Patients with manifest hepatic encephalopathy can reveal impaired thermal perception

Brenner, Meike; Butz, Markus; E, May; Kahlbrock, Nina; Kircheis, G.; Häussinger, Dieter; Schnitzler, Alfons

doi:10.1111/ane.12376

Cited by 9 publications

(6 citation statements)

References 20 publications

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“…Our results are in contrast with a previous study from Brenner et al [ 24 ] where the hand was used as the test site, the result of which found impaired thermal perception in grade 2 HE patients, but no differences in MHE patients. They concluded that these alterations emerge mainly in advanced stages of the disease.…”

Section: Discussioncontrasting

confidence: 99%

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Patients with Minimal Hepatic Encephalopathy Show Altered Thermal Sensitivity and Autonomic Function

Rega

Aiko

Peñaranda

et al. 2021

JCM

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Cirrhotic patients may experience alterations in the peripheral nervous system and in somatosensory perception. Impairment of the somatosensory system could contribute to cognitive and motor alterations characteristic of minimal hepatic encephalopathy (MHE), which affects up to 40% of cirrhotic patients. We assessed the relationship between MHE and alterations in thermal, vibration, and/or heat pain sensitivity in 58 cirrhotic patients (38 without and 20 with MHE according to Psychometric Hepatic Encephalopathy Score) and 39 controls. All participants underwent attention and coordination tests, a nerve conduction study, autonomic function testing, and evaluation of sensory thresholds (vibration, cooling, and heat pain detection) by electromyography and quantitative sensory testing. The detection thresholds for cold and heat pain on the foot were higher in patients with, than those without MHE. This hyposensitivity was correlated with attention deficits. Reaction times in the foot were longer in patients with, than without MHE. Patients with normal sural nerve amplitude showed altered thermal sensitivity and autonomic function, with stronger alterations in patients with, than in those without MHE. MHE patients show a general decrease in cognitive and sensory abilities. Small fibers of the autonomic nervous system and thermal sensitivity are altered early on in MHE, before large sensory fibers. Quantitative sensory testing could be used as a marker of MHE.

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Section: Discussioncontrasting

confidence: 99%

“…Previous studies using neurophysiological methods have found impairments in both central and peripheral parts of the somatosensory system in patients with liver cirrhosis and overt HE [ 24 ].…”

Section: Introductionmentioning

confidence: 99%

Patients with Minimal Hepatic Encephalopathy Show Altered Thermal Sensitivity and Autonomic Function

Rega

Aiko

Peñaranda

et al. 2021

JCM

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“…Our results demonstrate that this disease-related impairment does also span the somatosensory modality, and particularly the temporal discrimination of tactile stimuli. This finding tallies with early work showing both sensory impairments on the behavioral level in HE ( Brenner et al, 2015 ) and slowing of cortical oscillatory activity within the somatosensory system in this patient population ( May et al, 2014 ). Moreover, the correlation of CFF and criticalSOA implies that the severity of the impairment of tactile temporal perception parallels the impairments of visual temporal perception.…”

Section: Discussionsupporting

confidence: 89%

Impaired Tactile Temporal Discrimination in Patients With Hepatic Encephalopathy

et al. 2018

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The sensory system constantly receives stimuli from the external world. To discriminate two stimuli correctly as two temporally distinct events, the temporal distance or stimulus onset asynchrony (SOA) between the two stimuli has to exceed a specific threshold. If the SOA between two stimuli is shorter than this specific threshold, the two stimuli will be perceptually fused and perceived as one single stimulus. Patients with hepatic encephalopathy (HE) are known to show manifold perceptual impairments, including slowed visual temporal discrimination abilities as measured by the critical flicker frequency (CFF). Here, we hypothesized that HE patients are also impaired in their tactile temporal discrimination abilities and, thus, require a longer SOA between two tactile stimuli to perceive the stimuli as two temporally distinct events. To test this hypothesis, patients with varying grades of HE and age-matched healthy individuals performed a tactile temporal discrimination task. All participants received two tactile stimuli with varying SOA applied to their left index finger and reported how many distinct stimuli they perceived (“1” vs. “2”). HE patients needed a significantly longer SOA (138.0 ± 11.3 ms) between two tactile stimuli to perceive the stimuli as two temporally distinct events than healthy controls (78.6 ± 13.1 ms; p < 0.01). In addition, we found that the temporal discrimination ability in the tactile modality correlated positively with the temporal discrimination ability in the visual domain across all participants (i.e., negative correlation between tactile SOA and visual CFF: r = −0.37, p = 0.033). Our findings provide evidence that temporal tactile perception is substantially impaired in HE patients. In addition, the results suggest that tactile and visual discrimination abilities are affected in HE in parallel. This finding might argue for a common underlying pathophysiological mechanism. We argue that the known global slowing of neuronal oscillations in HE might represent such a common mechanism.

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“…The present observations revealed enhanced PTN and RNA oxidation in brain regions of Glul fl/fl × Alb-Cre + mice, whose function is compromised in HE. Functions affected in HE include memory formation in the hippocampus (44); processing of sensory stimuli, such as perception, in the somatosensory cortex (45); and motor functions in the cerebellum (46). Interestingly, in the cerebellum of mice lacking hepatic GS, we identified exceptionally high levels of oxidized RNA in Purkinje cells, which critically control motor functions (30).…”

Section: Discussionmentioning

confidence: 95%

Hyperammonemia in gene-targeted mice lacking functional hepatic glutamine synthetase

Qvartskhava

Lang

Görg

et al. 2015

Proc. Natl. Acad. Sci. U.S.A.

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Urea cycle defects and acute or chronic liver failure are linked to systemic hyperammonemia and often result in cerebral dysfunction and encephalopathy. Although an important role of the liver in ammonia metabolism is widely accepted, the role of ammonia metabolizing pathways in the liver for maintenance of whole-body ammonia homeostasis in vivo remains ill-defined. Here, we show by generation of liver-specific Gln synthetase (GS)-deficient mice that GS in the liver is critically involved in systemic ammonia homeostasis in vivo. Hepatic deletion of GS triggered systemic hyperammonemia, which was associated with cerebral oxidative stress as indicated by increased levels of oxidized RNA and enhanced protein Tyr nitration. Liver-specific GS-deficient mice showed increased locomotion, impaired fear memory, and a slightly reduced life span. In conclusion, the present observations highlight the importance of hepatic GS for maintenance of ammonia homeostasis and establish the liver-specific GS KO mouse as a model with which to study effects of chronic hyperammonemia.hepatic encephalopathy | metabolic zonation | oxidative stress | RNA oxidation | glutamine

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Patients with manifest hepatic encephalopathy can reveal impaired thermal perception

Cited by 9 publications

References 20 publications

Patients with Minimal Hepatic Encephalopathy Show Altered Thermal Sensitivity and Autonomic Function

Patients with Minimal Hepatic Encephalopathy Show Altered Thermal Sensitivity and Autonomic Function

Impaired Tactile Temporal Discrimination in Patients With Hepatic Encephalopathy

Hyperammonemia in gene-targeted mice lacking functional hepatic glutamine synthetase

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