“Life at the end, caring in the face of loss” – Notes from video

Last year I came across information about a short documentary film called “Life @ the end, caring in the face of loss.”  You might be able to find the 28-minute video online but local support group member Denise recommends not taking the time to watch it.  She says that there’s not much new information in the video.

Instead, she shares the “good reminders” the film raises, including:

* 40% of caregivers die before care recipients
* there are a diversity of approaches to caregiving
* how difficult the transition back to a normal life can be

Here’s what Denise says about the film….



Denise’s notes on

Life @ the end, caring in the face of loss
documentary film by Jennifer Molina & Farah Dosani, 2011
Distributed by Health News from Florida Public Media
Running Time: 28 minutes

“Love knows not its own depth until the hour of separation.” Khalil Gibran

That’s a quote from a touching video Robin asked me to review. It really reiterates what we already know about caregiving, because we are caregivers, and this is just interviews with caregivers. There’s no new information here. I wouldn’t recommend taking the time to watch it, but there are a few good reminders.

Nearly 1/4 of the population in the U.S. is engaged in family caregiving. As the title of the film denotes, it is because of love – even in the midst of mourning. But sometimes the motivation for uber-caring is to avoid any guilt after the person’s passing. You must feel you did everything you could, right? Be careful. Remember that the physical, emotional and financial stress of caregiving causes 40% to die before the person they’re caring for. If you don’t look after yourself, you may not survive them.

We commonly think of spousal caregiving or parent/child situations, but the face of caregiving is diverse. This video shares a same sex couple dealing with HIPAA rules, a family in which the ill father and his wife must care for two small children and himself simultaneously, and the impact on extended family who step in to support a primary caregiver.

Worth thinking about is that the diversity of people engaged in caregiving means there is also diversity of approaches to it, and ways of coping with the illness itself. The diagnosis, and finding how to live with it, clarifies and forever changes who each of you are. You may find yourself intensely worried about your partner and what the future holds, while they take their own therapies and symptoms in stride. You may become annoyed that a respite volunteer doesn’t do things the way you do, when you should be enjoying the respite, itself. You may need some support to handle your differences.

Finally, there will be an adjustment to life after caregiving. If its been all-consuming for you, it will leave an enormous vacuum when its over. One of the film’s subjects found that sharing with friends and family, during their journey through illness, all she had learned while caregiving, gave value to the loss of her partner. It perpetuated her identity as a caregiver but offered social interaction, support and transition back to a ‘normal’ life.


“An Introduction” to MSA by Gary Rose

Gary Rose is 60 years old.  He was diagnosed with multiple system atrophy (MSA) about 3.5 years ago.  Symptoms began over 7 years ago.  He lives in Washington state.  He is the facilitator of the monthly national support group “meeting” (online meeting or conference call) for those with MSA.

In honor of March being MSA Awareness Month, he wrote this article for the CurePSP (psp.org) March/April 2012 newsletter.  Amazingly for me, I can’t find anything in the article that I disagree with or think is inaccurate.  It’s the best lay article I’ve read on MSA!

Gary’s article is copied below.

I am very impressed that Gary referred to the “Clinical Outcomes” research article.  The article examines the clinical records of 83 people with autopsy-confirmed MSA.  It’s the best source of information on “survival time” and “diagnostic accuracy” in MSA.

You can read my notes on the “Clinical Outcomes” paper here:


Good job, Gary!



www.psp.org/file_download/b9b6fe18-8ac0-4354-8e23-b35734be1767  (this is a PDF; article starts on page 1)

Multiple System Atrophy: An Introduction
by Gary L. Rose
CurePSP Newsletter
March/April 2012, Issue 8

March is Multiple System Atrophy (MSA) Awareness month, so I am happy to introduce you to MSA. This article is a primer and will not delve too deeply into MSA.

I am a 60 year old man with MSA. I’d like to share the story of my diagnosis. I first went to the local urgency care clinic with symptoms more than seven years ago. I had been waterskiing with my adult daughter. I got up, but the water ski just didn’t feel right – it felt ‘slippery’. At the time, I was aware that I had a balance problem, but figured it was temporary – perhaps it was an ear infection. Of course, it turned out to not be an ear infection at all. I saw many healthcare professionals (including three neurologists) until my diagnosis, about three and a half years later. It is common for people with MSA to go years with no diagnosis, or to be misdiagnosed. Upon diagnosis with MSA, it is common for people with MSA or their loved ones to think further back and find MSA symptoms long before the diagnosis – that also was true for me. I remembered having problems roller skating. I had blamed it on the new skates. I sold the skates and stopped skating! Now I realize my balance had been off and that it was due to MSA.

MSA is a progressive brain disorder caused by loss of nerve cells in specific areas of the brain. The areas of the brain affected are the basal ganglia, the brain stem, or the cerebellum. Depending on the area of the brain most affected, symptoms can be stiffness, slowness and freezing (typical Parkinson’s Disease symptoms when the basal ganglia is affected); autonomic features like bladder control, low blood pressure, constipation, erectile dysfunction, body temperature regulation and loss of ability to sweat (symptoms when the brain stem is affected); and balance, coordination, and impaired speech (symptoms when the cerebellum is affected). There are two types of MSA: MSA-P, the parkinsonian type, and MSA-C, the cerebellar type. All people with MSA are thought to develop autonomic features, at some time.

The technical definition of MSA, according to Parkinson Society Canada:

“MSA was previously known as Shy-Drager syndrome, striatonigal degeneration and sporadic olivopontocerebellar atrophy. Researchers have learned that there is a common underlying cause in all three disorders, so they are now referred to as MSA. In MSA, brain cells in the affected areas shrink (atrophy). This can sometimes be seen on MRI scans. When brain tissue is examined under a microscope, structures called glial inclusion bodies can be seen; they contain a protein called alpha-synuclein. It is the presence of these inclusion bodies in the movement, balance and autonomic control centers of the brain that confirms a diagnosis of MSA.”

MSA is thought to be sporadic – that is non-hereditary. It is considered rare – about 4 or 5 people in 100,000 have it. MSA is rarer than progressive supranuclear palsy (PSP). MSA is slightly more common in men than women, but it is almost 50/50. It usually starts in a person’s 50s, although it can affect people younger and older than this. The cause of MSA is unknown. Some researchers believe that certain people can be genetically predisposed to the disease, even though a trigger still has to occur. The trigger is unknown, but suspected by some researchers to be an environmental factor of some kind. Environmental toxins and brain trauma as potential triggers are currently being researched.

MSA manifests itself differently in every individual – the speed of progression and types of symptoms vary from person to person. MSA is a progressive brain disease, but that is about all that can be said about it. Symptoms will change over time, and decline happens more rapidly than in Parkinson’s Disease.

Currently, there is no treatment to slow the progression of MSA. Each of the many symptoms of MSA should be treated by a neurologist (ideally, a movement disorder specialist), general (family) doctor, urologist, clinical nurse or physician’s assistant, speech-language pathologist, physical therapist, or occupational therapist.

After diagnosis, some patients have difficulty in finding out what the future holds. Often, the patient (or a loved one) discovers that MSA is terminal by searching the internet. Then the question becomes, “how long do I have?” Because MSA is highly individualized, it is dangerous to base one’s future (and expectations of MSA) on the anecdotal experiences of others. Unique experiences are just that – unique. For this reason, articles like “Clinical Outcomes of Progressive Supranuclear Palsy and Multiple System Atrophy can be much more helpful.” This particular study is based on a large number of MSA cases (83) and diagnoses that were pathologically confirmed. The study found that 7.9 years, plus or minus 2.8 years, is the average time of disease duration.

For more information on MSA, see these organizations/websites:

• The National Institute of Neurological Disorders and Stroke at the NIH:

• The Shy-Drager/Multiple System Atrophy Support Group, Inc.:

• The MSA Trust: www.msatrust.org.uk

Further reading:

• Second Consensus Statement on the Diagnosis of MSA:

• Clinical Outcomes of PSP and MSA:

Mass Genl researchers look at anesthesia and cognitive dysfunction

This post may be of interest to those who have a loved one with dementia, or those contemplating surgery with general (inhaled) anesthesia.

A Boston Globe newspaper article I circulated back in 2007 was about hospital-induced delirium.  In that article, Massachusetts General Hospital researchers drew attention to the anesthetic isoflurane as part of the cause of delirium.

Last week Massachusetts General Hospital distributed a press release on isoflurane; it causes Alzheimer’s-like changes in mammalian brains.  Researchers mention an anesthetic that may be safer — desflurane.

The full press release is copied below.




Massachusetts General Hospital Press Release
Study reveals how anesthetic isoflurane induces Alzheimer’s-like changes in mammalian brains
MGH researchers find desflurane may be safer anesthetic option for patients with Alzheimer’s disease

The association of the inhaled anesthetic isoflurane with Alzheimer’s-disease-like changes in mammalian brains may by caused by the drug’s effects on mitochondria, the structures in which most cellular energy is produced.  In a study that will appear in Annals of Neurology and has received early online release, Massachusetts General Hospital (MGH) researchers report that administration of isoflurane impaired the performance of mice on a standard test of learning and memory – a result not seen when another anesthetic, desflurane, was administered.  They also found evidence that the two drugs have significantly different effects on mitochondrial function.

“These are the first results indicating that isoflurane, but not desflurane, may induce neuronal cell death and impair learning and memory by damaging mitochondria,” says Yiying (Laura) Zhang, MD, a research fellow in the MGH Department of Anesthesia, Critical Care and Pain Medicine and the study’s lead author. “This work needs to be confirmed in human studies, but it’s looking like desflurane may be a better anesthetic to use for patients susceptible to cognitive dysfunction, such as Alzheimer’s patients.”

Previous studies have suggested that undergoing surgery and general anesthesia may increase the risk of Alzheimer’s, and it is well known that a small but significant number of surgical patients experience a transient form of cognitive dysfunction in the postoperative period.  In 2008, members of the same MGH research team showed that isoflurane induced Alzheimer’s-like changes – increasing activation of enzymes involved with cell death and generation of the A-beta plaques characteristic of the disease – in the brains of mice.  The current study was designed to explore the underlying mechanism and behavioral consequences of isoflurane-induced brain cell death and to compare isoflurane’s effects with those of desflurane, another common anesthetic that has not been associated with neuronal damage.

In a series of experiments, the investigators found that the application of isoflurane to cultured cells and mouse neurons increased the permeability of mitochondrial membranes; interfered with the balance of ions on either side of the mitochondrial membrane; reduced levels of ATP, the enzyme produced by mitochondria that powers most cellular processes; and increased levels of the cell-death enzyme caspase.  The results also suggested that the first step toward isoflurane-induced cell death was increased generation of reactive oxygen species – unstable oxygen-containing molecules that can damage cellular components. The performance of mice on a standard behavioral test of learning and memory declined significantly two to seven days after administration of isoflurane, compared with the results of a control group.  None of the cellular or behavioral effects of isoflurane were seen when the administered agent was desflurane.

In another study by members of the same research team – appearing in the February issue of Anesthesia and Analgesia and published online in November – about a quarter of surgical patients receiving isoflurane showed some level of cognitive dysfunction a week after surgery, while patients receiving desflurane or spinal anesthesia had no decline in cognitive performance.  That study, conducted in collaboration with investigators from Beijing Friendship Hospital in China, enrolled only 45 patients – 15 in each treatment group – so its results need to be confirmed in significantly larger groups.

“Approximately 8.5 million Alzheimer’s disease patients worldwide will need anesthesia and surgical care every year,” notes Zhongcong Xie, MD, PhD, corresponding author of both studies and director of the Geriatric Anesthesia Research Unit in the MGH Department of Anesthesia, Critical Care and Pain Medicine.  “Developing guidelines for safer anesthesia care for these patients will require collaboration between specialists in anesthesia, neurology, geriatric medicine and other specialties.  As the first step, we need to identify anesthetics that are less likely to contribute to Alzheimer’s disease neuropathogenesis and cognitive dysfunction.”  Xie is an associate professor of Anesthesia at Harvard Medical School (HMS)

Additional co-authors of the Annals of Neurology study are Zhipeng Xu, MD, PhD, Hui Wang, MD, and Yuanlin Dong, MD, MGH Anesthesia; Rudolph Tanzi, PhD, MGH Neurology; Hai Ning Shi, DVM, PhD, MGH Pediatrics; Deborah Culley, MD, and Greg Crosby, MD, Brigham and Women’s Hospital;  and Edward Marcantonia, MD, MS, Beth Israel Deaconess Medical Center.  The study was supported by grants from the National Institutes of Health, the American Geriatrics Society, the Alzheimer’s Association and the Cure Alzheimer’s Fund.

Massachusetts General Hospital, founded in 1811, is the original and largest teaching hospital of Harvard Medical School. The MGH conducts the largest hospital-based research program in the United States, with an annual research budget of more than $750 million and major research centers in AIDS, cardiovascular research, cancer, computational and integrative biology, cutaneous biology, human genetics, medical imaging, neurodegenerative disorders, regenerative medicine, reproductive biology, systems biology, transplantation biology and photomedicine.

“Mind, Mood & Memory” booklet

This terrific booklet, Parkinson’s Disease: Mind, Mood & Memory, was published several years ago by the National Parkinson Foundation (parkinson.org).  I hand it out to all newcomers to our Lewy Body Dementia caregiver-only support group meetings.  It has a wonderful chapter (five) focused on Dementia with Lewy Bodies.

The booklet makes the important point that there’s a delicate balance between treating psychosis (hallucinations and delusions) and treating parkinsonian motor symptoms.

Here’s a link to it:


I hope you value this booklet as much as I do!