Venous Infarction of Developmental Venous Anomaly: A Case Report with Perfusion Imaging

Abstract

Developmental venous anomaly (DVA) is a common congenital venous malformation characterized by dilated medullary veins in caput medusa configuration and a draining vein. Despite the high incidence of DVAs, they are benign anatomic variations and rarely cause symptoms. Here, we report computed tomography and magnetic resonance imaging findings with perfusion images of acute infarction from underlying DVA in a 63-year-old female patient who presented with acute onset of neurologic symptoms and recovered without any neurologic deficit. Index terms

A proposed framework for cerebral venous congestion

“…71 Typically seen, developmental venous anomalies (DVAs), characterized by fusing large draining transmedullary venous networks into a single venous collector, can cause local venous congestion with abnormal mean transit time, cerebral blood volume and cerebral blood flow. 72 DVAs can become symptomatic by thrombosing and bleeding, as well as causing venous infarcts 73 in much the same way as cortical or deep vein thrombosis can cause injury. 74 In addition to these intrinsic and extrinsic venous pathologies, there is a spectrum of hydrovenous disorders, particularly in pediatric populations, associated with dural arteriovenous fistulae (DAVF) and arteriovenous malformations (AVMs), first described by Lasjaunias, as impaired resorption of CSF or interstitial fluid due to markedly severe venous hypertension, resulting in increased ICP, hydrocephalus, or syringomyelia.…”

An Illustrative Review of the Pathomechanisms of Symptomatic Developmental Venous Anomalies

“…As is the case of any single-compartment system, the optimal pressure is dictated by the balance between the inflow and outflow pathways. Potential imbalance at either end may aggravate the neuroparenchymal injury associated with venous hypertension, whether it is due to increased inflow secondary to arterialization due to microshunts or an AVM nidus upstream of the DVA or reduced outflow secondary to thrombosis/stenosis of the collector vein or downstream venous sinuses or deep venous system 15,17,19 . Spontaneous intracerebral hemorrhage, subarachnoid hemorrhage, venous infarcts, and focal gliosis/scarring represent a spectrum of neuroparenchymal signal changes induced by flow-related alterations 20 …”

“…Potential imbalance at either end may aggravate the neuroparenchymal injury associated with venous hypertension, whether it is due to increased inflow secondary to arterialization due to microshunts or an AVM nidus upstream of the DVA or reduced outflow secondary to thrombosis/stenosis of the collector vein or downstream venous sinuses or deep venous system. 15,17,19 Spontaneous intracerebral hemorrhage, subarachnoid hemorrhage, venous infarcts, and focal gliosis/scarring represent a spectrum of neuroparenchymal signal changes induced by flow-related alterations. 20 The native parenchymal framework of DVA is composed of thick hyalinized venous channels with walls inherently devoid of elastic lamina, and sparse smooth muscles likely predispose these vascular variants to succumb at lower thresholds to hemodynamic insults.…”

“…These thereby translate into venous hypertension-induced focal neurological deficits brought about by spontaneous intracranial hemorrhage, including intraparenchymal, subarachnoid, venous infarcts, outflow obstruction-induced gliosis, tumefactive demyelination, and more 16–18 …”

“…These thereby translate into venous hypertension-induced focal neurological deficits brought about by spontaneous intracranial hemorrhage, including intraparenchymal, subarachnoid, ve-nous infarcts, outflow obstruction-induced gliosis, tumefactive demyelination, and more. [16][17][18] Through this series, we intend to illustrate the conventional cross-sectional imaging and perfusion abnormalities of DVA and thereby extend the scope in diagnosing the arterialized, transitional, and resistive variants.…”