Syria civil war: Outcomes of humanitarian neurosurgical care provided to Syrian wounded refugees in Israel.

BACKGROUND: As an expected consequence of the civil war in Syria, emergent neurosurgical care for battlefield trauma has been provided for severely head-injured Syrians transferred to Northern Israel. METHODS: Sixty-six patients suffering from brain injury were brought to the border and then referred to the institution after initial resuscitation. Both the time and type of injury were recorded based on paramedic testimony, forensic material or on details provided by patients. A retrospective analysis of all medical charts and imaging material was performed. RESULTS: Most injuries were combat-related, either caused by blast (13.6%), shrapnel (24.2%), assault (28.8%) or gunshot wound (15.2%). Only a minority of patients (18.2%) suffered from injuries that were not directly caused by weapon. A total of 55 surgical procedures were performed in 46 out of 66 patients, including craniotomies in 40 patients, burr hole alone for placement of intraparenchymal intracranial pressure (ICP) sensor in nine instances and ventricle peritoneal shunt in two patients. Decompressive craniectomy was used only for the treatment of gunshot wound and was performed in eight out of 10 patients. The most common complication consisted in cerebrospinal fluid fistulas (16.7%). Post-operative infections occurred in seven patients (10.6%). Short-term outcomes were favourable in 60.7%, with a mortality rate of 4.5%. DISCUSSION: The present findings suggest that aggressive surgery and neuro-intensive care measures may lead to good functional results, even in the presence of seemingly devastating injuries in some selected patients.

Investigation of the mechanisms of neuroprotection mediated by Ro5-4864 in brain injury.

Increasing evidence has established the involvement of the 18-kDa translocator protein (TSPO) in the process of mitochondrial membrane permeabilization and subsequent apoptosis through modulation of the mitochondrial permeability transition pore. Recent studies have shown that treatment with Ro5-4864, a TSPO ligand, resulted in a neuroprotective effect in traumatic brain injury. Yet, the nature of this effect remained uncertain as mature neurons are considered to be lacking the TSPO protein. In order to investigate the mechanism of Ro5-4864-mediated neuroprotection, the neuro-inflammatory and neurosteroid response to cortical injury was tested in sham-operated, vehicle, cyclosporine A (CsA) and Ro5-4864-treated rats. As anticipated, the levels of interleukin 1ß and tumor necrosis factor α, as well as the astrocyte and microglia cellular density in the injured area were all decreased by CsA in comparison with the vehicle group. By contrast, no visible effect could be observed in Ro5-4864-treated animals. None of the groups showed any significant difference with any other in respect with the expression of brain-derived neurotrophic factor. Double immunofluorescence staining with NeuN and TSPO confirmed the absence of TSPO in native neurons though showed clear evidence of co-localization of TSPO in the cytoplasm of NeuN-stained injured neurons. Altogether, this study shows that the neuronal protection mediated by Ro5-4864 in brain injury cannot be solely attributed to an indirect effect of the ligand on glial TSPO but may also represent the consequence of the modulation of upregulated TSPO in injured neurons. This observation may be of importance for future pharmacological research in neurotrauma.