OBJECTIVELittle is known regarding the natural history of posttraumatic vasospasm. The authors review the pathophysiology of posttraumatic vasospasm (PTV), its associated risk factors, the efficacy of the technologies used to detect PTV, and the management/treatment options available today.METHODSThe authors performed a systematic review in accordance with the PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) guidelines using the following databases: PubMed, Google Scholar, and CENTRAL (the Cochrane Central Register of Controlled Trials). Outcome variables extracted from each study included epidemiology, pathophysiology, time course, predictors of PTV and delayed cerebral ischemia (DCI), optimal means of surveillance and evaluation of PTV, application of multimodality monitoring, modern management and treatment options, and patient outcomes after PTV. Study types were limited to retrospective chart reviews, database reviews, and prospective studies.RESULTSA total of 40 articles were included in the systematic review. In many cases of mild or moderate traumatic brain injury (TBI), imaging or ultrasonographic studies are not performed. The lack of widespread assessment makes finding the true overall incidence of PTV a difficult endeavor. The clinical consequences of PTV are important, given the morbidity that can result from it. DCI manifests as new-onset neurological deterioration that occurs beyond the timeframe of initial brain injury. While there are many techniques that attempt to diagnose cerebral vasospasm, digital subtraction angiography is the gold standard. Some predictors of PTV include SAH, intraventricular hemorrhage, low admission Glasgow Coma Scale (GCS) score (< 9), and young age (< 30 years).CONCLUSIONSGiven these results, clinicians should suspect PTV in young patients presenting with intracranial hemorrhage (ICH), especially SAH and/or intraventricular hemorrhage, who present with a GCS score less than 9. Monitoring and regulation of CNS metabolism following TBI/ICH-induced vasospasm may play an important adjunct role to the primary prevention of vasospasm.

Bilateral carotid cavernous fistulas are rare entities that can cause debilitating symptoms and can lead to more severe consequences if left untreated. Therefore, the recognition and adequate treatment of these pathologies is very important. We present 2 cases of bilateral carotid cavernous fistulas that arose as a result of cavernous sinus thrombosis. We review the literature and discuss the pathophysiology, symptomatology, management, and treatment of bilateral carotid cavernous fistulas. Within our own cases, treatment of the patients was varied. The patient in case 1 was successfully treated with endovascular therapy after a failed trial of anticoagulation. The patient in case 2 demonstrated resolution of bilateral carotid cavernous fistulas after anticoagulation therapy. Case 2 highlights the fact that certain cases of bilateral carotid cavernous fistulas due to cavernous sinus thrombosis may benefit from extensive anticoagulation therapy. If anticoagulation therapy is unsuccessful, endovascular therapy may prove beneficial in resolving the fistulous shunt.

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Atherogenesis and atherosclerosis have long been thought to be a major inciting factor responsible for the formation of aneurysms in the cerebral vasculature. We propose that inception of side-wall aneurysms occurs in hemodynamic environments that promote an atheroprotective endothelial phenotype and that the atheroprotective phenotype is therefore aneurysmogenic.