Each year in the USA, more than 1 million patients undergo medical evaluation and treatment for acute head injury [1]. In the USA there were an average of 53,288 annual traumatic brain injury (TBI)-related deaths from 1989 to 1998, or 19.3 per 10,000 [2]. In Germany, the TBI death rate in 1996 was 11.5 per 10,000, with a total of 9415 deaths [3]. A 15-year study in Denmark showed that the mortality of children after TBI was 22%, and among those survivors of severe head injury, significant numbers were found to have serious neurological disabilities [4]. A regional population-based study in France showed that the mortality of hospitalized TBI patients was as high as 30.0% [5]. Similar data can be found in studies from a variety of demographic and cultural settings [6, 7]. Acute and long-term care of TBI patients has become a significant social and economic burden around the world [8-10].
The neurological outcome of TBI victims depends on the extent of the primary brain insult caused by trauma itself, and on the secondary neurochemical and pathophysiological changes occurring as a consequence of the mechanical injury, which leads to additional neuronal cell loss. Although a long list of experimental studies suggest that reduction or prevention of secondary brain injury after TBI is possible, clinical trials have failed to show benefit from therapeutic strategies proven to be effective in the laboratory [11-13]. This might reflect the diverse nature of clinical TBI and/or perhaps an incomplete understanding of the mechanisms of secondary neuronal loss.
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Two waves of neuronal cell death occur after TBI. Immediately after mechanical trauma due to impact or penetration, neurons can die by necrosis caused by membrane disruption, irreversible metabolic disturbances and/or excitotoxicity [14]. Early application of neuroprotective protocols seems critical for any possibility of reducing neuronal necrosis; however, this is beyond the scope of the current review. The second wave of neuronal death occurs in a more delayed fashion, with morphological features of apoptosis (or programmed cell death). This second wave of neuronal cell death presents within a time window that may be responsive to targeted therapies [15]. The current review summarizes clinically related investigation of apoptosis after TBI, as well as potential therapeutic interventions for altering apoptosis to improve neurological outcome.
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