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Neurophysiological investigations of hepatic encephalopathy: ISHEN practice guidelines
Authors:Jean‐Michel Guerit  Aldo Amantini  Catherine Fischer  Peter W. Kaplan  Oriano Mecarelli  Alfons Schnitzler  Emilio Ubiali  Piero Amodio
Affiliation:1. Neurology Clinique Edith Cavell, Bruxelles, Belgium;2. Department of Neurological Sciences, Neurophysiopathology, University Hospital of Florence, Florence, Italy;3. Neurological and Neurosurgical Hospital, Lyon, France;4. Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, USA;5. Department of Neurological Sciences, Neurophysiopathology, Sapienza University, Rome, Italy;6. Department of Neurology, Heinrich‐Heine University, Düsseldorf, Germany;7. Neurophysiology Unit, United Hospitals of Bergamo, Bergamo, Italy;8. Department of Clinical and Experimental Medicine, University of Padua, Padua, Italy
Abstract: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.
Keywords:acute liver failure  cirrhosis  electro‐encephalogram  encephalopathy  evoked potentials  neurophysiology
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