Rajiv Gandhi University of Health Sciences,



Rajiv Gandhi University of Health Sciences,

Bangalore, Karnataka

ANNEXURE II

Proforma for registration of subjects for Dissertation

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|1. |Name of the Candidate and Address |NITHIN KRISHNA K |

| | |SHREE DEVI COLLEGE OF PHYSIOTHERAPY, MANGALORE. |

| | |SHREE DEVI COLLEGE OF PHYSIOTHERAPY, BALLALBAGH, |

|2. |Name of the Institution |MANGALORE- 575003. |

| | |MASTER OF PHYSIOTHERAPY(MPT) |

|3. |Course of study and subject |2 YEARS DEGREE COURSE. |

| | |(NEUROLOGICAL AND PSYCHOSOMATIC DISORDERS) |

|4. |Date of Admission to Course |5TH NOVEMBER 2009. |

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|5. |Title of the Topic: “PREVALENCE OF ASYMPTOMATIC |

| |NEUROPATHY AMONG CHRONIC |

| |ALCOHOLICS” |

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|6. |Brief resume of the intended work : |

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| |6.1 Need for the study |

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| |Ethanol is one of the most commonly used drugs worldwide. Alcohol abuse is defined as the continued use of the alcohol despite the |

| |development of social, legal or health problems. Alcoholism, also known as alcohol dependence syndrome or alcohol addiction is a chronic |

| |disease involving strong need to drink, the inability to stop drinking, the occurrence of withdrawal symptoms and tolerance. Alcoholism |

| |is often progressive.1 |

| |WHO estimates there are about 2 billion people worldwide who consume alcoholic beverages and 76.3 million with diagnosable alcohol use |

| |disorders. Overall there is a causal relationship between alcohol consumption and more than 60 types of disease and injury. Alcohol |

| |consumption has been steadily increasing in developing countries like India. The total recorded alcohol per capita consumption in litres |

| |of pure alcohol is 0.82 in India for people above 15 years.2 There are about 62.5 million alcohol users estimated in India.3 |

| |Alcohol is the drug that has been used from many years. There are various causes of alcoholism. Most of them drink alcohol for |

| |recreational purposes. People also consume alcohol because of social, psychological, personal matters. Changing social norms, |

| |urbanization, increased availability, high intensity mass marketing and relaxation of overseas trade rules along with poor level of |

| |awareness related to alcohol has contributed to increased alcohol use.3 |

| |Alcohol consumption has health, economic and social consequences via intoxication, alcohol dependence and other biochemical effects of |

| |alcohol. Alcohol effects various systems of the body. It is associated with liver damage, which can take the form of |

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| |inflammation (alcoholic hepatitis) or liver scarring (fibrosis or cirrhosis). It can cause oesophagal cancer, pancreatitis, gastritis. |

| |High concentration of alcohol interferes with the pumping action of heart. People who drink heavily suffer more infectious diseases. Long|

| |term alcoholism can also disrupt the functioning of the endocrine system.1 Alcohol withdrawal is associated with tachycardia, elevated |

| |blood pressure, excessive sweating, seizures etc and in very severe cases hallucinations and delirium tremens.4 |

| |Alcohol has numerous effects on the central nervous system. A blood alcohol level of 500 mg/dl is usually fatal. It can cause wernick’s |

| |encephalopathy, cerebellar degeneration, korsakoff’s psychosis, alcoholic dementia and central pontine myelinolysis. Acute confusion |

| |state because of alcoholism is characterized by inattention, disorientation and sleepiness. Hypothalamic involvement can cause |

| |hypotension or hypothermia. |

| |Peripherally it can cause alcoholic myopathy and polyneuropathy. Polyneuropathy is one of the usual complications of alcoholism. It |

| |corresponds to the pattern of dying back type of distal axonopathy predominantly involving the lower limbs and is characterized by axonal|

| |degeneration and demyelination. It is often asymptomatic and demonstrable only on electroneurographic investigations. In severe cases, it|

| |is characterized by paresthesias, pain and weakness especially in the feet. Dysesthesias can be so severe that they interfere with |

| |walking. There will be reduced pain and temperature sensation and also distal muscle weakness. Deep tendon reflexes are reduced.5 |

| |The pathogenesis of neurological damage in chronic alcoholism remains obscure. Although previously it was thought that alcoholic |

| |neuropathy was mainly due to associated malnutrition or a specific lack of thiamine6,7, recent studies show that Total Lifetime Dose of |

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| |Ethanol (TLDE) is an important factor in determining neuropathy.8 |

| |Frequency of neuropathy among alcoholics varies. A.Ammendola et al. found neuropathy in 67.7% of the chronic alcoholics in their study.9 |

| |Vittadini et al. found 48.6% of alcoholics who showed electroneurographic signs of neuropathy when only 16.2% showed its symptoms.10 |

| |Recovery in abstinent patients is slow and often incomplete requiring weeks to months. So, it is necessary to identify the neuropathy in |

| |subclinical stage and to prevent the complications therefore. |

| |Polyneuropathy is therefore an important complication of alcoholism. The purpose of this study is to evaluate the incidence of |

| |asymptomatic polyneuropathy in a group of alcoholic subjects and thereby educate the people on the harmful effects of alcohol. |

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| |Research Question |

| |Whether there is any statistically significant difference in the nerve conduction studies of chronic alcoholics when compared with normal|

| |values. |

| |Null hypothesis |

| |There will be no significant difference in nerve conduction studies of chronic alcoholics when compared with normal values. |

| |Alternate hypothesis |

| |There will be a significant difference in nerve conduction studies of chronic alcoholics when compared with normal values. |

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| |6.2 Review of literature |

| |A study done on chronic alcoholics with or without minimal evidence of neuropathy showed that sensory nerve action potentials may be |

| |reduced in amplitude in most distal parts of the nerves in the arm at a time when proximal segments are normal. This study suggested |

| |axonal degeneration of nerves.11 |

| |A retrospective cross sectional study of 62 chronic alcoholics (44 males and 18 females) was conducted, the subjects used to consume |

| |atleast 100 grams of ethanol/day for over two years. Neuropathy was found in 67.7% of subjects. Sensory alterations (sural sensory evoked|

| |potential amplitude) were most frequent in lower limbs. The study correlated the risk factors of neuropathy with the occurrence of the |

| |disease and found that frequency of neuropathy rose in proportion to total life time dose of ethanol. Malnutrition was not significantly |

| |correlated with neuropathy. The study also suggested a greater sensitivity of females to the toxic effect of alcohol on the peripheral |

| |nerves.9 |

| |Another study was done on 296 chronic alcoholic subjects who consumed atleast 100 grams of ethyl alcohol/day. The study found neuropathy |

| |in 48.6% of subjects and then classified neuropathy on the basis of electroneurographic signs. 33.3% of subjects who had severe |

| |polyneuropathy according to electroneurographic signs were asymptomatic when 85.4% of subjects were asymptomatic who had mild |

| |polyneuropathy. This study supported the view that polyneuropathy increases with duration of alcoholism. According to the study |

| |subjective symptoms can occur after 1-5 years of misuse and symptoms increase as the age increases. Mean age was higher in subjects with |

| |neuropathy. Study also showed that signs are more frequent in subjects consuming wine or wine in combination with other alcoholic |

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| |beverages.10 |

| |H.Koike et al. (2001) studied on chronic alcoholics who had normal thiamine status. The subjects were consuming 100 grams of daily |

| |ethanol for atleast ten years. Most of the subjects had involvement of all sensory modalities with nociception being severely impaired.|

| |This study says that pathologically there is relatively selective small fibre loss although large myelinated fibres decreased to a lesser|

| |extent.12 Thomas Zambelis et al found neuropathy in 58.2% of subjects among 98 chronic alcoholics in which 11.2% were asymptomatic and |

| |45.9% were symptomatic. Their results were based on summation of data obtained on Neuropathy Symptom Score (NSS), Neurological disability|

| |score (NDS), Nerve conduction velocity (NCV) and Quantitative Sensory Testing (QST). There was significant co relation of neuropathy with|

| |age and with duration of alcoholism. Although both small and large fibres were involved, the difference was not significant.13 |

| |36.8% of neuropathics were found in a study of 107 alcoholics among which only 20.6% were symptomatic. Total Lifetime Dose of Ethanol was|

| |the only one factor significantly associated with presence of neuropathy. No other factors were related. The study suggested a direct |

| |toxic effect of alcohol on nerve fibres.8 |

| |Another study found neuropathy in 67.1% of their subjects while 36.8% were subclinical. They studied the effect of different risk factors|

| |for neuropathy on chronic alcoholics. Mean age was higher in subjects with neuropathy. They suggested that total lifetime dose of ethanol|

| |is a risk factor than malnutrition. They also suggested that duration of alcoholism has a role in alcoholic neuropathy.14 |

| |Current literatures say that diagnosis of alcoholic neuropathy is mainly through |

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| |electroneurographic investigations. Lower limbs are predominantly involved. Sensory signs are more commonly seen than motor signs. |

| |Sensory action potential amplitude and sensory conduction velocity are altered more than motor action potential amplitude and motor |

| |conduction velocity. In severe cases upper limbs are involved.9,13,14 |

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| |6.3 Objectives of the study |

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| |To find out the prevalence of asymptomatic neuropathy among chronic alcoholics. |

| |To know whether there is any relation between the number of years of alcohol consumption and the presence or the absence of neuropathy. |

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|7. |Materials and methods : |

| |7.1 Source of data |

| |Alcoholics from in and around mangalore. |

| |Community health centres. |

| |Social organizations. |

| |7.2 Method of collection of data |

| |60 individuals who are chronic alcoholics with no symptoms of neuropathy will be selected for the study. |

| |Inclusion Criteria: |

| |Age: between 30 years to 50 years. |

| |Both the sex will be included. |

| |Chronic alcoholics for more than three years. |

| |Exclusion criteria: |

| |Current or past neuropathies. |

| |Orthopaedic problems that might involve peripheral nerve. (eg: Osteoarthritis of spine) |

| |Serious physical illness. (eg: Diabetes mellitus, Cancer etc) |

| |Pregnant women. |

| |Any other neurological disorder. |

| |Nerve entrapment syndromes in lower limb. |

| |Symptomatic persons. |

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| |Study Design: |

| |Cross Sectional Study. |

| |Sampling: |

| |Judgement sampling is used. |

| |Statistical Test: |

| |Arithmatic mean, standard deviation and percentages will be used to describe baseline characteristics such as age, number of years of |

| |alcohol consumption and to calculate the number of individuals with neuropathy. |

| |‘Z’ test will be used to test the significance of difference in the mean values of different nerve conduction studies of chronic |

| |alcoholics with that of population mean. |

| |Chi-square test will be used to test whether there is any significant relation of number of years of alcohol consumption and the presence|

| |or absence of neuropathy. |

| |Outcome measure: |

| |Compound action potential amplitude of common peroneal nerve. |

| |Nerve conduction velocity of common peroneal nerve. |

| |Amplitude of sural nerve action potential. |

| |Nerve conduction velocity of sural nerve. |

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| |METHODOLOGY: |

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| |60 individuals who meet the inclusion criteria will be selected for the study. An informed consent will be obtained from all the |

| |subjects. A detailed neurological examination will be done. The assessments of subjects will also include the duration of alcoholism, |

| |amount of alcohol intake per day, type of alcoholic beverage, dominant side, daily dietary intake and weight. The subjects will also be |

| |given ‘Subjective Peripheral Neuropathy Screen Questionnaire’ to rule out existing neuropathy. |

| |Electrophysiological testing of the individuals: |

| |Electrophysiological testing of these individuals will be done using the Neurocare-2000 EMG/NCV/EP system. As the lower limbs usually get|

| |involved in alcoholic neuropathy, only lower limb nerve conduction studies will be conducted. Sural nerve and common peroneal nerve will |

| |be tested. Electrodes will be soaked in isotonic saline solution and a conducting gel applied to the skin to maximize conductivity. |

| |Testing will be done bilaterally. Values obtained from the best of three repetitions will be considered for the study. |

| |For common peroneal nerve conduction study, surface recordings are obtained from extensor digitorum brevis. The patient will be in supine|

| |lying and the stimulations will be given at the ankle and at the neck of fibula. Amplitude of compound muscle action potential is |

| |measured and nerve conduction velocity calculated. |

| |Nerve conduction of sural nerve is recorded by the surface electrode between lateral malleolus and tendoachilles. The patient is in |

| |lateral position and the leg completely relaxed. The nerve is stimulated antidromically 10-16 cm proximal to the recording electrode, |

| |distal to the lower border of gastrocnemius at the junction of middle and lower third of leg. |

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| |Sural nerve conduction velocity and amplitude of sensory nerve action potential is measured. |

| |The values thus obtained will be seen for abnormalities by comparing with the standard normal values obtained by Jun Kimura.15 An |

| |alteration in any two of the above parameters (amplitude of compound muscle action potential, motor nerve conduction velocity, amplitude |

| |of sensory nerve action potential, sensory nerve conduction velocity) will be considered as having neuropathy. The results will be |

| |statistically tested to know the effect of number of years of alcoholism on neuropathy. |

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| |MATERIALS: |

| |1) NCV Apparatus (Neurocare 2000. NCV/EMG. Ser. No. 1023) |

| |2) Electrodes |

| |3) Gel, Cotton |

| |4) Spirit |

| |7.3 Does the study require any investigations or interventions to be conducted on patients or other humans or animals? If so, please |

| |describe briefly. |

| |Yes. |

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| |Nerve conduction studies of common peroneal and sural nerve. |

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| |7.4 Has ethical clearance been obtained from your institution in case of 7.3? |

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| |Yes. |

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|8. |List of References: |

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| |Boggan W, Ed Drexler, Erwin VG, Marshall J, Nicholas G, Olney J. Understanding alcohol: Investigations into biology and behavior. |

| |Colorado: BSCS; 2003. |

| |Global status report on alcohol. Geneva: World Health Organization; 2004. |

| | accessed on 20/5/2010. |

| |Becker HC. Alcohol dependence, withdrawal and relapse. Alcohol Res Health 2008; 31(4): 348-61. |

| |Diamond I, Messing RO. Neurological effects of alcoholism. West J Med 1994; 161 (3): 279-287 |

| |Victor M, Adams RD. Symposium on neurologic and hepatic complications of alcoholism: On the etiology of alcoholic neurologic diseases. Am|

| |J Clin Nutr 1960; 9(4): 379-397 |

| |Koike H, Sobue G. Alcoholic neuropathy. Curr Opin Neurol 2006; 19(5): 481-6. |

| |Monforte R, Estruch R, Valls-Sole J, Nicolas J, Villalta J, Urbano-Marquez A. Autonomic and peripheral neuropathies in patients with |

| |chronic alcoholism: A dose-related toxic effect of alcohol. Arch Neurol 1995 Jan; 52(1): 45-51 |

| |Ammendola A, Gemini D, Iannaccone S, Argenzio F, Ciccone G, Ammendola E, et al. Gender and peripheral neuropathy in chronic alcoholism: a|

| |clinical-electroneurographic study. Alcohol Alcohol 2000; 35(4): 368-71. |

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| |Vittadini G, Buonocore M, Colli G, Terzi M, Fonte R, Biscaldi G. Alcoholic polyneuropathy: a clinical and epidemiological study. Alcohol |

| |Alcohol 2001; 36(5): 393-400 |

| |Casey EB, Pamela M. Lequesne. Electrophysiological evidence for a distal lesion in alcoholic neuropathy. J Neurol Neurosurg Psychiatry |

| |1972; 35: 624-630 |

| |Koike H, Mori K, Misu K, Hattori N, Ito H, Hirayama M, et al. Painful alcoholic polyneuropathy with predominant small-fiber loss and |

| |normal thiamine status. Neurology 2001; 56: 1727-32. |

| |Zambelis T, Karandreas N, Tzavellas E, Kokotis P, Liappas J. Large and small fiber neuropathy in chronic alcohol-dependent subjects. J |

| |Peripher Nerv Syst 2005; 10: 375-381 |

| |Ammendola A, Tata MR, Aurilio C, Ciccone G, Gemini D, Ammendola E, et al. Peripheral neuropathy in chronic alcoholism: A retrospective |

| |cross- sectional study in 76 subjects. Alcohol Alcohol 2001; 36(3): 271-275 |

| |Kimura J. Electrodiagnosis in diseases of nerve and muscle: Principles and practice. 2nd ed. Philadelphia: F.A. Davis; 1989. |

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|9. |Signature of the Candidate | |

|10. |Remark of the Guide | |

|11. |Name and Designation of |HARIPRIYA S. |

| |(In Block Letters) |ASST. PROFESSOR, |

| |11.1 Guide |SHREE DEVI COLLEGE OF PHYSIOTHERAPY, MANGALORE. |

| |11.2 Signature | |

| |11.3 Co-guide |S. SUKUMAR |

| | |ASST. PROFESSOR, |

| | |SHREE DEVI COLLEGE OF |

| | |PHYSIOTHERAPY, MANGALORE- 3. |

| |11.4 Signature | |

| |11.5 Head of department |DR. S. PADMAKUMAR |

| | |PRINCIPAL, |

| | |SHREE DEVI COLLEGE OF |

| | |PHYSIOTHERAPY, MANGALORE- 3. |

| |11.6 Signature | |

|12. | 12.1 Remark of the Chairman and Principal | |

| |12.2 Signature | |

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