Clinical features associated with internal carotid artery occlusion do not correlate with MRA cerebropetal flow
K J van Everdingen1, L J Kappelle, C J Klijn
1Department of Radiology, E01.132 University Hospital Utrecht, Heidelberglaan 100, 3584 CX Utrecht, The Netherlands. K.vanEverdingen@azu.nl
Insights
Internal carotid artery (ICA) occlusion affects cerebropetal blood flow but doesn't explain differing neurological symptoms. Low N-acetylaspartate/choline ratios indicate hemispheric ischemia, not ICA occlusion itself.
Area of Science:
- Neurology
- Vascular Medicine
- Medical Imaging
Background:
- Internal carotid artery (ICA) lesions can cause neurological symptoms via thromboembolic or hemodynamic mechanisms.
- Understanding the relationship between blood flow changes and clinical presentation in ICA disease is crucial.
Purpose of the Study:
- To assess if altered cerebropetal blood flow due to ICA occlusion impacts clinical symptoms and cerebral metabolism.
- To investigate the correlation between ICA occlusion, blood flow dynamics, and neurological deficits.
Main Methods:
- Magnetic Resonance Angiography (MRA) was used to measure total cerebropetal flow and middle cerebral artery flow in 43 patients with ICA occlusion and 34 controls.
- Proton MR spectroscopy determined cerebral metabolic changes in the middle cerebral artery territory.
Main Results:
- Low total cerebropetal flow and low middle cerebral artery flow were observed in patients with ICA occlusion but did not correlate with their clinical syndrome.
- Patients with hemispheric ischemia showed decreased cerebral N-acetylaspartate/choline ratios, but this metabolic change did not correlate with the presence of ICA occlusion or low flow.
Conclusions:
- Neurological deficits in hemispheric ischemia are linked to reduced N-acetylaspartate/choline ratios.
- Cerebropetal blood flow, as measured by MRA, does not explain the varying neurological features observed in patients with similar carotid artery disease.
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.
