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A Study of 9 Cases

Jean-Marie Annoni, MD; Asaid Khateb, PhD; Sandrine Gramigna, MA; Fabienne Staub, MA; Antonio Carota, MD; Philippe Maeder, MD; Julien Bogousslavsky, MD

Arch Neurol. 2003;60:1439-1443.

Background  The occlusion of the lateral thalamic arteries leads to infarcts of ventrolateral thalamic nuclei, the ventroposterior nucleus, and the rostrolateral part of pulvinar, and produces hemisensory loss with or without hemiataxia. Cognitive impairment after such strokes has not been systematically studied.

Objective  To determine the nature and the extent of long-lasting cognitive deficits following lateral thalamic strokes.

Design  Case series.

Setting  Neurology department, Lausanne University Hospital, Lausanne, Switzerland.

Patients  Nine patients with hemisensory loss due to an isolated laterothalamic infarct.

Main Outcome Measures  Three to 6 months after stroke onset, standard neuropsychologic evaluation, including testing of language, ideomotor and constructive praxis, visual gnosis, spatial attention, learning abilities, and executive functions.

Results  Six of 9 patients showed some degree of cognitive impairment. Executive functions tasks, particularly verbal fluency, were impaired in 5 patients (4 with right and 1 with left lesion). Learning and delayed recall in visuospatial and verbal tasks, but not in recognition, were impaired in 3 patients (2 with right and 1 with left lesion). Difficulties in visual gnosia were observed in 1 patient with right lesion while word-finding difficulties were observed in 1 patient with left lesion.

Conclusions  Our observations show that while learning, naming, and gnosic difficulties fit with the classical verbal/nonverbal dichotomy (left and right hemisphere, respectively), executive dysfunctions, including verbal fluency tasks, were more dominant after right thalamic infarcts. Although the observed deficits appeared to be less severe than those generally found with dorsomedial and polar thalamic strokes, the dominance of executive dysfunction suggests that ventrolateral thalamic lesions may disrupt frontothalamic subcortical loops.

From the Departments of Neurology (Drs Annoni, Carota, and Bogousslavsky, and Mss Gramigna and Staub), Diagnostic and Interventional Radiology (Dr Maeder), Lausanne University Hospital, Lausanne; Neuropsychology Unit, Department of Neurology, Geneva University Hospital, Geneva (Drs Annoni and Khateb), Switzerland.

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