Dementia thiamin deficiency

As might be predicted from these similarities between PNS and CNS, many disease entities can affect both these tissues. It should be noted, however, that the clinical expression of such diseases is variable and is sometimes restricted to the PNS. For example, patients with thiamine deficiency may display symmetrical distal sensorimotor polyneuropathy without accompanying CNS degeneration. Untreated infection with human immunodeficiency virus (HIV) may cause early polyneuropathy, with dementia appearing months or years later. Similarly, patients with sulfatidase deficiency or adrenoleukodystrophy may present initially with polyneuropathy, while their CNS dysfunction remains clinically undetectable. 

Nutritional Deficiency-Related Dementias. We have already mentioned that chronic alcoholics are subject to thiamine deficiency that can cause dementia. It usually occurs only after heavy, prolonged abuse of alcohol. In developed countries, the other key nutritional concern is vitamin deficiency. Vitamin deficiency can surprisingly strike even those with a healthy diet. Such people are missing a vital protein, intrinsic factor, which would enable them to absorb it from their digestive tract. 

An alcohol-related thiamine deficiency, Wemicke-Korsakojf Syndrome, is caused by inadequate intake of thiamine as well as impaired absorption and storage, and is the common cause of dementia. 

Thiamine, also known as vitamin B, is fairly ubiquitous. Thiamine deficiency is uncommon except in alcoholics as a result of nutritional deficiencies and malabsorption. The classic clinical triad of dementia, ataxia (difficulty with walking), and eye findings may be seen, but more commonly, only forgetfulness is noted. Sometimes, thiamine deficiency can lead to vague symptoms such as leg numbness or tingling. Because thiamine is water soluble, it can be added to intravenous fluids and administered in that way. Other manifestations include beri beri, which is cardiac involvement leading to a high cardiac output, and vasodilation. Affected patients often feel warm and flushed, and they can have heart failure. 

Gold, M., Chen, M.F., and Johnson, K., 1995. Plasma and red blood cell thiamine deficiency in patients with dementia of the Alzheimer s type. Archives of Neurology. 52 1081-1086. 

There is a claim that low TDP in blood may be a laboratory marker for alcoholism and a predictor for overt thiamine deficiency (Ceccanti et al. 2005). However, this marker is apparently secondary to earlier, direct and diverse elfects of ethanol on all systems of the human body which pave the road to alcoholic-TD encephalopathies of the Wernicke-Korsakolf type (Tables 33.1 and 33.2) (Pitel et al. 2011). Therefore, preventive measures are undertaken in several countries, including mandatory supplementation of bread flour with thiamine. However, there is no evidence as to whether such treatment delays onset of dementia in the population of alcoholics. 

Thiamine (Bl) is a coenzyme in the reaction to convert pyruvate to acetyl CoA, which enters the TCA cycle. Diet-related thiamine deficiency causes beri-beri, which may manifest as infantile, acute cardiac or chronic dry. Alcohol-related thiamine deficiency causes micke-Korsakoff syndrome, which is the third most common cause of dementia in the US. Alcohol consumption causes anorexia and the inhibition of active transport of thiamine across the intestinal wall as well as the conversion of thiamine to its active form, thiamine pyrophosphate. 

The long-term effects of alcohol on the nervous system can be debilitating and irreversible. In the periphery, there can be a loss of sensation, or paraesthesia, which begins in the extremities of the limbs. Depression can also be found in chronic alcoholics but a more severe central effect is Wernicke s encephalopathy. This acute condition, associated with thiamine deficiency, is characterised by relaxation of eye muscles, confusion and ataxia. It can be fatal if untreated but can be partially reversed by thiamine injections. However, a degree of memory impairment and confusion can be permanent and form part of the syndrome called Korsakoff s psychosis. Alcoholics may also suffer from dementia in the later stages of their illness. 

Substance-Induced Dementias. Substances of abuse can also cause dementia. The most common is alcohol-related dementia. Chronic alcoholism leads to dementia in several ways. The poor diet of the alcoholic causes a deficiency of certain essential nutrients such as thiamine. The alcoholic often suffers recurrent head injuries from falls or altercations. Alcohol-induced liver failure can expose the brain to toxic injury. Finally, the direct toxic effects of alcohol itself on the brain can lead to dementia. In addition to alcohol, the abuse of inhalants such as paint thinner and... 

In addition, other possible causes of dementia also need to be excluded, especially the treatable forms of cognitive impairment, such as that due to depression, chronic drug intoxication, chronic central nervous system infection, thyroid disease, vitamin deficiencies (i.e.. Bn and thiamine), central nervous system angitis, and normal-pressure hydrocephalus (Bird, 2008). Individuals who do not meet these criteria but have short-term memory loss and have only minimal impairment in other cognitive abilities and are not functionally impaired at work or at home are considered to have mild cognitive impairment (Petersen et al., 2001). 

Importance of thiamine An important water-soluble vitamin used as a cofactor in enzymatic reactions involving the transfer of an aldehyde group. Without thiamine, individuals can develop dementia, macrocytic anemia (folate deficiency), gastritis, peptic ulcer disease, liver disease, depression, nutritional deficiencies, cardiomyopathy, and pancreatitis. 

Concomitant deficiencies of other B vitamins, notably thiamine and pyridoxine, probably participate in the pathogenesis of the dementia of pellagra. Pyridoxine deficiency is associated with a peripheral neuropathy in adults and seizures in infants. Victor and Adams (1956) found that pyridoxine-depleted monkeys develop diffuse cerebral pathology similar to, but not absolutely the same as, that found in human pellagra. 

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