Cognitive impairment in patients with symptomatic carotid artery occlusion

Abstract

Background Although transient ischemic attacks (TIAs) by definition do not cause neurologic deficits, cognitive impairment has been suggested in patients with carotid artery disease (CAD) and ipsilateral TIAs. The cause of this impairment has not been elucidated yet. Thrombo-embolism, but also chronic cerebral hypoperfusion have been suggested to play a role. In this light, surgical interventions that improve the blood flow towards the brain have been promoted to halt or even reverse cognitive deterioration in patients with symptomatic CAD. However, studies on the effect of revascularization surgery on cognition have yielded conflicting results. Before conclusions can be drawn, knowledge is required on the natural history of cognitive impairment in these patients. Methods Between September 1995 and July 1998, 113 patients with TIAs or moderately disabling stroke attributable to an angiographically proved carotid artery occlusion were recruited from consecutive patients referred to the departments of Neurology or Vascular Surgery of the University Medical Center Utrecht. Neuropsychological assessment, MR investigations (MRI, 1H-MRS, MRA), TCD ultrasonography (CO2 reactivity) and investigations of health-related quality of life (SF-36) and depressive mood took place at three points in time: after inclusion in the study, and 6 and 12 months thereafter. Spouses of the patients were asked to cooperate with the neuropsychological assessment, thus providing a healthy control group. Results At baseline, 40% of patients with TIAs, and 70% of patients with minor stroke were cognitively impaired. Cognitive ipairment was non-specific in nature, and mild to moderate in severity. Impairment was not restricted to patients with MRI-detected lesions. Mean flow and mean CO2 reactivity ipsilateral to the carotid occlusion were decreased, as well as the median NAA/creatine ratio in non-infarcted white matter. Lactate in non-infarcted white matter was present in 27% of the patients with TIAs, and 47% of the patients with minor stroke. In patients with TIAs, the presence of lactate was a better indicator of cognitive impairment than MRI-detected lesions. In both patients with TIAs as those with stroke, cognitive functioning did not correlate with CO2 reactivity. At follow-up, cognitive functioning improved, but only in patients without lactate in white matter, and without recurrent TIAs at follow-up. A minority of patients underwent carotid endarterectomy (CEA) for stenosis of the contralateral carotid artery. Although CEA led to improved CO2 reactivity and MCA flow on the side of the carotid occlusion, it had no impact on cognitive functioning. Self-perceived quality of life (QoL) was affected, both in patients with TIAs and in those with minor stroke. Depressive mood was associated with impaired QoL on all the subscales of the SF-36, disability according to the modified Rankin scale correlated only with self-perceived physical functioning, whereas cognitive impairment had no impact on QoL. Conclusions A substantial portion of patients with symptomatic carotid artery occlusion is cognitively impaired. Cognitive functioning may improve in the 1.5 years after the occurrence of ischemia, if symptoms do not recur. Severity and course of cognitive impairment correlate with measures of metabolism, but not with quantitative flow and CO2 reactivity. CEA for contralateral carotid stenosis results not in improvement of cognitive functioning within one year.