Great review of neuropathogenesis and neurologic manifestations of #covid19 published in JAMA Neurology on May 29 by @SpudichLabYale (THREAD, 1/10) 
How does #sarscov2 get into the CNS? ACE2 receptors are expressed in multiple regions & on multiple cels of the human brain. (2/10)
Viral invasion of the CNS could happen in one of three ways. Nr 1: via the olfactory nerve (i.e., the transcribrial route). Olfactory nerve infection could also explain the common findings of loss of smell (anosmia) and loss of taste (ageusia). (3/10)
However, olfactory sensory neurons do not express ACE2, suggesting that #sarscov2 cannot gain access to nerve cells through this route. Damage to olfactory epithelium more likely to cause anosmia. To be investigated... (4/10)
Mechanism of CNS entry–Nr 2: via endothelial cells, then passed on to glial cells. (5/10)
Mechanism of CNS entry–Nr 3: the “Trojan Horse“ mechanism where infected leukocytes, which also express ACE2, cross the blood brain barrier into the CNS. (6/10)
Common CNS-related manifestations of #covid19 include: headache likely via neuroinflammatory mechanisms mediated by cytokines and chemokines that trigger nociceptive sensory neurons. (7/10)
Other common manifestations of #covid19: anosmia & ageusia. Present in 5.1-5.6% (Wuhan), 19.4% (Italy), 79.7% (Germany). (8/10)
Another common manifestation: impaired consciousness (est. 37% of hosp pts). Likely mediated through one of several mechanisms: toxic-metabolic encephalopathy, encephalitis, exacerbated by electrolyte disturbances, kidney or liver disease. (9/10)
Also common manifest: stroke (5% of hosp pts). Usually accompanied by elevated inflammatory markers and hypercoagulability. More common in older age but young pts also at risk. (10/10)
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