In the present study the cognitive performance of 25 patients with Cushing's disease (CD) was extensively evaluated in comparison with normal control subjects, matched one by one. The results indicate a selective impairment of memory functions: the number of patients showing a significantly impaired mnesic performance increases with age. Moreover, the neuropsychological impairment tends to recover in those cases who underwent further controls after surgical treatment. The neuropsychological data are discussed in the light of recent evidence in the literature concerning the effects of adrenal steroids on the brain.
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"There are clinical evidences that high levels of cortisol alter memory function. Patient populations with chronically elevated levels of cortisol, such as Cushing's syndrome, major depression, and schizophrenia, as well as asthmatic patients treated with the glucocorticoid prednisone are characterized by impaired memory function [50,51]. Experimental studies of acute stress and memory have been carried out in animals , and several well-controlled studies have recently been conducted in humans. "
"Little is known on the impact of hypercortisolism control on cognitive function. Partial improvement of several memory functions have been observed in small groups [121, 125], correlated in one study with recovery of hippocampus volume , but not in the other . Another study only found improvement in a visuospatial organization task . "
[Show abstract][Hide abstract]ABSTRACT: It was assumed that resolution of hypercortisolism in Cushing syndrome (CS) was followed by normalization of morbidity; however, in the last decade evidence is accumulating that patients with cured CS still have increased morbidity and mortality after the biochemical control of hypercortisolism. Patients with CS have an increased cardiovascular and metabolic risk and persistent accumulation of central fat, with an unfavorable adipokine profile, not only during the active phase of the disease but also long after biochemical remission. Clinical management should be particularly careful in identifying global cardiovascular risk, as a primary goal during the followup of these patients, aimed at improving global vascular morbidity. Moreover bone mass is reduced not only due to the endogenous hypercortisolism but also due to duration and dose of exogenous glucocorticoid (GC) replacement therapy after surgery. Thus, therapy in operated patients with inhibition of the hypothalamic-pituitary-adrenal axis should be reduced to the lowest dose and duration possible. Specific treatments should be considered in patients with decreased bone mass, aimed at reducing the increased fracture incidence. Finally, cognitive and health related quality of life impairments, described in active disease, are still abnormal after endocrine cure. Thus, residual morbidity persists in cured CS, suggesting irreversibility of GC-induced phenomena, typical of chronic hypercortisolism.
"Acute administration of exogenous corticosteroids in humans is associated with reversible decline in declarative memory performance (de Quervain et al., 2000; Newcomer et al., 1999). Cushing's disease is associated with memory impairment (Mauri et al., 1993) and hippocampal atrophy (Starkman et al., 1992) that is, at least partially, reversible with normalization of cortisol levels (Starkman et al., 1999; Starkman et al., 2003). We reported that patients receiving long-term prescription corticosteroid therapy had poorer declarative memory, decreased hippocampal volume and decreased temporal lobe levels of N-acetyl aspartate as compared to controls with similar medical histories but minimal corticosteroid exposure (Brown et al., 2004). "
[Show abstract][Hide abstract]ABSTRACT: An extensive animal literature suggests that stress or excessive corticosteroid exposure is associated with changes in hippocampal function and memory. These findings are pertinent to psychiatric disorders with elevated cortisol, Cushing's disease and the millions of patients receiving prescription corticosteroids. In animals, agents that decrease glutamate release attenuate the effects of corticosteroids on the hippocampus. Minimal data are available on preventing or reversing the effects of corticosteroids on the human hippocampus. We previously reported improvement in memory in corticosteroid-treated patients given lamotrigine. In this report, we examined the impact of lamotrigine on task-related hippocampal activation in patients taking prescription corticosteroids.
A total of 28 outpatients taking long-term oral prednisone for medical conditions, such as renal transplant rejection, were randomized to lamotrigine or placebo for 24 weeks. Hippocampal activation in response to a visual memory task was assessed with blood oxygenation level dependent (BOLD) functional magnetic resonance imaging (fMRI).
Consistent with a reduction in glutamate release, the right posterior hippocampus showed a significant decrease in task-related activation in the lamotrigine group as compared to the placebo group.
The modest sample size and an assessment period of only 24 weeks are study limitations.
Between-group differences in hippocampal activation were observed. The results suggest that an agent that modulates glutamate may modify the effects of long-term corticosteroid exposure on the human hippocampus.
Full-text · Article · Nov 2010 · Journal of Affective Disorders