Myasthenia gravis (MG) is an autoimmune, neuromuscular disorder that produces disabling weakness through a compromise of neuromuscular transmission. The disease fulfills strict criteria of an antibody-mediated disease. Close to 90% of patients have antibodies directed towards the nicotinic acetylcholine receptor (AChR) on the post-synaptic surface of skeletal muscle and another 5% to the muscle-specific kinase, which is involved in concentrating the AChR to the muscle surface of the neuromuscular junction. Conventional treatments of intravenous immunoglobulin and plasma exchange reduce autoantibody levels to produce their therapeutic effect, while prednisone and immunosuppressives do so by moderating autoantibody production. None of these treatments were specifically developed for MG and have a range of adverse effects. The extensive advances in monoclonal antibody technology allowing specific modulation of biological pathways has led to a tremendous increase in the potential treatment options. For MG, monoclonal antibody therapeutics target the effector mechanism of complement inhibition and the reduction of antibody levels by FcRn inhibition. Antibodies directed against CD20 and signaling pathways, which support lymphocyte activity, have been used to reduce autoantibody production. Thus far, only eculizumab, an antibody against C5, has reached the clinic. We review the present status of monoclonal antibody-based treatments for MG that have entered human testing and offer the promise to transform treatment of MG.

Throughout this pandemic, neurology resident education and service has, and will continue to be, affected during this unprecedented time. Balancing the safety of our residents as well as the anticipated inpatient service demands, we have, and continue to, make changes to meet the needs of our community. Education certainly has been affected but we have made great effort to maintain normalcy. We are leveraging web-based technologies to continue formal didactics. The American Academy of Neurology has provided program directors with various tools to share to provide high-yield academic education. AAN Synapse, distance learning modules, and podcasts are a few examples. Each residency training program will likely face different challenges depending on location and community structure. We have an obligation to help all of our colleagues in the hospital in providing quality and compassionate care during this time of need. Our training and education will only benefit from this experience teaching us lessons on adaptability, the importance of teamwork, and self-sacrifice.

Myasthenia gravis (MG) is an uncommon autoimmune, postsynaptic neuromuscular disorder, characterized clinically by variable and fluctuating weakness of ocular, bulbar, respiratory, and limb muscles. c Targeted immunotherapies, directed against immune checkpoint modulators such as cytotoxic T-lymphocyte-associated protein 4 (CTLA-4), programmed cell death protein 1 (PD-1), and the PD-1 ligand (PD-L1), have become an important treatment modality for malignancies; while effective, these novel therapies have been associated with autoimmunerelated adverse events. c Exacerbations of preexisting MG, as well as de novo presentations of MG, have been reported after the initiation of these agents; to date in the literature, pembrolizumab (Keytruda) has been associated with 3 exacerbations and 7 de novo presentations of MG. c It is imperative to be acquainted with immune checkpoint modulator complications, as while they are effective in otherwise treatment-resistant malignancies, they may also produce severe adverse effects including exacerbation or induction of autoimmune disorders including devastating neurologic diseases and endocrinopathies.

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Achieving sustained seizure freedom following epilepsy surgery remains a challenge in some patients. Lesional temporal lobe epilepsy (TLE), for example, in patients with mesial temporal sclerosis or other MRI abnormalities, carries a good prognosis for seizure freedom compared to significantly lower chances of seizure freedom in patients with non-lesional epilepsy. However, even in some lesional TLE cases, persistent post-operative seizures suggest seizure onset from a brain region that is clinically and electrographically silent but manifests only after propagation to the temporal lobe. A notable example of such a brain region is the parietal lobe, which has extensive connectivity to various brain regions. While certain seizure semiologies, for example, sensory seizures, suggest parietal lobe onset, some medial parietal seizures may be semiologically indistinguishable from temporal lobe seizures. Here, we report a patient with focal impaired awareness seizures that manifested semiologically and electrographically as left TLE but proved to originate from the contralateral medial parietal lobe. We discuss putative seizure propagation pathways.