Thirty-three patients with liver cirrhosis were investigated clinically and electrophysiologically. Nerve-conduction abnormalities were present in 24 (73%) patients compared with 71% reported in a recent study. The reported incidence in the earlier literature varies from no neuropathy to over 90%. ,4-8,20] This might be due to differences in patient selection or variation in the criteria used for the definition of neuropathy. The neuropathy was subclinical or mild, and in most of the patients, detected only on electrophysiological testing, as reported earlier.[4,5,6] Only a few patients had signs or symptoms of neuropathy. They were mainly in the form of distal sensory loss, parasthesias, absent ankle jerks and, in two patients, mild motor weakness. The nerve-conduction abnormalities were present diffusely in all nerves, conforming to a polyneuropathic pattern. Most of the patients had mildly reduced conduction velocities and decreased amplitudes. Only two patients had markedly decreased conduction velocities, suggesting demyelination. Some reduction in conduction velocity can be the result of axonal damage. Thus, the predominant pattern of neuropathy in our patients was of the axonal type. This is similar to a recent study, but unlike most of the earlier studies,[5,6,7,8] where a demyelinating neuropathy was reported.
Some diseases producing liver dysfunction can independently cause peripheral neuropathy. Hence, a cause and effect relationship between liver disease and neuropathy has been questioned. Alcohol consumption is one such hypothesis. Keeping this in mind, we analyzed our results separately in alcohol-related and non-alcohol-related cirrhosis. There were comparable numbers of patients in both the groups (i.e. alcohol-related (17) and non-alcohol-related (16) cirrhosis). As far as individual nerves were concerned, the incidence of conduction abnormalities was generally slightly higher in the alcohol group. The overall incidence of nerve-conduction abnormalities in the alcohol group was 88% compared with 56% in the non-alcohol group. The mean neuropathy score was 3 ± 0.44 in the alcohol group compared with 1.7 ± 0.62 in the non-alcohol group. These difference, despite being nearly significant, had a P-value more than 0.05. This shows that a significant number of patients with non-alcohol-related cirrhosis had neuropathy and that the neuropathy was probably the effect of liver cirrhosis itself, rather than just being a concomitant finding. The incidence and severity of neuropathy was also evaluated in patients with different severities of liver disease, as defined by Child-Pugh grading. Seventy-one per cent of patients with Child's class B had abnormal nerve-conduction results compared with 75% patients in class C. The mean neuropathy score in patients of Child's class B and class C were 2.3 ± 0.56 and 2.4 ± 0.59, respectively. None of these two observations had any significant difference. A recent study by Chaudhry et al reported more severe neuropathy in Child's class-C than in class-B cirrhosis.
Portosystemic shunting has been thought to be one of the factors in the pathogenesis of hepatic neuropathy. However, Chari et al. did not find a higher incidence of neuropathy in patients with portocaval shunts. Hindfelt et al. proposed hepatocellular failure as the main pathophysiological mechanism for neuropathy in a study done of rats with portocaval anastomosis. In our study, the incidence of nerve-conduction abnormalities in patients with and without history of encephalopathy was equal (73%) and the mean neuropathy score in these two groups was 2.0 ± 0.68 and 2.5 ± 0.48, respectively, which was not statistically significant. The severity of neuropathy in all patients was generally mild, with 11 (33%) patients having no neuropathy, 21 (64%) having grade-1 neuropathy (mild) and one (3%) having grade-II (moderate) neuropathy. None of the patients had grade-III (severe) neuropathy. Similar findings were reported in another recent study. The various mechanisms postulated for this hepatic neuropathy are metabolic inhibition of the axonal membrane function, metabolic damage to Schwann cells and even a possible disordered insulin metabolism, something similar to diabetic neuropathy. These changes could be occurring in the early stages of cirrhosis as the incidence and severity of neuropathy was not significantly different in patients with Child's B- and Child's C-class cirrhosis.
In conclusion, this study revealed that many patients with liver cirrhosis have an associated peripheral neuropathy, which is usually subclinical or mild, that is better assessed on electrophysiological testing. This is a diffuse motor-sensory polyneuropathy that is predominantly axonal in nature. The neuropathy is present regardless of the etiology of the cirrhosis. The incidence and severity of this neuropathy is not significantly related to the severity of liver cirrhosis. The cause of the neuropathy is probably the liver disease itself as the incidence and severity of the neuropathy in alcohol-related cirrhosis, although higher, was not significantly different from the non-alcohol-related cases.
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Dr S Prabhakar, Professor and Head, Department of Neurology, Postgraduate Institute of Medical Education and Research, Chandigarh 160012, India. E-mail: email@example.com
J Gastroenterol Hepatol. 2003;18(8) © 2003 Blackwell Publishing
Cite this: Peripheral Neuropathy in Liver Cirrhosis - Medscape - Aug 01, 2003.