Clinical features associated with internal carotid artery occlusion do not correlate with MRA cerebropetal flow measurements
- aDepartment of Radiology, E01.132 University Hospital Utrecht, Heidelberglaan 100, 3584 CX Utrecht, The Netherlands, bDepartment of Neurology
- Dr K J van EverdingenK.vanEverdingen{at}azu.nl
- Received 6 September 1999
- Revised 25 August 2000
- Accepted 6 November 2000
Abstract
OBJECTIVES The aetiology of clinical symptoms in patients with severe internal carotid artery (ICA) lesions may be thromboembolic or haemodynamic. The purpose was to assess whether changes in cerebropetal blood flow caused by an ICA occlusion have an effect on clinical symptoms and cerebral metabolism.
METHODS Forty three patients with an ICA occlusion who had hemispheric ischaemia (transient ischaemic attack or stroke), retinal ischaemia, or without symptoms, and 34 patients without significant ICA lesions with either hemispheric ischaemia or no symptoms were studied. Magnetic resonance angiography (MRA) was used to investigate total cerebropetal flow (flow in the ICAs plus basilar artery) and the flow in the middle cerebral arteries. Cerebral metabolic changes in the flow territory of the middle cerebral artery were determined with proton MR spectroscopy.
RESULTS Low total cerebropetal flow (r=−0.15, p<0.05) and low middle cerebral artery flow (r=−0.31, p<0.001) were found in patients with an ICA occlusion, but did not correlate with the clinical syndrome. By contrast, patients with prior symptoms of hemispheric ischaemia had decreased cerebral N-acetylaspartate/choline ratios (r=−0.35, p<0.001). However, the presence of an ICA occlusion (and subsequent low flow) did not correlate with low N-acetylaspartate/choline ratios.
CONCLUSION Neurological deficit caused by (transient) hemispheric ischaemia is associated with low N-acetylaspartate/choline ratios, whereas prior clinical features are not associated with low cerebropetal blood flow, as measured with MR angiography. As a result, differences in cerebropetal flow cannot explain why patients with similar carotid artery disease experience different neurological features.
