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September 1987

Normal Memory After Damage to Medial Thalamus

Author Affiliations

From the Department of Neurology, Division of Behavioral Neurology, University of Iowa College of Medicine, Iowa City. Dr Kritchevsky is now with the Veterans Administration Medical Center, San Diego.

Arch Neurol. 1987;44(9):959-962. doi:10.1001/archneur.1987.00520210055019

• We studied two patients with nonhemorrhagic infarcts of the thalamus and assessed their cognitive functions comprehensively using standardized neuropsychological probes. Neither patient had any discernible memory impairment for verbal or nonverbal material. Analysis of magnetic resonance images with a stereotaxic method revealed that one subject had a right-sided lesion involving about 15% of the dorsomedial nucleus (DM). The other had bilateral lesions that affected about 15% of the left DM and less than 5% of the right DM. The mamillothalamic tract appeared intact in both patients. Considering that medial thalamic lesions commonly cause amnesia in human beings as well as nonhuman primates, there are two possible reasons, alone or in combination, that may explain why these patients failed to have amnesia: the amount of DM damage was less than required to cause amnesia; or the amnesia related to thalamic lesions requires damage to a second structure, such as the mamillothalamic tract or the anterior nucleus.

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