User:MRH2002!/Wernicke encephalopathy/Delbel4567 Peer Review

Edits:

WE was (were) first identified in 1881 by the German neurologist Carl Wernicke, although the link with thiamine was not identified until the 1930s.

In a series of autopsy studies held in Recife, Brazil, it was found that only 7 out of 36 had consumed excessive amounts of alcohol, and only a small minority had malnutrition. In a review ed of 53 published case reports from 2001 to 2011, the relationship with alcohol was also about 20% (10 out of 53 cases).

WE related to alcohol misuse is more common in males and tends to be more common in females when WE is not related to alcohol misuse. In alcohol-related cases WE patients average the age of 40 and non-alcohol-related cases occur in younger people.

Pathological anatomy (Section)

Despite its name, WE is are not related to Wernicke's area, a region of the brain associated with speech and language interpretation.[ citation needed]

Brain lesions in  identifying what this stands for '(WE)'' are often credited to focal lactic acidosis. When thiamine is not available to facilitate pyruvate conversion through the same as above what is this TCA cycle, pyruvate accumulates within the cell. The concentrations of pyruvate and lactate are normally at equilibrium, and an increase in pyruvate causes a subsequent increase in lactate concentration.[1]'''

In most, early lesions are completely reversed with immediate and adequate supplementation.[ citation needed] (Delete and replace with the sentence below)

Lesions can be reversed in most cases with immediate supplementation of thiamine. citation needed

what is the they here They are usually symmetrical in the periventricular region, diencephalon, the midbrain, hypothalamus, and cerebellar vermis. Brainstem lesions may include cranial nerve III, IV, VI, and VIII nuclei, the medial thalamic nuclei, and the dorsal nucleus of the vagus nerve. Oedema may be found in the regions surrounding the third ventricle, and the fourth ventricle, also appearing as petechiae and small hemorrhages.[2] Chronic cases can present the atrophy of the mammillary bodies.[3]

Endothelial proliferation, hyperplasia of capillaries, demyelination and neuronal loss can also occur.[ citation needed](DELETE)

'''The idea that disruption of the blood–brain barrier may be a cause of WE lesions was first introduced in 1949. Increased permeability of the blood–brain barrier can allow large proteins not normally found in the central nervous system to pass into the brain and puts neurological tissue at risk of toxic effects. Several regions of the brain typically found to have lesions in WE are at the blood–brain barrier junctions.[1]'''

An altered blood–brain barrier may cause a perturbed response to certain drugs and foods.

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