Traumatic Brain Injury: Current Treatment Strategies and Future Endeavors

Abstract

Traumatic brain injury (TBI) presents in various forms ranging from mild alterations of consciousness to an unrelenting comatose state and death. In the most severe form of TBI, the entirety of the brain is affected by a diffuse type of injury and swelling. Treatment modalities vary extensively based on the severity of the injury and range from daily cognitive therapy sessions to radical surgery such as bilateral decompressive craniectomies. Guidelines have been set forth regarding the optimal management of TBI, but they must be taken in context of the situation and cannot be used in every individual circumstance. In this review article, we have summarized the current status of treatment for TBI in both clinical practice and basic research. We have put forth a brief overview of the various subtypes of traumatic injuries, optimal medical management, and both the noninvasive and invasive monitoring modalities, in addition to the surgical interventions necessary in particular instances. We have overviewed the main achievements in searching for therapeutic strategies of TBI in basic science. We have also discussed the future direction for developing TBI treatment from an experimental perspective. Keywords traumatic brain injury, management, intracranial hypertension, treatment strategies Epidemiology of Traumatic Brain Injury (TBI)TBI continues to plague millions of individuals around the world on an annual basis. According to the Centers for Disease Control, the total combined rates for TBI-related emergency department visits, hospitalizations, and deaths have increased in the decade 2001-2010. 1 However, taken individually, the number of deaths related to TBIs has decreased over this same period of time likely secondary in part to increased awareness, structuralizing management and guidelines, and significant technological advancements in current treatment regimens. We should also acknowledge that there is a certain percentage of TBIs that never reach medical care, hence, the overall rates for TBIs are likely underreported. 2The highest rates of TBI tend to be in a very young agegroup (0-4 y) as well as in adolescents and young adults (15-24 y). There is another peak in incidence in the elderly (>65 y). The 2 leading causes of TBI overall are falls and motor vehicle accidents.3 As a result of an overall increased number of TBIs, but lower rate of related deaths, we have a growing population of individuals living with significant disabilities directly related to their TBI. Pathophysiology of TBITBI pathogenesis is a complex process that results from primary and secondary injuries that lead to temporary or permanent neurological deficits. The primary deficit is related directly to the primary external impact of the brain. The secondary injury can happen from minutes to days from the primary impact and consists of a molecular, chemical, and inflammatory cascade responsible for further cerebral damage. This cascade involves depolarization of the neurons

Hypothermia for the Management of Intracranial Hypertension in Severe Brain Trauma: The Paradigm is Broken?

“…In the last decade, a clear trend has been demonstrated towards deterioration in patients with severe TBI, in which the whole brain is affected precisely because of the characteristics and degree of injury. This deterioration may be associated with a loss of autoregulation due to the lack of reactivity of cerebral vascular pressure, resulting in hyperemia, interstitial edema and subsequent intracranial hypertension (ICH) 5,6) .Normal intracranial pressure in adults is less than 15 mm Hg, values that remain above 20 mm Hg are considered pathological and are an indication for intensified treatment in patients with TBI 7) . It is important to consider that ICH can result from primary injury (hematoma expansion) or secondary damage (water accumulation, impaired autoregulation, ischemia, and contusion expansion).…”

“…In the last decade, a clear trend has been demonstrated towards deterioration in patients with severe TBI, in which the whole brain is affected precisely because of the characteristics and degree of injury. This deterioration may be associated with a loss of autoregulation due to the lack of reactivity of cerebral vascular pressure, resulting in hyperemia, interstitial edema and subsequent intracranial hypertension (ICH) 5,6) .…”