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E P Pepin

Publications and source records attributed to E P Pepin.

3 recordsLinked to original sources

Selective dorsolateral frontal lobe dysfunction associated with diencephalic amnesia.

We report three cases with unilateral thalamic ischemic lesions that resulted in lasting material-specific memory impairments and concomitant selective frontal lobe-related cognitive deficits. In two cases the lesions were limited to the left thalamus, and in the third the right thalamus was involved. These deficits were associated with ipsilateral diencephalic, striatal, and dorsolateral prefrontal hypoperfusion. The damage implicated the ventral anterior nucleus, the mamillothalamic tract, and the rostroventral internal medullary lamina. These findings suggest that medial thalamic damage involving the ventral and rostral sector of the dorsal thalamus will concurrently affect functionally and neurally distinct limbodiencephalic pathways and diencephalic connections with the frontal cortex. A review of the neuropsychological and neuroimaging findings from previously reported cases with vascular lesions of the thalamus further supports this contention. The presence of frontal lobe-related cognitive deficits, though not obligatorily related to the memory problems, may contribute to some aspects of the memory deficits and affect the nature of the memory disorder observed in some cases with diencephalic amnesia.

Aged

Verbal memory decline in Alzheimer's disease: a multiple-processes deficit.

Memory dysfunction is a primary diagnostic criterion and one of the earliest clinical manifestations of dementia of the Alzheimer type (DAT). The profile of progression of this memory deficit is assumed to represent a unitary decline. We studied the profile of verbal memory decline using an immediate free recall learning task in 18 DAT patients judged to be at 3 different stages of severity (mildly, moderately, and severely affected), using the serial-position function as the dependent measure. Results showed that the pattern of performance of DAT patients depended upon the severity of the disease. With mild dementia, the U-shaped curve was qualitatively similar to that observed in normals (presence of primacy and recency effects). With increasing severity of dementia, there was a consistent modification of the serial-position function with, in moderately affected subjects, a progression toward a unimodal curve devoid of a primacy effect and, later on, a decrease of the recency effect. These findings suggest that the serial-position function shows dynamic changes across stages of DAT. These dynamic changes may imply distinct disturbances of 2 or more learning-memory processes in this condition. The processes involved presumably reflect the temporal nature of the pathologic involvement of distinct neural systems, both structural and neurochemical.

Alzheimer Disease