Injury to the brain occurs when neurons that require high amounts of energy from thiamine dependent enzymes are not supplied with enough energy and die.Brain atrophy associated with WKS occurs in the following regions of the brain: 

the mammillary bodies,
the thalamus,
the periaqueductal grey,
the walls of the 3rd ventricle,
the floor of the 4th ventricle,
the cerebellum, and
the frontal lobe.In addition to the damage seen in these areas there have been reports of damage to cortex, although it was noted that this may be due to the direct toxic effects of alcohol as opposed to thiamine deficiency that has been attributed as the underlying cause of Wernicke-Korsakoff Syndrome.The amnesia that is associated with this syndrome is a result of the atrophy in the structures of the diencephalon (the thalamus, hypothalamus and mammillary bodies), and is similar to amnesia that is presented as a result of other cases of damage to the medial temporal lobe. It has been argued that the memory impairments can occur as a result of damage along any part of the mammillo-thalamic tract, which explains how WKS can develop in patients with damage exclusively to either the thalamus or the mammillary bodies. Diagnosis
Diagnosis of Wernicke–Korsakoff syndrome is by clinical impression and can sometimes be confirmed by a formal neuropsychological assessment. Wernicke encephalopathy typically presents with ataxia and nystagmus, and Korsakoffs psychosis with anterograde and retrograde amnesia and confabulation upon relevant lines of questioning.Frequently, secondary to thiamine deficiency and subsequent cytotoxic edema in Wernicke encephalopathy, patients will have marked degeneration of the mammillary bodies.
Additionally, the study included a category for classifying "bizarre" answers, which included any answer that was far outside of the normal range of expected responses. WKS patients did give answers that could fall into such a category and these included answers such as 15s or 1 hour for the estimated length of a shower, or 4 kg or 15 tonnes as the weight of a car. Memory deficits
As mentioned previously, the amnesic symptoms of WKS include both retrograde and anterograde amnesia. The retrograde deficit has been demonstrated through an inability of WKS patients to recall or recognize information for recent public events. The anterograde memory loss is demonstrated through deficits in tasks that involve encoding and then recalling lists of words and faces, as well as semantic learning tasks. WKS patients have also demonstrated difficulties in perseveration as evidenced by a deficit in performance on the Wisconsin Card Sorting Test. The retrograde amnesia that accompanies WKS can extend as far back as twenty to thirty years, and there is generally a temporal gradient seen, where earlier memories are recalled better than more recent memories. It has been widely accepted that the critical structures that lead to the memory impairment in WKS are the mammillary bodies, and the thalamic regions. Despite the aforementioned memory deficits, non-declarative memory functions appear to be intact in WKS patients. This has been demonstrated through measures that assess perceptual priming.Other studies have shown deficits in recognition memory and stimulus-reward associative functions in patients with WKS.