Few reports describe the clinical course and acute-care management of patients with recurrent multi-antibody paraneoplastic encephalitis. We describe a rare case of a patient having thymoma with multiple paraneoplastic syndromes who was found to have antibodies to α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) followed by N-methyl-d-aspartate (NMDA) receptor in the setting of residual thymic tissue. He initially presented to the hospital with severe, rapidly progressive encephalitis with simultaneous antibodies to AMPA and voltage-gated potassium channel complex receptor. Brain magnetic resonance imaging revealed scattered white matter hyperintensities and an enhancing lesion adjacent to the left caudate. Computerized tomography showed an anterior mediastinal mass that was resected and revealed to be a thymoma. He was refractory to treatment with intravenous immunoglobulin, high-dose steroids, and plasmapheresis. He was then started on monthly cyclophosphamide. After 3 cyclophosphamide infusions, he began to show improvement in his alertness, ability to speak, and capacity to follow commands. One month later, he was readmitted to the hospital for new and unusual behavioral outbursts and agitation. He was found to have new anti-NMDA receptor antibodies in his cerebrospinal fluid in the setting of residual hyperplastic thymic tissue that required another resection. He was treated with rituximab and then cyclophosphamide (due to an infusion reaction with rituximab) with positive outcomes. The presence of multiple antibodies may be associated with poor prognosis, requiring prompt recognition and aggressive immunosuppressive treatment. New neurological symptoms should prompt a search for residual pathologic tissue or tumor recurrence causing new autoantibodies and additional paraneoplastic syndromes.

Neuromyelitis Optica Spectrum Disorder (NMOSD) is an inflammatory autoimmune disorder of the central nervous system, with optic neuritis and transverse myelitis as its most common presentations. Although immunomodulatory treatment options for NMOSD have expanded, preventing reactivation of latent infections in patients can be both a therapeutic challenge and a special consideration for the neurohospitalist in an inpatient setting. We present a challenging case of a NMOSD patient who presented to the emergency department with worsening weakness and numbness in the setting of an NMOSD pseudo-relapse, later found to have untreated latent tuberculosis (TB) and chronic hepatitis B (HBV). She was briefly treated with high-dose IV methylprednisolone, which was stopped after her symptoms and imaging became more consistent with a pseudo-relapse. After confirmation that neither HBV nor TB had reactivated, the patient was discharged on isoniazid and entecavir. A month later, the patient’s symptoms were stable, and she was started on inebilizumab for relapse prevention of NMOSD. This case report is the first to highlight the therapeutic complexities of managing NMOSD that requires immunosuppression in the setting of preventing reactivation of both TB and HBV.

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Patients with severe obesity tend to have higher rates of morbidities which can complicate and even lengthen their hospital admission course. Hospitals which do not have the resources to efficiently manage bariatric patients due to equipment weight-restrictions should be proactive in their care and knowledgeable about their options to avoid long delays in treatment. Amid this obesity epidemic, the neurologist plays a role in the inpatient management of patients with severe obesity and could serve as a channel to improve the quality of care and reduce the length of stay. We present a case of a patient with severe obesity who presented with visual loss secondary to idiopathic intracranial hypertension. The patient’s treatment was delayed several weeks from the time of admission until his weight decreased enough to safely undergo CT imaging in the operating room, developing complications throughout the course of his stay. This paper highlights the identified barriers of care and potential solutions to ensure improvement in the quality of care of patients with severe obesity, in order to reduce preventable complications.

Syphilitic myelitis is an unusual manifestation of neurosyphilis, rarely reported in the literature. The best management approach remains unclear in severe cases with longitudinally extensive spinal cord lesions. We describe a 29-year-old man with a history of incompletely treated syphilis after a high-risk sexual encounter, who presented two years later with several weeks of progressive numbness and weakness in both legs. MRI spine showed significant cord expansion from the craniocervical junction to T6 with patchy cord enhancement. He was diagnosed with syphilitic myelitis given his history of inadequately treated syphilis, positive serum rapid plasma reagin at a high titer, and CSF pleocytosis with elevated protein along with a reactive CSF Venereal Disease Research Laboratory test. Alternative infectious or immunological etiologies were excluded. He was treated with IV penicillin and pulse steroid therapy with IV methylprednisolone 1 g daily for 3 days with improvement. However, he was soon readmitted with recurrent weakness requiring an additional course of pulse steroid therapy followed by a short prednisone taper. Afterward, his symptoms recurred with worsened cord expansion on imaging. He was re-treated with IV penicillin and pulse steroid therapy with a more prolonged prednisone taper. The patient subsequently improved and had no further recurrent symptoms on extended outpatient follow-up. This report illustrates the importance of keeping syphilitic myelitis on the differential as a treatable cause of longitudinally extensive myelopathy. The patient may have benefited from high-dose IV steroids with a prolonged taper while waiting for the full treatment effect of antibiotics.