Studying the complex molecular mechanisms involved in traumatic brain injury (TBI) is crucial for developing new therapies for TBI. Current treatments for TBI are primarily focused on patient stabilization and symptom mitigation. However, the field lacks defined therapies to prevent cell death, oxidative stress, and inflammatory cascades which lead to chronic pathology. Little can be done to treat the mechanical damage that occurs during the primary insult of a TBI; however, secondary injury mechanisms, such as inflammation, blood-brain barrier (BBB) breakdown, edema formation, excitotoxicity, oxidative stress, and cell death, can be targeted by therapeutic interventions. Elucidating the many mechanisms underlying secondary injury and studying targets of neuroprotective therapeutic agents is critical for developing new treatments. Therefore, we present a review on the molecular events following TBI from inflammation to programmed cell death and discuss current research and the latest therapeutic strategies to help understand TBI-mediated secondary injury.

Spontaneous Intracerebral hemorrhage (ICH) is a devastating injury that accounts for 10–15% of all strokes. The rupture of cerebral blood vessels damaged by hypertension or cerebral amyloid angiopathy creates a space-occupying hematoma that contributes toward neurological deterioration and high patient morbidity and mortality. Numerous protocols have explored a role for surgical decompression of ICH via craniotomy, stereotactic guided endoscopy, and minimally invasive catheter/tube evacuation. Studies including, but not limited to, STICH, STICH-II, MISTIE, MISTIE-II, MISTIE-III, ENRICH, and ICES have all shown that, in certain limited patient populations, evacuation can be done safely and mortality can be decreased, but functional outcomes remain statistically no different compared to medical management alone. Only 10–15% of patients with ICH are surgical candidates based on clot location, medical comorbidities, and limitations regarding early surgical intervention. To date, no clearly effective treatment options are available to improve ICH outcomes, leaving medical and supportive management as the standard of care. We recently identified that remote ischemic conditioning (RIC), the non-invasive, repetitive inflation-deflation of a blood pressure cuff on a limb, non-invasively enhanced hematoma resolution and improved neurological outcomes via anti-inflammatory macrophage polarization in pre-clinical ICH models. Herein, we propose a pilot, placebo-controlled, open-label, randomized trial to test the hypothesis that RIC accelerates hematoma resorption and improves outcomes in ICH patients. Twenty ICH patients will be randomized to receive either mock conditioning or unilateral arm RIC (4 cycles × 5 min inflation/5 min deflation per cycle) beginning within 48 h of stroke onset and continuing twice daily for one week. All patients will receive standard medical care according to latest guidelines. The primary outcome will be the safety evaluation of unilateral RIC in ICH patients. Secondary outcomes will include hematoma volume/clot resorption rate and functional outcomes, as assessed by the modified Rankin Scale (mRS) at 1- and 3-months post-ICH. Additionally, blood will be collected for exploratory genomic analysis. This study will establish the feasibility and safety of RIC in acute ICH patients, providing a foundation for a larger, multi-center clinical trial.

Trigeminal neuralgia (TN) is a chronic pain condition causing lancinating pain in the distribution of one or more divisions of the trigeminal nerve. Gamma knife stereotactic radiosurgery (GKSRS) is a surgical option for TN refractory to medical therapy. To report our experience and to analyze the reasons for the variance in radiosurgery outcomes between patients in our diverse population, we conducted a retrospective analysis of a prospectively created database. The 178 patients completed a pain assessment questionnaire before surgery, and at 1 and 2 year follow-ups. We used the “Trigeminal Neuralgia Gamma Knife Outcome Scale” (TN GKOS) to report the response. At 1-year, 35.4% of patients had grade 1A outcome (pain-free and off all pain medications), 24.7% had grade 1B (pain-free on pain medications), 24.2% had grade 1C (some pain but improved with radiosurgery), 12.9% had grade 2 (same as before radiosurgery) and 2.8% had grade 3 (worse pain compared to before radiosurgery). At 2 years, 42.3% had grade 1A, 20.5% had grade 1B, 19.2% had grade 1C, 14.1% had grade 2 and 3.8% had grade 3 outcome. Remarkably, a statistically significant association was found between GKOS and age, racial background and obesity.

Background: Primary pituitary lymphomas are uncommon neoplasms that are typically derived from a B-cell lineage. Extranodal natural killer (NK)/T-cell lymphoma is distinct from B- and T-cell lymphomas and is associated with Epstein–Barr virus infection. Primary central nervous system (CNS) presentations of this neoplasm are exceptionally rare. Here, we report the case of extranodal NK/T-cell lymphoma presenting as a pituitary mass and review the literature related to this rare clinical entity. Case Description: A 31-year-old previously healthy male presented with 2 weeks of progressive headaches and ophthalmoplegia. Imaging revealed a large intrasellar mass with retroclival extension and involvement of the sphenoid and cavernous sinuses. An endoscopic biopsy of the sphenoidal mucosa was performed, and pathological examination was consistent with extranodal NK/T-cell lymphoma. Despite treatment with chemo- and radiotherapy, the patient died approximately 8 months after initial presentation due to systemic disease progression with multiorgan failure. Conclusion: The presentation of extranodal NK/T-cell lymphoma as a pituitary lesion is very rare, having been reported only twice in the previous literature. Patients with primary CNS extranodal NK/T-cell lymphoma typically experience an aggressive clinical course with a poor prognosis, as in our case.