Neuroimmunologic influences in neuropsychiatric and psychophysiologic disorders.
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Top down central nervous system (CNS) influences on the immune system and bottom up immune system influences on the CNS take part in a complex feedforward and feedback loop which may be responsible for initiating events and perpetuating circumstances in the course of neuropsychiatric as well as immune system diseases. In this paper the authors examine the neuroendocrine-neuroimmune stress response system, the concept of autoimmunoregulation, and recent studies of immune and pharmacological dysregulation in neuropsychiatric and psychosomatic illnesses. The authors review the recent English language literature on these subjects. Support for the hypothesis that macrophages play an important role in neurodevelopment and in the pathophysiology of various neuropsychiatric conditions is found. The interplay between neurologic and immune systems may help to uncover the pathophysiologies of certain neuropsychiatric systems. This may provide new strategies for pharmacologic anti inflammatory treatments. The monocyte /macrophage, which crosses the blood brain barrier is an essential candidate cell in the study of psychoneuroimmunology. (+info)
Cognitive behavioral therapy and fasting therapy for a patient with chronic fatigue syndrome.
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Cognitive behavioral therapy temporarily alleviated symptoms of a chronic fatigue syndrome patient but the anxiety about rehabilitation into work became stronger and his symptoms worsened. This patient was successfully rehabilitated by fasting therapy. Natural killer cell activity and serum acylcarnitine levels recovered after fasting therapy. Though fasting therapy transiently increased physical and mental subjective symptoms, the patient gained self-confidence by overcoming difficulties after fasting therapy. A combination of cognitive behavioral therapy and fasting therapy is promising as a treatment for chronic fatigue syndrome. (+info)
Chronic fatigue and anxiety/depression: a twin study.
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BACKGROUND: Up to three-quarters of patients with fatigue syndromes have comorbid mood or anxiety disorders, suggesting that chronic fatigue is a forme fruste of anxiety or depressive states. AIMS: To establish whether the association of chronic fatigue with psychological distress is causal or due to a common genetic or environmental factor. METHOD: 69 monozygotic (MZ) and 31 dizygotic (DZ) female twin pairs, with only one co-twin reporting at least 6 months of fatigue, completed questions on fatigue, the General Health Questionnaire (GHQ) and a structured psychiatric interview. We examined the effects of three progressively more stringent definitions of chronic fatigue on four GHQ sub-scales. RESULTS: Fatigued MZ and DZ twins by all definitions were significantly more depressed, anxious, somatically preoccupied and socially dysfunctional than their non-fatigued co-twins. Intrapair differences were similar in DZ and MZ twins, but non-significant differences were observed for the somatic symptoms and anxiety/insomnia sub-scales. CONCLUSIONS: In this sample, chronic fatigue and psychological distress are strongly associated without evidence for genetic covariation, implying that the association is environmental, or due to overlapping definitions. Any genetic covariation missed is likely to involve anxiety rather than depression. (+info)
Family cognitive behaviour therapy for chronic fatigue syndrome: an uncontrolled study.
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AIM: To examine the efficacy of family focused cognitive behaviour therapy for 11-18 year olds with chronic fatigue syndrome. METHODS: Twenty three patients were offered family focused cognitive behaviour therapy. The main outcome was a fatigue score of less than 4 and attendance at school 75% of the time. RESULTS: Twenty patients completed treatment. Eighteen had completed all measures at six months follow up; 15 of these (83%) improved according to our predetermined criterion. Substantial improvements in social adjustment, depression, and fear were noted. CONCLUSIONS: Family focused cognitive behaviour therapy was effective in improving functioning and reducing fatigue in 11-18 year olds. Gains were maintained at six months follow up. (+info)
Cellular immunity in monozygotic twins discordant for chronic fatigue syndrome.
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Studies elsewhere have suggested that immune dysfunction may be common in patients with chronic fatigue syndrome (CFS). The objective of this study was to assess the nature and extent of abnormalities in lymphocyte cell surface markers and NK cell activity in patients with CFS while controlling for genetic factors. A co-twin control study of immune system parameters was conducted for 22 pairs of monozygotic twins discordant for CFS and 9 healthy pairs of twins. The CFS twins had greater numbers of CD62L(+) T cells in several T cell subsets, although these differences did not achieve statistical significance. Significantly greater variability was noted in twins discordant for CFS than in the concordant healthy twins for 20 of 48 variables examined. The monozygotic co-twin control design is of unique value because of its ability to control for genetic influences on CFS; however, additional studies will be required to further assess immune dysregulation in this illness. (+info)
Chronic fatigue syndrome: evaluation and treatment.
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Severe fatigue is a common complaint among patients. Often, the fatigue is transient or can be attributed to a definable organic illness. Some patients present with persistent and disabling fatigue, but show no abnormalities on physical examination or screening laboratory tests. In these cases, the diagnosis of chronic fatigue syndrome (CFS) should be considered. CFS is characterized by debilitating fatigue with associated myalgias, tender lymph nodes, arthralgias, chills, feverish feelings, and postexertional malaise. Diagnosis of CFS is primarily by exclusion with no definitive laboratory test or physical findings. Medical research continues to examine the many possible etiologic agents for CFS (infectious, immunologic, neurologic, and psychiatric), but the answer remains elusive. It is known that CFS is a heterogeneous disorder possibly involving an interaction of biologic systems. Similarities with fibromyalgia exist and concomitant illnesses include irritable bowel syndrome, depression, and headaches. Therefore, treatment of CFS may be variable and should be tailored to each patient. Therapy should include exercise, diet, good sleep hygiene, antidepressants, and other medications, depending on the patient's presentation. (+info)
Ribonuclease L proteolysis in peripheral blood mononuclear cells of chronic fatigue syndrome patients.
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A 37-kDa binding polypeptide accumulates in peripheral blood mononuclear cell (PBMC) extracts from chronic fatigue syndrome (CFS) patients and is being considered as a potential diagnostic marker (De Meirleir, K., Bisbal, C., Campine, I., De Becker, P., Salehzada, T., Demettre, E., and Lebleu, B. (2000) Am. J. Med. 108, 99-105). We establish here that this low molecular weight 2-5A-binding polypeptide is a truncated form of the native 2-5A-dependent ribonuclease L (RNase L), generated by an increased proteolytic activity in CFS PBMC extracts. RNase L proteolysis in CFS PBMC extracts can be mimicked in a model system in which recombinant RNase L is treated with human leukocyte elastase. RNase L proteolysis leads to the accumulation of two major fragments with molecular masses of 37 and 30 kDa. The 37-kDa fragment includes the 2-5A binding site and the N-terminal end of native RNase L. The 30-kDa fragment includes the catalytic site in the C-terminal part of RNase L. Interestingly, RNase L remains active and 2-5A-dependent when degraded into its 30- and 37-kDa fragments by proteases of CFS PBMC extract or by purified human leukocyte elastase. The 2-5A-dependent nuclease activity of the truncated RNase L could result from the association of these digestion products, as suggested in pull down experiments. (+info)
Long-term follow-up of patients from the 1989 Q fever outbreak: no evidence of excess cardiac disease in those with fatigue.
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BACKGROUND: In 1989, an outbreak of Q fever (C. burnetii infection) with 147 confirmed cases occurred in Solihull, West Midlands. Three patients developed cardiomyopathy in the subsequent 10 years. The cohort has been followed up with respect to the development of fatigue and, in this instance, cardiac effects after the original infection. AIM: To determine whether persisting fatigue after Q fever represented sub-clinical cardiomyopathy. DESIGN: Prospective follow-up study. METHODS: All traceable subjects from the original outbreak, and community age-, sex- and smoking-matched controls, were studied. Questionnaires for idiopathic fatigue, 12-lead ECG, echocardiography, spirometry and shuttle walk distance were undertaken, and a subset with CDC-defined chronic fatigue syndrome had gated cardiac scans. RESULTS: Of the original cohort, 19 had died, three had emigrated and 10 were untraceable. Of the remaining 115, 108 responded to a mailed questionnaire and 87 were investigated further, of whom 85 provided complete data. Two developed aortic valve vegetations, one of whom died. Chronic fatigue syndrome was found in 20% of cases and 5.3% of controls (including those with co-morbidities), falling to 8.2% and 0 when excluding those with co-morbidities. There were no significant differences in ECG and echocardiographic investigations or shuttle-walk distance between those with fatigue and those without. Six of the seven patients with CFS had gated cardiac scans: all were within normal limits. CONCLUSIONS: These findings do not support the existence of a sub-clinical cardiomyopathy in the patients in this cohort who suffer from fatigue after acute Q fever, although endocarditis can occur after acute infection. (+info)