Patients were excluded if they were obeying commands within 12 hours (indicating a non-severe TBI) or died within 12 hours of admission, as these patients were likely to succumb irrespectively of hemoglobin level.
Apoptosis was observed in the injured brain cortex and white matter in a study using mild TBI models, indicating that TBI was a cause of cell death [30].
These findings indicate that TBI alters the levels of neuroactive steroids in the brain with independence of its plasma levels and suggest that the pharmacological increase in the brain of the levels of progesterone and DHEA may result in the improvement of neurological recovery after TBI.
We included ICD-9-CM 959.01 indicating a head injury not otherwise specified to prevent under-estimation of TBI as recommended by the US Centers for Disease Control and Prevention CDCC) (Barell et al. 2002; United States Centers for Disease Control and Prevention 1997; Bazarian et al. 2006).
If both reasons were all reasonable, we may suggest that the decreased FA probably indicated the original damage to the axon and the increased one indicated the recovery; we also suggested that an increase in FA may indicate more severe TBI correlated with poor clinical outcomes.
In contrast, no significant difference was found between sham-TBI and PGI-02776 treated groups in either analysis indicating an improvement in cognitive performance with PGI-02776 treatment.
TBI is also associated with elevated NO levels in remote organs, indicating that TBI can induce systemic changes in NO regulation, which can be either beneficial or detrimental.
These results indicated that TBI can induce autophagy and GSK-3 β activation.
Patients who suffered TBI due to RTA, assault, or fall all showed increased mean PAD scores (5.93, 6.15, and 4.11 for GM; 7.52, 4.42, and 6.51 for WM), indicating that TBI patients' brains appeared to be older, irrespective of the cause of injury (see Fig 5C, D).
If confirmed in a larger sample, these results indicate that a significant subset of dysarthric children post TBI are at an increased risk for reduced language function, particularly impacting on sentence production.
