Neuroimaging of Wernicke’s Encephalopathy and Korsakoff’s Syndrome

There is considerable evidence that neuroimaging findings can improve the early diagnosis of Wernicke’s encephalopathy (WE)
in clinical settings. The most distinctive neuroimaging finding of acute WE are cytotoxic edema and vasogenic edema, which
are represented by bilateral symmetric hyperintensity alterations on T2-weighted MR images in the periphery of the third ventricle,
periaqueductal area, mammillary bodies and midbrain tectal plate. An initial bout of WE can result in Korsakoff’s syndrome
(KS), but repeated bouts in conjunction with its typical comorbidity, chronic alcoholism, can result in signs of tissue degeneration
in vulnerable brain regions. Chronic abnormalities identified with neuroimaging enable examination of brain damage in living
patients with KS and have expanded the understanding of the neuropsychological deficits resulting from thiamine deficiency,
alcohol neurotoxicity, and their comorbidity. Brain structure and functional studies indicate that the interactions involving
the thalamus, mammillary bodies, hippocampus, frontal lobes, and cerebellum are crucial for memory formation and executive
functions, and the interruption of these circuits by WE and chronic alcoholism can contribute substantially to the neuropsychological
deficits in KS.