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 – just click on the headings below to go to the relevant section.
We know that SARS-Cov-2 is a non-segmented positive-sense RNA virus. It is a Betacoronavirus of the family Coronaviridae, belonging to the order Nidovirales. Bats are possibly its natural host. It uses the angiotensin converting enzyme (ACE2) receptor for cell entry.
We know that SARS-Cov-2 is transmitted by droplets at close contact. It can also be spread via contaminated surfaces, and by the faeco-oral route.
We know that the incubation period for SARS-Cov-2 is usually 3-7 days, with a typical range of 1-14 days. In some cases, the incubation period has been as long as 24 days.
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 also know that SARS-COv-2 causes central nervous system autoimmune disorders such as central nervous system vasculitis and anti-NMDAR autoimmune encephalitis.
11. Olfactory and gustatory impairment
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.
We know that headache is the presenting feature of SARS-Cov-2 infections in 6-10% of cases, and it may affect the whole head or be localised to one side, or to the occipital (back) region. We now know that the headache may be worsened by physical exertion and head movements, and it responds poorly to analgesics. People who wear personal protective equipment are also at risk of what is now known as PPE headache.
13. MRI brain signal abnormalities
We know that SARS-Cov- 2 infection can give rise to high signal changes in various parts of the brain. These white matter hyperintensities have been reported in the medial temporal lobe, thalamus, globus pallidum, and corpus callosum.
We now know that SARS-Cov-2 can affect the muscles, presenting as myalgia (muscle aches), and an elevation of the level of the muscle enzyme creatinine kinase. SARS-COv-2 may also cause rhabdomyolysis, severe muscle breakdown that could threaten kidney function. It is thought that the muscle manifestations of SARS-Cov-2 are a result of necrotizing autoimmune myositis (NAM). In people admitted to the intensive care unit, there is at least one report of critical illness myopathy.
We are almost certain now that SARS-Cov-2 does not cause Guillain Barre syndrome (GBS). Whilst there are countless case reports of COVID19 associated with GBS, as well as its variant Miller Fisher syndrome (MFS), there is a clear sense that the incidence is not higher than it would have been had SARS-Cov-2 never reared its head. It is therefore possible that the association is correlative rather than causative. The same goes for reports of SARS-Cov-2 with peripheral neuropathy, neuralgic amyotrophy, and myasthenia gravis (MG). It is also reassuring that GBS is not a consequence of vaccination for COVID19.
16. COVID vaccine complications
We know that the COVID vaccines cause neurological complications, the most significant being cerebral vein thrombosis (CVT). This develops 5-24 days after vaccination, and it is associated with adenovirus vector vaccines. It is often the result of vaccine induced thrombotic thrombocytopenia (VITT), and this is caused by antibodies to platelet factor 4 (PF4). Treatment includes various forms of anticoagulation and immunomodulation. COVID vaccination may also rarely manifest with other neurological complications such as dizziness and headache, and systemic complications such as myocarditis and thrombosis.
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