Subject(s)
Facial Muscles/physiopathology , Muscle Weakness/diagnosis , Tetanus/diagnosis , Trismus/diagnosis , Anti-Bacterial Agents/therapeutic use , Bell Palsy/diagnosis , Debridement , Diagnosis, Differential , Facial Injuries/complications , Facial Injuries/therapy , Female , Humans , Immunoglobulins/therapeutic use , Lacerations/complications , Lacerations/therapy , Metronidazole/therapeutic use , Middle Aged , Muscle Weakness/etiology , Muscle Weakness/physiopathology , Tetanus/etiology , Tetanus/physiopathology , Tetanus/therapy , Tetanus Toxoid/therapeutic use , Trismus/etiology , Trismus/physiopathologyABSTRACT
Chronic alcohol use induces silent changes in the structure and function of the central and peripheral nervous systems that eventually result in irreversible, debilitating repercussions. Once identified, nutritional supplementation and cessation measures are critical in preventing further neurologic damage. The proposed mechanisms of neuronal injury in chronic alcohol abuse include direct toxic effects of alcohol and indirect effects, including those resulting from hepatic dysfunction, nutritional deficiencies, and neuroinflammation. Clinical manifestations include cerebellar ataxia, peripheral neuropathy and Wernicke-Korsakoff encephalopathy. Continued exploration of the pathophysiologic mechanisms may lead to the discovery of early interventions that can prevent permanent neurologic injury.
