[非a -非b型暴发性肝炎致急性肝性脑病的视觉P300:原位肝移植前后病程分析]。

C F Kügler, A Taghavy, W E Fleig, E G Hahn
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引用次数: 0

摘要

PFP300 (Pattern Flash induced P300)被应用于评价一名58岁女性(H. C.)因暴发性非a -非b型肝炎引起的肝功能衰竭的动态变化。在第一次检查时,她抱怨有轻微的记忆缺陷,并根据parsons - smith等人的诊断显示有肝性脑病I级的迹象(胆红素26.0 mg/dl, NH3 102微克/dl,电解质和血糖正常)。心理测试:数字连接测试(NCT): 54秒(28-53秒,大于2sd);综合征- kurz - test (SKT):总分= 9(0-4),符合轻微的“器质性脑综合征”。PFP300: N250延迟343.5 ms(276.4±14.7 ms,大于4sd);pfp300延迟:442.5 ms(326.9 +/- 14.7,大于7sd);PFP300幅值:16.0 microV (14.4 +/- 8.4, +/- 1sd),提示有严重的视觉辨别障碍,但无视觉注意缺陷。由于肝功能进行性恶化,患者不得不接受原位肝移植。四周后再次对患者进行调查。临床及实验室检查均正常,临床及心理测试均未发现肝性脑病征象。PFP300复合物的参数也完全恢复正常:N250-latency: 273.0 ms(小于1sd);PFP300-latency: 348.0 ms(小于1sd)。这一观察结果表明,P300的分析可以帮助检测和跟踪急性肝性脑病患者的轻微认知缺陷。它进一步强调了肝脏病因以及这种脑病的潜在可逆性。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
[Visual P300 in acute hepatic encephalopathy resulting from non-A-non-B fulminant hepatitis: analysis of the course before and after orthotopic liver transplantation].

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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