Acute Demyelinating Encephalomyelitis (ADEM) in COVID-19 infection: A Case Series

ObjectiveTo report three patients infected with COVID-19 with severe respiratory syndrome requiring intubation, who developed acute demyelinating encephalomyelitis (ADEM).MethodPatient data were obtained from medical records from the North Memorial Health Hospital, Robbinsdale, MN, USAResultsThree patients (two men and one woman, aged 38 - 63) presented with fatigue, cough and fever leading to development of acute respiratory distress syndrome secondary to COVID-19 infection requiring intubation and ventilatory support. Two patients were unresponsive, one with strong eye deviation to the left and the third patient had severe diffuse weakness. MRI in all patients showed findings consistent with ADEM. CSF showed elevated protein in all patients with normal cell count and no evidence of infection, including negative COVID-19 PCR. All three of the patients received Convalescent plasma therapy for COVID-19. All patients were treated with intravenous corticosteroids and improved, although two responded minimally. Two patients treated with IVIG showed no further improvement.ConclusionNeurological complications from COVID-19 are being rapidly recognized. Our three cases highlight the occurrence of ADEM as a postinfectious/immune mediated complication of COVID-19 infection, which may be responsive to corticosteroid treatment. Early recognition of this complication and treatment is important to avoid long term complications.

Pediatric Inflammatory and Autoimmune Neurologic Disorders at a Tertiary Medical Center

Objectives: To describe the spectrum of pediatric inflammatory neurologic diseases and compare the sensitivity of ancillary testing for these diagnoses. Methods: We analyzed clinical features and outcomes of 98 children with an immune-mediated central nervous system disorder. We compared sensitivities of each diagnostic modality. Results: We identified the following diagnoses: acute cerebellar ataxia (n = 14; 14.3%), acute demyelinating encephalomyelitis (n = 13; 13.3%), multiple sclerosis (MS) (n = 18; 18.4%), anti- N-methyl-d-aspartate receptor encephalitis (anti-NMDAR encephalitis) (n = 15; 15.3%), encephalitis not otherwise specified (n = 12; 12.2%), and “Other” (n = 26; 26.5%). “Other” included acute transverse myelitis, neuromyelitis optica, central nervous system lupus, primary central nervous system vasculitis, Rasmussen encephalitis, opsoclonus myoclonus ataxia syndrome, and clinically isolated syndrome. The mean age of onset of all diagnoses was 7.9 ± 5.5 years. The diagnostic sensitivity of magnetic resonance imaging (MRI) for acute demyelinating encephalomyelitis and multiple sclerosis was 92.3% and 94.4%, respectively. Cerebrospinal fluid was sensitive for multiple sclerosis in 92.3%, where 75% of patients had cerebrospinal fluid oligoclonal bands. Electroencephalogram (EEG) coupled with cerebrospinal fluid studies was highly sensitive for anti-NMDAR encephalitis (100%). EEG was sensitive for acute demyelinating encephalomyelitis and encephalitis not otherwise specified (77.8% and 80%). No diagnostic studies were sensitive for acute cerebellar ataxia. Seventy-three percent of patients with multiple sclerosis had residual deficits. Thirty-six percent of anti-NMDAR encephalitis patients were nonverbal and wheel-chair bound. Conclusions: We found that MRI is useful for detecting multiple sclerosis and acute demyelinating encephalomyelitis, cerebrospinal fluid is helpful in diagnosing multiple sclerosis and anti-NMDAR encephalitis, and EEG is often abnormal in suspected anti-NMDAR encephalitis, acute demyelinating encephalomyelitis, and encephalitis not otherwise specified. Neurologic outcome at follow-up was unfavorable in patients with multiple sclerosis and anti-NMDAR encephalitis.

The occurrence of acute demyelinating encephalomyelitis after respiratory viral infection (clinical observation)

This article examines the development of acute demyelinating encephalomyelitis against a background of a viral infection in a clinical case. Based on the literature review, it is known that acute disseminated encephalomyelitis is an immuno-mediated single-phase inflammatory demyelinating disorder of white matter of the brain and spinal cord. It is noted that one of the proposed mechanisms of pathogenesis is that myelin autoantigens, such as myelin main protein, proteolipid protein and myelin oligodendrocyte protein, have antigenic determinants with the infecting agent. Antiviral antibodies or cell-mediated cross-reacting pathogens respond to myelin autoantigens, resulting in acute demyelinating encephalomyelitis. Acute demyelinating encephalomyelitis has been found to be associated with increased vascular permeability and accumulation of circulating immune complexes or other humoral factors that develop after exposure to a foreign antigen introduced by infection or vaccination. This process then leads to infiltration of the walls of the vessels by mononuclear cells with subsequent swelling and periodic hemorrhage. Microglia, lymphocytes, and phagocytes appear throughout the day, ultimately leading to demyelination and possible gliosis and necrosis. The degree of demyelination and subsequent glial and neural changes explain the difference between clinical features and disease prognosis. In clinical case, we have demonstrated the appearance of this disease, which developed in close temporal connection with infectious disease. Positive meningeal signs, tenderness and limited movements of the eyeballs, diplopia when viewed sideways, decreased convergence, horizontal nystagmus when viewed sideways, symptoms of oral automatism, decreased muscle strength diffuse, tendons and tendons = D, average liveliness; from the feet S> = D, average liveliness, tremor of the hands. The MRI findings, in addition to the clinical picture, helped to establish the diagnosis. As a result of this, a cure for the disappearance of a neurological deficit was achieved. Thus, this clinical case proves that disseminated encephalomyelitis proceeds by type of acute disease with rapid increase of symptoms and their subsequent regression.