Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085437 (bacterial meningitis)
 4,038 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We observed 37 patients (mean age at onset, 48.5 years; range, 13 to 84 years) with segmental myoclonus (18 branchial, 19 spinal). Etiologies for branchial myoclonus included brain-stem demyelination, cerebrovascular disease, Meige's syndrome, cerebral arteritis secondary to bacterial meningitis, central nervous system Whipple's disease, acute cervicomedullary trauma, and cerebellar degeneration. Spinal myoclonus was associated with laminectomy, remote effect of cancer, spinal cord injury, post-operative pseudomeningocele, laparotomy, thoracic sympathectomy, poliomyelitis, herpes myelitis, lumbosacral radiculopathy, spinal extradural block, and myelopathy due to demyelination, electrical injury, acquired immunodeficiency syndrome, and cervical spondylosis. The latency between the predisposing condition and the onset of myoclonus ranged from immediate to 33 years (mean, 2.9 years). In six patients, the myoclonus was the presenting symptom of a serious underlying disease. Treatment with clonazepam, tetrabenazine hydrochloride, or other medications provides a satisfactory control in most patients.
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PMID:Segmental myoclonus. Clinical and pharmacologic study. 375 63

The concentration of alpha 1-microglobulin (alpha 1-m) in sera and cerebrospinal fluids (CSF) was measured in 121 patients with various neurological disorders. Using single radial immunodiffusion, its serum level was determined. No significant difference was found between the patients (29.1 +/- 4.3 mg/l; mean +/- 1 SD) and normal control group (23.7 +/- 4.6 mg/l). The level of CSF alpha 1-m was determined by the radioimmunoassay of solid antibody system. Its CSF level in the control group was 34.8 +/- 16.0 micrograms/l, while it was significantly increased in the patients with viral meningitis (p less than 0.01) and cerebral infarct (p less than 0.05). The level was also elevated in some cases of brain tumor, bacterial meningitis, cerebral hemorrhage, cervical spondylosis, and acute lymphocytic leukemia. There was a positive correlation between alpha 1-m and albumin levels in CSF. The analysis by CSF/serum albumin ratio and alpha 1-m ratio suggested that the increase of alpha 1-m in CSF could be explained mainly by an increase in permeability of the serum alpha 1-m through damaged blood brain barrier under these pathological conditions. Its local production within the central nervous system, however, could not be ruled out in these disorders.
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PMID:Human alpha 1-microglobulin levels in neurological disorders. 618 15

To evaluate significance of superoxide dismutase in neurological diseases, we measured cerebrospinal fluid (CSF) levels of copper-zinc superoxide dismutase (Cu/Zn SOD) and manganese superoxide dismutase (Mn SOD) using enzyme immunoassay methods in 181 neurological patients and 43 controls. The mean level of Cu/Zn SOD in CSF of controls was 54.4 +/- 28.7 ng/ml, and that of Mn SOD 8.1 +/- 2.5 ng/ml, although other methods have reported that Mn SOD is undetectable in CSF. Cu/Zn SOD or Mn SOD showed no statistical difference in age or sex of the controls. The elevation of both SOD levels was marked in acute diseases such as cerebrovascular diseases (CVD), bacterial meningitis and encephalitis, but mild in aseptic meningitis. The elevation of Cu/Zn SOD level was more prominent than that of Mn SOD in CVD, whereas vice versa in bacterial meningitis and encephalitis. In neurodegenerative diseases and cervical spondylosis, only Mn SOD level was significantly elevated. To examine the source of CSF SOD, we compared it with CSF levels of neuron-specific enolase (NSE) and S-100b protein (S-100b) in cerebral infarction and bacterial meningitis. Both SOD levels were correlated with NSE and S-100b levels in patients with cerebral infarction, but in bacterial meningitis no significant relationship was found among SOD levels, NSE and S-100b levels. This means that elevations of SODs in CSF may be due to not only damage of the nervous tissues but also the other mechanisms, as induction of SOD in the lesions.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Superoxide dismutase in cerebrospinal fluid in patients with neurological diseases]. 833 70