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Objective: Giant aneurysms are infrequently complicated with obstructive hydrocephalus (HC), however, when concurrent, effective treatments are unestablished. There are incredibly few reports of HC due to basilar artery giant aneurysms and fewer reports regarding ventriculoperitoneal (VP) shunt complications in these patients. Case presentation: We report the case of a gentleman in his 70 s who presented with a fusiform aneurysm of the entire basilar artery and mild intra-aneurysmal thrombosis. HC, secondary to the aneurysm, indicated VP shunt placement. Within 12 h following shunt placement, however, the patient deteriorated rapidly due to complete basilar artery occlusion and widespread brainstem ischemia. Endovascular intervention was unsuccessful due to extremely high clot burden. He unfortunately expired 2 days afterwards. Conclusion: Hydrocephalus due to aneurysms is not uncommon, and VP shunt placement should be optimized to avoid unforeseen complications like the one described. We suspect that the shunt placement aggravated the already aberrant flow within the aneurysm, propagating a pro-thrombotic environment. With further reports of this complication, a standardized method to place VP shunts for patients with giant aneurysms while minimizing the risk of thrombotic occlusion could be established.

Abstract Background The concept of a Hybrid Angio-Surgical Suite (HASS) has emerged as a solution to the complexity of cerebrovascular surgery and the need for immediate intraoperative feedback. When to use it, what cases are suitable for its use, who can use it and how to use it remain debatable. Objective Provide the information regarding the application of the HASS for hospital, neurosurgeon and interventionalist. Methods We review the literatures of case reports and studies on the use of the hybrid angio-sugical suite along with application of HASS in our own practice. Results Indications for using HASS on different types of cerebral vascular disease, including cerebral aneurysm, AVM, DAVF, carotid and vertebral stenosis/occlusion, are addressed. The application of HASS for other non-cerebral vascular diseases, such as trauma, spine and skullbase cases, is reviewed and discussed. Conclusion HASS has made many surgical procedures safer and many difficult or previously untreatable conditions much more tractable and cost-effective. Other than used in cerebral vascular disease, HASS has much more applications, such as trauma, spine and other neurosurgical diseases.

Despite mounting evidence of a massive peripheral inflammatory response accompanying stroke, the ability of intracerebrally transplanted cells to migrate to the periphery and sequester systemic inflammation remains unexamined. Here, we tested the hypothesis that human bone marrow mesenchymal stromal cells intracerebrally transplanted in the brain of adult rats subjected to experimental stroke can migrate to the spleen, a vital organ that confers peripheral inflammation after stroke. Sham or experimental stroke was induced in adult Sprague-Dawley rats by a 1 hour middle cerebral artery occlusion model. One hour after surgery, rats were intracerebrally injected with human bone marrow mesenchymal stromal cells (3×105/9 μL), then euthanized on day 1, 3, or 7 for immunohistochemical assays. Cell migration assays were performed for human bone marrow mesenchymal stromal cells using Boyden chambers with the bottom plate consisting of microglia, lymphatic endothelial cells, or both, and treated with different doses of tumor necrosis factor-α. Plates were processed in a fluorescence reader at different time points. Immunofluorescence microscopy on different days after the stroke revealed that stem cells engrafted in the stroke brain but, interestingly, homed to the spleen via lymphatic vessels, and were propelled by inflammatory signals. Experiments using human bone marrow mesenchymal stromal cells co-cultured with lymphatic endothelial cells or microglia, and treated with tumor necrosis factor-α, further indicated the key roles of the lymphatic system and inflammation in directing stem cell migration. This study is the first to demonstrate brain-to-periphery migration of stem cells, advancing the novel concept of harnessing the lymphatic system in mobilizing stem cells to sequester peripheral inflammation as a brain repair strategy.

We propose that stem cell therapy may be a potent treatment for metastatic melanoma in the brain. Here we discuss the key role of a leaky blood-brain barrier (BBB) that accompanies the development of brain metastases. We review the need to characterize the immunological and inflammatory responses associated with tumor-derived BBB damage in order to reveal the contribution of this brain pathological alteration to the formation and growth of brain metastatic cancers. Next, we discuss the potential repair of the BBB and attenuation of brain metastasis through transplantation of bone marrow-derived mesenchymal stem cells with the endothelial progenitor cell phenotype. In particular, we review the need for evaluation of the efficacy of stem cell therapy in repairing a disrupted BBB in an effort to reduce neuroinflammation, eventually attenuating brain metastatic cancers. The demonstration of BBB repair through augmented angiogenesis and vasculogenesis will be critical to establishing the potential of stem cell therapy for the treatment/prevention of metastatic brain tumors. The overarching hypothesis we advanced here is that BBB breakdown is closely associated with brain metastatic cancers of melanoma, exacerbating the inflammatory response of the brain during metastasis, and ultimately worsening the outcome of metastatic brain cancers. Abrogating this leaky BBB-mediated inflammation via stem cell therapy represents a paradigm-shifting approach to treating brain cancer. This review article discusses the pros and cons of cell therapy for melanoma brain metastases.

Moderate to severe traumatic brain injury (TBI) often results in malformations to the skull. Aesthetic surgical maneuvers may offer normalized skull structure, but inconsistent surgical closure of the skull area accompanies TBI. We examined whether wound closure by replacement of skull flap and bone wax would allow aesthetic reconstruction of the TBI-induced skull damage without causing any detrimental effects to the cortical tissue. Adult male Sprague-Dawley rats were subjected to TBI using the controlled cortical impact (CCI) injury model. Immediately after the TBI surgery, animals were randomly assigned to skull flap replacement with or without bone wax or no bone reconstruction, then were euthanized at five days post-TBI for pathological analyses. The skull reconstruction provided normalized gross bone architecture, but 2,3,5-triphenyltetrazolium chloride and hematoxylin and eosin staining results revealed larger cortical damage in these animals compared to those that underwent no surgical maneuver at all. Brain swelling accompanied TBI, especially the severe model, that could have relieved the intracranial pressure in those animals with no skull reconstruction. In contrast, the immediate skull reconstruction produced an upregulation of the edema marker aquaporin-4 staining, which likely prevented the therapeutic benefits of brain swelling and resulted in larger cortical infarcts. Interestingly, TBI animals introduced to a delay in skull reconstruction (i.e., 2 days post-TBI) showed significantly reduced edema and infarcts compared to those exposed to immediate skull reconstruction. That immediate, but not delayed, skull reconstruction may exacerbate TBI-induced cortical tissue damage warrants a careful consideration of aesthetic repair of the skull in TBI.