Clinical study on electrophysiological evaluation of asymptomatic neuropathy in alcohol dependence syndrome

 

 

Abstract              Background: Alcohol consumption results in multiple end-organ damages. Alcoholic neuropathy is the most common deleterious effect of excessive alcohol intake. The incidence of alcoholic neuropathy in the general population is not accurate as the percentage varies widely depending on the definition of chronic alcoholism and the criteria used to detect and classify neuropathy. Few studies suggest that the incidence of peripheral neuropathy is higher in alcoholic patients who have a family history of alcohol dependence syndrome. Aims And Objectives: To detect the prevalence of asymptomatic neuropathy in Alcohol dependent syndrome patients Vinayaka missions’ hospital Salem. Materials And Methods: A cross-sectional study with 100 cases was done. Alcohol-dependent syndrome patients were chosen based on CAGE criteria. Patients with normal RBS and other possible causes for neuropathy were ruled out history-wise. Clinical examination was done to rule out patients with neuropathy findings. Results: Findings in NCS show that there was a significant reduction in the action potential of median, ulnar and peroneal motor nerves. Prolongation of latency and action potential was found to be reduced in sural nerves. Axonal neuropathy was the predominant pathology. A cut-off value for developing neuropathy was found. Age>43 years, Duration of alcohol 12 years, Units per week 25 units /week. Finally, a statistically significant correlation was found between neuropathy and age of the study population, duration, and units of alcohol consumption, CAGE criteria (p value= <0.001) was established in the present study. Conclusion: Common peroneal and sural nerves are the most common nerves to be involved in neuropathy. Predominantly axonal degeneration is the main pathology. Units of alcohol and CAGE criteria score has a 100% specificity in detecting patients prone for neuropathy So the implementation of suitable preventive measurement and therapy methodologies can be applied to decrease the complications of alcohol.

Keywords: Alcohol dependence syndrome, alcohol use disorder, alcoholic neuropathy, alcohol-related neuropathy, CAGE, SAD-Q.

 

INTRODUCTION

The incidence of alcoholic neuropathy in the general population is not accurate as the percentage varies widely depending on the definition of chronic alcoholism and the criteria used to detect and classify neuropathy.¹ According to DSM-IV, studies involving clinical and electrodiagnostic criteria prove that neuropathy is present in 25-66% of chronic alcoholics. Neuropathy due to alcohol consumption depends on the duration and extent of the total lifetime of alcohol consumption. Cultural and racial factors also play a role in the development of alcohol neuropathy.² Alcohol consumption results in multiple end-organ damages. Chronic alcoholic consumption results in multiple organ damage among which the central nervous system is affected in the form of Wernicke encephalopathy, Korsakoff psychosis, cerebellar ataxia and, peripheral neuropathy and, sensory ataxia.³ Alcohol-related peripheral neuropathy is a potentially irreversible complication of alcoholism that results in sensory, motor, autonomic dysfunction which commonly presents as pain, paraesthesia, sensory ataxia. The exact prevalence of people affected by this condition is not known, however, studies have shown that approximately 66% of chronic alcoholics are found to have peripheral neuropathy. Alcoholic neuropathy is the most common manifestation of excessive alcohol intake.⁴ Alcohol-related neuropathy can be differentiated from other causes of neuropathy by eliciting detailed history and conducting a thorough physical examination. Previously conducted studies have used nerve conduction study of all motor and sensory nerves to diagnose neuropathy in symptomatic patients. Neuropathy sets in much earlier before the onset of symptoms. However, there is limited⁵ knowledge on the prevalence of neuropathy in asymptomatic chronic alcoholics. Earlier detection of neuropathy and advocation of abstinence of alcohol can alter the course of illness and gerund further nerve injury.⁶ This study is intended to detect asymptomatic neuropathy in alcohol dependence syndrome patients using nerve conduction studies and to correlate the presence of neuropathy to the duration and quantity of alcohol consumption in asymptomatic alcohol dependence syndrome patients.⁷ Uniqueness in our study is we have used SAD-Q scoring a higher sensitive and specific scoring for screening for dependence which has been used less commonly in previous studies Predominantly the nervous system is affected in the form of Wernicke encephalopathy, Korsakoff psychosis, cerebellar ataxia, and peripheral neuropathy.^8,9,10

 

MATERIALS AND METHODS

A Cross-sectional study was done in the Department of General Medicine, Vinayaka Mission’s Medical College and Hospitals, Salem, Tamil Nadu. totally 100 patients were included in the study. Alcohol-dependent syndrome patients were selected based on CAGE criteria. In these patients, diabetes mellitus and other possible causes for neuropathy were ruled out by history and clinical examination. All the patients were subjected to a nerve conduction study. Inclusion Criteria: Patient fulfilling the criteria of alcohol-dependent syndrome without symptoms of neuropathy. Ageabove18 years. Patients are willing to participate in the study. Exclusion Criteria: Patients suffering from neuropathy of other causes (infectious or noninfectious) Patients with symptoms of neuropathy. Patients are unwilling to participate in the study. History regarding alcohol habituation, the duration and quantity of consumption, symptoms of neuropathy, and history concerning other possible causes of neuropathy were taken and physical examination was done. The diabetic and Thyroid status of the patients were evaluated by checking their HbA1C, Random Blood Sugar, and Thyroid Profile. Patients with alcohol dependence syndrome confirmed through questionnaires like CAGE score (2 or more) and SAD-Q score(16 and above), who had alcohol habituation for more than two years and were asymptomatic for neuropathy were included in this study. The sensory and motor components of the Median, Ulnar, Sural, Superficial Peroneal, and the Tibial nerves were studied under Latency(ms), Amplitude(mV), and Conduction velocity(m/s), and the results were validated by the neurologist. Patients with neuropathy were compared with duration and quantity of alcohol consumption for any significant correlation. Similarly, neuropathy was compared with the CAGE and SAD-Q scores of the patients for correlation. Patients with neuropathy were treated as per the neurologist’s advice.

STATISTICAL ANALYSIS

A pilot study was done to ascertain the prevalence of alcohol-dependent syndrome patients. The above-said information was the base idea for the workup of sample size calculation based on this prevalence, sample size was calculated with the confidence interval being 95% and using the following calculation. Sample size n = (DEFF*Np(1-p)/ (d2/Z2 1- alpha/2 * (N-1) + p*(1-p).Using this formula, the number of people to be included in the study was estimated to be 100. Comparison of categorical variables was done by using a chi-square test based on the number of observations. Data entry was done in an MS Excel spreadsheet. Data analysis and validation were carried out by SPSS software version 17.

DISCUSSION

Early identification of alcohol-induced peripheral neuropathy and initiation of its treatment is very important to prevent disabilities in chronic alcoholics. Awareness of physicians has a key role to play in detecting and managing peripheral neuropathy. The mean age group of alcoholic patients in our study was 46.16± 7.5 years. This has similarities to an earlier study by John Rebecca et al. that showed the average age was 39.9 ± 7.5 years.¹¹ The present study indicated a positive correlation between age and the development of neuropathy with a p value< 0.001. Earlier studies have not postulated a correlation between age and neuropathy probably because as age increases the prevalence of neuropathy increases with alcohol being the additive effect and not the sole reason for neuropathy.¹² Hence to consider the establishment of age and the prevalence of neuropathy as a significant correlation is controversial. Also in our study after the age of 60 years percentage of the absence or presence of neuropathy was equal. This could be explained by the probability of complications and higher mortality rates due to alcohol consumption in the age group of more than 60 years.¹³ A statistical significance was found for correlation between units of alcohol consumption and development of neuropathy with a p value<0.001. Various studies done are controversial to the findings in our study.¹⁴ The first study to be mentioned here is a study done by Kawada T et al. states that the development of neuropathy does not correlate with age, units of alcohol, or nutritional factors.¹⁵ According to the previous studies, the most common electrodiagnostic finding in patients with alcohol abuse is symmetrical axonal sensory-motor neuropathy in the form of decreased amplitude, sensory and compound motor action potential, and decreased velocity.¹⁶ In our study comparison of the motor nerve parameters in left and right showed that there was a significant reduction in action potential in median, ulnar and peroneal nerves. This is similar to the study done in Vishakhapatnam which indicated a decrease in amplitude of compound muscle action potential of the common peroneal nerve.¹⁷ In another study, Mayfield et al. found a decrease in Motor nerve conduction velocity and terminal latencies in alcoholics. Comparing the sensory nerves in both left and right shows that latency is prolonged and action potential is reduced in sural nerves but previous studies show that there was a decrease in amplitude of sensory nerve action potential in radial nerves.¹⁸ In our study patients, clinically there was no evidence of neuropathy but NCS revealed conduction velocity to be decreased in motor and distal sensory nerves which were similar to the study by McKnight, J et al. where alcoholic patients who clinically had no evidence of neuropathy were investigated and found that there was a decrease in conduction velocity of motor and sensory nerves. The prevalence of alcoholic neuropathy in our study was 72%.¹⁹ Møller, Aage R et al. reported that 67.7% of the chronic alcoholics in his study population had evidence of neuropathy. In our study group, axonal neuropathy was found to be the most common mechanism possible for neuropathy in alcoholics.²⁰ Walsh and McLeod found histological changes of axonal degeneration in sural nerves in chronic alcoholics. Similarly in our study amongst the sensory nerves, action potential was delayed and the possible mechanism was postulated to be axonal degeneration. Abnormalities seen in alcoholics could be attributed to a direct toxic effect of ethanol or its metabolites on peripheral and autonomic nerves.²¹ Thiamine was thought to play a leading cause in the pathogenesis of alcoholic peripheral neuropathy. Constant use of alcohol contributes to metabolic changes in the nerve cells and degeneration of the nerves. As the disease progresses, the axonal flux becomes less and less efficient, and the degeneration begins to prolong to portions of the axons nearer to the cell body and is accompanied by the destruction of the myelin sheaths.^22,23

 

CONCLUSION

Electrophysiological tests like nerve conduction studies can be used to detect subclinical central and peripheral neuropathy at an early stage of alcohol intoxication. So the implementation of suitable preventive measurement and therapy methodologies can be applied to decrease the complication of alcohol. Furthermore, studies are needed to establish the development of neuropathy in pure alcoholic cases excluding other confounding factors being a nutritional deficiency.

 

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