, 35% was male with mean age at 53 years (range from 15-85 years).The shunt locations were cavernous sinus ( 55.17%), transverse-sigmoid sinus (27.16%), superior sagittal sinus (7.83%), torcula (3.89%), superior petrosal sinus(0.86%), inferior petrosal sinus(0.86 %), condylar vein(2.16%), and cortical vein(0.86%), osteodural site 0.86%, posterior mesencephalic vein 0.43%. Multiple shunts were 26.2%. According to Davies classification: 50 % were benign type, whereas 11.11% had retrograde sinus drainage, 50% were aggressive type whereas 2.78% had spinal cord venous drainage. Associated sinus thrombosis were found in 26.11%. One hundred and thirty one patients (72.78%) had endovascular embolization, 8/131 had further surgery due to inadequate or failed embolization. Forty nine patients ( 27.22%) had conservative treatment or clinical observation. Thirty-one patients(17.22%) were lost to follow up. The clinical outcome of 149 patients with the follow up period ranging from 2 months to 12 years, were favorable in 135 patients ( 90.60%), unchanged in 6(4.03 %), unfavorable in 8 ( 5.37%). Among 135 favorable outcomes, 111 patients( 82.22%) had successful treatment, 25 (18.52 %) had observation due to benign type. One patient had unchanged clinical blindness due to chronic increased intracranial pressure although the shunts were completely eradicated. Three patients with unfavourable outcome had initial hemorrhage and/or severe chronic venous congestion. Seven patients had procedural complications.
Conclusion
The favorable or good clinical outcome of cranial dural AV shunts are predicable in benign type, single shunt and successful treatment. The aggressive clinical symptoms of intracranial venous congestion are reversible, following an effective treatment. The poor outcomes are related to aggressive type with initial intraparenchymal hemorrhage, or papilloedema from increased intracranial pressure or prolonged venous congestion. Although the anatomical cure had been achieved, the functional impairment had been irreversible.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):132.
Purpose
The distal dural ring (DDR) plane separates the intradural from extradural paraclinoid internal carotid artery (ICA) aneurysm. The purpose of this study was to evaluate the feasibility of the localization of the distal dural ring (DDR) plane drawn by the bony landmarks in patients with paraclinoid ICA aneurysms at 3D rotational angiography (RA).
Materials and Methods
13 consecutive patients who underwent a 3D RA for the evaluation of 16 paraclinoid ICA aneurysms were reviewed retrospectively. 3D RA was performed on an Axiom Artis Zee Angiography System (Siemens, Medical Solutions, Forchheim, Germany) with a flat panel detector. On a dedicated workstation, a multiplanar reconstruction (MPR) image along the virtual plane of DDR was reconstructed from the mask run image of the 3D RA. Three bony landmarks were used to locate the virtual plane of DDR: tuberculum sellae, inferior root of anterior clinoid process (ACP) and superio-medial aspect of the optic strut. The MPR image along the virtual plane of DDR was fused with the 3D volume-rendered reconstruction angiographic image by dual volume visualization. The locations of the paraclinoid aneurysms were categorized into indradural, transdural, and extradural. The distance between the origin of ophthalmic artery and virtual DDR plane was measured.
Results
In all cases, the DDR plane was identified and the relationship between the DDR plane and the paraclinoid aneurysm was successfully determined on dual volume visualization image of 3D RA mask and contrast runs. The aneurysm locations determined with 3D RA were 8 intradural, 6 transdural and 2 extradural. The measured distance between the origin of ophthalmic artery and the DDR plane ranged -4.96 mm to 1.95 mm.
Conclusion
Visualization of virtual plane of DDR and localization of the paraclinoid ICA aneurysm in relation to the DDR is feasible with 3D RA by dual volume visualization, and it helps to decide the management strategy of these lesions.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):132.
Purpose
To analyse radiation doses for diagnostic and therapeutic neurointerventional procedures of intracranial aneurysms.
Materials and Methods
Dose-area product (DAP) measurements of 96 patients were retrospectively assessed for biplane angiographic units. Fluoroscopic and radiographic exposure parameters (kVp, mAs, fluoroscopic time, number of radiographic runs and frames) of each procedure were also recorded by the biplane angiographic unit. Radiation doses and exposure parameters were analysed for three groups: diagnostic procedure only (n=55), therapeutic procedure only (n=32), and diagnostic and therapeutic procedure in the same session(n=9).
Results
Total mean DAP values were 171 Gy-cm2 for diagnostic procedures, 195 Gy-cm2 for therapeutic procedures, and 262 Gy-cm2 for both procedures in the same session. Mean flurosopic time in each group was 12.8 min, 57.0 min, 41.8 min, respectively. For the diagnostic procedures, total fluoroscopic time was correlated with patient's age (r=0.544, p<0.01). Proportion of fluoroscopic DAP in each procedure was 26.7% for diagnostic only, 84.8% for therapeutic only, and 44.9% for both in the same session.
Conclusion
The complexity of the diagnostic and therapeutic procedure is responsible for the high radiation dose to the patient. Fluoroscopic time correlates with patient's age for the diagnostic procedure. Highest proportion of fluoroscopic time occurs with the therapeutic procedure. Interventional radiologists should measure patient doses for their procedures.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):133.
Purpose
The Axium coils were developed to improve durability of embolized cerebral aneurysms by increasing coil packing density. The purpose of this prospective and multicenter registry was to evaluate the safety and short- term durability of the Axium detachable coils.
Methods
One hundred twenty-six patients (mean, 55 years; 51 men and 75 women), harboring 135 aneurysms ≤ 15mm in size, were treated by coil embolization with bare platinum coils including more than 50% of Axium coils. Balloon was permitted for adjuvant device but stent was not. The characteristics of aneurysms, complications, packing density, immediate and short-to-midterm follow-up results were prospectively collected and retrospectively evaluated.
Results
Mean aneurysm diameter was 6 mm (range, 2 - 15 mm; 118 small aneurysms < 10mm and 17 large ones ≥ 10mm). Eighty-three aneurysms were unruptured and 52 were ruptured. Immediate post-procedure control angiography revealed complete occlusion in 80 (59.3%), neck remnant in 47 (34.8%), and incomplete occlusion in 8 (5.9%). Mean aneurysm packing density was 42.8% (range, 9.5 - 82%) and mean % Axium coil length of total coil length was 87.9%. Packing density was significantly higher in balloon-remodeling technique (mean, 47.9%) than in single or multi-catheters technique (mean, 40.7%) and was also significantly higher in small aneurysms (mean, 44.1%) than in large ones (33.6%). The rate of any procedure-related complication was 13.6%. Procedure-related permanent morbidity and mortality rates were 3.8% and 0.8%, respectively. Imaging follow-up with catheter angiography or MR angiography was available in 101 aneurysms (mean diameter, 5.9mm; 90 small and 11 large aneurysms; mean packing density, 42.3%) at 6 - 15 months (mean, 7.7 months). Follow-up imaging revealed stable/improved occlusion in 95 aneurysms and recanalization in 6 aneurysms (5.9%). Large aneurysm was the only significant predictor for recurrence on univariable analysis and multivariable logistic regression analysis (p <.05).
Conclusions
In this prospective and multicenter registry, Axium coils showed a relatively low rate of recanalization rate on short-to-midterm follow-up imaging with acceptable periprocedural safety profile, compared to those reported for the other bare platinum coils. These results may warrant further study for long-term efficacy of Axium coils in larger populations.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):134.
Purpose
Acute thromboembolism is a frequently encountered complication occurring during endovascular procedures. The abciximab is used as a rescue agent in the thromboembolic events complicating interventional procedures. We report our experience of intraarterial administration of abciximab in various clinical settings.
Materials and Methods
We retrospectively reviewed thirty-two cases (mean age: 60 years, range: 28 to 85 years) in which abciximab was intraarterially administered for the treatment of acute thrombosis during neurointervention in our institution between 2005 and 2008. 18 patients were treated with coiling/stent-assisted coil embolization (ruptured: 8, unruptured: 10). 13 patients were treated with elective stenting for atherosclerotic stenosis (four patients had underlying acute or subacute infarct).
Results
In all cases, successful recanalization of the thrombosed artery was achieved. Complete angiographic improvement was seen during the procedure in 26 cases or on follow up angiography (mean days: 7.6 days, range: 4 to 14 days) in 6 cases. Total mean dose of used abxicimab was 9.6 mg; range 4 to 20 mg. One subdural hematoma was demonstrated on CT after the procedure, however there was recent trauma in this case. There was no parenchymal or subarachnoid hemorrhage in any patient.
Conclusion
Abciximab was safe and effective when used as a rescue agent for thromboembolic complications encountered during endovascular treatment, even if there is concomitant ruptured aneurysm or recent infarction.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):135.
Purpose
Restenosis is a major late complication after stenting of intracranial atherosclerotic stenosis. Little attention has been given to the issue of treatment of intracranial restenosis. The authors report their clinical experience of endovascular treatment for intracranial restenosis.
Methods
From January 2000 to October 2009, 13 patients (7 men and 6 women; mean age 53.4 years, range 37~71 years) underwent endovascular treatment for intracranial restenosis. Middle cerebral artery restenosis was found in nine patients, supraclinoid internal carotid artery in two, basilar artery in one, and intracranial vertebral artery in one. Balloon angioplasty was performed in nine patients and double-stenting was done in four patients. Clinical and angiographic follow-ups were done.
Results
12 patients (92.3%) patients were successfully treated. One patient died due to arterial perforation and subsequent in-stent occlusion. Angiographic follow-up (mean 12.3 months with a range of 2 to 28 months) was available in nine patients. Re-restenosis (rate >50%) was observed in three patients (33.3%). All re-restenoses were observed in patients treated with balloon-assisted angioplasty. One patient with double-stenting using a drug eluting stent presented with very late stent thrombosis at the 28th month after double-stenting, which was correlated with the discontinuation of dual antiplatelet agents.
Conclusions
These results show a relatively good midterm results of endovascular treatment for intracranial restenosis. More clinical experience is warranted.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):136.
Purpose
Early arterial recanalization is crucial to the treatment of acute ischemic stroke. Intravenous tissue-plasminogen activator (IV t-PA) is known as the primary treatment method, however, its recanalization rate is not satisfactory and additional treatment modalities are needed. The authors report early clinical experience of emergent primary stenting after IV t-PA in patients with acute ischemic stroke.
Methods
From January 2009 to June 2009, 11 patients (M:F = 10:1, mean age 61.9 with a range of 47 to 73) underwent emergent primary stenting after IV t-PA to treat acute ischemic stroke. IV t-PA was given within 3 hours after ictus in all patients. Cervical carotid occlusion was identified in three patients, tandem occlusion (cervical carotid with MCA and V4 with basilar tip) in two, basilar artery in two, ICA terminus in two, V4 in one, and MCA in one. Initial, 30-day, and 6-month clinical outcomes were assessed using NIHSS score and modified Rankin scale (mRS).
Results
Stent placement was successful in all patients. Ten patients gained successful (TIMI 2 or 3) recanalization and one patient (ICA terminus occlusion) achieved partial (TIMI 1) recanalization. In the two patients with tandem occlusions, thrombi in the distal occluded lesion autolyzed shortly after stent implantation in the proximal occluded site. 30-day and 6-month clinical follow-up results exhibited good neurologic outcomes (mRS ≤3) in nine patients, but two patients (one with basilar artery occlusion and the other with ICA terminus occlusion with TIMI 1) remained severely disabled.
Conclusion
In this study, emergent primary stenting after IV t-PA was a feasible and effective therapeutic modality to treat acute ischemic stroke. Although our early results are promising, more clinical experiences are warranted.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):137.
Purpose
The true pathomechanism of hemorrhage in cerebral cavernoma is still to be elucidated. Bleeding cavernomas occurred in our three patients with dural arteriovenous malformation (DAVM) within the subsequent interval during follow up imaging following the treatment of DAVM. Therefore, a retrospective review and literature search have been conducted to find out the possible pathomechanism of bleeding frm cavernoma.
Method
A retrospective review of three patients with DAVM who were referred to interventional neuroradiology service from year 2003 to 2009 with subsequent studies showing bleeding cavernomas was performed. Medline and literature search also have been conducted.
Results
Bleeding cavernoma is known to often co-exist with the developmental venous anomaly (DVA) in approximately 30%, although the pathogenesis of bleeding cavernoma is in a matter of debate. Dural arteriovenous shunts are invariably recognized as a cause of cerebral venous hypertension due to draining disturbance of the other veins into dural sinuses. Consequently, functional venous out flow impairment may occur resulting in the brain suffering from the devastating hemorrhagic venous infarction. In our series, DAVM at the posterior cranial fossa is the primary presentation of all the three cases. All cavernomas existed in the cerebellum, either hemispheric sides or vermis which are seen in the follow up MRI studies. All of the cavernomas appeared hypersignal in T1 and invariably hypersignal in T2 with the hypointense T2 rim which were not apparent in previous MR imaging. We also found transcerebellar DVAs as coincidental findings in two cases. There are two symptomatic cases which ataxic gait being the patient's deficit. Increase venous pressure in DAVM, venous flow imbalance and outflow restriction could be one of the pathomechanism of cerebellar cavernoma hemorrhage.
Conclusion
Although, the true cause of bleeding cavernoma and its association with the dural arteriovenous malformation are unknown, flow imbalance and venous outflow restriction could play important roles of the bleeding cavernoma. For better understanding and proper management, further study of pathomechanism are needed.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):138.
Objective
Cerebral aneurysms which cause third cranial nerve (CN) palsy, are frequently found with a daughter sac or lobe from the dome of the aneurysm. When the daughter sac is located at the very distal part of the dome from the neck, we can assume that the third CN might be compressed by the daughter sac. We thought that it would be more helpful not to fill the daughter sac with coils than vice versa, during endovascular embolization for recovering from third CN palsy, because it may give a chance for the daughter sac to shrink by itself later. We reviewed the long-term results of our initial experience of such cases.
Materials and Methods
Out of a series of 255 cerebral aneurysms treated endovascularly in our institution, 9 (8 unruptured, 1 ruptured) were accompanied by third CN palsy. All of the aneurysms were found in the distal internal carotid artery and most of them (7/9, 6 unruptured, 1 ruptured) showed a daughter sac which was expected to compress the third CN on the pre-embolization angiogram. During embolization we tried to fill the main dome completely and tightly and spare the daughter sac from coil filling to increase the possibility of decompression. We evaluated the long- term effectiveness of this concept using medical records and angiograms.
Results
For the 7 aneurysms with daughter sacs, we used a single microcatheter in 1 case, double microcatheter in 5, and stent-assisted technique in 1 for coil packing. After initial embolization, all of the third CN palsies caused by unruptured aneurysms (6/6) were resolved completely after variing periods (1 day ~ 2 months) of time. No adverse effects were noted during and after the procedures except for one case of harmless coil stretching during coil filling using double microcatheter. During the follow-up periods (6 unruptured, 5 ~ 26 months, mean 16.2 months), no recurrence of third CN palsy was detected but one patient who showed mild compaction of coil mass at the 6-month follow-up MRA underwent re-embolization under local anesthesia. The patient with the ruptured aneurysm (1/1) died 2 months later due to medical problem without improvement in third CN palsy.
Conclusion
During the coil embolization of the cerebral aneurysm causing third CN palsy, sparing the daughter sac from coil packing while tightly packing the main dome, can be helpful in increasing the effectiveness of decompression.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):139.
Purpose
To demonstrate the changes of regional cerebral blood volume (rCBV), regional cerebral blood flow (rCBF) and mean transit time (MTT) in patients with unilateral extracranial and intracranial arterial occlusion using brain CT perfusion.
Methods
Twenty four patients with CT angiography documented unilateral intracranial arterial occlusion (n=10, aged 61.9±13.2 years, range 40-78 years) and unilateral extracranial internal carotid occlusion (n=14, aged 61.0±9.8, range 44-77 years) were selected retrospectively. Visual analysis of images of CBV, CBF and MTT map were applied and regions of prolonged MTT mapping were determined by two neuroradiologists through consensus. All perfusion data in chosen regions were compared to those on their mirror sites in each group by the Wilcoxon signed rank test. Regional cerebral blood volume ratios of lesion sites to mirror sites were obtained in both patient groups. Hypoperfusion or decreased rCBV ratio was defined as a rCBV ratio less than or equal to 0.8. The analysis of group differences in the perfusion parametric ratios was carried out by means of the Mann-Whitney U test.
Results
Increased MTT and decreased rCBF values were observed in both patient groups (P< 0.001), but reduced rCBV values were not significant (P> 0.05). All six patients with decreased rCBV are due to intracranial arterial occlusion. The difference of decreased rCBV ratios in these two groups is significant with P value of 0.0104. Vascular occlusion results in prolonged MTT and decreased regional CBF value in both patient groups.
Conclusion
These findings are in accordance with current concept that MTT and CBF are more sensitive indicators to identify the extent of regional abnormalities on perfusion. Although the decrease of regional CBV value is not statistically significant in each group, decreased regional CBV ratios are significant in patients with intracranial arterial occlusion. This may suggest that CBV is less affected by extracranial internal carotid artery occlusion than intracranial artery occlusion.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):140.
Purpose
To report long-term clinical and angiographic outcomes of stenting for patients with symptomatic intracranial stenosis using drug-eluting stents (DES) versus bare metal stents (BMS).
Materials and Methods
Between May 1998 and Sep.2008, stent-assisted angioplasty was performed on 179 patients (mean age:63.2 years) with 196 symptomatic intracranial stenosis (MCA:61, ICA:75, VBA:60). DES were used in 33 of the total 196 cases (MCA:17, ICA:4, VBA:12). The DES sizes used were 2.25mm in six, 2.5mm in 24, and 2.75mm in three cases. We retrospectively analyzed the technical success, procedure-related complications, clinical and angiographic outcomes between two groups.
Results
Technical success was achieved in 100% for the DES and in 95.1% for the BMS. The 30day and periprocedural complication rate was 9.1% in the DES and 4.5% in the BMS. Angiographic follow-up was available in 19 of 33 cases for the DES (range:3-37, mean:10.7months) and in 75 of 155 cases for the BMS (range:3-55,mean:13.3months). Restenosis rate was 0% in the DES and 17.3% in the BMS (28.6% in cases less than 3mm in diameter and 7.5% in cases equal to or more than 3mm in diameter).Clinical follow-up was available in 33 patients for the DES (range: 3-42,mean:18.4 months) and 139 patients for the BMS (range: 3-107,mean:41.8 months). Ipsilateral stroke or death rate was 0% in the DES and 2.88% in the BMS. Overall vascular events or death rate was 3% in the DES group and 10.1% in the BMS group.
Conclusion
Stent-assisted angioplasty for symptomatic atherosclerotic intracranial artery stenosis is feasible and safe with favorable long term outcomes .Drug-eluting stents could be recommended for stenotic vessel less than 3mm in diameter.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):141.
Purpose
To evaluate the therapeutic strategies and outcome of patients with cavernous sinus dural arteriovenous fistula (DAVFs)
Methodology
The clinical presentation, angiographic findings, modalities of treatment and clinical outcome of the cavernous DAVFs cases at Ramathibodi Hospital between January 1998 and December 2009 were retrospective reviewed. Within the total of 213 patients with intracranial DAVFs 124 were located at the cavernous sinus (39 male, 85 female). The patients' ages ranged from 8 to 80 years.
Results
A total of 124 cases of cavernous DAVFs patients were evaluated for the clinical signs and symptoms including exophthalmos (74.19%), arterialization of conjunctival veins and chemosis (63.7%), diplopia (18.55%), impaired vision (14.52%), eye pain (12.10%), headache (8.06%), bruit (5.65%), rectus palsy (2.42%), dizziness (2.42%), facial palsy (1.61%), ptosis (0.81%) and hemorrhagic venous infarction (0.81%). Angiography revealed superior and inferior ophthalmic drainage in 92.8%, cortical drainage in 24.19%, and posterior fossa drainage in 7.26% of the patients. Therapeutic strategies were 56.45% endovascular treatment alone (14.52% transarterial embolization and 41.94% transvenous embolization alone (11.29% transvenous coils embolization through the visualized Inferior Petrosal sinus- IPS, 27.42% re-opening IPS embolization, 3.23% tranvenous embolization through facial vein), 16.13% manual eye compression [8.87% partial thrombosis of the cavernous sinus, 7.26% fail transarterial and/or transvenous embolization (included transvenous embolization through facial vein)], conservative treatment (2.42%) and spontaneous thromboses (3.22%), and 22.58% multimodality treatments. Multimodality treatments were the combination of transarterial, tranvenous, eye compression, radiosurgery or conservative treatments. There were 78% successful rate of re-opening IPS transvenous coils embolization, 22% fail re-opening IPS and 2.06% fail transarterial embolization. 99.2% of patients were angiographic ally and clinically cured, 100% closure of the malignant reflux and improvement of the clinical symptoms. In our series there were immediate complication of about 4.84% including 2 recoverd strokes; 2 visual loss; 1 ecchymosis and 1 trigeminal neuralgia.
Conclusions
Endovascular treatment plays major role in treatment of DAVFs. Transvenous embolization is the most successful route and multimodality treatments are useful in the treatment of complicated cases. Cavernous DAVFs with cortical and posterior fossa refluxes should be considered for urgent treatment aiming to close the malignant reflux. Transvenous access of the IPV could be very effective and successful under full venous anatomical analysis and cautious skill.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):142.
Two weeks before admission an otherwise healthy 22 year old woman suffered from severe headaches; due to them she had to come home from school. She took birth control pills.
A CT scan was carried out as there was a question of a subarachnoidal hemorrhage. She was admitted under neurosurgery. MR revealed thrombosis of the deep venous system with bilateral thalamic infarctions and edema of the basal ganglia. At this time she became sleepy and was transferred to our hospital where mechanical thrombectomy with the Merci device (V3, stiff, 3 mm) was used to recanalize the straight sinus and then continual infusion of 1 mg of rtPA per hour for 24 hours. The patient recovered and remained without any neurological deficit in one month follow up.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):143.
Purpose
Simultaneous multiple intracranial carotid injuries (ICIs) following head trauma are rarely referred for treatment and are often fatal. The purpose of the current study was to describe the potential angiographic pitfalls in diagnosis of multiple ICIs and to report the principles of endovascular management in 15 patients with 34 ICIs.
Methods
In the past 12 years, a total of 315 patients with blunt ICIs were referred to our institute for endovascular treatment. Of them, 15 patients (8 men and 7 women) with 34 ICIs were managed by endovascular treatment. Of the 34 ICIs, there were 22 traumatic carotid-cavernous fistulas (TCCFs), 6 traumatic carotid aneurysms (TCAs), 5 meningeal arteriovenous fistulas (MAVFs) and one traumatic occlusion of carotid artery. Transarterial endovascular embolization was performed in 32 ICIs.
Results
Four TCAs, 4 MAVFs and a second hole of the TCCF were missed in early detection by initial cerebral angiograms. The causes of missed early detection of ICIs in angiograms were attributed to occur with TCCFs in the ipsilateral ICA territory due to overlooking (n=4), overlap with nearby carotid artery and/or fistula drains of TCCFs (n=2), steal phenomenon (n=2) and/or a latent period of ICI (n=1). Successful occlusion of 32 ICIs was achieved. On the modified Rankin scale applied in follow-up, 14 patients were assessed as stable clinical status.
Conclusions
Early initial detection of ICIs in cerebral angiograms may be difficult if ICIs occur in the same carotid artery, particularly when they coexist with TCCF. However, as soon as TCCFs are occluded, post-embolization angiograms should be scrutinized to find the potential associating ICIs, and endovascular management should be performed promptly.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):144.
Purpose
To report our experience regarding in-stent restenosis in the carotid arteries with special focus on angiographic morphology , clinical factors contributing to the development of in-stent restenosis, to profile the patients at greatest risk, and to review the treatment modalities evolved from our experience.
Methods
Between July 2003 and August 2007, 245 CAS procedures were performed in 243 patients (172 men and 71 women). Stenting for de novo stenoses was performed in 214 (87.3%) carotid arteries and 31 (12.7%) vessels were treated due to postsurgical restenosis . 76.3% of all patients (n=187), were symptomatic. Patients were evaluated at 3 and 6 months and at 6-month intervals thereafter with duplex ultrasonography. Symptomatic or significant (≥70%) recurrent lesions detected on the ultrasound scan were an indication for further balloon dilation with or without stent placement.
Results
During the follow-up period with a median duration of 821 days (range: 62-1750 days) surveillance for all 245 survivors), there were 10 deaths, all non-procedure related. Stent restenosis (first end point) was defined as more than 30% stenosis and could be detected in 35 (14.3%) patients (.31 after surgery and 4 after CAS). Retreatment was indicated in 16 (6.5%) patients. The 35 lesions with restenosis were differentiated into, 3 types of restenosis. Tandem type restenosis, encountered in (5/35) patients; secondly, the more common type (n = 18/35) was the "in- stent" restenosis. The third type was seen in 12 patients and was localized at the distal end of the stent ("end-stent" restenosis). Interventions, either dilation alone (n=12) or dilation with restenting (n=4) for restenosis were performed with one procedure-related dysphasia that resolved in 30 days. Female sex, hypercholesterolemia, PVD, preprocedural stenosis severity, and carotid artery surgery were considered to be predictors for restenosis that developed serious re-restenosis.
Conclusions
The present study may highlight on a serious restenosis subtype that develope after surgical endarterectomy which could represent a retreatment resistant subtype specially to CAS retreatment.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):145.
P urpose
Safety and gentleness to the vascular wall are required for a guiding catheter, especially in neuroendovascular treatments. Therefore, the new guiding catheter with a highly efficient silicone made balloon has been developed. Here we introduce a feature of this new instrument.
Materials and Methods
As compared with other balloon-catheters, on account of the silicone made balloon, our new catheter called CELLO (Fuji Systems Corporation, Tokyo, Japan) can provide a lot of usefulness; high conformability for fitting to a vascular wall gently, no fragmentation in case of burst although a balloon can be inflated to 16mm-diameter, easy and certain removing of all air. Also there will be a low risk of catheter-induced damage on the vascular wall, because the tip of the catheter is covered fully with a silicon made balloon.
Results
We are developing a various sizes of catheters from 5Fr to 10Fr. The shaft of smaller catheters, such as 5 or 6Fr, is softer and more flexible to be used for occlusion of internal carotid artery and vertebral artery. The larger catheters, such as 9Fr or 10Fr, which have more stability and trackability for cases such a carotid artery stenting or needing proximal common carotid artery occlusion. Moreover, these will be applicable to cases needing percutaneous transluminal angioplasty and thrombectomy.
Conclusion
Our new balloon-catheter, CELLO can be used for wide range of neuroendovascular treatment. This will provide us more surefire and safer procedure.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):146.
Introduction
Percutaneous angioplasty and carotid artery stenting (CAS) is a minimal invasive alternative to carotid artery endarterectomy. But thrombembolic events have to be minimized. Therefore several filter-systems are used to capture the embolic material in the blood stream distal to the site of the procedure to lower neurological complication rates. Although no large randomised trial has been carried out to this issue, there are hints that especially the rate of major strokes associated with the procedure can be reduced by the use of these devices. An important issue is not to increase the complication rate due to additional technical manipulations by using protection devices. Therefore we want to introduce a simple and quick way to retrieve these filters without being obliged to further introduce retrieval devices.
Method
In our institution carotid artery stenting was performed via a 6F flexible catheter system (Envoy, Cordis, J&J), constantly being flushed with heparinized saline (1000 IE heparin/500ml saline). Prior to stenting a filter device (EPI Filterwire) was passed through the stenosis and deployed in the ICA, rarely a 2mm balloon had to be used for predilatation. For stenting carotid Wall stents were used. Once the self-expandable stent is in place, post dilatation with a balloon was performed.
At the end of the procedure the deflated PTA balloon is left in place, just sticking out of the proximal end of the stent. With this guidance by the balloon avoiding a calibre difference or step between catheter and balloon, the stent could be passed easily, because the catheter could not get captured by the mesh of the stent. The coaxial catheter was advanced to the filter device. After stopping the flushing of the coaxial-system to prevent antegrade flow in the catheter, the balloon and the filter were simulanously pulled into the catheter and removed. No exchange of the balloon and no insertion of a retrieval device was needed.
The interventions were performed by the department of Neuroradiology, the patients were hospitalized and examined before and after stenting in the Neurological clinic of our university hospital.
Results
120 patients were intended to treat; it was successful in 117 (97,5%), in 3 patients CAS was abandoned. In 2 patients an ordinary filter removal device was necessary due to aortic elongation. No technical complications occurred. One permanent neurological deficit appeared one day after stenting, most probabely due to heart embolism with small infarctions in the ipsilateral and the posterior circulation, one patients experienced a TIA, one patient suffered MI after stenting and recovered, one patient needed coronary angiography but did not develop MI, no patient died within 30 days (complication rate of death, stroke and MI 2,5 %).
Discussion
Using small flexible coaxial catheters as a retrieval device shortens the intervention time, is easier to perform and increases procedural safety.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):147.
Purpose of Study
The purpose of our retrospective study was to investigate the relationship between MR findings using DWI- ASPCT score on admission and long-term clinical outcome following emergency reperfusion therapy (ERT).
Methods
Inclusion criteria for retrospective analysis were patients 1) who were admitted to our institution during the period from October 2006 to August 2009, 2) who presented serious neurological symptoms of GCS of 12 or less and of NIHSS score of 10 or more, 3) who had total occlusion of intracranial major arteries displayed by MRA on admission, and 4) who underwent emergency intravenous rt-PA or endovascular treatment within 6 hours from stroke onset. We assessed patient's age, sex, DWI-ASPECT score, MRA findings, stroke subtype, onset-to-treatment time (OTTT), mRS before admission, mRS on admission (AD-mRS), mRS on the 10th day, mRS at 3 months (3M- mRS), NIHSS score on admission (AD-NIHSS), NIHSS score on the 7th day (7D-NIHSS), cerebral hemorrhage within 7days from onset, and hospitalization period. According to DWI-ASPECT score, patients were classified into two groups; patients with 8 or more of score into S group and others into L group.We defined good clinical outcome as improving of mRS at 3 months compared to mRS on admission.
Results
Fifty-two patients were included for our analysis. Age (median) was 76 years, twenty nine patients(55.8%) were men, NIHSS score on admission (median) was 19.5, DWI-ASPECT score (median) was 7.5, and OTTT (median) was 3.16 hrs. Among them, 36 patients underwent intravenous rt-PA and other 16 patients endovascular treatment.Three-month investigation showed that there were 9 (17.4%) in mRS of 0 and 1, 15 (28.8%) in mRS of 2 and 3, 13 (25.0%) in mRS of 4 and 5, and 15 (28.8% ) in mRS of 6. Intracerebral hemorrhage occurred in 5 patients (9.6%) within 7 days of onset. Among 52 patients, 26 belonged to S group and others to L group. In group S and L, 7D-NIHSS (median) was 7 and 17 (p<0.01), 3M-mRS (median) was 3 and 5 (p<0.05), the number of patients with good clinical outcome was 20 and 9 (p<0.01), respectively. Logistic regression analysis demonstrated that younger age(OR0.84 95%CI;0.74-0.96 P<0.01), lower point of AD-NIHSS (OR0.87;95%CI;0.77-0.98, p<0.05), and 8 or more of DWI-ASPECT score (OR 0.135 95%CI;0.02-0.90,p<0.05) were the independent predictors of good clinical outcome.
Conclusions
DWI-ASPECT score of 8 or more was the independent predictor of favorable clinical outcome in acute stroke patients who had major intracranial artery occlusion and underwent emergency perfusion therapy within 6 hours.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):148.
Purpose
To report two cases with large vertebral artery AV fistula with marked cervical spinal epidural varix. Because of very high flow shunt of these lesions, we applied technigues in combination (hybrid) including coils, stenting, vascular plug and NBCA embolization to complete preservation or trapping of the vertebral arteries according to each patient's condition.
Summary of Case 1
A 51 year-old female suffered from right side pulsatile tinnitus and right upper limb numbness. MRI and angiogram revealed a right proximal VA large fistula with multiple paraspinal and epidural venous drainage. A small dissecting aneurysm was noted at the distal VA. Embolization was performed by occlusion of the distal dissecting aneurysm and vertebral artery with coils first. A vascular plug (Amplatzer, AGA) was then deployed above the fistula segment in an attempt to trap the VA with coils. But in vain due to very high flow of fistula the undetached coil was pushed into heart. A Zilver stent (Cook) was deployed across the fistula segment of VA to prevent the coils migration and finally the VA was trapped with intra-stent detachable coils and pushable coils. Follow-up angiogram showed complete occlusion of the A-V fistula.
Summary of Case 2
A 35 year-old female presented with neck pain and progressive gait disturbance, weakness and numbness of right limbs. MRI and angiogram revealed bilateral extracranial vertebral artery dissection with a large A-V fistula at the right VA with marked epidural venous drainage causing spinal cord edema due to compression. Stent graft placement was planned to treat the dissection and fistula and preserve both VA. Because of high flow of VA fistula, NBCA intravenous injection was performed to improve the apposition of stent graft and prevent an endoleak. Follow-up angiogram half year later showed complete obliteration of the A-V fistula with patency of bilateral vertebral arteries.
Conclusion
High flow vertebral artery A-V fistula sometimes can't be totally treated by only one method (materials). Combination (hybrid) of coils, stents, NBCA and other occlusion device may be an efficient technique to deal with these lesions.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):149.
Purpose of Study
We report a case of 66 years old woman with diagnosis of dural expansion on magnetic resonance imaging (MRI ) and of dural arteriovenous malformation (AVM) on follow up spinal angiography. Surgical decompression and endovascular treatment were performed. Control MRI showed only lipoma.
Methods
Only five cases of vascular malformation of spinal cord and myeloschizis including myelomeningocele, lipoma or lipomyelomeningocele have been reported in literature. In our case, a 66 years old white woman noted a 4 months history of lower extremity paresthesia progressed to symetric paraparesis. On initial MRI there was described dural expansion in level L1 - L4. Spinal angiography showed spinal dural arteriovenous malformation with Anson-Spetzler classification of conus lesions type I - dorsal intradural arteriovenous fistula. It was supplied by the lumbal arteries and drained by tortuos perimedullary veins. 2 days after neurosurgical decompression endovascular treatment was performed. Through the left L3 artery, a diagnostic cathether, SIM 2 and then a microcathether, Magic 1.2 with microwire Sor 007 were placed. The mixture of Lipiodol - Histoacryl 5 : 1 was used for embolisation. The control MRI after 3 months showed only lipoma in level L1 - 2, the previous AV malformation was completly occluded.
Conclusion
Early diagnosis and good choice of endovacular and surgical treatment in the case of dural expansion combined with arteriovenous malformation were crucial for managment of progressive paraparesis .
interv neuroradiol. 2010 Mar 23;16(Suppl 1):150.
Purpose of Study
Extend of carotid artery stenosis is one of the most important factor in decision about the method of stenosis treatment (medical, surgical endarterectomy or intravascular carotid artery stenting). The preciseness of carotid artery stenosis measurement based on different imaging modalities is compared with histological specimens obtained by endarterectomy.
Material and Method
103 patients with carotid artery stenosis were investigated by digital subtraction angiography (DSA), Doppler ultrasonography (DUS) and magnetic resonance angiography (MRA). Assessment of carotid artery stenosis was performed by each modality. All patients were operated. During carotid endarterectomy (CEA) the whole atherosclerotic plaque was removed in one piece, preserving walls of the plaque. Specimens were fixed with formaldehyde, transversally cut and processed by routine paraffin technique. The minimal diameter and the whole plaque diameter were measured. In all 103 cases the above mentioned measurements were obtained. Comparison of preoperative measurements and histological findings was performed.
Results
Mean differences between preoperative measurements and histological measurement are very interesting: DSA underestimates histological measurement by 14,4 %, MRA by 0,7 % and DUS overestimates by 6,7%. The results in mild stenoses 30 - 49 % are as follows: DSA measurement underestimate histological measurement by 24,7 %, MRA by 7,6 % and DUS overestimates by 3,3 %. The results in moderate stenoses 50 - 69 % are as follows: DSA measurement underestimates histological measurement by 12,3 %, MRA overestimates by 0,2 % and DUS overestimates by 6,3 %. The results in high grade stenoses ≥ 70 % are as follows: DSA measurement underestimates histological measurement by 2,3 %, MRA overestimates by 12,2 % and DUS overestimates by 11,3 %.
Conclusion
Study confirms that: DSA is most accurate in high grade stenose (underestimates moderate and mild carotid artery stenose). DUS is most accurate in mild stenose (slightly overestimates moderate and more significantly high grade stenose). MRA is most precise in moderate stenose (slightly underestimates mild and overestimates high grade stenose). These discrepancies should be aware in decision between medical and surgical/intravascular treatment of carotid artery stenoses.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):151.
Background
Whole brain perfusion CT images have recently been made available in Australia, with Monash Medical Centre acquiring the first such scanner. In this study we described our initial experiences with this new CT scanner.
Method
We used a 320 multirow detector Toshiba CT scan to obtain whole brain perfusion images in patients with cerebrovascular diseases. This type of scanning has the advantage of simultaneously acquiring dynamic CT angiography and CT perfusion images in one bolus contrast injection. In this mode, 19 frames were acquired in less than 60 seconds. The voxels have dimensions of 0.5 mm x 0.5 mm x 0.5 mm in all directions. The CT perfusion images were analysed using deconvolution method (PMA software).
Results
We analysed the CT angiography and perfusion images in selected patients with cerebrovascular diseases to illustrate the utility of this form of imaging. The images provide excellent anatomical data on the arterial and venous phase of the cerebral circulation. The studies illustrated perfusion deficit in a patient with ischaemic stroke, venous occlusion and perfusion deficit in a patient with venous stroke, perfusion deficit from vasospasm in aneurysmal subarchnoid haemorrhage and Sturge Weber syndrome
Discussion
Whole brain perfusion images and dynamic angiography data can be obtained on CT scans. These images provided invaluable functional and anatomical information on patients with cerebrovascular diseases.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):152.
Background
There is recent interest in the role of carotid bifurcation anatomy, geometry and hemodynamic factors in the pathogenesis of carotid artery atherosclerosis. Investigators have drawn parallel between certain anatomical and geometric configuration at the carotid bifurcation and its exposure to disturbed flow. An intriguing idea is that the vascular dimensions of the intracranial carotid artery may be optimally designed such that there is minimum work to maintain blood and pump it through a vascular system. It has been proposed that this occurs when the exponent power relationship between the radii of the parent artery and the daughter arteries is 3. In this study, we evaluate if the dimensions of bifurcation of the extracranial carotid artery follows this principle of minimum work.
Methods
This study involved subjects who had CT angiography at Monash Medical Centre between 2006-2007. Subjects with luminal stenosis > 30% were excluded. Following segmentation of the carotid artery, the radii and areas of the common carotid/parent artery and the two daughter arteries (internal and external carotid arteries) were determined. A non-linear equation solver was used to determine the optimum value of power n.
Results
When the equation was solved for radius, the value of n ranged from 1.4 to 1.8.
Conclusion
Our findings indicate that the principle of minimum work (as defined by power n of 3) may not apply at the carotid bifurcation and may suggest that additional factors play a role in the relationship between the parent and daughter vessels radii.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):153.
Background
The correlation an difference between penumbra and regional risk of infarction in MCA stroke has been described only in terms of volume but not at a voxel level. In this study we investigate the differences between maps of penumbral region and infarcts in the MCA territory.
Method
64 multirow detector CT scan was used to acquire 8 cm coverage of the brain in the vertical dimension. Twelve patients, with middle cerebral artery (MCA) occlusion, were studied within 6 hours of stroke onset. Penumbra voxels were defined as voxels > 4 sec on mean transit time (MTT) map and <2.5 ml/100 g on cerebral blood volume (CBV) map. MCA infarct was defined on FLAIR images in patients with MCA occlusion. The difference between the Penumbra and the Infarct map at a voxel level was calculated using the Fisher exact test and Z score. The Fisher exact map provides an index of probability of the difference between the two maps. The Z score map provides a normalised distance between the Penumbral and Infarct maps at a given voxel
Results
Perfusion abnormalities within the MCA territory were heterogenous, reflecting the different regions at higher risk of ischaemia. The Penumbral and Infarct maps provide complementary information on the differences between Penumbra and Infarct maps. These maps show that deep compartment of the MCA territory has lowest probability (<0.0001on Fisher exact test) of being penumbra tissue and that certain parts of the superficial compartment has high normalised distance (Z score > 2) between penumbra tissue and the risk of infarction.
Discussion
The Fisher exact probability map and the Z score map may be useful determining the significance of Penumbra voxel.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):154.
Purpose
To compare the quality of immediate anatomical results after the endovascular treatment of ruptured aneurysms using GDC and Matrix coils in CLARITY series.
Methods
Postoperative anatomical results were evaluated on DSA, anonymously and independently by two experienced neuroradiologists. Two different scales were used: the Montreal scale and a new scale specifically designed for the present study (Clarity scale).
Results
401 aneurysms were treated using GDC coils and 373 using Matrix coils. Immediate anatomical results (Montreal scale) were not significantly different with GDC or Matrix coils. In GDC group, result was complete occlusion for 197 aneurysms (49.1%), neck remnant for 155 aneurysms (38.7%), and aneurysm remnant for 49 aneurysms (12.2%). In Matrix group, result was complete occlusion for 168 aneurysms (44.9%), neck remnant for 171 aneurysms (45.7%), and aneurysm remnant for 35 aneurysms (9.4%). Similar results were obtained using Clarity scale. The factors affecting the quality of aneurismal occlusion have been studied in both GDC and Matrix groups.
Conclusions
The postoperative occlusion after endovascular treatment of ruptured aneurysms is satisfying with a high percentage of complete occlusion or neck remnant in both GDC (87.8%) and Matrix (90.6%) groups.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):155.
Purpose
To evaluate the clinical results of the endovascular treatment of ruptured intracranial aneurysms using GDC and Matrix coils.
Materials and Methods
A prospective, multicenter registry was conducted in France from October 2006 to June 2007 in 19 neurointerventional centers to compare the endovascular treatment of ruptured aneurysms with GDC and Matrix coils. 405 patients were treated with GDC coils and 377 with Matrix coils.
Results
Endovascular treatment failed in 3/405 cases (0.7%) in GDC group and in 2/377 cases (0.5%) in Matrix group. Adverse events related to the treatment were encountered in 71/405 patients (17.5%) in GDC group and in 68/377 patients (18.0%) in Matrix group. Thromboembolic events were encountered in 54/405 patients (13.3%) in GDC group and 45/377 patients (11.9%) in Matrix group, intraoperative rupture in 15/405 patients (3.7%) in GDC group and 19/377 patients (5.0%) in Matrix group, and early rebleeding in 2/405 patients (0.5%) in GDC group and 4/377 (1.1%) in Matrix group. Finally morbidity and mortality of the treatment were respectively 4.0% (16/405) and 1.5% (6/405) in GDC group and 4.0% (15/377) and 1.3% (5/377) in Matrix group.
Conclusion
Clarity study demonstrates that the immediate safety of the endovascular treatment of ruptured intracranial aneurysms using GDC and Matrix coils is similar with low morbidity and mortality with both types of coils.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):156.
Background
Juvenile Paget Disease (JPD) is a rare genetic bone disorder, also affecting the immune and vascular systems. We describe the first ever case of JPD associated with bilateral giant cavernous carotid artery aneurysms in a child and the treatment for this condition using both endovascular and neurosurgical bypass techniques.
Purpose of Study
Description of an association between osteoprotegerin and its involvement in cerebral aneurysm formation as described in a young child with juvenile Paget disease
Case Description
A child with known JPD presented with left abducens nerve palsy and a CT angiogram revealed bilateral giant cavernous carotid artery aneurysms. He underwent a left sided superficial temporal artery to middle cerebral artery bypass and endovascular carotid artery occlusion, followed by an identical procedure on the right side 3 months later and made an event-free recovery without any new neurological deficits.
Conclusion
This previously unreported association poses the question of determining the optimal management strategy for such cases. The pathophysiology and clinical features of JPD are discussed, with special emphasis on the management of giant cavernous carotid aneurysms in this sub-group of individuals and also gives insight in the treatment of bilateral giant carotid aneurysms in children and the various modalities of treatment available.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):157.
Purpose of Study
To evaluate vessels recanalization and clinical outcome in severe acute stroke patients after thrombolysis therapy and balloon angioplasty
Methods
11 patients with acute major arterial occlusion January 2008 – August 2009 were included. All patients were confirmed by preliminary CT Angiography. Vessels recanalization was defined as TIMI (Thrombolysis in myocardial infaction) grade 2 to 3 flow. Outcomes were categorized using modified Rankin Scale (mRS). Follow up CT Angiography was performed in all cases.
Results
Patients age range 52-75 years, range of National Institutes of Health Stroke Scale (NIHSS) score was 13-23. The occlusion sites were: internal carotid artery (ICA) terminus (four patients), M1 segment (five patients) and basilar artery (two patients). Thrombolysis therapy included intravenous (IV) t-PA and intraarterial (IA) Streptokinase (one patient), IV and IA t-PA (eight patients) and IA t-PA only (two patients). Range time to treatment was 2.5 to 8 hours. There was no procedure related morbidity. Overall recanalization rate (TIMI grade 2 to 3) was 90.9%. Follow up CTA confirmed patency of all the recanalized vessels. There were 2 asymptomatic hemmorrhage (hemmorhagic infarction HI type I). Outcome at 90 days were independent (six patients) and dependent (four patients). One dead was due to pulmonary emboli event.
Conclusion
Combined balloon angioplasty and thrombolysis therapy is an effective and safe treatment modality, and produce high recanalization rates with better outcomes.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):158.
Purpose: Case report
Methods
A 52-year-old woman presentied with headache and vertigo. During investigations she underwent a brain CT scan that showed a right occipital mass suggesting either a meningioma or a vascular lesion. Angiography was performed and a tentorial fistula was found. This fistula was fed by petrosal branches of the middle meningeal and occipital arteries which drained into a huge venous pouch that later emptied into the right sigmoid sinus. An embolisation was subsequently performed with Onyx via boththe middle meningeal and occipital arteries. A complete occlusion of the fistula was achieved with almost no contamination of the huge pouch. The patient woke up well, without any focal deficits.
Results
In the 5th day after treatment she went into an abrupt coma. CT scan showed thrombosis of the venous pouch surrounded by edema. The patient underwent surgical resection of the thrombosed pouch and progressively recovered, although there is residual paresis of the left arm and a left hemianopsia.
Conclusion
In such cases should post embolisation surgical resection be anticipated or wouldsimple anti-coagulation be enough to prevent these acute venous thrombosis?
interv neuroradiol. 2010 Mar 23;16(Suppl 1):159.
Introduction
To evaluate the safety and efficacy of multimodal treatment of symptomatic vasospasm after aneurysmal subarachnoid hemorrhage
Methods
Between March 2007 and November 2009, a total of 116 ruptured cerebral aneurysms were treated. 22 (18.9%) patients developed symptomatic cerebral vasospasm; 17 in the clipping group) and 5 in the coiling group. All patients were treated by therapeutic Triple H therapy and endovascular treatment. .
Results
Ninety two procedures were performed in 22 patients (balloon angioplasty in 14 sessions, IA chemical angioplasty in 77 sessions).
In cases of refractory vasospasm after IA chemical angioplasty, we performed balloon angioplasty in 14 sessions. Clinical improvement after endovascular treatment for symptomatic vasospasm was observed in 22 (100%), of whom 19 improved dramatically. One patient expired. After follow-up at 3 months, 19 (90.1%) of the 21 patients had a favorable outcome (modified Rankin scale of 0-2).
Conclusions
Multimodal treatment with IA chemical and balloon angioplasty is an effective and safe method for the treatment of symptomatic vasospasm after aneurysmal subarachnoid hemorrhage.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):160.
Purpose of Study
Orbital lymphatic-venous malformation (LVM) is rare and successful treatment of orbital LVM has eluded the physician until now. We report three cases of orbital LVM - all of the patients have clinically improved and significant lesions size regression after percutaneous intralesional bleomycin injection.
Brief Statement of Methods
Three cases, who have been diagnosed as orbital LVM, two have received surgical treatment in vain and vision loss of their affected eyes, one with normal visual acuity but poor eye movement. After diagnostic angiography to rule out abnormal high flow arteriovenous shunting within the lesions, fluoroscopic guided percutaneous intralesional bleomycin injection (10mg/10mL) were accomplished under general anesthesia.
Summary of Results
All the patients have clinically improved after 3 weeks. The lesions size were significantly regressed and elucidated in the follow-up imaging. The patient with normal visual acuity was preserved and the affected eye movement was improved.
Conclusion
Percutaneous bleomycin sclerotherapy can be used as one of the treatment alternatives encountered with orbital LVM because it is relative safe, effective and less impairment to the vision.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):161.
Purpose
The purpose of this study is to analyze the clinical presentation, morphological characteristics, angioachitecture, and outcome of veretbrobasilar artery dissection in the pediatric population.
Methods
We retrospectively reviewed 29 consecutive children (less than 16 years old) diagnosed with symptomatic vertebrobasilar artery dissections (sVBAD) according to the patient's age, gender, clinical history, associated underlying disease, symptoms (headache, vertigo), location of dissection and imaging appearance.
Results
Mean age was 8.24 years (range 2months-15 years), there was an overall 3:1 male predominance, however, in children older than 8 years, girls and boys were similarily affected. Hemorrhagic dissections occurred in 10/29 cases. In non-hemorrhagic dissections stroke occurred in 16 cases with the most common presenting symptoms being headaches and vertigo, in the final three patients, mass effect due to a chronic dissecting aneurysm was present. In 7 children an underlying vessel wall disease was found. Locations of the dissections were extradural in 11 cases and intradural in the remainder, there was no preference of one side, the basilar artery was affected in 9 patients.
Conclusions
sVBAD have a different imaging and clinical appearance in the pediatric population compared to adults. Boys are more often affected, esp. at a younger ages, and hemorrhagic presentation is more common, owing presumably to the fact that the basilar artery is more commonly involved. Depending on the underlying pathomechanism of the dissection, different clinical symptoms will evolve necessitating an individually tailored treatment.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):162.
Purpose
We analyzed the impact of anatomical variations of the parent arteries on the incidence and recurrence rate following coiling of aneurysms of the anterior (AcoA), posterior communicating artery (PcoA) and basilar tip (BA).
Methods
202 (96AcoA, 67PcoA and 29BA) aneurysms in 200 patients were treated with coiling between January 2000-April 2008. Parent artery variations at each location were classified as: AcoA: A1-aplasia vs. hypoplasia vs. symmetrical size; PcoA: fetal origin vs. medium vs. small size, BA: cranial vs. caudal vs. asymmetrical fusion. Incidence of aneurysms and difference between recurrence rates for each group were recorded on follow-up.
Results
AcoA, PcoA and BA-aneurysms were more often associated with embryonically earlier vessel wall dispositions (A1-aplasia, fetal PcoA, asymmetrical fusion). Two of these variations were also associated with aneurysm recurrence following coiling: asymmetrical A1 segment (P=.01), and asymmetrical BA tip (P=.02).
Conclusions
AcoA, PcoA and BA tip aneurysms tend to occur more often in anatomically variant parent artery dispositions, some of which are related to aneurysm recurrence following coiling. This may relate to embryologically younger and therefore less mature vessel dispositions or to altered hemodynamics secondary to the anatomical variations.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):163.
Background and Purpose
Intracranial stenting has been applied in acute ischemic stroke as a rescue regimen although a significant rate of symptomatic intracranial hemorrhage due to antiplatelet therapy. Recently there are some case reports about 'temporary endovascular bypass technique' using a self-expandable stent for therapy of acute ischemic stroke, which recanalized an occluded intracranial artery without stenting. The purpose of this study is to evaluate feasibility, efficacy and safety of temporary endovascular bypass technique for treatment of acute ischemic stroke using a self-expandable stent.
Methods
All patients who were treated with temporary endovascular bypass technique for acute ischemic stroke were included. All the procedures consist of temporary stenting and retrieval of a self-expandable stent with intraarterial thrombolytics. Recanalization was evaluated with post-procedural angiography immediately after the procedure. Complications related to the procedure and outcome at 3 months were assessed.
Results
Ten patients (median NIHSS 13, mean age 65 years, male: female=5:5) were treated with temporary endovascular bypass technique for acute cerebral artery occlusion. Occlusion segment were located in the anterior circulation (n= 6) and the posterior circulation (n= 4). This procedure was feasible in all the patients and achieved in partial or complete recanalization (TIMI 2/3) in 90%. There was no complication related to the procedure. Nine patients (90%) had a good outcome (mRS 0 to 2) and one patient (10%) a poor outcome (mRS 4 to 6).
Conclusion
Temporary endovascular bypass technique is feasible and may be safe in treatment of acute embolic cerebral artery occlusion.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):164.
Purpose of Study
Despite of approved safety, various reports agree on minor technical failure rate of Perclose® Proglide™ Suture- Mediated Closure system(Abbott Vascular, IL, USA). The purpose of this study is to decrease the failure rate of Perclose® system after neurovascular procedures via femoral artery. The efficacy of new innovative method of ours, namely "Four hands halo technique", is evaluated.
Brief Statement of Methods
From June to October 2009, total 310 cases of neuro-angiography were performed. Besides manual compression and other closing devices, in 152 cases, Perclose® system was used for hemostasis. Retrospective review of manufacturer's original method revealed most of failure and complications were related to inexact tension onto the femoral puncture site. The new "Four hands halo technique (FHHT)" was introduced to reduce impingement of soft tissue during needle sting-docking stage of Perclose®. Briefly, at the stage of introduction of Perclose® system into femoral artery by the operator, the assistant retracted and widened the skin and soft tissue of puncture site. Just before sting-docking procedure, both of them double checked complete free margin around puncture site, namely "halo". The first author started this FHHT since 2009 September. We compared the failure rates between traditional technique (TT) of manufacturer's recommendation and new FHHT method.
Summary of Results
The TT was used in 87 cases and failure was occurred in 11 cases (12.6%). Among them, 2 cases were related to innate faulty instrument problem and beginner's error, respectively. Remaining 9 cases (10.3%) were caused by sting-docking failure, docking removal failure or loose knot. Impingement of soft tissue was primary reason. To exclude individual technical bias, the cases performed by first author were selected separately and the failure rate of TT and FHHT were 5/78 (6.4%) and 0/65 (0%), respectively.
Conclusion
Impingement of soft tissue can elicit failure of Perclose® system with the incidence of 6-10%. Operator and assistant co-work, namely Four hands halo technique (FHHT) can decrease this failure rate.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):165.
Purposes
Percutaneous vertebroplasty usually is performed under local anesthesia and light neuroleptic sedation. Sometimes, the patient became more and more anxious during the procedure, especially when several vertebral bodies are to be treated in one session. We evaluated the clinical application of epidural anesthesia for percutaneous vertebroplasty.
Methods
The preparation including scrub of skin and draping was the same as percutaneous vertebroplasty. We used a lumbar puncture needle to do epidural anesthesia, under bi-plane fluoscopic monitoring. We studied the curvature of the spine, and decide which level of interspace is best to achieve anesthesia for levels of vertebral body to be treated.
Summary of Results
We performed epidural anesthesia for 15 patients in the past half a year. Levels of vertebral bodies treated were in the lower thoracic and lumbar regions. After a needle entered the epidural space, contrast media was injected to confirm its location and to see contrast media spreading. Then we injected IV form of xylocaine 2.5-5cc according to scope of spreading in the epidural space. The effect of anesthesia began about 5-15 minutes in most patients. Therefore, we did not need to give local anesthesia for the 2nd vertebral body and later levels to be treated. Two patients had temporary paraplegia most likely due to intradural leakage of xylocaine. Five patients had drop in BP, four of these rapidly recovered after intravenous fluid replacement. One of these five had severe BP drop to 50mmHg systolic, associate with nausea, cold sweating, temporary loss of vision, paraplegia and nervous extremely. The condition improved after intravenous fluid replacement and legs raising.
Conclusion
Epidural anesthesia may be helpful for percutaneous vertebroplasty. However, avoiding intradural leakage of anesthetics and being ready for control of BP drop are necessary.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):166.
Purpose
To present an unusual method to retrieve a stretched coil by advance of the microcatheter in embolization of a case of traumatic carotid-cavernous fistula (CCF).
Summary of Case
A middle-aged female suffered from a traffic accident and traumatic intracranial hemorrhage was noted in the initial brain CT scan. Eyelid swelling and ecchymosis were noted during the hospitalization and bilateral direct CCFs were diagnosed by angiography. Endovascular embolization for CCFs was requested. During the embolization of one side CCF, coil stretching was noted while retrieval a suboptimal-sized coil (Boston Scientific). Part of the stretched coil located in the cavernous sinus and residual part of the coil remained in the microcenter. The attempt to withdraw the stretched coil alone or to withdraw the coil and the microcatheter as a unit was failed. The coil was still in the same location and dislodgement of the microcatheter tip into the parent internal carotid artery was noted. By careful advance of the microcatheter using the stretched coil as a microguidewire, the tip of microcatheter was repositioned into cavernous sinus until the whole stretched coil was retrieved in the microcatheter. Then the whole unit was withdrawn.
Conclusion
There are several ways to manage the stretched coils and the coils may be retrieved. However, the time and complexity of procedure increase in dealing with coil stretching. Prevention of stretching is a better strategy.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):167.
Propose
To evaluate the natural history, imaging features, treatment strategies and outcomes of intracranial giant aneurysms
Methodology
A retrospective review of 24 collected cases of giant intracranial aneurysms (external radial dimension diameter equal or more than 25 millimeters) at Ramathibodi Hospital between July 2002 to December 2009(6 males; 18 females; mean age: 52 years; range 19 to 73 years), in terms of aneurysm locations, presenting symptoms, noninvasive and angiographic imaging features, associated pathologies, therapeutic methods, complications, and clinical outcomes.
Results
Twenty four giant aneurysms were found; the locations were cavernous ICA (42%), basilar artery (25%), supraclinoid ICA (12.5%). vertebral artery (12.5%), MCA bifurcation (4%), trigeminal artery (4%). Three different mechanisms of primary presenting symptoms were found; localized mass effect to adjacent structures (83.3%), ischemia (12.5%) and aneurysmal rupture (8.3%). The symptoms related to aneurysm mass effect were cranial nerve dysfunction, dementia, headache, hemiparesis and ataxia. The aneurysm features found were partial thrombosis (71%), calcified wall (37.5%), swelling of adjacent brain (21%). Angiographically the aneurysms patent lumen morphology was saccular (46%), fusiform (37.5%), and serpentile (4%). Spontaneous complete thromboses of the aneurysm lumen angiographically were found in three cases, two at the time of first diagnosis and one after three years of follow up. The treatment strategy and clinical outcome history were unretrievable in four cases. The treatment strategies were endovascular aneurysmal coiling (7 cases), balloon sacrifice of the parent artery (2 cases), surgical aneurysmal clipping and aneurysmectomy (4 cases), conservative treatment (7 cases) by steroid, antiplatelet and surgical ventriculostomy. One of the two cases of aneurysmal rupture died from massive subarachnoid hemorrhage despite adequate coiling of the aneurysm. The remaining eight cases treated endovascularly and four cases treated surgically showed clinical improvement within one to six months. Recanalization of the coiled aneurysm was found in only one case. Two treatment complications were found, watershed infarction after balloon sacrifice of the patent artery and propagation of clot from the cavernous ICA aneurysm into the more distal artery after surgical clamping of the patent artery.
Conclusion
Intracranial giant aneurysms carry a variety of natural history; mostly the symptoms are from the mechanism of aneurysm mass effect. Endovascular treatment either aneurysmal coiling or parent artery sacrification when feasible has a high successful rate and good outcome.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):168.
Background
Therapeutic external beam irradiation is frequently used as first-line treatment of head and neck malignancies. This is especially true for nasopharyngeal carcinoma (NPC) which is prevalent in South East China. Among several complications associated with irradiation, carotid artery steno-occlusive disease is a significant cause of morbidity and mortality. The purpose of this study is to compare the clinical presentation as well as the radiological features of critical carotid artery stenosis between patients previously exposed to external beam irradiation and those without. In addition, comparisons of the following outcomes: post-stenting re-stenosis, added neurological deficit and National Institutes of Health Stroke Scale (NIHSS) were made.
Methods
This is a retrospective observational study of 72 patients (56 male, 16 female with mean age of 66 years) who were diagnosed to have critical carotid artery stenosis from August 1999 to September 2009 at Hong Kong's largest neurosurgical centre. The mean time of follow-up was 53 months. Carotid arterial stenting was done in 69 patients with a total of 99 stents deployed. 58 patients were analyzed of which 25 patients had previously received cervical radiotherapy (RT) for treatment of head and neck malignancies (21 patients had NPC). The mean cervical RT dose was 42 Gy and the mean duration from RT-to-carotid stenting was 18.6 years.
Results
Patients with critical irradiation induced carotid artery stenosis were more likely to be younger than 60 years old compared with those patients who did not receive previous RT (p= 0.005). There was no significant difference in clinical presentation (e.g. carotid bruits, ischemic stroke) between those who were exposed to RT and those who were not (p=1.75). Angiographically, there was no difference in the degree of carotid stenosis as measured by the North American Symptomatic Carotid Endarterectomy Trial (NASCET) method (p=0.69). However, RT exposed patients had more extensive longitudinal arterial involvement (p<0.05) and the stenosis was predominantly located in the sub-bifurcation segment of the common carotid artery (p=0.001). There was no difference in outcomes between the two groups in terms of post-stenting re-stenosis, added neurological deficit and NIHSS score. Among RT exposed patients logistic regression analysis revealed that a time interval of > 15 years from RT- to-stenting was an independent clinical factor (p<0.043) and bilateral disease was an independent angiographic factor (p<0.046) for re-stenosis.
Conclusions
Most patients treated in this centre with irradiation-induced carotid arterial stenosis have a history of NPC and are relatively young. For these patients the time interval from RT-to-stenting and bilateral disease are independent risk factors for re-stenosis.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):169.
Purpose
To evaluate the rebleeding rate and time distribution of aneurysmal SAH.
Materials and Method
From June, 2007 to May, 2009, total 158 consecutive patients underwent four-section CT angiography in the emergency room of our hospital, a tertiary refer center. The indications in most cases are severe explosive headache with or without conscious change and SAH in the plain CT presumed to be aneurysm rupture. The patients with aneurysmal SAH confirmed by angiography or consensus by two neuro-interventionalists are included. Active bleeding as contrast extravasation and the hematoma volume difference between the plain and postcontrast enhanced CT scans are reviewed.
Results
According to the inclusion criteria, total 84 patients of which had 101 aneurysms are included. Among them, three patients with contrast extrasavation and three patients with hematoma progression (maximal diameter change > 3mm between the plain and postcontrast CT scans) are found. The average time interval between plain CT and CTA is 47 minutes (8-83 minutes). The location of re-ruptured aneurysm are three in middle cerebral artery, two in anterior communicating artery and one in intradural VA. The clinical outcome of hemorrhagic events are 3 deaths, one modified Rakin scale(mRS) 5, one mRS 3 and one mRS 2.
Conclusion
Rebleeding rate of aneurysmal SAH in the hyperacute stage < 2 hours is 7.1% per patient and 5.9% per aneurysm with dismal prognosis in this case series.
interv neuroradiol. 2010 Mar 23;16(Suppl 1):170.
Purpose
The aim of the study is to introduce a new strategy in the endovascular treatment of ruptured small intracranial aneurysm
Methods
From 2008 to 2010, we use the coil assisted method in the treatment of ruptured small intracranial aneurysm. Total three patients suffered from ruptured small (<3mm) intracranial aneurysm with SAH presentation. All patients were female patient, ranged from 40-60 years old. Standard endovascular treatment was offered and difficult to put the small coils within the aneurysm due to easy herniated into the parent artery. One basket coil (complex coil) was put into the parent artery at the aneurysm level to enhance the coil stability and safety.
Results
All three procedures were done smoothly without any procedure related complication. The initial easy herniated ultrasoft coil was put into the aneurysm sac successfully with help of neck bridge effect from the complex basket coil in the parent artery. The embolized coils were the ultrasoft coil (Boston Sci) and the neck bridge coils were the complex coil (Microvention).
Conclusion
The coil assisted single coil embolization is the easy and feasible technique in the treatment of ruptured small intracranial aneurysm when the coil was difficult to put into aneurysm sac successfully.