Objective: Acute encephalopathy may occur in COVID-19-infected patients. We investigated whether medically indicated EEGs performed in acutely ill patients under investigation (PUIs) for COVID-19 report epileptiform abnormalities and whether these are more prevalent in COVID-19 positive than negative patients. Methods: In this retrospective case series, adult COVID-19 inpatient PUIs underwent EEGs for acute encephalopathy and/or seizure-like events. PUIs had 8-channel headband EEGs (Ceribell; 20 COVID-19 positive, 6 COVID-19 negative); 2 more COVID-19 patients had routine EEGs. Overall, 26 Ceribell EEGs, 4 routine and 7 continuous EEG studies were reviewed. EEGs were interpreted by board-certified clinical neurophysiologists (n = 16). EEG findings were correlated with demographic data, clinical presentation and history, and medication usage. Fisher's exact test was used. Results: We included 28 COVID-19 PUIs (30-83 years old), of whom 22 tested positive (63.6% males) and 6 tested negative (33.3% male). The most common indications for EEG, among COVID-19-positive vs COVID-19-negative patients, respectively, were new onset encephalopathy (68.2% vs 33.3%) and seizure-like events (14/22, 63.6%; 2/6, 33.3%), even among patients without prior history of seizures (11/17, 64.7%; 2/6, 33.3%). Sporadic epileptiform discharges (EDs) were present in 40.9% of COVID-19-positive and 16.7% of COVID-19-negative patients; frontal sharp waves were reported in 8/9 (88.9%) of COVID-19-positive patients with EDs and in 1/1 of COVID-19-negative patient with EDs. No electrographic seizures were captured, but 19/22 COVID-19-positive and 6/6 COVID-19-negative patients were given antiseizure medications and/or sedatives before the EEG. | 315GALANOPOULOU et AL. | METHODS | Study design, inclusion and exclusion criteria

Ohtahara syndrome and early myoclonic encephalopathy are the earliest presenting of the epileptic encephalopathies. They are typically distinguished from each other according to specific clinical and etiologic criteria. Nonetheless, considerable overlap exists between the two syndromes in terms of clinical presentation, prognosis, and electroencephalographic signature. Newer understandings of underlying etiologies of these conditions may support the previously suggested concept that they represent a single spectrum of disease rather than two distinct disorders. We review both syndromes, with particular focus on the underlying genetics and pathophysiology and implications regarding the classification of these conditions.

In the past, West Nile fever has manifested as a systemic illness involving acute fever, myalgia, headache, lymphadenopathy, and maculopapular rash. 2 However, in 1 to 40% of cases there has been infection of the neuroaxis, including encephalitis, meningitis, myelitis, radiculopathy, and peripheral neuropathy. 3,4 We describe an adolescent with West Nile encephalitis with brainstem manifestations.Case report. A healthy 15-year-old boy presented with a 3-day history of fever, headache, vomiting, and confusion. Recent history was remarkable for multiple insect bites while living in the Bronx and during a visit to Rhode Island in July 1999. History was negative for immunosuppression, systemic illness, rashes, vaccinations, trauma, or drug use. The patient was hospitalized in the Bronx on September 5, 1999. Pertinent laboratory investigations included abnormal CSF results, with 98 white blood cells/mm 3 , 498 red blood cells/mm 3 , protein count of 84 mg/dL, and glucose count of 65 mg/dL. The differential showed 8% polymorphonuclear cells, 86% lymphocytes, and 6% monocytes. The Center for Disease Control and Prevention documented an elevated immunoglobulin M (IgM) count in the high positive category for West Nile virus in the CSF and blood. Serum Lyme titer was negative, and no other serology workup was performed. Hematologic and blood chemistries were normal. Before the diagnosis, sedimentation rate and antinuclear antibody tests were not ordered. A CT scan of the brain was normal. No electrophysiologic studies were performed. During the hospitalization, the patient required a nasogastric tube, as he was unable to swallow.Six weeks postadmission, the patient was seen in a pediatric neurology clinic. He had bifacial weakness, depressed gag reflex, and tongue fasciculations. Also, there was bilateral appendicular and truncal ataxia. The tendon reflexes were mildly increased, with the right side greater than left. One month later, he improved with a more ellicitable gag reflex, less ataxia, a decrease in tongue fasciculations, less drooling, better swallowing, and efficient feeding. Brain MRI at that time was normal. Six months after the illness, neurologic examination was normal.