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The syndrome of posterior choroidal artery territory ifarction
Author(s) -
Neau JeanPhilippe,
Bogousslavsky Julien
Publication year - 1996
Publication title -
annals of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.764
H-Index - 296
eISSN - 1531-8249
pISSN - 0364-5134
DOI - 10.1002/ana.410390614
Subject(s) - thalamus , anterior choroidal artery , medicine , posterior cerebral artery , infarction , stroke (engine) , anatomy , cardiology , surgery , ischemia , radiology , middle cerebral artery , myocardial infarction , internal carotid artery , mechanical engineering , engineering
Abstract Posterior choroidal artery (PChA) territory infarcts remain the least well‐known type of thalamic infarcts. Our study of 10 personal cases, selected from 2,925 stroke patients admitted consecutively to a community‐based primary care center, and 10 published cases of unilateral PChA territory infarct suggests that they can often be differentiated clinically from other thalamic infarcts. Patients with PChA territory infarct associated with superficial posterior cerebral artery territory infarct or with another infarct were excluded. Damage was characteristically limited to the lateral geniculate body, pulvinar, posterior thalamus, hippocampus, and parahippocampal gyrus, without involvement of the upper midbrain and the anterior nucleus of thalamus. In lateral PChA territory infarct, the most common clinical manifestations included homonymous quadrantanopsia, with or without hemisensory loss and neuropsychological dysfunction (trans‐cortical aphasia, memory disturbances). A homonymous horizontal sectoranopsia is exceptional but particularly suggestive of the involvement of the lateral geniculate body in this territory. Medial PChA territory infarct was less frequent. Its neurologic picture was dominated by eye movement disorders not particularly suggestive of thalamic involvement. Late disability was usually absent or slight, being related to pain and delayed abnormal movements. The most common stroke etiology was presumed small‐vessel occlusive disease.