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Anterior inferior cerebellar artery territory infarcts. Mechanisms and clinical features
P Amarenco1, A Rosengart, L D DeWitt
1Department of Neurology, New England Medical Center, Tufts University, Boston, Mass.
Insights
Anterior inferior cerebellar artery (AICA) territory infarcts in hypertensive patients are linked to atherosclerosis. Isolated infarcts suggest small artery disease, while widespread infarcts point to basilar artery occlusion.
Area of Science:
- Neurology
- Vascular Neurology
- Neuroimaging
Background:
- Anterior inferior cerebellar artery (AICA) territory infarcts have been primarily described in necropsy studies.
- Limited large clinical series exist for AICA territory infarcts, hindering understanding of their mechanisms and clinical presentation.
Observation:
- Nine patients with AICA territory infarction confirmed by MRI and angiography were studied.
- Atherosclerosis was identified as the sole cause in all patients, who were also hypertensive.
Findings:
- Four patients with pure AICA territory infarcts were diabetic, with occlusion likely due to basilar artery plaques or microatheroma at the AICA origin; they reported minimal or no prodromal symptoms.
- Five patients with AICA plus infarcts showed basilar artery occlusion at the AICA with distal reconstitution via collaterals; most had prodromal symptoms.
- Cranial nerve involvement suggesting lateral pontine lesions occurred in seven patients. The complete AICA syndrome was rare, and isolated vertigo was absent.
Implications:
- Isolated unilateral AICA infarcts in diabetic hypertensive patients likely result from small artery atherosclerotic disease.
- Widespread infarcts involving the AICA territory suggest underlying basilar artery occlusive disease.
- Clinical presentation and prognosis vary based on the extent of infarction and underlying vascular pathology.
Abstract:
Arterial lesions, mechanisms, territory, and clinical features of anterior inferior cerebellar artery (AICA) territory infarcts are only based on necropsy cases. To our knowledge, no large clinical series has been reported. We selected nine consecutive patients with AICA territory infarction confirmed by magnetic resonance imaging and angiography. Atherosclerosis was the only cause and all patients were hypertensive. Patients with pure AICA territory infarcts (n = 4) were diabetic and likely had basilar branch occlusion due to basilar artery plaques that extended into the AICA or microatheroma that blocked the AICA origin. These patients had no or had only recently had (1 day) prodromata. Patients with AICA plus infarct (n = 5) had basilar artery occlusion at the AICA and reconstitution of the distal basilar artery by collaterals through hemispheric anastomoses from the posterior inferior cerebellar arteries and posterior communicating arteries. All these patients except one had prodromata. In seven of nine patients, cranial nerve involvement indicated a lateral pontine lesion in the territory supplied by the AICA. Only two patients had the complete AICA syndrome, and none of the patients had isolated vertigo. The outcome was good in seven of nine patients. Isolated unilateral AICA infarcts should be regarded as most likely due to small artery atherosclerotic disease in diabetic patients. More widespread infarctions that include that AICA territory are due to basilar artery occlusive disease.