تجزیه و تحلیل منابع EEG از سندرم خستگی مزمن
|کد مقاله||سال انتشار||مقاله انگلیسی||ترجمه فارسی||تعداد کلمات|
|33158||2010||10 صفحه PDF||سفارش دهید||9168 کلمه|
Publisher : Elsevier - Science Direct (الزویر - ساینس دایرکت)
Journal : Psychiatry Research: Neuroimaging, Volume 181, Issue 2, 28 February 2010, Pages 155–164
Sixty-one dextral, unmedicated women with chronic fatigue syndrome (CFS) diagnosed according to the Fukuda criteria (1994) and referred for investigation by rheumatologists and internists were studied with quantitative EEG (43 channels) at rest with eyes open and during verbal and spatial cognitive activation. The EEGs from the patients were compared with recordings from 80 dextral healthy female controls. Only those subjects who could provide 20 1-s artefact-free segments of EEG were admitted into the study. The analysis consisted of the identification of the spatial patterns in the EEGs that maximally differentiated the two groups and the estimation of the cortical source distributions underlying these patterns. Spatial patterns were analyzed in the alpha (8–13 Hz) and beta (14–20 Hz) bands and the source distributions were estimated using the Borgiotti–Kaplan BEAMFORMER algorithm. The results indicate that the spatial patterns identified were effective in separating the two groups, providing a minimum correct retrospective classification rate of 72% in both frequency bands while the subjects were at rest to a maximum of 83% in the alpha band during the verbal cognitive condition. Underlying cortical source distributions showed significant differences between the two groups in both frequency bands and in all cognitive conditions. Lateralized cortical differences were evident between the two groups in the both frequency bands during both the verbal and spatial cognitive conditions. During these active cognitive conditions, the CFS group showed significantly greater source-current activity than the controls in the left frontal–temporal–parietal regions of the cortex.
Fukuda et al. (1994) have provided a modern operational definition of chronic fatigue syndrome (CFS): 6 months or more of increased fatigue, severe enough to reduce daily activity below 50% of premorbid level with at least four of the following symptoms present for at least 6 months or more: mild fever, painful lymph nodes, myalgia, nonexudative pharyngitis, sleep disturbance (insomnia or hypersomnia), migratory arthralgia, memory dysfunction, post-exertional fatigue for more than 24 h. The above, of course, requires that no primary medical or psychiatric illness be present that could account for the symptomatology. Fibromyalgia (FM) differs from CFS in that pain at particular trigger points is found, whereas fatigue dominates the clinical picture in CFS, but the symptomatic overlap in the two conditions is striking (Goldenberg, 1989). It has now been well established that no single virus is etiological in CFS, but in 70% of cases it is triggered by a viral “flu-like” illness. A preexisting immune vulnerability is probable, given the overwhelming female susceptibility, women being more prone to autoimmune diseases than men, for example, Hashimoto's thyroiditis, lupus, rheumatoid arthritis, Sjogren's syndrome, antiphospholipid syndrome, Graves' disease/hyperthyroiditis, scleroderma, myasthenia gravis, and multiple sclerosis. That the immunologic system is involved is shown by increase in activated T lymphocytes, increase in cytotoxic T cells, increase in circulating cytokines and poor cellular function: low natural killer cell cytotoxicity, poor response to mitogens in culture and frequent immunoglobulin deficiencies: IgG1 and IgG3 (Landay et al., 1991 and Lloyd et al., 1988). In recent years it has become increasingly recognized that the brain and the immune system interact in a bidirectional chemical communication through neurotransmitters and cytokines modulating corticotropin releasing factor, in turn regulating the hypothalamic–pituitary–adrenal axis (Black, 1995). One of the most important conveyors of immunological information to the central nervous system (CNS) is the polypeptide cytokine interleukin-1 (Ur et al., 1992). At the subjective level, cognitive impairment is emphasized in patients with CFS, “mental fog”, impaired concentration, poor memory and frequent word finding difficulties. Numerous neuropsychological studies have confirmed the presence of CNS dysfunction, essentially deficits in information processing, memory impairment, and poor learning of information (Marcel et al., 1996, Altay et al., 1990, DeLuca and Schmaling, 1995 and Moss-Morris et al., 1996). Michiels and Cluydts, 2001 and Tiersky et al., 1997 have reviewed these findings. Joyce et al. (1996) further found that patients with CFS were also impaired on verbal tests of unrelated word association learning and letter fluency. Interestingly, Lange et al. (2005) found in a functional magnetic resonance imaging (fMRI) study of verbal working memory that although individuals with CFS could process auditory information as accurately as controls, they utilized more extensive regions of the network associated with the verbal working memory system and that mental fatigue accounted largely for the increased blood-oxygen-level-dependent (BOLD) signal change in the left superior parietal region as well as increased activation bilaterally in the supplementary and premotor regions. Numerous publications document a downregulation of the hypothalamic–pituitary–adrenal axis in chronic fatigue (Parker et al., 2001, Demitrack et al., 1991, Demitrack, 1994, Bearn et al., 1995 and Poteliakhoff, 1981). Some 30–40% of CFS patients have hypocortisolism. Abnormalities in serotonin neurotransmission have been found in CFS: serotonin agonists lead to an increase in serum prolactin in CFS that is not seen in depressed or healthy controls, i.e. in CFS there is an up-regulation of serotoninergic neurotransmission, while in depression the opposite is found, hypercortisolism and suppressed serotonin-mediated prolactin response (Demitrack and Crofford, 1995). Excellent reviews of the general characteristics of CFS have been provided by Wessely, 1995, Afari and Buchwald, 2003 and Prins et al., 2006. There are three diseases characterized by symptomatology that is remarkably similar to that of chronic fatigue syndrome: Addison's disease, Rickettsial diseases (Scientific American Medicine, 1987. 7:XVII: 1–10), and glucocorticoid deficiency. For example, Addison's disease is of sudden onset with an overrepresentation of middle-aged women and presents with the following general symptoms: persistent fatigue, debilitation after exercise, weakness, fever, enlarged lymph nodes, myalgia, arthralgia, flu-like symptoms, sore throat, headaches, and dizziness upon standing (Baschetti, 2000). Hypotension and reduced aldosterone are an integral part of Addison's disease, and it is probably not coincidental that postural hypotension (Bou-Holaigah et al., 1995) and symptomatic relief with fludrocortisone (Florinef) have been described in CFS. Remarkably, Scott et al. (1999) administered the adrenocorticotropin (ACTH) stimulation test in 30 patients with CFS, in each case triggered by a viral influenza-type illness, and found eight who had a blunted response to 1 μm intravenously, i.e. failure to achieve a peak cortisol level greater than 600 nmol/l 30 min later. In all these subjects both adrenal glands were 50% smaller than in controls on examination with computed tomography (CT). Some neurological illnesses may provide insight into the pathogenesis of CFS: measles encephalomyelitis is a neurological disorder of abrupt onset that starts, on average, 5 days after the rash with headaches, generalized seizures, confusion, and motor deficits. The virus is not detected in the brain where the neuropathological changes are similar to those seen in experimental allergic encephalomyelitis, suggesting an autoimmune pathogenesis (Johnson et al., 1984). There was in the small locality of Akureyri in Iceland an epidemic CNS illness in the winter of 1948–49 characterized by low grade fever (not higher than 37.8 °C) with painful muscles, weakness, nervousness and extreme fatigue. Seven years later, 75% had persistent symptoms, 52% had muscle weakness and 65% had clear CNS signs (Goodnick and Sandoval, 1993).