Resources and Tips from Occupational Therapist

This post is of general interest to both caregivers and those with neurological disorders.

PPSG (Parkinson’s Patients Support Groups, ppsg.org) held its annual “Caregiver and Volunteer Appreciation Luncheon” in September 2008 in Fremont.  One of the speakers wrote a summary of her luncheon presentation — Julie Groves, an occupational therapist.  Julie runs an outfit called Therapy in Your Home, therapyinyourhome.net. Therapy in Your Home provides OT, PT, and ST services in San Mateo, Santa Clara, and Santa Cruz counties at $100-125/visit.  You can also gain access to Julie Groves, as an occupational therapist, through CareSouth Home Health (408/871-9860) if you are in Santa Clara County (and have Medicare home health benefits).

Julie’s summary of her September presentation was published in the latest edition of the PPSG Newsletter, available online.  I’ve copied the text below.

I especially liked this comment:  “Compensate for decreased judgment, memory and comprehension rather than expecting the old level of participation and understanding.”

And the Resources section is terrific.

I’ve copied the summary below.

Robin

—————————-

www.ppsg.org/PPSG_2/Docs/December%202008.pdf  (the summary starts on page 3)

Volunteers Appreciation Luncheon: OT says “Thank You!”
A Speech Summary from Julie Groves, OT
PPSG Newsletter
November/December 2008

– I spoke of my love for my profession of Occupational Therapy with an emphasis on DOING, ENGAGING, CHALLENGING, ADAPTING, COMPENSATING, and making the task ENJOYABLE. Those words describe OT as well as what you do. I spoke of the neuro-research that supports why DOING at the right level of challenge is effective. As Dr. Liang also reiterated, since 1998 we know that brain cells can re-grow, grow more connections and have more efficient synapses. Although some cells may be damaged by PD, you are never too old to learn new techniques. And you, volunteers, might want to go back to school to be an OT!

We discussed specifically:

– Dexterity and using large arm movements: Using art work, washing windows, shooting the rubber band from the morning paper.

– Rhythm: Clapping, drumming, listening and responding to music, applying these concepts to mobility, and dancing (in a wheel chair, behind a wheelchair, both of you holding a walker, rocking arm in arm), and the PD Tango Class at Avenidas Senior Center in Palo Alto.

– Facial exercise and swallow skills: Laugh with the funny faces, use your hands to encourage those muscles to move, pause long enough for a response, sing, and yell.  Make poetry with the KKK and GGG sounds which help the swallow muscles.

– Breathing: Again, yell and sing for fun! Use your hands on the rib cage, encourage breathing into your hands and help expel the air with a firm pressure. Touch almost always makes an activity more meaningful and enjoyable. And while you are at it, be sure to breath out long and slowly yourself!

– Move more: From the audience came discussions of Tai Chi and of the Wii, both known to be beneficial for people with PD. The Parkinson’s Institute is planning training in use of the Wii; call to get on their list. The Wii is the ultimate biofeedback machine, encourages challenge, participation, adaptation for different levels of participation and skill. The grandkids or friends or significant others can play it with you. We discussed Wii sports, Wii dance and Wii Fit. Wii is like your grandkids’ Xbox but interactive. It’s not cheap, but the benefits may make it worth it. Hook up the box to your TV and hold the wireless controller. The TV/box senses how you move (swing a bat, change your balance, launch a bowling ball) and shows the result on the TV screen, giving you immediate feedback and you just WANT to do it again better.

– Finally: take care of yourself. Besides all the usual ways, we discussed:
* Anticipate change, prepare
* Accept help, ask for help
* Compensate for decreased judgment, memory and comprehension rather than expecting the old level of participation and understanding
* Be ready to say “no.” Look ahead; will you be able to do this next year? What will you do on a bad day? Adapt, before you need to, before you get worn down and grumpy. Think through your options, talk about them with your support system.

A question was raised later in the program about why the healthcare community doesn’t address all the other symptoms of PD: constipation, lack of concentration, stiffness and fatigue, depression. Research shows healthcare providers are not comfortable or skilled at talking about these subjects. If you can bring up the subject it is more likely to be discussed, and we are more likely to learn more about how PD is impacting you.

Some resources that were requested:

Places to get equipment and ideas:
* Abledata.com, 1-800-227-0216: ABLEDATA provides objective information about assistive technology products and rehabilitation equipment available from domestic and international sources. Although ABLEDATA does not sell any products, they can help you locate the companies that do. Hint: call and ask, don’t just use the online version.
* SammonsPreston.com
* Ncmedical.com
* Alimed.com

Resources about attending to all the other needs of the person with PD:
* “My Mother, Your Mother” by Dennis McCullough.  “Slow Medicine” advocates for careful anticipatory “attending” to an elder’s changing needs rather than waiting for crises that force acute medical interventions–an approach that improves the quality of elders’ extended late lives without bankrupting their families financially or emotionally
* Handbook for Mortals by Diane Lynn, available in full online
* CodaAlliance.org and the Go Wish Cards for facilitating difficult conversations.

Finally, consider asking for Occupational and Physical therapy each time there is a change of condition. Your insurance probably covers therapy, and it is available through Outpatient or, if you are homebound, through Home Health. In some cases you might need to pay privately for therapy at $80 to $130 an hour. Be sure to explain to the therapist what the problems are that you are experiencing and ask for (demand?) practical solutions, not just more exercises. Help the therapist understand your individual needs.

Thank you, again.
Julie Groves, Therapy in Your Home — OT, PT, ST

 

“Handbook for Mortals”

This publication — “Handbook for Mortals” — was recently recommended to me. It is available for free online at: 

http://www.growthhouse.org/educate/flash/mortals/layouts/frameset1.html


Or you can purchase it from amazon.com for about $15. 

The chapter on “Controlling Pain” is particularly good. This topic is covered from the point of view of end-of-life pain but of course many people in our group experience pain and are not at the end of life. 

Advance care directives and related topics about forgoing medical treatment are discussed*. 

Happy Thanksgiving! 

Robin 


* The table of contents includes: 

1. Living With Serious Illness 
2. Enduring And Changing 
3. Finding Meaning 
4. Helping Family Make Decisions And Give Care 
5. Getting The Help You Need 
6. Talking With Your Doctor 
7. Controlling Pain 
Types of pain 
Choosing the right pain medicine 
Different ways to take pain medicine 
Doses of pain medicine 
A few rules about pain medicine 
How often to take pain medicine 
Fear of addiction 
Side effects of pain medication 
More medications that relieve pain 
8. Managing Other Symptoms 
9. Learning About Specific Illnesses 
10. Planning Ahead 
11. Forgoing Medical Treatment 
Thinking about the issues 
Stopping treatment 
Time-limited trials 
When food seems like love 
The benefits of dehydration at the end of life 
Tube feeding and the dementia patient 
Artificial feeding and the permanently unconscious patient 
Choosing to stop eating and drinking 
Decisions about ventilators 
Decisions about resuscitation 
The many meanings of “DNR” 
Other decisions to forgo treatment 
12. Hastening Death 
13. Coping With Events Near Death 
14. The Dying Of Children 
15. Dying Suddenly 
16. Enduring Loss

5 CBD research grants; NAP is focus of UCSF, UPenn, MayoRoch

In August ’08, it was announced that the Pollin family had given over $1 million to CurePSP to fund CBD research. (We discussed that here: http://forum.psp.org/viewtopic.php?t=7499)

CurePSP recently announced that a total of $1.15 million in research grants have been given to:
* Mt. Sinai School of Medicine, NY, Dr. Giulio Pasinetti
* University of South Florida, Tampa, Dr. Chad Dickey
* UCSF, San Francisco, Dr. Adam Boxer
* Duke University Med Ctr, Durham, Dr. Hana Dawson
* Cleveland Clinic, Cleveland, Dr. Kiran Bhaskar
(See http://www.psp.org/doc_library/1226690767/cbd%20pr.pdf for the short press release.)

The remainder of this post is about the research that will be conducted at UCSF, UPenn, and Mayo Rochester, hopefully beginning in April ’09.

Dr. Boxer, a neurologist at UCSF’s Memory & Aging Clinic, said that in the spring of 2009 UCSF intends to conduct a trial in CBD (and FTLD) patients with a drug called NAP. He needs to go through the UCSF IRB first as well as the FDA. The research project that Dr. Boxer will manage will potentially include two additional sites — UPenn (with whom UCSF has a close working relationship) and Mayo Rochester. UPenn and Mayo Rochester will also have to go through their IRBs.

(CBD folks can see some preliminary details that I posted recently on the CBD-related Yahoo!Group.)

I posted in late July about news out of the Alzheimer’s conference regarding the experimental drug Rember. (To re-live that news, see http://forum.psp.org/viewtopic.php?p=39893)

Like Rember, NAP is a tau-busting drug. It was also announced at the Alzheimer’s conference (ICAD) in Chicago. A trial of a NAP-derived compound called AL-108 was organized by a Duke University researcher. The drug was administered via a nasal spray for a twelve-week period in those with aMCI (amnesic mild cognitive impairment), thought to be a possible precursor to Alzheimer’s Disease. After four weeks of using the nasal spray, aMCI patients showed improvements in the ability to count backwards and to remember four objects. Here’s a short Good Morning America (ABC News) clip on this treatment from 7/29/08:
http://abcnews.go.com/GMA/story?id=5469940 (you may have to click on “Reload” to get this page to load properly)

The MD interviewed by GMA, Dr. Marie Savard, notes that it may be several years before we know if this treatment will be proven effective. This is still very early in the research into this drug. The GMA clip suggests people look on clinicaltrials.gov for trial info. I’m not sure why. The Duke-managed trial is listed but nothing else.

There is no published data on the Duke-managed human trial. There is published data on the mouse trial. You can find the abstract on pubmed.gov using PubMed ID# 18199809. (You can pay $10 to access the full journal article online.)

Allon Therapeutics, a Canadian company, is the manufacturer of AL-108. Here’s the company’s 7/30/08 press release on the AL-108 research:
http://www.allontherapeutics.com/ir_jul30_2008.html
You can also dig around on their website to find their ICAD ’08 presentation.

For an outside perspective, this Medscape Medical News article is worth reading:
http://www.medscape.com/viewarticle/578314
The article points out that the results of the “12-week, phase 2a, double-blind, placebo-controlled study to evaluate the safety and tolerability of AL-108…showed that the drug had a positive effect on memory that was durable at 16 weeks in subjects randomized to the high-dose group (15 mg twice daily). However, the trial missed its primary efficacy end point — a composite of cognitive memory scores from the memory components of 4 cognitive tests — but did show a trend toward efficacy at weeks 8 and 16.” An Alzheimer’s researcher at Mayo Rochester was asked to comment on the trial. He noted that “(phase) 2 trials are not powered to show efficacy”; rather, they are designed to show if a medication is safe and tolerated.

Robin

“Unraveling PSP” article (by Houghton/Litvan)

In this short abstract, the authors state: “Etiology remains elusive, but a variable combination of genetic, environmental, oxidative stress, and inflammatory factors may all contribute.” (etiology = cause)
Robin

Parkinsonism & Related Disorders. 2007;13 Suppl 3:S341-6.

Unraveling progressive supranuclear palsy: from the bedside back to the bench.

Houghton DJ, Litvan I.
Division of Movement Disorders, Department of Neurology, University of Louisville, Louisville, KY, USA.

Progressive supranuclear palsy (PSP) typically presents with a gradual onset and progressive course of symmetric levodopa-unresponsive parkinsonism characterized by postural instability with falls, supranuclear vertical gaze palsy, dysarthria, dysphagia, and cognitive and behavioral disturbances.

Though the clinical course is variable, the typical presentation is usually associated with mortality at 5-9 years after symptom onset.

The pathological hallmark of PSP is widespread neuronal cell loss with deposition of aggregated hyperphosphorylated tau, particularly within the midbrain.

Etiology remains elusive, but a variable combination of genetic, environmental, oxidative stress, and inflammatory factors may all contribute.

Genetic advances have confirmed the H1 tau haplotype on chromosome 17q21.31 to be associated with PSP, while the H2 haplotype seems protective. With greater knowledge of the molecular and genetic aspects of PSP, we can expect future diagnostic and therapeutic challenges to be more effectively met.

PubMed ID#: 18267262 (see pubmed.gov for abstract only)

Brain-Computer Interface for Communication (60 Minutes10/31)

A local support group member sent me this link to an amazing “60 Minutes” segment from last Sunday called “Brain Power.” A man with ALS (diagnosed in ’99) and a woman who had a stroke — both of whom are “locked-in” (fully functioning minds locked in disabled bodies) — are shown using their thoughts to communicate and use a computer. The man, Dr. Scott Mackler*, is a neuroscientist who is still able to run a research lab at the University of Pennsylvania. The woman also uses her mind to operate a wheelchair. It’s incredible.

The link is: (you may have to cut and paste to get the link to fit on one line)
http://www.cbsnews.com/stories/2008/10/ … 0940.shtml

Robin

* Someone on an MSA-related discussion group posted these two links for previous media coverage of Dr. Mackler:

http://www.alsphiladelphia.org/NetCommu … Doc?id=198

http://www.philadelphiaweekly.com/view.php?id=9839

NPH Commonly Misdiagnosed as PD, Atypical Parkinsonism or AD

Good Morning America (on ABC) had a segment this Thursday on NPH (normal pressure hydrocephalus). (Janet Edmunson alerted me to this segment.) Common symptoms in NPH are gait problems (shuffling), urinary incontinence, memory problems, and slowed thinking. Some of these symptoms can also be found in the four atypical parkinsonism disorders. I have occasionally read about people being diagnosed with PSP, CBD, MSA, or LBD initially, and then MDs figure out it is actually NPH. (I’ve probably read about more cases that go the other way: initial diagnosis of NPH, and a later diagnosis of an atypical parkinsonism disorder.) According to this GMA segment, NPH can be misdiagnosed as Alzheimer’s or Parkinson’s Disease. An MRI is critical in diagnosing NPH. This is one of the few dementia-causing conditions that is treatable.

Here’s a link to the video of the GMA segment:
http://abcnews.go.com/Video/playerIndex?id=6196343
(You’ll have to watch a short commercial beforehand. And the volume is set *very* high for both the ad and the segment; you can turn it down.)

At the bottom of this post is a transcript of the Good Morning America segment. Here’s a link to the transcript:
http://abcnews.go.com/GMA/OnCall/story? … 680&page=1

Finally, you can locate info on NPH here:
http://www.lifenph.com/
http://www.emedicine.com/neuro/topic277.htm

Is It Really Alzheimer’s?
NPH Commonly Is Misdiagnosed as Alzheimer’s Disease
By JUJU CHANG, THEA TRACHTENBERG and IMAEYEN IBANGA
Good Morning America (ABC News)

Nov. 6, 2008 —

When 74-year-old Phil Myers was barely able to walk and his memory seemed to be going quickly, his wife, Shirley Myers, was terrified. She watched as the man she loved and was married to for 54 years slipped away, with thoughts of the two children they’d raised clearly in her mind.

“At first I was scared,” Shirley Myers said. “He took care of his family. He was just a family man. That was it. And he did so much for me.”

Is It Alzheimer’s?
“The doctors kept saying, ‘Oh, he’s OK. He’s OK,’ but then things kept getting worse — like dragging his feet. And then he started kind of forgetting where he was at,” Shirley Myers said.

The first diagnosis doctors gave Phil Myers was devastating; they believed it was a form of Alzheimer’s.

“When they told me it was Alzheimer’s, I couldn’t believe it because he was only 70 years old and it just didn’t seem like it was his time yet,” Shirley Myers said.

So the two went to see neurologist Mark Luciano from the Cleveland Clinic. He suspected it wasn’t Alzheimer’s at all, but rather something called normal pressure hydrocephalus, or NPH.

What Is NPH?
According to “Good Morning America” medical editor Dr. Tim Johnson, NPH can begin at age 55 and no one knows why.

The condition occurs when cerebral spinal fluid accumulates in the brain. The extra fluid pushes the brain against the nerves that affect memory, walking and balance, and bladder control.

“Hydrocephalis just means water inside the brain. It’s when water builds up and starts pressing on the brain itself,” Luciano said.

“The symptoms come on very gradually and they can be very subtle,” he said. “A gait problem, a problem with your bladder control, a problem with your memory, those are all very common symptoms in our elderly population.”

Other symptoms include problems with thinking, a slowing down of the thought process. Since the symptoms are so common, the condition is often misdiagnosed.

That happens in part because the warning signs come on very gradually and they can be very subtle, Johnson said. Also, in the elderly population, loss of memory, walking slowly, bladder control problems are all very common problems, so it looks like many other diseases, such as Parkinson’s, Alzheimer’s or dementia, he added.

“It is one of the only treatable forms of dementia or memory loss. It can be not only treated, but in many cases reversed to a great extent just by removing the fluid,” Luciano said.

An MRI of the brain will show the enlarged ventricles and is a way for doctors to properly diagnose the condition, Johnson said.

Treatment of NPH
Treatment for NPH is a relatively simple operation.

“When they told us it was — it would be treatable, it was like a miracle,” Shirley Myers said. “We all felt like it’s a miracle.”

A shunt is implanted in the brain and leads the excess fluid away from the brain and into the abdomen.

“Quite honestly, we weren’t sure that fluid removal was going to help him,” Luciano said.

Four months ago, Phil Myers had the operation to implant the shunt, four years after his symptoms first appeared.

Now the man, who once had tremendous trouble walking, travels with much more ease.

“It was quite, quite nice to be able to do the things you want to do,” he said.

Phil Myers remains in recovery and Luciano said it can take up to a full year to see all the effects of the procedure.

“The improvement that we see now, we hope, that he has for many years,” Luciano said.

“He still has a ways to go on some issues, but his walking is terrific. And that’s what the doctor was looking for I think. And his balance has improved,” Shirley Myers said.

Click here to get more information about NPH: http://www.lifenph.com/

“Tau forms in CSF as a reliable biomarker” for PSP

This is a GREAT Italian study (just published last week) on the use of CSF (cerebrospinal fluid) in diagnosing PSP. The researchers found: “Truncated tau production, which selectively affects brainstem neuron susceptibility, can be considered a specific and reliable marker for PSP.”

“A total of 166 subjects were included in the study (21 PSP, 20 corticobasal degeneration syndrome, 44 frontotemporal dementia, 29 Alzheimer disease, 10 Parkinson disease, 15 dementia with Lewy bodies, and 27 individuals without any neurodegenerative disorder). Each patient underwent a standardized clinical and neuropsychological evaluation. In CSF, a semiquantitative immunoprecipitation was developed to evaluate CSF tau 33 kDa/55 kDa ratio. MRI assessment and VBM analysis was carried out.” Researchers concluded that “Tau form ratio was the lowest in progressive supranuclear palsy with no overlap with any other neurodegenerative illness.”

If this can be duplicated and if the clinical diagnoses of the 166 subjects involved in the study can be confirmed on post-mortem analysis, we will have a biomarker for diagnosing PSP.

I’m pretty sure this is the paper that Dr. Golbe was referring to in the PSP/CBD webinar a few weeks ago.

Robin

Neurology. 2008 Oct 29. [Epub ahead of print]

Tau forms in CSF as a reliable biomarker for progressive supranuclear palsy.

Borroni B, Malinverno M, Gardoni F, Alberici A, Parnetti L, Premi E, Bonuccelli U, Grassi M, Perani D, Calabresi P, Di Luca M, Padovani A.

From the Centre for Aging Brain and Dementia (B.B., A.A., E.P., A.P.), Department of Neurology, University of Brescia; the Centre of Excellence for Neurodegenerative Disorders and Department of Pharmacological Sciences (M.M., F.G., M.D.), University of Milan; the Section of Clinical Neuroscience (L.P., P.C.), University of Perugia; Department of Neurology (U.B.), University of Pisa; Department of Health Sciences (M.G.), Section of Medical Statistics & Epidemiology, University of Pavia; and the Vita-Salute San Raffaele University and Scientific Institute San Raffaele (D.P.), Milan, Italy.

OBJECTIVE: In CSF, extended (55 kDa) and truncated (33 kDa) tau forms have been previously recognized, and the tau 33 kDa/55 kDa ratio has been found significantly reduced in progressive supranuclear palsy (PSP) vs in other neurodegenerative disorders.

The aim of this study was to evaluate the diagnostic value of the CSF tau form ratio as a biomarker of PSP and to correlate the structural anatomic changes as measured by means of voxel-based morphometry (VBM) to CSF tau form ratio decrease.

METHODS: A total of 166 subjects were included in the study (21 PSP, 20 corticobasal degeneration syndrome, 44 frontotemporal dementia, 29 Alzheimer disease, 10 Parkinson disease, 15 dementia with Lewy bodies, and 27 individuals without any neurodegenerative disorder). Each patient underwent a standardized clinical and neuropsychological evaluation. In CSF, a semiquantitative immunoprecipitation was developed to evaluate CSF tau 33 kDa/55 kDa ratio. MRI assessment and VBM analysis was carried out.

RESULTS: Tau form ratio was significantly reduced in patients with PSP (0.504 +/- 0.284) when compared to age-matched controls (0.989 +/- 0.343), and to patients with other neurodegenerative conditions (range = 0.899-1.215). The area under the curve (AUC) of the receiver operating characteristic analysis in PSP vs other subgroups ranged from 0.863 to 0.937 (PSP vs others, AUC = 0.897, p < 0.0001). VBM study showed that CSF tau form ratio decrease correlated significantly with brainstem atrophy.

CONCLUSIONS: Truncated tau production, which selectively affects brainstem neuron susceptibility, can be considered a specific and reliable marker for PSP. Tau form ratio was the lowest in progressive supranuclear palsy with no overlap with any other neurodegenerative illness.

PubMed ID#: 18971445 (see pubmed.gov for abstract only)