Wernicke’s encephalopathy is caused by thiamine (vitamin B1) deficiency and his manifest by a clinical triad of encephalopathy, ocular motor dysfunction, and gate ataxia.  Encephalopathy is characterized by disorientation, indifference and inattentiveness.  Oculomotor abnormalities include nystagmus, lateral rectus palsy and conjugate gaze palsies. Gait ataxia is manifest as walking with a wide-based gait and slow short steps.  Treatment involves intravenous or intramuscular thiamine depending on the severity of the symptoms.
 
Korsakoff’s syndrome is a later neuropsychiatric manifestation of Wernicke’s encephalopathy characterized by striking anterograde and retrograde amnesia with relative preservation of long-term memory and other cognitive skills.  Patients usually do not fully recover.
 
Ventricular enlargement and cognitive dysfunction: Up to 50-70% of chronic alcohol abusers have cognitive deficits.  The ventricle and sulci abnormalities seen in alcoholics decrease with abstinence. There are also micro structural abnormalities in white matter tracks of alcohol abusers.
 
Alcoholic cerebellar degeneration  is a syndrome manifest with gait ataxia where there is degeneration of Purkinje cells in the cerebellar cortex. This usually occurs after 10 or more years of excessive alcohol intake.
 
Marchiafava-Bignami disease is a rare disorder with demyelination or degeneration of the corpus callosum occurring in malnourished alcoholics.  This is manifest by dementia, dysarthria, spasticity and an inability to walk.
 
Peripheral neuropathy is a gradual progressive disorder of sensorimotor and autonomic nerves.  Abnormalities are usually symmetric and predominately distal. Symptoms include numbness, paresthesias, burning sensations, pain, weakness, muscular cramps and gate ataxia.
 
Myopathy is observed in up to 60% of hospitalized alcohol users following muscle biopsy.   It can evolve acutely or over weeks or months.