Catecholamines predict outcome in traumatic brain injury

Abstract

Activation of the sympathetic nervous system attends traumatic brain injury, but the association of the severity of neurological impairment and recovery with the extent of sympathetic nervous system stimulation is poorly defined. In this study, plasma norepinephrine (NE), epinephrine (E), and dopamine (DA) levels were measured serially in 33 patients with traumatic brain injury and compared with the Glasgow Coma Score (GCS), which was obtained concurrently. A catecholamine gradient that reflected the extent of brain injury was demonstrated within 48 hours of the injury. In patients with a GCS of 3 to 4, NE and E levels increased four- to fivefold and the DA level increased threefold above normal (NE, 1686 +/- 416 pg/ml; E, 430 +/- 172 pg/ml; DA, 236 +/- 110 pg/ml), while patients with mild brain injury (GCS, greater than 11) had slightly elevated or normal levels. Patients with marked (GCS, 5 to 7) and moderate (GCS, 8 to 10) traumatic brain injuries had intermediate levels. The prognostic value of determining admission levels of NE was shown in patients with an admission GCS of 3 to 4 1 week after injury. Patients with severe and unchanging neurological impairment 1 week after injury had markedly elevated initial NE levels (2,176 +/- 531 pg/ml), whereas initial NE levels (544 +/- 89 pg/ml) were only mildly elevated in patients who improved to a GCS of greater than 11. These data indicate that markedly elevated NE levels predict outcome in patients with comparable neurological deficits. Thus levels of circulating catecholamines are excellent endogenous and readily quantifiable markers that appear to reflect the extent of brain injury and that may predict the likelihood of recovery.

Alcohol and mortality after moderate to severe traumatic brain injury: a meta-analysis of observational studies

“…5,15 Trauma in general is followed by a catecholamine surge due to sympathetic activation, and a prolonged hyperadrenergic state, which may impair the outcome of TBI patients. 8,11 It has been shown that alcohol administration can blunt this surge and possibly improve outcome in patients with TBI. 52 However, high BAC (exceeding 2.0%), appears to be associated with impaired outcome.…”

“…14,30 It has been postulated that one of the main reasons why the NMDAR antagonists have failed are due to the tight time-window for neuroprotection after brain injury. 11,15,21,53 Patients with positive BAC on injury overcome this dilemma by already having the NMDAR antagonist present prior to injury. Administration of NMDAR antagonists prior to TBI have been shown to prevent neuronal death, possibly explaining some of the positive effects of alcohol.…”

Development of electrochemical methods to enzymatically detect traumatic brain injury biomarkers

“…Generally, asymptomatic levels of the catecholamines are 0 nM to 10 nM (0-1750 pg/mL) in urine and 0.19 nM to 11 nM (33.25-1925 pg/mL) in blood (Kumar et al, 2011;Mayo Clinic Laboratories, 2012). As a result of trauma, catecholamine blood concentrations fluctuate and can reach levels of 29 nM (49 ng/mL) or higher, depending on severity (Hamill et al, 1987). However, the current method to measure catecholamine levels is conducted in clinical laboratories by high-performance liquid chromatography (HPLC) on blood or urine samples (Mayo Clinic Laboratories, 2012;Tsunoda et al, 2009).…”

Plasma catecholamines: follow-up on 10-year study in health and cardiovascular disease

“…Neil-Dwyer et al [16] reported higher concentrations of urinary catecholamines among patients with high plasma renin activity, which they found to be statistically significantly associated with a higher incidence of morbidity and mortality in patients after a subarachnoid hemorrhage. Hamill et al [17] also conclude that markedly elevated concentrations of plasma NE predict outcome in patients with traumatic brain injury.…”