Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Local hypothermia was used to manage motor disorders in infantile cerebral paralysis. Ice was applied to muscles being the key factors in the pathologic muscular synergies and determinants of the level of motor disorders at the residual stage of infantile cerebral paralysis. The hypothermic method is given in detail with respect to different pathologic muscle synergies and infantile cerebral paralysis syndrome peculiarities: spastic diplegia varying in severity, hyperkinetic syndrome. EMG investigations yielded results correlating with a positive clinical effect. The EMG data indicated that deprivation of pathologic muscle afferentation not only reduced the muscle spasticity but also led to functional reconstruction in the spinal motoneuron pool.
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PMID:[Artificial local hypothermia in the treatment of children with cerebral palsy]. 319 81

Besides oxygen administration and immaturity of the premature retinal vessels, there are other risk factors for retrolental fibroplasia: (1) respiratory distress syndrome; (2) multiple episodes of bradycardia apnoea; (3) exchange transfusions; (4) hyaline membrane disease; (5) anemia of prematurity; (6) hyperbilirubinemia; (7) avitaminosis E; (8) cardiovascular defects; (9) infectious diseases; (10) multiple births; (11) hypocalcemia; (12) hypothermia; (13) hemorrhagic tendency; (14) delayed coaptation of the retina, and (15) spastic diplegia.
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PMID:Risk factors for retrolental fibroplasia. 668 25

Cerebral palsy (CP) is a group of disorders of movement and posture resulting from nonprogressive disturbances of the fetal or neonatal brain. More than 80% of cases of CP in term infants originate in the prenatal period; in premature infants, both prenatal or postnatal causes contribute. The most prevalent pathological lesion seen in CP is periventricular white matter injury (PWMI) resulting from vulnerability of the immature oligodendrocytes (pre-OLs) before 32 wk of gestation. PWMI is responsible for the spastic diplegia form of CP and a spectrum of cognitive and behavioral disorders. Oxidative stress and excitotoxicity resulting from excessive stimulation of ionotropic glutamate receptors on preOLs are the most prominent molecular mechanisms for PWMI. Asphyxia around the time of birth in term infants accounts for less than 15% of CP in developed countries but the incidence is higher in underdeveloped areas. Asphyxia causes a different pattern of brain injury and CP than is seen after preterm injuries. This type of CP is associated with the clinical syndrome of hypoxic-ischemic encephalopathy shortly after the insult, and the cortex, basal ganglia, and brainstem are selectively vulnerable to injury. Experimental models indicate that neurons in the neonatal brain are more likely to die by delayed apoptosis extending over days to weeks than those in the adult brain. Neurons die by glutamate-mediated excitotoxicity involving downstream caspase-dependent and caspase-independent cell death pathways. Recent reports indicate that males and females preferentially utilize different pathways. Clinical trials indicate that mild hypothermia reduces death or disability in term infants following asphyxia and basic research suggests that this approach might be combined with pharmacological strategies in the future.
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PMID:Cerebral palsy. 1702 68