It is a fact that excessive alcohol consumption causes disorders, acute or chronic, of the central nervous system and, in particular, of the brain, such as Wernicke-Korsakoff syndrome; however, until the nineteenth century this knowledge did not begin to become We do not yet know the mechanisms by which alcohol produces brain syndromes associated with its consumption.
Traditionally, alcohol psychopathology was considered only as a result of the direct and exclusive action of this substance on the central nervous system, but over time, the impact of malnutrition associated with excessive alcohol consumption has been fundamental in the manifestations of some of these. Next, we’ll examine one of the most well-known disorders caused by excessive alcohol consumption: Wernicke-Korsakoff syndrome.
- Wernicke encephalopathy and Korsakoff syndrome are different conditions.
- But they often occur together; when that happens.
- We’re talking about Wernicke-Korsakoff syndrome.
- As we’ll see later.
- One of the causes is thiamine deficiency (vitamin B).
Lack of vitamin B is common in people with alcoholism, but it doesn’t just happen in these people. It is also common in people whose bodies do not absorb food properly (malabsorption). This can sometimes occur as a result of a chronic illness or after surgery to treat obesity.
Korsakoff syndrome or psychosis tends to develop as symptoms of Wernicke syndrome go away. Wernicke’s encephalopathy causes brain damage to the lower parts of the brain, thalamus and hypothalamus. Korsakoff psychosis is the result of permanent injuries to the areas of the brain involved in memory. separately about Wernicke’s encephalopathy and Korsakoff’s amnesia syndrome to better understand what we’re talking about.
This condition was first described by Wernicke in 1885 and occurs in alcoholics with chronic malnutrition. Wernicke’s encephalopathy causes symmetrical lesions of the brain structures surrounding the third ventricle, aqueduct, and fourth ventricle.
Specifically, these structures are the bodies of the nipple, the dorsolateral thalamus, the locus coeruleus, the periacucual grey substance, the motor nucleus of the eye and the vestibular nucleus; Similarly, cerebellar lesions have been reported in 50% of cases, consisting of selective lesions loss of Purkinje neurons. Perhaps the most typical neurological sign of this encephalopathy is the atrophy of the nipple bodies, which occurs in approximately 80% of cases.
Clinically, these patients are disoriented and careless, many of them show a decrease in levels of consciousness and, if not treated, can cause stupor, coma and death.
Other associated symptoms are obvious: nystagmus (involuntary, rapid and repetitive eye movements), ataxia (difficulty coordinating movements) and ophthalmoplegia (inability to voluntarily move the eyeball), as well as lesions of the oculomotor, abducent and vestibular nuclei.
Its etiology is due to the lack of thiamine or vitamin B, as we have said above, this thiamine deficiency is common in people who consume alcohol frequently and in those who have developed some dependence.
Vitamin B deficiencies in alcoholics are the result of a combination of malnutrition, reduced gastrointestinal absorption of this vitamin and decreased storage and liver use, the latter factors induced by chronic alcohol consumption.
Deficiencies in vitamin B processes can be genetic or acquired, these differences could explain why not all alcoholics develop this encephalopathy.
This syndrome is characterized by a severe deterioration of the functions of an anograde and retrograde memory (inability to learn new things and remember old things). It is also characterized by apathy. On the other hand, sensory and intellectual abilities are often preserved.
Korsakoff amnesia syndrome may be associated with Wernicke’s encephalopathy, which occurs in 80% of people who have recovered from this encephalopathy; however, Korsakoff amnesia has been observed in people who have never had Wernicke encephalopathy.
Korsakoff syndrome is not common in non-alcoholic people who have had encephalopathy, suggesting that alcohol-induced neurotoxicity has a specific impact on the cause of this syndrome.
The neurons most affected by neurotoxic action are cholinergic neurons of the basal complex, neurons that appear to be reduced in patients with Korsakoff. Thiamine deficiencies can lead to the loss of neurotransmitters, especially neurons, whose arousal is related to acetylcholine, so this deficiency also contributes to memory loss.
Injuries to the body of the nipple, thalamus, dorsolateral and anterior thalamus can also cause serious memory problems. As we have seen, the distinction between Korsakoff syndrome and Wernicke encephalopathy is not necessarily clear and accurate. From a pathological point of view, there is an overlap between the affected areas in both syndromes.
Due to this lack of clear demarcation between the two diseases, several authors have proposed using the term “Wernicke-Korsakoff syndrome”, which would describe both syndromes.
Belloch, A. , Sandon, B. y Ramos, F. Manuel of Psychopathology. Revised edition. Mc Graw Hill, Madrid.