Topography of cerebral infarction associated with carotid artery dissection.

Because the pathogenesis of cerebral ischaemia in internal carotid artery dissection (ICAD) is controversial we studied the topography of cerebral infarction that results from ICAD according to pathophysiology of embolic and haemodynamic stroke. Sixty-four patients with 67 ICADs diagnosed by angiography, Doppler duplex sonography and magnetic resonance imaging (MRI) were studied prospectively during the past decade. According to current pathophysiological concepts, cortical territorial infarcts and large subcortical lenticulostriate infarcts revealed by CT or MRI were classified as embolic, while smaller infarcts in the subcortical junctional zone and infarcts in the cortical borderzone between the middle (MCA) and anterior cerebral artery were interpreted as haemodynamic infarcts. Of the 67 dissections 37 (55%) were associated with brain infarcts, of which territorial MCA infarcts of variable size accounted for 60%. These were combined with infarcts of the anterior and posterior cerebral artery in 5%; 8% of the patients had complete MCA infarction. Large lenticulostriate infarcts were present in 11%. Haemodynamic infarcts involved the subcortical junctional zone in 16% but never the anterior cortical borderzone. Although different abnormal Doppler findings indicated haemodynamically significant carotid obstruction in all symptomatic ICADs, only the characteristic high-resistance Doppler signal was significantly associated with the occurrence of brain infarction (in 66%, P < 0.01). The angiographic features of ICAD did not correlate with the incidence or with the topography of cerebral infarction. Patterns of infarction in ICAD indicate a predominantly embolic causation probably due to thrombus formation in the dissected carotid artery in the presence of severe haemodynamic obstruction, as demonstrated by Doppler sonography.