Published August 2008; EPNN Journal - European Parkinson’s Nursing Network

PD BASICS 

            Physiologically, PD in the adult demonstrates a drop in dopamine levels in the brain.  Dopamine, a neurotransmitter, appears to regulate the level of neural activity needed to start or end a movement.  Lack of dopamine leads to inadequate muscle activation resulting in slowness of movement (bradykinesia), or incompletion of a movement (hypokinesia).  It also interferes with the ability to maintain upright posture resulting in poor balance.  However, people with PD retain the ability to increase muscle activation and can learn to perform larger and faster movements using conscious

effort. ^2,3

  RESEARCH

           A growing body of scientific evidence indicates that physical activity has a neuroprotective effect on the brain and nervous system.  In the animal model, studies reveal that exercise works at the molecular level to inhibit the death of dopamine-producing cells, concurrently increasing synaptic activity thereby maintaining the level of dopamine utilized in the brain. ^4,5,6  The result is improvement of the motor impairments associated with PD.

The details of these studies are exciting.  A group of rats injected with a toxin that induced PD, experienced a resultant loss of brain cells mimicking that in a human with the disease.  The rats were then divided into two groups; one group was forced to perform motor exercise daily (treadmill running), and the other group was rested.  During exercise, the rodents avoided motor impairment associated with PD. When they stopped exercising symptoms reappeared.  These findings suggest regular physical activity is needed to prevent PD symptoms from developing and progressing. ¹   Brain examination showed that in the exercised group of rats, there was only a 6% loss of brain cells containing Dopamine, compared to an 87% loss of cells in the rested group.  Treadmill running enhanced the survival of dopaminergic neurons and their fibers. ^5,12  It is reasonable to hypothesize that this data translates to human PD models, and holds promise for every individual diagnosed with PD.

The timing and intensity of exercise intervention also appears to be important.  In the animal model, the degree of neuroprotection and neurorecovery is dependent upon how early exercise is started in the course of the disease.  ^6,7,8  This suggests a need for regular activity to commence at the time of diagnosis to provide optimum results. This data is compelling enough to lead researchers to suggest that early physical training interventions may actually halt the progression of the disease. ^8,9,10  Clinical trials are presently ongoing to help elucidate exercise parameters, intensity, difficulty and repetition that may achieve the most robust effects on symptoms. 

Currently published human PD studies report outcomes including improved axial rotation, flexibility, balance, muscle strength, short-step gait, and overall mobility with routine exercise.  Improvement was measured using a variety of standardized tests and mobility scales. Results support that individuals with PD enhance their activities of daily living and physical performance through exercise. ¹¹  Grizzle and Newhouse suggest in a study performed in Ontario, Canada that future research should include the development of a standardized exercise program specific for problems associated with PD.

Human studies performed to date suggest that exercise is beneficial for individuals with PD, but no study can definitively make this claim.  Major study weaknesses include the short duration of exercise intervention and the fact that individuals were not tested while they were off their PD medications.  If the study participant is evaluated while on their meds, it is unclear exactly what effect the exercise is truly having on the disease.  The NIH is currently funding a study at the University of Illinois ( Julie A. Robichaud, PT, Ph.D., Daniel Corcos, Ph.D., principal investigator)  evaluating the effect of exercise on PD.  The Parkinson’s specific exercise programs are measuring tremor, gait, balance, cognitive and quality of life parameters.  The double-blinded study is ongoing for a period of 2 years and tests patients both on and off their medication. Conclusions drawn from this study will be exciting and helpful to the neurologist in recommending the exact type of activity most beneficial for the patient with PD. 

            The idea that something as simple as exercise may be neuroprotective is an exciting breakthrough.  With overwhelming scientific evidence and convincing patient testimonials, there doesn’t seem to be a reason not to start an exercise program when diagnosed with PD.  This treatment does not require FDA approval, is readily available and can safely be combined with medications.  Most importantly, it empowers the individual to take control of the disease with a proactive approach.  You may have Parkinson’s disease, but it does not have you.

   References

 

1. Farley BG.  Developing Parkinson’s-specific exercise programs.  The Journal on Active Aging. 2004; Sept-Oct:22-28.
2. Behrman AL, Teitelbaum P, Cauraugh, JH.  Verbal instructional sets to normalize the temporal and spatial gait variables in Parkinson’s disease.  Journal of Neurology, Neurosurgery and Psychiatry. 1998; 65:580-582
3. Bond J,  Morris M.  Goal-directed secondary motor tasks:  their effects on gait in  subjects with Parkinson’s disease. Archives of Physical Medicine and Rehabilitation. 2000;81:110-116   
4. Jankowec MW, Fisher B, Nixon K, Hogg E, Meshul C, Bremmer S, Mcneil T, Petzinger G.  Neuroplasticity in the MPTP-lesioned mouse and nonhuman primate.  Annals of the New York Academy of Sciences. 2003;991:298-301           
5.  Tillerson J, Caudle WM, Reveron ME, Miller GW.  Exercise induces behavioral recovery and attenuates neurochemical deficits in rodent models of Parkinson’s disease.  Neuroscience 2003;119 (3):899-911
6. Tillerson J, Cohen AD, Philhower J, Miller GW, Zigmond MJU, Schallert T.  Forced limb-use effecs on the behavioral and neurochemical effects of 6-hydroxydopamine. Journal of Neuroscience. 2001;21(12):4427-4435 
7. Tillerson J, Cohen AD, Caudle WM, Zigmond MJ, Schallert T, Miller GW. Forced nonuse in unilateral parkinsonian rats exacerbates injury. Journal of Neruoscience. 2002;22(15):6790-6799 
8.  Farley BG, Fox CM, Ramig LO, McFarland, D.  Intensive amplitude-specific therapeutic approaches for Parkinson disease:  Toward a neuroplasticity-principled rehabilitation model.  Topics in Geriatric Rehabilitation.  2008, February
9. Kleim J, Jones T, Schallert T. Motor enrichment and the induction of plasticity before or after brain injury. Neruochem Res. 2006; 11:1757-1769  
10. Smith AD, Zigmond MJ. Can the brain be protected through exercise? Lessons from an animal model of parkinsonism. Exp Neurol. 2003;184:31-39
11. Grizzle AM, Newhouse IJ. Is physical exercise beneficial for persons with Parkinson’s disease? Clin J Sport Med. 2006 Sept;16(5):422-5

Editor’s Note: Many of the attendees of the OSU PEAC Exercise program will recognize this author’s name. Jackie is a familiar face at the Friday exercise class located at The Highland building. She works closely with David Zid, spreading the word about the exciting news of the potential neuroproductive benefits of exercise. She and David have been to many speaking engagements throughout the United States talking, and demonstrating, exercises to benefit individuals with PD. She also collaborated with David to create "Delay the Disease: Exercise and Parkinson’s Disease" book and companion DVD.

For information about the classes offered contact the office, or view the information on the second page of any newsletter. For information about the Exercise Book and DVD, go to www.delaythedisease.com, send an email to delaythedisease1@aol.com, or contact our office toll free at 866.920.6673