M ultiple sclerosis (MS) is a chronic autoimmune disease of the central nervous system. A secondary progressive clinical course develops in many individuals with MS, typically 20 years after onset, and sustained disability leads to impaired mobility and cognition (1).Conventional MRI (ie, T2-or proton densityweighted, T2-weighted fluid-attenuated inversion recovery [FLAIR], or unenhanced and contrast materialenhanced T1-weighted imaging) is the main tool used in the diagnosis and routine surveillance of abnormal changes in patients with MS (2,3). Lesion measures (ie, number of new or enlarging or contrast-enhanced lesions and their respective volumes) enable quantitative assessment of active inflammation. They have been largely used as primary and secondary end points in many clinical trials (3,4). Monitoring the appearance of new lesions and their enlargement is routinely used as an indicator of disease activity and treatment efficacy in a clinical routine. However, the association between lesion MRI markers and MS clinical worsening or transition to secondary progressive MS (SPMS) disease course is weak to modest (5,6).Assessment of brain atrophy is considered a more robust outcome reflecting neurodegeneration, the end

Background: Pathologic changes in cortical gray matter (GM) and leptomeninges contribute to disability worsening in patients with multiple sclerosis (MS), but there is little evidence whether disease-modifying treatments can slow down cortical pathology in MS. Objectives: To investigate the effect of teriflunomide (TFM) and dimethyl fumarate (DMF) in reducing cortical pathology, as determined by percentage cortical volume change (PCVC) and leptomeningeal contrast enhancement (LMCE) on MRI. Methods: This was a retrospective, single-center, observational study that selected 60 TFM- and 60 DMF-treated MS patients over 24 months. Results: TFM had a lower rate of PCVC compared to DMF over 24 months (−0.2% vs. −2.94%, p = 0.004). Similar results were observed for percentage GM volume change over 0–12 (p = 0.044) and 0–24 (−0.44% vs. −3.12%, p = 0.015) months. No significant differences were found between the TFM and DMF groups in the frequency and number of LMCE foci over the follow-up. TFM showed a numerically lower rate of whole brain atrophy over 24 months (p = 0.077), compared to DMF. No significant clinical or MRI lesion differences between TFM and DMF were detected over follow-up. Conclusions: These findings suggest that TFM has a superior effect on the preservation of cortical GM volume, compared to DMF.

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After prompt diagnosis, severe myasthenia gravis and Guillain-Barré syndrome (GBS) usually require management in the intensive care unit. In the myasthenic patient, recognition of precipitating factors is paramount, and frequent monitoring of bulbar, upper airway, and/or respiratory muscle strength is needed to identify impending myasthenic crisis. Noninvasive ventilation can be attempted prior to intubation and mechanical ventilation in the setting of respiratory failure. Cholinesterase inhibitors should be discontinued, but resumed prior to extubation, and steroid dosage could be increased once the airway is secured. In GBS, hemodynamic and respiratory monitoring are essential; however, respiratory failure can develop rapidly and intubation with mechanical ventilation is often required and can be prolonged. Guillain-Barré syndrome can also be complicated by dysautonomia necessitating specific therapies. Prompt recognition and initiation of immunotherapy including intravenous immunoglobulin or plasmapheresis, together with supportive care including treatment of underlying infections and physical therapy, can improve outcomes in both myasthenic crisis and GBS.