Article on Alternative Therapies and PD

PSP Forum –
Sorry for the screwy formatting of this post. These are two emails below that I sent in August ’06 to the local (SF Bay Area) support group on “alternative therapies” (including CoQ10) and Parkinson’s Disease. (I thought the author worked at Scripps but the institution is Cedars-Sinai.) It’s just easier to copy-and-paste rather than re-work the two emails. If you are interested in seeing these sorts of posts from me, note that I am a regular poster on (Yahoo!Groups). I don’t regularly come to the Forum (because I dislike using anything but email to post and read).

Date: Wed, 23 Aug 2006 18:38:47 -0700
To: Local Support Group
From: Robin Riddle <[email protected]>
Subject: Fwd: “Alternative Therapies” & PD (Co-Q10, vitamin C, creatine, etc)

This updated email will be of interest to those considering NADH, glutathione, massage therapy, and exercise. There’s also a resource list for additional info on alternative therapies.

The “Alternative Therapies” article provided answers to seven questions. I found an earlier article by the same author, Dr. Jill Marjama-Lyons, that had ten questions. Perhaps three questions were eliminated to fit the article on one page in the APDA Newsletter Spring 2006. The earlier article was written perhaps in 2004 or early 2005. Here are the three new questions along with the exercise question answered again (because the earlier article gave a longer answer), a resource list (books, etc) for holistic therapies (“holistic” is the preferred term), and some info on the author:

Should persons with PD take NADH? Similar to Co-Q10, NADH (nicotinamide adenine dinucleotide hydrogen) is an enzyme that is involved in energy production of living cells. NADH is not a proven treatment for Parkinson’s disease. Several open-label (patients and examiners were not blinded) studies have shown motor improvement in persons with PD who took NADH. One small double-blinded, controlled study of 10 persons with Parkinson’s disease who took intravenous NADH did not indicate that any improvement occurred in patients.

Should a person take IV(intravenous) glutathione for Parkinson’s? Glutathione is not an approved treatment for Parkinson’s disease. Similar to Co-Q10, glutathione levels have been shown to be lower in persons with PD. Despite many personal stories of patients feeling better with use of IV glutathione, currently there are no published controlled studies proving or disproving it as a therapy for PD.

Can massage therapy help people with Parkinson’s disease? Some persons with PD report massage therapy to lessen muscle stiffness (rigidity) and pain, though the benefit is often transitory and last a few hours or days.

Does exercise really make a difference? Exercise of any kind that does not increase one’s risk of falling is always recommended to increase endurance, improve delivery of oxygen to the brain, heart and muscles, increase muscle strength and mass, and improve coordination, balance and flexibility. Exercises such as yoga and tai chi focus on the mind-body connection and improve balance and mobility for persons with Parkinson’s and many PD centers and health clubs offer these exercise classes. Even for someone with advanced Parkinson’s disease, exercise can make a big difference; chair and bed/floor stretches/movements as well as swimming can be performed by almost anyone. (Note from Robin: the last sentence is not in the APDA Newsletter Spring ’06.)

Resource List for Holistic Therapies
(Note from Robin: the author of the article has a book listed below – third item down. It was recommended to me by someone who used to work with Dr. Marjama-Lyons at Cedars-Sinai Medical Center.)

The American Holistic Health Association’s Complete Guide to Alternative Medicine, by William Collinge, M.P.H., Ph.D.

Alternative Medicine: The Definitive Guide, edited by Burton Goldberg (Future Medicine, 1998), features over 400 holistic practitioners

What Your Doctor May Not Tell You About Parkinson’s Disease: A Holistic Program for Optimal Wellness, by Jill Marjama-Lyons, MD and Mary Shomon (Warner Books, 2003)

PDR for Herbal Medicine, (First Edition, 1999) Medical Economics Company

Prescription for Nutritional Healing, by James Balch, MD and Phylis Balch (Avery Penguin Putnam, 2000)

Tyler’s Herbs of Choice: The Therapeutic Use of Phytomedicinals, by James E. Robbers and Varro E. Tyler

Eat Well, Stay Well With Parkinson’s Disease,by Kathrynn Holden, M.S., R.D. (Five Star Living, 1998)

The Brain Wellness Plan, by Jay Lombard, M.D. and Carl Germono

American Holistic Health Association P.O. Box 17400, Anaheim, California 92817 / (714-779-6152/

NIH National Center for Complementary and Alternative Medicine (NCCAM) 888-644-6226 /

Mind Body Medical Institute 110 Francis St., Boston, Massachusettes 02215 / (617-632-9530) /

American Association of Oriental Medicine 433 Front St., Catasauqua, Pennsylvania 18032 / (888-555-7999) /

Acupuncture Page Listing licensed acupuncturists in each state,

The Homeopathy Home Page

Nutritional Web Site

About the Author: Dr. Marjama-Lyons received her bachelors degree in psychology from the University of North Carolina in Chapel Hill and her medical degree from S.U.N.Y Health Sciences Center in Syracuse, NY. She completed her internship at the University of Rochester and her neurology residency at the University of Arizona followed by a fellowship in Parkinson’s disease at Kansas University. She was assistant professor and medical director of The Parkinson Center at the University of Florida in Jacksonville, and currently is regional director of PADRECC (Parkinson Disease Research Education and Clinical Center) at the Albuquerque VA Hospital, Director of the NPF Parkinson Outreach Program serving Navajo persons with Parkinson’s and medical director of a new Deep Brain Stimulation program in Albuquerque. She is co-author of What Your Doctor May Not Tell You About Parkinson’s Disease: A Holistic Program for Optimal Wellness published by Warner Books (February 2003) and author of the National Parkinson Foundation Medication and Deep Brain Stimulation Manuals. She is dedicated to patient education and believes in a holistic approach to care and life.

(Note from Robin: The author’s name was misspelled in the APDA Newsletter Spring ’06.)

3 Forms of PSP – RS, PSP-P, and PPFG

The Society for PSP had an International PSP Resarch Symposium on 11/17/05, right after the annual meeting of the Society for Neuroscience in Washington, DC.  The latest issues of the PSP Advocate has an interesting series of articles on some of the presentations made by scientists at the Symposium.

One scientific abstract I found worthwhile was written by David Williams, MBBS, FRACP, of the Queen Square Brain Bank (QSBB), the Sara Koe PSP Research Center, etc., London.

Dr. Williams said that clinicians can use some key differences between PD and some types of PSP in differentiating PD from some types of PSP in a clinical setting.  Specifically, the “timing of falls, the presence of visual hallucinations and testing of smell should be helpful in distinguishing PSP-P and PPFG from PD.”  (PD patients start falling later, nearly half have sustained visual hallucinations, and a decreased sense of smell.)

Also, he identified three distinct types of PSP:

  • Richardson’s Syndrome (RS):  early onset of postural instability and falls, gaze difficulties, and dementia.  54% of cases in the study.
  • PSP-parkinsonism (PSP-P):  non-symmetrical symptom onset, tremor, and a moderate initial therapeutic response to levodopa.  32% of cases in the study.  Obviously this type is often confused with Parkinson’s Disease.
  • Primary progressive freezing gait (PPFG):  early onset of gait freezing without other neurological signs. 4% of cases in the study.

Here are some excerpts from the scientific abstract about survival time and other symptoms:

“…We have recently identified two apparently distinct clinical types of PSP by analyzing clinical case notes of patients with a pathological diagnosis, archived at the Queen Square Brain Bank, London. We have named these two clinical types: Richardson’s syndrome (RS) and PSP-Parkinsonism (P).

Disease duration in RS was shorter (average 5.9 vs. 9.1 years), falls occurred earlier and age at death was younger (72.1 vs. 75.5 years) than in PSP-P. …

Primary progressive freezing gait (PPFG) … had longer disease duration (average 12.8 years) and late onset of gaze palsy and dementia compared with RS.

Other clinical analysis at QSBB has shown that sustained visual hallucinations are exceedingly rare in PSP (3%), but relatively common in Parkinson’s disease (PD, 49%). A decreased sense of smell is usual in Parkinson’s disease but not common in PSP. The time from symptom onset to first fall is early in PSP: 57% of patients with PSP fall within two years, 
compared to 6% with PD. The timing of falls, the presence of visual hallucinations and testing of smell should be helpful in distinguishing PSP-P and PPFG from Parkinson’s disease in the clinic…”

You can find this scientific abstract and the related lay abstract along with all the other articles online at:



“Foiling Chemical Event May Combat Brain Breakdown”

This post is about an interesting article on preventing misfolded protein accumulations (which occurs in AD, PD, and many related diseases), protecting an enzyme (called called protein disulphide isomerase), and stopping a chemical (nitric oxide) from wreaking havoc in the brain.

The Bloomberg News article talks about a study just published in the journal Nature. The aarticle notes:

“While previous studies showed that nitric oxide can be involved in the degeneration of brain cells through a variety of mechanisms, the new study shows a previously unrecognized relationship between the chemical and protein misfolding.”

Here’s a link to the article:

Foiling Chemical Event May Combat Brain Breakdown, Study Says
May 24, 2006

“A Surprising Clue to Parkinson’s” (MIT Technology Review)

I saw an article in the May/June ’06 issue of Technology Review, an MIT publication, related to protein aggregations in those with PD and other diseases. What I found interesting was the fact that there is not scientific agreement over whether abnormal protein aggregations in the brain are a bad thing. The author says that the MIT biotechnology study demonstrates “that increased protein aggregation can improve the health of cells modeling neurodegenerative disease.”

That led to a related article published on the Technology Review’s website on 3/7/06. Excerpts from that March article:

“It’s easy to distinguish a healthy person from a person with advanced Parkinson’s: the Parkinson’s sufferer has large clumps of proteins in his or her brain cells. Scientists disagree, however, about the nature of these clumps. Some contend that they lead to the massive neuronal cell death and resulting movement disorders in Parkinson’s, others that the clumps are merely a byproduct of the disease — and some scientists contend that the clumps are actually protective, sequestering toxic proteins so they can’t hurt the cell. Mounting evidence points to the last possibility.”

“Existing research already suggests that the biggest clumps, known as inclusions, are helpful. Cells that form clumps of the mutant Huntington protein, for example, survive longer than clump-free cells. Now MIT scientists have discovered a compound that increases clumps in cell models of Huntington’s and Parkinson’s disease and makes the cells healthier. Scientists aren’t sure how the compound works, but they think it might be helping cells get rid of toxic forms of the proteins floating around in the cell by isolating them into clumps.”

Here’s a link to the older article:

A Surprising Clue to Parkinson’s
Drugs that boost the protein clumping that occurs during neurodegenerative disease could provide a new route to treatment.
Technology Review (MIT)
By Emily Singer
March 7, 2006

And a link to the newer article:

A Curious Clue to Parkinson’s
Drugs that boost protein aggregation could provide a new route to treatment
Technology Review (MIT)
May/June 2006

Journal article on MRIs to distinguish PSP, MSA, and PD

This article in the Movement Disorder Society magazine (of the UK) is on using MRIs to distinguish between Progressive supranuclear palsy (PSP), Multiple system atrophy (MSA), and Parkinson’s disease (PD). Apparently the technique is most (only?) effective in later stages. This was published online on 4/6/06. The abstract is below.



Regional brain volumes distinguish PSP, MSA-P, and PD: MRI-based clinico-radiological correlations
Dominic C. Paviour, MRCP, Shona L. Price, BSc, Marjan Jahanshahi, PhD , Andrew J. Lees, MD, FRCP , Nick C. Fox, MD, FRCP

Progressive supranuclear palsy (PSP) and multiple system atrophy (MSA) are neurodegenerative disorders, each with a prevalence of around 5 per 100,000. Regional brain atrophy patterns differ in the two disorders, however, and magnetic resonance imaging is sometimes helpful in distinguishing them in the later stages. We measured whole brain and regional volumes, including cerebellum, pons, midbrain, superior cerebellar peduncle (SCP), and ventricular volumes as well as frontal and posterior-inferior cerebral regions in 18 subjects with PSP, 9 with MSA-P (parkinsonian phenotype), 9 with Parkinson’s disease (PD), and 18 healthy controls. Associations between these volumes, cognitive profiles, and clinical measures of disease severity and motor disability were assessed. Mean midbrain volume was 30% smaller in PSP than in PD or controls (P < 0.001) and 15% smaller than in MSA-P (P = 0.009). The mean SCP volume in PSP was 30% smaller than in MSA-P, PD, or controls (P < 0.001). Mean cerebellar volumes in MSA-P were 20% smaller than in controls and PD and 18% smaller than in PSP (P = 0.01). Mean pontine volume in MSA-P was 30% smaller than in PD or controls (P < 0.001) and 25% smaller than in PSP (P = 0.01). Motor disability was most strongly associated with midbrain volume, and more severe executive dysfunction was associated with reduced frontal volume. These distinct patterns of cortical and subcortical atrophy, when considered together rather than independently, better differentiate PSP and MSA-P from each other and also from healthy controls. © 2006 Movement Disorder Society

“Applause sign” to diagnose PSP?

The “applause sign” test is useful in diagnosing progressive supranuclear palsy (PSP), according to recent research.  The “applause sign” is where you ask someone who might have PSP to clap.  While clapping, you tell them to stop.  The person with PSP continues to clap; it takes them awhile to stop.

In a study done by Dubois, 30 out of 42 patients diagnosed with PSP could not stop applauding immediately after being told to stop.  None of those with frontotemporal dementia (FTD) or Parkinson’s Disease (PD) had trouble stopping.

So I guess the part of the brain that controls this process is not affected by PD or FTD…?  The “applause sign” is an indication of “motor perseveration.” Perhaps this is controlled by the frontal lobe so interesting that it’s not affected in FTD.

I’ll ask the neurologist to do this in Dad’s next appt.  I’m interested in seeing this.

Copied below is part of the abstract of the Dubois article (published 6/05 in Neurology) from PubMed (



“Applause sign” helps to discriminate PSP from FTD and PD

The “applause sign” is a simple test of motor control that helps to differentiate PSP from frontal or striatofrontal degenerative diseases. It was found in 0/39 controls, 0 of 24 patients with frontotemporal dementia (FTD), 0 of 17 patients with Parkinson disease (PD), and 30/42 patients with progressive supranuclear palsy (PSP). It discriminated PSP from FTD (p < 0.001) and PD (p < 0.00). The “three clap test” correctly identified 81.8% of the patients in the comparison PSP and FTD and 75% of the patients in the comparison of PSP and PD.

NIH/NINDS Creatine Study Press Release

If you are interested in research going on in the Parkinson’s world that might affect the atypical parkinsonism disorders, this post may be of value to you.

The National Institute of Neurological Disorders and Stroke (NINDS) of the National Institutes of Health (NIH) has organized a nationwide effort called NET-PD (Neuroprotection Exploratory Trials in Parkinson’s Disease), a randomized, double-blind futility trial, to study compounds that may slow the clinical decline of Parkinson’s disease.  Creatine and the antibiotic minocycline were identified as agents worthy of preliminary study.

In a press release on the study that was released in conjunction with the World Parkinson Congress in Feb ’06, the lead investigator said that a “clinical trial with 200 Parkinson’s disease patients has shown that creatine and minocycline may warrant further consideration for study in a large trial.”

Here’s a link to the press release titled
“Preliminary Results Shows Creatine and Minocycline May Warrant Further Study in Parkinson’s Disease”:

The bottom line is this:

“The trial investigators note that while encouraging, this pilot study does not have sufficient numbers of patients or duration of follow-up to recommend that patients with Parkinson’s take either agent.  In fact, the investigators caution Parkinson’s patients and their physicians not to interpret the results of this study as suggesting such a course of treatment.  Further study is required before the researchers can conclude whether creatine or minocycline is in fact helpful, harmful or has no significant impact.”


Points from an expert physical therapist – on PD and parkinsonism

I attended Marilyn Basham’s presentation this afternoon on “Caregiving Made Easy for Parkinson’s Individuals.”  She’s the physical therapist (PT) at The Parkinson’s Institute (TPI).  I picked up a few tidbits at the presentation that I thought I’d pass along.  As the presentation was focused on Parkinson’s Disease (PD), not everything applied to the situations we are dealing with but there were still many interesting points that apply.

Here are the points I found interesting….  (with some of my comments in parantheses)

People with PD and Parkinsonism MUST use a walker or wheelchair to make them as safe as possible.  It’s very important to have mobility and postural strategies worked out with a physical therapist and/or neurologist.

PD is evident when 60-80% of the cells in the basal ganglia have died.

The “automatic motor programs” we have are stored in the basal ganglia.  One of these “programs” is what tells us that to stand up from a low chair, we need to scoot to the edge, put our feet underneath us, lean forward, and push up.  PD folks must either receive cues as to the steps of these programs, or they must practice it so many times that doing it becomes somewhat automatic again.

To overcome freezing (called “gait initiation failure”), you can put masking tape on the floor to provide a visual cue.  Put the tape at thresholds or where ever the person often has the freezing problem.  (Of course this won’t work for those with PSP who have downward gaze palsy.)

A suggested verbal cue to give someone who wants to speak is:  “Swallow.”  (pause to let the person swallow)  “Take a deep breath in and then, at the top of your breath tell me what you want.”  (pause to let this happen)  Swallowing is important because fluid accumulates in the back of the throat and those with PD are not aware of it.  You can give them gum to initiate a swallow response.

Before someone with MSA (or PD with blood pressure fluctuations) stands up, give them a glass of water with salt in it or Gatoraid.  This will increase the blood pressure.  Obviously the person’s diet and blood pressure medication needs to be taken into account before following this suggestion.

We must give time for those with these diseases to process information!  Be patient!  Give long pauses.  Don’t overload them.  Don’t give them more than one complex task at a time.  Walking is a complex task.

(Some of you know that my father and I communicate by our holding up fingers to designate an answer.  Example, “do you want 1 for coffee, 2 for tea, or 3 for nothing,” and I hold up 1, 2, and 3 fingers.  He answers by holding up fingers.  Long after the fingers come up, he may try to verbalize the answer.)  I asked Marilyn why my father could hold up fingers faster than he could verbalize a response.  Marilyn said she didn’t know why but pointed out that parents of small children teach their children sign language long before the children can verbalize.

Dementia is rare in PD.  (It’s definitely common in the Atypical Parkinsonism diseases.)  PD folks may lose their keys but they still remember what keys are and how to use them.  (I thought that was a good story for remembering what dementia is.  My dad, for example, cannot remember how to use an ATM card.  I see the dementia very clearly.)

A patch for Sinemet is in the works.  (Some of your loved ones take Sinemet.)

The head of TPI thinks that PD is the most curable of all the neurodegenerative diseases.  (Let’s hope he’s right because hopefully those diseases related to PD can be cured quickly too.)


Two distinct types of PSP – RS and PSP-parkinsonism

Here’s the citation to a very important paper published recently on progressive supranuclear palsy (PSP):

Brain. 2005 Jun;128(Pt 6):1247-58. Epub 2005 Mar 23. 
Characteristics of two distinct clinical phenotypes in pathologically proven progressive supranuclear palsy: Richardson’s syndrome and PSP-parkinsonism.
Williams DR, de Silva R, Paviour DC, Pittman A, Watt HC, Kilford L, Holton JL, Revesz T, Lees AJ.
The Queen Square Brain Bank for Neurological Disorders, University College London, UK.

Dr. David Williams and others from The Queen Square Brain Bank in London examined the brains and clinical records of 103 people with autopsy-confirmed PSP.  They discovered two key clinical types of PSP:  Richardson’s Syndrome and PSP-parkinsonism.

The authors described Richardson’s Syndrome (RS) as follows:

“The core clinical features of PSP appears to be bradykinesia, rigidity and postural instability, and are almost always present later in the disease.  Together with the supranuclear vertical ophthalmoplegia, dementia, dysarthria and pseudobulbar palsy, they form the classic features of PSP.  When these features appear in the first 2 years, a diagnosis of RS is most likely.”

The authors described the PSP-parkinsonism type as follows:

“The features which most clearly differentiate this syndrome from RS appear to be an asymmetric onset, extra-axial dystonia, tremor and benefit from levodopa.  Early bradykinesia appears to be essential for the diagnosis, but does not adequately differentiate it from RS, especially later in the disease course.  Disease duration in PSP-P is significantly longer than in RS, and to our knowledge exceeds median survival in all clinicopathological PSP case series.”

Here’s the abstract to this important paper:  (broken into paragraphs)

“The clinical diagnosis of progressive supranuclear palsy (PSP) relies on the identification of characteristic signs and symptoms. A proportion of pathologically diagnosed cases do not develop these classic features, prove difficult to diagnose during life and are considered as atypical PSP. The aim of this study was to examine the apparent clinical dichotomy between typical and atypical PSP, and to compare the biochemical and genetic characteristics of these groups.

In 103 consecutive cases of pathologically confirmed PSP, we have identified two clinical phenotypes by factor analysis which we have named Richardson’s syndrome (RS) and PSP-parkinsonism (PSP-P). Cases of RS syndrome made up 54% of all cases, and were characterized by the early onset of postural instability and falls, supranuclear vertical gaze palsy and cognitive dysfunction. A second group of 33 (32%) were characterized by asymmetric onset, tremor, a moderate initial therapeutic response to levodopa and were frequently confused with Parkinson’s disease (PSP-P). Fourteen cases (14%) could not be separated according to these criteria. In RS, two-thirds of cases were men, whereas the sex distribution in PSP-P was even. Disease duration in RS was significantly shorter (5.9 versus 9.1 years, P < 0.001) and age at death earlier (72.1 versus 75.5 years, P = 0.01) than in PSP-P.

The isoform composition of insoluble tangle-tau isolated from the basal pons also differed significantly. In RS, the mean four-repeat:three-repeat tau ratio was 2.84 and in PSP-P it was 1.63 (P < 0.003). The effect of the H1,H1 PSP susceptibility genotype appeared stronger in RS than in PSP-P (odds ratio 13.2 versus 4.5). The difference in genotype frequencies between the clinical subgroups was not significant. There were no differences in apolipoprotein E genotypes.

The classic clinical description of PSP, which includes supranuclear gaze palsy, early falls and dementia, does not adequately describe one-third of cases in this series of pathologically confirmed cases. We propose that PSP-P represents a second discrete clinical phenotype that needs to be clinically distinguished from classical PSP (RS). The different tau isoform deposition in the basal pons suggests that this may ultimately prove to be a discrete nosological entity.”

From my reading, the PSP-parkinsonism type of PSP looks like Parkinson’s Disease and may look like MSA, specifically the parkinsonism type (MSA-P).

According to the full article, some people with PSP actually had a response to levodopa therapy!  Do the diagnostic criteria need to be changed to accommodate this finding?


Update from 2007:

This important paper is now available online at no cost.

Here’s the direct link to the Brain ’05 article:

And I think the commentary is worth reading too:


Disclose early, find roses, and hope in Parkinson’s (2005 article)

I’ve been reading about the importance of hope, and ran across this article from The Washington Post, published last week. It’s certainly worth reading. The author, Daniel Stark, has written extensively about his battle with Parkinson’s Disease (PD). Though it’s about PD, I think the principles apply to any neurodegenerative disorder.

Here’s a link:

Living Large With Parkinson’s
It’s A Messy Path Ahead, the Author Finds — But Better With a Map
By Daniel Stark
Special to The Washington Post
Tuesday, June 21, 2005; Page HE01