ABSTRACT
BACKGROUND: Bipolar electrocautery systems used during neurosurgical procedures have been shown to induce thermal injury to surrounding tissue. The goal of this study was to compare the thermal injury induced by two different systems commonly used in neurosurgical procedures (Silverglide by Stryker Corporation and SpetzlerMalis by Codman Neuro), with that of a newly introduced device (TRIOwand by NICO Corporation). METHODS: A farm swine underwent craniectomy and durotomy with subsequent exposure of cortical brain tissue. Electrocoagulation for the duration of 3 s was conducted with three different bipolar systems under comparable power settings. The maximal depth of thermal injury and mean area of injury in Hematoxylin and Eosin stained slides were quantified using Image J. The tissues were evaluated for vacuolization and ischemic damage. One-way ANOVA followed by post hoc Tukey test was utilized for statistical analysis. Alpha level was set at 0.05. RESULTS: TRIOwand lesions showed less depth of injury when compared to both Spetzler-Malis (P < 0.001) and Silverglide lesions (P = 0.048). Silverglide lesions showed significantly less depth of injury when compared to SpetzlerMalis lesions (P < 0.001). The injury area induced by the TRIOwand was significantly less than that of Spetzler-Malis (P < 0.001) and Silverglide systems (P < 0.001). Ischemic changes and vacuolization were seen in all three groups. CONCLUSION: Thermal damage is induced to varying extents by all bipolar systems. In this porcine model and under the conditions tested, bipolar cauterization with the TRIOwand resulted in less depth and decreased mean area of injury. Further studies are needed to characterize the injury caused by different bipolar systems with other settings and under surgical conditions in humans.
ABSTRACT
BACKGROUND: Aneurysmal subarachnoid hemorrhage (aSAH) continues to be a devastating neurological condition with a high risk of associated morbidity and mortality. Inflammation has been shown to increase the risk of complications associated with aSAH such as vasospasm and brain injury in animal models and humans. The goal of this review is to discuss the inflammatory mechanisms of aneurysm formation, rupture and vasospasm and explore the role of sex hormones in the inflammatory response to aSAH. METHODS: A literature review was performed using PubMed using the following search terms: "intracranial aneurysm," "cerebral aneurysm," "dihydroepiandrosterone sulfate" "estrogen," "hormone replacement therapy," "inflammation," "oral contraceptive," "progesterone," "sex steroids," "sex hormones" "subarachnoid hemorrhage," "testosterone." Only studies published in English language were included in the review. RESULTS: Studies have shown that administration of sex hormones such as progesterone and estrogen at early stages in the inflammatory cascade can lower the risk and magnitude of subsequent complications. The exact mechanism by which these hormones act on the brain, as well as their role in the inflammatory cascade is not fully understood. Moreover, conflicting results have been published on the effect of hormone replacement therapy in humans. This review will scrutinize the variations in these studies to provide a more detailed understanding of sex hormones as potential therapeutic agents for intracranial aneurysms and aSAH. CONCLUSION: Inflammation may play a role in the pathogenesis of intracranial aneurysm formation and subarachnoid hemorrhage, and administration of sex hormones as anti-inflammatory agents has been associated with improved functional outcome in experimental models. Further studies are needed to determine the therapeutic role of these hormones in the intracranial aneurysms and aSAH.
