There continues to be debate about the long-term neuropsychological impact of mild traumatic brain injury (MTBI). A meta-analysis of the relevant literature was conducted to determine the impact of MTBI across nine cognitive domains. The analysis was based on 39 studies involving 1463 cases of MTBI and 1191 control cases. The overall effect of MTBI on neuropsychological functioning was moderate (d = .54). However, findings were moderated by cognitive domain, time since injury, patient characteristics, and sampling methods. Acute effects (less than 3 months postinjury) of MTBI were greatest for delayed memory and fluency (d = 1.03 and .89, respectively). In unselected or prospective samples, the overall analysis revealed no residual neuropsychological impairment by 3 months postinjury (d = .04). In contrast, clinic-based samples and samples including participants in litigation were associated with greater cognitive sequelae of MTBI (d = .74 and .78, respectively at 3 months or greater). Indeed, litigation was associated with stable or worsening of cognitive functioning over time. The implications and limitations of these findings are discussed.
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.
Both glial fibrillary acidic protein (GFAP) and S100β are found in glial cells and are released into serum following a traumatic brain injury (TBI), however, the clinical utility of S100β as a biomarker has been questioned because of its release from bone. This study examined the ability of GFAP and S100β to detect intracranial lesions on computed tomography (CT) in trauma patients and also assessed biomarker performance in patients with fractures and extracranial injuries on head CT. This prospective cohort study enrolled a convenience sample of adult trauma patients at a Level I trauma center with and without mild or moderate traumatic brain injury (MMTBI). Serum samples were obtained within 4 h of injury. The primary outcome was the presence of traumatic intracranial lesions on CT scan. There were 397 general trauma patients enrolled: 209 (53%) had a MMTBI and 188 (47%) had trauma without MMTBI. Of the 262 patients with a head CT, 20 (8%) had intracranial lesions. There were 137 (35%) trauma patients who sustained extracranial fractures below the head to the torso and extremities. Levels of S100β were significantly higher in patients with fractures, compared with those without fractures (p<0.001) whether MMTBI was present or not. However, GFAP levels were not significantly affected by the presence of fractures (p>0.05). The area under the receiver operating characteristics curve (AUC) for predicting intracranial lesions on CT for GFAP was 0.84 (0.73-0.95) and for S100β was 0.78 (0.67-0.89). However, in the presence of extracranial fractures, the AUC for GFAP increased to 0.93 (0.86-1.00) and for S100β decreased to 0.75 (0.61-0.88). In a general trauma population, GFAP out-performed S100β in detecting intracranial CT lesions, particularly in the setting of extracranial fractures.
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