iarjcrIARJCRIARJCR2789-6064https://doi.org/10.47310/iarjcr.2022.v02i02.005The Spectrum of Neuro-COVID is Broader than PresumedJosefFinstererFulvioAScorzaNeurology & Neurophysiology Center, Postfach 20, 1180 Vienna, AustriaDepartment of Neuroscience. University of Sao Paolo (UNIFESP/EPM). Sao Paulo, BrazilWe read with interest the review article by Wan et al. about the neurological complications of COVID-19 and its mechanisms of infection by SARS-CoV-2 [1]. It was concluded that SARS-CoV-2 may enter the brain via pathways other than invasion of the olfactory nerve, inflammatory responses disrupting the blood-brain-barrier (BBB), or infection of vascular endothelial cells [1]. The study is appealing but raises concerns and comments. The main shortcoming of the review is that the number of neurological complications after SARS-CoV-2 infections is incomplete. The authors did not consider various central nervous system (CNS) disorders, such as cerebellitis, ventriculitis, cerebral vasculitis, giant cell arteritis, transverse myelitis, optic neuritis, hypophysitis, cerebral vasoconstriction syndrome, pontine myelinolysis, and venous sinus thrombosis (VST) as manifestations of neuro-COVID. Missing are also some manifestations of neuro-COVID in the peripheral nervous system (PNS), such as cranial neuritis, myasthenia, myasthenic syndrome, and Parsonage-Turner syndrome. The various pathophysiological models according to which the virus allegedly enters the brain are nice but unsupported by real world data. For example, in almost all patients with SARS-CoV-2 associated GBS, SARS-CoV-2 could not be detected within the cerebro-spinal fluid (CSF) [2], suggesting that the virus not necessarily needs to invade the CNS to cause CNS damage. We do not agree with the statement that “cerebro-vascular disease is characterised by damage to brain tissue due to intra-cranial blood circulation disturbances” [1]. Cerebro-vascular disease may also derive from damage to extra-cranial arteries, from cardiac abnormalities, and even from disease of the peripheral veins in case of a patent foramen ovale. The cardiac origin of cerebro-vascular disease is crucial to encounter as the heart can be affected by the SARS-CoV-2 infection as well and may secondarily lead to cerebro-vascular disease. Cardiac abnormalities that have been reported in SARS-CoV-2 infected so far include endocarditis, which is usually secondary due to infectious agents other than SARS-CoV-2, myocarditis, which is usually immune-mediated and responds to immune-suppressive treatment [3], and Takotsubo syndrome, a stress-related transient heart failure. All these conditions may be complicated by intra-ventricular thrombus formation and thus a risk of cardio-embolism.