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Case Reports
. 1991 Dec;22(4):259-63.

[Visual P300 in acute hepatic encephalopathy resulting from non-A-non-B fulminant hepatitis: analysis of the course before and after orthotopic liver transplantation]

[Article in German]
Affiliations
  • PMID: 1786789
Case Reports

[Visual P300 in acute hepatic encephalopathy resulting from non-A-non-B fulminant hepatitis: analysis of the course before and after orthotopic liver transplantation]

[Article in German]
C F Kügler et al. EEG EMG Z Elektroenzephalogr Elektromyogr Verwandte Geb. 1991 Dec.

Abstract

The method of Pattern Flash elicited P300 (PFP300) has been applied to evaluate the dynamic alterations in cognitive function of a 58 year old woman (H. C.) presenting with hepatic failure due to fulminant hepatitis Non-A-Non-B. At the time of the first investigation she complained about slight memory deficits and revealed signs of hepatic encephalopathy grade I according to Parson-Smith et al. (bilirubin 26.0 mg/dl, NH3 102 micrograms/dl, electrolytes and blood sugar normal). Psychometric tests: Number connection test (NCT): 54 s (28-53 s, greater than 2sd); Syndrom-Kurz-Test (SKT): total score = 9 (0-4), compatible with a slight "organic brain syndrome". PFP300: N250 latency 343.5 ms (276.4 +/- 14.7 ms, greater than 4sd); PFP300-latency: 442.5 ms (326.9 +/- 14.7, greater than 7sd); PFP300 amplitudes: 16.0 microV (14.4 +/- 8.4, +/- 1sd), indicating severe disturbance in visual discrimination without visual attention deficits. Due to progressive deterioration of liver function the patient had to undergo orthotopic liver transplantation. The patient was reinvestigated four weeks later. The clinical and laboratory status were normal and no signs of hepatic encephalopathy could be detected clinically or by means of the psychometric tests. The parameters of the PFP300 complex had also completely returned to normal: N250-latency: 273.0 ms (less than 1sd); PFP300-latency: 348.0 ms (less than 1sd). This observation suggests that the analysis of P300 can help to detect and follow minor cognitive deficits in cases of acute hepatic encephalopathy. It further underscores the hepatic etiology as well as the potential reversibility of this type of encephalopathy.

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