• W Chong, H Patel, and M Holt.
• Interventional Neuroradiology Unit, Diagnostic Imaging, Monash Medical Centre; Melbourne, Australia - winston.chong@southernhealth.org.au.
• Neuroradiol J. 2011 Mar 29;24(1):59-70.

PurposeThe 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.Materials & MethodsThe pathophysiology of DVAs were analysed with CT perfusion (CTP), 4 dimensional dynamic computed tomography angiography (4D CTA) and catheter digital subtraction angiography.ResultsSymptomatic 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.ConclusionWe 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.

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