Giving PSPers balance exercises w/and w/o eye exercises

This is an interesting little study done in Beaverton, OR and published last week in the journal “Physical Therapy.”  Ten people with the clinical diagnosis of progressive supranuclear palsy (PSP) were given balance training and eye movement exercises (“treatment group”) while nine people with PSP were given balance training only (“comparison group”).

Results were:

“The within-group analysis revealed significant improvements in stance time and walking speed for the treatment group, whereas the comparison group showed improvements in step length only.”

The abstract is copied below.

Robin
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Physical Therapy 2008 Oct 23. [Epub ahead of print]

Balance and Eye Movement Training to Improve Gait in People With Progressive Supranuclear Palsy: Quasi-Randomized Clinical Trial.

Zampieri C, Di Fabio RP.
Neurological Science Institute, Oregon Health and Science University, Beaverton, OR.

BACKGROUND AND PURPOSE: Although vertical gaze palsy and gait instability are cardinal features of progressive supranuclear palsy (PSP), little research has been done to address oculomotor and gait rehabilitation for PSP.

The purpose of this study was to compare the benefits of a program of balance training complemented with eye movement and visual awareness training versus balance training alone to rehabilitate gait in people with PSP.

Participants Nineteen people moderately affected by the disease were assigned to either a treatment group (balance plus eye movement exercises, n=10) or a comparison group (balance exercises only, n=9) in a quasi-random fashion.

METHODS: The baseline characteristics assessed were diagnosis (possible versus probable), sex, age, time of symptom onset, dementia, and severity of symptoms. Within-group, between-group, and effect size analyses were performed on kinematic gait parameters (stance time, swing time, and step length) and clinical tests 8-ft [2.4-m] walk test and Timed “Up & Go” Test).

RESULTS: The within-group analysis revealed significant improvements in stance time and walking speed for the treatment group, whereas the comparison group showed improvements in step length only. Moderate to large effects of the intervention were observed for the treatment group, and small effects were observed for the comparison group. The between-group analysis did not reveal significant changes for either group.

DISCUSSION AND CONCLUSION: These preliminary findings support the use of eye movement exercises as a complementary therapy for balance training in the rehabilitation of gait in people with PSP and moderate impairments. Additional studies powered at a higher level are needed to confirm these results.

PubMed ID#: 18948373  (see pubmed.gov for the abstract only)
 

How MDs complete death certificates and “old age” not a cause of death

Given our efforts with brain donation, we are often asked by families how they can get a certain “cause of death” listed on the death certificate (DC) and what that means.

Since a brain autopsy or body autopsy cannot be done in time for the death certificate, what is placed on the DC is largely up to the hospice MD, MD in the hospital, MD who most recently treated the patient, or coroner.  Of course families often can influence this.  And, once a brain autopsy report has been received, families can petition to have the DC modified to reflect the confirmed neurological diagnosis.  (There can be a fee associated with this.)

The topic of “cause of death” is raised in a recent blog post in the New York Times.  The author is frustrated that “old age” cannot be listed as a cause of death on a DC.  The author states:

Instead, every death must be attributed to a single disease, which is the immediate cause of death. A second disease may be cited as the intermediate cause, and a third as the underlying condition. Even in situations “when a number of conditions or multiple organ/system failure resulted in death,” the C.D.C. instructs that “the physician, medical examiner or coroner should choose…a clear and distinct etiological sequence,” a “chain of morbid events.”

The author believes that this “biomedical world view” distorts the reality that people do die of old age!

Here’s a link to the article:

newoldage.blogs.nytimes.com/2008/10/23/the-immediate-cause-of-death/

The Immediate Cause of Death
New York Times
By Jane Gross
October 23, 2008 6:12 am

Robin

Notes from PSP/CBD Webinar (10/14/08)

I thought the webinar was excellent. I hope many of you were able to attend either by the combo of web and phone, or by phone alone (as I did).

Apparently CurePSP intends to post Dr. Golbe’s PowerPoint presentation to its website some time soon. I do not believe a recording of the webinar was made, unfortunately.

“PSP” was mentioned much more often than CBD. It was unclear if some of the information was PSP-only or applied equally to both PSP and CBD. I think each item would need to be addressed with Dr. Golbe.

The following are some notes I took during the presentation. The notes include what I could recall of the questions and answers. If any of you attended the webinar, please share your notes and key take-aways!

There are two types of PSP: Richardson’s Syndrome and PSP-Parkinsonism. The most common type is RS. One-third of those with PSP have PSP-Parkinsonism (PSP-P). PSP-Parkinsonism looks like Parkinson’s Disease. People with PSP-P live longer. They are less likely to have dementia or visual problems, and they are less likely to fall. Those with PSP-P are more likely to experience tremor. (Robin’s note: If the head of the CurePSP Scientific Advisory Board is using the “two types of PSP” terminology, I conclude that it has gained acceptance among PSP experts.)

On average, those with PSP live 7 years after symptom onset. Broken down, those with RS live 5.9 years after symptom onset and those with PSP-P live 9.1 years after symptom onset. On average, those with PSP are diagnosed 3.5 years after symptom onset. This does not allow for much time for treatment. If you have an earlier age of onset, you survive longer.

In order to get people diagnosed earlier, we need to educate MDs. If MDs see unexplained falls, they should immediately think of PSP. MDs should check for eye movement problems.

There’s a list of supportive features. These are not required for a PSP diagnosis. They are simply “common symptoms” that can be “helpful clues” to an MD in making a diagnosis. (Examples: symmetric bradykinesia, retrocollis.)

In all his years caring for those with PSP, Dr. Golbe has never seen someone with Whipple’s Disease, though it is commonly screened for as part of the PSP diagnosis.

A defect in the protein tau causes: 1) disintegration of microtubules, and 2) clumping. The disintegration of microtubules causes problems in the brain. The tau tangles are the result of problems with tau.

There are three key issues in PSP:
1) too much 4-repeat tau is produced.
2) there is too much oxidation. (Rusting is one form of oxidation.) Too much oxidation damages molecules.
3) the mitochondria is not working properly.

These three key issues lead to the creation of tau tangles. Any treatment in PSP likely to have some success in slowing the disease progression needs to effect one of these three key problems.

The incidence of PSP is 1 per 100,000 people. The prevalence of PSP is 6 per 100,000 people. By comparison, Alzheimer’s Disease is 800 per 100,000 people. (Robin’s note: I believe 800 is a prevalence number.) The incidence of CBD is thought to be less than 1 per 100,000 but the incidence and prevalence of CBD have never been studied.

Of the brains at the PSP Brain Bank where the patients was diagnosed in life with PSP, only 70% actually had PSP. Those who were misdiagnosed actually had: CBD (8%), a continuum of DLBD/PD (3%), ALS (1%), and FTD (1%). FTD is “another tau disorder.” (Robin’s note: Some FTD disorders are not tau disorders but are ubiquitin disorders, so Dr. Golbe’s comment is confusing to me.)

In looking at first-degree relatives of those with PSP, 39% showed abnormalities on various rating scales. This 39% figure suggests that something genetic is going on.

There is evidence of environmental toxins. An example of this is tropical fruit. There is currently research going on into the dietary habits of those with PSP.

In research conducted 20 years ago, there was a *slim* suggestion that those with PSP were less likely to be educated, and more likely to be a factory worker or exposed to toxins used on a farm.

We can’t biopsy the brain and diagnose PSP or CBD. Confirmation of the diagnosis is only possible on post-mortem exam of brain tissue. (Robin’s note: It seems that one or two people on the CBGD_support Yahoo!Group have indicated that their loved ones *did* receive a biopsy and CBD was confirmed.)

A research paper will be published soon looking at the use of CSF (cerebrospinal fluid) in diagnosing PSP.

A family with a history of PSP was studied. We know the general location but not the specific gene associated with PSP.

Standard medication given to those with PSP and CBD includes levodopa (Sinemet) and amantadine. Levodopa sometimes helps with the slowness and stiffness. Amantadine can help sometimes for a few months.

Other medication has unproven benefits:
* amitriptyline (Elavil). Due to side effects from this medication, Dr. Golbe has stopped using it.
* ChEIs. Sometimes these help with dementia.
* SSRIs can help disinhibition.
* CoQ10 is focused on slowing the progression of PSP. It does *not* help with symptoms.

Namenda seems to be poorly tolerated in those with PSP.

Not all symptoms progress at the same rate. There is huge variability.

Sense of smell is reduced a little in PSP.

There are PSP animal models in a type of fish, fly, and worm, and in rats.

An ’05 study showed that lithium reduced hyperphosphorylation of tau. The NIH decided to fund a lithium trial in PSP and CBD. No site involved in the study has received approval yet to proceed recruiting patients. It was noted that the info on the NIH-funded lithium trial is not on the curepsp.org website.

CurePSP is funding the PSP Genetics Consortium. The goal was to have 1000 PSP brains to include in the study. They’ve ended up with 1300 brains. This is a DNA study, a genome study.

There was a question about estimating survival time in someone with PSP. Dr. Golbe replied that the best tool for prognosticating is the PSP Rating Scale he developed. Generally, patients decline at a rate of 10-12 points per year. When a patient gets to 70 points, they usually live for six months. Often the issue is the immobility leads to medical complications. (Robin’s note: You can find the PSP Rating Scale on the CurePSP website — https://www.psp.org/materials/rating_scale.pdf I used this with my dad and found it accurate.)

There was a question about the experimental drug Rember that was discussed at a recent Alzheimer’s Disease conference. Dr. Golbe said he and others are skeptical of the results reported at the conference. There are problems with the design of the trial and the data. The analysis was also suspect. The principal investigator of the trial has a conflict of interest.

There was a question about stem cell research. (Robin’s note: I’m not confident I got all of Dr. Golbe’s statements down correctly so if others listened in please help me out here!) Dr. Golbe noted that there are currently no treatment trials for stem cell therapy. We can’t replace all the dead cells in the brain. He said that stem cell therapy in the early stages of PD is relevant to the PSP world. The closest approach with relevance to PSP is to encourage cells to produce chemicals.

Rare disease of PSP affects only 5 or 6 per 100,000 people

My online friend Joe Blanc posted this article about a New Jersey man with progressive supranuclear palsy to the Society for PSP’s Forum recently.

Robin


PSP: A rare disease 
Brain ailment affects only 5 or 6 per 100,000 people, including John Tartis of Glen Gardner
BY Jeff Weber, staff writer
October 14, 2008

You likely have heard of Parkinson’s disease, Alzheimer’s disease and Lou Gehrig’s disease (also known as amyotrophic lateral sclerosis, or ALS).

What do they have in common? Each affects the brain and can cause anything from loss of memory and/or motor function to even death.

But there is another brain disease, one that affects far fewer people — only five or six per every 100,000 — but is just as potent, about which many people are not aware. It’s called progressive supranuclear palsy, or PSP, and like those other diseases, it has no cure.

There are treatments for Parkinson’s, Alzheimer’s and ALS, but none yet exists for PSP. Those suffering from the neurodegenerative ailment must work hard to live through it — usually for six to 10 years, according to the Society for PSP — until finally succumbing to it.

That’s just what 71-year-old John Tartis of Glen Gardner has been doing since being diagnosed with PSP in October 2004.

Tartis doesn’t speak much these days, finding it difficult to join conversations, but he has made one thing clear: “I feel helpless and can’t figure things out anymore.”

Tartis originally was misdiagnosed with Parkinson’s disease — a common occurrence for those with PSP, according to www.curepsp.org — but thanks to neurologist Dr. Lawrence Golbe of Robert Wood University Hospital in New Brunswick, at least he’s aware of what he has.

But that peace of mind still doesn’t help quell myriad symptoms.

“I am tired all the time but can’t sleep at night,” said Tartis, who had a scale of one to 100 devised for him by Golbe to track the progress of the disease. When first diagnosed, Tartis registered at 14. He now is at 63. “I miss being able to fool around with the car and do things myself (because) I can’t move or walk by myself.”

Tartis — a retired Newark Deputy Fire Chief who used to enjoy skiing, golf, tennis, sailing, biking and camping — also suffers from a lack of concentration and often shows disinterest in conversation. Still, he never is unpleasant nor exhibits any level of frustration.

When asked how he’s doing, Tartis simply says, “Good,” and his wife, Carol, believes he doesn’t truly understand that PSP is fatal. In fact, after a few visits to Golbe, Tartis asked, “When am I going to get better?”

Golbe’s response? “There may be a trial some time that you could participate in; otherwise, the disease will slowly progress.”

And it has. Tartis sometimes falls backward. At first, he needed only a cane. Then came a walker and now a wheelchair. He can barely write, and when he does, the penmanship often is illegible. Tartis even has difficulty feeding himself, since he cannot focus or see the food on the plate.

October is National PSP Awareness Month, and the Society for PSP and www.curepsp.org hope to get the word out about their mission of finding treatment and ultimately a cure. If there were a cure, Tartis once again could enjoy the things he loves, such as skiing, instead of watching on TV and saying, “I wish I could still do that.”

More information is available by calling 800-457-4777 or by visit the Web site.

Vivimind for dementia (available OTC in Canada)

This will only be of interest to those dealing with memory loss who are willing to obtain/try a supplement available over the counter in Canada.

There’s a psychiatrist who goes by the name “Dr. David” who was recently diagnosed with Lewy Body Dementia. He studied in the SF Bay Area. On his blog today (10/12/08), he posted about a new agent called Vivimind, recommended to him by a neurologist at the University of Pittsburgh. Vivimind is based on homotaurine. Here’s a link to the web page and most of the text of today’s blog: (I think the last two paragraphs are from Vivimind marketing materials.)

http://knittingdoc.wordpress.com/2008/1 … r-12-2008/

I told you in the last post about a new agent on the market for dementia! I present this info with tongue in cheek and only after serious thought and consideration. But there’s more.

On my recent visit with my neurologist, Oscar L. Lopez, M.D., several weeks ago, he informed me of a new chemical agent called VIVIMIND™. He said he was very familiar with it and “you should look into it on the Internet. It’s just now being released as an OTC (Over the Counter) agent in Canada. Gosh, what was I supposed to think? I’m really not one to take just any substance which someone mentions just because ‘it’s supposed to be good’ or ‘Hey, this stuff really works.’ So, yes, I do believe in vitamins, minerals and other natural substances. But I like to make sure that I know what the substance is, what it does and to have some scientific evidence before ingesting it.

So here I was, leaving his office with the name of this drug written on a piece of paper. I didn’t know what to think. It this some new fad? Is this some kind of snake oil? I knew he was highly involved with dementia research, etc. as well as being affiliated with the University of Pittsburgh Medical Center’s Neurology Department. But was he really serious?? Pam and I talked about it on the way home. She felt very encouraged by it. As for me, I was the “doubting Thomas.” Yes, please excuse the pun!

Ok, David. At least be fair. So I did a Google search on Dr. Lopez. Gee whiz! He is very nice, warm, explains things, isn’t arrogant and snooty and he listens. And low and behold, there were hundreds of links for him! He definitely is more modest than one would ever expect.

All right then. Maybe I should take this a bit more seriously. I came home and looked up the Vivimind stuff of which I am showing some info a few lines below in this blog. After much discussion with my wife, a couple friend of ours and with me, I came to this conclusion. It could be nothing and if I get it I’d be spending a lot of $$$ on nothing. But if I don’t get it, I’ll always wonder later on down the road why I didn’t get it. Maybe it’ll prove to be something over the next few years. Maybe it’ll give me many more years with a better mind. After all, I’m taking Aricept and Namenda. Each of them has a different mechanism of action which works well when taken in combination. It sounds like the Vivimind could function in yet a 3rd way. But I vacillated day after day until I knew I had to make some kind of a decision.

The 180 mile trek to Niagara Falls is the closest part of Canada to us; I called some pharmacies there and asked one of them to hold the Vivimind for me. We decided to make a ‘day trip’ and left on Friday, October 10, 2008 with Pam’s friend, Darlene. Thanks to Lewy Land, I FORGOT to print out a map from MapQuest to the pharmacy. Needless to say we got lost and were able to see some beautiful scenery along the way. Any my bladder was about to give way. We were near some trees so………….let your imagination take over at this point. I guess Pam and Darlene got a real laugh as I was trying to walk fast — they said between my balance and gait problems and trying to hold things in, I looked like a ‘contorted’ person which would scare most people away. We need to use humor with this disease. All I could think of was “Oh God. I don’t want to get arrested in a foreign country. Please don’t let any police drive by!”

After getting some directions, we finally found the pharmacy and bought some of this ‘magic potion.’ And then left to visit the Falls.

We came home and went straight to bed…..fatigued to the max. So I took Saturday off from writing on the blog. I took the first Vivimind pill on Saturday morning. I will gradually increase the dose slowly with Dr. Lopez’ guidance.

After hundreds of millions of dollars invested and 15 years of rigorous scientific research, including clinical testing with over 2,000 individuals in 68 European, 50 U.S. and 17 Canadian medical centers, VIVIMIND™ is now available for consumers.

Welcome to a new generation of memory protection. For an aging population, VIVIMIND™ represents a breakthrough in one of the key consequences of getting older – memory loss. VIVIMIND™ is a science-based natural health product that has been shown to protect memory function based on the naturally occurring ingredient, homotaurine.

Dr. David

Pain in PD

Here’s a WebMD article on some research that shows that PD is associated with pain. “The type of pain that the Parkinson’s patients most reported was related to ‘dystonia’ — involuntary muscle contractions.” Many list members here experience this sort of pain.

Here’s a link to the WebMD article and the full text:

http://www.webmd.com/parkinsons-disease … ns-sets-in

Pain Shows Up as Parkinson’s Sets In
Study Shows Pain Is Felt at Onset of Parkinson’s Disease

By Kelley Colihan
WebMD Health News
Reviewed by Louise Chang, MD

Sept. 8, 2008 — Parkinson’s disease has no known cure, although it is treated with several medicines. The movement disorder takes its time developing; it can go unnoticed for years, or show up initially as just a small shaking in your hand.

New research shows that another thing to look for as Parkinson’s takes hold is pain.

The study, led by Giovanni Defazio, MD, of the University of Bari, shows that people with Parkinson’s have more pain than those who are disease-free.

Researchers found that the pain seems to show up with the onset of the disease or shortly thereafter.

The research team looked at 402 patients who had Parkinson’s disease, comparing them to 317 people who did not have the disorder.

The groups were similar in ages (mid-60s) and the proportion of men and women.

However, more Parkinson’s participants had depression and medical conditions associated with pain symptoms, such as diabetes and herniated discs.

Taking into account age, sex, depression, and other medical conditions associated with pain, 70% of the Parkinson’s patients said they experienced pain lasting at least three months, compared with 63% of the comparison group.

The type of pain that the Parkinson’s patients most reported was related to “dystonia” — involuntary muscle contractions.

Among the Parkinson’s patients, 17% had dystonia. Dystonic pain was more commonly located in the leg, foot, neck, or shoulders.

When it came to pain that was nondystonic, rates were similar between Parkinson patients and the comparison group.

The researchers write that the brain area damaged in Parkinson’s is also involved in pain perception, so this “might at least partly account for the increased risk of pain.”

The average age for the onset of Parkinson’s disease was 60.

The researchers write that pain should be considered an important feature of Parkinson’s disease since it often begins at the onset of the disease or soon after.

They add that the findings could help lead to better treatment strategies for people with the disorder.