A Cerebellar Tumor-to-Tumor Metastasis in a Patient With Von Hippel-Lindau Disease.

Tumor-to-tumor metastasis in the central nerve system is uncommon in our routine practice. Most reports include metastatic breast cancer into meningioma. Here we report a metastatic clear cell renal cell carcinoma (ccRCC) into a cerebellar hemangioblastoma in a patient with von Hippel-Lindau (VHL) disease. Imaging cannot distinguish metastatic ccRCC from primary cerebellar hemangioblastoma. Immuno-molecular studies are proven to be diagnostic. We also reviewed previously documented tumor-to-tumor metastasis of ccRCC to cerebellar hemangioblastoma in VHL disease. Lastly, we discussed potential mechanisms involved in the metastasis of ccRCC to hemangioblastoma in the cerebellum in patients with VHL.

Neurovascular Syndromes.

Patients with cerebrovascular syndromes are at risk for additional concerns associated with their syndrome. A wide variety of syndromes are associated with cerebrovascular diseases. Multidisciplinary care is helpful to ensure comprehensive evaluation and management. Precise diagnosis and appreciation for the underlying syndrome is critical for effective cerebrovascular and broader care. This text focuses on these conditions with a focus on underlying pathophysiology and associated genetics, presentation, diagnosis, and management of each disease.

Spontaneous Atraumatic Subdural Hematoma Related to Methamphetamine Use.

There are multiple risk factors associated with spontaneous subdural hematoma (SDH), including substance abuse, hypertension, vascular abnormalities, and neoplasms. The illicit drugs typically cited as risk factors for spontaneous SDH are alcohol and cocaine. We report a rare case of spontaneous, significant SDH associated exclusively with methamphetamine. Although it is unclear whether the underlying pathophysiology involves vasculitis, sympathomimetic-induced hypertension, or a combination of both, this case further illustrates the risks of methamphetamine abuse.

COVID-19 and stroke: A review.

COVID-19 patients have presented with a wide range of neurological disorders, among which stroke is the most devastating. We have reviewed current studies, case series, and case reports with a focus on COVID-19 patients complicated with stroke, and presented the current understanding of stroke in this patient population. As evidenced by increased D-dimer, fibrinogen, factor VIII and von Willebrand factor, SARS-CoV-2 infection induces coagulopathy, disrupts endothelial function, and promotes hypercoagulative state. Collectively, it predisposes patients to cerebrovascular events. Additionally, due to the unprecedented strain on the healthcare system, stroke care has been inevitably compromised. The underlying mechanism between COVID-19 and stroke warrants further study, so does the development of an effective therapeutic or preventive intervention.

Animal Models of Post-Traumatic Epilepsy.

Traumatic brain injury is the leading cause of morbidity and mortality worldwide, with the incidence of post-traumatic epilepsy increasing with the severity of the head injury. Post-traumatic epilepsy (PTE) is defined as a recurrent seizure disorder secondary to trauma to the brain and has been described as one of the most devastating complications associated with TBI (Traumatic Brain Injury). The goal of this review is to characterize current animal models of PTE and provide succinct protocols for the development of each of the currently available animal models. The development of translational and effective animal models for post-traumatic epilepsy is critical in both elucidating the underlying pathophysiology associated with PTE and providing efficacious clinical breakthroughs in the management of PTE.

T-cell Dysfunction in Glioblastoma: Applying a New Framework.

A functional, replete T-cell repertoire is an integral component to adequate immune surveillance and to the initiation and maintenance of productive antitumor immune responses. Glioblastoma (GBM), however, is particularly adept at sabotaging antitumor immunity, eliciting severe T-cell dysfunction that is both qualitative and quantitative. Understanding and countering such dysfunction are among the keys to harnessing the otherwise stark potential of anticancer immune-based therapies. Although T-cell dysfunction in GBM has been long described, newer immunologic frameworks now exist for reclassifying T-cell deficits in a manner that better permits their study and reversal. Herein, we divide and discuss the various T-cell deficits elicited by GBM within the context of the five relevant categories: senescence, tolerance, anergy, exhaustion, and ignorance. Categorization is appropriately made according to the molecular bases of dysfunction. Likewise, we review the mechanisms by which GBM elicits each mode of T-cell dysfunction and discuss the emerging immunotherapeutic strategies designed to overcome them. Clin Cancer Res; 24(16); 3792-802. ©2018 AACR.

High Frequency of Pre-Existing Type 2 Diabetes in a Series of Pregnant Women Referred for "Gestational Diabetes" in a Large Canadian Indigenous Community.

We examined the referral processes and true diagnostic classifications for diabetes complicating pregnancy in a series of 62 pregnant women consecutively referred to a diabetes education and treatment centre in a large Indigenous community in Alberta, Canada. The referrals were made over a 5-year period (2010 to 2015). The main findings of this analysis were the high frequency (38.7%) of pre-existing type 2 diabetes and previously undiagnosed or unrecognized overt diabetes and the deficiencies in early testing and recognition.