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  Vol. 49 No. 10, October 1992 TABLE OF CONTENTS
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Contributions of the Left Intralaminar and Medial Thalamic Nuclei to Memory

Comparisons and Report of a Case

Mark Mennemeier, PhD; Eileen Fennell, PhD; Edward Valenstein, MD; Kenneth M. Heilman, MD

Arch Neurol. 1992;49(10):1050-1058.


Abstract

• A patient complained of memory disturbance after a small left thalamic infarction. Neuropsychological testing revealed her memory to be normal provided that she was allowed to rehearse or use semantic encoding strategies. When these strategies were prevented, her performance was impaired. Mapping of the lesion demonstrated involvement of the caudal intralaminar nuclei (centre médian and parafascicular nuclei), and portions of the medial nuclei (medioventral [reuniens], centromedial, and the most inferior aspect of the mediodorsal nucleus). The majority of mediodorsal nucleus, the mammillary bodies, the mammillothalamic tract, and the anterior thalamic nuclei, were spared. A comparison among our patient's performances and those of alcoholic Korsakoff patients, patient NA, and amnestic patients with circumscribed diencephalic lesions suggests that there are two distinct behavioral and anatomic types of memory impairment associated with diencephalic lesions. The severe amnesia associated with damage to the mammillary bodies, midline nuclei, mammillothalamic tract, and/or dorsomedial nucleus of the thalamus (eg, Korsakoff and NA) is characterized by encoding deficits that never approximate normal performance. The memory disturbance associated with damage to the intralaminar and medial nuclei of the thalamus is milder and is characterized by severe distractibility.



Author Affiliations

From the Department of Veterans Affairs Medical Center (Drs Mennemeier, Valenstein, and Heilman); Department of Neurology, Center for Neuropsychological Studies (Drs Mennemeier, Fennell, Valenstein, and Heilman); and Department of Clinical and Health Psychology (Dr Fennell), University of Florida College of Medicine, Gainesville.


Footnotes

Accepted for publication June 10, 1992.

Reprint requests to Department of Neurology, University of Florida, Box J-236, Gainesville, FL 32610 (Dr Mennemeier).



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