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Frequently, secondary to thiamine deficiency and subsequent cytotoxic edema in Wernicke encephalopathy, patients will have marked degeneration of the mammillary bodies. Thiamine (vitamin B 1) is an essential coenzyme in carbohydrate metabolism and is also a regulator of osmotic gradient. Its deficiency may cause swelling of the intracellular ...
Damage to the mammillary bodies due to thiamine deficiency is implied in pathogenesis of Wernicke–Korsakoff syndrome.Symptoms include impaired memory, also called anterograde amnesia, suggesting that the mammillary bodies may be important for memory.
Korsakoff syndrome (KS) [1] is a disorder of the central nervous system characterized by amnesia, deficits in explicit memory, and confabulation.This neurological disorder is caused by a deficiency of thiamine (vitamin B 1) in the brain, and it is typically associated with and exacerbated by the prolonged, excessive ingestion of alcohol. [2]
Wernicke encephalopathy (WE), also Wernicke's encephalopathy, [1] or wet brain is the presence of neurological symptoms caused by biochemical lesions of the central nervous system after exhaustion of B-vitamin reserves, in particular thiamine (vitamin B 1). [2]
Wernicke syndrome is an ambiguous term. It may refer to: Wernicke aphasia: the eponymous term for receptive or sensory aphasia.; Wernicke encephalopathy: an acute neurological syndrome of ophthalmoparesis, ataxia, and encephalopathy brought on by thiamine deficiency.
Alcoholic Korsakoff syndrome occurs when a chronic alcoholic patient suffers from poor nutrition and specifically develops a thiamine deficiency. Usually with this disease, there are widespread abnormalities in the Papez and fronto-cerebellar circuits. [16] The mammillary bodies are an important part of the Papez circuit.
Individuals with Korsakoff's syndrome, the result of thiamine deficiency in chronic alcoholics, have damage to the dorsomedial nucleus of the thalamus and the mammillary nuclei, as well as degeneration of the frontal lobes. [1] They display both amnesia and poor metamemory.
Transneuronal degeneration is the death of neurons resulting from the disruption of input from or output to other nearby neurons. [1] It is an active excitotoxic process when a neuron is overstimulated by a neurotransmitter (most commonly glutamate) [2] causing the dysfunction of that neuron (either damaging it or killing it) which drives neighboring neurons into metabolic deficit, resulting ...