Encephalopathy alcoholism

Stendig-Lindberg, G., 1974, Hypomagnesemia in alcohol encephalopathies, Acta Psychiat. Scand. 50 465. 

Beri-beri or clinically manifest thiamin deficiency exists in several subforms infantile beri-beri and adult beri-beri. Infantile beri-beri occurs in exclusively breastfed infants of thiamin-deficient mothers. Adults can develop different forms of the disease, depending on their constitution, environmental conditions, the relative contribution of other nutrients to the diet as well as the duration and severity of deficiency. First of all, there is a so called dry or atrophic (paralytic or nervous) form, including peripheral degenerative polyneuropathy, muscle weakness and paralysis. Second, a wet or exudative (cardiac) form exists. In this form, typical symptoms are lung and peripheral oedema as well as ascites. Finally, there is a cerebral form, that can occur as Wernicke encephalopathy or Korsakoff psychosis. Tli is latter form mostly affects chronic alcoholics with severe thiamin deficiency. 

Behar KL, Rothman DL, Petersen KF, et al Preliminary evidence of low cortical GABA levels in localized 1FF-MR spectra of alcohol-dependent and hepatic encephalopathy patients. Am J Psychiatry 136 952-954, 1999... 

Thiamin deficiency can result in three distinct syndromes a chronic peripheral neuritis, beriberi, which may or may not be associated with heart ilure and edema acute pernicious (fulminating) beriberi (shoshin beriberi), in which heart failure and metabolic abnormalities predominate, without peripheral neuritis and Wernicke s encephalopathy with KorsakofPs psychosis, which is associated especially with alcohol and dmg abuse. The central role of thiamin diphosphate in... 

Corticosteroid therapy for patients with alcoholic hepatitis (steatonecrosis) with or without hepatic encephalopathy... 

Wernicke s encephalopathy A neurological condition characterised by visual disturbances, motor dysfunction and confusion which, like Korsakoff s syndrome, is commonly associated with long-term alcohol misuse. 

Thiamine deficiency results in early decreases in activity of the mitochondrial enzyme a-ketoglutarate dehydrogenase in brain. Wernicke s encephalopathy, also known as the Wernicke-Korsakoff syndrome is a neuropsychiatric disorder characterized by ophthalmoplegia, ataxia and memory loss. Wernicke s encephalopathy is encountered in chronic alcoholism, in patients with HIV-AIDS and in other disorders associated with grossly impaired nutritional status. The condition results from thiamine deficiency. 

In addition to epilepsy, reduced GABA has been recorded in patients with unipolar depression, following alcohol withdrawal and in hepatic encephalopathy. The finding that the concentration of GABA is reduced in depression is unexpected as there is no evidence that the disorder is associated with an increased cortical excitability. One possibility is that the reduction in GABA is a reflection of a decreased availability in its excitatory amino acid precursor glutamate. 

Scientific procedures for risk assessment include assessment of risk for human health as well as risk for the environment. A substantial part of the EU risk assessment work was in 1997 delegated to the DG SANCO, in relation to the scandal surrounding BSE (bovine spongiform encephalopathy or mad cow disease ). Risk assessment work not under DG SANCO includes pharmaceuticals, working environment, and health effects caused by lifestyle factors such as diet, smoking, and alcohol consumption (EU 2006f). 

Inadequate nutrition and conditions which are complicated by malabsorption may lead to thiamine deficiency. Beriberi, a diet-deficiency disease, is especially prevalent in those parts of the East where the diet consists mainly of polished rice. The disease is characterized by neuritis but may also lead to serious heart failure. Recovery is prompt when adequate amounts of vitamin B1 are restored to the diet. Severe deficiency as can occur in alcoholics may lead to Wernicke s encephalopathy, often accompanied by Korsakoff s syndrome. Care should be taken with intravenous substitution with thiamine in these cases to prevent serious complications like vascular collapse with hypotension, respiratory distress or an-gioedema. 

Where patients are at risk of Wernicke s encephalopathy - for example, because of chronic alcohol abuse, hyperemesis gravidarum, or malnutrition - they should be given thiamine. In many countries no intravenous preparation of thiamine alone is available, and the compound preparations that are available are prone to cause anaphylactoid reactions, so they should be given by slow infusion, and with adequate facilities for resuscitation. A high potency preparation (Pabrinex ) that contains thiamine 250 mg in 10 ml with ascorbic acid, nicotinamide, pyridoxine and riboflavin, can be given by intravenous infusion over 10 min. 

A variety of pathological problems involving the CNS have been described in chronic alcoholics, the main ones being Wernicke s encephalopathy and Korsakoff s psychosis Brain damage from chronic ethanol consumption can be especially severe in the elderly and may accelerate aging. 

The spectrum of cognitive deficits associated with chronic alcohol use extends to the extreme of Wernicke s encephalopathy and Korsakoff s psychosis. Wernicke s encephalopathy is an acute neurologic syndrome caused by thiamine deficiency. Symptoms include mental confusion, ophthalmoplegia, and ataxia. Many of these symptoms reverse with administration of thiamine however about 50% of patients are left with some degree of ataxia. Left untreated, Wernicke s encephalopathy can progress to stupor, coma, and death. Approximately 80% to 90% of alcoholics treated for Wernicke s encephalopathy are left with Korsakoff s psychosis, a syndrome of impaired learning and recent memory produced by lesions of the medial dorsal nuclei of the thalamus. 

Ethanol-related cognitive deficits in the absence of Wernicke s encephalopathy also improve with extended abstinence. Most functional neuroimaging studies of abstinent alcoholics have shown decreases in both cerebral glucose metabolism and blood flow, with the decreases being greatest in the frontal lobes (Netrakom et ah, 1999). 

It is indicated in wet beriberi, dry beriberi, Wernicke s encephalopathy, prophylaxis of thiamine deficiency, hyperemesis gravidarum, Korsakoff s syndrome, chronic alcoholics, multiple neuritis, toxic and confusional states, delirium tremens and anorexia nervosa. 

In addition, the alcohol addicts are liable to other neuropsychiatric syndrome (Korsakoff s psychosis) which is associated with hallucination, suicidal tendencies and encephalopathy. They may also suffer from hyperlipidemia, hyperuricemia, pancreatitis and hepatitis. 

In this chapter Case studies levels 1-3 explore the management of a patient with alcoholic liver disease. The patient has alcoholic liver cirrhosis and first presents with alcohol withdrawal (Case study level 1), then the patient s risk of bleeding and treatment for the maintenance of alcohol abstinence are considered (Case study level 2). The patient then goes on to develop encephalopathy (Case study level 3). Case studies levels Ma and Mb consider two patients one presents with TB and the other liver failure. 

Cirrhosis is often asymptomatic until complications of liver disease are present. Mrs MW may present with itching, jaundice, dark urine, pale fatty stools, abdominal pain, nausea, fatigue, bleeding - such as nose bleeds, hepatic encephalopathy, hepatomegaly, ascites, distended abdominal veins, spider angiomata, palmar erythema and asterixis. She may also present with the signs and symptoms of alcohol withdrawal, which include irritability, anxiety, tachycardia, tremor, sweating, confusion and hallucinations. 

Thiamine is given for alcohol-induced liver toxicity (to prevent Wernicke s encephalopathy). 

A 31-year-old man developed priapism after taking zuclopenthixol 30 mg/day for 8 days, the dose having been increased to 75 mg the day before, while he was still taking oral carbamazepine 600 mg/day and clora-zepate dipotassium 30 mg/day. He had a history of perinatal anoxic encephalopathy with severe motor sequelae and dyslalia, alcohol dependence, and a personality disorder. On the day before the priapism occurred, he had been physically restrained and given an extra dose of intramuscular clorazepate dipotassium 50 mg. When priapism occurred, all drugs except clorazepate were withdrawn and about 6 hours later the corpora cavernosa were washed and infused with noradrenaline in glucose (8 doses of 40 pg), after which the priapism resolved. 

A 33-year-old chronic alcoholic with hepatitis C developed acute liver and renal insufficiency with grade III encephalopathy. Hemodialysis was begun and emergency liver transplantation was performed. The explanted liver showed marked diffuse macrovesicular steatosis with massive coagulative-type necrosis. The postoperative course included a persistently raised gamma-glutamyltransferase, but he recovered fully after 60 days. 

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