16 research outputs found

    Central pathways causing fatigue in neuro-inflammatory and autoimmune illnesses

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    A Comparison of Neuroimaging Abnormalities in Multiple Sclerosis, Major Depression and Chronic Fatigue Syndrome (Myalgic Encephalomyelitis): is There a Common Cause?

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    Personality dimensions in chronic fatigue syndrome and depression.

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    Chronic fatigue syndrome (CFS) is a poorly understood condition. Possible etiological factors include infectious agents, psychiatric disorders, and personality characteristics. We examined personality dimensions in 30 nondepressed patients with CFS, 20 patients with major depressive disorder (MDD), and 15 healthy controls. On the NEO-FFI, patients with CFS scored significantly lower than healthy controls on the extroversion subscale. On the neuroticism dimension of the Eysenck Personality Questionnaire (EPQ), patients with MDD scored higher than those with CFS, who in turn scored significantly higher than the healthy controls. CFS patients rated themselves as higher on neuroticism and less extroverted when ill than when they were well. Our results suggest that high scores on neuroticism and low scores on extroversion in CFS could be a reaction to chronic illness

    Cerebral perfusion in chronic fatigue syndrome and depression.

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    BACKGROUND: Patients with chronic fatigue syndrome (CFS) and depressive illness share many, but not all, features. AIMS: To test the hypothesis that patients with CFS have abnormal cerebral perfusion, that differs from that in patients with depressive illness. METHOD: We recruited 30 patients with CFS who were not depressed, 12 depressed patients and 15 healthy volunteers. Regional cerebral perfusion at rest was assessed using region of interest (ROI) and voxel-based statistical parametric mapping (SPM) techniques. RESULTS: On SPM analysis there was increased perfusion in the right thalamus, pallidum and putamen in patients with CFS and in those with depressive illness. CFS patients also had increased perfusion in the left thalamus. Depressed patients differed from those with CFS in having relatively less perfusion of the left prefrontal cortex. The results were similar on ROI analysis. CONCLUSIONS: Abnormal cerebral perfusion patterns in CFS subjects who are not depressed are similar but not identical to those in patients with depressive illness. Thalamic overactivity may be a correlate of increased attention to activity in CFS and depression; reduced prefrontal perfusion in depression may be associated with the greater neuropsychological deficits in that disorder

    Depression after stroke and lesion location: a systematic review.

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    BACKGROUND: There is conflicting evidence on the hypothesis that the risk of depression after stroke is influenced by the location of the brain lesion. We undertook a systematic review to examine the hypotheses that depression is more commonly associated with left-hemisphere strokes than with right-hemisphere strokes and with lesions of the left anterior brain than with other regions. METHODS: We did a computer-aided search of MEDLINE, BIDS ISI, and PsychLit databases supplemented by hand searches of key journals. We included all reports on the association of depression after stroke with the location of the brain lesion. Studies were systematically and independently examined by two investigators. Fixed-effects and random-effects meta-analyses were done. FINDINGS: 143 reports were identified by the search strategy. 48 were eligible for inclusion. Not all reports included original data. Only two reports of original data supported the hypotheses and seven clearly did not. The pooled (random-effects) relative risk of depression after a left-hemisphere stroke, compared with a right-hemisphere stroke, was 0.95 (95% CI 0.83-1.10). For depression after a left anterior lesion compared with all other brain areas the pooled (random-effects) relative risk was 1-17 (0.87-1.62). Restriction of the analyses to reports from high-quality studies or major depressive disorder did not substantially affect the findings. Nor were they affected by stratification of the time between stroke and the assessment of depression. Multiple publications from the same samples of patients were apparent. INTERPRETATION: This systematic review offered no support for the hypothesis that the risk of depression after stroke is affected by the location of the brain lesion
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