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

P4 (P14 in adults), N' (N18) and N1' (the negative wave after cortical N1, obtained until late infancy) of short-latency somatosensory evoked potentials (S-SEPs) by median nerve stimulation were studied in 13 selected patients. Of these, 12 patients were suggested to have brain-stem lesions responsible especially for the cardinal symptoms and at the same time showed abnormal S-SEPs characteristically between P3 (P13) and N1 (N20). Another patient showed no cortical response with multilocular cystic encephalopathy. Each wave component could be identified by the same methodology as in controls from neonates to adults. In the normal subject the wave forms of P4 and N' were slightly influenced by sleep level. The abnormal S-SEP findings could be classified by an increase and decrease in the wave amplitudes or by a shortening and prolongation in the peak latencies. Upon these classifications we tried to delineate the pathophysiology underlying abnormalities of S-SEPs between P3 and N1. In addition, a negative wave after N1, compatible with N1', was identified in a case without cortical response. Evidence suggests that the origins of P4 and N' may include not only the lemniscal pathway but partly also the extra-lemniscal synapses in the brain-stem. The neural source of N1' seems to be partly in the subcortical structures. As for the clinical significance of S-SEPs in children, the features of P4 and N' are influenced both by the distribution of the affected lesions and by the underlying pathophysiology.
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PMID:Origin and clinical significance of subcortical components in short-latency somatosensory evoked potentials in children. 245 1

Median somatosensory and brainstem auditory evoked potentials (SEP and BAEP) were studied in chronic alcoholics with and without complications of alcoholic liver disease. The alcoholics were divided into 4 groups: Group 1 with minimally abnormal liver function tests; Group 2 with hepatic failure; Group 3 with mild to moderate hepatic encephalopathy; and Group 4 with severe encephalopathy. A control group consisted of age-matched normal subjects. In the alcoholic groups, BAEPs showed a significant prolongation in the latencies of peaks III to VI and interpeaks I-III, III-V, and I-V. The peak latency prolongation was associated with a reduction in all peak amplitudes. In median SEPs, the cervical N13 and cortical N20 latencies were significantly delayed in the alcoholic groups. The amplitude of all cortical SEP components within 150 msec analysis time was also significantly reduced. In addition, the alcoholic groups had slowing in median nerve conduction and prolongation in central conduction time (N13 to N20 interpeak latency). In both BAEPs and SEPs, there were no differences in the peak amplitude and the peak latency among the alcoholic groups except for the late cortical SEP components which showed progressive prolongation and eventual absence from Groups 2 to 4. The present data indicate that chronic alcoholics have subclinical dysfunction in the central somatosensory and brainstem auditory pathways irrespective of the complications of alcoholic liver disease. However, the late components of the cortical SEPs can be affected in hepatic failure and hepatic encephalopathy.
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PMID:Somatosensory and brainstem auditory evoked potentials in alcoholic liver disease with and without encephalopathy. 362 89

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

BAEPs and SEPs were studied in 25 patients of enteric encephalopathy in acute phase and the results were compared with 25 healthy control persons. In the study the important observations of BAEPs were delayed peak latency of wave III, wave V and delayed ILP I-V, and of SEPs was prolonged peak latency of N20. The electrophysiological evidence suggests metabolic cause for the coma and the SEP changes were similar to those observed in cerebral malaria reported earlier in this laboratory.
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PMID:Brainstem auditory evoked potentials (BAEPs) and somatosensory evoked potentials (SEPs) in enteric encephalopathy (EE). 940 31

Myoclonus, defined as shock-like involuntary movement, may be physiological or caused by a very wide variety of hereditary and acquired conditions. Because myoclonus can originate from different disorders and lesions affecting quite varied levels of the central and peripheral nervous systems, it represents from many points of view a diagnostic challenge. Moreover, new entities have been recently individualized, such as cortical tremor, which deserve renewed attention. The aim of this review is to propose a rationale for a diagnostic approach based on clinical and electrophysiological grounds. In this setting, we successively address 1) the clinical features allowing a positive diagnosis of myoclonus; 2) the clinical clues to the etiology; 3) the relevance of the clinical context to the diagnosis; and 4) the contribution of neurophysiology. Differentiating myoclonus from tics, spasm, chorea and dystonia can be difficult, and a careful reappraisal of clinical features allowing precise identification is presented. Moreover, the topographical distribution of myoclonus, the temporal pattern of muscle recruitment, the condition of occurrence and the rhythm of the event, may provide clinical clues relevant to the diagnosis. Myoclonus without associated epilepsy, myoclonus with epilepsy, myoclonus with encephalopathy, parkinsonism and/or dementia represent overlapping clinical categories, although they remain useful for the diagnostic approach. Using electrophysiology (including back-averaging EEG, MEG, SEP, C-reflex studies) to determine the origin of myoclonus may not allow us to focus on the underlying condition. Indeed, in many instances, the myoclonus is cortical in origin, but the pathology is found elsewhere.
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PMID:[Myoclonus in the adult: diagnostic approach]. 1128 Oct 67