First They Got COVID-19. Then Came the Parkinson’s Symptoms.
In March, a 45-year-old man from Israel took a week-long trip to the United States. On the flight home, he sat in front of a passenger who coughed repeatedly. Two days later, coronavirus symptoms appeared: a dry cough, muscle pain. He also lost his sense of smell.
He tested positive for the coronavirus, was briefly hospitalized with fatigue, shortness of breath, and chest pain, and was released into quarantine just a few days later. But in the three weeks that followed, new symptoms began to appear. His handwriting grew less legible. He began to have difficulty speaking, difficulty texting. He was having tremors in one hand, his movements slowed, and he observed his cognitive performance was a bit off.
This particular combination of symptoms was familiar—and alarming: The doctors who published the case report this October called it “a case of probable Parkinson’s.”
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Meanwhile, in Brazil, a 35-year-old woman with COVID-19 displayed hypophonia (slowness of speech) and bradykinesia (slowness of movement) and other examples of parkinsonism—the bucket of a couple-dozen symptoms associated with the neurodegenerative disease. Then there was the 58-year-old male COVID-19 patient in Madrid who experienced movement-related symptoms, including tremors and eye movement abnormalities—yet more parkinsonism.
A recent paper in The Lancet analyzed these case reports, noting the research community’s eager interest in a novel coronavirus/Parkinson’s link. So far, instances number only three—far from enough data to establish a causal link, the paper’s authors stressed. But that hasn’t stopped speculation after speculation after speculation by neurodegenerative disease experts asking: Could this coronavirus cause parkinsonism? And if so, will it lead to a spike in cases of Parksinson’s disease years from now?
These questions have much broader implications. Past pandemics have helped researchers establish that viral infections aren’t just about physical symptoms—they can change our brains. At one end of the spectrum, viruses have been linked to temporary mood changes, anxiety, and insomnia. At the most extreme, researchers aren’t sure what is possible. Some evidence points to the possibility of permanent brain disorders like Parkinson’s and schizophrenia. Significant data on COVID-19 parkinsonism, should it develop, could confirm some of the most terrifying working theories about viruses and neurodegeneration.
“The distinction between parkinsonism and Parkinson’s disease is important to make,” Dr. Emily Troyer, a psychiatrist and neuropsychiatry researcher at University of California San Diego, told The Daily Beast. “A number of things can cause parkinsonism, including certain medications, exposures, and several types of illnesses. Parkinson’s disease, on the other hand, refers to a specific illness with a well-defined set of symptoms, disease mechanisms, potential treatments. With that said, I'm not surprised that we are seeing case reports of parkinsonism that are temporally associated with COVID-19.”
For one thing, Troyer said, 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 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 to be carriers of past coronavirus antibodies, hinting at a link.
Then, there are the “psychoses of influenza.”
Neuropsychiatric complications from coronavirus infections—which range from headaches, dizziness, and behavioral changes to life-threatening neurophysical events like seizures, comas, and strokes—are reported in many patients. This follows past examples of virus-related psychoses, like SARS-CoV-1, the coronavirus behind the 2003 SARS epidemic, which led to higher rates of PTSD and depression among survivors.
And looking even farther back, as Troyer discussed in a July paper she co-authored (titled “Are We Facing a Crashing Wave of Neuropsychiatric Sequelae of COVID-19?”), these neuropsychiatric conditions could last for years, decades, or even generations. The survivors of the Spanish flu epidemic of 1918 had double the chance of developing Parksinson’s disease later in life as those who had not come in contact with the virus. Long-term effects didn’t stop there: Those survivors’ grandchildren were also more likely to develop schizophrenia.
The most pointed example of a link between parkinsonism and influenza also comes from 1918, in the pages of case reports detailing encephalitis lethargica, a brain disease discovered among Spanish flu patients. During the acute phase of encephalitis lethargica, patients experienced neuroinflammation, or swelling of the brain—which is also thought to play a role in both COVID-19 and in Parkinson’s disease. With that condition came some of the same symptoms observed in the Brazil, Spain, and Israel coronavirus cases: ocular motility disorders, tremors, movement disorders.
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Years later, 1918 flu survivors were observed to have developed chronic postencephalitic parkinsonism. Some autopsy studies on these patients found accumulation of protein plaques and tangles in the parts of the brain that are helpful for controlling movement, much like the ones that form in the brains of people with Parkinson’s. But without knowing the mechanisms by which Parkinson’s, or something like it, would occur in a coronavirus infection, Troyer said key questions remain unanswered about duration, treatment, and other factors. Would it resurface as Parkinson’s later in life? Or is it something different altogether?
“Luckily, we have much more advanced biomedical research tools this time around,” she said. “But we still have a lot of work to do in determining how it is that COVID-19 infection could cause the neuropsychiatric symptoms with which it’s being associated.”
The large-scale observational studies that could shed light on whether there is indeed a causal link, she said, will take years.
Parkinson’s is the second most common neurodegenerative disorder after Alzheimer’s, and the most rapidly growing. The global burden of the disease has more than doubled since 1990 and is expected to double again by 2040. If the coronavirus may increase that burden, the medical community wants a head start in confronting the outcome.
But Benjamin Stecher, patient advocate for the longitudinal Cincinnati Cohort biomarker Program study on aging and co-author of Brain Fables: The Hidden History of Neurodegenerative Diseases and a Blueprint to Conquer Them, hopes researchers’ fixation on the appearance of parkinsonism won’t distract them from the bigger picture.
“If I put on my cynical hat for a moment, most of the interest in this connection is coming from the Parkinson’s research community. It’s a means to drive research, and interest, and funding for more Parkinson’s research,” he told The Daily Beast. “That’s not to say that it shouldn’t be done—obviously it should. But personally, I think it should be done in a much more agnostic fashion.”
“There's a pretty clear link between viral infections and a whole range of neurodegenerative diseases,” said Stecher, who was diagnosed with Parkinson’s seven years ago, at age 29. “It would be much more beneficial to society if we started to study that link, rather than this link between infection and this amorphous thing we term Parkinson’s.”
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