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п»ї<title>Do you know about Wernicke-Korsakoff syndrome?</title>
It is a fact that excessive alcohol intake causes disorders, acute or chronic, of the central nervous system, and in particular of the brain such as Wernicke-Korsakoff syndrome. However, it was not until the 19th century that this knowledge began to be systematized. Even today we still do not know the mechanisms by which alcohol produces the brain syndromes associated with its consumption.
Traditionally, the psychopathology of alcohol was considered to be none other than the consequence of the direct and exclusive action of this substance on the central nervous system. However, over time, the repercussions of malnutrition associated with excessive alcohol consumption have proven to be decisive in the manifestations of some of these disorders. We will now take a look at one of the most well-known disorders caused by excessive alcohol consumption: Wernicke-Korsakoff syndrome.
Wernicke-Korsakoff's syndrome
Wernicke's encephalopathy and Korsakoff's syndrome are different conditions, but they often occur together. When this occurs, we speak of Wernicke-Korsakoff syndrome. As we will see below, one of the causes is thiamine (vitamin
deficiency.
Vitamin B deficiency is common in people with alcoholism, but it is not unique to these people. It is also common in people whose bodies do not absorb food properly (malabsorption). This can sometimes occur as a result of chronic illness or after surgery for obesity.
Korsakoff's syndrome or psychosis tends to develop as the symptoms of Wernicke's syndrome disappear. Wernicke's encephalopathy causes brain damage in the lower parts of the brain, thalamus and hypothalamus. Korsakoff's psychosis results from permanent damage to the areas of the brain involved in memory. Let's look at Wernicke's encephalopathy and Korsakoff's amnesic syndrome separately to better understand what we are talking about.
Wernicke's encephalopathy
It was first described by Wernicke in 1885. It occurs in chronic alcoholics with poor nutrition. In Wernicke's encephalopathy there are symmetrical lesions of the brain structures surrounding the third ventricle, the aqueduct and the fourth ventricle.
Specifically, these structures are the mammillary bodies, dorsolateral thalamus, locus coeruleus, periaqueductal gray matter, ocular motor nucleus and vestibular nucleus. Likewise, cerebellar lesions consisting of a selective loss of Purkinje neurons have been described in 50% of cases. Perhaps the most typical neurological sign of this encephalopathy is atrophy of the mammillary bodies, which occurs in approximately 80% of cases.
Symptoms of Wernicke's encephalopathy
Clinically, these patients are observed to be disoriented and inattentive. Many of them present with decreased levels of consciousness and, in the absence of treatment, stupor, coma and death may result.
Other associated symptomatology is evident: nystagmus (involuntary, rapid and repetitive eye movement), ataxia (difficulty in coordinating movements) and ophthalmoplegia (inability to voluntarily move the eyeball), with lesions in the oculomotor, abducens and vestibular nuclei.
Causes of Wernicke's encephalopathy
Its etiology is due to a lack of thiamine or vitamin B, as mentioned above. This thiamine deficiency is common in people who consume alcohol frequently and for which they have developed a certain dependence.
Vitamin B deficiencies in alcoholics are the result of a combination of malnutrition, reduced gastrointestinal absorption of vitamin B and decreased hepatic storage and utilization. The latter factors are induced by chronic alcohol consumption.
Deficiencies in vitamin B processes could have a genetic or acquired origin. These differences could explain why not all alcohol addicts develop this encephalopathy.
Korsakoff's amnesic syndrome
This syndrome is characterized by a strong impairment in the functions of anterograde memory and retrograde memory (inability to learn new things and to remember old ones). It is also characterized by apathy. On the other hand, sensory and other intellectual abilities are usually preserved.
Korsakoff's amnesic syndrome may be linked to Wernicke's encephalopathy, being evident in 80% of subjects who have recovered from this encephalopathy. However, Korsakoff's amnesia has been observed in individuals who have never had Wernicke's encephalopathy.
It is not usual that in non-alcoholic individuals, but who have had an encephalopathy, Korsakoff's syndrome is present. This suggests that alcohol-induced neurotoxicity plays a specific role in the cause of this syndrome.
Alterations due to Korsakoff's syndrome
The neurons most affected by the neurotoxic action are the cholinergic neurons of the basal complex, neurons that appear reduced in patients with Korsakoff's syndrome. Deficiencies in thiamine can cause loss of neurotransmitters, in particular of neurons whose excitation involves acetylcholine. Thus, this deficiency also contributes to memory loss.
Lesions of the mammillary bodies, dorsolateral thalamus, dorsolateral thalamus and anterior thalamus can also cause severe memory deficits. As we have seen, the distinction between Korsakoff's syndrome and Wernicke's encephalopathy is not necessarily clear and precise. From the pathological point of view there is an overlapping of the affected areas in the two syndromes.
Because of this lack of clear demarcation between the two diseases, it has been proposed, by several authors, to use the term Wernicke-Korsakoff syndrome, which would describe the two syndromes.
Bibliographic references
Belloch, A., SandГn, B. and Ramos, F. Manual de psicopatologГa. Revised edition. Mc Graw Hill. Madrid.
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