No abstract

We compared Wisconsin Card Sorting Task (WCST) performance in 19 obsessive-compulsive disorder (OCD) patients and 19 individually matched healthy controls. Measures of intelligence and mood were taken into account for all participants. Within the patient group, factors such as duration and severity of symptoms (as assessed using the Yale-Brown Obsessive-Compulsive Scale, Y-BOCS) were considered. We explored the relationship between OCD WCST errors and regional cerebral blood flow (rCBF) on brain dedicated, high resolution, single photon emission tomography (SPET). We used uptake of 99mTc-hexamethylpropylamine oxime (HMPAO) on SPET to estimate rCBF, and regional values were quantified as ratios of cerebellar blood flow. WCST results confirmed OCD patients were significantly impared when compared with age- and sex-matched healthy volunteers. Patients made significantly more trials, more preseverative errors, and more null-sorts. OCD patients Y-BOCS 'obsessive' subtotal significantly correlated with many WCST errors. Furthermore OCD WCST null-sorts correlated significantly with SPET OCD left inferior frontal cortical rCBF (r(18) = .47, p = .05) and left caudate rCBF (r(18) = .72, p = .01). The implications of these findings are discussed in the context of other studies which examine functional imaging and neuropsychology in OCD.

SYNOPSIS Abnormalities in central serotonin function have been implicated in the pathogenesis of anorexia nervosa. It is difficult, however, to separate neuroendocrine abnormalities induced by weight loss and malnutrition from those related primarily to the disorder itself. To minimize these influences, this study assessed long-term weight restored anorexics. A correlation between persistent eating-related psychopathology, co-morbid illness and serotonin dysfunction was sought. Nine female weight-restored out-patients who had previously fulfilled DSM-III-R criteria for anorexia nervosa and nine healthy controls participated. Following baseline estimation, prolactin and cortisol responses to 30 mg p.o. of D-fenfluramine were measured over a 5 h period. Eating related psychopathology was assessed using the Eating Disorders Inventory and Eating Attitudes Test. Depressive and obsessional symptoms were measured using the Beck Depressive and Maudsley Obsessive-Compulsive Inventories respectively. The Tridimensional Personality Questionnaire assessed impulsivity. The weight-restored anorexic group exhibited persistent eating-related psychopathology and significant co-morbid symptomatology. There was no difference between long-term weight restored anorexics and controls in their endocrine response to D-fenfluramine. Long-term weight-recovered anorexic subjects continued to exhibit behavioural and attitudinal disturbances characteristic of anorexia nervosa. The results suggest that abnormalities in 5HT activity do not contribute significantly to trait status in anorexia nervosa.

Background Immune system dysfunction is implicated in the pathophysiology of major depression, and is hypothesized to normalize with successful treatment. We aimed to investigate immune dysfunction in melancholic depression and its response to ECT. Methods 55 melancholic depressed patients and 26 controls participated. 33 patients (60%) were referred for ECT. Blood samples were taken at baseline, one hour after the first ECT session, and 48 hours after ECT series completion. Results At baseline, melancholic depressed patients had significantly higher levels of the pro-inflammatory cytokine IL-6, and lower levels of the regulatory cytokine TGF-β than controls. A significant surge in IL-6 levels was observed one hour after the first ECT session, but neither IL-6 nor TGF-β levels normalized after completion of ECT series. Seventy per cent (n=23) of ECT recipients showed clinical response and 42% (n=10) reached remission. Neither IL-6 nor TGF-β changes correlated with clinical improvement following ECT. No significant changes in IL-10, TNF-α and CRP levels were found in relation to melancholia or response to ECT. Limitations As a naturalistic study, some potential confounders could not be eliminated or controlled, including medication use. Conclusions Melancholic depressed patients demonstrated a peripheral increase in IL-6 and reduction in TGF-β, which did not normalize despite clinical response to ECT. These findings may be consistent with emerging hypotheses of the role of inflammation in mediating neurotropin expression. The implications of chronic inflammation in the melancholic depressed population for future medical health, particularly cardiovascular risk, are largely unknown and warrant further investigation.

These preliminary results are consistent with previous research implicating limbic cortical regions in the pathophysiology of schizophrenia, suggesting that reduced inhibitory GABAergic tone in these areas may contribute to the appearance of schizophrenic symptoms.