Acute Infarction Limited to the Lenticular Nucleus: Clinical, Etiologic, and Topographic Features | Cerebrovascular Disease | JAMA Neurology | JAMA Network
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Original Contribution
March 2003

Acute Infarction Limited to the Lenticular Nucleus: Clinical, Etiologic, and Topographic Features

Author Affiliations

From the Departments of Neurology (Drs Russmann, Vingerhoets, Ghika, and Bogousslavsky) and Radiology (Dr Maeder), Centre Hospitalier Universitaire Vaudois, Lausanne, Switzerland.

Arch Neurol. 2003;60(3):351-355. doi:10.1001/archneur.60.3.351

Background  Chronic diseases involving the putamen and globus pallidus induce parkinsonism and other movement disorders. Sensory and motor dysfunction from deep middle cerebral artery infarction is usually due to an involvement of the internal capsule. The clinical picture associated with isolated infarction of the lenticular nucleus is less well established.

Objective  To analyze clinical features, topographic correlations, and cause of purely lenticular ischemic infarction.

Patients and Methods  We reviewed 820 consecutive patients with deep hemispheral infarct included in the Lausanne Stroke Registry between 1986 and 1998 and selected those with isolated lenticular involvement on computed tomography or magnetic resonance imaging.

Results  Thirteen patients had pure lenticular infarction. All had faciobrachiocrural hemisyndrome, while none showed acute or delayed parkinsonism or abnormal movement. Nine patients had a lesion restricted to the putamen. Two of them had ataxic motor hemisyndrome and 7 had sensorimotor hemisyndrome (with ataxia in 4, left hemineglect in 1, and deep pain in the arm and leg in 1). Four patients had a lesion of putamen and globus pallidus externus.Three of them had motor hemisyndrome (with nonfluent aphasia in 2 and ataxia in 1) and 1 had ataxic sensorimotor hemisyndrome. All infarcts were in the territory of the medial perforating branches of the medial cerebral artery. Presumed cause of stroke was small-artery disease in 5, artery-to-artery embolism in 4, cardioembolism in 3 and undetermined in 1.

Conclusions  Acute lenticular infarction induces mainly hemiparesis but no movement disorder. Associated sensory deficits, aphasia, and hemineglect underline clinically the function of the lenticular nucleus in connection with the prefrontal, temporal, and parietal cortices.