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COVID19 and the brain
Acute symptoms of COVID19 act on the lung, but with time many other organs become involved. Increasing evidence suggests that COVID19 causes both acute and chronic neurological[1] or psychological symptoms[2]. These symptoms result from multiple different factors. Coronavirus-2 (CoV-2) directly infects olfactory neurons (smell) and nerve cells expressing taste receptors. Although these cells communicate directly with the brain, the virus does not exhibit strong infection of other nerve cells in the central nervous system. Many of the neurological sequelae appear to result from damage to the vascular cells of the brain or from damage resulting from hypoxia (i.e., limitations in the oxygen supply for the brain). Chronic effects of COVID19 can lead to a prolonged inflammatory state, which can increase symptoms resembling an autoimmune disorder [1]. Many patients with COVID19 experience psychological symptoms that can arise either from the direct actions of the virus, the chronic increase in inflammation or secondary effects, such as post-traumatic stress disorder [2].
Acute Effects of COVID19 on the Brain
Epidemiology
It is important to note that only about 20% of patients who are infected with Coronavirus-2 (CoV-2) exhibit the clinical syndrome, known as COVID19 [1]. About 35% of patients appear to have some type of neurological complication [3][1]
Symptoms:
Loss of taste, smell. Roughly 81% of patients with clinical COVID19 experience disorders of disorders of smell (46% anosmia,
29% hyposmia, and 6% dysosmia) [1]. Similarly for taste, disorders of taste occur in 94% of patients (ageusia 45%, hypogeusia 23%, and dysgeusia
26%) [1]. Importantly, most patients recover their sense of taste or smell within 8 days [1].
headache, nausea, vomiting, impaired consciousness, encephalitis and acute cerebrovascular disease including stroke, venous sinus
thrombosis and intracerebral haemorrhage [1][4]. Encephalopathy is more common in patients with severe disease [1].
Several cases of necrotizing encephalitis have been reported, but such cases are rare [1].
Increasing attention is being given to children with COVID19 who develop Kawasaki disease, which is a multi-system inflammatory syndrome that also cerebrovascular disease and neurologic involvement [1].
Cerebrovascular accidents (e.g., stroke) are reported in up to 5% of hospitalized patients, and occur in both old and young patients
Guillain–Barre Syndrome, acute myelitis and encephalomyelitis have been reported. The cases of myelitis could arise from direct infection of muscle via local Ace2 [4].
Reported prevalence of mental health disorders vary depending on the study. In one review, anxiety, depression, insomnia and distress are reported in up to 35% patients had mild, and 13% of patients had moderate to severe psychological symptoms[3]. Another review reports frequencies of depression and anxiety of 47% and 37% [2]. These psychological symptoms correlate with blood based biomarkers, such as C-reactive protein, which is an inflammatory protein.
Medical Tests
Etiology/Mechanisms
PCR can detect CoV-2 in the brain and cerebrospinal fluid (CSF) acutely, and is thought to enter via the olfactory system. Cranial nerve (including facial nerve and vagus nerve, which mediate taste) provides an additional route of entry [4].
Endothelial cell infection (hematogenous route) putatively shown by EM, but EM is not as definitive as PCR [4].
Infected immune cells from lungs and other sites provide an additional source of entry
Cytotoxic autoimmune based antibodies against CoV-2 have been observed in COVID19 patients with encephalitis [4]
Therapeutic Approaches
Chronic Effects of COVID19 on the Brain
Epidemiology
Symptoms
Post-infectious complications of COVID19 can include Guillain-Barre Syndrome, which presents as bilateral multi-limb flaccid weakness with areflexia; sometimes this also presents with facial weakness [1].
Medical Tests
Etiology/Mechanisms
Increasing evidence suggests that COVID19 causes chronic disruption of the neurovascular unit, leading to leakage of plasma into the brain, which damages neurons.
Therapeutic Approaches
Neuropathology:
The most common observations are hypoxic damage, which is attributable to use of ventilators. However, many patients who died exhibited perivascular T cells (55%) and microglial cell activation (50%) [3].
References
- ^ a b c d e f g h i j k l Koralnik, Igor J.; Tyler, Kenneth L. (2020). "COVID ‐19: A Global Threat to the Nervous System". Annals of Neurology. 88 (1): 1–11. doi:10.1002/ana.25807. ISSN 0364-5134. PMC 7300753. PMID 32506549.
{{cite journal}}: CS1 maint: PMC format (link) - ^ a b c Hossain, Md Mahbub; Tasnim, Samia; Sultana, Abida; Faizah, Farah; Mazumder, Hoimonty; Zou, Liye; McKyer, E. Lisako J.; Ahmed, Helal Uddin; Ma, Ping (2020-06-23). "Epidemiology of mental health problems in COVID-19: a review". F1000Research. 9: 636. doi:10.12688/f1000research.24457.1. ISSN 2046-1402. PMC 7549174. PMID 33093946.
{{cite journal}}: CS1 maint: PMC format (link) CS1 maint: unflagged free DOI (link) - ^ a b c Mukerji, Shibani S.; Solomon, Isaac H. (2021). "What can we learn from brain autopsies in COVID-19?". Neuroscience Letters. 742: 135528. doi:10.1016/j.neulet.2020.135528. ISSN 1872-7972. PMC 7687409. PMID 33248159.
- ^ a b c d e Al‐Sarraj, S.; Troakes, C.; Hanley, B.; Osborn, M.; Richardson, M. P.; Hotopf, M.; Bullmore, E.; Everall, I. P. (2021). "Invited Review: The spectrum of neuropathology in COVID‐19". Neuropathology and Applied Neurobiology. 47 (1): 3–16. doi:10.1111/nan.12667. ISSN 0305-1846.