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Claudia J. Chaves, MD; Irina Staroselskaya, MD; Italo Linfante, MD; Rafael Llinas, MD; Louis R. Caplan, MD; Steven Warach, MD, PhD

Arch Neurol. 2003;60:237-242.

Background  The importance of hemodynamic factors in the pathophysiology of stroke and transient ischemic attacks in patients with internal carotid artery (ICA) stenosis or occlusion remains controversial.

Objective  To investigate whether perfusion-weighted imaging (PWI) could identify pathophysiologically meaningful categories in patients with symptomatic and asymptomatic ICA occlusive disease.

Methods  Thirty-eight consecutive patients with occlusion (22 patients) or severe stenosis (16 patients) of the ICA, determined by ultrasonography or magnetic resonance angiography, were identified from the Beth Israel Deaconess Medical Center Stroke Database, Boston, Mass. Thirty-five patients were symptomatic (29 who had strokes and 6 who had transient ischemic attacks) and 3 were asymptomatic. All symptomatic patients underwent PWI within the first 24 hours after symptom onset. The patterns of PWI were analyzed according to the degree of ICA stenosis and the clinical presentation.

Results  Three patterns of perfusion abnormalities were identified: extensive hypoperfusion involving the middle cerebral arterial and/or anterior cerebral arterial territories (25 patients), localized perfusion deficits involving predominantly the ipsilateral border zone areas (8 patients), and normal perfusion (5 patients). All 3 patterns were found whether or not the ICA was occluded. Patients who had acute stroke most frequently had extensive perfusion deficits involving 1 or 2 territories while patients who had transient ischemic attacks often had hypoperfusion affecting the border zone regions. All asymptomatic patients had normal perfusion.

Conclusions  In our sample the pattern of PWI related to the clinical presentation but not to the degree of ICA disease (occlusive vs severe stenosis). Our study findings add further support to the hypothesis that hypoperfusion is a major contributing factor in the pathophysiology of carotid artery occlusive disease.

From the Department of Neurology, Lahey Clinic, Burlington, Mass (Dr Chaves); the Department of Neurology, Beth Israel Deaconess Medical Center, Boston, Mass (Drs Staroselskaya, Linfante, Llinas, and Caplan); and the National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Md (Dr Warach).

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