Abstract
Background
Early anatomists suspected that the radiculomedullary veins draining the spinal cord had valves preventing their retrograde filling with anatomical casting material. Modern investigations have discarded the presence of true valves and introduced instead the notion of a pseudo-valvular configuration for which the term antireflux mechanism was coined in the 1970s. The angiographic anatomy of the antireflux mechanism has not been well documented so far.
Methods
This article discusses anatomical and clinical features of the antireflux mechanism with a series of 12 angiographic observations documenting the antireflux mechanism under normal and pathological circumstances.
Results
The antireflux mechanism divides radiculomedullary veins into intradural and extradural segments. While the structure of the antireflux mechanism is not yet fully clarified, it includes at least a tight narrowing of the radiculomedullary vein at its point of passage through the thecal sac, which is angiographically detectable and likely protects the intradural venous system from transient or persistent surges in venous pressure (e.g. sneezing, pregnancy). This tight narrowing of the antireflux mechanism likely also represents an obstacle to normal anterograde flow, potentially leading to venous stagnation and thrombosis.
Conclusions
The antireflux mechanism includes at least a tight narrowing of the radiculomedullary vein, which likely influences the development and clinical expression of low-flow spinal arteriovenous fistulas and might impact the spinal venous drainage even in the absence of arteriovenous shunts.
Keywords: Spinal veins, spinal angiography, spinal vascular malformations, spinal vascular anatomy, radiculomedullary veins
Having noted the lack of intradural progression of casting material forcefully injected into extradural veins, past anatomists postulated that valves were protecting the veins of the spinal cord. In Breschet’s words, intradural veins1:
[…] isolated as they are by the meningeal sheath from both the internal and external veins of the vertebral column, cannot be injected, easily at least, through these, and they are most commonly found empty amidst the best injections of the veins located outside the meningeal canal. [author transl.]
Interest in these hypothetical valves temporarily faded before being revived by the investigations of Clemens,2 Gillilan,3 Dommisse,4 and Crock and Yoshizawa5 (Figure 1). In a series of articles published between 1979 and 1985, Tadié et al.6–8 established the existence of a valve-like arrangement near the distal end of radiculomedullary veins (RMV), for which the term antireflux mechanism (ARM) was coined. This article discusses the angiographic and clinical features of the ARM.
Figure 1.
Artistic representation of the antireflux mechanism as a segmental narrowing of the radiculomedullary vein (based on Crock and Yoshizawa5).
Methods
Conventional spinal angiography (SA) and flat-panel catheter angiotomography (FPCA) were both performed in a biplane neuroangiography suite (Artis Zee, Siemens, Germany). Spinal FPCA used three-dimensional datasets generated from rotational angiograms of intersegmental arteries. Venous phase documentation required the addition of a 10-s delay to the standard 20-s rotational FPCA acquisition.9 Secondary reconstructions were produced and analyzed using a commercially available software (Osirix, Pixmeo, Switzerland). All studies were obtained during routine clinical investigations for which patients gave written informed consent.
Illustrative cases
Cases illustrating the normal angiographic anatomy of the antireflux mechanism
Case 1—Anatomy of the ARM in a 74-year-old man. The information provided by the venous phase of spinal angiography (SA) is limited by the small size of the vessels investigated, the thickness and radio-opacity of the surrounding tissues, and respiratory and peristaltic artifacts (Figure 2(a) and (b)). FPCA complements SA with a venous analysis comparable to the venous phase of cerebral angiography9 (Figure 2(c) and (d)).
Figure 2.
Angiographic anatomy of the antireflux mechanism in a 74-year-old man. (a) DSA, left L1 injection (arterial phase), posteroanterior projection, documenting the artery of Adamkiewicz (large white arrow) and the anterior spinal artery (small white arrow). (b) DSA, left L1 injection (venous phase), posteroanterior projection, showing the anteromedian spinal vein (small black arrow) and a left L1 radiculomedullary vein (RMV) (large black arrow). (c) FPCA, left L1 injection, oblique reconstruction along the plane of the artery of Adamkiewicz; note the course of the vessel between its take-off from the left L1 intersegmental artery (arrowhead) and its intradural segment (arrow). (d) FPCA, left L1 injection, oblique reconstruction along the plane of the left L1 RMV. The RMV drains into the internal vertebral venous plexus (black asterisk), which is connected to the external vertebral venous plexus (white asterisk) by the intervertebral veins crossing the neural foramen (gray arrowhead). The RMV is divided into intra- and extradural segments (black and gray arrows) by the ARM located at its point of passage through the thecal sac (bracket). As shown in this example, the ARM commonly appears as a focal opacification defect indicating the minute caliber of its lumen.
Case 2—Anatomy of the ARM in a 28-year-old woman illustrating regional variations in length and orientation (Figure 3).
Figure 3.
Angiographic anatomy of the antireflux mechanism in a 28-year-old woman. FPCA, left T12 injection, oblique reconstruction along the plane of a right T11 posterior radiculomedullary vein (RMV), showing the near horizontal course of its terminal segment (black arrow) and the focal opacification defect indicating its transdural passage (white arrow) shortly before reaching the internal vertebral venous plexus (asterisk). The extradural segment of the RMV is, in that case, short.
Cases illustrating the role of the antireflux mechanism in RMV occlusion and in the formation of the so-called “arrow-tipped” anastomotic loop
Case 3—Anatomy of the ARM in a 52-year-old man depicting an RMV with multiple roots (Figure 4).
Figure 4.
Angiographic anatomy of the antireflux mechanism in a 52-year-old man. FPCA, oblique reconstruction of an RMV with anterior (black arrow) and posterior (white arrow) roots joining immediately before their passage thought the thecal sac (arrowhead) to join the internal vertebral venous plexus (asterisk). The common distal segment of an RMV with multiple roots can vary in length; it can be very short, as illustrated here.
Case 4—RMV occlusion in a 75-year-old man. Distal occlusion is appreciated angiographically when a multirooted RMV takes the shape of a so-called “arrow-tipped anastomotic loop” (Figure 5).
Figure 5.
“Arrow-tipped” anastomotic loop in a 75-year-old man. DSA, posteroanterior projection, magnified view documenting a portion of the perimedullary venous drainage of a lumbar spinal arteriovenous fistula. The occluded distal segment of a multirooted radiculomedullary vein (RMV) (a) is identified thanks to persistent flow within its dual roots. The dotted line shows the approximate location of the lateral edge of the thecal sac, the upper dashed line represents the occluded RMV segment. This configuration—sometimes called an “arrow-tipped” anastomotic loop and believed to represent an anatomic variant—is in fact an angiographic marker of RMV occlusion.10 The lower dashed line depicts the hypothetical location of an occluded single-rooted RMV (b); the absence of that vessel would be angiographically undetectable.
Cases illustrating the impact of high-flow pathologies on the antireflux mechanism
Case 5—Angiographic appearance of the ARM in an 8-year-old boy with a high-flow perimedullary fistula (PmAVF) (Figure 6).
Figure 6.
8-year-old boy with a high-flow perimedullary arteriovenous fistula. (a) 3D-DSA, left L2 injection, coronal MIP reconstruction (thickness=4 mm), showing the arteriovenous shunt (gray arrow) with its posterior spinal feeding artery (small white arrow) and draining vein (small black arrow); the lesion is supplied by a left L2 posterior radiculomedullary artery (large white arrow) and drains into a right L1 RMV (large black arrow) into the internal vertebral venous plexus (asterisk). (b) 3D-DSA, left L2 injection, coronal MIP reconstruction (thickness=0.4 mm); this thinner reconstruction offers a better appreciation of the termination of the right L1 RMV (black arrow) into the internal vertebral venous plexus (asterisk). Measurements of the RMV caliber proximal to and at the ARM are indicated; the relative stenosis is slightly above 50%.
Case 6—Angiographic appearance of the ARM in a 57-year-old woman with a spinal hemangioblastoma (Figure 7).
Figure 7.
57-year-old woman with a spinal hemangioblastoma. DSA, right T10 injection, posteroanterior projection, venous phase. The hypervascular tumor (asterisk) drains into a dilated left L1 RMV (black arrow); a focal opacification defect indicates the site of the ARM (white arrow).
Case 7—Angiographic evaluation of a 60-year-old man with a high-flow sacral spinal extradural arteriovenous fistula (SEAVF) draining intradurally after the failure of the ARM (Figure 8).
Figure 8.
60-year-old man with a high-flow sacral spinal extradural arteriovenous fistula (SEAVF). (a) MRI, sagittal T2-weighted image documenting a large retrosacral arterialized epidural pouch (asterisk) and multiple intrathecal flow voids. (b) DSA, right internal iliac artery injection, posteroanterior projection, arterial phase, showing two arterialized epidural pouches (asterisks) supplied by a massively dilated lateral sacral artery (arrow). (c) DSA, right internal iliac artery injection, posteroanterior projection, early venous phase. The main drainage of the arteriovenous fistula is via the left common iliac vein (a) and inferior vena cava (b). (d) DSA, right internal iliac artery injection, posteroanterior projection, late venous phase. The vena cava is still opacified (b). In addition, dilated intrathecal veins are now visible (arrow).
Cases illustrating the role of the antireflux mechanism in the clinical expression of low-flow spinal epidural arteriovenous fistulas
Case 8—Angiographic evaluation of a 73-year-old woman with a low-flow SEAVF draining intradurally after the failure of the ARM (Figure 9).
Figure 9.
73-year-old woman with a spinal extradural arteriovenous fistula (SEAVF). (a) DSA, left L4 injection, posteroanterior projection, arterial phase, showing early opacification of an isolated epidural venous pouch (large arrowheads) draining into a left L3 radiculomedullary vein (RMV) (small arrowheads) with a focal narrowing (arrow). (b) FPCA, coronal MIP reconstruction of a left L4 injection; the fistulous pouch (large arrowheads) and the left L3 draining RMV (small arrowheads) are visible. The ARM—ineffective in this instance—is indicated by a focal narrowing (arrow). (c) FPCA, sagittal reconstruction of a left L4 injection better delineating the connection of the epidural pouch (large arrowhead) and draining RMV (small arrowhead); the arrow points at the focal narrowing marking the incompetent ARM (arrow).
Case 9—Angiographic evaluation of a 46-year-old patient with a low-flow SEAVF; a functional ARM prevents retrograde intradural drainage (Figure 10).
Figure 10.
Angiographic evaluation of a 46-year-old patient with a low-flow spinal extradural arteriovenous fistula (SEAVF). (a) DSA, right T4 injection, posteroanterior projection, arterial phase, showing early opacification of an epidural venous pouch (arrow). A prominent anterior radiculomedullary artery (artery of von Haller) is noted (white arrowhead). There is no evidence of retrograde intradural venous drainage. (b) FPCA, coronal reconstruction of a right T4 injection; the fistulous epidural pouch (arrow) and the artery of von Haller (white arrowhead) are documented. In addition, a second channel is seen paralleling the radiculomedullary artery (black arrowhead). This vessel—not visible in the arterial angiographic phase (see A)—corresponds to a posterior RMV. (c) FPCA, oblique reconstruction of a right T4 injection; this thinner and slightly oblique reconstruction shows the connection of the posterior RMV (black arrowhead) to the fistulous epidural pouch (arrow). Despite being connected to the fistula, the RMV appears protected from retrograde flow by a still functional ARM. This situation may represent an early stage of evolution of SEAVFs, with subsequent failure of the ARM leading to retrograde intradural drainage and the development or worsening of spinal venous hypertension.
Cases illustrating the role of the antireflux mechanism in the development and expression of spinal dural arteriovenous fistulas
Case 10—Angiographic evaluation of a 78-year-old man with a typical SDAVF (Figure 11).
Figure 11.
Angiographic evaluation of a 78-year-old man with a typical spinal dural arteriovenous fistula (SDAVF). (a) DSA, left T6 injection, posteroanterior projection, arterial phase, showing a left T6 radiculomeningeal artery (large arrow) supplying a SDAVF draining into a left T6 radiculomedullary vein (RMV) (gray arrowhead). The arteriovenous shunt (small arrow) rests on the inner aspect of the thecal sac, which is delineated by meningeal feeding branches from both T6 (white arrowhead) and T5 (black arrowhead). (b) DSA, same injection, nonsubtracted view; the dotted line indicates the location of the thecal sac (inferred from the position of the meningeal branches in (a). The shunt of the SDAVF—located along the inner side of the dura mater11—is intimately associated with the antireflux mechanism (ARM).
Case 11—Angiographic evaluation of a 62-year-old man with an atypical SDAVF draining both intra- and extradurally (Figure 12).
Figure 12.
Angiographic evaluation of a 62-year-old man with an atypical right T12 SDAVF. (a) DSA, superselective injection of a T12 radiculomeningeal artery, posteroanterior projection, early arterial phase. The feeding artery provides two small feeding branches (black arrowheads) that converge towards the site of the arteriovenous shunt (black arrow). The intradural segment of the draining radiculomedullary vein (RMV) has started to opacify (white arrow). (b) Same injection, posteroanterior projection, late arterial phase. The intradural segment of the RMV is completely opacified (white arrow) and some perimedullary veins are visible (small white arrowheads). The extradural segment of the RMV is also visible (gray arrow). The direction of the venous drainage from the arteriovenous shunt (black arrow) to the RMV is bidirectional, i.e. retrograde in its intradural segment and antegrade in its extradural segment. (c) Same injection, posteroanterior projection, early venous phase. Both the intra- (white arrow) and extradural (gray arrow) segments of the RMV are now completely opacified. They respectively drain into the perimedullary venous system (small arrowheads) and the internal vertebral venous plexus (large arrowhead). Note that the arteriovenous shunt is immediately proximal to the focal narrowing of the RMV (bracket) corresponding to the location of the ARM.
Case illustrating the possible role of the antireflux mechanism in the development of myelopathies without arteriovenous shunt
Case 12—Angiographic evaluation of a 57-year-old man with a progressive myelopathy and prominent perimedullary veins on MRI without arteriovenous shunt on SA (Figure 13).
Figure 13.
Angiographic evaluation of a 57-year-old man with prominent perimedullary veins. (a) DSA, left L1 injection, posteroanterior projection, arterial phase, documenting the artery of Adamkiewicz (gray arrow) and the anterior spinal artery (gray arrowhead). There is no arteriovenous shunt. (b) DSA, left L1 injection, posteroanterior projection, venous phase, showing delayed and stagnant opacification of dilated venous structures including the anteromedian spinal vein (white arrow) connected to the posteromedian spinal vein (black arrow) by a lateral anastomosis (white arrowhead); both veins are draining into a left T11 posterior radiculomedullary vein (RMV) (black arrowhead). (c) FPCA, sagittal reconstruction of a left L1 injection, depicting the dilated anteromedian spinal vein (white arrow), lateral anastomosis (white arrowhead), and posterior perimedullary veins (black arrow). (d) FPCA, coronal reconstruction of a left L1 injection; this reconstruction along the posterior aspect of the spinal cord documents multiple posterior perimedullary veins (small black arrows) converging towards a segment of posteromedian spinal vein (large black arrow) draining into a left posterior T11 RMV (black arrowhead). (e) FPCA, oblique reconstruction of a left L1 injection; a magnified reconstruction along the plane of the left T11 RMV (arrowhead)—which appears to be the sole drainage pathway for the conus medullaris—better illustrates the tight narrowing at its point of passage through the thecal sac (arrow).
Discussion
The spinal venous system
The thecal sac divides the spinal venous system into intradural and extradural compartments; the intradural compartment consists of intrinsic and perimedullary veins, the extradural compartment includes the internal and external vertebral venous plexuses. RMVs are likewise divided into intra- and extradural segments; the length of each segment varies regionally, but the extradural segment is typically short (Figure 14). The intradural compartment and the internal vertebral venous plexus are valveless but their interface—i.e., the point of passage of each RMV through the dura—acts a valve-like structure, the ARM.
Figure 14.
Organization of the spinal venous system. The intradural (red) and extradural (blue) venous systems are demarcated by the passage of the RMV through the thecal sac. The RMV has a long intradural and a short extradural component. The extradural venous system includes the internal vertebral venous plexus (i.e. the anterior and posterior epidural veins) and the external vertebral venous plexus (e.g. the lumbar and thoracic intersegmental, ascending lumbar, azygos and hemiazygos veins). The internal and external vertebral venous systems are interconnected by valveless anastomotic pathways such as the intervertebral veins and vertebral osseous network.
The antireflux mechanism
Oswald and Clemens described “valves” at or near the point of termination of RMVs into the epidural venous plexus in the early 1960s.2,12,1 In 1970, Gillilan3 introduced the notion of multifactorial venous backflow protection:
These valves, the relatively small caliber of the medullary veins, and the acute angle of their entrance into the plexus are factors which limit the backflow of venous blood into the spinal cord.
Five years later, Dommisse4 postulated a “valve-like mechanism” rather than actual valves:
[…] the axillary pouches of the dural sac, at which the veins make their exit in the company of the segmental nerve roots, appear to serve the function of venous valves. (p. 88)
The nature of these pseudo-valves was clarified by Tadié et al.,6–8 who coined the term antireflux mechanism (dispositif protecteur anti-reflux) to characterize the configuration they observed in anatomical specimen:
[…] an obstacle caused by a very significant and inextensible narrowing of the vein in its course within the dura mater [with a] clear and constant modification of the wall of the vein precisely where it crosses the dura mater.
Van der Kuip et al.13 validated Gillilan’s multifactorial hypothesis in 1999:
Intravenous dural folds, meandrous configuration and widening of the extradural part of the radicular veins, narrowing of the transdural part of these veins, and the presence of large amounts of smooth muscle cells in the venous walls suggest the existence of a—at least in part—dynamic reflux regulating mechanism.
Objections to the antireflux mechanism
Thron et al.14 confirmed a “special arrangement” of the transdural segment of the RMV, principally a focal narrowing, without true valves or “dural folds”. They reported, besides the “slit” type” configuration linked to the oblique course of the RMV within the thecal sac, a less frequent arrangement in which the RMV was encapsulated by a fibrous or dural nodule (“bulge” type”). The “slit” type was mainly seen in the vicinity of nerve roots and the “bulge” type with veins crossing the dura at some distance from nerve roots. The authors attempted to inject 14 RMVs retrogradely but were successful in two instances only; they suggested that retrograde filling of RMVs might result from postmortem thrombus formation and that “reflux from the epidural plexus to radicular veins is not reliably stopped at the dural level and possibly physiological”. They emphasized the latter point by mentioning the retrograde filling of RMVs reported during spinal phlebography. Such reflux was occasionally observed by Moret and Theron,15 in 15% of cases by Meijenhorst,16 but never by Vogelsang (personal communication to Meijenhorst).16 It is worth noting that Vogelsang17 used intraosseous phlebography rather than the more recently introduced transcatheter technique. The inconstant efficacy of adjuvant techniques used during spinal phlebography—e.g. “vigorous compression of the inferior vena cava”16—may also partially explain discrepancies. We cannot exclude either that some of these patients—investigated in the pre-MRI era—harbored undiagnosed low-flow SEAVFs.
Retrograde filling was noted in two recent anatomical studies using an epoxy resin as casting material in specimens injected beforehand with a thrombolytic solution;13,18 in one of these studies, van der Kuip et al.13 observed retrograde passage of epoxy in all instances (involving between 1 and 15 RMVs per specimen) and suggested that the various backflow-restricting factors they documented constituted a regulating rather than an antireflux mechanism.
Importantly, none of these situations were physiological as they involved the injection of contrast agents or anatomical material under artificial pressure and various adjuvant maneuvers. In postmortem studies, the lack of normal venous and cerebrospinal fluid pressure may also play a role. In our experience, material injected extradurally with sufficient pressure can occasionally overcome the resistance of the ARM (San Millan, unpublished data).
Overall, these studies suggest that the ARM probably involves physiological factors (e.g. muscular tone, CSF pressure, etc.) besides the purely morphological barrier established by the narrowing of the RMV at its point of transdural passage.
The antireflux mechanism and high-flow spinal vascular anomalies
High-flow vascular anomalies impact the ARM differently depending on their intra- or extradural location. High-flow intradural anomalies with antegrade venous drainage seem able to distend the focal narrowing of the RMV to a degree possibly proportional to the increase in venous pressure. This phenomenon is illustrated with two high-flow lesions, a high-pressure PmAVF (Case 5) and a low-pressure hemangioblastoma (Case 6): the ARM is reduced to a mild narrowing in the first case (Figure 6) but remains a tight stenosis in the second (Figure 7). This pressure-dependent distension of the ARM needs confirmation since factors such as patient’s age and duration of the pressure elevation may also play a role.
The ARM has an important protective function in cases of high-flow, high-pressure extradural anomalies. High-flow SEAVFs, which usually affect young patients, are not in our experience associated with intradural drainage and spinal venous hypertension (SVH) despite the severe and diffuse epidural dilation they induce. On the other hand, intradural drainage may occasionally be observed with long-standing high-flow extradural anomalies likely wearing down the effectiveness of the ARM (Case 7, Figure 8).
The antireflux mechanism and spinal venous thrombosis
While the protection afforded by the ARM against potentially harmful surges in intradural venous pressure is important, the presence of a tight narrowing proximal to the termination of RMVs into the epidural plexus may have a negative effect upon the normal antegrade spinal cord drainage. This seems particularly concerning in the lower thoracic and lumbosacral regions, where the long, near vertical course of RMVs must represent a risk factor for venous stagnation and thrombosis in the seating or standing postures. This phenomenon might explain the age-related loss of draining RMVs suggested by prior authors,19,20 which influences both the development and the clinical expression of low-flow spinal arteriovenous fistulas.
A thrombus forming at the site of the ARM propagates retrogradely, leaving the occluded RMV angiographically undetectable (Figure 5, lower dashed line). When the terminal segment of a multirooted RMV fills with thrombus, on the other hand, its roots remain patent and form an “arrow-tipped anastomotic loop,” a pseudo-variant acting as an angiographic marker of RMV thrombosis10 (Figure 5, upper dashed line).
It is conceivable that the chronic drainage impairment associated with the ARM might lead to SVH in the absence of arteriovenous shunt. This hypothesis must be envisaged prudently considering recent controversial associations made between venous stenoses and inflammatory cerebral disorders.21 Nonetheless, we have investigated several myelopathic patients referred for suspicion of low-flow spinal arteriovenous fistulas, in whom SA documented dilated perimedullary veins secondary to drainage impairment without arteriovenous shunt (e.g. Case 12). It is not clear whether these observations represent extreme variations of the norm, a specific disorder (i.e. spinal venous insufficiency), or the initial stage of the SVH seen with low-flow spinal arteriovenous fistulas (“prefistulous” stage).
The antireflux mechanism and low-flow spinal arteriovenous fistulas
SDAVFs and low-flow SEAVFs with intradural drainage typically present with a progressive myelopathy secondary to SVH. These acquired lesions generally occur in older men, likely in relation to a progressive loss of functional RMVs, although it is difficult to establish whether the paucity of RMVs leads to the formation of the arteriovenous shunt or results from the hemodynamic alterations induced by these anomalies (or both). As noted earlier, both the formation and expression of low-flow spinal arteriovenous fistulas appear mediated by thrombotic phenomena. The role played by a lack of drainage pathways on the development of SVH was emphasized by Logue in 1979.20 Merland et al. noted in 1980 that:19
[…] the dilatation of these veins, which is considerable in both diameter and extent, cannot be explained by arterialization alone. It is probably due to concomitant impairment in medullary venous return associated to the absence of veins draining into the dorsolumbar epidural space.
Regarding SDAVFs, it appears likely that RMV thrombosis precedes the formation of the arteriovenous shunt in a manner similar to the development of cranial dural arteriovenous fistulas.22 An attempt at recanalizing the thrombosed intradural segment of an RMV by radiculomeningeal arteries would account for the mode of drainage of these lesions, retrograde and through a single channel. Rare instances of SDAVFs with dual intra- and extradural drainages confirm that the shunt sits near the point of passage of the RMV through the thecal sac (Case 11).23 This hypothesis is also consistent with the histological studies of SDAVFs conducted by Takai et al., which found the feeding arteries within the two layers of the thecal wall and the arteriovenous shunt on its inner aspect.11
The shunt of low-flow SEAVFs typically involves an isolated pouch of epidural plexus. The irregular appearance of this arterialized venous pouch and its partial or complete disconnection from the rest of the internal and external vertebral venous plexuses again implies a context of venous thrombosis. Low-flow SEAVFs typically become symptomatic when a connection with one or more RMVs leads to retrograde intradural drainage. The development of SVH is, here again, facilitated by a lack of functional drainage pathways.
Low-flow SEAVFs without intradural venous drainage are typically incidental observations, although back and/or radicular pain may occur. Even when an RMV connects the arterialized pouch to the intradural venous system, retrograde drainage may still be prevented by a functioning ARM (Case 9). Subsequent failure of the ARM may be facilitated by angioarchitectural features such as the lack of alternate drainage pathways towards the external vertebral venous plexus (Case 8).
A note on bridging veins
The term bridging vein is used at the cranial level to characterize vessels crossing the subdural space to connect the superficial venous network to dural sinuses.24 For example, bridging veins of the medulla oblongata, which are topographically and developmentally close to spinal cord veins,25 “connect the median anterior medullary vein with the sinuses around the jugular foramen.26 By analogy, the term bridging vein has been introduced at the spinal level. Like RMVs, spinal bridging veins drain the perimedullary venous system into the epidural plexus but are distinguished by their point of passage through the thecal sac: RMVs cross the dura along the nerve root, laterally to the medial interpedicular line, while spinal bridging veins pierce the dura in between two spinal nerves, medially to the medial interpedicular line.27
However, this difference could be semantic and indicate a variability in the course of vessels with common developmental origin:
The radiculomedullary veins […] follow a nerve root and descend to an intervertebral foramen where they pierce the wall of the dural sac close to the nerve root in about 70%, but their exit may be completely independent from the nerve root in 30%.28
We adopt, in this article, the notion that spinal bridging veins are RMV variants rather than separate anatomical entities, possibly with a modification of their antireflux mechanism structure (i.e. slit versus bulge types). We therefore suggest that the concept of antireflux mechanism equally applies to RMVs and bridging veins.
Conclusions
The ARM divides RMVs into intradural and extradural segments. While the structure of the ARM is not yet fully clarified, it includes at least a tight narrowing of the RMV at its point of passage through the thecal sac, which is angiographically detectable and likely protects the intradural venous system from transient or persistent surges in venous pressure (e.g. sneezing, pregnancy). But this tight narrowing of the ARM also represents an obstacle to normal anterograde flow, potentially leading to venous stagnation and thrombosis. RMV thrombosis and the resulting loss of functional drainage pathways are likely involved in the development of SDAVFs and are known to influence the clinical expression of both SDAVFs and SEAVFs. Chronic spinal drainage impairment caused by the ARM in the absence of arteriovenous shunt, which could be viewed as a spinal form of the “idiopathic intracranial hypertension” caused by transverse sinus stenoses, is speculative but not inconceivable.
All studies used in this report are routine clinical investigations for which patients gave written informed consent.
Note
The author unfortunately could not obtain a copy of Oswald’s thesis, quoted here based on Clemens’ citation.
Footnotes
Declaration of conflicting interests: 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) disclosed receipt of the following financial support for the research, authorship, and/or publication of this article: The author is a consultant for Cerenovus and received research grant money from Siemens Medical.
ORCID iD: Philippe Gailloud https://orcid.org/0000-0003-0768-3273
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