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Cognitive impairment in patients with carotid artery occlusion and ipsilateral transient ischemic attacks

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Abstract.

Although transient ischemic attacks (TIAs) by definition do not cause lasting neurological deficits, cognitive impairment has been suggested in patients with carotid artery disease who have suffered from a TIA. The purpose of our study was to assess whether patients with carotid artery disease and TIAs are cognitively impaired, to describe the frequency, nature and severity of this impairment, and to search for associated patient characteristics.

Thirty-nine consecutive patients with carotid occlusion and ipsilateral cerebral or retinal TIAs, and 46 healthy controls underwent extensive neuropsychological assessment. Performances were compared group-wise with analysis of variance. In addition, the presence of cognitive impairment in the individual patient was determined. Associations between illness characteristics and cognitive impairment were explored with regression analysis.

Fifty-four percent of patients were cognitively impaired. Cognitive deficits were non-specific in nature and mild in severity. Impairment occurred also in patients with isolated retinal symptoms and in those without visible ischemic brain lesions on MRI. Neither the presence of any vascular risk factor, the side of the symptomatic carotid occlusion, the uni- or bilaterality of carotid occlusion, nor the number of cerebral ischemic lesions were predictors of cognitive impairment.

We conclude that about half of the patients with carotid artery occlusion and ipsilateral TIAs are cognitively impaired. The presence of cognitive deficits in patients with isolated retinal symptoms and in those without cerebral ischemic lesions on MRI argues against an exclusive role for structural brain damage in the pathogenesis of these deficits.

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Correspondence to Floor C. Bakker.

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Bakker, F.C., Klijn, C.J.M., Jennekens-Schinkel, A. et al. Cognitive impairment in patients with carotid artery occlusion and ipsilateral transient ischemic attacks. J Neurol 250, 1340–1347 (2003). https://doi.org/10.1007/s00415-003-0222-1

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  • DOI: https://doi.org/10.1007/s00415-003-0222-1

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