Blood flow velocity and vasomotor reactivity in patients with arteriovenous malformations. A transcranial Doppler study.

BACKGROUND AND PURPOSE

A large percentage of patients with a cerebral arteriovenous malformation (AVM) show focal neurological signs or have a history of intracranial hemorrhage. The present study used transcranial Doppler sonography to assess the clinical significance of hemodynamic disturbances in the intracranial arteries of patients with an AVM.

METHODS

Eighteen patients with untreated AVMs were examined clinically, angiographically, and with transcranial Doppler sonography (blood flow velocity measurement and vasomotor reactivity in all main intracranial arteries).

RESULTS

A pathological increase in blood flow velocity (57.6%) and a decrease in vasomotor reactivity (72.7%) were frequently found in AVM feeding arteries. Vasomotor reactivity was also reduced in several nonfeeding arteries both ipsilateral (53.3%) and contralateral (30.8%) to the AVM. AVM size was a poor predictor of pathological transcranial Doppler results. Vasomotor reactivity of arteries ipsilateral to an AVM in patients with a history of hemorrhage was significantly higher (2.10 +/- 1.66% per mm Hg; mean +/- SD) than in patients with no history of bleeding (1.12 +/- 1.48% per mm Hg; P < .05). In patients with focal neurological signs but no history of hemorrhage, the percentage of arteries ipsilateral (100%) and contralateral (63.6%) to an AVM showing a pathological vasomotor reactivity was significantly larger than in nonhemorrhagic patients without focal signs (66.7% and 22.2%, respectively; both P < .05).

CONCLUSIONS

Our results suggest two distinct relations between transcranial Doppler results and clinical findings: (1) Relatively normal vasomotor reactivity values in arteries ipsilateral to an AVM indicate a high-pressure AVM with an increased risk of hemorrhage. (2) A strongly pathological vasomotor reactivity in arteries ipsilateral and contralateral to an AVM indicates a low-pressure AVM with a higher prevalence of hemodynamically induced neurological signs.