Cerebral metabolic dysfunction has been shown to extensively mediate the pathophysiology of brain injury after subarachnoid hemorrhage (SAH). The characterization of the alterations of metabolites in the brain can help elucidate pathophysiological changes occurring throughout SAH and the relationship between secondary brain injury and cerebral energy dysfunction after SAH. Cerebral microdialysis (CMD) is a tool that can measure concentrations of multiple bioenergetics metabolites in brain interstitial fluid. This review aims to provide an update on the implication of CMD on the measurement of metabolic dysfunction in the brain after SAH. A literature review was conducted through a general PubMed search with the terms “Subarachnoid Hemorrhage AND Microdialysis” as well as a more targeted search using MeSh with the search terms “Subarachnoid hemorrhage AND Microdialysis AND Metabolism.” Both experimental and clinical papers were reviewed. CMD is a suitable tool that has been used for monitoring cerebral metabolic changes in various types of brain injury. Clinically, CMD data have shown the dramatic changes in cerebral metabolism after SAH, including glucose depletion, enhanced glycolysis, and suppressed oxidative phosphorylation. Experimental studies using CMD have demonstrated a similar pattern of cerebral metabolic dysfunction after SAH. The combination of CMD and other monitoring tools has also shown value in further dissecting and distinguishing alterations in different metabolic pathways after brain injury. Despite the lack of a standard procedure as well as the presence of limitations regarding CMD application and data interpretation for both clinical and experimental studies, emerging investigations have suggested that CMD is an effective way to monitor the changes of cerebral metabolic dysfunction after SAH in real-time, and alternatively, the combination of CMD and other monitoring tools might be able to further understand the relationship between cerebral metabolic dysfunction and brain injury after SAH, determine the severity of brain injury and predict the pathological progression and outcomes after SAH. More translational preclinical investigations and clinical validation may help to optimize CMD as a powerful tool in critical care and personalized medicine for patients with SAH.

Background: Fibrous dysplasia (FD) is often difficult for skull base surgeons to address. FD arises due to the abnormal proliferation of fibroblasts, ultimately resulting in immature osseous tissue replacing normal cancellous bone. When the skull base is involved, it can result in cranial nerve compression. FD affecting the optic canal and optic nerve is the most concerning as new onset of vision loss is considered a surgical emergency. The prevalence of FD is approximately 3.6 per 1,000,000. The most severe implications of this disease are neurological deficits due to cranial nerve compression, cosmetic appearance, and high recurrence rates even in the setting of surgical and medical therapy interventions. Methods: A PubMed search of “pediatric fibrous dysplasia management” using MESH Terms was conducted. Articles were excluded for non-English languages, inaccessibility, and events/erratum/letters to the editor. Included articles were in English, as well as encompassed pediatric FD case reports or comprehensive reviews of FD that discussed pediatric presentations. Results: A total of 109 articles were reviewed, and 44 were included in the final review. Most articles were case reports. There is a clear need for guidelines regarding surgical intervention, especially in the pediatric population, where hormonal fluctuation can influence rates of recurrence and bony deformity. Overall, most surgeons recommend close observation with biomarkers and radiographic imaging for asymptomatic patients until at least the age of 16 years old. Conservative methods, such as RANK-L inhibitors, can be utilized to decrease growth with some success, especially in older adolescents. Conclusion: This review is an update on this disease and its presentations, imaging findings, and treatment options. The current literature lacks clear guidance on management, especially in regard to surgical intervention or recurrence monitoring algorithms.