Venous Infarction Of Developmental Venous Anomaly: A Case ...

DISCUSSION

Currently, DVAs are regarded as a primary dysplasia of capillaries and small transcerebral veins or a compensatory mechanism caused by an arrest of normal venous development during-embryogenesis (7). They are thought to represent variations of parenchymatas' venous drainage and surgical resection should be avoided, because when they are drained no other normal venous discharging system exists (1, 2).

Despite the DVAs' high incidence, they are benign anatomic variations and rarely cause symptoms due to either mechanical compression to adjacent intracranial structures, which may result in hydrocephalus, tinnitus, hemifacial spasms, and trigeminal neuralgia or a misbalance of the blood flow (4). Flow related complications can be characterized as a misbalance of the blood's in- and outflow in the DVA system, which raises the pressure in the DVAs, either due to an increase of the former or a restriction of the latter (4). They may also give rise to acute symptoms which can mimic arterial stroke due to the draining vein's restricted outflow and venous congestion, which might cause an increase of complications such as hemorrhages or infarctions. Ruíz et al. (8) reported complications in 19 cases with symptomatic DVAs (venous ischemic infarction. 53%, parenchymal hemorrhage, 37%, and subarachnoid and intraventricular hemorrhages, 5%). DVAs also frequently coexist with other types of vascular malformations, such as cavernous ones and they may be associated with a higher hemorrhagic risk. There are several reported cases of DVAs with thrombotic obstruction of draining veins, resulting in venous infarction with or without parenchymal hemorrhage (5, 6, 8). Thrombosis of an DVA's draining vein leading to venous brain infarction is a rare complication and an infarction remained nonhemorrhagic, if early recanalization is ach-ieved (9).

According to Pereira et al. (4), mechanical and increased inflow types of flow-related symptomatic DVA can be excluded in our case, since there was no intracranial structure causing mechanical compression or cerebral arteriovenous malformation which may also result in an increased inflow of DVA. In our case, there was no discernible venous thrombosis as found in the imaging studies and we assumed there a possibility of venous infarction with early recanalization of thrombosed vein might exist; this implies a decreased outflow type of flow-related symptomatic DVA, considering that there is no hemorrhage associated with infarction and that the acute onset of the patient's symptoms happened without a significant past medical history.

DVAs are thought to lack smooth muscle cells and elastic connective tissue resulting in less flexibility to changes of hemodynamic disturbances (5, 6). Truwit (1) reported that a focal stenosis of the draining vein is possible at the point where it penetrates the dura which can cause lessened compliance, increased resistance to flow, and reduced capacity of the vessel for pressure change adjustments. In addition, a relative volume overload, previous hemorrhages, and chronic cerebral ischemia or venous hypertension can result when a large parenchymal territory is drained by a DVA. As a result, it has been suggested that imaging abnormalities of high SI on T2 FLAIR images, higher ADC values, and perfusion alterations in the DVAs' vicinity can be explained by chronic cerebral ischemia, resulting from venous congestion (10). The pattern of perfusion abnormalities in our case was similar to previously reported results, e.g., an increased rCBV and rCBF with prolonged MTT and TTP, implicating venous congestion with delayed perfusion (10).

Regarding DWI and ADC maps, focal SI change of diffusion restriction may be indistinguishable from arterial infarction, but underlying DVA can be identified by enhanced T1-weighted images. In addition, DVA-associated perfusion abnormalities may represent its role regarding venous congestion.

Treatment principles of acute infarctions related to DVA have not been established, but a number of case series has reported favorable outcomes after anticoagulation therapy, particularly in instances of the draing vein associated with thrombus (5, 6, 7). Due to differences in the pathophysiology of venous and arterial stroke, venous infarction may not have the same prognostic value as the arterial infarct and it may be completely reversible (6).

In conclusion, even though DVAs commonly encounter insignificant anatomic variants, they rarely cause venous infarction with acute neurologic symptoms; characteristics of imaging features by perfusion studies may provide a clue to diagnosis. The understanding of and familiarity with imaging findings of complicated DVAs is essential for accurate diagnoses with different kinds of management of and prognoses about arterial infarction.