Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085584 (encephalopathy)
 18,178 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The improved technique of cardiopulmonary resuscitation (CPR) resulted in survival of many patients who had experienced cardiopulmonary arrest (CPA). However, when the recovery of brain function is poor, patients suffer from severe neurological sequelae, including persistent vegetative state. There have been no conclusive methods to predict the outcome of anoxic encephalopathy after CPR. Madl et al (1993) recorded cortical SEP over the parietal scalp electrodes after bilateral median nerve stimulation at the wrists in anoxic patients experiencing CPR. Their results indicated that the median SEP is useful for the early prediction of neurological prognosis after CPR. We studied short and long latency cortical SEPs evoked by the left median nerve stimulation in 18 consecutive anoxic patients within 48 hours after CPR. The absence of N20, N35, P45 indicated mortality of 86.4% (100% in Madl's results). Preserved N60 peak indicated the recovery of consciousness, while Madl's results showed that patients did not regain consciousness when the N60 latency was longer than 121 ms. Neurological prognosis showed the significant correlation with N20, P25 amplitude and not with amplitude ratio (N20 P25/P15 N20). Reduced amplitude of N20 P25 was consistent with the high score of GOS. N20 P25 was greater than 3.7 microV in all patients who regained consciousness. Recording of cortical SEP within 48 hours after CPR was useful for the prediction of neurological outcome.
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PMID:[Use of cortical SEP for the prediction of neurological prognosis after cardiopulmonary resuscitation]. 904 24

Hypoxic encephalopathy is a common cause of neonatal seizures and long-term neurological cognitive deficits. In rats at postnatal days 10-12 (P10-P12), global hypoxia induced spontaneous seizures and chronic brain injury, mimicking clinical aspects of neonatal hypoxia. Synaptic Ras-GTPase activating protein (SynGAP) has important roles in RAS/MAPK-dependent synaptic plasticity and mammalian learning. We investigated possible alterations of SynGAP expression occurring in memory-impaired animals previously exposed to perinatal hypoxia insults. We also evaluated the therapeutic efficacy of A68930, a selective agonist of dopamine D1/D5 receptors, on perinatal hypoxia insults. In the hippocampal CA1 region, perinatal hypoxia insults (P10) led to a reduction in SynGAP expression associated with impairment in long-term spatial learning and memory performance at P45. The use of A68930 (at a dose of 1, 2, 3mg/kg, P17-P23) effectively attenuated the deleterious effects as described above. Our results may indicate the involvement of SynGAP in certain forms of brain injury, leading to long-term learning and memory deficits. A68930 may have clinical potential as a therapeutic agent for alleviation of long-term cognitive deficits in rats and other animal models.
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PMID:Impaired SynGAP expression and long-term spatial learning and memory in hippocampal CA1 area from rats previously exposed to perinatal hypoxia-induced insults: beneficial effects of A68930. 1550 Sep 70