Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0003129 (Anoxia)
 551 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Five hundred and forty four cases of cerebral palsy were studied to find the etiology. Male to female ratio was 1.9:1. Prenatal, natal and postnatal factors were found in 42 (7.72%), 238 (43.75%) and 142 (26.1%) cases respectively. Only 79 (14.52%) cases were found to have more than one factor which could have contributed to brain damage. In 43 (7.9%) cases the prenatal, natal and postnatal history were normal and the cause was not known. Toxemia (1.29%) cases and microcephaly (1.84%) cases were the most common etiological factors in the prenatal category. Among the natal causes, birth anoxia was the most common etiological factor and was observed in 24.45% cases. Infections of the central nervous system comprised the major etiopathogenetic factors of the postnatal causes--11.95% cases had encephalitis, while 5.15% cases had meningitis. In cases where more than one etiology was present, the most frequent causes were a combination of prematurity or birth anoxia in association with toxemia, antepartum hemorrhage, prolonged labour, twins, forceps or caesarean delivery. Anoxia was consistently the most common etiological factor in those cases of monoplegia paraplegia, quadriplegia, diplegia, and ataxia, i.e. in 0.55%, 1.29%, 11.76%, 6.07% and 0.55% cases respectively. The present study reveals that majority of the cases were found to have natal or post natal etiology.
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PMID:Cerebral palsy--an etiological study. 134 Aug 61

The detection of neuron-specific enolase in biological fluids has been investigated as an indirect marker of neuronal damage in man. This protein was measured by a sandwich enzymoimmunoassay in serums and cerebrospinal fluids from patients with consciousness disorders of various aetiologies. Neuron-specific enolase level was significantly increased in sera from patients with comas resulting from anoxemia, head injury, septic state, cirrhosis and fulminant hepatitis. On the other hand, patients with meningitis (affection not normally accompanied with neuronal lesion) exhibited no change of this marker level. The statistical analysis of our results suggests that, in neurological disorders, the neuron-specific enolase levels in cerebrospinal fluid could have some prognostic value. The correlation between its level in cerebrospinal fluid and in serum was also demonstrated. Neuron-specific enolase increase in biological fluids thus represents a useful and promising marker to biochemically characterize various strokes possibly resulting in neuronal damage.
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PMID:Neuron-specific enolase as a marker of neuronal lesions during various comas in man. 2048 94