As the dust clears, and the froth settles, the picture of how COVID 19 impacts the nervous system is taking form. As eager neuroscientists track down case reports and carry out surveys, gently winnowing out the chaff from the wheat, a clearer picture is beginning to emerge. As the neurological cartographers map the path of SARS-Cov-2 in the brain, and pin its locations in the nerves and muscles, we are learning a lot about how it inflicts its terror on the nervous system. We don’t have all the answers yet, but the sinister machinations of one of the most aggressive viruses nature has ever unleashed are unravelling.
A lot has changed since we published our first checklists on COVID19. Then, we had only four checklists on a puzzling infection which was shrouded in uncertainty. Then, the landscape was riddled with rapidly churned-out case reports, and the expert opinions were just that…opinions. But now, with more reliable data from dependable studies, and with more verifiable case reports, the mist is clearing. We have therefore thoroughly revised and updated our COVID19 checklists, inevitably increasing the number of checklists from 4 to 12. With some degree of certainty and confidence, here are 15 things we now know about COVID-19 and the nervous system. You don’t have to memorise these – all the information and references are accessible from Neurochecklists.
We know that the respiratory system is the major target organ of SARS-Cov-2, causing cough, shortness of breath, chest pain, and, in severe cases, acute respiratory distress syndrome (ARDS). Less common respiratory features are sore throat, rhinorrhoea (running nose), sputum production, wheezing, and pneumothorax (air around the lungs).
We know that SARS-Cov-2 can infect almost any organ in the body, causing such severe disorders as acute myocardial infarction, multi-organ failure, and a Kawasaki-like disease in children called multisystem inflammatory syndrome in children (MIS-C). Conjunctivitis, various skin rashes, abnormal clotting, autoimmune anaemia, and low sodium are amongst its many other systemic manifestations.
We know that SARS-Cov-2 is a cause of ischaemic stroke. The incidence is 1.4%, in people who get COVID19. We also now know that it is the result of large vessel occlusion frequently involving the vertebrobasilar territory (the large blood vessels supplying the back of the brain). The pathology is called a thrombotic microangiopathy, and this results from endotheliopathy (abnormality of the inner lining of the blood vessels). We also know that COVID19 stroke is associated with elevated d-dimer levels of ≥1000μg/L. Thrombolysis (clot busting) treatment has also been reported to be safe and effective in COVID19 stroke.
We know that SARS-Cov-2 results in a myriad of haemorrhagic (bleeding) brain lesions, from intracerebral haemorrhage (ICH) and subarachnoid haemorrhage (SAH), to subdural haematoma (SDH) and intraventricular haemorrhage (IVH). SARS-Cov-2 has also been reported to cause haemorrhagic posterior reversible encephalopathy syndrome (PRES), haemorrhagic venous infarction, and anticoagulation related haemorrhage.
We know that COVID causes direct infection of the brain manifesting as meningoencephalitis, steroid-responsive encephalitis, and post-infectious brainstem encephalitis.
We know that SARS-Cov-2 causes a wide range of inflammatory brain lesions, and these include COVID encephalopathy, acute disseminated encephalomyelitis (ADEM), and tumefactive demyelination.
We know that SARS-Cov-2 frequently impairs the senses of smell and taste. We know that smell and taste are both affected in more > 50% of COVID19 cases, and this occurs within 4 days of infection. We also know that taste impairment may manifest as the complete loss of taste, or alteration of taste to metallic, bitter, or salty. Most people will recover their taste and smell, but smokers are less likely than non-smokers to do so.
There is more to SARS-COv-2 and the nervous system; for a practical handle on these, and everything else neurological, check out Neurochecklists.com.