Vernike's encephalopathy
Contents:
- Description
- Symptoms of Encephalopathy of Vernike
- Reasons of Encephalopathy of Vernike
- Treatment of Encephalopathy of Vernike
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see also:
- Atherosclerotic encephalopathy of Binswanger
- Encephalopathy
- Hepatic encephalopathy
- Distsirkulyatorny encephalopathy
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Description:
Vernike's encephalopathy (acute upper hemorrhagic polioencephalitis of Gayet-Vernique) - the damage of a brain in a rezultataa of deficit of thiamin which is usually arising at an alcoholism is more rare at pernicious vomiting, unbalanced parentalny food.
Symptoms of Encephalopathy of Vernike:
The classical triad of symptoms - an ophthalmoplegia, an ataxy, confusion of consciousness - is available only in a third of cases. Most of patients are deeply disoriented, apathetic, are not capable to concentration, the delirium with excitement as display of an alcoholic abstinence syndrome is sometimes observed. Without treatment the sopor and a coma can develop and to come death. Oculomotor frustration include a horizontal nystagmus at a look in the parties, paralysis of an outside direct muscle of an eye (usually bilateral), disorder of the consensual movements of eyes, occasionally a ptosis. The ataxy (preferential an abasia) is caused by a combination of polyneuropathy, a cerebellar and vestibular ataxy. Pupils are, as a rule, not changed, but at late stages of a disease can be narrowed.
Vernike's encephalopathy (MRT picture)
Reasons of Encephalopathy of Vernike:
Vernike's encephalopathy is caused by B1 avitaminosis. B1 vitamin serves as a cofactor of several enzymes, including transketomanholes, pyruvatedehydrogenases and alpha кетоглутаратдегидрогеназы. At avitaminosis of B1 glucose utilization by neurons decreases and mitochondrions are damaged. Accumulation of a glutamate as a result of decrease of the activity alpha кетоглутаратдегидрогеназы against the background of deficit of energy has neurotoxic effect. At rats with B1 avitaminosis at a submicroscopy it is possible to see morphological features of neurotoxic action of exciting mediators: destruction of mitochondrions, aggregation of chromatin and swelling of neurons with degeneration signs in diencephalon kernels. The degeneration of neurons can be suspended introduction of antagonists of glutamate NMDA receptors.
Treatment of Encephalopathy of Vernike:
Vernike's encephalopathy - the emergency state. Urgently enter thiamin, 50 mg in/in or in oil. Further the drug in the same dose is administered daily before transition of the patient to a normal diet. Thiamin needs to be entered to glucose in/in as it can provoke Vernike's encephalopathy or a fulminant (cardial) form of beriberi, and at an initial stage of these states - to weight them. Therefore, appointing the alcoholic glucose in/in, it is necessary to enter thiamin at first.