Literature DB >> 18702680

A clinical profile of memory impairment in humans due to endogenous glucocorticoid excess.

José León-Carrión1, Ainara Madrazo Atutxa, Miguel Angel Mangas, Alfonso Soto-Moreno, Alfonso Pumar, Antonio Leon-Justel, Juan Francisco Martín-Rodriguez, Eva Venegas, M Rosario Domínguez-Morales, Alfonso Leal-Cerro.   

Abstract

OBJECTIVE: Glucocorticoid excess is commonly related to neuropsychiatric and neurological disorders, with memory impairment typically found among these disorders. The objective of this study is to offer a clinical profile of memory deficits resulting from exposure to chronic stress-level elevations of endogenous glucocorticoids in patients with Cushing's Syndrome (CS). STUDY
SUBJECTS: Thirty female participants of matching age and education level were studied: 15 had untreated CS (mean age 38 +/- 14) and 15 were healthy. In all patients, CS was confirmed by histology of the lesion after surgery.
DESIGN: Different learning and memory processes were assessed using an adapted version of Luria's Memory Words-Revised task (LMW-R). Participants' performances were measured in an immediate condition and, 30 min later, in a delayed condition. Attentional and executive functions were also evaluated.
RESULTS: Our data show that chronic exposure to elevated levels of cortisol is clinically associated with significant working memory deficits, which included less shot-term memory volume, slow learning rate, memory contamination and no accurate perception of own performance. Patients also show impairment in the delayed recall task. No relation was detected between learning and delayed conditions. CS group did not differ significantly from control group in basic attentional and executive functioning.
CONCLUSIONS: Our clinical profile of memory deficits related to CS relates chronic exposure to hypercortisolemia to impaired attentional-dependent working memory and delayed recall process, suggesting that cortisol levels play a critical role in the modulation of learning and memory. Possible damage to hippocampus and extrahippocampal areas is discussed.

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Year:  2008        PMID: 18702680     DOI: 10.1111/j.1365-2265.2008.03355.x

Source DB:  PubMed          Journal:  Clin Endocrinol (Oxf)        ISSN: 0300-0664            Impact factor:   3.478


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