In 46 patients experiencing traumatic brain injury, we studied the interactions of alcohol intoxication and severity of neurologic dysfunction on the resulting sympathetic nervous system activation. Sixty percent of the variation in norepinephrine (p < 0.0001) and more than 50% of the variation in epinephrine (p < 0.0001) were due to the initial ethanol concentrations and extent of brain injury assessed by the admission Glasgow Coma Score (GCS). As brain function deteriorated plasma cathecholamines rose (p < 0.0001), but ethanol qualitatively and quantitatively modified this observation. The magnitude of the sympathetic response to worsening neurologic function was progressively diminished in association with increasing ethanol levels, i.e., the inverse relationship of GCS values with both norepinephrine and epinephrine was flattened. In comatose patients (GCS < B) increasing ethanol levels was associated with progressively decreasing norepinephrine and epinephrine responses (p < 0.04), such that catecholamines were reduced by 80 to 90% at ethanol concentrations approaching 400 mg/dl (87.0 mmol/l). However, the impact of ethanol on the degree of sympathetic nervous system activation depended upon the degree of injury; the apparent ethanol suppression was greatest in patients with the most severe neurologic dysfunction (GCS 3 or 4), but it diminished as neurologic function improved. We conclude that the presence of alcohol appears to modify the rise in catecholamine levels following traumatic brain injury in a dose‐dependent manner and alters the relationship between neurologic dysfunction and SNS activation. These alterations may have profound effects on patient morbidity in the immediate post‐accident period.
|Original language||English (US)|
|Number of pages||5|
|Journal||Alcoholism: Clinical and Experimental Research|
|State||Published - Apr 1990|
ASJC Scopus subject areas
- Medicine (miscellaneous)
- Psychiatry and Mental health