Neurological Effects

The many neurological effects of acute and chronic alcohol abuse can be categorized as those related directly to alcohol, those secondary to chronic liver disease, and those mediated by thiamine deficiency. The stages of acute alcohol toxicity progress upward from legal intoxication with reduced reaction time and judgment, as occurs with blood levels greater than 0.08 g dl-1 that usually define legal intoxication, to coma and death with levels greater than 0.4 g dl-1. While mild intoxication is common with social drinking, coma and death have been described among college age males who consume excessive amounts of alcohol in a very short period of time. Automobile accidents, which account for a large portion of alcohol-related deaths, are more common in drunken pedestrians than drivers. Intoxication also leads to frequent falls and head trauma, and subdural hematoma can present with delayed but progressive loss of cognition, headaches, and eventual death. Chronic alcoholics are prone to episodes of alcohol withdrawal, which can be characterized according to stages of tremulousness, seizures, and delirium tremens with hyper-excitability and hallucinations at any time up to 5 days after the last drink. This state of altered consciousness is distinct from hepatic encephalopathy, which results from diversion of toxic nitrogenous substances around the scarred cirrhotic liver and is associated with progressive slowing of cerebral functions with stages of confusion, loss of cognition, and eventual coma and death. Progressive altered cognition and judgment can also result from cerebral atrophy following years of heavy drinking, and may also be mediated by thiamine deficiency as described in greater detail below.

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