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Query: UMLS:C0085584 (encephalopathy)
 18,178 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Recovery functions of somatosensory evoked potentials were studied by the paired stimulation technique in 61 patients with various neurological disorders. A less suppressive or hyperexcitable phase at short intervals, which had been shown in myoclonic patients, was seen in 22 patients. This abnormality was observed even in patients without myoclonus or involuntary movements, which suggests that this phenomenon is not mainly due to some dysfunction causing myoclonus or movement disorders. Less suppression at short intervals was observed for both N20-P25 and P25-N33 components in most of them. Less suppressive recovery of the N20-P25 component with normal recovery of the P25-N33 component was shown only in 3 patients with subcortical lesions with relative sparing of the cortical elements (Binswanger's subcortical encephalopathy). We conclude that less suppressive recovery of only the N20-P25 component suggests the presence of subcortical lesions.
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PMID:Somatosensory evoked potential recovery (SEP-R) in various neurological disorders. 896 65

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

Brainstem auditory evoked potentials (BAEP), visual evoked potentials (VEP) and short latency somatosensory evoked potentials (SSEP) were examined in 30 nonalcoholic liver cirrhotics without clinically detectable hepatic encephalopathy and 30 healthy controls. In the cirrhotics, all peak latencies of the three kinds of evoked potentials, the interpeak latencies (IPLs) I-V, III-V of BAEP and the IPLs N13-N20, N13-P25 of SSEP were significantly prolonged compared with the controls, respectively. The amplitudes of P100, N125 of VEP were significantly lowered in the cirrhotics than those of the controls. Abnormal BAEP test and abnormal SSEP test results were found in both 60% of the cirrhotics, while VEP tests showed abnormalities in only 36.7%. In total, abnormal evoked potential test of one or more kinds were found in 90% of the cirrhotics. It is concluded that in cirrhotic patients, before the appearance of clinically encephalopathy, there were already brain evoked potential abnormalities or brain function changes. Our results argue in favor of the three kinds of evoked potential as the combined investigation for the sensitive and objective diagnosis of subclinical hepatic encephalopathy in patients with nonalcoholic cirrhosis.
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PMID:[Evaluation of brain evoked potentials in the detection of subclinical hepatic encephalopathy in cirrhotics]. 936 85