I would like to thank them for supporting me during my whole professional career and for numerous stimulating discussions on vascular problems of the brain. Forsting and I. Capillary Telangiectasia. Cognard, L.
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Spelle, and L. Clinical Presentation. Wanke, A. In contrast, DVAs must be considered as unusual, but nonpathological, venous drainage and an embryologically determined variant of venous drainage. In my experience, another factor contributing to the DVA-related confusion is that many radiologists and clinicians just see abnormal vessels on magnetic resonance imaging MRI scans, immediately tell the patient something about a vascular malformation, and refer the patient for neurosurgical extirpation of the lesion.
However, if you are reporting about a DVA, it is usually necessary to explain what this is. And this is a good reason to read the upcoming chapter. Saito and Kobayashi et al. This hypothesis is supported by the absence of normal draining veins in the region of the large draining collector vein. Another assumption is that an in-utero acquired venous occlusion maintains the intrinsic venous anastomoses within the white matter. The DVA then expresses an early collateral adaptation, but develops on a preexisting venous system that has been transformed.
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However, the majority of DVAs are not associated with any sort of neural tissue damage or dysfunction. Furthermore, the fact that DVAs do not exist in the diencephalon, brain stem, or spinal cord and are only encountered where tectum derivates exist, excludes DVAs from the group of pathological malformations Lasjaunias The association of venous malformations with other vascular malformations gave further room for speculation.
Mullan et al. However, these are nice theories, but do not have any impact on diagnostic work-up or patient management, nor are they supported by any study. Kilic et al. Whereas AVM and cavernomas had expression of vascular endothelial growth factor, DVAs did not express any of the studied growth factors and mainly consisted of structural proteins of angiogenically mature tissue. Wanke 2 the venous drainage instead of being a true vascular malformation. In contrast, the relationship of DVAs with cavernous hemangiomas has been well documented Abe et al.
There are also reports about de novo formation of cavernous hemangiomas in the vicinity of DVAs Ciricillo et al. The close relationship of mixed malformations may be related to venous hypertension within the regional microenvironment with erythrocyte diapedesis and angiogenic growth factor release Cirillo et al. However, we have to accept the coincidence between DVAs and cavernomas, but have to admit that we do not have any substantial hypothesis what the pathogenetic origin of this coincidence is.
The histologic examination does not reveal any vessel abnormality.
Cerebral Arteriovenous Malformation from Classification to the Management
The vessel wall is completely normal in DVAs. The anomaly in DVAs is the course of the draining vein. There is no arterial component in this entity. Intervening brain tissue is present between the veins compromising the lesion, and this brain tissue is usually normal without evidence of hemosiderin staining or gliosis. On MRI, there is sometimes a high T2-signal visible around the draining vein. The lesion consists of a tuft of abnormally enlarged medullary venous channels that are radially arranged around, and drain into a central venous trunk.
This should be of particular interest when surgery has to be performed around the draining vein, e. In these patients, it is of the utmost importance to preserve the draining vein and to remove only the cavernoma see Fig. Garner et al. This range of hemorrhage risk is within the range we expect from cavernous hemangiomas alone.
Based on these data and on hemodynamics, one might already conclude that hemorrhages in the presence of a DVA are not related to the DVA itself, but in nearly all patients related to an associated cavernous angioma! My opinion is that the risk of hemorrhage b Fig. Axial a and sagittal b contrast-enhanced T1-weighted magnetic resonance imaging with a typical right frontal developmental venous anomaly.
Conspicuous on both views is the transcerebral draining vein. However, this is not evidence-based, just a simple clinical impression gained over the years. In all cases mentioning a pure DVA as the cause of an ICH, imaging was not optimal and did not rule out the more common constellation with an associated cavernoma. The coincidence of DVAs and cavernomas, however, is evidence-based and therefore has to be taken into consideration whenever facing a cavernoma or a DVA.
Up to one third of DVAs are associated with cavernomas see Figs. Axial contrast-enhanced T1-weighted magnetic resonance imaging with a developmental venous anomaly located in the left cerebellar hemisphere. Again, the transparenchymal draining vein is the most striking sign. On b , the Medusa head is clearly visible.
There is no need for an additional digital subtraction angiography A major problem of most studies reporting hemorrhages due to a DVA is how they ruled out an associated cavernoma. It is clearly not enough just to perform T2-weighted images in patients with DVAs. However, having in mind the association of caverb 4 M. Wanke a b c d Fig. Note the enlarged perivascular space around the vein on T2 image a and the coronal T1 image without contrast enhancement d. In , McLaughlin and colleagues published their series of 80 patients with DVAs focused on the prospective natural history of cerebral developmental venous malformations.
Two patients presented with trigeminal neuralgia and a single patient with an extrapyramidal movement disorder. Korinth et al. After microvascular decompression, the typical symptoms of the neuralgia disappeared completely. In three patients, there was an association of the DVA with a cavernous hemangioma. McLaughlin and colleagues did excellent work while collecting all these data and it is clearly one of the most important papers dealing with DVAs.
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However, it is questionable whether the symptoms of the patients were really related to the DVA. It is not surprising that a substantial proportion of patients with these lesions reaching neurosurgical centers had some history of associated neurologi- Developmental Venous Anomalies cal events. Such selection bias is not unusual and is likely to overestimate the risk of any associated neurological manifestation.
Another problem of the study is that imaging was not optimized to get maximal sensitivity for cavernomas. Symptoms like bleeding, seizures, and headache are known to be associated with cavernomas.
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Another interesting hypothesis of theirs is that association of a cavernoma and a DVA may increase the probability of a cavernoma-related hemorrhage. Comey et al. Other surgeons Little et al. The typical transcerebral draining vein is diagnostic. However, the epileptic seizures of the patient are not associated with the DVA. This cellular migration disorder is the cause of the seizures b c 6 M. The patient was referred with the diagnosis of an arteriovenous malformation as causative for his temporal lobe epilepsy.
Therefore, it might indeed be possible that venous hypertension in association with DVA can predispose a cavernoma to bleed. Because of their eloquent location, it is likely that smaller hemorrhages in the posterior fossa manifest overt symptoms and may hence be detected clinically. In 12 patients, an associated cavernoma was found. And again: there was no hemorrhage in a patient with a pure DVA. All hemorrhages were due to an associated cavernoma. All hemorrhages are related to an associated cavernoma. In both groups, there were a lot of patients with headaches and epilepsy; in fact, these two groups represented the main referral reason in Developmental Venous Anomalies both groups.
In general, there are two explanations for the coincidence of headaches and DVAs in the same patient. Second, a small subgroup of patients with DVA and headache might have an additional cavernoma located near the surface of the brain. Some of these patients suffer from headache due to subarachnoid microhemorrhages.
If this is true, one should take a careful look for an associated cavernoma, cavernomas being known to cause different types of epilepsy, mainly due to their content of hemosiderin. Lasjaunias pointed Fig.