Importance of PT + Exercise in Neurodegenerative Disorders

This article was published in the latest issue (Fall ’07) of the Parkinson’s Disease Foundation newsletter. Here’s a link to the article and the full text: … id=3030787 –> this article –> Fall ’07 newsletter

Current Research Highlights Importance of Physical Therapy and Exercise For People with PD
By Mark A. Hirsch, Ph.D. and
David A. Lehman, Ph.D., P.T.

From the Fall 2007 issue of PDF News & Review
Published by the Parkinson’s Disease Foundation

The traditional view of how to treat people with neurodegenerative conditions is that exercise has little or no effect, or that it can actually worsen the disease! However, recent research in both humans and animal models suggests that physical therapy — including gait and balance training with external cues to improve walking, resistance training for the lower extremity muscles, balance training, and regular exercise — can be an important component of an exercise program that may help improve or hold the signs and symptoms of Parkinson’s disease (PD) at bay.

Gait and balance

Gait and balance impairments are cardinal symptoms of PD. If left untreated, impairment in walking or balance can lead to falls, fractures, hospitalization and loss of independence. In fact, roughly 40 percent of nursing home admissions are preceded by a fall, and falls occur more frequently in people with Parkinson’s than they do among other individuals.

Recently, a large number of studies have focused on improving gait in people with Parkinson’s disease through a training exercise known as “cueing.” People with PD sometimes have difficulty generating internal cues to take a step. They may “freeze” while standing or walking, which in turn can cause falls and injuries. External cues, such as providing a cane to trigger a stepping movement, placing horizontal lines on the floor, giving instructional cues (such as asking the person to “take long steps”) or walking to a rhythmic metronome, can all improve a person’s stride length and walking velocity, and reduce shuffling and freezing.

It is encouraging that many of these studies were carried out in the home environments of the study participants. This means that individuals who do not have direct access to a rehabilitation center or wellness facility can benefit from training that is provided in the home.

In one such study conducted by physical therapists in England, Belgium and Holland — the largest study on gait training to date — cueing training was used to improve walking in participants’ home environments. The study included 153 people who received a three-week home cueing program, followed by three weeks during which no training was done. The results, though modest, showed measurable improvements in gait and balance, as well as reduced freezing and greater confidence to carry out functional activities. However, after the training ended, the improvements were gradually lost, reminding us that it is important to continue exercising if those improvements are to be long lasting.

Improving strength

Studies have generally shown that exercise improves speech and swallowing, posture, tremor, dexterity, cognition and depression. Other studies have shown that treadmill training, and lower extremity resistance and balance training, can be effective at improving muscle strength, gait and balance.

There has been considerable interest recently in therapies designed to increase muscle mass, known as “muscle hypertrophy.” Several studies have shown that individuals who improved the size of their muscles also demonstrated improvements in functional activities such as climbing or descending stairs or balancing. Muscles shrink when they are not used; conversely, muscle tissue increases in girth with intense resistance training. As we age, we often become more sedentary and muscle loss becomes inevitable ­ underscoring the need for exercise.

During the 1970s and 1980s studies showed that aging triggers a gradual and inevitable decline in function, and therefore it was believed that older adults could not improve strength or muscle girth with training. Many studies had shown that while aerobic fitness in older adults could be improved with training, muscle strength could not. Later examination showed that these early studies included biases about older adults and aging that affected the study design, and therefore the conclusions. Most of the earlier studies, it turned out, had used a very low intensity of training (e.g., rubber bands or very light weights) because the researchers feared that heavier weights would cause injuries among their older study participants. Since the participants did not improve in muscle strength it was concluded, wrongly, that “seniors” could not improve strength.

In the late 1980s, studies began to show that older adults — many already in their 80s and 90s, and some of them in nursing homes — could improve strength, muscle bulk and function in response to high-intensity resistance training. Despite this new evidence — and because some researchers and therapists believed that resistance training might itself increase muscle stiffness — strengthening was not advised for people with PD out of fear that it might be harmful.

More recent studies have further challenged this view. Results of one study of people with mid-stage Parkinson’s suggest that high-intensity resistance training results in a six percent increase in muscle volume, 17 percent improvement on how far participants could walk in six minutes, and a 22 percent and 13 percent improvement in stair descent and ascent time. In another study, high-intensity resistance training for the lower extremity muscles was found to improve balance and to reduce the occurrence of falls.

While resistance training does pose risks that other types of training do not (e.g., risk of hernias and other musculoskeletal injuries), the risks of not participating in such a program and remaining sedentary are not insignificant.

Animal studies on exercise and the PD brain

In addition to helping with movement, researchers now believe that exercise may influence the progression of Parkinson’s disease. While the mechanism for these effects in Parkinson’s are poorly understood, researchers and therapists are coming to believe that when a person with PD engages in a novel activity such as beginning an exercise program — especially when there are opportunities to interact socially — changes in the structure and function of the brain may result. Most of this research is based on animal models of Parkinson’s but some of the findings may apply to humans. Recent studies of PD with rat models suggest that intense sensory motor training triggers the creation of nerve connections (synaptogenesis) and new nerve cells (neurogenesis). Apparently it is never too late for the brain to change its structure and function in response to stimulating environments.

The timing of training in relation to a Parkinson’s diagnosis may also be relevant. In a recent series of studies, rats were forced to rely on an impaired forelimb during exercise, while their less impaired forelimb was restricted from movement by a cast. In these studies, animals forced to exercise immediately after the PD lesion demonstrated greater retention of the nerve cells that produce dopamine and less severe symptoms down the road. Rats that began the exercise program later (three to seven days after the PD lesion) fared far worse. They had more pronounced Parkinson’s symptoms and showed greater PD-related damage in the brain. In other words, the earlier the training is begun after a diagnosis, the better.

In another animal study, it was shown that exercise (represented by rats running on a wheel) increased the number of new dopamine-producing neurons as compared to rats that did not exercise. In these animal models of Parkinson’s, exercise seems to have a neuroprotective effect on the brain. Studies showing the effect of exercise and physical therapy on the human PD brain structure and function are forthcoming.

What does this mean for people with PD?

If the animal studies are found to hold up in humans, it would appear that early referral to a physical therapist or exercise program may prevent or delay some disabling aspects of the disease. We will not know this for sure until more human trials have been done. What we do know is that people with Parkinson’s disease are well advised to begin or continue exercise and therapy after a diagnosis has been made.

A major problem in getting people with PD to exercise is that many medical professionals still do not understand the value of exercise. Education of patients and families could certainly improve this situation, as could the increased availability of community-based health clubs or wellness facilities that are equipped to provide services for special populations, such as people with Parkinson’s. It is important to remember to ask your physician for a referral for physical therapy, as it may be essential to obtain coverage from insurance or Medicare.

In addition, motivating older adults to exercise and to stay physically fit requires skills on the part of the practitioner that are not traditionally taught in allied healthcare programs. People with PD often require hands-on guidance during exercise in order to minimize the occurrence of injuries, to stay motivated and to continue with a program. Of course, anyone thinking of beginning an exercise program should consult with his or her physician beforehand to make sure that it is safe.

Both younger and older people with a diagnosis of Parkinson’s disease can benefit from physical and occupational therapies, or a home-based exercise program. Neither the age of the patient nor the stage of their Parkinson’s disease should be seen as limiting factors in the decision to exercise. The results of studies to date are encouraging and the message to people with Parkinson’s is clear: look for opportunities to exercise!

Dr. David Lehman is Associate Professor at Tennessee State University with an emphasis in neurorehabilitation and Parkinson’s disease. He is President-elect for the Middle Tennessee Chapter of the American Parkinson Disease Association. Dr. Mark A. Hirsch is on the faculty of the Department of Physical Medicine and Rehabilitation at Carolinas Rehabilitation in Charlotte, NC, and has worked extensively in motor therapy. He is a Board member of the Parkinson Association of the Carolina’s.

Indiana family struggling with rare diagnosis (PSP)

My online friend Joe Blanc posted this article today to the Society for PSP’s Forum. The article is about an Indiana family coping with progressive supranuclear palsy (PSP). The wife was diagnosed with anxiety, Alzheimer’s, and, finally, PSP. Swallowing is described as the main complication with PSP.

The concept of brain autopsy is raised in the article:

“Dr. Alberto Espay, assistant professor of Neurology at the University of Cincinnati, said it is very difficult to pinpoint PSP, and the only way to positively confirm a diagnosis is by an autopsy.”

If you are interested in making arrangements for a family member’s brain donation (or your own brain donation), please let me know. I can help!


Difficult Diagnosis 

Struggle with rare, fatal disease compels family to raise awareness
By Rebecca L. Sandlin

Chris Ryan doesn’t want other families to have to go through what hers suffered when her mother, Augie O’Herren, slowly began to deteriorate.
Augie and her husband, Roger O’Herren, had lived in Noblesville for years, and she was active in the community, Ryan said. But in 1994, at the age of 62, she began to have mysterious symptoms of “light-headedness,” followed by failing eyesight, poor balance and slowed speech. “It was such a long battle of trying to figure out what’s wrong,” Ryan said. “That’s the sad state. … So many different doctors’ opinions. It’s a science – nothing perfect.”

Augie was diagnosed with everything from anxiety to Alzheimer’s disease. But the family wasn’t satisfied with the doctors’ diagnoses.
Finally, they took Augie for an evaluation at the University of Chicago. There, a doctor told them her symptoms appeared in a pattern that suggested she had progressive supranuclear palsy, or PSP – a form of Parkinson’s disease.

According to a PSP Web site, PSP is a fatal, degenerative brain disease that has no known cause, treatment or cure. It causes complete disability by progressively impairing all movement, balance, vision, speech and swallowing. PSP patients may often show alterations of mood and behavior, including depression and progressive dementia.
It is estimated between 5,000 and 10,000 people are currently afflicted with the disease and as many as 10,000 more are undiagnosed or misdiagnosed.

Dr. Alberto Espay, assistant professor of Neurology at the University of Cincinnati, said it is very difficult to pinpoint PSP, and the only way to positively confirm a diagnosis is by an autopsy.

“We don’t have a readily-available blood test that we could use and say, ‘Yes – that’s what you have,” Espay said. “A high proportion of people that end up developing full-blown PSP may be misdiagnosed early on as Parkinson’s disease.”

Espay said the treatment of suspected PSP patients would be nearly the same as for Parkinson’s disease.

“We can then counsel patients as to what to expect, what to watch for so that the main sources of potential complications – namely, difficulty with swallowing … can be monitored and ideally kept at a point where they are not going to be losing the patient to complications,” he said.

Espay suggests patients go to a clinic that is dedicated to PSP research for a second opinion if they are uncomfortable with a doctor’s diagnosis.
Augie O’Herren finally succumbed to the disease in August 2006 at the age of 74. Her daughter, Kathleen O’Herren Huston, said she’s now “dancing, eating and reading – all the things she loved to do before this horrible disease took it away from her.”

Ryan said she hopes her family’s trial will help others with loved ones who are struggling with mysterious symptoms.

“Don’t give up – don’t just listen to one doctor, if your senses are telling you something different and what you’re reading is contrary,” Ryan said. “It did bring us some relief to know that we were not crazy – that all of her symptoms that she’s been complaining about actually do fit into something. … Keep on believing.”

Symptoms of PSP:
Gradual loss of certain brain cells causes slowing of movement and reduced control over walking
Balance problems
Difficulty speaking or thinking
Slow eye movement; complaints of not being able to read
Difficulty swallowing
Tight, small script when writing
On the Web
You can learn more about progressive supranuclear palsy by visiting The O’Herren family journal is located at visit/augieoherren.

Neuroleptics and anticholinergics can be catastrophic in LBD

I recently came across an article in the Human Givens Journal ( from 2003 on the use of neuroleptics (anti-psychotics) with sometimes disastrous results in Lewy Body Dementia (LBD). A warning is also shared for anticholinergics.

In this article, the term “neuroleptics” refers to both typical and atypical anti-psychotics.

The article notes that those with LBD should avoid anticholinergics in any form, even over-the-counter cold remedies. One example of an anticholinergic that is a cold remedy is Benadryl. And usually sleeping aids have anticholinergic properties along with anti-bladder spasm meds. And on and on….

I have never found a complete list of all meds with anticholinergic properties but a website such as or do mention these problems in the “Side Effects” section.


“To drive or not to drive, that is the question…1 solution”

I’m forwarding this email mostly for the good laugh but it does contain a very clever suggestion!


(From the LBDA Forum)

Posted by: Linda
Posted: Mon Sep 03, 2007 5:49 pm
Post subject: To drive or not to drive, that is the question… 1 solution

Dad wad driving. He LOVED his keys. We really thought we would have to take the car away from both mom and dad to get him to stop. He came to visit us in Florida and got the car stuck in the mulch. We decided to just leave it there. After 3 or 4 days we started talking about how bad his vision was. (He WAS seeing things that were not there.) Then we brought up the fact that maybe it was time to let mom drive. It was MUCH easier than we thought. BUT, we knew when he returned to NC, he was going to make a break for it. SO, I went to the key store and had them make a key for the ignition that would NEVER start the car. We left the key to open the doors and trunk on his ring and replaced the ignition key with the dummy. Sure enough, when he returned home, he tried to start the car. Every time he comes in and says the car won’t start, we just point out the fact that he agreed not to drive because his eyes are so bad.

Back in February, I took him to the beach. On the way home, I needed to stop at the grocery store. He said he would wait in the car. He was in the passenger seat. “Don’t leave me, Dad.” (Famous last words.) When I came out, no dad! I just started laughing. I should have known better. After a while, I spotted the car at the far end of the strip mall. I ran as fast as I could, pushing the cart. When I almost reached the car. He took off. This happened two or three times before I caught him. I almost believed he was doing it just for fun. I just thought I’d share this, since so many days with LBD are so tough. Some things that happen are a blessing. When dad is gone, I’ll remember the day he exercised me at the grocery store.
Father has LBD, lives 400 miles away

American Family Physicians article on DLB

I ran across this 2006 article today in the American Family Physician journal. It’s a good, short description of dementia with Lewy bodies, intended for use by family practic physicians.

You can get the article free online at: –> in HTML –> in PDF

You might provide this article to your general/family practice MD!

The diagnostic criteria listed in Table 1 of the article is from 1996. The diagnostic criteria was updated in 2005. (The latest criteria are: McKeith IG, Dickson DW, Lowe J, et al. Diagnosis and management of dementia with Lewy bodies: third report of the DLB consortium. Neurology 2005;65:1863­72.)

Figure 1 offers a good comparison of AD and DLB.

In the section on pharmacological treatment of DLB, the authors state: “Patients with significant visual hallucinations are reported to have better response to cholinesterase inhibitor therapy than other patients with dementia; these medications improve fluctuating cognition, hallucinations, apathy, anxiety, and sleep disturbances.” (ChEIs include Aricept, Exelon, and Razadyne.)

And: “Patients who have dementia with Lewy bodies should not be given the older, typical D2-antagonist antipsychotic agents such as haloperidol (Haldol), fluphenazine (Prolixin), and chlorpromazine (Thorazine). Patient records should document this and caregivers should be informed. As many as one half of patients who have dementia with Lewy bodies who receive neuroleptic medications experience life-threatening adverse effects characterized by sedation, rigidity, postural instability, falls, increased confusion, and neuroleptic malignant syndrome, with an associated two- to threefold increase in mortality. Atypical antipsychotics may be tried in low doses, but these can cause similar adverse effects and increase the risk of stroke.”

The associated summary handout for patients and families is very disappointing:

Copied below is the abstract of the article.



American Family Physician. 2006 Apr 1;73(7):1223-9.

Dementia with Lewy bodies: an emerging disease.Neef D, Walling AD.
Via Christi Family Medicine Residency, Wichita, Kansas 67218, USA.

Dementia with Lewy bodies appears to be the second most common form of dementia, accounting for about one in five cases. The condition is characterized by dementia accompanied by delirium, visual hallucinations, and parkinsonism. Other common symptoms include syncope, falls, sleep disorders, and depression. The presence of both Lewy bodies and amyloid plaques with deficiencies in both acetylcholine and dopamine neurotransmitters suggests that dementia with Lewy bodies represents the middle of a disease spectrum ranging from Alzheimer’s disease to Parkinson’s disease. The diagnosis of dementia with Lewy bodies is based on clinical features and exclusion of other diagnoses. Individualized behavioral, environmental, and pharmacologic therapies are used to alleviate symptoms and support patients and their families. Cholinesterase inhibitors are more effective in patients who have dementia with Lewy bodies than in those with Alzheimer’s disease. Conversely, patients who have dementia with Lewy bodies do not respond as well to antiparkinsonian medications. Anticholinergic medications should be avoided because they exacerbate the symptoms of dementia. Traditional antipsychotic medications can precipitate severe reactions and may double or triple the rate of mortality in patients who have dementia with Lewy bodies.

PubMed ID#: 16623209 (see for abstract)