Cerebrovascular reactivity in the caudate nucleus, lentiform nucleus and thalamus in patients with carotid artery disease
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2017-03-01
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Abstract
Background and purpose To assess the effect of unilateral large vessel disease upon the cerebral hemodynamic autoregulatory status in the basal ganglia of patients with steno-occlusive internal carotid artery (ICA) disease. Materials and methods Twenty-five healthy volunteers and 38 patients with a unilateral symptomatic steno-occlusive ICA lesion and were investigated; 20 with a stenosis > 50% and 18 with an occlusion. Cerebral blood flow (CBF) and cerebrovascular reactivity (CVR) were assessed with pseudo-continuous arterial spin labeling (ASL) magnetic resonance (MR) imaging before and after administration of acetazolamide. Results When compared to controls, the CVR in patients with ICA stenosis was significantly lower in the middle cerebral artery (MCA) territory (P < 0.05), and in the caudate (P < 0.05) and lentiform nucleus (P < 0.05) of the hemisphere ipsilateral to the stenosis. The CVR in the caudate nucleus contralateral to the stenosis was significantly lower (P < 0.05) as well. In patients with ICA occlusion, the CVR in the hemisphere ipsilateral to the occlusion as well as in the contralateral hemisphere was significantly lower in the MCA territory (P < 0.05), the caudate (P < 0.05) and lentiform nucleus (P < 0.05), and in the thalamus (P < 0.05). Conclusion Perfusion ASL MR imaging shows impaired cerebral hemodynamic autoregulation of the basal ganglia in patients with steno-occlusive ICA disease both in the hemisphere ipsilateral as well as in the hemisphere contralateral to the stenosis or occlusion.
Keywords
Carotid artery disease, Cerebrovascular reactivity, Magnetic resonance imaging, Perfusion, Taverne, Journal Article
Citation
Hartkamp, NS, Bokkers, R P H, van Osch, M J P, de Borst, G J & Hendrikse, J 2017, 'Cerebrovascular reactivity in the caudate nucleus, lentiform nucleus and thalamus in patients with carotid artery disease', Journal of neuroradiology, vol. 44, no. 2, pp. 143-150. https://doi.org/10.1016/j.neurad.2016.07.003