Neuropathies associated with nutritional deficiencies are routinely encountered by the practicing neurologist. Although these neuropathies assume different patterns, most are length‐dependent, sensory axonopathies. Cobalamin deficiency neuropathy is the exception, often presenting with a non–length‐dependent sensory neuropathy. Patients with cobalamin and copper deficiency neuropathy characteristically have concomitant myelopathy, whereas vitamin E deficiency is uniquely associated with a spinocerebellar syndrome. In contrast to those nutrients for which deficiencies produce neuropathies, pyridoxine toxicity results in a non–length‐dependent sensory neuronopathy. Deficiencies occur in the context of malnutrition, malabsorption, increased nutrient loss (such as with dialysis), autoimmune conditions such as pernicious anemia, and with certain drugs that inhibit nutrient absorption. When promptly identified, therapeutic nutrient supplementation may result in stabilization or improvement of these neuropathies.
Current therapeutic development in amyotrophic lateral sclerosis (ALS) relies on individual randomized clinical trials to test a specific investigational product in a single patient population. This approach has intrinsic limitations, including cost, time, and lack of flexibility. Adaptive platform trials represent a novel approach to investigate several interventions for a single disease in a continuous manner. Already in use in oncology, this approach is now being employed more often in neurology. Here, we describe a newly launched platform trial for ALS. The Healey ALS Platform Trial is testing multiple investigational products concurrently in people with ALS, with the goal of rapidly identifying novel treatments, biomarkers, and trial endpoints.
Serogroup B meningitis represents 30% of American meningococcal infections and had no commercially available vaccine in the USA until 2013 when the FDA made an expanded allowance for importation of the MenB-4C vaccine for outbreaks at two American universities. Infections of Neisseria meningitidis, notably meningococcal meningitis represent a continued, lethal threat to the pediatric and adolescent populations and those with primary or acquired complement component deficiencies, largely mitigated by the quadrivalent meningococcal conjugated vaccine against serogroups A, C, W, and Y (MenACWY).
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