Posted by admin on September 25th, 2009

25
Sep

Older bipolar disorder patients have a similar cognitive profile to that of younger patients with the disease, say Swiss scientists, who suggest that processing speed and episodic memory are two core deficits in elderly patients.

Previous studies have indicated that bipolar disorder patients have impairments in processing speed, working memory, episodic memory, and executive function. However, these investigations have largely focused on young and middle-aged patients and all have shown that the severity of cognitive deficits increase with illness duration.

To examine cognitive deficits in older patients, Christophe Delaloye, from University Hospitals of Geneva in Chêne-Bourg, and colleagues administered a comprehensive neuropsychological battery to 22 euthymic elderly bipolar disorder patients with an average age of 68.45 years and 22 gender-, age-, and education-matched controls.

In comparison with controls, bipolar disorder patients were found to have significantly slower processing speed, lower working memory scores, lower episodic memory scores, and verbal fluency scores, at r-value effect sizes of 0.44, 0.44, 0.48, and 0.38, respectively.

There were no significant differences between the two groups in terms of executive function, and duration of illness had no impact on cognitive performance.

Processing speed was found to explain 19% of the variance in working memory scores, 14% of the verbal fluency composite scores, and 23% of the variance in episodic memory scores in hierarchical regression analysis. After controlling for processing speed, only episodic memory had a persistent group effect, explaining 10% of the variance in scores.

The team writes in the journal Bipolar Disorders: “Euthymic elderly BD patients had reduced performance in measures of processing speed, working memory, verbal fluency, and episodic memory compared to controls. This pattern of cognitive deficits is largely comparable to the one reported in younger BD cohorts.

“Moreover, the length of illness was not associated with cognitive performance in our elderly BD group, suggesting that longstanding BD is not associated with an increase in cognitive decline.”

MedWire (www.medwire-news.md) is an independent clinical news service provided by Current Medicine Group, a part of Springer Science+Business Media. © Current Medicine Group Ltd; 2009

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Posted by admin on June 22nd, 2009

22
Jun

Dopamine release in the prefrontal cortex increases flattening of the glucocorticoid rhythm, which may underpin prefrontal dysfunction in bipolar disorder patients, conclude researchers.

Previous studies have shown that bipolar disorder patients have abnormal glucocorticoid secretion, dopaminergic neurotransmission, and prefrontal cortex function, explain Sarah Gartside, from Newcastle University in the UK, and colleagues.

Believing that flattening of the diurnal glucocorticoid rhythm, which is common in bipolar disorder, modulates dopaminergic transmission in the prefrontal cortex, leading to functional abnormalities, the team administered corticosterone 50 µg/ml or 0.5% ethanol vehicle to the drinking water of male rats for 13??”15 days.

Compared with animals given vehicle, those treated with corticosterone had a flattened diurnal rhythm in blood corticosterone concentrations, with levels significantly lower before the diurnal peak and significantly higher at the nadir of the rhythm, and significant adrenal gland atrophy.

Corticosterone-treated animals had significantly increased basal dopamine levels compared with those given vehicle, the team reports in the journal Neuropsychopharmacology. Analysis revealed that depolarization-evoked release was also enhanced, while local blockade of terminal D2 autoreceptors failed to normalize release to control values.

In the ventral tegmental area, levels of mRNAs coding tyrosine hydroxylase and the vesicular monoamine transporter 2, as measured using in situ hybridization, were significantly increased in rats treated with corticosterone compared with vehicle-treated rats.

“The finding of increased dopamine release in the prefrontal cortex suggests a causal link between the neuroendocrine abnormalities observed in mood disorders, and some of the cognitive symptoms of these conditions: the prefrontal cortex plays a key role in cognitive functions including working memory, selective attention, goal directed behavior, and behavioral inhibition with prefrontal dopaminergic neurotransmission strongly influencing these functions,” the researchers write.

MedWire (www.medwire-news.md) is an independent clinical news service provided by Current Medicine Group, a part of Springer Science+Business Media. © Current Medicine Group Ltd; 2009

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