Raphe nucleus encephalopathy (myalgic encephalomyelitis, epidemic neuromyasthenia)

Maurizi, C.P.

doi:10.1016/0306-9877(85)90053-2

Cited by 4 publications

(2 citation statements)

References 22 publications

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“…It has already been suggested that damage to the serotoninergic central raphe neurons of the brain stem might underlie CFS [86], although the evidence reviewed here supports the idea that more laterally situated brain stem lesions might be responsible. MRI of the highest quality is needed, followed up by more detailed SPECT scans, perhaps with the use of one of the new imaging agents for serotonin receptors [168].…”

Section: Discussionmentioning

confidence: 39%

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Chronic fatigue syndrome—aetiological aspects

Dickinson

1997

Eur J Clin Investigation

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The chronic fatigue syndrome (CFS) has been intensively studied over the last 40 years, but no conclusions have yet been agreed as to its cause. Most cases nowadays are sporadic. In the established chronic condition there are no consistently abnormal physical signs or abnormalities on laboratory investigation. Many physicians remain convinced that the symptoms are psychological rather than physical in origin. This view is reinforced by the emotional way in which many patients present themselves. The overlap of symptoms between CFS and depression remains a source of confusion and difficulty. But even if all CFS patients were rediagnosed as depressives, this would not negate the possibility of an underlying organic cause for the condition, in view of the growing evidence that depression itself has a physical cause and responds best to physical treatments. There is some evidence both for active viral infection and for an immunological disorder in the CFS. Many observations suggest that the syndrome could derive from residual damage to the reticular activating system (RAS) of the upper brain stem and/or to its cortical projections. Such damage could be produced by a previous viral infection, leaving functional defects unaccompanied by any gross histological changes. In animal experiments activation of the RAS can change sleep state and activate or stimulate cortical functions. RAS lesions can produce somnolence and apathy. Studies by modern imaging techniques have not been entirely consistent, but many magnetic resonance imaging (MRI) studies already suggest that small discrete patchy brain stem and subcortical lesions can often be seen in CFS. Regional blood flow studies by single photon-emission computerized tomography (SPECT) have been more consistent. They have revealed blood flow reductions in many regions, especially in the hind brain. Similar lesions have been reported after poliomyelitis and in multiple sclerosis--in both of which conditions chronic fatigue is characteristically present. In the well-known post-polio fatigue syndrome, lesions predominate in the RAS of the brain stem. If similar underlying lesions in the RAS can eventually be identified in CFS, the therapeutic target for CFS would be better defined than it is at present. A number of logical approaches to treatment can already be envisaged.

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Section: Discussionmentioning

confidence: 39%

“…Several 'unifying hypotheses' have already been proposed to explain chronic fatigue syndrome [86][87][88], although none has achieved substantial acceptance. All have been lacking in detail.…”

Section: Towards a Unifying Hypothesismentioning

confidence: 99%

Chronic fatigue syndrome—aetiological aspects

Dickinson

1997

Eur J Clin Investigation

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Serotonin turnover rate in raphe and cortex of mice infected with Venezuelan equine encephalomyelitis virus

Lima

Walder

Obregón

et al. 1987

J of Neuroscience Research

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The turnover of serotonin (5HT) was determined in the raphe area and cortex of mice infected with Pixuna, a strain of intermediate virulence of Venezuelan equine encephalomyelitis virus (VEEV). NMRI-mice, 24 days old, were inoculated intracerebrally (ic) with 300 LD50 of the virus. The animals were sacrificed 4, 7, 15, 21, 30, and 60 days postinoculation. 5HT and 5-hydroxyindoleacetic acid (5HIAA) in raphe and cortex were determined by high performance liquid chromatography (HPLC) with electrochemical detection. Turnover rate of 5HT was determined by the administration of pargyline, p-chlorophenylalanine, and probenecid. The content of 5HT or 5HIAA and 5HT/5HIAA ratios were not significantly different in infected compared with control mice. However, a decrease of 5HT turnover rate, determined after pargyline treatment, was observed in the raphe and not in the cortex of infected mice at 4 and 7 days after the inoculation. The turnover rate/(5HT)0 in raphe is decreased in infected mice with signs of illness, suggesting a lower density of 5HT innervation in this brain area. The administration of p-chlorophenylalanine and probenecid showed that the cortex is also affected, but the synthesis is less modified than metabolism or elimination. Cell bodies of 5HT neurons seem to be more susceptible than projections to infection by Pixuna strain of VEEV.

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