Intro: COVID-19 has been associated with neurological manifestations such as headaches, insomnia, and strokes. However, it is unclear if COVID-19 directly attacks the CNS or if it is the body’s response to the virus. Experiments were conducted to address this issue. Study: by the New England Journal of Medicine in Boston, MA. Sample: 18 patients who died at a single teaching hospital from April 14, 2020, to April 29, 2020. All patients were positive for SARS-CoV-2. Fourteen out of eighteen (14/18) patients were males. Neurologic symptoms include myalgia (n=3), headaches (n=2), and decreased sense of taste (n=1). Comorbidities include Diabetes Mellitus (n=12), hypertension (n=11), cardiovascular disease (n=5), hyperlipidemia (n=5), chronic kidney disease (n=4), prior stroke (n=4), dementia (n=4), and treated anaplastic astrocytoma (n=1). Eleven patients were placed on mechanical ventilation. Method: Used Neuropathological methods that combine immunochemistry techniques, Reverse transcriptase PCR (RT-qPCR) to examine postmortem tissue. Results: Neuropathological analysis of brain tissue showed hypoxic injury in the cerebellum in all patients. The analysis also showed the loss of neurons in the cerebral cortex, hippocampus, and cerebral Purkinje cell layer. There were no thrombi or vasculitis detected in these areas. However, immunochemistry and RT-qPCR showed minimal traces of SARS-CoV-2 in the brain. There were two rate foci of perivascular lymphocytes detected in n=2 brains.
Focal leptomeningeal inflammation was detected in n=1 of the brains. The study concluded that hypoxic changes in the brain are attributed to patient-specific comorbidities or secondary effects of the virus.