I just returned from my neurologist visit. Last visit was in January. He reported that I am unchanged since January and I am still at Level 1 "way ahead of the curve". He said that people are normally at Level 2 by three years into the disease. I'm at five years. I've been able to cycle nearly every day since getting home a week ago. He suggested I return to ReQuip XL 4 mg (I had raised it to 6) since I'm able to be back on the bike.

For those of you who are in the area and are so inclined, I've been asked to speak three places in the next few weeks as follows:

1. Thursday, Sept 16, Mill Creek, WA to the Washington Academy of Family Physicians, 7:15 p.m. at the Capri Restaurant in the Mill Creek Town Center.

2. Thursday, October 4, Rush University Medical Center, 1725 W. Harrison, Professional Building, Suite 755, Young Onset Support Group, 6:30-8:30 p.m.

3. Friday, October 5, Cliffbreakers Hotel, 700 W. Riverside Blvd., Rockford, Illinois, , Parkinson's Conference that lasts from 9-1.

Please introduce yourself if you come from this forum!

Wow! This thread got me poking about and I just found a motorized "bike" for about $115. Hmmm...70 RPM...I understand, thus far, the exercise must be forced (you don't effort) and at 80 to 90 RPM. Well, the Cleveland Clinic's the protocol Jan would like to try, but cost is prohibitive. So, this?

http://www.therapy-cycle.com/cycle_therapy.html

Thanks, Nan!

TrishaPDX

Here is info on the Motomed Viva 2:

http://en.motomed.com/medizin_01_gb/...parkinson.html

Found one of these in Oregon a few weeks ago at Portland Providence Medical Center's Acute Rehabilitation Center, where Jan just spent 10 days being tuned up. Alas, the PT wasn't familiar with the PD & Forced Motion Cycling reseach and wouldn't allow a 80 rpm trial. Today, Jan was evaluated by a physical therapist who say her hip flexors are A-OK for a trial of the forced rpm that's being studied.

Off to the races!

The following piece is part of an article written by Dr. Jay Alberts that addresses your issues. Forced Exercise (FE) is different from Voluntary Exercise (VE). As you can see from the article, FE is not just sitting on a cycle that turns one's legs around at a specific rpm. The patient is an active participant in the exercise. On a tandem the patient provides at least 25% of the power in order to achieve results. From reading the Therapy-Cycle website, it appears that there is a hodgepodge of partial information and data, all designed to part the patient from their $. I have written to Dr. Alberts to ask about the Motomed and will let you know when I hear from him. I hope this helps. I'm eager for Dr. Albert's cycle to be generally available, but I firmly believe that testing, gathering data, and evaluating it are of primary importance.

Here are the parts from his 2011 article:
"FE, in this case, is defined operationally as a mode of aerobic exercise in which exercise rate is augmented mechanically to assist the participant in achieving and maintaining an exercise rate that is greater than their preferred voluntary rate of exercise. It is important to note that during FE, the participant is contributing actively to the exercise; they are not being moved through the motion passively. Our data indicate that FE leads to a global improvement in PD motor function and an alteration in the CNS [Central Nervous System] function (22). These global changes in motor function and altered activation patterns provide strong evidence for the hypothesis that for patients with PD to derive motor benefits from exercise, assistance is required to achieve a rate of exercise that triggers the release of neurotrophic factors or possibly dopamine.

FUTURE DIRECTIONS AND SUMMARY
A randomized controlled trial currently is underway as a follow-up to the initial tandem cycling study. Subjects are randomized to one of three groups: no exercise, VE, and FE. However, in the current trial, a motor-driven cycle, which we have developed is being used to safely deliver FE. A model- based controller was developed to replicate the ‘‘feel’’ of the human interaction that occurs during tandem cycling (e.g., real-time alteration of motor contribution, pedaling rate, and monitoring of heart rate). The controller model approximates the dynamics of the cycle interacting with the rider during an exercise session. This trial includes clinical testing and neuroimaging 8 wk after exercise cessation to help determine the long-term effects of FE and VE in patients with PD. We also are engaged in a preliminary study with deNovo patients with PD in which they will exercise for 6 months in their home. Weekly cognitive and motor assessments will be made and compared with a group of deNovo patients with PD who are not exercising. Collectively, these studies will provide greater information regarding the potential mechanisms underlying any improvements in cognitive or motor function in patients with PD after FE or VE, the possible duration of motor or symptom benefits and initial data regarding the potential for exercise to slow the progression of PD.
Although the exact components and dosage of optimal exercise interventions have not been determined for patients with PD, evidence from the animal studies and our data suggests that intensive aerobic FE may have neurorestorative and neuroprotective properties possibly through the endogenous release of neurotrophins or alteration of dopamine. Animal and our preliminary human data suggest the ability to influence cognition, metabolism, and potentially, the progression of neurodegenerative diseases through these mechanisms. Even the hint of neurorestoration associated with FE warrants the testing of this intervention in other neurologic conditions such as stroke and Alzheimer disease, as the ‘‘side effects’’ of exercise include improved cardiovascular fitness and increased energy. Future studies will help delineate the optimal dosage of FE or VE for neurologic patients. Furthermore, a clearer understanding of the use of FE as a neuroprotective or neurorestorative adjunct to pharmacological or surgical interventions offers these patients a rare opportunity to participate actively in the treatment of their disease with minimal risks or side effects."

Copyright © 2011 by the American College of Sports Medicine

I'm quite alarmed at the hype coming from THERACYCLE, I get an email a week from them promoting their device and now i can even talk to people who have tried it.

i'm anxious to see the results from roberts next trial, anyone know if it has started?

the benefit appears to be transient, it goes away if you stop cycling. but according to alberts study lasted weeks after the participants stopped. so either those neurotrophic factors have a long half life or there were temporary changes at the DNA level to produce these factors or do something that temporarily changed the dopamine system, either create more dopamine, produce a few more dopamine cells from stem cells, increase dopamine receptors? seems end game would be find drugs/gene therapy that could do the same thing as vigorous excercise.

There is already one treatment in trial and another that has shown long term benefit over course of four years.


The PicoTesla Magnetic Resonator is entering Phase III trials. It reduces symptoms for months. http://www.pico-tesla.com/#

Light therapy shows improvement of symptoms over course of four years.

http://informahealthcare.com/doi/abs...20520701420717

I honestly think that if they compared the longer term treatments like this, including cycling and DBS, to see what is that extra thing that we seem to need beyond dopamine replacement we would be making some real progress.

I am a bit confused now: https://www.michaeljfox.org/foundati...=95&category=3

By 'level' 1 could he mean the same thing as 'stage' 1?

For Laura and Soccertese:

Jay thinks that the mechanism is neuroregeneration, i.e., the part of the substantia nigra that is still alive somehow is creating new neurons due to the forced pace cycling. Why or how is not at all clear. This is an hypothesis, not a conclusion. I type this with great hesitation as it is not my place to speak for him.

Laura, I think you're spot on. What are the commonalities and how can they translate them into treatments?

To respond to pwpboy:

I have two take away points on this:

1. If you sit on your duff waiting for the perfect definitive "best" form of exercise, you're shooting yourself in the foot. Choose a form of exercise that you like and will make part of your daily life, then DO IT!

2. The exercise that has been clinically shown (although with a small sample) to have an average of 35% reduction in PD symptoms is forced paced cycling. If you can safely do that, and WILL do it consistently, go for it. Medicine lasts for hours at best, whereas forced pace cycling has residual benefits of up to four weeks.

To rempatterson:

Sorry I wasn't clear. He said that 1 means that I have unilateral symptoms: everything happens on my right side. Now and then my left ring finger cramps for a moment, but the few symptoms that I still have are on the right. My penmanship has gone from bad to scratch; typing with the right hand is compromised; needlework is much harder, i.e., all fine motor skills with the right hand are compromised. The rest is pretty good.