Increased Intracranial Pressure in Myelin-Oligodendrocyte Glycoprotein Antibody-Associated Disease.

Objectives: To assess characteristics of increased intracranial pressure (ICP) in myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD).

Methods: This is a multicenter retrospective review of 84 MOGAD cases at the University of Florida, Baylor College of Medicine, the University of California San Diego, and Providence Health and Services, Portland, Oregon, to identify cases with a documented increased opening pressure >25 cm H2O. A literature review was conducted to identify previously reported MOGAD cases with an opening pressure >25 cm H2O.

Frequency, characteristics, predictors and treatment of relapsing myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD).

Background: Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) may have a monophasic or relapsing disease course. To date, factors that may predict a relapsing disease course remain largely unknown and only limited data exist regarding the efficacy of different utilized immunotherapy regimens at preventing or reducing relapses.

Objectives: To assess the characteristics, predictors, and immunotherapy of relapsing MOGAD.

Health Disparities in Multiple Sclerosis among Hispanic and Black Populations in the United States.

Multiple sclerosis (MS) is an acquired demyelinating disease of the central nervous system (CNS). Historically, research on MS has focused on White persons with MS. This preponderance of representation has important possible implications for minority populations with MS, from developing effective therapeutic agents to understanding the role of unique constellations of social determinants of health.

Immunopathogenesis, Diagnosis, and Treatment of Multiple Sclerosis: A Clinical Update.

Multiple sclerosis (MS) is the most prevalent nontraumatic disabling neurologic condition among young adults worldwide. The diagnosis and management of MS is complex. The goal of this review is to provide an updated and practical approach to the diagnosis and treatment approaches in MS, emphasizing current understanding of immunopathogenesis, recent advances, and future directions, for both MS and non-MS clinicians.

Elsberg syndrome following acute immunosuppressive treatment for multiple sclerosis relapse.

First described more than 80 years ago, Elsberg Syndrome (ES) continues to be an under-recognized cause of cauda equina syndrome (CES). ES is an infectious disorder that presents with lower thoracic and/or lumbosacral myelitis in conjunction with CES, and most often occurs in the setting of herpes simplex virus 2 (HSV-2) reactivation (Savoldi et al., 2017; Eberhardt et al.

Multiple Sclerosis in a Multi-Ethnic Population in Houston, Texas: A Retrospective Analysis.

Multiple Sclerosis (MS) is a progressive neurodegenerative disease that affects more than 2 million people worldwide. Increasing knowledge about MS in different populations has advanced our understanding of disease epidemiology and variation in the natural history of MS among White and minority populations. In addition to differences in incidence, African American (AA) and Hispanic patients have greater disease burden and disability in earlier stages of disease compared to White patients.

Current Advances in Pediatric Onset Multiple Sclerosis.

Multiple sclerosis (MS) is an autoimmune inflammatory disease affecting the central nervous system leading to demyelination. MS in the pediatric population is rare, but has been shown to lead to significant disability over the duration of the disease. As we have learned more about pediatric MS, there has been a development of improved diagnostic criteria leading to earlier diagnosis, earlier initiation of disease-modifying therapies (DMT), and an increasing number of DMT used in the treatment of pediatric MS.

Stem Cell-Based Therapies for Multiple Sclerosis: Current Perspectives.

Multiple sclerosis (MS) is an inflammatory and neurodegenerative autoimmune disease of the central nervous system (CNS). Disease-modifying therapies (DMT) targeting inflammation have been shown to reduce disease activity in patients with relapsing⁻remitting MS (RRMS). The current therapeutic challenge is to find an effective treatment to halt disease progression and reverse established neural damage.

Multipotent adult progenitor cells prevent macrophage-mediated axonal dieback and promote regrowth after spinal cord injury.

Macrophage-mediated axonal dieback presents an additional challenge to regenerating axons after spinal cord injury. Adult adherent stem cells are known to have immunomodulatory capabilities, but their potential to ameliorate this detrimental inflammation-related process has not been investigated. Using an in vitro model of axonal dieback as well as an adult rat dorsal column crush model of spinal cord injury, we found that multipotent adult progenitor cells (MAPCs) can affect both macrophages and dystrophic neurons simultaneously.

Adult NG2+ cells are permissive to neurite outgrowth and stabilize sensory axons during macrophage-induced axonal dieback after spinal cord injury.

We previously demonstrated that activated ED1+ macrophages induce extensive axonal dieback of dystrophic sensory axons in vivo and in vitro. Interestingly, after spinal cord injury, the regenerating front of axons is typically found in areas rich in ED1+ cells, but devoid of reactive astrocyte processes. These observations suggested that another cell type must be present in these areas to counteract deleterious effects of macrophages.

PTPsigma is a receptor for chondroitin sulfate proteoglycan, an inhibitor of neural regeneration.

Chondroitin sulfate proteoglycans (CSPGs) present a barrier to axon regeneration. However, no specific receptor for the inhibitory effect of CSPGs has been identified. We showed that a transmembrane protein tyrosine phosphatase, PTPsigma, binds with high affinity to neural CSPGs.

Activin acutely sensitizes dorsal root ganglion neurons and induces hyperalgesia via PKC-mediated potentiation of transient receptor potential vanilloid I.

Pain hypersensitivity is a cardinal sign of tissue damage, but how molecules from peripheral tissues affect sensory neuron physiology is incompletely understood. Previous studies have shown that activin A increases after peripheral injury and is sufficient to induce acute nociceptive behavior and increase pain peptides in sensory ganglia. This study was designed to test the possibility that the enhanced nociceptive responsiveness associated with activin involved sensitization of transient receptor potential vanilloid I (TRPV1) in primary sensory neurons.