Furthermore, infections are usually present in pediatric cases.In the last stage other symptoms may occur: hyperthermia, increased muscle tone, spastic paralysis, choreic dyskinesias and coma.Because of the frequent involvement of heart, eyes and peripheral nervous system, several authors prefer to call it Wernicke disease rather than simply encephalopathy.Early symptoms are nonspecific, and it has been stated that WE may present nonspecific findings. In Wernicke Korsakoffs syndrome some single symptoms are present in about one-third. Location of the lesion
Depending on the location of the brain lesion different symptoms are more frequent:
Brainstem tegmentum. - Ocular: pupillary changes. Extraocular muscle palsy;  gaze palsy: nystagmus. Hypothalamus. Medulla: dorsal nuc. of vagus. - Autonomic dysfunction: temperature; cardiocirculatory; respiratory. Medulla: vestibular region. Cerebellum. - Ataxia. Dorsomedial nuc. of thalamus. Mammillary bodies. - Amnestic syndrome for recent memory.Mamillary lesion are characteristic-small petechial hemorrhages are found. Diffuse cerebral dysfunction.- Altered cognition: global confusional state. Brainstem: periaqueductal gray.- Reduction of consciousness
Hypothalamic lesions may also affect the immune system, which is known in people who consume excessive amounts of alcohol, causing dysplasias and infections. Korsakoff syndrome
Korsakoff syndrome, characterised by memory impairment, confabulation, confusion and personality changes, has a strong and recognised link with WE. A very high percentage of patients with Wernicke–Korsakoff syndrome also have peripheral neuropathy, and many people who consume excess alcohol have this neuropathy without other neurologic signs or symptoms. Korsakoffs occurs much more frequently in WE due to chronic alcoholism. It is uncommon among those who do not consume excessive amounts of alcohol.
Up to 80% of WE patients who misuse alcohol develop Korsakoffs syndrome. In Korsakoffs, is usually observed atrophy of the thalamus and the mammillary bodies, and frontal lobe involvement. In a study, half of Wernicke-Korsakoff cases had good recovery from the amnesic state, which may take from 2 months to 10 years. Risk factors
Wernicke encephalopathy has classically been thought of as a disease solely of people who drink excessive amounts of alcohol, but it is also found in the chronically undernourished, and in recent years had been discovered post bariatric surgery. Without being exhaustive, the documented causes of Wernicke encephalopathy have included:

pancreatitis, liver dysfunction, chronic diarrhea, celiac disease, Crohns disease, uremia, thyrotoxicosis
vomiting, hyperemesis gravidarum, malabsorption, gastrointestinal surgery or diseases
incomplete parenteral nutrition, starvation/fasting
chemotherapy, renal dialysis, diuretic therapy, stem cell/marrow transplantation
cancer, AIDS,  Creutzfeldt–Jakob disease, febrile infections
this disease may even occur in some people with normal, or even high blood thiamine levels, are people with deficiencies in intracellular transport of this vitamin. Selected genetic mutations, including presence of the X-linked transketolase-like 1 gene, SLC19A2 thiamine transporter protein mutations, and the aldehyde dehydrogenase-2 gene, which may predispose to alcohol use disorder. The APOE epsilon-4 allele, involved in Alzheimers disease, may increase the chance of developing neurological symptoms. Pathophysiology
Thiamine deficiency and errors of thiamine metabolism are believed to be the primary cause of Wernicke encephalopathy. Thiamine, also called B1, helps to break down glucose. Specifically, it acts as an essential coenzyme to the TCA cycle and the pentose phosphate shunt.