The cerebral vascular malformations are mostly classified into four categories: Developmental venous anomaly (DVA), arteriovenous malformation (AVM), capillary telangiectasia, and cavernous angioma (CA) [12, 13]. Of these, DVA is the most common one, constituting about 60% of all vascular malformations, especially with the progresses of MR imaging and is mostly incidental on neuroimaging [14]. Hammoud et al. [15] thought that DVAs are benign entities and likely to become asymptomatic, although headache and epilepsy were reported.
The exact prevalence of DVA is nearly unidentified, but autopsy studies had reported an incidence of 2–3% in the general population [16]. In our study, DVAs were demonstrated a 2.8% incidence, which is also like those observed by Cho et al. [1], who reported a 2.6% incidence in 1068 brain MR examinations.
DVAs are characterized by a cluster of venous radicles that converge into a draining vein, resulting in the typical caput medusae or umbrella-like appearance. To join either the superficial or deep venous system, the collecting vein crosses a variable length of cerebral or cerebellar parenchyma [17].
Several studies thought that the incidence of two or more DVAs existing in different regions of the brain simultaneously about 1.2–16.3% of cases [18]. Most our studied cases were noted with a single DVA with the prevalence of double DVAs was only 3.4%, which is in accordance with Lee et al. [19], who found that 1.6% of their cases had three DVAs. Faure et al. [3] also reported that most DVAs were solitary.
Of the total 29 DVA cases, DVAs are mostly located in the supratentorium (86.2%), with a clear frontal predominance (48.3%). The parietal lobe showed the second most frequent location representing about 31%. While the temporal lobe showed only 6.9% with no occipital or basal ganglia DVAs were noted. Regarding the infratenotrial region, DVAs were accounted about 13.8% with only cerebellar location. Various articles exhibited similar findings to our study. The study by Garner et al. [20], of 100 cases with DVA diagnosed by DSA, CT, and MRI examinations, showed that DVAs are predominant in the frontal location (42%), while the parietal and cerebellar locations representing about 24% and 14% respectively. To Huang et al. [21], DVAs were frequently been found in the frontal lobe (40%) and the cerebellum (27%) and were less often in the parietal lobe (15%). Wilms et al. [22] reported that the prevalence of DVA locations to be as follows: the frontal (38%), the cerebellar (38%), the parietal (10%), and the occipital regions (10%).
DVAs can be located subcortically, juxtacortically, and deeply (or paraventricularly) with the corresponding cases for each area; 9/29 (31.1%), 7/29 (41.1%), and 13/29 (44.8%) respectively. This categorization was first suggested by Valavanis et al. [23] and Ostertun et al.’s [24] studies. Both showed that DVA caputs were localized predominantly in the subcortical region representing 57.1% and 61.9% respectively. However, our findings were matched with the study performed by Gökçe et al. [13], who observed predominant deep parenchymal DVA location, 54.5%, followed by the subcortical area, 17%.
Various parenchymal abnormalities and lesions can accompany DVAs [13]. The parenchymal abnormalities within our study are relatively few, but it may be related to selection bias and sample size. In our study, three of 29 DVA cases (10.3%) displayed hyperintensity on FLAIR sequence within the drainage territory of a DVA with no identified diffusion restriction. Few previous studies have estimated this association. In a study performed by Ruiz et al. [25], signal-intensity abnormalities in the drainage territory was 28.3% of 60 DVAs evaluated by MRI, more than twice the frequency reported in our study. However, the etiology of signal-intensity abnormalities related to DVAs is relatively unclear; Santucci et al. [4] reported that the abnormal FLAIR high signal intensity may represent edema or gliosis caused by chronic mild venous congestion and hypertension as a result of the anomalous venous drainage.
Our study showed no evidence of accompanying brain pathologies such as intracerebral hemorrhage, cerebral infarction, or leukomalacia. Also, no calcification deposit was noted in the surrounding brain parenchyma or the walls of the DVA.
To Ku et al. [26], intracerebral hemorrhage is a rare DVA complication and predominately described in patients with coexisting vascular malformations. McLaughlin et al. [27], in their observational study of 80 patients with symptomatic DVAs, found an annual hemorrhage rate of 0.68% per year retrospectively and 0.34% per year in the prospective study. Garner et al. [20] revealed that the hemorrhages that associated with DVA are usually small and do not lead to high mortality. The previous studies are matched with our results regarding unidentified cerebral hemorrhage within our DVA cases.
DVAs were found to be rare before the developments in MR imaging, as had to be undetectable on unenhanced MRI as well as on MRA image, unless they were associated with a CM. Nowadays, they are seen with high frequency as incidental finding at contrast-enhanced MRI [28].
Susceptibility-weighted imaging (SWI), an increasingly used MR sequence in recent years with a high sensitivity effect, can better detect vascular anomalies such as the DVA and has been shown to be more sensitive than conventional T2* sequence in the detection of vascular structures [10]. SWI can demonstrate the whole vascular structure well and typically have a low signal intensity due to the blood oxygen level-dependent (BOLD) effect in the dilated medullary and draining veins [4].
We consider that SWI has a high potential for the detection of non-complicated DVAs including the small lesions without contrast-enhanced MR study. SWI in our study showed 100% true positive result with consequent high global diagnostic accuracy. So, invasive imaging as conventional cerebral angiography as well as contrast-enhanced MR imaging are not required for their confirmation and mostly reserved for complicatd cases or to exclude associated vascular lesions.
