Cognitive event-related potential in hepatic encephalopathy

Gallai, Virgilio; Alberti, Andrea; Balò, Sofia; Clerici, Carlo; Gentili, Giorgio; Firenze, Caterina; Morelli, Antonio

doi:10.1111/j.1600-0404.1995.tb07021.x

Cited by 16 publications

(14 citation statements)

References 24 publications

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“…70,72 The use of P300 latency elicited by active auditory oddball paradigm was advocated as a tool to detect the onset of HE in several studies. 38,[73][74][75][76][77][78] Present knowledge supports the conclusion that in HE P300 latency is significantly more prolonged in HE then in normal subjects and, therefore the stimulus categorization time is prolonged. However, the value of P300 prolongation as a marker of the risk of the occurrence of overt HE in the follow up was found to be lower than that of the EEG (positive predictive value 53 vs. 75%, negative predictive value 81 vs. 86%).…”

Section: Motor Evoked Potentials (Meps)supporting

confidence: 76%

Clinical Neurophysiology of Hepatic Encephalopathy

Amodio

Montagnese

2015

Journal of Clinical and Experimental Hepatology

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Background/Objectives: Hepatic encephalopathy (HE) has relevant impact on the quality of life of patients and their caregivers and causes relevant costs because of hospitalizations and work days lost. Its quantification is important to perform adequate clinical trials on this relevant complication of cirrhosis and portal-systemic shunting. Clinical neurophysiology, which detects functional alterations of the nervous system, has been applied to the study of HE for over 60 years. This review aims at summarizing and clarifying the role of neurophysiologic techniques in the study of HE. Methods: A narrative review was performed aiming at interpreting the cited papers and the techniques on the basis of their physiological and pathophysiological meaning. Results: The potential role of EEG, quantified EEG, evoked potentials-both exogenous, endogenous and motor-have been clarified to the reader that may be unfamiliar with neurophysiology. Conclusions: The EEG, reflecting the oscillatory changes of neural network is the preferable tool to detect and monitor HE, with the exception of its most severe stage, when EEG flattens. SSEP and MEP have indication to detect and monitor transmission alterations that are likely related to myelin changes and microedema. ( J CLIN EXP HEPATOL 2014;5:S60-S68)

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Section: Motor Evoked Potentials (Meps)supporting

confidence: 76%

Clinical Neurophysiology of Hepatic Encephalopathy

Amodio

Montagnese

2015

Journal of Clinical and Experimental Hepatology

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“…The use of a fixed cutoff will overrate the prevalence of alterations in old patients and underrate that in young patients. [41–46] So a battery of psychometric tests is recommended by Ferenci et al . [47] for the diagnosis of MHE.…”

Section: Discussionmentioning

confidence: 99%

Predictors of minimal hepatic encephalopathy in patients with cirrhosis

Sharma

2010

Saudi J Gastroenterol

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Background/Aim:Minimal hepatic encephalopathy (MHE) impairs patient’s daily functioning of life. Predictors of MHE in cirrhotic patients have not been evaluated.Patients and Methods:A total of 200 cirrhotic patients (Child A, 74 [37%]; Child B, 72 [36%]; Child C, 54 [27%]) were evaluated by psychometry, P300 auditory event-related potential (P300ERP) and critical flicker frequency (CFF). MHE was diagnosed by abnormal psychometry (>2 S.D.) and P300ERP (>2.5 S.D.). Univariate and multivariate logistic regression analyses were performed to determine the predictors of MHE.Results:Eighty-two (41%) patients were diagnosed to have MHE – 26/74 (35%) in Child A, 26/72 (36%) in Child B and 30/54 (56%) in Child C. Ninety-seven (48.5%) patients had abnormal psychometric tests, and 96 (48%) had prolonged P300ERP (>358 ms). Sixteen (16.5%) patients with abnormal psychometry had P300ERP < 358 ms, and 15 (14.5%) patients with normal psychometry results had P300ERP > 358 ms. One hundred and three patients had CFF value < 39 Hz with specificity of 86.6% and sensitivity of 72.9% for MHE. Model for end-stage liver disease (MELD) (17.9 ± 5.7 vs. 13.4 ± 4.2, P = 0.005), Child-Turcotte-Pugh (CTP) score (8.4 ± 2.5 vs. 7.7 ± 2.2, P = 0.02), ammonia (104.8 ± 37.9 vs. 72.5 ± 45.2 µmol/L, P = 0.001) and CFF (37.0 ± 2.8 vs. 41.0 ± 3.4 Hz, P = 0.001) were significantly higher in MHE as compared to non-MHE patients. Ninety-one (45.5%) patients had MELD > 15.5, 115 (57.5%) had CTP score > 7.5, while 93 (46.5%) had venous ammonia > 84.5 µmol/L. On univariate analysis, MELD (8.52 [95% CI, 4.46-16.26; P = 0.001]), CFF (17.34 [95% CI, 8.16-36.85; P = 0.001]) and venous ammonia (7.80 [95% CI, 4.11-14.81; P = 0.003]) were associated with MHE; while CTP score (1.51 [95% CI, 0.85-2.69; P = 0.30]) was not significant. On multivariate analysis, MELD, CFF and venous ammonia were predictive of MHE.Conclusion:Prevalence of MHE in this study was 41%; and MELD > 15.5, CFF < 39 Hz and venous ammonia > 84.5 µmol/L were predictive of MHE.

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“…The latency of the P300 wave has been studied in various conditions (such as hepatic encephalopathic patients (26), major depression (7) and dementia (12)) where cognitive ability is affected. Whereas previous findings indicate the clinical usefulness of P300 latency prolongation as an objective parameter in several disorders with impaired cognitive function, further placebo-controlled trials with sufficient numbers of patients need to be done for the clinical application of this parameter in GHD.…”

Section: Discussionmentioning

confidence: 99%

Utility of P300 auditory event related potential latency in detecting cognitive dysfunction in growth hormone (GH) deficient patients with Sheehan's syndrome and effects of GH replacement therapy

Gölgeli

Tanrıverdi

Süer

et al. 2004

European Journal of Endocrinology

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Objective: Impaired cognitive function has been demonstrated in adults with growth hormone (GH) deficiency (GHD) by using different neuropsychological tests. Despite several studies, present knowledge about the impact of GHD and GH replacement therapy (GHRT) on cognitive function is limited. P300 event-related potential (ERP) application is a well-established neurophysiological approach in the assessment of cognitive functions including the updating of working memory content and the speed of stimulus evaluation. GHD is a well-known feature of Sheehan's syndrome and cognitive changes due to GHD and the effects of GHRT remain to be clarified. The present study was designed to investigate the effects of GHD and 6 months of GHRT on cognitive function in patients with Sheehan's syndrome by using P300 latency. Design and methods: The study comprised 14 patients with Sheehan's syndrome (mean age, 49.5^7.8 years) and 10 age-, education-and sex-matched healthy controls. With hormone replacement therapy, basal hormone levels other than GH were stable before enrollment and throughout the GHRT. The diagnosis of GH deficiency was established by insulin-tolerance test (ITT), and mean peak level of GH in response to insulin hypoglycemia was 0.77^0.35 mIU/l. Treatment with GH was started at a dose of 0.45 IU (0.15 mg)/day in month 1, was increased to 0.9 IU (0.30 mg)/day in month 2 and was maintained at 2 IU (0.66 mg)/day. Initially baseline auditory ERPs in patients and controls were recorded at frontal (Fz), central (Cz), and parietal (P3 and P4) electrode sites. In the patient group, ERPs were re-evaluated after 6 months of GH replacement therapy. During each session P300 amplitude and latency were measured. Results: Mean serum insulin-like growth factor-I (IGF-I) concentration in the patient group before GHRT was 23^13 ng/ml. After 6 months of GH therapy mean IGF-I significantly increased to an acceptable level, 234^71 ng/ml (P , 0.05). The mean latencies (at all electrode sites) of the patients before GHRT were found to be significantly prolonged when compared with those of normal controls (P , 0.05). After 6 months of GHRT mean P300 latencies (at all electrode sites) were decreased significantly when compared with latencies before treatment (P , 0.05). Conclusions: The present study, using P300 ERP latencies, therefore suggests an impairment of cognitive abilities due to severe GHD in patients with Sheehan's syndrome and an improvement of cognitive function after 6 months of physiological GHRT. Moreover, this was a novel application of P300 ERP latencies in cognitive function detection in patients with GHD. Further studies with different patient groups need to be done to assess the clinical use of this electrophysiological method in the diagnosis of cognitive dysfunction due to GHD. European Journal of Endocrinology 150 153-159

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Cognitive event-related potential in hepatic encephalopathy

Cited by 16 publications

References 24 publications

Clinical Neurophysiology of Hepatic Encephalopathy

Clinical Neurophysiology of Hepatic Encephalopathy

Predictors of minimal hepatic encephalopathy in patients with cirrhosis

Utility of P300 auditory event related potential latency in detecting cognitive dysfunction in growth hormone (GH) deficient patients with Sheehan's syndrome and effects of GH replacement therapy

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