{"id":31331,"date":"2020-03-28T10:08:04","date_gmt":"2020-03-28T10:08:04","guid":{"rendered":"http:\/\/biomedpharmajournal.org\/?p=31331"},"modified":"2020-04-22T12:42:31","modified_gmt":"2020-04-22T12:42:31","slug":"electrophysiological-evaluation-of-peripheral-neuropathy-in-chronic-alcoholic-patients","status":"publish","type":"post","link":"https:\/\/biomedpharmajournal.org\/staging\/vol13no1\/electrophysiological-evaluation-of-peripheral-neuropathy-in-chronic-alcoholic-patients\/","title":{"rendered":"Electrophysiological Evaluation of Peripheral Neuropathy in Chronic Alcoholic Patients"},"content":{"rendered":"

Introduction<\/strong><\/p>\n

Alcohol is a psychoactive substance and its consumption is harmful to human health and it represents 5.9% of worldwide deaths. The alcohol causes more than two hundred diseases and various conditions such as cancer of the mouth, esophagus and larynx, liver cirrhosis, pancreatitis etc. (1) India’s annual alcohol intake increased by 38 per cent between 2010 and 2017 and\u00a0 alcohol consumed globally per year has risen by 70 per cent since 1990. (2) Chronic consumption of alcohol leads to advent of peripheral neuropathy(3) Polyneuropathy has been reported to be present in 13%\u201366% of chronic alcoholics(4). Even in clinically evident polyneuropathy the prognosis often can be established on the basis of electrodiagnostic findings. Furthermore, the electromyographer can readily identify other primary or superimposed disorders, such as polyradiculopathy, that may be clinically indistinguishable from polyneuropathy . .In present study patients\u00a0 consuming alcohol and clinically\u00a0 suspected or diagnosed as a peripheral neuropathy were evaluated. Hypothesis for present research work is, alcohol damages peripheral nerves and more is the duration of alcohol intake more is the damage.\u00a0 So aim of present research work is to find out type of neuropathy, extent of damage and effects of\u00a0 long\u00a0 duration of alcohol intake on peripheral nerves with the help of\u00a0 nerve conduction studies. Knowledge of present research work will be\u00a0 useful for determination of prognosis and\u00a0 better\u00a0 management of neuropathy patients.<\/p>\n

Materials and Methods<\/strong><\/p>\n

It was a cross sectional, comparative study .Present research work was carried out in department of physiology KIMS. karad. Patients from Krishna hospital who were willing to participate in study were included in present study.\u00a0 Study duration was\u00a0 from\u00a0 Nov. 2018 to March. 2019. Institutional Ethics committee permission was taken. (KIMSDU\/IEC\/06\/2018).<\/p>\n

55 patients clinically\u00a0 suspected or diagnosed of peripheral neuropathy and taking alcohol\u00a0 which were referred to department of Physiology were investigated.<\/p>\n

Inclusion Criteria for Controls <\/strong><\/p>\n

Apparently healthy individuals (non diabetic, Non Alcoholic ) between the\u00a0 age of 40 years to 60 years\u00a0\u00a0 willing to participate in\u00a0 the study. No history suggestive of\u00a0\u00a0 exposure to heavy metals and neurotoxic industrial agents like , lead. Etc.<\/p>\n

Inclusion Criteria for Alcoholic Patients <\/strong><\/p>\n

Patients between age of 40 years to 60 years willing to participate in study. , Patients taking alcohol and\u00a0 Clinically diagnosed or\u00a0 suspected patients of poyneuropathy.<\/p>\n

Nerve conduction study was also performed on\u00a0 apparently healthy 60 age matched controls who were non diabetic non alcoholic\u00a0 and not having any major illness .Alcoholic patients were divided into three groups depending upon number of years , taking alcohol.( Group A): up to Two years( Sample size 20)\u00a0 .( Group B):More than two years to\u00a0 Four\u00a0 years( Sample size 20),\u00a0 ( Group C) More than four years up to\u00a0 six years or\u00a0 more( Sample size 15).\u00a0 Average age of patients was 53 years and all were male patients. Average age of controls was 52 years, and all were male subjects.<\/p>\n

Exclusion Criteria for Patients<\/strong><\/p>\n

Patients not Willing to participate in study, having any major illness\u00a0 or endocrinal disorder like\u00a0 diabetes mellitus or\u00a0 renal failure etc.\u00a0 Patients having\u00a0 history suggestive of\u00a0\u00a0 exposure to heavy metals and neurotoxic industrial agents like , lead. Etc were excluded from the study.<\/p>\n

Institutional ethical committee approval was taken for the study. Patients and subjects were informed the detailed procedure of nerve conduction study and written consent was taken.\u00a0 Electro diagnostic study included motor and sensory nerve conduction of Median , Ulnar\u00a0 Peroneal , Tibial, and sural\u00a0 nerves\u00a0 by conventional method .(4) For stimulation supra maximal strength was used.\u00a0 For recording sensory and motor nerve conduction, surface metal electrodes were used.\u00a0 For recording motor conduction , recording electrode was placed close to the motor point and reference electrode three centimeter distal to it .\u00a0 For median nerve stimulation , stimulus was given at wrist and at elbow near volar crease of brachial pulse. For recording motor conduction of Ulnar nerve, Abductor Digiti Minimi\u00a0 muscle was used. Stimulus was given at wrist and at elbow in cubital tunnel behind medial epicondyle. For ulnar nerve stimulation at elbow arm position was maintained at 1350 <\/sup>\u00a0. <\/sup>(5,6). For motor conduction of Peroneal nerve, Extensor Digitorum Brevis (EDB) muscle and\u00a0 for motor conduction of Tibial nerve\u00a0 Adductor Hallucis (AH)\u00a0 muscles were selected. Reference electrode was placed\u00a0 three centimeter distal to recording electrode.<\/p>\n

For Sensory conduction of median nerve\u00a0 surface recording electrode was placed three centimeter\u00a0 proximal to distal wrist crease on median\u00a0 nerve.\u00a0 For\u00a0 Sensory conduction of ulnar nerve\u00a0 surface recording electrode was placed three centimeter\u00a0 proximal to distal wrist crease on ulnar\u00a0 nerve.\u00a0\u00a0 Reference electrode was placed three centimeter\u00a0 proximal to recording electrode.\u00a0 For sensory conduction of Sural nerve the surface recording electrode was placed midway between heel and lateral malleolus and reference electrode was placed\u00a0 three centimeter distal to recording electrode.\u00a0 For\u00a0 sensory nerve\u00a0 conduction study , twenty supramaximal stimuli were delivered and average was recorded. Ground electrode was placed between recording and stimulating electrodes.<\/p>\n

For each motor nerve studied following parameters were measured:<\/p>\n

Distal motor latency ( DML).\u00a0 milliseconds.( ms.)<\/p>\n

Compound muscle action potential amplitude\u00a0 ( CMAP) . mill volt. ( MV)<\/p>\n

Motor Nerve\u00a0 conduction velocity( MNCV) . Meters \/Sec. ( M\/S)<\/p>\n

For each sensory nerve studied following parameters were measured:<\/p>\n

Distal sensory latency ( DSL). milliseconds.( ms.)<\/p>\n

Sensory\u00a0 Nerve action potential . ( SNAP)\u00a0 Microvolt\u2019s. (\u00b5V)<\/p>\n

Sensory Nerve\u00a0 conduction velocity ( SNCV) . Meters \/Sec. ( M\/S)<\/p>\n

During nerve conduction study, laboratory temperature was maintained between 21o <\/sup>C to 230<\/sup>C. When skin temperature of limb was below 340<\/sup>C, the limb was immersed in a warm water to correct the temperature.\u00a0 (4,7) For nerve conduction studies, Recorder and Medicare System (RMS) machine from Chandigarh (India) was used.<\/p>\n

Statistical Analysis<\/strong><\/p>\n

Statistical analysis was performed using SPSS, version 20.0. Data was summarized into mean \u00b1 S.D. One way ANOVA was used for multiple group comparisons followed by post hoc Tukey\u2019s test. P>0.05 Not significant (\u00a0 NS. ) ,P<0.05 was said to be significant.*, P < 0.01\u00a0 highly significant ** ,P < 0.001\u00a0 very highly significant ***<\/p>\n

Results<\/strong><\/p>\n

Table 1: Mean and SD. Values of DMLs, CMAPs,\u00a0 and MNCVs of\u00a0 <\/strong>upper extremity nerves<\/strong>:<\/p>\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n
\u00a0Nerve<\/strong><\/td>\nGroups<\/strong><\/td>\nDML.( ms.)<\/strong><\/p>\n

Mean & SD.<\/strong><\/td>\n

CMAP( MV)<\/strong><\/p>\n

Mean & SD<\/strong><\/td>\n

NCV. ( M\/S)<\/strong><\/p>\n

Mean & SD<\/strong><\/td>\n<\/tr>\n

Median nerve.<\/p>\n

(Motor)<\/td>\n

Control ( N=60)<\/td>\n2.88 \u00b1.41<\/td>\n15.89\u00b1 3.1<\/td>\n57\u00b15.4<\/td>\n<\/tr>\n
two years alcoholic(N=20)<\/td>\n2.78\u00b1.42<\/td>\n14.19\u00b15.2<\/td>\n57.11\u00b14.6<\/td>\n<\/tr>\n
four\u00a0 years alcoholic(N=20)<\/td>\n2.22\u00b1.41<\/td>\n14.12\u00b14.4<\/td>\n56.18\u00b13.71<\/td>\n<\/tr>\n
six years alcoholic(N=15)<\/td>\n2.61\u00b1.35<\/td>\n14.14\u00b13.4<\/td>\n56.11\u00b14.11<\/td>\n<\/tr>\n
\u00a0ANOVA\u00a0\u00a0 F Value<\/p>\n

P Value<\/td>\n

14.179<\/p>\n

<0.0001 ***<\/td>\n

2.11<\/p>\n

0.102 NS<\/td>\n

0.267<\/p>\n

0.84 NS<\/td>\n<\/tr>\n

ulnar nerve.<\/p>\n

(Motor)<\/td>\n

Groups<\/td>\nDML.( ms.)<\/p>\n

Mean & Sd.<\/td>\n

CMAP( MV)<\/p>\n

Mean & Sd.<\/td>\n

NCV<\/p>\n

Mean & Sd.<\/td>\n<\/tr>\n

control(N=60)<\/td>\n2.82 \u00b1.41<\/td>\n15.82\u00b1 2.8<\/td>\n57.88\u00b15.88<\/td>\n<\/tr>\n
two years alcoholic(N=20)<\/td>\n2.79\u00b1.11<\/td>\n14.87\u00b13.1<\/td>\n56.11\u00b1511<\/td>\n<\/tr>\n
four\u00a0 years alcoholic(N=20)<\/td>\n2.66\u00b1.14<\/td>\n14.11\u00b13.1<\/td>\n55.14\u00b15.12<\/td>\n<\/tr>\n
six years alcoholic(N=15)<\/td>\n2.67\u00b1.11<\/td>\n14.00\u00b13.2<\/td>\n55.11\u00b15.14<\/td>\n<\/tr>\n
\u00a0ANOVA\u00a0\u00a0 F Value<\/p>\n

P Value<\/td>\n

1.901<\/p>\n

0.1136 NS<\/td>\n

2.66<\/p>\n

0.051 NS<\/td>\n

1.924<\/p>\n

0.84\u00a0 NS<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n

 <\/p>\n

Table 2:<\/strong> \u00a0Mean and SD. Values of DSL, SNAP and SNCV of <\/strong>upper extremity nerves<\/strong>:<\/p>\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n
\u00a0Nerve<\/strong><\/p>\n

Median nerve.<\/strong><\/p>\n

\u00a0(Sensory)<\/strong><\/td>\n

Groups<\/td>\nDSL.( ms.)<\/p>\n

Mean & SD<\/td>\n

SNAP. (\u00b5V)<\/p>\n

Mean & SD<\/td>\n

NCV. ( M\/S)<\/p>\n

Mean & SD<\/td>\n<\/tr>\n

control(N=60)<\/td>\n2.52 \u00b1.34<\/td>\n12.68\u00b1 2.44<\/td>\n53.21\u00b15.22<\/td>\n<\/tr>\n
two years alcoholic(N=20)<\/td>\n2.51\u00b1.33<\/td>\n11.98\u00b11.44<\/td>\n54.21\u00b13.18<\/td>\n<\/tr>\n
four\u00a0 years alcoholic(N=20)<\/td>\n2.49\u00b1.41<\/td>\n9.11\u00b11.22<\/td>\n54.14\u00b14.1<\/td>\n<\/tr>\n
six years alcoholic(N=015)<\/td>\n2.30\u00b1.11<\/td>\n7.14\u00b11.33<\/td>\n53.14\u00b15.11<\/td>\n<\/tr>\n
ANOVA\u00a0\u00a0 F Value<\/p>\n

P Value<\/td>\n

1.81<\/p>\n

.149\u00a0 NS<\/td>\n

39.875<\/p>\n

<.0001 ***<\/td>\n

1.924<\/p>\n

0.772 NS<\/td>\n<\/tr>\n

Nerve<\/strong><\/p>\n

 <\/p>\n

Ulnar nerve.<\/strong><\/p>\n

\u00a0(Sensory)<\/strong><\/td>\n

Groups<\/td>\nDSL.( ms.)<\/p>\n

Mean & SD<\/td>\n

SNAP(\u00b5V)<\/p>\n

Mean & SD<\/td>\n

NCV( M\/S)<\/p>\n

Mean & SD<\/td>\n<\/tr>\n

control(N=60)<\/td>\n2.71 \u00b1.55<\/td>\n13.22\u00b1 2.58<\/td>\n53.27\u00b14.44<\/td>\n<\/tr>\n
two years alcoholic(N=20)<\/td>\n2.68\u00b1.14<\/td>\n12.14\u00b13.11<\/td>\n53.14\u00b14.12<\/td>\n<\/tr>\n
four\u00a0 years alcoholic(N=20)<\/td>\n2.70\u00b1.17<\/td>\n8.12\u00b11.14<\/td>\n53.44\u00b13.12<\/td>\n<\/tr>\n
<\/td>\n<\/td>\n<\/td>\n<\/td>\n<\/tr>\n
six years alcoholic(N=15)<\/td>\n2.80\u00b1.11<\/td>\n6.11\u00b12.71<\/td>\n52.17\u00b13.17<\/td>\n<\/tr>\n
ANOVA\u00a0\u00a0 F Value<\/p>\n

P Value<\/td>\n

.271<\/p>\n

.846\u00a0 NS<\/td>\n

44.19<\/p>\n

<0.0001 ***<\/td>\n

.345<\/p>\n

0.794 NS<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n

 <\/p>\n

Table 3: \u00a0Mean and SD. Values of\u00a0 DMLs, DSLs, CMAPs ,SNAPs,\u00a0 MNCVs and SNCVs<\/strong>. of\u00a0 <\/strong>lower extremity nerves<\/strong>:<\/p>\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n
 <\/p>\n

Peroneal nerve.<\/strong><\/p>\n

(Motor)<\/strong><\/td>\n

Groups<\/td>\nDML.( ms.)<\/p>\n

Mean & SD<\/td>\n

CMAP ( MV)<\/p>\n

Mean & SD<\/td>\n

NCV ( M\/S)<\/p>\n

Mean & SD<\/td>\n<\/tr>\n

control(N=60)<\/td>\n3.22 \u00b1.76<\/td>\n7.88\u00b1 2.2<\/td>\n47.55\u00b13.56<\/td>\n<\/tr>\n
two years alcoholic(N=20)<\/td>\n3.14\u00b1.77<\/td>\n5.14\u00b11.2<\/td>\n46.81\u00b13.77<\/td>\n<\/tr>\n
four\u00a0 years alcoholic(N=20)<\/td>\n4.12\u00b1.17<\/td>\n4.18\u00b11.4<\/td>\n46.11\u00b13.17<\/td>\n<\/tr>\n
<\/td>\n<\/td>\n<\/td>\n<\/td>\n<\/tr>\n
<\/td>\n<\/td>\n<\/td>\n<\/td>\n<\/tr>\n
six years alcoholic(N=15)<\/td>\n5.21\u00b1.11<\/td>\n3.11\u00b11.1<\/td>\n41.17\u00b12.18<\/td>\n<\/tr>\n
ANOVA\u00a0\u00a0 F Value<\/p>\n

P Value<\/td>\n

45.89<\/p>\n

<.0001 ***<\/td>\n

41.36<\/p>\n

<.0001 ***<\/td>\n

14.34<\/p>\n

<.0001 ***<\/td>\n<\/tr>\n

Tibial nerve.<\/strong><\/p>\n

(Motor)<\/strong><\/td>\n

Groups<\/td>\nDML .( ms.)<\/p>\n

Mean & SD<\/td>\n

CMAP( MV)<\/p>\n

Mean & SD<\/td>\n

NCV( M\/S)<\/p>\n

Mean & SD<\/td>\n<\/tr>\n

control(N=60)<\/td>\n3.64 \u00b1.58<\/td>\n12.97\u00b1 4.21<\/td>\n47.12\u00b13.56<\/td>\n<\/tr>\n
two years alcoholic(N=20)<\/td>\n3.54\u00b1.28<\/td>\n10.11\u00b15.12<\/td>\n47.14\u00b14.44<\/td>\n<\/tr>\n
four\u00a0 years alcoholic(N=20)<\/td>\n4.12\u00b1.44<\/td>\n8.12\u00b12.31<\/td>\n46.14\u00b13.11<\/td>\n<\/tr>\n
six years alcoholic(N=15)<\/td>\n5.12\u00b1.14<\/td>\n6.14\u00b13.14<\/td>\n45.11\u00b14.12<\/td>\n<\/tr>\n
ANOVA\u00a0\u00a0 F Value<\/p>\n

P Value<\/td>\n

43.80<\/p>\n

<.0001***<\/td>\n

17.03<\/p>\n

<.0001 ***<\/td>\n

1.405<\/p>\n

.24 NS<\/td>\n<\/tr>\n

\u00a0(Sensory)<\/strong><\/p>\n

sural nerve.<\/strong><\/td>\n

Groups<\/td>\nDSL .( ms.)<\/p>\n

Mean & SD<\/td>\n

SNAP. (\u00b5V)<\/p>\n

Mean & SD<\/td>\n

NCV( M\/S)<\/p>\n

Mean & SD<\/td>\n<\/tr>\n

control(N=60)<\/td>\n2.22 \u00b1.36<\/td>\n13.45\u00b1 3.11<\/td>\n50.21\u00b13.12<\/td>\n<\/tr>\n
two years alcoholic(N=20)<\/td>\n2.11\u00b1.34<\/td>\n11.11\u00b12.12<\/td>\n50.41\u00b14.12<\/td>\n<\/tr>\n
four\u00a0 years alcoholic(N=20)<\/td>\n3.11\u00b1.25<\/td>\n10.11\u00b13.11<\/td>\n50.17\u00b13.17<\/td>\n<\/tr>\n
six years alcoholic(N=15)<\/td>\n4.14\u00b1.33<\/td>\n7.14\u00b13.17<\/td>\n48.11\u00b12.37<\/td>\n<\/tr>\n
ANOVA\u00a0\u00a0 F Value<\/p>\n

P Value<\/td>\n

159.84<\/p>\n

<.0001 ***<\/td>\n

24.34<\/p>\n

<.0001 ***<\/td>\n

1.904<\/p>\n

.113\u00a0 NS<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n

 <\/p>\n

Discussion <\/strong><\/p>\n

In present study all were male patients. In present study when two year alcohol\u00a0 intake group (A), was compared with control group\u00a0 , no significant differences were observed\u00a0 for sensory and motor nerve conduction velocities, and Distal motor latencies , distal sensory latencies of upper extremity and lower extremity nerves. .( P>.05 not. Sig)<\/em>).However When four year alcohol\u00a0 intake group (B) , was compared with control group , significant decrease in Amplitudes of CMAPs and SNAPs and significant increase in DSLs were observed for lower extremity nerves. When six\u00a0 year alcohol\u00a0 intake group\u00a0 (C) was compared with control , no significant differences were observed\u00a0 for sensory and motor nerve conduction velocities of up.( Table 1 )per limbs. However significant decrease\u00a0 in SNAPs were observed in upper extremity sensory nerves. Very\u00a0 Significant decrease in sensory and motor nerve conduction velocities, Amplitudes of CMAPs and SNAPs were very significantly decreased\u00a0 in lower extremity nerves.( P < .001 )<\/em>. ( Table 3) Distal motor latencies , distal sensory latencies of lower\u00a0 limb nerves were very significantly increased.( P < .001 )<\/em> . Our study showed that lower extremity nerves were initially affected\u00a0 than upper extremity nerves.( Table 1, 2 ,3) Our study showed that\u00a0 the amplitudes of CMAPs and SNAP s were significantly reduced\u00a0 earlier than conduction velocities, Which indicates that\u00a0 alcoholic neuropathy is mainly because of axonal loss. Due to alcohol there is\u00a0 metabolic alterations in the nerve cells and degeneration of the axial flux. Each axon begins to degenerate from the most distal sections of the cell body whose integrity depends on the consistency of the streams. This explains why the longest axons are the first to be involved. Lower extremity nerves are longest so these nerves show earlier changes. (8)<\/p>\n

Sensory and motor nerves were equally affected. More is the duration of alcohol intake more is deterioration in nerve conduction study.\u00a0 ( Table 3) When all parameter were compared within the two year, four year and six year alcohol intake groups\u00a0 DMLs and DSLs\u00a0 were significantly increased and NCVs were decreased. When fast conducting axons get\u00a0 degenerated then nerve conduction velocities\u00a0 decreases .(9) Self reported history of alcohol intake of all the patients for type of alcohol and frequency and quantity of alcohol intake\u00a0\u00a0 was variable and unreliable so it is difficult to correlate. The cause for polyneuropathy in alcoholics is\u00a0 multifactorial , from both nutritional deficiencies and alcohol metabolism’s direct toxic effects on neurons.\u00a0 History, physical examination and nerve conduction study can help to differential this condition from other forms of neuropathy. No specific lab test is available for diagnosis. .(10, 11, 12)Thiamine deficiency, direct toxicity of alcohol and\u00a0 Vitamin B12 deficiency is associated with alcoholic polyneuropathy. . (2,7,8,13,14,15). So further research is required to find out exact effects of alcohol , toxic ingredients in alcohol , associated vitamin and nutrition\u00a0 deficiencies responsible for polyneuropathy. .<\/p>\n

Implications<\/strong><\/p>\n

Knowledge of present research work will be useful to study\u00a0 prognosis of disease, planning treatment of alcoholic neuropathy patients. . Knowledge of present research work will be also \u00a0useful for planning\u00a0 further research in alcoholic neuropathy to find out exact effects of alcohol , toxic ingredients in alcohol , associated vitamin and nutrition\u00a0 deficiencies.<\/p>\n

Limitations<\/strong><\/p>\n

History of alcohol intake like\u00a0 exact duration of alcohol intake, type of alcohol intake is as per patients history .Effects of alcohol , toxic ingredients in alcohol , associated vitamin and nutrition\u00a0 deficiencies are not separately studied.<\/p>\n

Acknowledgement<\/strong><\/p>\n

The authors gratefully acknowledge the\u00a0\u00a0 medical director of Krishna hospital. for permitting the research work.<\/p>\n

Financial Support and Sponsorship<\/strong><\/p>\n

Nil<\/p>\n

Conflicts of Interest<\/strong><\/p>\n

There are no conflicts of interest.<\/p>\n

Conclusion<\/strong><\/p>\n

Based on the results observed in our study, we conclude that the\u00a0 axonal\u00a0 loss is the main cause of poly neuropathy mainly affecting lower extremity nerves .More is the duration of alcohol intake more is deterioration in nerve conduction.<\/p>\n

References<\/strong><\/p>\n

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