Monthly Archives: March 2009

Atypical Parkinsonism – Breakout session notes (3/12/09)

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On Thursday 3/12/09 at the Victory Summit (Symposium for People Living with Parkinson’s Disease) in San Jose, there was a one-hour breakout session on “Atypical Parkinson’s Disease.” There were two presenters:
* Grace Liang, MD, Neurologist/Movement Disorder Specialist, The Parkinson’s Institute
* Amy Manning-Bog, PhD, Researchers, The Parkinson’s Institute

In a one-hour period, I thought they gave a great summary of the clinical picture of the four atypical parkinsonism disorders, and of the basic research underway that pertains to these disorders with particular attention to MSA. The Q&A was especially good; there were many in the audience who grasped even the challenging research update. I shared the draft of my notes with Dr. Manning-Bog, and she kindly corrected them and expanded the explanation in a few places. Also, support group member Helen added many points I had missed. Here are our combined notes from the presentations and the Q&A…

Notes from Dr. Liang’s Presentation

In order to know what “atypical PD” is, we must first review what “typical PD” is. Typical PD:
* usually starts on one side
* usually has a resting tremor
* includes Lewy body pathology
* slow progression (several decades)
* responds to medications

Common parkinsonian motor signs include:
* bradykinesia (slowed movements)
* tremor
* rigidity
* balance difficulty/gait instability

Other motor signs of PD include:
* hypophonia
* freezing
* stooped posture
* decreased facial expression

There are many non-motor symptoms of PD:
* constipation
* sleep disorders
* depression

These additional non-motor symptoms are prominent in atypical PD:
* blood pressure fluctuations
* swallowing difficulties
* urinary symptoms
* change in thinking and memory abilities

Parkinsonism can include the following diagnoses:
* Drug-induced Parkinsonism: may be caused by dopamine blocking drugs (examples – Haldol, Reglan, Risperdal, Depakote); reversible to some extent; these medications should be avoided by those with PD or parkinsonism
* Vascular Parkinsonism: caused by loss of blood flow to certain regions of the brain; minimal response to medication

NPH (normal pressure hydrocephalus):
* symptoms include shuffling gait, urinary incontinence, and dementia
* very rare
* not easy to diagnose
* treated with surgery but not that the surgical results are variable

DLB (dementia with Lewy bodies):
* second most common dementia (after AD)
* early notable cognitive changes (can be before or after motor symptoms start; the “time course” determines whether we call this PDD or DLB)
* visual hallucinations are common and are made worse by medication
* fluctuating mental alertness
* delusions

DLB – treatment:
* there is a balance between motor and cognitive symptoms
* dementia drugs can be helpful (examples – Aricept, Exelon, Razadyne, Namenda)
* minimize factors that can increase confusion and hallucinations
* use antipsychotics sparingly for delusions and hallucinations. Note the FDA black-box warning on antipsychotics. The care team must balance the patient’s (and caregiver’s) quality of life with the risks of this type of medication.

MSA (multiple system atrophy):
* often called “Parkinson’s Plus”
* autonomic dysfunction (orthostatic hypotension or low blood pressure upon standing, urinary incontinence, erectile dysfunction)
* there is also a cerebellar form (where balance is a problem)

MSA – treatment:
* there is not usually a strong or prolonged response to PD medication
* to support blood pressure: increase fluid intake, increase salt intake, wear support stockings
* muscle exercises to improve tone and circulation (this can be something as simple as keeping the feet moving throughout the day)
* balance exercises
* evaluate whether there are sleep problems

PSP (progressive supranuclear palsy):
* named for eye movement problem: it’s hard to look up and down
* early balance problems (falls) and gait freezing
* swallowing difficulties
* speech changes
* impulsive behavior

PSP – treatment:
* PD meds may not improve symptoms (and can make balance worse)
* evaluate for speech and swallowing problems
* physical therapy and fall precautions
* dystonia and contractures might be treatable with botox injections

CBD (corticobasal degeneration):
* rare
* usually starts with loss of function of one limb
* apraxia (examples: forgotten how to put clothes on correctly; forgotten how to brush teeth correctly)
* dystonia (involuntary muscle contractions) may occur
* cognitive changes (decreased ability to interpret visual or sensory signs; language difficulty) (example of a sensory sign: the patient can’t tell if he/she is holding a dime or a nickel)

CBD – treatment:
* variable results
* might try dementia medication (Namenda or AChEIs such as Aricept, Exelon, and Razadyne)
* physical therapy is important
* speech therapy is important

“Helpers” or Important resources:
* grab bars
* walker (actually, people can become *more* mobile by using a walker)
* shower seat
* reacher (pick-up stick)
* special eating utensils with big grips and bendable metal
* gait belt
* thickener (example: ThickIt)

Fall prevention:
* remove throw rugs and clutter on floor
* don’t use a step stool
* put things at eye level rather than reaching up for things
* hold onto hand rails and don’t carry a load of things while using stairs

Key points:
* be observant
* control the environment
* protect your brain — reduce risk factors
* nutrition: consider vitamin B, fish oil, Mediterranean diet, CoQ10?, creatine. (Both CoQ10 and creatine are being studied in PD and atypical PD.)
* exercise, exercise, exercise. This is great for the mind, body, and spirit
* do something you enjoy each day

Organizational resources:
LBDA.org
curepsp.org
shy-drager.org
ppsg.org
wemove.org
caregiver.org
nfacares.org
pdtrials.org
atypical parkinsonism support group organized by Robin Riddle

Notes from Dr. Manning-Bog’s presentation:

Changes in brain tissue overlap between the atypical diseases:
* loss of dopaminergic neurons
* depletion
* presence of cytosolic inclusions

A “Lewy body inclusion” is an abnormal deposit of protein. Many proteins are included but it’s mostly alpha-synuclein.

Alpha-synucleinopathies (PD, MSA, LBD) can either be familial or sporadic.

There are modifiers:
* genetics
* environment
* aging

Alpha-synuclein comprises up to 2% of total brain protein in normal brains.

Alpha-synuclein can self-aggregate or bind itself to form multimers of the protein and even alpha-synuclein fibrils.

Alpha-synuclein aggregation (or clumping) could be due to:
* increased expression
* decreased degradation (ie, the cell doesn’t get rid of the protein)
* exposure to toxicants that can stimulate alpha-synuclein to bind itself

In the last few years, a transgenic mouse model was developed for MSA (by Eliezer Masliah’s group at UC San Diego). This is an exciting tool because researchers can isolate and manipulate the alpha-synuclein gene! Now that Dr. Masliah has generated these MSA mice, there is a tool that we can use to study mechanisms to disaggregate and clear alpha-synuclein from cells (i.e. neurons in PD and oligodendroglia in MSA). We can use this tool to test therapeutics in a pre-clinical environment.

Images were shown of alpha-synuclein fibrils in test tubes. This research was done at UC Santa Cruz. This research is promising. Researchers could disintegrate the fibrils (although not always completely) and may leave some toxic synuclein species.

Eliezer Masliah’s group at UC San Diego tried to target the aggregation of synuclein and increase the degradation of synuclein by giving the drug rifampicin to MSA mice. This partially worked. Results were promising — less cell death and alpha-synuclein deposition were apparent in mice treated with rifampicin.

Dr. Manning-Bog’s research approach is to deliver alpha-synuclein to where it needs to go. The goal is to restore alpha-synuclein trafficking via the lipid raft.

If researchers find a mechanism that prevents alpha-synuclein build-up in cells, these agents can be tested in animal models of other diseases that involve alpha-synuclein (including the MSA model or a mouse model of alpha-syn build-up in neurons).

>From this standpoint, any work that is done on these aspects of alpha-synuclein is important to any PD form that has alpha-synuclein pathology. (For example, the alpha-synuclein trafficking arm of my research program, for example, is relevant to any PD form with alpha-synuclein pathology.)

[I asked Dr. Manning-Bog why she talked about the MSA mouse model during her presentation. She replied: “While putting together my talk for the symposium, I asked Dr. Brandabur what types of Atypical PD were most commonly treated at the Institute. She informed me that MSA is one of the more predominant Atypical PD forms of the Institute’s patient population. For this reason, I focused on the research of other labs, because it would be so directly relevant to many patients. Patients with atypical PD are starved for information, so I thought that I should try to tailor the presentation to their interests.”]

Dr. Manning-Bog is also at step one of some tau research. (She has an intern working on this.) She’s seen toxic tau protein changes in DJ1 transgenic mice. This may be a good model for researching Parkinson’s Disease Dementia. This is a first step.

[Robin’s note: PD, DLB and MSA are disorders of alpha-synuclein. They are called alpha-synucleinopathies. Any of the alpha-synuclein research should help these disorders. Of these, only PD and DLB are Lewy body diseases. AD, PSP and CBD are disorders of tau. They are called tauopathies. Any of the tau research should help these disorders. Because DLB typically appears with Alzheimer’s pathology – the so-called “Lewy body variant of Alzheimer’s disease” – tau research may help the DLB community as well.]

Notes from the Q&A:

Q: Can you have the other symptoms of PSP without having the eye movement problem?
A by Dr. Liang: Yes.

Q: What’s the story about statins?
A by Dr. Manning-Bog: Statins have been studied in a few models and seem to be neuroprotective. (See note 1 below.)
A by Dr. Liang: Statins can effect muscle tissue. The atypical PD disorders are neurological disorders, not muscular disorders, so statins are not implicated in the decline seen in these disorders.

Q: When do you get Lewy bodies?
A by Dr. Manning-Bog: Lewy bodies develop throughout the brain predominantly in disease conditions.
A by Dr. Liang: But it could be that Lewy bodies are part of normal aging. We don’t know.
A by Dr. Manning-Bog: We don’t know yet if Lewy bodies are toxic. Currently, we don’t think they cause the disease. They may serve to sequester toxic synuclein. It may be that when synuclein is not sequestered into a Lewy body, it’s toxic.
A by Dr. Manning-Bog: In PD, Lewy bodies start in the brain stem and progress to midbrain, then cortex. In DLB, there are Lewy bodies in the brain’s cortex.

Q: Can imaging see Lewy bodies?
A: No, Lewy bodies are only detectable upon autopsy.

Q: What’s the prevalence of dementia in these disorders?
A by Dr. Liang: The studies vary between 30% and 80% of those with PD getting dementia. It depends on what tests are given to research participants and the definition of “dementia.”

[Answer by Robin:
DLB: 100% of those with DLB have dementia; “progressive dementia” is a “central feature” of DLB (according to the diagnostic criteria)
MSA: none of those with MSA have dementia; according to the diagnostic criteria, dementia is an exclusionary criterion for MSA
PSP: according to the latest clinicopathological correlations, 54% to 62% of those with PSP had dementia as a primary symptom
CBD: there have been no studies on this; my impression is that the percentage for CBD is roughly the same as for PSP; however, it seems from Dr. Liang’s presentation that the percentage may be higher]

Q: What about stem cell research?
A by Dr. Manning-Bog: In research using iPS (induced pluripotent stem cells) to create dopmainergic neurons, the yield is only two percent! This means that iPS isn’t an efficient means of treatment currently. But iPS offers a great way to study the disease mechanism. Before any iPS cells are transplanted into patients, we need to study teratomas, the tumors that can grow.

Q: Are you hopeful about the research?
A by Dr. Manning-Bog: Yes, I’m hopeful!

Note 1:
Dr. Manning-Bog provided two references on statin studies. You can look up the abstracts on pubmed.gov by using the PubMed ID#.

1. The 3-hydroxy-3-methylglutaryl-CoA reductase inhibitor lovastatin reduces severity of L-DOPA-induced abnormal involuntary movements in experimental Parkinson’s disease.
Schuster S, Nadjar A, Guo JT, Li Q, Ittrich C, Hengerer B, Bezard E.
J Neurosci. 2008 Apr 23;28(17):4311-6.
PubMed ID#: 18434508

2. Simvastatin is associated with a reduced incidence of dementia and Parkinson’s disease.
Wolozin B, Wang SW, Li NC, Lee A, Lee TA, Kazis LE.
BMC Med. 2007 Jul 19;5:20.
PubMed ID#: 17640385

New book by Parkinson’s Plus Patient Dan Brooks

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Dan Brooks started a blog about his life with Parkinson’s Plus in December 2006. (Ru posted about this on The Back Porch.) The blog — at http://wewillgoon.blogspot.com/ — has grown into a book, which has just been published! The book, “I Will Go On: Living with a Movement Disorder,” is available online through Amazon* for $16. Here’s some info from amazon.com about the book:

“Dan was a 50-year-old husband, father and district-level administrator in a public school system, when he first noticed pronounced tremors, speech difficulties and walking problems developing. In this book, Daniel chronicles his life with a Parkinson’s Plus syndrome and explains how he dealt with the neurological decline that resulted. Read a user-friendly, patient’s explanation of the defining symptoms of these atypical Parkinsonism disorders and find out how this neurodegenerative disease progressed in Dan’s case. This book addresses the many facets of neurodegenerative diseases, while primarily focusing on Atypical Parkinsonian disorders, namely PSP, MSA, and CBD. Parkinson’s Disease is also discussed in depth. Dan tells a compelling and inspirational story of how he maintained his faith in God, while courageously facing life with a movement disorder.”

Dan’s goal is to encourage and inspire patients or caregivers as they face the challenges posed by neurodegenerative illness. He wrote to me: “Sometimes this medical condition is overwhelming, as you know, but I have adjusted and learned to accept what is happening. There is still a lot of life to live and I am very energized right now by this book project. … I am very pleased to have finished [the book]. My hope is that patients and caregivers will appreciate the patient’s viewpoint from which I write. … If I help one person with this book, it will have been worth the effort.”

You can read an overview about the book and learn more about Dan at his blog http://wewillgoon.blogspot.com/ I’m sure you will agree that he’s a remarkable person! Many of us count ourselves lucky that our paths have crossed with his.

Robin

* Link to amazon.com for “I Will Go On: Living with a Movement Disorder”
http://www.amazon.com/Will-Go-Living-Mo … 597&sr=8-1

FDA warning – transdermal patches with metallic backings

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This advisory came out today. I have confirmed with Novartis that the Exelon patch does not contain a metallic backing. (Exelon is a dementia medication.) I don’t know about Fentanyl or scopolamine. Maybe someone else can find out??

http://www.fda.gov/cder/drug/advisory/t … lpatch.htm

FDA Public Health Advisory
Risk of Burns during MRI Scans from Transdermal Drug Patches with Metallic Backings
Dated 3/5/09

The FDA has been made aware of information about certain transdermal patches (medicated patches applied to the skin) that contain aluminum or other metals in the backing of the patches. Patches that contain metal can overheat during an MRI scan and cause skin burns in the immediate area of the patch.

Transdermal patches slowly deliver medicines through the skin. Some patches contain metal in the layer of the patch that is not in contact with the skin (the backing). The metal in the backing of these patches may not be visible. The labeling for most of the medicated patches that contain metal in the backing provides a warning to patients about the risk of burns if the patch is not removed before an MRI scan. However, not all transdermal patches that contain metal have this warning for patients in the labeling.

FDA is in the process of reviewing the labeling and composition of all medicated patches to ensure that those made with materials containing metal provide a warning about the risk of burns to patients who wear the patches during an MRI scan.

Until this review is complete, FDA recommends that healthcare professionals referring patients to have an MRI scan identify those patients who are wearing a patch before the patients have the MRI scan. The healthcare professional should advise these patients about the procedures for removing and disposing of the patch before the MRI scan, and replacing the patch after the MRI scan. MRI facilities should follow published safe practice recommendations concerning patients who are wearing patches.1,2

Until this safety issue is resolved, FDA recommends that patients who use medicated patches (including nicotine patches) do the following:

* Tell the doctor referring you for an MRI scan that you are using a patch and why you are using it (such as, for pain, smoking cessation, hormones)

* Ask your doctor for guidance about removing and disposing of the patch before having an MRI scan and replacing it after the procedure.

* Tell the MRI facility that you are using a patch. You should do this when making your appointment and during the health history questions you are asked when you arrive for your appointment.

The FDA urges health care professionals and patients to report possible cases of skin burns while wearing patches during an MRI to the FDA through the MedWatch program by phone (1-800-FDA-1088) or by the Internet at http://www.fda.gov/medwatch/index.html.

(1) Kanal, et. al, “ACR Guidance Document for Safe MR Practices: 2007,” AJR 2007; 188:1­27.
(2) Guidelines for Screening Patients For MR Procedures and Individuals for the MR Environment, Institute for Magnetic Resonance Safety, Education, and Research, www.imrser.org, 2009.

Five types of PSP and diagnostic challenges

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This is an interesting article by perhaps the top two PSP researchers in the world — Lees of the old guard and Williams of the new guard.

When looking at the brains of those with a pathological diagnosis of progressive supranuclear palsy (PSP), there are some differences:
(a) in the severity of pathology in the brain,
(b) in the distribution of pathology in the brain, and
(c) clinical features

Presumably three of the disease “subgroups” the authors refer to include: Richardson’s Syndrome (described elsewhere as “classic PSP”), PSP-Parkinsonism, and primary progressive freezing gait (PPFG). I’m unclear if “pure akinesia with gait freezing” (PAGF) is another PSP subgroup or not. (Or if it’s the new name for PPFG. So many acronyms!)

This review article addresses these differences.  You’ll have to check out the full article to see all the differences.  In this post, I’m only sharing the differences in “clinical features” or symptoms.

The authors describe five clinical subgroups or types of PSP:

#1- Richardson’s syndrome (“classic PSP”)

Symptoms include:  lurching gait; postural instability; unexplained backwards falls; personality change; cognitive decline; slowing of vertical saccadic eye movements (“an early telltale sign”); eyelid abnormalities; severely impaired spontaneous blink rate; slow, slurred, growling speech; swallowing difficulties; overactivity of the frontalis; surprised, worried facial appearance; muscle tone can be normal; acoustic startle response absent in most patients; auditory blink reflex absent in most patients.

“The median survival in the original series was 5 years from disease onset; in larger, more recent studies, disease durations to death of 5 to 8 years have been reported.”

#2- PSP-Parkinsonism (PSP-P)

Symptoms include:  limb bradykinesia; limb rigidity is more common and severe than in patients with Richardson’s syndrome; jerky postural tremor; 4-6 Hz rest tremor; asymmetry of limb signs in some cases; axial rigidity; “moderate or good improvement in bradykinesia and rigidity” following levodopa therapy, “although the response is rarely excellent”; acoustic startle response absent in most patients; auditory blink reflex preserved in all patients.

Those with PSP-P are “commonly misdiagnosed with Parkinson’s disease.”

“Falls and cognitive dysfunction occur later in PSP-P than they do in Richardson’s syndrome and, perhaps as a consequence, the time for disease duration to death is about 3 years longer in PSP-P.”

PSP-P compared to other disorders:

(a) “PSP-P and Richardson’s syndrome can be distinguished by their different clinical pictures in the first 2 years; however, there is clinical overlap, and after 6 years of follow up the clinical phenomenology might become similar.”

(b) auditory blink reflex “was absent in most patients with Richardson’s syndrome but was preserved in all patients with PSP-P”

(c) “[We] emphasize the difficulty in separating these [PSP-P] patients from those with [PD]. Early pointers that might help a clinical diagnosis of PSP-P could include rapid progression, prominent axial symptomatology, or a poor response to levodopa…”

“In a few patients, a purely parkinsonian syndrome predominates until death, and abnormalities of eye movement or other characteristics of Richardson’s syndrome might never appear. A sustained response to levodopa and drug-induced choreic dyskinesias with a long duration of disease seem to characterise these patients.”

The prevalence of the PSP-P type seems to be between 8% and 32% of those with PSP pathology.

#3 – PSP-Pure akinesia with gait freezing (PSP-PAGF)

Symptoms include:  “progressive onset of gait disturbance with start hesitation and subsequent freezing of gait, speech, or writing”; “without rigidity, tremor, dementia, or eye movement abnormality during the first 5 years of the disease”; no benefit to levodopa therapy; acoustic startle response present in all patients; auditory blink reflex preserved in all patients.

PAGF was “first described in 1974 in two patients who developed freezing of gait, writing, and speech, with paradoxical kinesia. At presentation, these patients were cognitively intact, had no abnormalities of eye movement, and, as is the case in many patients, there was a long disease duration without the development of other parkinsonian features.”

“The median duration of disease was 11 years.”

Fewer than 1% have this type of PSP.

#4- PSP-Corticobasal syndrome (PSP-CBS)

Symptoms include:  asymmetric limb dystonia; apraxia; alien limb. “An increase in latency to initiate saccadic eye movements, which leads eventually to compensatory head tilts, is the most common eye movement abnormality and is typically more pronounced on the side on which the apraxia predominates. The distinction between this and the typical slowness of saccadic eye movements in Richardson’s syndrome can be difficult to make early in the course of the disease.”

“Most patients with PSP-CBS eventually develop postural instability but this occurs much later in Richardson’s syndrome.”

“Pathological series have indicated that only 50% of patients with CBS have pathology that is typical of corticobasal degeneration… Cerebrovascular disease, Alzheimer’s disease, and progressive supranuclear pathology account for most of the other patients.”

“PSP-CBS seems to be a rare presentation of PSP-tau pathology; only five patients from a pathological series of 160 patients with PSP was identified with asymmetric limb dystonia, apraxia, and alien limb phenomena.”

#5- Progressive non-fluent aphasia (PNFA)

Symptoms include:  non-fluent spontaneous speech, with hesitancy; agrammatism; “phonemic errors that require substantial effort in speech production.”

“In a small case series, five of seven patients who presented with PNFA and prominent early apraxia of speech had underlying PSP-tau pathology. The other two patients had Pick’s disease and corticobasal degeneration… The apparent specificity of prominent early apraxia of speech for tauopathies, particularly PSP-tau pathology, has [led] to the suggestion that this syndrome should be regarded as a clinical subtype of PSP. Patients who present with prominent early apraxia of speech do so at similar ages of onset or disease duration as patients with Richardson’s syndrome.”

Conclusions.  In the conclusion to the review article, the authors state:

“The early recognition of patients with Richardson’s syndrome, PSP-P, PSP-CBS, PAGF, or PSP-PNFA would be enhanced by biomarkers for tauopathies and clinical criteria with a high positive predictive value for Parkinson’s disease, which is the main differential diagnosis for these conditions and is 30 times more prevalent than PSP.”

And:

“Clinical features, such as visual hallucinations, drug-induced dyskinesias, hyposmia, and a prolonged sustained response to levodopa are uncommon in PSP, but have not yet been prospectively assessed in PSP-P, PAGF, or PSP-CBS.”

This sentence of the abstract is important, given that it is in conflict with the “typical”(?) patient’s desire to have a diagnosis:

“[For] patients for whom the diagnosis is unclear, clinicians must continue to describe accurately the clinical picture of each individual, rather than label them with inaccurate diagnostic categories, such as atypical parkinsonism or PSP mimics.”

Copied below is the abstract.

Robin

Lancet Neurology. 2009 Mar;8(3):270-9.

Progressive supranuclear palsy: clinicopathological concepts and diagnostic challenges.

Williams DR, Lees AJ.
Faculty of Medicine (Neurosciences), Monash University, Melbourne, Australia; Reta Lila Weston Institute of Neurological Studies, University College London, London, UK.

Progressive supranuclear palsy (PSP) is a clinical syndrome comprising supranuclear palsy, postural instability, and mild dementia. Neuropathologically, PSP is defined by the accumulation of neurofibrillary tangles. Since the first description of PSP in 1963, several distinct clinical syndromes have been described that are associated with PSP; this discovery challenges the traditional clinicopathological definition and complicates diagnosis in the absence of a reliable, disease-specific biomarker.

We review the emerging nosology in this field and contrast the clinical and pathological characteristics of the different disease subgroups. These new insights emphasise that the pathological events and processes that lead to the accumulation of phosphorylated tau protein in the brain are best considered as dynamic processes that can develop at different rates, leading to different clinical phenomena.

Moreover, for patients for whom the diagnosis is unclear, clinicians must continue to describe accurately the clinical picture of each individual, rather than label them with inaccurate diagnostic categories, such as atypical parkinsonism or PSP mimics. In this way, the development of the clinical features can be informative in assigning less common nosological categories that give clues to the underlying pathology and an understanding of the expected clinical course.

PubMed ID#: 19233037  (see pubmed.gov for this abstract)

 

Foster independence and offer respect (advice for caregivers)

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Local support group member and volunteer Denise is reading the book How to Care for Aging Parents.  She is offering occasional reports on the highlights of the book.  She has read the second chapter, which is about the caregiving role.  Here are Denise’s take-aways.  Other than the first paragraph of Denise’s notes (which applies to adult children caregivers), all of the rest of the information applies to all caregivers.

Robin

*******************************

Denise’s Notes to

Chapter two – “Your Parent and You”
of the book “How to Care for Aging Parents”
by Virginia Morris and Robert Butler
2004

Chapter 2 acknowledges how common it is to still feel the push and pull of the parent/child relationship, no matter how old you are. It recommends hiring a good therapist to tackle those issues, but goes into some detail as to how to approach them on your own. At a minimum you must find ways to set aside your parent’s ability to push your buttons so you can do an effective job of caregiving with as little frustration as possible.

It also has some good words of advice for ALL caregivers.

The first is to foster independence wherever possible. It is difficult to watch a loved one struggle with tasks that were once easy for them. Sometimes we worry about symptoms or frailty contributing to an injury, but we all need exercise. Any amount of movement helps maintain flexibility, balance, even good bowel health. Doing for oneself is also good for the brain. Maintaining one’s identity and dignity can help ward off depression and, possibly, the onset of dementia. It actually takes more patience, time and effort for you, as a caretaker, if the person is slow or messy about some tasks, but it does worlds of good if you are both willing.

Try not to be overprotective of the person you care for. If you feel they are taking excessive risks, start by expressing your concerns rather than bossing around a grown adult. Perhaps your elderly mother doesn’t know breaking a hip can be fatal. Offer solutions to reduce the risk and still allow the activity to continue. If you’re worried she isn’t steady enough on the stairs, suggest moving her bedroom downstairs to avoid them all together. Remember, you only have so much influence dealing with a competent adult. We all have the right to make risky decisions. We do it every day when we get in the car, smoke a cigarette, even eat fatty foods. Some people would rather die living fully than live longer, just like the saying:

*** Life is not a journey to the grave with the intention of arriving safely in a pretty, well preserved body, but rather to skid in broadside, thoroughly used up, totally worn out, and loudly proclaiming, “Wow! What a ride!!!” ***

There are times when it is appropriate to step in and forbid someone from exercising their independence. If the safety and/or health of themselves and/or those around them are seriously threatened you have an obligation to intervene. If you find medication is being misused, you should take steps to dispense them properly. You may find it necessary to pay bills to prevent utilities being shut off or turn off the gas when someone is incompetent to use the stove. Many of us have had to take away car keys. Its not easy. Enlist the assistance of a doctor, if you are unable to manage it on your own. They can report to the DMV, which will suspend or revoke the license, depending on the doctor’s statement.

If you find yourself in doubt about where to draw the line; whether to step in and, if so, how; seek advice from someone with experience. Since this book is all about helping aging parents, it suggests asking a Geriatric Care Manager, Hospital Social Worker or Geriatric Department, an Area Agency on Aging, or Adult Protective Services, which is part of the Department of Social Services.

The second bit of good advice for all caregivers is a big reminder to offer respect. Remember, you may be in their shoes one day. Some suggestions to that end are:

– If the person you’re caring for is inactive, take the time to ask their opinion on various topics to keep them involved in daily life around them. If they’re up to it, read the newspaper, magazines or pick out a recipe together. Don’t forget to listen to their comments and answers.

– If they are unable to speak, assume he or she understands. Explain what’s going on and reassure that his or her needs and preferences are being considered at every point. This is where having those conversations ahead of time come in handy.

– Never speak about someone as if they aren’t present, when they are.

– Don’t be afraid to ask that other caregivers do the same. Correct them if they are behaving in a disrespectful way or doing anything you feel the patient would feel uncomfortable with, if they could speak for themselves.

Keep in mind that IF you’re dealing with someone who is exceptionally difficult you could be dealing with a bigger problem. For instance:

– Unremitting orneriness, social withdrawal, or refusal to eat can be signs of depression. Seek medical advice.

– Complaining, calling constantly, or becoming sick at just the wrong moment (like when you’re about to leave on vacation) can be a way to control you. Get a reliable backup caregiver so you have respite.

– Between 2-5% of elderly people living in the community (not long term care facilities) are excessively suspicious or paranoid. Seek a psychiatrist with elder experience. Treatment is usually carefully balanced medication.

– At least 5% of people age 65 and older suffer hypochondria or undifferentiated somatoform disorder. In the former, a person is obsessed with the idea they have a serious illness. In the latter, a person complains about symptoms (fatigue, loss of appetite, abdominal pain) that have no medical basis. Psychotherapy doesn’t help either of these conditions. Your best bet is a good, firm doctor to sort out the real medical issues and be firm about the imaginary ones.

-Denise