There is increasing evidence of the neurotropic and neuroinvasive nature of SARS-CoV-2.
Taxonomically similar viruses like SARS and MERS were associated with neuropsychiatric symptoms.
SARS-CoV-2 has 96% genomic sequence homology with a bat CoV found in a cave in Yunnan province, China (which does not infect humans) – raising the possibility that the virus originated in bats. However, the infectious nature indicates another intermediate host which has not been identified.
SARS-CoV-2 uses the ACE2 receptor for entry. The ACE2 receptor is found in many organs in the body (eyes, nose, kidneys, liver, brain, endothelium, lungs) and this likely contributes to the multiorgan involvement in COVID.
Dysregulation of the ACE2 receptor leads to inflammation, fibrosis and vasoconstriction.
Another core feature of the illness is hypercoagulability.
The virus entry in the brain is through a number of direct and indirect mechanisms
1. Olfactory network
2. Medullary respiratory network
3. Enteric nervous system
Indirect mechanisms include
1. Myeloid cell trafficking (Trojan horse mechanisms)
2. Cytokine storm
3. Neuroinflammation
4. Gut-brain translocation
CNS manifestations include
1. Encephalopathies
2. Meningoencephalitis
3. Psychiatric disorders – host immune response and psycho-social factors
4. Peripheral NS disorders – e.g GBS, neuropathy
5. Myopathies
6. Anosmia and Ageusia
We discuss the role of the psychiatrist in more detail, taking a bio-psychosocial perspective.
We cover management principles for psychiatrists based on currently available treatments. Drug interactions with antiretrovirals, steroids and N-P side effects of Interferon, Chloroquine and Hydroxychloroquine are discussed.
COVID-19 challenges the mind-body dichotomy. Psychiatrists will play an important role in bridging the gap by addressing the short and long term biological, psychological and social consequences of the condition. A truly multidisciplinary effort is required.
