Developmental Venous Anomalies (DVA): What are they really?
OBJECTIVE
The aim of this paper is to analyse the pathophysiology of 3 DVA cases from our institution, review the literature and propose a classification of these lesions.


METHODS
The pathophysiology of DVAs were analysed with CT perfusion (CTP), 4 dimensional dynamic computed tomography angiography (4D CTA) and catheter digital subtraction angiography.


RESULTS
Symptomatic DVAs may be caused by associated lesions and compression of neural structures by the DVAs. The imbalance between the inflow and outflow of these lesions, including venous ischaemia, has also been postulated as a cause. Our analysis showed that increased cerebral blood flow (CBF) and cerebral blood volume (CBV) and decreased mean transit time (MTT) and time to peak (TTP) were found in DVAs with micro arteriovenous shunting. DVAs without shunting had raised MTT and TTP instead.


CONCLUSIONS
We postulate that the arteriovenous shunting resulted in arterial steal and chronic hypoxia which could be a pathophysiological mechanism for symptomatic DVAs. CTP and 4D CTA are effective non invasive tools to study DVAs. A classification is proposed.
Interventional Neuroradiology Unit, Diagnostic Imaging, Monash Medical Centre; Melbourne, Australia - winston.chong@southernhealth.org.au.
W
W
Chong
H
H
Patel
M
M
Holt