A 40-Year-Old Woman With COVID-19 and Bilateral Vision Loss.

Mucormycosis is a fast-spreading angioinvasive fungal infection with a very high mortality rate. It is associated with immunodeficiency, diabetes mellitus, iron overload, stem cell transplantation and the use of steroids. As cultures and histopathological biopsy may have low yield in invasive fungal infections, new generation sequencing of cfDNA (cell free deoxyribonucleic acid) has become a cornerstone for diagnosis. Over the past 18 months, increasing reports of COVID-19 associated Mucormycosis have emerged, most specifically in India and other nearby developing countries. Awareness and knowledge of this newly discovered association is of high importance and clinical relevance as the global COVID-19 pandemic continues. Herein, we present a case of a patient who was treated with steroids for COVID-19 in the outpatient setting and presented with unilateral periorbital pain and blurry vision. She progressively developed bilateral vision loss, fixed bilateral mydriasis, ophthalmoplegia and coma. Imaging findings included leptomeningeal, vascular, and subcortical enhancement accompanied with multifocal infarction. Subsequent biopsy of the paranasal sinuses revealed broad type fungal elements and cfDNA sequencing identified the pathogen as Rhizopus species. She was treated with intravenous amphotericin B, but succumbed to the infection.

Rituximab in Refractory Myositis and Acute Neuropathy Secondary to Checkpoint Inhibitor Therapy.

Checkpoint inhibitor immunotherapies have been one of the latest advances through the last decade in the treatment of various cancers. As their use is increasing so is the knowledge of their complications which can affect various organ systems including the central and peripheral nervous systems. Management of these complications requires stopping the offending agent and in some cases treating with immunosuppressive agents like intravenous steroids. Physicians can face challenging situations if patients are unresponsive to steroids, intravenous immunoglobulins (IVIG), and plasmapheresis (PLEX). There are no formal guidelines to help in the management of such patients.  We present an 85-year-old male with a past medical history of renal cell carcinoma status post nephrectomy who was admitted with diplopia, eyelid ptosis, dysphagia, dysphonia, dyspnea, and generalized weakness. He was started on nivolumab and ipilimumab 10 days prior to presentation. Laboratory studies showed an elevated erythrocyte sedimentation rate, C-reactive protein, and creatine phosphokinase, and an unrevealing lumbar puncture. Acetylcholine receptor (AChR) and muscle-specific kinase (MuSK) antibodies were negative. Electromyography and nerve conduction studies showed axonal and demyelinating sensorimotor neuropathy with no significant decrement on 3 Hz repetitive stimulation. Thyroid function tests were concerning for thyroiditis and anti-thyroid peroxidase antibodies were positive. Together, these findings led to the diagnosis of refractory myositis and acute neuropathy along with autoimmune thyroiditis from nivolumab and ipilimumab immunotherapy. His symptoms were unresponsive to a 5-day course of steroids, intravenous immunoglobulins, and plasmapheresis. He was then started on rituximab with significant improvement in ptosis, dysphagia, dysphonia, and proximal weakness. Immune checkpoint inhibitors (ICI) are associated with an increased risk for the development of various autoimmune conditions. Treatment involves discontinuation of the offending drug and initiation of immunosuppressive therapy. This case is interesting as it demonstrates the importance of the awareness of the neurological complications of the checkpoint inhibitor therapies and the beneficial role of rituximab in patients who are unresponsive to initial immunosuppressive therapies including steroids, IVIG, and PLEX.

Nonepileptic, Stereotypical, and Intermittent Symptoms After Subdural Hematoma Evacuation.

Transient neurological deficits can occur in the setting of subdural hemorrhages with subsequent unremarkable electrodiagnostic and radiological evaluation. This scenario is rare and can be difficult for physicians to interpret. These transient neurological deficits are thought to result from relative ischemia, secondary to a lesser-known concept known as cortical spreading depolarization. These transient neurological deficits are thought to result from relative ischemia, secondary to a lesser-known concept known as cortical spreading depolarization, which may present clinically as nonepileptic, stereotypical, and intermittent symptoms (NESIS). In these instances, patients are often misdiagnosed as epileptics and committed to long-term antiseizure drugs. We present a 51-year-old patient developing acute global aphasia following the evacuation of a subdural hematoma, with no significant findings on laboratory, microbiological, electrodiagnostic, or radiological evaluation. The patient experienced spontaneous improvement and returned to baseline in the subsequent weeks. Increased awareness of NESIS as a cortical spreading depolarization phenomenon can improve patient care and prevent both unnecessary, extended medical evaluations and therapeutic trials.

Glioblastoma Multiforme Masquerading as Stroke.

Sudden-onset anomic aphasia is a unique symptom that is suggestive of an acute etiology. This case presents a sudden-onset focal neurological deficit with an underlying brain tumor. A 68-year-old female awoke with sudden-onset anomic aphasia, with mild hypertension as her only medical history. After an initial stroke workup was unremarkable, magnetic resonance imaging found a focal lesion on the left temporal lobe. An electroencephalogram showed lateralized periodic discharge and a focal area of increased epileptic potential in the left temporal lobe. Brain biopsy revealed World Health Organization grade IV glioblastoma, followed by resection. This case is an important reminder that chronic etiologies may present with acute symptoms.