Thiamine administration

Wernicke-Korsakoff syndrome is a relatively uncommon but important entity characterized by paralysis of the external eye muscles, ataxia, and a confused state that can progress to coma and death. It is associated with thiamin deficiency but is rarely seen in the absence of alcoholism. Because of the importance of thiamine in this pathologic condition and the absence of toxicity associated with thiamine administration, all patients suspected of having Wernicke-Korsakoff syndrome (including virtually all patients who present to the emergency department with altered consciousness, seizures, or both) should receive thiamine therapy. Often, the ocular signs, ataxia, and confusion improve promptly upon administration of thiamine. However, most patients are left with a chronic disabling memory disorder known as Korsakoff s psychosis. 

Severe thiamine deficiency is called beriberi. The major organs affected are the nervous system (in dry beriberi), the cardiova.scuIar system (in wet beriberi), and the gastrointestinal tract. Thiamine administration reverses the gasUointesli-nal and cardiovascular symptoms. The neurological danugc may be permanent, however, if the deficiency has been severe or of long duration. Thiamine hydrochloride is indicated... 

Thiamine deficiency resulting in beriberi usually occurs because of excessive alcohol intake, which interferes with thiamine absorption. In the early stages, the person tires easily and the limbs feel heavy and weak. In an advanced stage of wet beriberi,.symptoms include neuromuscular problems enlarged heart (with tachycardia), peripheral edema, and weakness and malaise. These symptoms usually respond to thiamine administration. 

Excessive CNS depression Intoxication due to acute ingestion of ethanol is managed by maintenance of vital signs and prevention of aspiration after vomiting. Intravenous dextrose is standard. Thiamine administration is used to protect against the Wemicke-Korsakoff syndrome, and correction of electrolyte imbalance may also be required. 

TD-induced behavioral deficits and neuronal loss can be reversed by the administration of thiamine if the treatment is provided early enough. For example, in mice, thiamine administration by day 7 of TD prevents TD-induced neuron loss and deficits in rotarod performance. If thiamine is administered later, the neuron loss is permanent (Ke et al., 2003). These straightforward studies are important from a mechanistic point of view because they indicate that certain irreversible steps in cell death occur by a defined time in the treatment. 

TD-Induced Neurological Deficits that are Not Reversed by Thiamine Administration... 

The archetype of primary thiamin deficiency disease is beriberi, a polyneuritis, rapidly reversible upon thiamin administration. 

AEDs administered with some effect. Later, when the diagnosis of vitamin deficiency was made, thiamine administration led to some neurologic improvement and fewer seizures. However, most of the children became persistently neurologic disabled and needed chronic therapy with AEDs (Fattal-ValevsM et al. 2009). 

Despite the equivalent amount of food consumed, thiamine decreased the extent of weight gain. This interesting finding could have great significance for reduction in obesity if thiamine administration shows a similar effect on human metabolism. We therefore examined other obesity parameters in detail, i.e. visceral fat mass and adipocyte size. 

Immune Anaphylaxis with cardiac arrest secondary to intravenous thiamine administration has been described [23 ]. 

The first case of angioneurotic oedema due to oral thiamine administration has been reported [24 ]. 

Alcoholism. Alcoholism or impaired nutrition severely affects the level of thiamine in brain. Thiamine deficiency strongly affects the activity of transketolase (TK) and often leads to the severe neurological disorder, Wemicke-Korsakoff syndrome (WKS). Although thiamine administration results in normalization of neurological symptoms, the TK activity does not completely recover in all regions of the brain [39],... 

Wernicke s syndrome is a serious consequence of alcoholism and thiamine (vitamin Bx) deficiency. Certain characteristic signs of this disease, notably ophtalmoplegia, nystagmus, and ataxia, respond rapidly to the administration of thiamine but to no other-vitamin. Wernicke s syndrome may be accompanied by an acute global confusional state that may also respond to thiamine. Left untreated, Wernicke s syndrome frequently leads to a chronic disorder in which learning and memory are strongly impaired. This so-called Korsakoff s psychosis is characterized by confabulation, and is less likely to be reversible once established. 

The identification of co-occurring medical problems is an important element in detoxification (Naranjo and Sellers 1986). Good supportive care and treatment of concurrent illness, including fluid and electrolyte repletion, are essential (Naranjo and Sellers 1986). Administration of thiamine (50—100 mg/day po or im) and multivitamins is a low-cost, low-risk intervention for the prophylaxis and treatment of alcohol-related neurological disturbances. 

True. Excessive alcohol use can lead to serious damage to mental health. Depression, anxiety, delusions and negative changes in personality can occur. Korsakoff s psychosis occurs in some excessive users of alcohol. This form of dementia results in disorientation, loss of memory and lowered intellectual abilities. It is reversible in some sufferers through the administration of thiamine (vitamin Bj. 

Rare patients respond to the administration of thiamine in large doses (10-30mg/day). The clinical course is even more mild than that of patients with intermittent disease. Thiamine is a cofactor for the branched-chain ketoacid dehydrogenase, and the presumed mutation involves faulty binding of the apoprotein to this vitamin. 

Classic beri-beri, rarely seen in the United States and Europe, except in alcoholism (P4), is endemic in the Far East because of the prevalent diet of decorticated rice (F6). It occurs in two forms wet beri-beri, characterized by edema and cardiovascular symptoms (G6), and dry beri-beri with peripheral neuritis, paralysis, and atrophy of the muscles. Conditions which may predispose to deficiency by increasing thiamine requirements are pregnancy (see section 2.4), and lactation, hyperthyroidism, malignant disease, febrile conditions, increased muscular activity, high carbohydrate diets, and parenteral administration of glucose solutions. A constant supply of thiamine is required for optimal nutrition because storage in the liver and elsewhere is limited. Thiamine is synthesized by bacteria in the intestinal tract of various animals, but this is not a dependable source for man. 

Psychoneuroses involving depression, irritability, anxiety, increased sensitivity to noise and painful stimuli, and uncertainty of memory have been induced in human patients as a result of thiamine deficiency. 22 It seems probable that the Wernicke type syndrome, which is more severe, can likewise be caused by thiamine deficiency. In all cases the psychological symptoms are eliminated or prevented by the administration of adequate amounts of thiamine. Here again is a clear-cut case in which mental disease can be caused by a nutritional deficiency and cured by supplying adequate amounts of the missing nutritional factor. 

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. 

After being found to be healthy on a thorough physical examination accompanied by a broad range of laboratory examinations, 22 men were used in studies of the renal clearance of I, after intravenous injection at 5 mg/kg under a variety of conditions.161 Alkaliniza-tion of the urine to a pH above 7.5 by administration of bicarbonate and acidification of the urine to a pH below 5.0 by administration of ammonium chloride both reduced urinary excretion of I. When 200 mg of thiamine was Injected intramuscularly 20-30 min before intravenous injection of I, urinary excretion of I during the 5 h after... 

During the first 3 h after Intravenous injection of 1 that followed administration of thiamine, urinary excretion of the oxime was about 12.7% below that during the corresponding period of the control experiment during the remainder of the run, it was 62.2% above that during the same period of the control experiment. Inasmuch as intravenous injection of 900 mg of sodium jg-aminohippurate with I decreased by only 6.3% the urinary excretion of I during the first 3 h after its administration, the tubular transport mechanisms for 1 and for jg-amino-hippurate probably are different. 

The Wernicke-Korsakofi syndrome consists of both an acute (i.e., Wernicke s encephalopathy) and a chronic phase (i.e., Korsakoff s psychosis). The acute encephalopathy may be precipitated or worsened by carbohydrates (including intravenous glucose) unless thiamine is also replenished before or during administration. Wernicke s encephalopathy may first be manifested by the following ... 

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