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September 1988

Lateral Thalamic Infarcts

Author Affiliations

From the Departments of Neurology (Drs Caplan, DeWitt, and Pessin) and Neuropathology (Dr Adelman), New England Medical Center, Tufts University, Boston, and the Departments of Neurology, Michael Reese Hospital, Chicago, and the University of Chicago (Dr Gorelick).

Arch Neurol. 1988;45(9):959-964. doi:10.1001/archneur.1988.00520330037008

• A patient with occlusion of the proximal posterior cerebral artery (PCA), a lateral thalamic infarct, and hemisensory loss later developed hemianopia and hemiparesis and had extensive PCA territory infarction in the midbrain, the lateral portion of the thalamus, and the occipital lobe noted at necropsy. Two other patients had lateral thalamic infarcts on computed tomography, normal angiographic findings, and presumed thalamogeniculate artery branch occlusion. There are three clinical syndromes associated with lateral thalamic infarction: (1) hemisensory loss, hemiataxia, and involuntary movements; (2) pure sensory stroke; and (3) sensory-motor stroke. Ataxia, adventitious movements, and sensory loss are due to infarction of the lateral, posterolateral, and posteromedial ventral nuclei caused by occlusion of the PCA proximal to the thalamogeniculate artery branches or by occlusion of large thalamogeniculate arteries. Pure sensory and sensory-motor strokes are due to smaller infarcts in the posterolateral-posteromedial ventral complex and adjacent internal capsule caused by occlusion of penetrating artery branches of the thalamogeniculate arteries.

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