This Article  • Full text  • PDF  • Reply to article  • Send to a friend  • Save in My Folder  • Save to citation manager  • Permissions  Citing Articles  • Citation map  • Citing articles on ISI (4)  • Contact me when this article is cited  Related Content  • Similar articles in this journal  Topic Collections  • Cerebrovascular Disease  • Stroke  • Alert me on articles by topic  Social Bookmarking   What's this?

Fabienne Perren, MD; Stephanie Clarke, MD; Julien Bogousslavsky, MD

Arch Neurol. 2005;62:1212-1216.

Background  Occlusion of the polar or the paramedian arteries of the thalamus usually leads to distinct infarcts with specific clinical and imaging correlates. However, vascular variation is such that in up to one third of humans, the polar artery is missing and its territory taken over by the paramedian arteries.

Objective  To provide attention to the corresponding stroke syndrome of combined polar and paramedian thalamic infarction.

Methods  We studied combined polar-paramedian thalamic infarction in 12 patients (6 right-sided lesions, 3 left-sided lesions, and 3 bilateral lesions) who were selected from 208 consecutively registered patients with thalamic strokes in the Lausanne Stroke Registry.

Results  The clinical manifestation included executive dysfunction, apathy, and memory impairment in all patients, with eye movement disturbances in 10 patients (5 with right-sided lesions, 2 with left-sided lesions, 3 with bilateral lesions); acutely impaired consciousness in 11 patients (5 with right-sided lesions, 3 with left-sided lesions, 3 with bilateral lesions); aphasic disturbances in 8 patients (2 with right-sided lesions, 3 with left-sided lesions, 3 with bilateral lesions), including nonfluent aphasia in 1 patient (with left-sided lesions); dysarthria in 5 patients (4 with right-sided lesions, 1 with bilateral lesions); constructional apraxia in 5 patients (with right-sided lesions); mild hemiparesis in 4 patients (2 with right-sided lesions, 2 with left-sided lesions); dyscalculia in 3 patients (1 with left-sided lesions,1 with right-sided lesions, 1 with bilateral lesions); limb dystonia or asterixis in 2 patients (1 with right-sided lesions, 1 with bilateral lesions); mild hemisensory loss in 2 patients (1 with right-sided lesions, 1 with left-sided lesions); hemiataxia in 1 patient (with right-sided lesions); and ideomotor apraxia in 1 patient (with left-sided lesions). Follow-up showed severely disabling, persistent amnesia in 7 patients (4 with right-sided lesions, 3 with bilateral lesions) and persistent eye movement dysfunction in 5 patients (2 with right-sided lesions, 1 with left-sided lesions, 2 with bilateral lesions). The most common etiology appeared to be cardioembolism, followed by artery-to-artery embolism and presumed small-artery disease.

Conclusions  Key features of this syndrome included amnesia preceded by a period of altered consciousness, and vertical eye movement disturbances. The severe and persistent amnesia may be due to coexisting damage to the anterior and dorsomedial nuclei.

Author Affiliations: Departments of Neurology (Drs Perren and Bogousslavsky) and Neuropsychology (Dr Clarke), Centre Hospitalier Universitaire Vaudois, Lausanne, Switzerland.

CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati     What's this?