Developmental venous anomaly

Clinical History

25-year-old man presented with recurrent attacks of headache and blurring of vision, no vomiting or other neurological deficit. His blood pressure as well as blood tests were normal. Non contrast CT brain was unremarkable.

Imaging Findings

Axial T2 and FLAIR images (Fig 1) reveal a left periventricular hyperintense linear structure (white arrow) that is perpendicular to the left lateral ventricle. T1 pre and post contrast images (Fig 2) show this structure to be of low signal in pre contrast and enhances avidly and homogenously in post contrast images. Because it is perpendicular to the sagittal plane it has a dot shape in sagittal images (red arrow). There is no perilesional oedema or mass effect seen. This structure traverses the white matter toward the lateral ventricle as seen in post contrast coronal image (Fig 2c).
Susceptibility weighted images (SWI) (Fig 3) clearly display this venous structure which arises from the surface of the left frontal lobe draining cortical veins, traverses the white matter of left frontal lobe and drains to the internal cerebral vein.

Discussion

Developmental venous anomalies (DVA), formerly known as venous angiomas, are the commonest cerebral congenital vascular malformation that are thought to be either due to primary dysplasia of the cerebral veins without the capillaries and arteries or in-utero thrombosis of normal venous pathway. They are usually asymptomatic, uncomplicated and don't require surgical intervention. [1, 2]
DVAs can be classified into juxtacortical which are within the grey matter and usually drain to cortical veins and dural sinuses, deep periventricular which are adjacent to the lateral or 3rd ventricles and drain to the subependymal veins and Galen system and subcortical which are just below the cortex but do not reach the ventricles and drain to either way. [1]
Furthermore, vascular malformation can be subdivided into high flow anomalies e.g. arteriovascular fistula and slow flow anomalies e.g. capillary telangectasia, cavernous malformation and DVAs. Slow flow anomalies may be missed in conventional imaging especially when uncomplicated, hence the need for a new technique to detect such abnormalities. [3]
Susceptibility weighted image (SWI) is the new technique that has high sensitivity to detect venous structures and low flow anomalies. It is high spatial resolution 3D gradient echo MR sequence that augments the magnetic susceptibility differences between tissues according to their oxy/deoxy haemoglobin and blood products contents. Paramagnetic blood products e.g. deoxygenated haemoglobin; intracellular methaemoglobin and haemosiderin create phase difference with adjacent tissues (which contain more oxygen) leading to signal loss. This is why the veins normally appear hypointense in SWI and when there is mechanical ventilation, which increases blood oxygenation level, the veins become less hypointense. [3, 4]
DVAs range from a single small draining vein to a large anomalous vein draining the entire hemisphere. On angiography they have caput medusae appearance where multiple small veins drain to a larger one. On MRI the anomalous vessel usually displays signal void in T1 and T2 WIs. Due to its slow flow, the vessel shows avid homogenous enhancement post contrast. [5] The appearance of DVA as a bright linear structure in T2 and FLAIR images, as in this case, is due to spatial misregistration artefact. This occurs when blood flow is oblique to the axis of phase encoding gradient that results in bright structure in spite of flow void. [6]
When DVA is found in setting of cerebral haemorrhage, an associated lesion e.g. cavernoma should be sought as the cause of bleeding because DVAs rarely bleed. [2]

Differential Diagnosis List

Final Diagnosis

Developmental venous anomaly

URL:	https://eurorad.org/case/11269
DOI:	10.1594/EURORAD/CASE.11269
ISSN:	1563-4086