impact of the covid-19 pandemic on neurological, psychological and other mental health outcomes impact of the covid-19 pandemic on neurological, psychological and other mental health outcomes there is increasing evidence suggesting that covid-19 causes both acute and chronic neurological or psychological symptoms. caregivers of covid-19 patients also show a higher than average prevalence of mental health concerns. these symptoms result from multiple different factors. for an associated topic, see mental health during the covid-19 pandemic. part of a series on thecovid-19 pandemicscientifically accurate atomic model of the external structure of sars-cov-2. each "ball" is an atom. covid-19 (disease) sars-cov-2 (virus) cases deaths timeline 2019 2020 january responses february responses march responses april responses may responses june responses july responses august responses september responses october responses november responses december responses 2021 january responses february 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football ice hockey motorsport rugby league impacts animals black people crime death rates by country disability domestic violence emergency evacuations education female environment hospitals language lgbt community long-term care media coverage mental health symptoms migration military notable deaths other health issues politics diplomacy popular culture protests pregnancy prisons religion catholic church hajj science and technology social media strikes suicides telehealth xenophobia and racism society ireland malaysia new zealand russia uk us covid-19 portal sars-coronavirus-2 (sars-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 covid-19 can lead to a prolonged inflammatory state, which can increase symptoms resembling an autoimmune disorder. many patients with covid-19 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. sars-cov-2 can be detected in the brain and cerebrospinal fluid (csf) acutely by pcr, 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. sars-cov-2 has been detected in endothelial cells by electron microscopy, although such a method provides evidence that demonstrates the presence of the virus, but does not convey the amount of virus that is present (qualitative rather than quantitative). acute covid-19 neurologic symptoms the fraction of subjects who experience symptoms following an infection with sars-cov-2 varies by age. between 10 and 20% of patients who are infected with sars-cov-2 generally exhibit the clinical syndrome, known as covid-19. the number of covid-19 infections are highest in subjects between ages 18–65, while the risk of severe disease or death jumps after age 50 and increases with age. about 35% of patients with symptoms of covid-19 experience neurological complications. neurological symptoms are not unique to covid-19; infection with sars-cov-1 and mers-cov also give rise to acute and delayed neurological symptoms including peripheral neuropathy, myopathy, guillain–barré syndrome and bickerstaff brainstem encephalitis. the influenza pandemic of 1918 was well known for producing post-viral parkinsonism, which was memorialized in the writings of oliver sacks and the movie awakenings. loss of the sense of taste or smell are among the earliest and most common symptoms of covid-19. roughly 81% of patients with clinical covid-19 experience disorders of smell (46% anosmia, 29% hyposmia, and 6% dysosmia). disorders of taste occur in 94% of patients (ageusia 45%, hypogeusia 23%, and dysgeusia 26%). most patients recover their sense of taste or smell within 8 days. delirium is also a common manifestation of covid-19 infection, particularly in the elderly. recent evidence from a longitudinal study supports an inflammatory basis for delirium. many patients with covid-19 also experience more severe neurological symptoms. these symptoms include, headache, nausea, vomiting, impaired consciousness, encephalitis, myalgia and acute cerebrovascular disease including stroke, venous sinus, thrombosis and intracerebral hemorrhage. increasing attention has focused on cerebrovascular accidents (e.g., stroke), which are reported in up to 5% of hospitalized patients, and occur in both old and young patients. guillain–barré syndrome, acute myelitis and encephalomyelitis have also been reported. guillain–barré syndrome arises as an autoimmune disorder, that leads to progressive muscle weakness, difficulty walking and other symptoms reflecting reduced signaling to muscles. the cases of myelitis could arise from direct infection of muscle via local angiotensin-converting enzyme 2, the receptor for sars cov-2. covid-19 can also cause severe disease in children. some children with covid-19 who develop kawasaki disease, which is a multi-system inflammatory syndrome that also cerebrovascular disease and neurologic involvement. disorders of smell (olfaction) and taste (gustation) as mentioned above, many covid-19 patients suffer from disorders of taste or smell. 41% to 62% of patients (depending on the particular study) have disorders of the sense of smell (olfaction), which can present as anosmia (loss of olfaction), hyposmia (reduced olfaction) or parosmia (distortion of olfaction). however, loss of olfaction is not unique to covid-19; approximately 13% of patients with influenza also lose olfaction, as do patients with mers-cov and ebola virus. among the patients with covid-19, 50% of patients recover olfaction within 14 days, and 89% of patients have complete resolution of their loss of olfaction within 4 weeks. only 5% of covid-19 patients experience a loss of olfaction lasting more than 40 days. structure of the olfactory epithelium. sars-cov-2 infects the support cells (sustentacular cells), which injures the olfactory neurons in the olfactory epithelium leading to loss of smell. new olfactory neurons regenerate from the basal cells. the sars-cov-2 virus appears to attack the sustentacullar cells (also referred to as "support cells"), which are the cells that surround and support olfactory receptor neurons. little if any virus directly infects the olfactory receptor neurons themselves. however, sars-cov-2 infection of the sustentacullar cells can lead to desquamation (shedding) of the olfactory epithelium, with collateral loss of olfactory receptor neurons and anosmia. however, the olfactory epithelium is continually regenerated, and neurons that are damaged are typically replaced in about 14 days. the nerve cells controlling taste, termed the gustatory nerve cells, turn over even faster, being renewed in about 10 days. clinical help exists for patients experiencing disorders of olfaction. patients who experience of loss of smell for longer than two weeks are recommended to obtain olfactory training. olfactory training helps to "teach" the new olfactory neurons how to link with the brain so that odors can be noticed and then recognized. personal accounts of the process of olfactory training post covid-19 infection have been covered in media outlets such as the new york times. patients experiencing loss of smell for more than 2 weeks are also recommended to obtain a referral to an ear nose and throat (ent) physician. oral corticosteroid therapy can help, but is optional. alpha-lipoic acid is another remedy that has been proposed, but the accumulated literature on this suggests that it does not improve symptoms or recovery. chronic covid-19 neurologic symptoms main article: long covid impact of covid-19 on neurological and psychiatric outcomes in the subsequent 6 months compared with other respiratory tract infections this section is an excerpt from long covid § epidemiology. estimates of the prevalence of long covid vary widely. the estimates depend on the definition of long covid and the population studied. an april 2022 meta-analysis estimated that the pooled prevalence of post-covid conditions was 43%, with estimates ranging between 9% and 81%. people who had been hospitalised with covid saw a higher prevalence of 54%, while this number dropped to 34% for nonhospitalised people. prevalence generally decreased with a longer follow-up time. in people age 0–18 years the prevalence of long covid conditions – like mood symptoms, cfs and sleep disorders – appears to be at ~25% overall. in a large population cohort study in scotland, 42% of respondents said they had not fully recovered after 6 to 18 months after catching covid, and 6% indicated they had not recovered at all. the risk of long covid was associated with disease severity; people with asymptomatic infection did not have increased risk of long covid symptoms compared to people who had never been infected. those that had been hospitalised had 4.6 times higher odds of no recovery compared to nonhopitalised people. in june 2022, a cdc study based on electronic health records showed that "one in five covid-19 survivors aged 18–64 years and one in four survivors aged ≥65 years experienced at least one incident condition that might be attributable to previous covid-19" or long covid. an analysis of private healthcare claims showed that of 78,252 patients diagnosed with 'long covid', 75.8% had not been hospitalized for covid-19. a study of 236,379 covid-19 survivors showed that the "estimated incidence of a neurological or psychiatric diagnosis in the following 6 months" after diagnosed infection was 33.62% with 12.84% "receiving their first such diagnosis" and higher risks being associated with covid-19 severity. neuroinflammation as a result of viral infection (e.g., influenza, herpes simplex, and hepatitis c) has been linked to the onset of psychiatric illness across numerous publications. coronavirus infections are defined as neurotropic viral infections (i.e., they tend to target the nervous system) which increases the risk of neuroinflammation and the induction of immune system dysfunction. psychotic disorders are characterized by neuroinflammation, more specifically maternal inflammation, and abnormally high mesolimbic dopamine (da) signaling. excess inflammation following a covid-19 infection can alter neurotransmitter signaling which contributes to development of psychotic and mood related disorders. a large study showed that post covid-19, people had increased risk of several neurologic sequelae including headache, memory problems, smell problems and stroke; the risk was evident even among people whose acute disease was not severe enough to necessitate hospitalization; the risk was higher among hospitalized, and highest among those who needed icu care during the acute phase of the infection. about 20% of covid-19 cases that pass through the intensive care unit (icu) have chronic neurologic symptoms (beyond loss of smell and taste). of the patients that had an mri, 44% had findings upon mri, such as a flair signal (fluid-attenuated inversion recovery signal), leptomeningeal spaces and stroke. neuropathological studies of covid-19 victims show microthrombi and cerebral infarctions. 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%). guillain–barre syndrome occurs in covid-19 survivors at a rate of 5 per 1000 cases, which is about 500 times the normal incidence of 1 per 100,000 cases. a related type of autoimmune syndrome, termed miller-fisher syndrome, also occurs. covid-19 patients who were hospitalized may also experience seizures. one paper suggests that seizures tend to occur in covid-19 patients with a prior history of seizure disorder or cerebrovascular infarcts, however no