M Müller1, K Schimrigk. 1. Department of Neurology, University Hospital of the Saarland, Homburg/Saar, Germany.
Abstract
BACKGROUND AND PURPOSE: The compromise of cerebrovascular autoregulation in severe occlusive carotid artery disease depends on the functional capacity of collateral pathways. In previous reports correlating hemodynamic disturbances with collateral pathways, collateral blood supply was often evaluated by invasive cerebral angiography. In this study noninvasive transcranial Doppler ultrasound was used to determine both collateral pathways and vasomotor reactivity. METHODS: With the use of blood flow direction, compression tests, and evident side-to-side asymmetries of blood velocities, the collateral supply through the anterior and posterior communicating arteries, the ophthalmic artery, and leptomeningeal anastomoses was evaluated by transcranial Doppler ultrasound in 48 patients (42 men, 6 women; mean +/- SD age, 59 +/- 9 years) with occlusion (n = 36) or stenosis of more than 90% (n = 12) of one internal carotid artery. Ipsilateral vasomotor reactivity was determined by the percent increase of middle cerebral artery mean blood velocity with the use of (1) the breath-holding maneuver and (2) acetazolamide (1 g IV) as vasodilatory stimulus. Additional stenoses (50% to < 90%) of the contralateral internal carotid artery were present in 20 of the 48 patients. RESULTS: Vasomotor reactivity was not affected by the presence of a contralateral internal carotid artery stenosis. Both vasodilatory stimuli similarly indicated poor vasomotor reactivity when an ophthalmic or a leptomeningeal pathway accompanied an anterior communicating artery pathway compared with a lone anterior communicating artery pathway (P < .05). The acetazolamide challenge indicated significantly better preserved vasomotor reactivity when blood supply was provided through a lone anterior communicating artery pathway (66 +/- 30%) than through an anterior and posterior communicating artery pathway (33 +/- 20%, P < .05), whereas the breathholding method failed to show such a difference. CONCLUSIONS: The presence of an ophthalmic artery pathway may provide the first evidence of disturbed vasomotor reactivity. The use of cerebral angiography to evaluate collateral pathways must be considered carefully since transcranial Doppler ultrasound is a reliable noninvasive alternative.
BACKGROUND AND PURPOSE: The compromise of cerebrovascular autoregulation in severe occlusive carotid artery disease depends on the functional capacity of collateral pathways. In previous reports correlating hemodynamic disturbances with collateral pathways, collateral blood supply was often evaluated by invasive cerebral angiography. In this study noninvasive transcranial Doppler ultrasound was used to determine both collateral pathways and vasomotor reactivity. METHODS: With the use of blood flow direction, compression tests, and evident side-to-side asymmetries of blood velocities, the collateral supply through the anterior and posterior communicating arteries, the ophthalmic artery, and leptomeningeal anastomoses was evaluated by transcranial Doppler ultrasound in 48 patients (42 men, 6 women; mean +/- SD age, 59 +/- 9 years) with occlusion (n = 36) or stenosis of more than 90% (n = 12) of one internal carotid artery. Ipsilateral vasomotor reactivity was determined by the percent increase of middle cerebral artery mean blood velocity with the use of (1) the breath-holding maneuver and (2) acetazolamide (1 g IV) as vasodilatory stimulus. Additional stenoses (50% to < 90%) of the contralateral internal carotid artery were present in 20 of the 48 patients. RESULTS: Vasomotor reactivity was not affected by the presence of a contralateral internal carotid artery stenosis. Both vasodilatory stimuli similarly indicated poor vasomotor reactivity when an ophthalmic or a leptomeningeal pathway accompanied an anterior communicating artery pathway compared with a lone anterior communicating artery pathway (P < .05). The acetazolamide challenge indicated significantly better preserved vasomotor reactivity when blood supply was provided through a lone anterior communicating artery pathway (66 +/- 30%) than through an anterior and posterior communicating artery pathway (33 +/- 20%, P < .05), whereas the breathholding method failed to show such a difference. CONCLUSIONS: The presence of an ophthalmic artery pathway may provide the first evidence of disturbed vasomotor reactivity. The use of cerebral angiography to evaluate collateral pathways must be considered carefully since transcranial Doppler ultrasound is a reliable noninvasive alternative.
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