Ethanol per se inhibits thiamine transport in the gastrointestinal system and blocks phosphorylation of thiamine to its cofactor form (ThDP).Following improved nutrition and the removal of alcohol consumption, some impairments linked with thiamine deficiency are reversed, in particular poor brain functionality, although in more severe cases, Wernicke–Korsakoff syndrome leaves permanent damage. (See delirium tremens.) Wet beriberi
Wet beriberi affects the heart and circulatory system. It is sometimes fatal, as it causes a combination of heart failure and weakening of the capillary walls, which causes the peripheral tissues to become edematous. Wet beriberi is characterized by:

Increased heart rate
Vasodilation leading to decreased systemic vascular resistance, and high-output heart failure
Elevated jugular venous pressure
Dyspnea (shortness of breath) on exertion
Paroxysmal nocturnal dyspnea
Peripheral edema (swelling of lower legs) or generalized edema (swelling throughout the body)
Dilated cardiomyopathy

Gastrointestinal beriberi
Gastrointestinal beriberi causes abdominal pain. It is characterized by:

Abdominal pain
Nausea
Vomiting
Lactic acidosis

Infants
Infantile beriberi usually occurs between two and six months of age in children whose mothers have inadequate thiamine intake. It may present as either wet or dry beriberi.In the acute form, the baby develops dyspnea and cyanosis and soon dies of heart failure.
As a result, the uncontrollable writhing motions witnessed with athetosis deal with the over-activity of synapses within the basal ganglia. Neonatal jaundice
Neonatal jaundice is the other chief complication that leads to the basal ganglia damage associated with this condition. Jaundice is caused by hyperbilirubinemia, or abnormally high levels of bilirubin in the blood. Bilirubin is usually bound to albumin immediately and sent to the liver. However, in neonatal jaundice, the concentration of bilirubin overwhelms that of albumin and some of the bilirubin remains unconjugated and can enter the brain through the blood–brain barrier. Normally bilirubin would not be able to diffuse across the blood–brain barrier, but in infants, the barrier is immature and has higher permeability. Bilirubin is toxic as it prevents the phosphorylation of many proteins, including synapsin I which binds vesicles in the presynaptic terminal. Therefore, it directly inhibits the exocytosis of neurotransmitters and severely hinders the synapses it affects. In autopsies of children who suffered from neonatal jaundice, chronic changes of neuronal loss, gliosis and demyelination were observed in the basal ganglia and more specifically within the globus pallidus. Thalamic stroke
Another study was done where the onset of athetoid movement followed a thalamic stroke. The thalamus is part of a pathway that is involved with the cortical feedback loop in which signals from the cortex are relayed through the striatum, pallidus and thalamus before making it back to the cortex. The striatum receives excitatory inputs from the cortex and inhibits the pallidum.