Korsakoff s psychosis

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. 

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. 

However, when used in excess it can lead to a wide range of physical and mental problems, e.g. heart and liver disease, cancers, increased risk of stroke, mood and personality changes and dementia (Korsakoff s psychosis). 

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. 

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. 

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 ... 

Ocular findings, including nystagmus (horizontal or vertical), weakness or paralysis of the lateral recti muscles, and weakness or paralysis of conjugate gaze Korsakoff s psychosis is most characterized 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 An organic brain syndrome associated with prolonged, heavy ingestion of alcohol. It is characterized by amnesia for recent events and an inability to memorize new information. 

Thiamin deficiency can result in three distinct syndromes a chronic peripheral neuritis, beriberi, which may or may not be associated with heart failure and edema acute pernicious (fulminating) beriberi (shoshin beriberi), in which heart failure and metabolic abnormalities predominate, with little evidence of peripheral neuritis and Wernicke s encephalopathy with Korsakoff s psychosis, a thiamin-responsive condition associated especially with alcoholism and narcotic abuse. 

Initially, there is a confused state, Korsakoff s psychosis, that 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. Postmortem examination shows hemorrhagic lesions in the thalamus, pontine tegmentum, and mammillary body, with severe damage to astrocytes, neuronal dendrites, and myelin sheaths. 

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. 

Perceptual Visual hallucinations, disordered thinking, psychosis, Korsakoff s psychosis, paranoia... 

Victor et al (1989), in classic studies, followed 186 alcoholic patients with Wernicke s encephalopathy for up to ten years and documented that 84% developed Korsakoff s syndrome. A subsequent study of 32 alcoholic patients followed for a period of 33 months showed the rate of progression to KP to be 56% (Wood et al, 1984). PuU recovery from Korsakoff s psychosis occured in only 20% the majority of KP patients required some level of supervision and social support (Reuler et al, 1985 Chamess, 2006). 

Wernicke s encephalopathy is associated with a mortality rate of 10-20%, predominantly as a result of sepsis, respiratory infection and decompensated liver disease Korsakoff s psychosis is associated with a mortality rate of approximately 17% (Harrison et al, 2006 Ogershok et al, 2002 Meikin-Zaborsky et al, 2001). 

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). 

Human brains show symmetrical necrotic lesions most consistently in the mammillary bodies but also in the periaqueductal midbrain, thalamus, and along the floor of the fourth ventricle. These are the lesions of the acute disease, not necessarily associated with disordered memory. The changes in patients from the Korsakoff end of the spectrum differ by virtue of consistent involvement of the diencephalon, particularly the medial dorsal nucleus of the thalamus. This structural lesion, rather than a reversible biochemical process, appears to be responsible for the memory loss. Thus, patients with third ventricular tumors, resection of inferomed-ial portions of the temporal lobes, or sequelae of herpes encephalitis may demonstrate classical signs of Korsakoff s psychosis (Victor et al., 1971). 

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