Over the last quarter century there has been significant progress toward identifying certain characteristics and patterns in GBM patients to predict survival times and outcomes. We sought to identify clinical predictors of survival in GBM patients from the past 24 years. We examined patient survival related to tumor locations, surgical treatment, postoperative course, radiotherapy, chemotherapy, patient age, GBM recurrence, imaging characteristics, serum, and molecular markers. We present predictors that may increase, decrease, or play no significant role in determining a GBM patient's long-term survival or affect the quality of life.

Balloon angioplasty is often performed for symptomatic vasospasm following aneurysmal subarachnoid hemorrhage. Angioplasty of the anterior cerebral artery (ACA), however, is perceived to be a challenging endeavor and not routinely performed due to technical and safety concerns. Here, we evaluate the safety and efficacy of balloon angioplasty of the anterior cerebral artery for vasospasm treatment. Patients with vasospasm following subarachnoid hemorrhage who underwent balloon angioplasty at our institution between 2011 and 2016 were retrospectively reviewed. All ACA angioplasty segments were analyzed for pre- and post-angioplasty radiographic measurements. The degree of vasospasm was categorized as mild (<25%), moderate (25–50%), or severe (>50%), and relative change in caliber was measured following treatment. Clinical outcomes following treatment were also assessed. Among 17 patients, 82 total vessel segments and 35 ACA segments were treated with balloon angioplasty. Following angioplasty, 94% of segments had increased caliber. Neurological improvement was noted in 75% of awake patients. There were no intra-procedural complications, but two patients developed ACA territory infarction, despite angioplasty treatment. We demonstrate that balloon angioplasty of the ACA for vasospasm treatment is safe and effective. Thus, ACA angioplasty should be considered to treat vasospasm in symptomatic patients recalcitrant to vasodilation infusion therapy.

Background: 5-Hydroxytryptamine (5HT) modulates N-methyl-D-aspartate (NMDA) depolarization. Results: 5HT2C co-immunoprecipitates with GluN2A and enhances NMDA motoneuronal depolarization through phosphorylation of Src . Conclusion: 5HT modulates NMDA through Src phosphorylation in a molecular complex that is localized in the processes of spinal neurons. Significance: 5HT2C modulation of NMDA excitation is coordinated by a molecular complex.

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