Abstract
Arachnoid cysts are the most common incidentally discovered intracranial lesions on imaging and the most common cystic intracranial lesions. They may be developmental or secondary. A relative lack of recent literature and any comprehensive radiological review on arachnoid cysts has led to a general lack of awareness among radiologists of symptomatic or complicated arachnoid cysts. This is particularly concerning in pediatric patients. While arachnoid cysts are asymptomatic in most cases, they can cause clinical symptoms in a minority of cases, especially when they occur in unusual sites. These include intraventricular locations where they may cause hydrocephalus, the basal cisterns where they may compress cranial nerves, the cerebellopontine angle where they have to be differentiated from a number of cystic lesions, the cavum septum pellucidum or cavum velum interpositum, the choroid fissure where they can entrap the temporal horn and compress the hippocampus, the posterior fossa where they need to be differentiated from other posterior fossa cystic lesions, and within the spinal canal where there is a concern for cord or nerve root compression. Larger cysts are more prone to complications such as mass effect, hemorrhage, and rupture. Hemorrhage and rupture often present with acute symptoms. Ruptured cysts lose their characteristic imaging appearance and can mimic several ominous pathologies. It therefore becomes vital to accurately diagnose these cases as complications of pre-existing arachnoid cysts for appropriate management. A detailed review of all diagnostic imaging aspects of arachnoid cysts will help fill in the existing information void on this important entity.
Keywords: Arachnoid cyst, cisternography, cranial nerve compression, posterior fossa cysts, spinal arachnoid cyst, arachnoid cyst hemorrhage, arachnoid cyst rupture
Introduction
Arachnoid cysts are the most common cystic intracranial lesions. 1 They are the most common incidentally discovered intracranial lesions on imaging and represent about 1% of all intracranial space occupying lesions. 2 They may present at any age, but clinically significant arachnoid cysts tend to present in the pediatric age group. There is a male preponderance reported in literature in the ratio of 2:1. 2 In recent years, there has been an increasing prevalence of arachnoid cysts discovered in the population due to the increasing use of imaging. The overall prevalence of arachnoid cysts has been estimated to be 1-1.5%. 1 Arachnoid cysts may be developmental or the result of inflammation, trauma, or surgery. In many instances, they are asymptomatic and not the primary cause of the symptoms that prompted imaging. However, in a minority of cases, arachnoid cysts do cause significant clinical symptoms. 3 A relative lack of recent literature and any comprehensive radiological review on this extremely common pathology has resulted in a tendency to underplay the importance of this entity. Complications such as rupture and hemorrhage, although uncommon, are often misdiagnosed due to a lack of awareness. They may be construed as ominous pathologies, often leading to extensive and invasive testing that leads to significant morbidity and financial burden for the patient. This is of particular concern in pediatric patients. To address these issues, we have presented a detailed review of arachnoid cysts including their diagnostic assessment, unusual locations, uncommon presentations, complications, various associations, and differential diagnoses in pediatric patients.
Etiopathogenesis
Arachnoid cysts may be primary or secondary to other causes such as inflammation or trauma. Majority of cases are primary or developmental in origin. These are hypothesized to form due to abnormalities in splitting of the arachnoid during embryogenesis leading to formation of a diverticulum from the arachnoid or even duplication of the arachnoid. 4 The cyst wall may be secretory in a few cases. Secondary arachnoid cysts may form due to injury or inflammation to the arachnoid and subsequent formation of adhesion membranes that trap cerebrospinal fluid (CSF). In some cases, a ball valve mechanism may occur, causing progressive enlargement of the arachnoid cysts and resulting in progressive mass effect with compression symptoms.
Clinical presentations
The vast majority of arachnoid cysts are asymptomatic and discovered incidentally. Even in patients imaged for symptoms typically attributed to arachnoid cysts, such as headaches, it is more likely that the cysts are incidental and not the cause of the symptoms. Arachnoid cysts in unusual locations are statistically more likely to produce clinical symptoms. Additionally, larger cysts are more likely to be associated with symptoms. They have been implicated in a wide array of symptoms including headache due to increased intracranial pressure, hydrocephalus leading to nausea and vomiting, cranial nerve palsies that may involve virtually any cranial nerve and even psychiatric symptoms such as depression. 5 Spinal canal arachnoid cysts may present with typical spinal compression or nerve root compression symptoms including weakness, paralysis, sensory or motor deficits, and bowel or bladder symptoms. Radicular pain and neurogenic claudication have also been reported. 6 Many of these could also have an acute presentation requiring emergency surgical treatment. Complications of arachnoid cysts such as rupture or hemorrhage are frequently symptomatic. The primary concern in such cases is that the appearance on imaging may be atypical and, in the absence of prior imaging, is prone to misdiagnosis.
Diagnostic evaluation of arachnoid cysts
Uncomplicated “typical” arachnoid cysts are characteristically simple cystic lesions which are anechoic on ultrasound, of CSF attenuation on computed tomography (CT) scans and follow signal intensity of CSF on magnetic resonance imaging (MRI) (Figure 1). They are hypointense on T1W and hyperintense on T2W with complete suppression on FLAIR sequence. There is no restricted diffusion or post contrast enhancement. The cyst wall is thin and often imperceptible on CT, with optimal visualization necessitating heavily T2W sequences. Scalloping of the inner table of the calvarium and mass effect on the underlying parenchyma are visible with larger cysts. The diagnosis is straightforward when such cystic lesions are located in sites commonly associated with arachnoid cysts. The most common location is in the middle cranial fossa anterior to the temporal lobes which accounts for 50–60% of cases. The second most common site is in the posterior fossa in a retrocerebellar location (10% of cases). 7 Other sites are considered uncommon or atypical and various differentials would need consideration depending on the location. Complicated cysts also pose a diagnostic dilemma and several differentials merit consideration. Differentiating arachnoid cysts from other entities is paramount in such cases for appropriate management and prognostication. Prenatal diagnosis of arachnoid cysts on obstetric ultrasound or fetal MRI is also possible.
Figure 1.
Coronal T2W (A), axial FLAIR (B), post contrast coronal T1W (C) and axial DWI (D) MRI brain of a 16-year-old patient shows a large middle cranial fossa arachnoid cyst which is hyperintense on T2W and completely suppressed on FLAIR without contrast enhancement or diffusion restriction (arrows).
Demonstrating communication of the arachnoid cyst with the CSF space is sometimes useful for planning management. This can be done by CT cisternography or MR cisternography. Intrathecal administration of contrast into the spinal canal is followed by positioning to fill the intracranial subarachnoid spaces and subsequent imaging. The timing and extent of filling can help guide management. Freely communicating cysts show early and complete filling and are generally not operated upon. 8 Non-contrast MRI techniques have also been used to evaluate communication between the cyst and CSF. Heavily T2W 3D sequences may show the site of communication as a jet of signal void. Phase contrast techniques have been similarly used. 9 However, these methods are less reliable than contrast cisternography techniques.
Galassi classification
Galassi et al. divided middle cranial fossa arachnoid cysts into three types: 10
(i) Type 1: Occupies only anterior part of the middle cranial fossa with free CSF communication on cisternography.
(ii) Type 2: Occupies anterior and middle part of middle cranial fossa with mild mass effect on temporal lobe and slow CSF communication on cisternography.
(iii) Type 3: Occupies most of the middle cranial fossa with significant mass effect on temporal lobe with minimal or no CSF communication on cisternography.
Unusual locations, presentations, and differential diagnosis
(i) Intraventricular: These are rare and may present with hydrocephalus due to obstruction of the ventricular outflow tracts (Figure 2).11,12 They can be missed since their signal matches that of CSF and can be especially difficult to visualize when the ventricles are dilated. Heavily T2W 3D sequences will demonstrate the cyst walls distinctly in most cases. Isolated dilatation of one of the horns of the lateral ventricles is particularly suspicious for intraventricular arachnoid cysts either distending these segments or obstructing the site of communication of the horn with the ventricle.
(ii) Cavum septum pellucidum: This may be difficult to visualize as the arachnoid cyst tends to conform to the shape of the septum pellucidum (Figure 3). These can also present with compressive symptoms due to compression of the commissural tracts or obstruction of the foramen of Monro. 13 Compression of the hypothalamo-septal triangle can present with visual, sensorimotor, autonomic, or behavioral symptoms. Any mass effect should prompt a high degree of suspicion for an arachnoid cyst as the normal cavum never causes compressive symptoms. Careful assessment of heavily T2W sequences to identify the cyst wall is again the key to correct diagnosis.
(iii) Cavum velum interpositum: These are very rare and tend to present with uncharacteristic symptoms such as memory loss when symptomatic, 14 presumably due to compression of the subiculum-retrosplenium continuum or the fornices. As with cavum septum pellucidum cysts, any mass effect should lead to suspicion and heavily T2W sequences can identify the cyst wall for diagnosis (Figure 4). Due to the characteristic location of the cavum velum interpositum, arachnoid cysts of the cavum velum interpositum tend to displace the splenium of corpus callosum posterosuperiorly. Pineal cysts are an important differential diagnosis but they are usually smaller and tend to displace the splenium superiorly.
(iv) Choroid fissure: They can present with symptoms such as memory loss due to hippocampal compression or headache due to ventricular obstruction. They tend to trap the temporal horn due to their characteristic location leading to isolated dilatation of the temporal horn (Figure 5). When small, they may be impossible to differentiate from choroid fissure cysts but any interval change in size or mass effect should prompt consideration of arachnoid cyst as the diagnosis. Such enlarging cysts also have a propensity to become symptomatic.
(v) Basal cisterns: Arachnoid cysts can occur in any of the basal cisterns with characteristic symptomatology in each cistern depending on the structures traversing them. These may be difficult to diagnose, especially when small in size. Heavily T2W 3D sequences are paramount, not only for cyst wall visualization, but also for visualization of the cranial nerves and of any compression by the cyst (Figures 6–10). The most common cistern involved is the suprasellar cistern, which may involve the Liliequist membrane. The structures affected by arachnoid cysts in various cisterns that subsequently lead to specific symptoms are tabulated in Table 1.15–18 Cerebellopontine angle cistern arachnoid cysts deserve special mention as they are much more common than in the other cisterns and should be differentiated from other cystic lesions that have a propensity to occur in the cerebellopontine cistern. 19 The differentials and differentiating features on imaging are tabulated in Table 2. Other cisterns such as the superior cerebellar cistern (Figure 11) may also be involved, but there is no cranial nerve compression in these locations.
(vi) Optic nerve sheath: This is an extremely rare entity with only a handful of cases having been reported in literature. 20 Optic nerve sheath arachnoid cysts can cause visual loss due to nerve compression. They can be very small (Figure 12) and careful assessment on heavily T2W thin section orbital scans with particular attention to any areas of abnormal focal displacement or angulation of the optic nerve is necessary for diagnosis.
(vii) Posterior fossa: Although these are not rare, differentiation from other cystic lesions of the posterior fossa is important. Arachnoid cysts typically show mass effect with compression of the morphologically normal vermis and cerebellum as well as the fourth ventricle (Figure 13). The tegmento-vermian angle is normal. There is no communication with the fourth ventricle. These features are in contrast to Dandy Walker cyst and Blake’s pouch cyst as well as vermian hypoplasia. Mega cisterna magna may be difficult to differentiate but lack of significant mass effect on the cerebellum and non-displaced dural leaflets of the falx cerebelli within are useful features pointing to mega cisterna magna. Rarely, cerebellar hypoplasia can also be associated with posterior fossa arachnoid cysts, complicating the diagnosis. In difficult cases, contrast cisternography can be definitive. 21
(viii) Spinal canal: These are rare in general. Within the spinal canal, they are most commonly located in the thoracic spinal canal and more likely to be located posterior to the spinal cord (Figure 14). They may present with symptoms of backache or symptoms of nerve root or cord compression. Spinal arachnoid cysts can be difficult to diagnose but any abnormally eccentric position of the cord or displacement of the nerve roots should raise suspicion. 6 Demonstration of the cyst wall on heavily T2W sequences confirms the diagnosis.
Figure 7.
Coronal T2W (A) and 3D BFFE(B) MRI brain of a 15-year-old patient with right oculomotor palsy shows a small arachnoid cyst (arrows in A and B) in the prepontine cistern compressing the root of the right oculomotor nerve.
Figure 8.
Sagittal T1W (A) and axial T2W (B) MRI brain of a 3-year-old patient shows two arachnoid cysts. One is located in the quadrigeminal cistern (arrows in A and B) compressing the aqueduct and causing hydrocephalus (block arrow in B). Another is located in the suprasellar cistern (curved arrows in A and B) causing mass effect upon the optic chiasm and tracts.
Figure 9.
Axial T2W (A) and coronal post contrast T1W (B) MRI brain of a 6-year-old patient shows an arachnoid cyst in the cerebellopontine angle cistern (arrows in A and B).
Figure 2.
3D BFFE MRI brain (A-D) of a 17-year-old patient shows a large arachnoid cyst in the fourth ventricle with the cyst membrane herniating through the foramina of Luschka (arrows in A) and foramen of Magendie (arrow in B) with obstruction to CSF flow causing hydrocephalus (arrow in D).
Figure 3.
T2W axial (A) and coronal (B) MRI brain of a 10-year-old patient show an arachnoid cyst (arrows) with distinct walls and mild expansion of the septum pellucidum and slight compression of the corpus callosum.
Figure 4.
T2W axial (A) and T1W post contrast sagittal (B) and coronal (C) MRI brain of a 7-year-old patient show an arachnoid cyst (arrows) in the cavum velum interpositum with compression of the splenium and retrosplenial region. The splenium is displaced posterosuperiorly, differentiating this from a pineal cyst in the same location.
Figure 5.
Post contrast coronal T1W (A), 3D BFFE (B), axial T2W (C) and axial SWI (D) MRI brain of an 8-year-old patient show a large arachnoid cyst in the left choroid fissure (arrows in A and B) causing entrapment and isolated dilatation of the temporal horn (arrow in C). Also seen is hemorrhage into the intact cyst with dependent blood products on SWI (arrow in D).
Figure 6.
Sagittal T1W (A) and axial T2W (B) MRI brain of a 5-year-old patient shows an arachnoid cyst in the suprasellar cistern (arrows in A and B) with associated Chiari 1 deformity of the hindbrain (curved arrow in A) and displacement of the optic chiasm and optic tracts (curved arrow in B).
Figure 10.
T2W coronal (A) and axial (B) MRI brain of an 8-year-old patient shows an arachnoid cyst in the cerebellomedullary cistern (arrows in A and B).
Table 1.
Locations of arachnoid cysts in basal cisterns and structures which may be compressed.
| Cistern involved | Common structures compressed | Symptoms |
|---|---|---|
| Suprasellar | Optic chiasm and tracts | Visual deficits |
| Prepontine | Oculomotor nerve | Oculomotor nerve palsy |
| Quadrigeminal cistern | Trochlear nerve, cerebral aqueduct | Superior oblique palsy, obstructive hydrocephalus |
| Cerebellopontine angle cistern | Trigeminal nerve, facial nerve, vestibulocochlear nerve | Sensory deficits of face and masticator muscle palsy, facial palsy, hearing and balance issues |
| Cerebellomedullary cistern | Glossopharyngeal nerve, vagus nerve | Swallowing and speech deficits |
Table 2.
Differential diagnosis for cystic lesions in the cerebellopontine angle cistern and their differentiating features from arachnoid cyst.
| Differential diagnosis | Differentiating features |
|---|---|
| Epidermoid cyst | Incomplete suppression on FLAIR with diffusion restriction |
| Dermoid cyst | Incomplete suppression on FLAIR with areas of fat signal within |
| Abscess | Variable signal with diffusion restriction and peripheral/meningeal enhancement |
| Racemose neurocysticercosis | Clustered multiple cysts with fluid signal in the subarachnoid space in contrast to a single large arachnoid cyst |
| Cystic meningioma or schwannoma | Peripheral or eccentric rind of enhancing tumor with predominantly cystic component |
Figure 11.
Sagittal T1W (A), axial T2W (B) and post contrast coronal T1W (C) MRI brain of a 19-year-old patient shows an arachnoid cyst in the superior cerebellar cistern (arrows) with mild scalloping of the superior cerebellar surface.
Figure 12.
3D BFFE (A and B), coronal STIR (C) and post contrast coronal T1W FS (D) MRI orbit of an 18-year-old patient with vision loss in the right eye shows a tiny arachnoid cyst causing focal medial deviation of the optic nerve with focal enlargement of the lateral subarachnoid space (arrows in A, B and C) of the optic nerve sheath just posterior to the globe without contrast enhancement (arrow in D).
Figure 13.
Axial T2W (A) and sagittal T1W (B) MRI brain of a 6-year-old patient shows a large arachnoid cyst in the posterior fossa (arrows in A and B) with mass effect upon the cerebellum and fourth ventricle and scalloping of the calvarium without any communication with the fourth ventricle or increase in the tegmento-vermian angle. Sagittal T1W (C) MRI brain in a 2-year-old patient shows a large arachnoid cyst in the posterior fossa (arrow in C) with similar features and with associated hydrocephalus (block arrow arrow in C).
Figure 14.
Axial T2W (A) and sagittal T2W (B) MRI cervicothoracic spine of a 35-year-old patient shows an arachnoid cyst in the upper thoracic spinal canal posteriorly (arrows in A and B) with discernable cyst walls causing significant spinal cord compression (curved arrow in B).
Complications of arachnoid cysts
(i) Mass effect: Most symptoms attributable to arachnoid cysts are due to compression of adjacent structures. The mass effect may lead to increased intracranial pressure which may present as headache, vomiting, or visual disturbances. Compression of underlying parenchyma may present with focal symptoms. As previously discussed, cysts in atypical locations are more likely to be symptomatic due to compression of vital structures such as commissural tracts, cranial nerves, hippocampus, brainstem, spinal cord, or nerve roots. Compression of the aqueduct or any other part of the ventricular drainage system can result in hydrocephalus. Scalloping of the overlying calvarium due to chronic pressure effects are typical for peripherally located arachnoid cysts.
(ii) Hemorrhage: Hemorrhage into an intact arachnoid cyst can occur due to the tendency for rupture of small bridging vessels in the wall of the arachnoid cyst (Figure 5). For the same reason, there is also an association between chronic subdural hematomas and arachnoid cysts. 3 In general, large cyst size and recent head trauma have been identified as major risk factors for hemorrhage and rupture of arachnoid cysts. 22 Mild focal peripheral enhancement of the cyst may occur at the site of hemorrhage. Combined with the internal hemorrhage, this may be mistaken for other pathologies in the absence of prior imaging unless the radiologist is aware of this entity and its imaging appearance.
(iii) Focal rupture: Focal rupture of the cyst may lead to partial decompression and often results in a subdural hygroma (Figure 15). 23 There may be associated intracystic hemorrhage or blood within the hygroma forming a subdural hematoma (Figure 16). Occasionally, emergency surgical treatment may be necessary. In focal cyst rupture, spontaneous decompression of the cyst may lead to difficulty in identifying the underlying ruptured cyst, which may be mistaken for a primary subdural hygroma or subdural hematoma, sometimes prompting detailed evaluation for child abuse. For unclear reasons, such spontaneous rupture is far more likely to occur in middle cranial fossa cysts than in posterior fossa cysts. 24 Any unexplained subdural collection should be carefully evaluated for telltale signs of a ruptured arachnoid cyst. Scalloping of the calvarium in peripherally located cysts is a useful feature to infer its prior presence in the absence of previous imaging. Heavily T2W imaging can sometimes delineate the wall of the remnant cyst.
(iv) Complete rupture: Complete rupture has an acute presentation with headache and vomiting with or without papilledema, often after trivial trauma in children. 25 This leads to complete decompression of the cyst which is no longer visible. Often there is associated subdural hygroma. 26 Collapsed and crumpled membranes that show post contrast enhancement and adjacent reactive meningeal enhancement (Figure 17) may be visualized and can easily be mistaken for meningitis with associated subdural hygroma. Heavily T2W sequences may show the multilayered collapsed membranes in some cases (Figure 18). This appearance of complete rupture has not been previously reported in literature. Subsequent lack of awareness among radiologists may lead to misdiagnosis in such cases, leading to invasive testing and mismanagement. Spontaneous resolution of arachnoid cysts due to rupture may be more common than previously reported, given the frequency of occurrence of arachnoid cysts.
Figure 15.
Axial T2W (A), coronal post contrast T1W (B), 3D BFFE (C and D) brain MRI of an 8-year-old patient shows a subdural hygroma (arrows) in the left fronto-temporo-parietal convexity with mild contralateral midline shift and scalloping of the overlying calvarium (block arrows in B, C and D) indicating presence of an underlying arachnoid cyst. The wall of the focally ruptured and partially decompressed arachnoid cyst is well seen on heavily T2W sequence (curved arrows in C and D).
Figure 16.
Axial T2W MRI brain (A) and axial CT brain (B) in a 19-year-old patient show a subdural collection in the right frontal convexity with dependent hemorrhage (arrows in A and B). Mild scalloping of the calvarium is better appreciated on CT (curved arrow in B) indicating the prior presence of an arachnoid cyst.
Figure 17.
T2W sagittal fetal MRI (A) shows a simple cystic lesion in the suprasellar region. Axial T2W MRI brain (B) of the same patient at 1-year of age shows an arachnoid cyst in the suprasellar cistern (arrow in A) involving the membrane of Liliequist. Postcontrast T1W (C) and 3D CISS (D) MRI brain of the same patient 2 years later performed for acute severe headache shows complete rupture of the cyst with collapsed and crumpled enhancing membranes (arrows in B and C).
Figure 18.
Axial T2W (A), axial FLAIR (B), 3D BFFE (C and D) MRI brain of a 9-year-old patient shows a small extra-axial collection with a linear hypointense structure within (arrows in A and B) which are seen to be crumpled membranes (arrows in C and D). Scalloping of the overlying calvarium (block arrows in A, C and D) indicates the prior presence of an arachnoid cyst.
Associations and secondary causes
Several anomalies are associated with arachnoid cysts. Those more commonly observed include septo-optic dysplasia (Figure 19), neural tube defects, Chiari 2 malformation (Figure 20) and Chiari 1 deformity (Figure 6). An association has also been reported between congenital melanocytic nevus syndrome and arachnoid cysts, particularly posterior fossa arachnoid cysts. 27 Spinal arachnoid cysts are developmentally associated with Chiari 2, but are also known to develop following posterior fossa decompression and neural tube defect closure procedures. Comparison with prior scans is essential to know the temporal sequence in such cases. Many other associations of arachnoid cysts have been described including microphthalmia, corpus callosum agenesis, gray matter heterotopia, Marfan’s syndrome and achondroplasia. 28 The cause-effect relationship is often not definite in such cases and it is unclear whether the underlying disorder predisposes to the development of arachnoid cysts. However, there are several reports in literature noting symptomatic improvement of associated anomalies following treatment of arachnoid cysts, possibly due to relief of compression on the brain parenchyma. This is particularly well established with Chiari malformations. 29
Figure 19.
Sagittal T1W (A) and coronal T2W (B) MRI brain of a 13-year-old patient shows a supracerebellar cistern arachnoid cyst (arrow in A) associated with absent septum pellucidum (arrow in B) and bilateral optic nerve thinning (not shown) consistent with septo-optic dysplasia.
Figure 20.
Sagittal T2W MRI cervicothoracic (A) and thoracolumbar (B) spine of a 11-year-old patient shows a cervicothoracic arachnoid cyst (arrow in A). Patient has evidence of posterior fossa decompression for Chiari 2 (curved arrow in A) and surgical neural tube defect closure (arrow in B). Whether the arachnoid cyst was developmental or a complication of these surgeries was not clear in this case due to non-availability of prior scans.
Arachnoid cysts may also develop as sequelae to head injury, meningitis, tumors, or surgery (Figure 20) due to arachnoid injury and fibrosis. These cysts show evolution from the time of initial imaging and may lead to compressive symptoms requiring surgical treatment. Delayed worsening of symptoms in any patient with a prior brain insult or surgery should lead to suspicion of development of a secondary arachnoid cyst. Significant improvement is usually expected following surgical treatment of the cyst in these cases.
Conclusion
Arachnoid cysts are the most common intracranial cystic lesions and are asymptomatic and innocuous in most cases. These are easily amenable to conservative management or surgical treatment with complete recovery, but accurate imaging diagnosis is paramount A relative lack of literature on this topic has led to a general lack of awareness among radiologists, thus resulting in increased risk of misdiagnosis and mismanagement of symptomatic or complicated arachnoid cysts. A detailed review of all diagnostic imaging aspects of arachnoid cysts will help fill in the existing information void on this important entity.
Footnotes
The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
Funding: The author(s) received no financial support for the research, authorship, and/or publication of this article.
ORCID iD
Venkatram Krishnan https://orcid.org/0000-0002-8945-2614
References
- 1.Al-Holou WN, Terman S, Kilburg C, et al. Prevalence and natural history of arachnoid cysts in adults. J Neurosurg 2013; 118(2): 222–231. [DOI] [PubMed] [Google Scholar]
- 2.Hall S, Smedley A, Sparrow O, et al. Natural history of intracranial arachnoid cysts. World Neurosurg 2019; 126: e1315–e1320. [DOI] [PubMed] [Google Scholar]
- 3.Logan C, Asadi H, Kok HK, et al. Arachnoid cysts-common and uncommon clinical presentations and radiological features. J Neuroimaging Psychiatry Neurol 2016; 1: 79–84. [Google Scholar]
- 4.Osborn AG, Preece MT. Intracranial cysts: radiologic-pathologic correlation and imaging approach. Radiology 2006; 239(3): 650–664. DOI: 10.1148/radiol.2393050823. [DOI] [PubMed] [Google Scholar]
- 5.Shettar M, Karkal R, Misra R, et al. Arachnoid cyst causing depression and neuropsychiatric symptoms: a case report. East Asian Arch Psychiatry 2018; 28(2): 64–67. [PubMed] [Google Scholar]
- 6.Garg K, Borkar SA, Kale SS, et al. Spinal arachnoid cysts - our experience and review of literature. Br J Neurosurg 2017; 31(2): 172–178. [DOI] [PubMed] [Google Scholar]
- 7.Carbone J, Sadasivan AP. Intracranial arachnoid cysts: review of natural history and proposed treatment algorithm. Surg Neurol Int 2021; 12: 621. DOI: 10.25259/SNI_946_2021. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 8.Wang X, Chen JX, You C, et al. CT cisternography in intracranial symptomatic arachnoid cysts: classification and treatment. J Neurol Sci 2012; 318(1-2): 125–130. [DOI] [PubMed] [Google Scholar]
- 9.Algin O. Evaluation of the communication between arachnoid cysts and neighboring cerebrospinal fluid spaces by T2W 3D-SPACE with variant flip-angle technique at 3 T. J Comput Assist Tomogr 2018; 42(5): 816–821. [DOI] [PubMed] [Google Scholar]
- 10.Galassi E, Tognetti F, Gaist G, et al. CT scan and metrizamide CT cisternography in arachnoid cysts of the middle cranial fossa: classification and pathophysiological aspects. Surg Neurol 1982; 17(5): 363–369. [DOI] [PubMed] [Google Scholar]
- 11.Park SW, Yoon SH, Cho KH, et al. A large arachnoid cyst of the lateral ventricle extending from the supracerebellar cistern - case report. Surg Neurol 2006; 65(6): 611–614. DOI: 10.1016/j.surneu.2005.07.069. [DOI] [PubMed] [Google Scholar]
- 12.Westermaier T, Vince GH, Meinhardt M, et al. Arachnoid cysts of the fourth ventricle - short illustrated review. Acta Neurochir 2010; 152(1): 119–124. [DOI] [PubMed] [Google Scholar]
- 13.Lancon JA, Haines DE, Lewis AI, et al. Endoscopic treatment of symptomatic septum pellucidum cysts: with some preliminary observations on the ultrastructure of the cyst wall: two technical case reports. Neurosurgery 1999; 45(5): 1251–1257. [DOI] [PubMed] [Google Scholar]
- 14.Funaki T, Makino Y, Arakawa Y, et al. Arachnoid cyst of the velum interpositum originating from tela choroidea. Surg Neurol Int 2012; 3: 120. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 15.Brewington D, Petrov D, Whitmore R, et al. De novo intraneural arachnoid cyst presenting with complete third nerve palsy: case report and literature review. World Neurosurg 2017; 98(873): e27–e31. [DOI] [PubMed] [Google Scholar]
- 16.Pagni CA, Canavero S, Vinci V. Left trochlear nerve palsy, unique symptom of an arachnoid cyst of the quadrigeminal plate. Case report. Acta Neurochir 1990; 105(3-4): 147–149. [DOI] [PubMed] [Google Scholar]
- 17.Gönül E, Izci Y, Onguru O. Arachnoid cyst of the cerebellopontine angle associated with gliosis of the eighth cranial nerve. J Clin Neurosci 2007; 14(7): 700–702. [DOI] [PubMed] [Google Scholar]
- 18.Olaya JE, Ghostine M, Rowe M, et al. Endoscopic fenestration of a cerebellopontine angle arachnoid cyst resulting in complete recovery from sensorineural hearing loss and facial nerve palsy. J Neurosurg Pediatr 2011; 7(2): 157–160. [DOI] [PubMed] [Google Scholar]
- 19.Bonneville F, Sarrazin JL, Marsot-Dupuch K, et al. Unusual lesions of the cerebellopontine angle: a segmental approach. Radiographics 2001; 21(2): 419–438. DOI: 10.1148/radiographics.21.2.g01mr13419. [DOI] [PubMed] [Google Scholar]
- 20.Touarsa F, El Ouali I, Elkettani N, et al. Incidental optic nerve sheath arachnoid cyst: A rare case finding with literature review, 10. Thousand Oaks, CA: Sage Open Med Case Rep, 2022, p. 2050313X221113261. DOI: 10.1177/2050313X221113261. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 21.Kollias SS, Ball WSJ, Prenger EC. Cystic malformations of the posterior fossa: differential diagnosis clarified through embryologic analysis. Radiographics 1993; 13(6): 1211–1231. DOI: 10.1148/radiographics.13.6.8031352. [DOI] [PubMed] [Google Scholar]
- 22.Cress M, Kestle JR, Holubkov R, et al. Risk factors for pediatric arachnoid cyst rupture/hemorrhage: a case-control study. Neurosurgery 2013; 72(5): 716–722. DOI: 10.1227/NEU.0b013e318285b3a4. [DOI] [PubMed] [Google Scholar]
- 23.Gelabert-González M, Fernández-Villa J, Cutrín-Prieto J, et al. Arachnoid cyst rupture with subdural hygroma: report of three cases and literature review. Childs Nerv Syst 2002; 18(11): 609–613. DOI: 10.1007/s00381-002-0651-7. [DOI] [PubMed] [Google Scholar]
- 24.Russo N, Domenicucci M, Beccaglia MR, et al. Spontaneous reduction of intracranial arachnoid cysts: a complete review. Br J Neurosurg 2008; 22(5): 626–629. [DOI] [PubMed] [Google Scholar]
- 25.Furtado LMF, Costa Val Filho JA, Ferreira RI, et al. Intracranial arachnoid cyst rupture after mild TBI in children: have we underestimated this risk? BMJ Case Reports CP 2019; 12: e228790. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 26.Hall S, Smedley A, Manivannan S, et al. Ruptured intra-cranial arachnoid cysts: a case series from a single UK institution. Br J Neurosurg 2021; 35(4): 462–466. DOI: 10.1080/02688697.2020.1862057. [DOI] [PubMed] [Google Scholar]
- 27.Fledderus AC, Widdershoven AL, Lapid O, et al. Neurological signs, symptoms and MRI abnormalities in patients with congenital melanocytic naevi and evaluation of routine MRI-screening: systematic review and meta-analysis. Orphanet J Rare Dis 2022; 17(1): 95. DOI: 10.1186/s13023-022-02234-8. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 28.Wang PJ, Lin HC, Liu HM, et al. Intracranial arachnoid cysts in children: related signs and associated anomalies. Pediatr Neurol 1998; 19(2): 100–104. [DOI] [PubMed] [Google Scholar]
- 29.Galarza M, López-Guerrero AL, Martínez-Lage JF. Posterior fossa arachnoid cysts and cerebellar tonsillar descent: short review. Neurosurg Rev 2010; 33(3): 305–1314. DOI: 10.1007/s10143-010-0262-9. [DOI] [PubMed] [Google Scholar]