Parky is not so Simpleby David Yon, revised July 21, 2019
Nothing is simple in this world anymore, but some things are complicated. Take for example Parkinson’s disease. Since I was diagnosed with the disease in 2012, approximately 400,000 people in the United States have been added to the list, with the total now approaching or exceeding 1,000,000 in the US and 6,000,000 worldwide. So far there is only one way off the list and that is not a very good option.
But that tells only part of the story as there are many things people diagnosed with Parkinson’s can do to maintain the quality of their life. Diagnosing and treating the disease, or at least the symptoms of the disease, is critical and difficult. That first step must be followed by a commitment to stay active, mentally and physically. Start every day by punching Parky and his demons square in the nose. Yes, he will hit back.
In 1817, physician James Parkinson, began to articulate the symptoms for what he called the Shaking Palsy in an essay. His observations included tremor, rigidity, slow movements and stooped gait. His famous essay also observed “there appears to be sufficient reason for hoping that some remedial process may ere long be discovered, by which, at least, the progress of the disease may be stopped.”
The following definition of Parkinson’s disease comes from the Michael J. Fox Foundation for Parkinson’s Research: “Parkinson’s disease (PD) occurs when brain cells that make dopamine, a chemical that coordinates movement, stop working or die. Because PD can cause tremors, slowness, stiffness, and walking and balance problems, it is called a ‘movement disorder.’ But constipation, depression, memory problems and other non-movement related symptoms also can be part of Parkinson’s. PD is a lifelong and progressive disease.”
There is good and bad in that. Diseases such as ALS, Alzheimer’s Disease and many types of cancer move in, torture their victims, and then snuff the life out of them. Parkinson’s does not deliver the death blow to anyone directly but given enough time it will leave someone virtually helpless. The goal of course is to put that time off for as long as possible, maybe even long enough for someone to find a cure.
The best tool available for keeping the disease manageable, for me at least, remains exercise. It is my weapon on the battlefield with the demon Parky. I can’t say for sure I ever win any ground against Parkinson’s by pushing through the heat and humidity of a 15-mile run in the summer. There is research suggesting that yes, I do push my enemy back when I push myself through intense exercise. I am certain that every time I roll over and pull the covers over my head Parky attacks.
Yet, the question always lingers in my mind – is exercise more than a placebo? Is there any strong evidence to show intense exercise can be neuroprotective? Reviewing the growing body of literature, gives me great hope and motivation.
The available research has increased substantially (thankfully) since 2012 and the complexity of it all can quickly overwhelm a lawyer. However, I still work hard to understand this demon that rattles my brain. One of the many sources I found during this search period was an article entitled: “Enhancing Neuroplasticity in the Basal Ganglia: The Role of Exercise in Parkinson’s Disease.” (Published in US National Library of Medicine, National Institutes of Health.)
The abstract from the paper provides:
Epidemiological and clinical trials have suggested that exercise is beneficial for patients with Parkinson’s disease (PD). … This review presents current findings from our laboratories …. The data indicate that alterations in both dopaminergic and glutamatergic neurotransmission, induced by activity-dependent (exercise) processes, may mitigate the cortically driven hyper-excitability in the basal ganglia normally observed in the parkinsonian state. These insights have potential to identify novel therapeutic treatments capable of reversing or delaying disease progression in PD.
Those are magic words: “capable of reversing or delaying disease progression in PD.” In the intro the review contains the following:
Exercise has been shown to be beneficial in PD, yet the question remains whether exercise leads to central nervous system (CNS) compensatory or neuroprotective changes with potential to alter the natural course of the disease. Studies have demonstrated that the adult brain is altered by experience including exercise. This phenomenon termed “activity-dependent neuroplasticity” is defined as modifications within the CNS, in response to physical activity that promotes a skill acquisition process.
These findings suggest that high intensity exercise leads to compensatory changes in dopamine handling and neurotransmission.
We have shown that exercise may influence activity-dependent processes in the basal ganglia through alterations in dopaminergic and glutamatergic neurotransmission. In addition, we demonstrate that exercise-induced behavioral benefits may be in part due to changes in cortical hyper-excitability normally observed in the dopamine depleted state, as in PD. A critical next step is to determine whether exercise induces or is associated with a disease modifying effect in PD. The implications for our understanding of the impact of exercise in PD are broad. Not only is there potential to develop new insights into mechanisms of neuroplasticity and motor recovery in PD, but also the study of exercise may lead to the development of novel therapeutics, perhaps even nonpharmacological approaches to delay or reverse disease progression in PD.
There are a lot of technical, complex words in that summary. (Thanks for the right click Smart Lookup option.) No worries, I think I will just go for a run now knowing that something good is happening, maybe.
Oh, one more thing before I leave for that run. Results from a recent study, Spinal Cord Stimulation Therapy for Gait Dysfunction in Advanced Parkinson’s Disease Patients” (Samotus et al., 2018), show promise of restored movement for people with Parkinson’s when an electrical implant is placed in their spine. The headline from the editors of the newsletter ParkinsonsDisease.net screamed: “Breakthrough Treatment…may Restore Movement…” The implant, developed by researchers in Canada, enables people with chronic Parkinson’s Disease to walk better. It works, as best I understand, by amplifying the signal between the brain and muscle to overcome the damage done to the usual dopamine delivery system by rogue proteins. Most efforts attempt to improve the signals the brain sends to the muscle telling it to move. However, this study focuses more on the signal from the muscle back to the brain. Without this return signal the brain does not know whether its first command was obeyed or ignored. The stimulators job is to communicate what happened to the brain and do it loudly. It should be noted that this research study was a pilot study with only 5 participants and much more research is needed to understand if this treatment option will work with others who have Parkinson’s. But the results in this study were very impressive.
Of importance to me, the researchers found that stride velocity improved by 42.3%, while mean step length improved by 38.8%. Stanley, watch out, with those numbers I may be coming after you soon.Dr. Okun, have you been holding out on me?
While my focus for this column was on exercise, another approach with promise is gene therapy, a subject for another day. There are many exciting possibilities for help and maybe even reason to think a cure might be just around the corner more than 200 years after its discovery.
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