COVID-19 may be related to spontaneous psychosis. Researchers try to find out why

In May 2020, a 33-year-old mother of three in North Carolina began developing symptoms of COVID-19. Four days later, another set of symptoms arose. She stopped sleeping well and developed paranoid delusions that people were following her on her cell phone – culminating in a hectic scene at a fast food restaurant, where she tried to pass her. children through the drive-through window, where they would be safe from the phones and other hazards.

A restaurant worker called 911 and emergency medical services arrived, gathered the family and rushed to the nearby emergency department of Duke University Medical Center in Durham, where the mother was quickly cared for by doctors. “She was physically in the room, but she wasn’t making consistent eye contact,” says Dr. Colin Smith, who is now the chief resident of the hospital’s internal psychiatry program but was a sophomore when he cared for the patient. “She wasn’t really exciting at all. Her thought processes were disorganized.”
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Despite this, the patient acknowledged two things to Smith and the other doctors: She knew her behavior was not right for her, and the changes all happened soon after she was diagnosed with COVID-19.

There is growing evidence that COVID-19 and new psychotic episodes are linked. The case in North Carolina, reported in the British medical journal in August 2020, joins a slew of case reports published in medical journals during the pandemic describing psychotic episodes following a COVID-19 diagnosis. In the July 2020 issue of BJPsyh Open, researchers reported that a 55-year-old woman in the UK, with no history of mental illness, arrived at a hospital days after she had recovered from a severe case of COVID-19 with delusions and hallucinations, convinced the nurses were fiends in disguise and that monkeys jumped out of doctors’ bags. In April 2021, other researchers submitted: BMJ Case Reports of a middle-aged British man, also with no previous mental illness, who had appeared in a London hospital having auditory and visual hallucinations and banging his head against walls until he bruised his skin. (Weeks earlier, he had recovered from a COVID-19 attack that had sent him to intensive care.) In yet another case, published in the Journal of Psychiatric Practice In March 2021, a 57-year-old man showed up at Columbia University’s New York Presbyterian Hospital and claimed that his wife poisoned him, that cameras were placed throughout his apartment, and that patients in the hospital’s emergency department were secretly were treated. murdered.

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“The situation was strikingly similar to one we would expect for someone with a schizophrenia spectrum disease,” said Dr. Aaron Slan, now a fourth-year psychiatry resident at Columbia University who cared for the patient and co-authored the report. . † But this patient, too, had no history of mental illness and was too old for a first case of schizophrenia, which usually occurs between the ages of 20 and 30 for men, Slan notes. What the patient did have, a hospital test showed, was COVID-19.

COVID-19-related psychotic interruptions are rare — although researchers say it’s too early to say exactly how rare — and many experts believe the link between the two conditions, if any, is not causal. In a review published in Neurological Letters in 2021, a group of researchers in the UK cast doubt on emerging body of work on the COVID-19 psychosis link as “suffering from both a small sample size and insufficient consideration of potential confounding factors, such as increased stress, substance abuse, and socioeconomic problems.

Still, researchers are investigating the link. A British study published in the Lancet in October 2020, they found that of the 153 people diagnosed with COVID-19 early in the pandemic, 10 suffered new psychotic episodes after their COVID-19 diagnosis, and seven had the onset of psychiatric disorders, including catatonia and mania.

A study published last August in General hospital psychiatry took a broad look at the phenomenon, analyzed 40 scientific papers, including 48 adults from 17 different countries who suffered from psychotic episodes related to COVID-19 infection, and tried to find similarities between them. As with the Neurological Letters paper, the authors of this study found numerous other variables that could obscure the link between COVID-19 and psychosis, such as stress, substance use, and medications, but the relationship persisted.

“We see post-infectious neuroinflammatory disorders associated with a variety of different viral diseases,” said Dr. Samuel Pleasure, a professor of neurology at the University of California, San Francisco (UCSF). “Normally we see it in very small numbers, but here we have [COVID-19] infect tens of millions of people at once.” Even rare cases of psychiatric disorders will begin to manifest when the sample of infected people is so large.

There are currently more questions than answers. It is still unclear whether the severity of the COVID-19 symptoms plays a role in the likelihood of a psychotic break. “There clearly seem to be cases of neuropsychiatric sequelae of COVID linked to cases that are not severe,” Pleasure says. “I believe the quality of the studies right now is so preliminary, and the ability to really commit these patients to study is really early on, so it’s hard to be definitive.” Likewise, Pleasure says, it’s impossible to say whether people suffering from Lung COVID — symptoms that last for months after the infection is over — are more prone to psychotic symptoms.

There are multiple possible mechanisms at work, each of which – or a combination – could contribute to the neuropsychiatric symptoms associated with COVID-19. The most obvious would be direct infection of brain tissue itself, Pleasure said. If so, the number of COVID-19 patients with loss of taste and smell would indicate that the brain’s olfactory bulb may be the first to be affected by the virus.

“There are documented cases where people early in the [COVID-19 disease] process and have seen some local inflammation in the olfactory bulb,” Pleasure says. “That further contributed to the idea that maybe that’s the gateway. Once that portal is breached, the brain in general can be exposed.”

How the COVID-19 infection reaches the brain is unclear, but Pleasure and his colleague Dr. Michael Wilson, an associate professor of neurology at UCSF, performed lumbar punctures on three teens with COVID-19 who had developed neuropsychiatric symptoms to examine their cerebrospinal fluid. In two cases, they found antibodies in the fluid that target neural antigens. That presented an apparent puzzle: the patients had SARS-CoV-2; if anything, they should show antibodies to the virus, not their own neural tissue. But Pleasure cites a study he conducted with a group from Yale University showing that antibodies specific for the coronavirus spike protein also cross-react with and attack nerve cells as well.

“There was molecular mimicry between the spike protein and a neural antigen,” he says. “One of the main hypotheses is that if there’s an antibody that targets the virus, you’re unlucky to see damage to the host as well.” In other words, he says, you start with an immune response that’s adapted to fighting the virus, and that turns into an autoimmune response.

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That’s just one theory. There are other routes by which COVID-19 can affect the brain. Upper respiratory infections can sometimes cause the immune system to become dysregulated and develop antibodies against parts of the brain known as NMDA (N-methyl-D-aspartate) receptors, the main excitatory receptors that respond to neurotransmitters . A broad attack on receptors scattered throughout the brain can lead to rapid and severe symptoms, says Dr. Mudasir Firdosi, a Consultant Psychiatrist with the Kent and Medway NHS and Social Care Partnership Trust and a co-author of the 2021 BMJ paper.

†[NMDA involvement] presents a very, very flowery way of being psychotic,” says Firdosi. Slan agrees, “When someone goes into psychosis abruptly after a viral illness, NMDA antibodies are often called out,” he says.

Yet another suspect in the development of neuropsychiatric symptoms is the so-called cytokine storm that often follows infection with SARS-CoV-2. Cytokines are proteins essential for cell signaling and are produced by the immune system and give rise to inflammation which in turn can fight infection. But if cytokine production spirals out of control, extreme inflammation could ensue all over the body, and brain tissue wouldn’t be spared the impact.

“The neurons themselves aren’t invaded,” Slan says, “but what happens is that the systemic inflammatory response causes stress as well as changes in signaling throughout the body. That includes the brain, and can cause these kinds of problems.” [psychotic] symptoms.”

Another piece of evidence linking COVID-19 to psychotic fractures comes not from current scientific literature, but from history. After the 1918 and 1919 flu pandemics, there was a spike in what was called encephalitis lethargica, which was essentially a form of early Parkinson’s disease that often didn’t show up until several years after infection, but left patients in the lurch. which was in fact a state of catatonia.

“That flu virus caused inflammation after infection that killed brain cells that in turn led to Parkinson’s disease,” Pleasure says. The book and the movie awakenon patients who temporarily regained consciousness and lucidity after treatment with l-dopa – a precursor to the neurotransmitter dopamine – was based on cases of people suffering from that form of Parkinson’s.

The good news is that, unlike more chronic forms of psychosis, most cases seemingly related to COVID-19 don’t seem to last. The symptoms may respond to antipsychotics such as Risperdal (risperidone) and Zyprexa (olanzapine), Smith and Slan say. Intravenous immunoglobulin infusions — which reduce the overall load of abnormal cells and inflammatory agents — and steroids, which also reduce inflammation, may also be effective.

In no case is the case closed for psychosis caused by a virus. Even Slan, who has first-hand experience treating a patient suffering from an apparently virus-related psychotic disorder, believes there is more work to be done — acknowledging the doubts of the researchers who believe other psychological factors may be involved. can play.

“Given the stress of COVID,” he says, “given the concerns about mortality and isolation, all of these things represent huge psychosocial stressors, and they have the potential to cause often short-lived psychotic symptoms.”

Of course, even a transient psychosis is still a psychosis – something no one wants to experience even fleetingly. That puts a premium on avoiding infection in the first place. “The best way to treat COVID-19 and the risk of psychosis is to prevent it,” Smith says. “Even if neurological complications are rare, vaccination remains the smartest choice.”

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