|Year : 1999 | Volume
| Issue : 1 | Page : 68--70
Huntington's disease and alcohol abuse.
SK Mattoo, H Khurana
Department of Psychiatry, Postgraduate Institute of Medical Education and Research, Chandigarh, U.T., 160012, India., India
S K Mattoo
Department of Psychiatry, Postgraduate Institute of Medical Education and Research, Chandigarh, U.T., 160012, India.
The dopamine, glutamate and GABA systems are known to mediate the effects of alcohol on the movement disorders, though their exact roles are not clear. Thus, use of alcohol has implications for pathogenesis as well as management of the movement disorders. These implications are discussed citing a patient who had a strong family history of Huntington«SQ»s disease and in whom movement disorder and behavioral problems were manifest under alcohol use and withdrawal, but not while being abstinent.
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Mattoo S K, Khurana H. Huntington's disease and alcohol abuse. Neurol India 1999;47:68-70
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Mattoo S K, Khurana H. Huntington's disease and alcohol abuse. Neurol India [serial online] 1999 [cited 2021 Jul 25 ];47:68-70
Available from: https://www.neurologyindia.com/text.asp?1999/47/1/68/1655
The research on alcohol abuse in Huntington's disease (HD) has, focused more on prevalence than the neurochemical link between the two. The etiological role of alcohol in inducing movement disorder in alcoholic patients, with or without a family history of HD, was first implicated in 1970s. But recently use of alcohol has been reported to possibly slow down the course of HD. Thus, the role of alcohol in HD remains controversial. We report a patient with a family history of HD, who manifested movement disorder and behavioral problems under alcohol use and withdrawal, but not during abstinence.
BS, a 40 year male, was referred to the de-addiction services in November 1993 following complete recovery from a drunken driving related head injury. The history revealed onset of alcohol use (42% v/v whisky) with 30-60 ml once a month in 1988 and gradually increasing to 180 ml twice a week by 1990. In 1991, when he got married, his wife noticed that after alcohol intake he would have abnormal movements and behaviour. The movements included jerky non-repetitive movements of limbs, excessive blinking and twitching of cheeks. The behaviour included suspecting wife's fidelity, consequent abusive and assaultive behaviour and threats of and attempts at committing suicide. Till 1993 he had attempted suicide 7-8 times, two of such attempts being reasonably serious. Since 1991 he had also been using 5-10 mg of oral diazepam two to three times a week to overcome his tensions at office and at home. Against the advice of the family members and the doctors his use of alcohol and diazepam persisted, without any evidence of withdrawal symptoms.
In October 1994 after one of his suicidal attempts, he was admitted to the indoor services about 12 hours after his last drink. The examination revealed bilateral increased blinking, occasional pill rolling movements of hands and mildly depressed affect. Personality assessment revealed marked schizoid features. He had a family history of HD in maternal grandfather, mother, 3 out of 9 maternal uncles and aunts, and three out of six siblings. One of his maternal cousins having HD was reported to have exacerbation of movement disorder on consuming alcohol.
The cranial CT scan of the patient showed a normal ventricular brain ratio and a frontal horn index of 1.78. The peripheral blood cytology, the serum protein profile, the liver function profile and the electrocardiogram were within physiological limits. The thin layer chromatography of urine for opioids, cannabinoids and benzodiazepines was negative. The psychometric examination revealed mild to moderate impairment of memory, intelligence and perceptuomotor functions.
The patient was maintained in a drug free and abstinent state for all 26 days of hospitalization. His abnormal movement subsided between 2nd and 3rd week, and a repeat psychometric examination in 4th week showed marked improvement in all areas. The patient and family members were counselled regarding his vulnerability to HD and behavioral problems, the need for abstinence from alcohol and drugs, and the coping skills to reduce interpersonal stress. With final diagnoses of harmful use of alcohol and benzodiazepines, schizoid personality disorder and HD (latent, manifest under alcohol intoxication and withdrawal) the patient was discharged in an asymptomatic and abstinent status, which he hasaintained till December, 1998.
In the absence of characteristic clinical and laboratory evidence, the movement disorder in our patient could not be attributed to hypomagnesemia, hepatic disorder, hypovitaminosis of B1, B2 and nicotinic acid, or drugs like antipsychotics. A strong family history of HD and a bifrontal index of 1.78 suggested a diagnosis of HD. But the absence of characteristic clinical picture, peripheral blood cytology and serum lipoprotein profile indicated that the patient had a latent state of HD. The temporal relation between alcohol use and the movement disorder implied that alcohol was the only factor that temporarily made the HD manifest through movement disorder.
Alcohol has been reported to induce movement disorders during intoxication and withdrawal, as well as to slow down the progression of movement disorder in HD. This state of contradiction urges one to have a fresh look at the known pathophysiological relationship between alcohol, movement disorder and HD.
The alcohol related, extrapyramidal movements in the patients on chronic neuroleptic treatment and in alcoholics have been explained by changes in dopamine receptor system. The changes reported, often contradictory, include decreased striatal release of DA, decreased DA induced adenylcyclase activity during intoxication or due to DA receptor supersensitivity during prolonged use or withdrawal. In our patient, the movement disorder and ideas of infidelity, but not the entire presentation, could be explained by DA dysfunction. However, the basal ganglion dysfunction during intoxication and withdrawal as well as the behavioral problems during intoxication, may also be attributed to alcohol induced general cerebral inhibition.
The glutamate excitotoxicity has been implicated in the pathophysiology of movement disorder and other manifestations of HD. The gamma-amino butyric acid (GABA) neuron loss in HD may also be secondary to glutamate excitotoxicity. Alcohol has been shown to inhibit N-methyl-D-aspartate (NMDA) receptors in rats and mice as well as to retard the progression of HD disorder in humans. But the chronic NMDA inhibition has also been reported to lead to NMDA upregulation, increasing the risk of glutamate excitotoxicity. Thus alcohol intake may initially inhibit NMDA receptors and mask the manifestation of HD; but chronic alcohol use may lead to receptor upregulation, resulting in NMDA excitotoxicity and manifestation of HD. In our patient, the movement disorder became manifest under alcohol intoxication and withdrawal, and disappeared during abstinence. Also, in his maternal cousin who had a manifest HD, the movement disorder used to worsen during alcohol intoxication. The findings in both these subjects cannot be explained entirely by the NMDA mechanism underlying the movement disorder.
Thus, one is forced to conclude in agreement with the opinion that exact pathophysiological relationship between alcohol and movement disorder is not yet clear. Hence, how so ever tempted one might feel by the reported beneficial effects of alcohol in HD, there is no room for therapeutic recommendation of alcohol in HD. In some cases, like ours, on the other hand advice against alcohol is clearly warranted .
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