Update on Neurological Manifestations of SARS-CoV-2

Abstract

Severe acute respiratory syndrome coronavirus 2, the source of COVID-19, causes numerous clinical findings including respiratory and gastrointestinal findings. Evidence is now growing for increasing neurological symptoms. This is thought to be from direct in-situ effects in the olfactory bulb caused by the virus. Angiotensin-converting enzyme 2 receptors likely serve as a key receptor for cell entry for most coronaviridae as they are present in multiple organ tissues in the body, notably neurons, and in type 2 alveolar cells in the lung. Hematogenous spread to the nervous system has been described, with viral transmission along neuronal synapses in a retrograde fashion. The penetration of the virus to the central nervous system (CNS) allows for the resulting intracranial cytokine storm, which can result in a myriad of CNS complications. There have been reported cases of associated cerebrovascular accidents with large vessel occlusions, cerebral venous sinus thrombosis, posterior reversible encephalopathy syndrome, meningoencephalitis, acute necrotizing encephalopathy, epilepsy, and myasthenia gravis. Peripheral nervous system effects such as hyposmia, hypogeusia, ophthalmoparesis, Guillain-Barré syndrome, and motor peripheral neuropathy have also been reported. In this review, we update the clinical manifestations of COVID-19 concentrating on the neurological associations that have been described, including broad ranges in both central and peripheral nervous systems.