Neurological Manifestations of COVID-19

By Dr. Mohammed M. Al-Qasmi, Neurologist

It’s been over a year since COVID-19 has been declared in the United States. 30 million plus people have been infected with the virus, and over 550,000 deaths nationwide. In Genesee county thus far we have we have over 28,000 confirmed cases with over 770 fatalities, this disease is no joke. The disease itself varies significantly in terms of symptoms and severity. The fatality also is quite variable amongst age groups ranging from 0.3 deaths per 1000 cases among patients aged 5 to 17 years to 304.9 deaths per 1000 cases among patients aged 85 years or older in the US. The disease commonly causes pneumonia and upper respiratory tract infections however Neurological symptoms have been commonly seen as well. It has been reported in up to 40% of COVID positive patients. Encephalopathy of some sort has commonly been described. Pooled prevalence of neurological manifestations are as follows; smell disturbances (35.8%), taste disturbances (38.5%), myalgia (19.3%), headache (14.7%), dizziness (6.1%), and syncope (1.8%). Pooled prevalence of acute cerebrovascular disease was (2.3%), of which majority were ischaemic stroke (2.1%), followed by haemorrhagic stroke (0.4%), and cerebral venous thrombosis (0.3%; 95% CI 0.1-0.6).  Guillain Barre Syndrome has also been reported.

Interestingly, it has been noted that most neurological manifestations occurred early on in the disease which may pose to be an important early predictor of future clinical deterioration. In a retrospective series by Chen et al from the city of Wuhan described that confusion (9%) and headache (8%) were symptoms reported by such patients with COVID infections; importantly however, neurological complaints were significantly less prevalent than the typical respiratory symptoms of cough (82%) and dyspnoea (31%).  More significant and potentially long lasting neurological complications of the disease were highlighted by Li et al in a study of 221 patients, and 6% developed severe neurological disease: ischaemic stroke, haemorrhage of cerebral vein thrombosis, of which a significant proportion died as a result. 

Current published studies have suggested that neurological involvement in the pathogenesis of COVID-19 does seem to be associated with a more “severe” infection and subsequent mortality. However currently, no direct cause and effect have been attributed to neurological deterioration in patients with COVID-19 and this relationship could just as plausibly be explained by association with other multi-organ system failures. The direct effect on mortality and morbidity in such “neurological involving” patients is yet to be elucidated.

It has been proposed that COVID-19, like other viruses such as avian influenza, can infiltrate the mammalian brainstem via trans-synaptic transfer which can lead to dysfunction of the cardiorespiratory centres of brainstem. It has therefore been suggested that CNS infiltration of the virus may explain the deterioration of some patient’s respiratory effort and their subsequent need for ventilation. Hence, close and serial neurological observations as an adjunct to routine serial observations may prove to be an early warning marker of impending deterioration. This of course needs further study


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