In March, a 45-year-old Israeli took a week-long trip to the United States. On the return flight, he sat in front of a passenger who coughed repeatedly. Two days later, symptoms of coronavirus appeared: dry cough, muscle pain. He also lost his sense of smell.
He tested positive for coronavirus, was briefly hospitalized with fatigue, shortness of breath and chest pain, and was returned to quarantine a few days later. But within three weeks, new symptoms started to appear. His handwriting has become less readable. He began to have difficulty speaking, texting. He had tremors in one hand, his movements were slowing down and he observed that his cognitive performance was a bit poor.
Meanwhile, in Brazil, a 35-year-old woman with COVID-19 presented with hypophonia (slowness of speech) and bradykinesia (slowness of movement) and other examples of parkinsonism – the bucket of a few dozen symptoms associated with neurodegenerative disease. Then there was the 58-year-old COVID-19 male patient in Madrid, who exhibited movement-related symptoms, including tremors and eye movement abnormalities – even more parkinsonism.
A recent article in The Lancet analyzed these case reports, noting the strong interest in the research community for a novel coronavirus / Parkinson’s link. So far, there are only three instances – far from sufficient to establish a causal link, the article’s authors point out. But that hasn’t stopped speculation after speculation after speculation from neurodegenerative disease experts asking: Could this coronavirus cause parkinsonism? And if so, will this lead to a spike in Parksinson’s disease cases years from now?
These questions have much broader implications. Past pandemics have helped researchers establish that viral infections aren’t just physical symptoms – they can change our brains. At one end of the spectrum, viruses have been linked to temporary mood swings, anxiety, and insomnia. At its most extreme, researchers don’t know what is possible. Some evidence points to the possibility of permanent brain disorders like Parkinson’s disease and schizophrenia. Important data on COVID-19 parkinsonism, if it develops, could confirm some of the most terrifying working theories about viruses and neurodegeneration.
“The distinction between parkinsonism and Parkinson’s disease is an important one to make,” Dr. Emily Troyer, psychiatrist and neuropsychiatry researcher at the University of California at San Diego, told The Daily Beast. “There are a number of factors that can cause parkinsonism, including certain medications, exposures, and many types of illnesses. Parkinson’s disease, on the other hand, refers to a specific disease with a well-defined set of symptoms, disease mechanisms, and potential treatments. That said, I am not surprised that we are seeing reports of cases of parkinsonism that are temporarily associated with COVID-19. “
On the one hand, said Troyer, parkinsonism has been reported after other viral infections, from the common flu to West Nile virus, herpes and HIV.. For another, researchers have found evidence of some sort of relationship between Parkinson’s disease and coronaviruses in the past: In the early 1990s, researchers learned that people with Parkinson’s disease were, mysteriously, more likely than people without Parkinson’s disease to have previous antibodies to the coronavirus, alluding to a link.
Then there are the “flu psychoses”.
Neuropsychiatric complications of coronavirus infections – which range from headaches, dizziness, and changes in behavior to life-threatening neurophysical events like seizures, coma and stroke – are reported in many patients. This follows past examples of virus-related psychoses, such as SARS-CoV-1, the coronavirus that caused the 2003 SARS epidemic, which led to higher rates of PTSD and depression. among survivors.
And looking back even further, as Troyer discussed in a July article she co-authored (titled “Are We Facing a Tidal Wave of Neuropsychiatric Sequelae from COVID-19?”), These Neuropsychiatric Conditions could last for years, decades, even generations. Survivors of the 1918 Spanish flu epidemic were twice as likely to develop Parksinson’s disease later in life as those who had not been in contact with the virus. The long-term effects did not end there: the grandchildren of these survivors were also more likely to develop schizophrenia.
The most glaring example of a link between parkinsonism and the flu also comes from 1918, in the pages of case reports detailing lethargic encephalitis, a brain disease discovered in Spanish flu patients. During the acute phase of lethargic encephalitis, patients presented with neuroinflammation or swelling of the brain – which is also believed to play a role in both COVID-19 and Parkinson’s disease. With this condition appeared some of the same symptoms seen in coronavirus cases in Brazil, Spain and Israel: eye motility disorders, tremors, movement disorders.
Years later, 1918 influenza survivors were observed to have developed chronic postencephalitic parkinsonism. Some autopsy studies on these patients have found a build-up of protein plaques and tangles in parts of the brain that are helpful in controlling movement, just like those that form in the brains of people with Parkinson’s disease. . But without knowing the mechanisms by which Parkinson’s disease, or something like that, would occur in a coronavirus infection, Troyer said key questions remain unanswered regarding duration, treatment and other factors. Would he come back with Parkinson’s disease later in life? Or is it something completely different?
“Fortunately, this time around we have much more advanced biomedical research tools,” she says. “But we still have a lot of work to do to determine how infection with COVID-19 might cause the neuropsychiatric symptoms it is associated with.”
Large-scale observational studies that could shed light on the existence of a causal link, she said, will take years.
Parkinson’s disease is the second most common neurodegenerative disease after Alzheimer’s disease and the fastest growing disease. The global burden of disease has more than doubled since 1990 and is expected to double again by 2040. While the coronavirus can increase that burden, the medical community wants to be ahead of the curve in dealing with the outcome.
But Benjamin Stecher, patient advocate for the longitudinal study of the Cincinnati Cohort Biomarker Program in Aging and co-author of Brain Fables: The Hidden History Of Neurodegenerative Diseases And A Plan To Beat Them, hopes that the researchers’ fixation on the onset of parkinsonism will not distract them from the bigger picture.
“If I put my cynical hat on for a moment, most of the interest in this regard comes from the Parkinson’s research community. It’s a way to stimulate research, interest and funding for more research on Parkinson’s disease, ”he told The Daily Beast. “That’s not to say it shouldn’t be done – obviously it should. But personally I think it should be done in a much more agnostic way.
“There’s a pretty clear link between viral infections and a whole range of neurodegenerative diseases,” said Stecher, who was diagnosed with Parkinson’s disease seven years ago, at 29. “It would be a lot more beneficial for society if we started to study this link, rather than this link between infection and this amorphous thing that we call Parkinson’s disease.
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