Highlights Neurological manifestations are increasingly being recognized in patients with COVID-19. The ExactMechanism of seizure is unkown. Managing Patients With Epilepsy (PWE) infected with COVID-19 can be challenging. Important to Consider drug-drug interactions between AEDs(Anti-epileptic drugs) and anti-COVID therapies.

Amyotrophic lateral sclerosis (ALS) is a clinically progressive neurodegenerative syndrome predominantly affecting motor neurons and their associated tracts. Riluzole and edaravone are the only FDA certified drugs for treating ALS. Over the past two decades, almost all clinical trials aiming to develop a successful therapeutic strategy for this disease have failed. Genetic complexity, inadequate animal models, poor clinical trial design, lack of sensitive biomarkers, and diagnostic delays are some of the potential reasons limiting any significant development in ALS clinical trials. In this review, we have outlined the possible reasons for failure of ALS clinical trials, addressed the factors limiting timely diagnosis, and suggested possible solutions for future considerations for each of the shortcomings.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) cases were first reported in Wuhan, Hubei province of China in December, 2019. SARS-COV-2 primarily affects the cardio-respiratory system. Over the last few months, several studies have described various neurological sequelae of SARS-COV-2 infection. Neurological complications are more frequent in patients with severe respiratory infections. In this review, we have analyzed the current literature on neuromuscular complications associated with SARS-COV-2 and highlighted possible mechanisms of neuromuscular invasion. We reviewed 11 studies describing 11 cases of Guillain Barre syndrome (GBS), and 1 case each of Miller Fisher syndrome, Polyneuritis Cranialis, Acute myelitis, Oculomotor paralysis and Bell's Palsy associated with SARS-COV-2 infection. Mean age of patients with GBS was 61.54 years, with standard deviation (SD) 14.18 years. Majority patients had fever and cough as the first symptom of SARS COV-2 infection. Mean time for onset of neurological symptoms from initial symptoms in 11 patients was 8.18 days, with SD of 2.86 days. Mean time to performing electrodiagnostic study from onset of neurological symptom was 6 days with standard deviation of 3.25. Six patients had demyelinating pattern, three had acute sensory motor axonal neuropathy, and one had acute motor axonal neuropathy on electrodiagnostic studies.

Background: Although established therapies are effective in most patients with generalized myasthenia gravis (gMG), some patients do not respond or they experience intolerable adverse events, highlighting the need for better tolerated targeted therapies for treatment-refractory gMG. Objective: To describe real-world experience with eculizumab in patients with treatment-refractory acetylcholine receptor antibody-positive (AChR+) gMG. Methods: Retrospective chart review of 15 patients with treatment-refractory AChR+gMG treated for 12 months with eculizumab (900 mg/week for 4 weeks then 1200 mg every 2 weeks). Outcome measures were Myasthenia Gravis–Activities of Daily Living (MG-ADL) scores, number of exacerbations, single-breath count test (SBCT) score, medication changes, selected Quantitative Myasthenia Gravis (QMG) evaluations, and adverse events. Data collected at 3-monthly intervals for 12 months before and after eculizumab initiation were analyzed. Results: Clinically meaningful reductions in total MG-ADL scores were observed at 3 months following eculizumab initiation and maintained up to 12 months in all patients. After 12 months’ eculizumab treatment, there was a significant reduction in the number of acute exacerbations; mean (SD) SBCT score improved from 28.13 (0.33) to 50.26 (2.86); most patients achieved a ‘none’ or ‘mild’ rating for QMG evaluations; all patients reduced their daily prednisone dose; and eight patients had discontinued pyridostigmine. At the end of treatment, intravenous immunoglobulin was discontinued in all six patients receiving this therapy at eculizumab initiation. Eculizumab was well tolerated. Conclusions: This real-world study demonstrated improvement in outcome measures and decreased concomitant drug requirement within 12 months of eculizumab initiation in patients with treatment-refractory AChR+gMG.

Delayed post-hypoxic leukoencephalopathy (DPHL) is a unique clinical entity that presents with cognitive impairment days to weeks after an episode of acute hypoxic brain injury. Frequently hypoxia is unrecognized as a mechanism for clinical decline and extensive workup ensues. We present two cases of DPHL highlighting the neuroimaging findings. In both patients, a cerebral hypoxic event was followed by a recovery phase with subsequent delayed clinical decline. Patient 1 suffered hypoxia from drug-induced respiratory depression and lack of post-operative positive airway pressure (PAP) support. Her neurological exam on follow-up revealed progressive cognitive decline. Magnetic resonance imaging (MRI) brain showed bilateral white matter changes involving the centrum semiovale. Patient 2 developed a generalized tonic-clonic seizure during an endobronchial biopsy procedure and was found to have multiple air emboli on computed tomography (CT) head scan. She was initially in a drug-induced coma for her seizures. Electroencephalography (EEG) on day 14 of admission showed changes consistent with diffuse encephalopathy. MRI brain showed bilateral white matter changes particularly at the watershed zones and in the centrum semiovale. DPHL is a rare and under-recognized clinical entity that requires clinical suspicion and detailed evaluation for diagnosis. Neuroimaging studies can provide prognostic information regarding the extent of neurological injury.