ABSTRACT
Traumatic brain injury (TBI) is a significant contributing factor to injury-related deaths worldwide. Despite the medical and fiscal importance of this subject, guidelines for the surgical management of closed and penetrating TBI are largely based on Level III evidence. Furthermore, the results of a large, costly trial designed to further elucidate the role of decompressive craniectomy, an important surgical intervention in patients with severe TBI and medically-refractory intracranial hypertension, have limited applicability. In this review, we summarize the existing guidelines for the surgical management of TBI, present an overview of the underlying pathophysiologic principles and neurophysiologic consequences relating to decompressive hemicraniectomy, highlight the history, relevant studies, and outcomes pertaining to decompressive craniectomy for patients with severe TBI, and discuss some of the current controversies in the surgical management of traumatic brain injury. Despite the varied outcomes seen in the literature, DC is indeed an important intervention in the management of TBI, as it is highly effective at reducing ICP and thus, an important higher-treatment strategy for patients with medically-refractory intracranial hypertension. There will continue to be unresolved controversies regarding decisions pertaining to defining an "optimal" surgical candidate, specific timing, techniques, and post-operative management of TBI patients who undergo surgery. New guidelines for the surgical management of TBI are forthcoming. Regardless, for neurosurgeons involved in the care of individuals with TBI, understanding the pathophysiologic and neurophysiologic consequences of surgical interventions, and gaining an understanding of the extant literature is imperative.
Subject(s)
Brain Injuries/surgery , Decompressive Craniectomy/methods , Brain Injuries/physiopathology , Humans , Practice Guidelines as TopicABSTRACT
INTRODUCTION: The mechanisms responsible for cognitive decline after traumatic brain injury (TBI) in pediatric patients are poorly understood. The present study examined the potential role of synaptic alterations in this process by using an animal model of immature head injury to define the impact of TBI on expression of the synaptic protein, synaptophysin. MATERIALS AND METHODS: After craniotomy, TBI was induced in postnatal day 17 (PND17) rats using controlled cortical impact delivered to the left hemisphere. NeuN, a neuronal marker, and synaptophysin expression were examined 1 day, 1 week, and 1 month after injury by immunohistochemistry and immunoblotting. RESULTS: There were significant decreases in both NeuN and synaptophysin after 1 day and 1 week but not 1 month after injury within the hippocampus and neocortex adjacent to the impact site compared to sham-injured controls. The decrease in synaptophysin and NeuN was also noted in the contralateral hippocampus by 1 day after injury and in the contralateral neocortex by 1 week, indicating that changes in protein expression were not solely localized to the injury site but occurred in more distant regions as well. DISCUSSION: In conclusion, the decrease and recovery in synaptophysin parallel the cognitive changes that occur after experimental TBI in the PND17 rat, which suggests that changes in this protein may contribute to cognitive declines after injury. The results also suggest that, in spite of the focal nature of the impact, diffuse alterations in protein expression can occur after immature TBI and may contribute to the subsequent cognitive dysfunction.
