Relation Between the Severity of Liver Cirrhosis and Neurological Symptoms, Nerve Conduction Study Results, and Motor Unit Number Estimation

Reem M Gabr; Dina A El Salmawy; Mye A Basheer; Marwa khairy; Saly H Elkholy

Disclosures

J Viral Hepat. 2021;28(9):1312-1318. 

In This Article

Abstract and Introduction

Abstract

Liver cirrhosis is a global health problem that can be associated with several neurological manifestations. We aimed to assessment of the relation between the severity of the liver cirrhosis and the neurological symptoms, nerve conduction studies (NCS), as well as detecting subclinical neuropathic affection using motor unit number estimation (MUNE) technique. This cross-sectional study was conducted on 56 cirrhotic patients and 61 age- and sex-matched healthy controls. Neurological manifestations, Child-Pugh classification, Model for End-Stage Liver Disease score, NCS and MUNE using a modified spike-triggered averaging technique were studied. Forty-five (80.3%) of the cirrhotic patients had neurological manifestations. Muscle cramps were the most frequently reported manifestation, followed by fatigue and then numbness. NCS abnormality was significantly related to the presence of neurological symptoms (p < 0.001) and not only to peripheral numbness. Only fatigue was significantly related to the lower MUNE values (p < 0.017). Child-Pugh classification progression was significantly related to the presence of fatigue and abnormal NCS results (p < 0.001); no similar relation was detected between the Child-Pugh classification and the MUNE value (p = 0.103). Higher MELD scores were significantly related to NCS abnormalities (p = 0.014) and negatively correlated, although not significantly, with the MUNE values (r = −0.246 and p = 0.067). The progression of liver cirrhosis was related to the presence of neurological manifestations and nerve conduction abnormalities. Nerve conduction abnormalities may be present even in the absence of clinical numbness. A decline in motor unit number could explain the pathophysiology of fatigue in cirrhotic patients.

Introduction

Liver cirrhosis is the final pathway of a wide variety of chronic liver diseases. Major causes of hepatic cirrhosis include hepatitis B (HBV) and hepatitis C (HCV) virus infection.[1] Egypt has been on a fast track to eliminate HCV because of the national HCV treatment programme.[2]

The most frequently reported neurological complications, in patients with liver cirrhosis, are peripheral neuropathy, fatigue, hepatic encephalopathy and muscle cramps.[3] The latter occur due to intramuscular nerve axonal hyperexcitability that can be related to ischaemia.[4]

Nervous dysfunction could be due to the association with abnormality of glucose metabolism and hence higher prevalence of diabetes mellitus among cirrhotic patients that may reach about 20–60% of patients.[5] Also, the evidence introduced by the nerve excitability studies in the cirrhotic patients suggests depolarization probably caused by ischaemia resulting from imbalance of potent vasoconstrictors (such as endothelin) and vasodilators (such as nitric oxide) resulting in poor nerve perfusion.[4]

Epidemiology as well as pattern of peripheral neuropathy in patients with liver diseases varies widely in the literature from 19% up to 100%. This variation may be due to the different electrophysiologic and/or clinical methods among studies.[6]

The prevalence of peripheral neuropathy was 72.3% and was affected mainly by the duration and severity of liver cirrhosis that was determined by Child-Pugh classification.[7] Close percentages were also found: 67.39%,[5] and 73%,[8] of cirrhotic patients despite different aetiologies of liver cirrhosis.

The associated peripheral neuropathy could impact the patient's condition and prognosis.[5] Autonomic neuropathy, in patients with chronic liver disease, is accompanied by failure of the compensatory mechanisms in the overwhelming stress, which may explain the apparent increase in mortality in those patients.[9]

Fatigue was present in approximately two-thirds of patients with chronic hepatitis C infection, even in the absence of considerable liver disease. Even after successful treatment of the HCV infection, disabling fatigue was still present in approximately 30% of the responders.[10,11]

Fatigue, in patients with liver disease, could be cause by excessive production of cytokines such as interferon (INF), interleukin-1 (IL-1) and tumour necrosis factor (TNF) may be involved in the development of chronic fatigue syndromes.[10] Other causes include altered central neurotransmission involving the serotonergic system, or increased incidence of neuromuscular dysfunction.[11]

The study aimed at assessing the relation between the severity of the liver cirrhosis and the presence of neurological symptoms, nerve conduction study results, as well as detecting subclinical neuropathy affection using motor unit number estimation (MUNE) technique.

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