Background and Objectives: The injury burden after head trauma is exacerbated by secondary sequelae, which leads to further neuronal loss. B-cell lymphoma 2 (Bcl-2) is an anti-apoptotic protein and a key modulator of the programmed cell death (PCD) pathways. The current study evaluates the clinical evidence on Bcl-2 and neurological recovery in patients after traumatic brain injury (TBI). Materials and Methods: All studies in English were queried from the National Library of Medicine PubMed database using the following search terms: (B-cell lymphoma 2/Bcl-2/Bcl2) AND (brain injury/head injury/head trauma/traumatic brain injury) AND (human/patient/subject). There were 10 investigations conducted on Bcl-2 and apoptosis in TBI patients, of which 5 analyzed the pericontutional brain tissue obtained from surgical decompression, 4 studied Bcl-2 expression as a biomarker in the cerebrospinal fluid (CSF), and 1 was a prospective randomized trial. Results: Immunohistochemistry (IHC) in 94 adults with severe TBI showed upregulation of Bcl-2 in the pericontusional tissue. Bcl-2 was detected in 36-75% of TBI patients, while it was generally absent in the non-TBI controls, with Bcl-2 expression increased 2.9- to 17-fold in TBI patients. Terminal deoxynucleotidyl transferase-mediated biotinylated dUTP nick-end labeling (TUNEL) positivity for cell death was detected in 33-73% of TBI patients. CSF analysis in 113 TBI subjects (90 adults, 23 pediatric patients) showed upregulation of Bcl-2 that peaked on post-injury day 3 and subsequently declined after day 5. Increased Bcl-2 in the peritraumatic tissue, rising CSF Bcl-2 levels, and the variant allele of rs17759659 are associated with improved mortality and better outcomes on the Glasgow Outcome Score (GOS). Conclusions: Bcl-2 is upregulated in the pericontusional brain and CSF in the acute period after TBI. Bcl-2 has a neuroprotective role as a pro-survival protein in experimental models, and increased expression in patients can contribute to improvement in clinical outcomes. Its utility as a biomarker and therapeutic target to block neuronal apoptosis after TBI warrants further evaluation.

Background

The occurrence of traumatic brain injury with spinal cord injury (SCI) in polytrauma patients is associated with significant morbidity. Clinicians face challenges from a decision-making and rehabilitative perspective. Management is complex and understudied. Treatment should be systematic beginning at the scene, focusing on airway resuscitation and hemodynamic stabilization, immobilization, and timely transport. Early operative interventions should be provided, followed by minimizing secondary pathophysiology. The authors present a case to delineate decision-making in the treatment of combined cranial and spinal trauma.

Observations

A 19-year-old man presented as a level I trauma patient after falling 30 feet as the result of scaffolding collapse. The patient was unresponsive and was intubated; he had an initial Glasgow Coma Scale score of 4. Computed tomography revealed multicompartmental bleeding and herniation, for which supra- and infratentorial decompressive craniectomies were performed. The patient also suffered from thoracic SCI that resulted in complete paraplegia. Multimodality monitoring was used. After stabilization and lengthy rehabilitation, the patient obtained significant functional improvement.

Lessons

The approach to initial management of concomitant head and spine trauma is to establish intracranial stability followed by intraspinal stability. Patients can make considerable recovery, particularly younger patients, who are more likely to benefit from early aggressive interventions and medical treatment.