Subcortical impairment in subclinical hepatic encephalopathy

Kono, Ichiyo; Ueda, Yoshihiko; Nakajima, Kenji; Araki, Kuniharu; Kagawa, Keiichiro; Kashima, Kei

doi:10.1016/0022-510x(94)90267-4

Cited by 16 publications

(9 citation statements)

References 15 publications

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“…[53][54][55][56][57] Somatosensory evoked potentials (SSEPs) SSEPs explore both nervous transmission from the medulla oblongata to the cortex (central conduction timei.e., the interpeak latency N13-N20-) and hemispheric transmission (middle components of the EP), therefore produce data related to the ones provided by BAEPs and fVEPs, respectively. A minor prolongation of central conduction time in cirrhosis, 37,58 and therefore an alteration in brainstem nervous transmission possibly due to myelopathy or edema was confirmed by SSEPs. However, the prolongation of the middle cortical components (after P25) was found to be much more evident and related with the impairment in neuropsychiatric status 37 and with the risk to develop overt HE in the follow up.…”

Section: Brainstem Auditory Evoked Potentials (Baeps)mentioning

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: Brainstem Auditory Evoked Potentials (Baeps)mentioning

confidence: 76%

Clinical Neurophysiology of Hepatic Encephalopathy

Amodio

Montagnese

2015

Journal of Clinical and Experimental Hepatology

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“…Motor-evoked potentials, as well as SSEPs and BAEPs, may reveal signs of brainstem dysfunction or myelopathy, even in patients considered to have minimal HE (18)(19)(20)(21)(22)(23), possibly linked to focal oedema occurring in this syndrome, or to concurrent disorders.…”

Section: Evoked Potentialsmentioning

confidence: 99%

Neurophysiological investigations of hepatic encephalopathy: ISHEN practice guidelines

Guérit¹,

Amantini²,

Fischer³

et al. 2009

Liver International

127

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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 4 100 ms) and somatosensory EPs (SEPs) (latency between 25 and 100 ms). Short-latency EPs (brainstem acoustic EPs, SEPs of a latency o 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, nonconvulsive 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.By studying neuronal activity through central or peripheral neuronal electrogenesis, neurophysiological investigations provide a functional assessment of the nervous system. Therefore, their domain is similar to that of the clinical examination and complementary to that of neuroimaging. When compared with the clinical examination, they provide a more quantitative assessment, potentially amenable for follow-up, and may remain interpretable in patients under muscle blockade, in whom clinical examination is not feasible.Because neuronal electrogenesis depends on neuronal activity that is sensitive to the influence of energyproviding metabolic systems as well as to the influence of those systems that are involved in electrolyte homoeostasis and clearance of toxic substances, clinical neurophysiology has been used for quantitative assessment and follow-up of metabolic encephalopathies (1). Neurophysiological techniquesTwo techniques are available for routine use, both in clinical and in experimental settings: the electroencephalogram (EEG) and evoked potentials (EPs). Recommendations for their execution are reported by Deuschl and Eisen (2). The grading of recommendations in this article was performed according to the EASL criteria (Table 1).The EEG primarily reflects cortical neuronal activity modulated by both physiological and pathological diencephalic and brainstem influences and by metabolic and toxic factors. Many abnormal EEG patterns are

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“…While the prolongation of the late compo nents suggests a dysfunction of the cerebral cortex, prolongation of the early components in short-latency somatosensory potentials sug gests a subcortical impairment [12], In order to circumvent the role of the exog enous component and to increase the sensitiv ity of the neurophysiological approach, eventrelated endogenous potentials have been eval uated [19]. Here, the stimulus (sound or sight) triggers additional electrical signals that are independent of the original inciting factor and that are subject to study.…”

Section: Subclinical Encephalopathymentioning

confidence: 99%

“…Abnormalities in these domains, commonly seen in entities such as Parkinson's disease [11], raise the possibility that subcorti cal pathways, namely basal ganglia, may be altered in SHE. Studies from a Japanese group also suggest a similar area of involve ment [12], Recent neuroanatomical data have also focused on subcortical areas: MRI has shown selective alterations in basal ganglia [ 13], manganese may be responsible for caus ing these changes [14] and alterations in the density of postsynaptic dopamine D> recep tors are seen in the globus pallidus of cirrhotic patients who died in hepatic coma [15], Another dimension for evaluation of SHE lies in neurophysiological testing. Electroen cephalograms do not have the sensitivity to detect changes in a subclinical state.…”

Section: Ia Gn O Sis Of Sh Ementioning

confidence: 99%

Subclinical Encephalopathy

Blei¹,

Córdoba²

1996

Dig Dis

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Subclinical hepatic encephalopathy (SHE) – cognitive deficits in the absence of overt encephalopathy – is frequently present in patients with cirrhosis. In the absence of biological correlates, diagnosis of SHE relies on psychometric tests. Attentional and motor abnormalities are the most common neurocognitive deficits. Sleep disturbances – a frequent complaint in cirrhosis – may be part of the spectrum of SHE. The impact of SHE on daily activities is controversial as patients may adapt their lives to cognitive limitations. Demanding activities, such as driving motor vehicles, may be impaired, though a blanket restriction appears premature. The benefit of treating SHE is not established. Antiencephalopathic drugs may be effective and can be considered in certain individuals.

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Subcortical impairment in subclinical hepatic encephalopathy

Cited by 16 publications

References 15 publications

Clinical Neurophysiology of Hepatic Encephalopathy

Clinical Neurophysiology of Hepatic Encephalopathy

Neurophysiological investigations of hepatic encephalopathy: ISHEN practice guidelines

Subclinical Encephalopathy

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