Thiamin psychosis

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. 

Thiamin has a very low toxicity (oral LD5o of thiaminchloride hydrochloride in mice 3-15 g/kg body weight). The vitamin is used therapeutically to cure polyneuropathy, beri-beii (clinically manifest thiamin deficiency), and Wernicke-Korsakoff Syndrome ( Wernicke encephalopathy and Korsakoff psychosis). In mild polyneuropathy, 10-20 mg/d water-soluble or 5-10 mg/d lipid-soluble thiamin are given orally. In more severe cases, 20-50 mg/d water-soluble or 10-20 mg/d lipid-soluble thiamin are administered orally. Patients suffering from beri-beri or from early stages of Wernicke-Korsakoff Syndrome receive 50-100 mg of thiamin two times a day for several days subcutaneously or intravenously until symptoms are alleviated. Afterwards, the vitamin is administered orally for several weeks. 

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. 

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... 

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. 

Thiamine deficiency is commonly seen in alcoholics, who may develop a complex of symptoms associated with Wernicke peripheral neuropathy and Korsakoff psychosis. Alcohol interferes with thiamine absorption from the intestine. Symptoms include ... 

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. 

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 ... 

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. 

Korsakoff s psychosis is considered by some to represent a progression of WE. It is characterized by a striking loss of working memory with relatively little loss of reference memory. Prompt treatment of Wernicke s syndrome with thiamine is believed to prevent the development of Korsakoffs syndrome, but the latter responds little if at all to treatment with thiamine. 

Thiamin deficiency in alcoholics may be caused by decreased intake, reduced absorption, and impaired ability to use ihe absorbed vitamin. The ataxia and ocular symptoms associated with the deficiency in alcoholics are known as Wernicke s disease. Vitamin therapy can provide relief from nystagmus within a few hours of treatment and from ataxia within several weeks. The treatment of alcoholics also involves the supply of other nutrients lacking in the diet, such as folate, vitamin B12, and protein. Left imtreated, patients suffering from Wernicke s disease continue to develop Korsakoff s psychosis, which involves amnesia and confusion. Only about 25% of patients with Korsakoff s psychosis can be completely cured by thiamin treatment, which must be continued for a few weeks or months. The two conditions just described constitute the Wemicke-Korsakoff syndrome. The S5mdrome was named after two researchers. Karl Wernicke, a German, noted impaired or paralyzed eye movements and imstable walking and disorientation in his patients, most of whom were alcoholics. Polyneuropathy, a weakness of the hands, calves, and feet, was also noted. Sergei Korsakoff, a Russian, observed amnesia and confusion and an inability to learn new names or tasks in alcoholic patients. 

This psychosis, along with beriberi and polyneuritis, results from a deficiency of thiamine, not of vitamin K. 

Nerve tissue is mainly dependent for ATP production on glucose metabolism via glycolysis to produce acetyl CoA by the PDH reaction for oxidation in Krebs cycle. Since thiamin is essential for PDH activity, thiamin deficiency, which can occur in malnourished alcoholics, results in PDH dysfunction and an energy deficit in nerve tissue. This causes hyperlactataemia and neuropathy, which can progress to Wernicke s encephalopathy and Korsakoff s psychosis (Chapter 53). 

Thiamine is the third B vitamin for which deficiency classically causes cognitive impairment. Wernicke s disease and Korsakoff s psychosis have been recognized since the 1880 s. Yet for years these conditions were... 

Korsakoff s psychosis represents an essentially irreversible extension of Wernicke s disease, which developed in 157 of 186 (84%) of such patients studied by Victor et al. (1971). The mental disorder is unique in that memory is deranged out of all proportion to other components of mentation and behavior. This memory disorder comprises the truly crippling aspect of the Wernicke-Korsakoff syndrome, since complete recovery occurred in only 21% of patients. Aggressive nutritional support beyond thiamine did not correlate with the partial recovery seen in another 25% of patients who ultimately were able to carry out routine tasks with supervision. Clinical experience in England suggests a more insidious onset with just as dismal a prognosis (Lishman, 1981). 

Thiamine deficiency is the established cause of Wernicke s encephalopathy (WE), an acute neurological disorder constituting one of two components of Wernicke-Korsakoff syndrome (WKS), a neuropsychiatric disorder characterized by ophthalmoplegia, gait ataxia and confusion/memory loss. Up to 80-90% of these patients with WE go on to develop the more debilitating chronic amnesic state, referred to as Korsakoff s psychosis. 

Wernicke s encephalopathy. This is most frequent clinical manifestation of thiamine deficiency in developed countries. It is frequently associated with alcoholism and other conditions impairing nutrition. This neuropsychiatric disorder is characterized by eye muscle paralysis, abnormal posture and gait, and impaired cognitive functions. Progressive deterioration of WE patients ends with KorsakofFs psychosis with manifestation of amnesia, stupor and loss of conceptual functions. 

Wernicke s encephalopathy with KorsakofFs psychosis, a thiamin-responsive condition associated especially with alcohol and narcotic abuse. 

While peripheral neuritis and acute cardiac beriberi with lactic acidosis occur in thiamin deficiency associated with alcohol abuse, the more usual presentation is as the Wernicke—Korsakoff syndrome, due to central nervous system lesions. Initially there is a confused state, Korsakoff s psychosis, which is characterized by confabulation and loss of recent memory, although memory for past events may be unimpaired. Later, clear neurological signs develop — Wernicke s encephalopathy. This is characterized by nystagmus and extraocular palsy. Post-mortem examination shows characteristic brain lesions. 

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