Coronavirus disease 2019 associated with aggressive neurolog
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A 68-year-old man temporarily lost consciousness, with a slight cough, vomiting, fatigue, and low fever. There was no apparent sputum production, sore throat, chest tightness, difficulty breathing, headache, or limb convulsion. Chest computed tomography (CT) showed ground-glass shadows in both lungs. He was recommended to isolate at home due to a suspicion of “new coronavirus pneumonia.” Aggravated fatigue accompanied by headache, dizziness, nausea, and coma occurred. Emergency craniocerebral CT revealed lacunar lesions in the left basal ganglia region and chest CT showed dispersive and patchy shadows bilaterally in the lungs with partial consolidation; the lesion had enlarged. The patient was clinically diagnosed with “new coronavirus pneumonia” and was hospitalized. He awoke 48 h later with headache and vomiting after antiviral treatment and fluid and nutritional support. During this period, the patient underwent 2 viral RNA tests by pharyngeal swab, both of which were negative. The patient once again slipped into a comatose state without any apparent cause. He woke up 4 days later unable to walk and with uroclepsia, coprolalia, and persecution delusion. He was transferred to our hospital.

The patient had a history of diabetes and hypertension under good control. His wife was also diagnosed with "new coronavirus pneumonia” a few days after his diagnosis. Her symptoms were mild without loss of consciousness or mental abnormalities. There was no reported history of mental disorders in the family. His blood oxygen saturation maintained above 95% without supplemental oxygen even in his poor condition after admission. Slight neck stiffness, trembling of the hands, and grade 4 muscle strength were detected. Laboratory investigations showed normal liver function, renal function, electrolyte level, and coagulation function. Leucocyte and lymphocyte count and percentage were all within a reasonable range. SARS-CoV-2 IgM antibodies in the plasma were slightly high and IgG antibodies in the plasma were within the normal range.

A repeated craniocerebral CT showed results similar to those obtained; another chest CT showed ameliorated lung opacities. The cerebrospinal fluid (CSF) was strongly positive for SARS-CoV-2 IgM antibodies and IgG antibodies (107.52 and 70.07, respectively). However, his swab and CSF RNA tests were consistently negative. The protein level in the CSF was significantly high (803.6 mg/L), but no obvious abnormality was found in routine examination. Craniocerebral magnetic resonance imaging and other further CSF tests could not be done at this hospital. After 18 days of routine antiviral treatment (0.1 g ibavirin per day for 7 days), immunoglobulin therapy (10 g per day for 5 days), and antipsychotic drug treatment, the neurological and mental abnormalities were greatly ameliorated. He was discharged with mild irritability, slight shaking of the hands, and walking fatigue.

This is the first case involving neural system injury in a patient who confirmed COVID-19 based on CSF antibody test results. Negative ribonucleic acid test results, strong positivity for antibodies, and high protein levels in the CSF suggest the possibility of autoimmune encephalitis secondary to COVID-19. This case highlights additional novel symptoms of COVID-19, and these data are important for the assessment and follow-up of COVID-19 patients.