Excitatory amino acids in cerebrospinal fluid of patients with acute head injuries.

BACKGROUND

The excitatory amino acids (EAAs) glutamate (Glu) and aspartate (Asp) play a role in the pathogenesis of postischemic and posttraumatic brain insult. The changes of EAAs in cerebrospinal fluid (CSF) of patients with traumatic brain injury are incompletely understood.

METHODS

We used reversed-phase HPLC with precolumn derivatization with o-phthalaldehyde and fluorescence detection to measure Glu and Asp in CSF of 42 patients with acute head injury and 9 control adults without neurologic diseases. We assessed the Glasgow Coma Scale (GCS) on admission, the main lesion patterns on computed tomography (CT) scan within 24 h post trauma, and the Glasgow Outcome Scale (GOS) 3 months post injury.

RESULTS

The mean concentrations of Glu and Asp in CSF in the brain-injured group were significantly higher than those of the control group (Glu, P <0.001; Asp, P <0.05). In patients admitted within 24 h after severe injury (n = 13), peak Glu values appeared within 48 h in 11 patients (85%), and the mean value remained higher than control values at day 7 (P <0.02). The concentrations of EAAs were higher in patients with severe injuries (GCS < or =8) than in those with milder injuries (Glu, P <0.001; Asp, P <0.05). GCS and peak EAAs correlated negatively (Glu, rs = -0.5706, P <0.001; Asp, rs = -0.5503, P <0.001). The patients with focal brain contusion on initial CT scan (n = 8) had a significantly lower peak Glu value than the patients with other patterns (n = 8-15; P <0.02 to 0.001). The peak value of EAAs in the poor-outcome group (including severe disability, vegetative state, and death) was significantly higher than in the good-outcome group (good recovery and moderate disability; Glu, P <0.001; Asp, P <0.01); GOS was closely correlated to the EAA values (Glu, rs = 0.5737, P <0.001; Asp, rs = 0.5470, P <0.001).

CONCLUSIONS

The EAA concentrations in CSF increase after acute head injury and remain higher for at least 1 week post injury in severely injured patients. The more severe the trauma, the more obvious the excitotoxicity induced by EAAs and the worse the outcome.