COVID-19 and Parkinson’s Disease: Is There a Link?
By: Shiva Gopal Vasishta
Tags: Coronavirus, Medical, Neurology, Covid 19, Doctors

As people continue to live longer, Parkinson’s disease, or PD, becomes more widespread. It is the fastest-growing neurological disorder. By 2040, the number of cases is expected to top 14 million worldwide. Scientists who study PD wonder if COVID-19 will compound the problem.

Photo by Markus Spiske on Unsplash

It is far too early to speculate about the long-term neurological effects, if there are any, of COVID-19. However, some symptoms of the viral respiratory illness worry researchers. Encephalitis, an inflammation of the brain, is one. The loss of taste and smell is another. They indicate that SARS-CoV-2 — the virus strain that causes COVID-19 — might be capable of invading the central nervous system.

Dr. Carla Alessandra Scorza is a professor of neurology at the Federal University of Sao Paulo in Brazil. In the Journal of Parkinson’s Disease, she recently weighed in on possible links between PD and viruses. She noted that the microanatomy and motor symptoms of PD share traits with several viruses. Examples include HIV, West Nile virus, Japanese encephalitis B, and H1N1, known as swine flu.

Scorza also pointed to telling studies. Patients with severe COVID-19 were more likely to develop problems that affect the brain’s blood supply. Brain scans of other patients showed evidence of altered brain structure and function. Still, other scans indicated intracerebral hemorrhage, which is bleeding on the brain.

Are these findings evidence of a viral neuro-invasion? Scorza and other scientists concede that only time will tell. However, the possibility has been discussed before.

Encephalitis lethargica, or EL, is a rare and serious inflammation of the brain. It was once known as sleeping sickness.

The deadly Spanish flu pandemic infected an estimated 500 million people through 1918 and 1919. An epidemic of EL followed. Dr. Ava Easton of the Encephalitis Society reports that EL affected up to a million or more people. A remarkable number of patients who survived developed a form of PD. At the time, many scientists blamed the Spanish flu virus, but the cause was never confirmed.

Scorza and others are revisiting that theory. Neurology has advanced by light-years since then, and COVID-19 sparks renewed interest in the role of viruses in PD.

Viruses might directly trigger PD by being physically present in the central nervous system.

COVID-19 patients struggle with shortness of breath and other respiratory issues. Scorza points out that the nuclei responsible for breathing rhythm are in the brain stem. If the virus took hold in the central nervous system, it would directly impact breathing.

Another possibility is that COVID-19 and similar viruses start a lengthy inflammatory process in the brain. PD is an indirect result.

Finally, lab studies show that other human coronaviruses may lie dormant in blood cells. They could potentially cause infections in the central nervous system much later. Coronavirus antibodies have turned up in the brain and spinal fluid of PD patients.

There is a reverse aspect to consider. Are people who already have PD at greater risk for contracting COVID-19? Will the virus affect them differently if they get it? No one knows for sure.

There is no evidence that having PD makes someone more susceptible to COVID-19 infection. Complications of the virus definitely increase for the elderly, diabetics, and people with heart or lung problems. No such data exists for PD patients.

Scientists can only study cases of PD patients who have had other viral respiratory illnesses. Their PD symptoms worsened, but just about any illness exacerbates symptoms. Some patients reported feeling stiffer and slower than usual. Others thought their medications didn’t work as well while they were sick. Recovery was drawn out.

Doctors assume that most PD patients who contract COVID-19 will have similar complaints. Symptoms might be much worse, though, for patients who also have restrictive lung disease. In that condition, the lungs never fully expand with air.

Until more is known, PD patients should do all they can to protect themselves. Safety guidelines vary almost by the community, so doctors advise erring on the side of caution. When in doubt, the experts agree, follow the most stringent guidelines.

Dr. Patrik Brundin is co-editor-in-chief of the Journal of Parkinson’s Disease. He hopes that neurology researchers closely monitor COVID-19 patients who recover. Infections and viral inflammation have already been linked to a higher risk for PD later in life.

Also, studies on animals show that viruses probably raise alpha-synuclein levels. Alpha-synuclein is a protein found in the heart, muscle, and stomach tissue. It is especially abundant in the brain.

Neurologists are not quite sure about all its functions. They do know that it plays a role in the release and regulation of dopamine. That is highly relevant to PD. Dopamine helps control the start and stop of both voluntary and involuntary movements.

Daniella Balduino Victorino was the lead author of the journal article. She remarked that the National Institutes of Health recently threw $6 billion at infectious disease research. Only $300 million went to PD research.

Victorino, Scoza, Brundin, and other scientists hope that PD soon gets its fair share. With well-funded research, the relationship between neurology, viruses, and PD will be much clearer.