Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038220 (status epilepticus)
 7,272 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We studied the P300 of two epileptic cases with almost continuous diffuse spike-wave discharges on sleep EEG: one with epilepsy with continuous spike-waves during slow wave sleep, and another with atypical benign partial epilepsy. These cases showed a marked prolongation of P300 latencies during nonconvulsive status epilepticus with continuous spike-waves during slow wave sleep. As they improved clinically and electroencephalographically, the latencies became normal. These findings indicate that P300 is a useful method to elucidate the pathophysiology of nonconvulsive status epilepticus with continuous spike-waves during slow wave sleep.
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PMID:[Event-related potential (P300) in two epileptic cases with continuous spike-waves during slow wave sleep]. 1065 51

By studying neuronal activity through neuronal electrogenesis, neurophysiological investigations provide a functional assessment of the nervous system and, therefore, has been used for quantitative assessment and follow-up of hepatic encephalopathy (HE). The different clinical neurophysiological approaches can be classified depending on the function to explore and their sensitivity to HE. The reliable techniques are those that reflect cortical function, i.e., cognitive-evoked potentials (EPs) (P300 paradigm), electroencephalogram (EEG), visual EPs (latency>100 ms) and somatosensory EPs (SEPs) (latency between 25 and 100 ms). Short-latency EPs (brainstem acoustic EPs, SEPs of a latency<25 ms) are in principle insensitive to HE, but can disclose brainstem conduction deficits due to oedema. SEPs and motor EPs can disclose myelopathies. Because of its parallelism to the clinical examination, clinical neurophysiology can complement the neurological examination: (i) to provide evidence of HE in patients who have normal consciousness; (ii) to rule out, at least under some conditions, disturbances of consciousness due to other causes (e.g. drug-induced disturbances, non-convulsive status epilepticus) with the reservation that the mildest degrees of encephalopathy might be associated with an EEG pattern similar to that induced by drugs; and (iii) to demonstrate the worsening or, conversely improvement, of HE in the follow-up period.
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PMID:Neurophysiological investigations of hepatic encephalopathy: ISHEN practice guidelines. 1963 7