Fluid percussion models produce brain injury by rapidly injecting fluid volumes into the cranial cavity. The authors have systematically examined the effects of varying magnitudes of fluid percussion injury in the rat on neurological, systemic physiological, and histopathological changes. Acute neurological experiments showed that fluid percussion injury in 53 rats produced either irreversible apnea and death or transient apnea (lasting 54 seconds or less) and reversible suppression of postural and nonpostural function (lasting 60 minutes or less). As the magnitude if injury increased, the mortality rate and the duration of suppression of somatomotor reflexes increased. Unlike other rat models in which concussive brain injury is produced by impact, convulsions were observed in only 13% of survivors. Transient apnea was probably not associated with a significant hypoxic insult to animals that survived. Ten rats that sustained a moderate magnitude of injury (2.9 atm) exhibited chronic locomotor deficits that persisted for 4 to 8 days. Systemic physiological experiments in 20 rats demonstrated that all levels of injury studied produced acute systemic hypertension, bradycardia, and increased plasma glucose levels. Hypertension with subsequent hypotension resulted from higher magnitudes of injury. The durations of hypertension and suppression of amplitude on electroencephalography were related to the magnitudes of injury. While low levels of injury produced no significant histopathological alterations, higher magnitudes produced subarachnoid and intraparenchymal hemorrhage and, with increasing survival, necrotic change and cavitation. These data demonstrate that fluid percussion injury in the rat reproduces many of the features of head injury observed in other models and species. Thus, this animal model could represent a useful experimental approach to studies of pathological changes similar to those seen in human head injury.

Objective This study examined whether serum levels of GFAP breakdown products (GFAP-BDP) were elevated in mild and moderate TBI compared to controls and if they were associated with traumatic intracranial lesions on CT scan (+CT) and having a neurosurgical intervention (NSI). Methods This prospective cohort study enrolled adult patients presenting to three Level 1 Trauma Centers following blunt head trauma with loss of consciousness, amnesia, or disorientation and a GCS 9–15. Control groups included normal uninjured controls and trauma controls presenting to the ED with orthopedic injuries or an MVC without TBI. Blood samples were obtained in all patients within 4 hours of injury and measured by ELISA for GFAP-BDP (ng/ml). Results Of the 307 patients enrolled, 108 were TBI patients (97 with GCS 13–15, and 11 with GCS 9–12) and 199 were controls (176 normal controls and 16 MVC controls and 7 orthopedic controls). ROC curves demonstrated that early GFAP-BDP levels were able to distinguish TBI from uninjured controls with an AUC of 0.90 (95%CI 0.86–0.94) and differentiated TBI with a GCS 15 with an AUC 0.88 (95%CI 0.82–0.93). Thirty two TBI patients (30%) had lesions on CT. The AUC for discriminating those patients with CT lesions versus those without CT lesions was 0.79 (95%CI 0.69–0.89). Moreover, the ROC curve for distinguishing NSI from no NSI yielded an AUC of 0.87 (95%CI 0.77–0.96). Conclusions GFAP-BDP is detectable in serum within an hour of injury and is associated with measures of injury severity including the GCS score, CT lesions and neurosurgical intervention. Further study is required to validate these findings before clinical application.

Forty-six patients with severe nonpenetrating brain injury [Glasgow Coma Scale (GCS) 4-7] were randomized to standard management at 37 degrees C (n = 22) and to standard management with systemic hypothermia to 32 to 33 degrees C (n = 24). The two groups were balanced in terms of age (Wilcoxon's rank sum test, p > 0.95), randomizing GCS (chi-square test, p = 0.54), and primary diagnosis. Cooling was begun within 6 h of injury by use of cooling blankets. Metocurine and morphine were given hourly during induction and maintenance of hypothermia. Rewarming was at a rate of 1 degree C per 4 h beginning 48 h after intravascular temperature had reached 33 degrees C. Muscle relaxants and sedation were continued until core temperature reached 35 degrees C. There were no cardiac or coagulopathy-related complications. Seizure incidence was lower in the hypothermia group (Fisher's exact text, p = 0.019). Sepsis was seen more commonly in the hypothermia group, but difference was not statistically significant (chi-square test). Mean Glasgow Outcome Scale (GOS) score at 3 months after injury showed an absolute increase of 16% (i.e., 36.4-52.2%) in the number of patients in the Good Recovery/Moderate Disability (GR/MD) category as compared with Severe Disability/Vegetative/Dead (SD/V/D) (chi-square test, p > 0.287). Based on evidence of improved neurologic outcome with minimal toxicity, we believe that phase III testing of moderate systemic hypothermia in patients with severe head injury is warranted.

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