Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0015674 (chronic fatigue syndrome)
 2,978 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

INTRODUCTION. This paper review the state of the art of alternating hemiplegia of childhood. This entity is a rare neurologic disorder of infancy characterize by transient hemiplegic spells shifting from one side to another, and occasionally affecting to both hemispheres at the same time. Usually start before 18 months, many cases exhibit neonatal symptoms related with the disorder. Early symptomatology include abnormal ocular movements, mainly nystagmus, and tonic or dystonic attacks generally beginning before 6 months of age. These symptoms are frequently misdiagnosis as epilepsy. Typical hemiplegic fits which disappeared when infant felt asleep appeared by 12 months of age. Diagnosis is on clinical basis after excluding any other causes of fluctuating and transitory hemiplegic attacks. Complementary investigations, such as electroencephalograms, TAC, MRI, angiographic MRI, CFS are strictly normal. Cerebral SPECT show controversial abnormalities in some studies. We perform SPECT study in a alert 12 months old girl during an interictal period resulting in a non significant asymmetry, with lesser perfusion in left frontal basal and anterior temporal gyrus. Nevertheless, we observed an striking hyperperfusion in middle occipital area. Treatment is symptomatic with flunarizine. Our patient experience a dramatic decrease in frequency, duration and severity of hemiplegic attacks.
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PMID:[Alternating hemiplegia in young babies]. 1198 11

Previous studies have provided evidence supportive of the clinical importance of widespread pain in patients with chronic fatigue syndrome (CFS): pain severity may account for 26-34% of the variability in the CFS patient's activity limitations and participation restrictions. The etiology of widespread pain in CFS remains to be elucidated, but sensitisation of the central nervous system has been suggested to take part of CFS pathophysiology. It is hypothesised that a nitric oxide (NO)-dependent reduction in inhibitory activity of the central nervous system and consequent central sensitisation accounts for chronic widespread pain in CFS patients. In CFS patients, deregulation of the 2',5'-oligoadenylate synthetase/RNase L pathway is accompanied by activation of the protein kinase R enzyme. Activation of the protein kinase R and subsequent nuclear factor-kappaB activation might account for the increased production of NO, while infectious agents frequently associated with CFS (Coxsackie B virus, Epstein-Barr Virus, Mycoplasma) might initiate or accelerate this process. In addition, the evidence addressing behavioural changes in CFS patients fits the central sensitisation-hypothesis: catastrophizing, avoidance behaviour, and somatization may result in, or are initiated by sensitisation of the central nervous system.
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PMID:Pain in patients with chronic fatigue syndrome: does nitric oxide trigger central sensitisation? 1561 66

We report a 41-year-old man with meningoencephalitis associated with herpes simplex virus type 1 (HSV-1). The patient developed fever, headache and dysuria followed by generalized convulsion and neck stiffness, and the CSF showed pleocytosis. The titers of enzyme-linked immunosorbent assay against HSV measured 6 days after onset showed a significant rise; IgG antibody 4.89 (<0.2) and IgM antibody 1.45 (<0.8) in CSF, IgG antibody 46.1 (<2.0) and IgM antibody 1.76 (<0.8) in the serum. The antibody index for IgG was 0.50, and that for IgM was 4.2. CFS neutralization test showed HSV-1 antibody of x16 and HSV-2 antibody of <x4. MRI showed atypical features: disseminated cortical lesions without massive hemispheric involvement. All of the cortical lesions were small and appeared to be located in the gray matter. The patient recovered with acyclovir. This report demonstrates that disseminated encephalitis can be a feature of acute HSV-1 infection.
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PMID:Herpes simplex virus type-1 meningoencephalitis showing disseminated cortical lesions. 1754 Dec 31