Neurophysiological investigations of hepatic encephalopathy: ISHEN practice guidelines

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 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

Clinical Neurophysiology of Hepatic Encephalopathy

“…81 In conclusion, despite its theoretical interest, P300 latency is not recommended as a routine technique to detect and monitor minimal or covert HE by the 'International Society for Hepatic Encephalopathy and Nitrogen Metabolism' (ISHEN) consensus. 82 Recently mismatch negativity was proposed as a good diagnostic tool for minimal HE, also because it is independence of age 79 and reflects a precocious phase of the attentional processes, and these are altered in minimal HE. 83 The clinical use of this potential is even more difficult and problematic than that of P300, since its elicitation is not constant and its measurement difficult.…”

P300 as an auxiliary method in clinical practice: A review of literature

“…Moreover, with P300 testing, damage of cognitive functions resulting from taking different medicines, especially antiepileptic drugs, can also be monitored (61)(62)(63). Additionally, P300 characteristics help diagnosing cognitive damage resulting from systemic diseases, such as anaemia, uremia (renal insufficiency), hepatic encephalopathy, systemic lupus erythematosus, diabetes mellitus, hypothyreosis, as well as COPD (64)(65)(66)(67)(68)(69)(70)(71)(72)(73)(74)(75)(76). Moreover, cognitive function damage in patients with HIV-1 neurologically asymptomatic seropositive can be assessed with P300 testing (78).…”

“…Cognitive damage in some systemic diseases can be assessed with CEP P300 (64)(65)(66)(67)(68)(69)(70)(71)(72)(73)(74)(75)(76)(77)(78). Improvements in the treatment and recovery can be followed in the same way.…”

Hepatic Encephalopathy and Sleepiness: An Interesting Connection?

“…[24][25][26] In addition, sleepiness has been shown to be more common in cirrhotic patients with a history of HE and documented portal-systemic shunt, 28 and to be positively correlated with the amount of slow activity on the wake EEG. 24 This is a well-established marker of HE, 29 and one of the neurophysiological correlates of sleepiness. 7 In a recent, large study, in which habitual daytime sleepiness was qualified as present/absent, its absence had a negative predictive value of 92% in relation to the occurrence of HE-related hospitalizations over the subsequent 8 months.…”