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The Shriver Report – Maria Shriver and the Alzheimer's Association

“I’m Maria Shriver, and I’m a child of Alzheimer’s.”

That’s how I introduced myself last year when I testified before the Senate Special Committee on Aging. I was there to support the Alzheimer’s Study Group, a blue-ribbon panel Congress had charged, at the request of the Alzheimer’s Association, with designing an action plan to deal with Alzheimer’s disease.

Alzheimer’s is an epidemic. Every minute or so—in fact, before you get to the end of this page—someone in this country will develop Alzheimer’s. Millions of people already have been formally diagnosed. Millions more are undiagnosed—or diagnosed with some form of dementia that could actually be Alzheimer’s. And with the 78 million baby boomers now moving into their later years, the cost of Alzheimer’s to American society is expected to be $20 trillion between now and the year 2050.1 That’s right—$20 trillion.

There’s no doubt about it. We are in the midst of a national emergency, and we’re woefully unprepared.

So there I was in that packed hearing room, sitting with Alzheimer’s Study Group members—former House Speaker Newt Gingrich, former Sen. Bob Kerrey, former Supreme Court Justice Sandra Day O’Connor (who had left the High Court to care for her husband with Alzheimer’s) and Larry Butcher, chairman of Alzheimer’s Community Care in Florida (who would lose his wife months later to youngeronset Alzheimer’s). We were all there to ask this powerful congressional committee to listen up, pay attention, increase funding and take on Alzheimer’s.

I must admit it was something of a surreal experience for me, because the truth is, for so many years it was my father, Sargent Shriver, who would be sitting in that chair, pleading with senators to listen up, pay attention and increase funding. My dad was the one who would go up to the Hill to testify for his beloved Peace Corps and for all the War On Poverty programs he started and fought for, including Head Start, Vista, Job Corps and Legal Services for the Poor. My father was legendary for the way he worked the Capitol. He knew every senator and congressman by name. He knew their careers, their interests, their politics and their soft spots. He was a brilliant, idealistic and optimistic public servant. My dad was sharp and witty, a walking encyclopedia—his mind a beautifully-tuned instrument that left people in awe and inspired.

That was then. Today he doesn’t know I’m his daughter, and he doesn’t even know my name. To be honest, it’s still really difficult to wrap my own mind around that. But so goes the reality and the heartbreak of Alzheimer’s. It’s a mind-blowing disease—not just for the people who get it, but for everyone around them. That’s why I’m so passionate about defeating it

As one of my dad’s doctors told me, “Once you’ve seen one case of Alzheimer’s, you’ve seen…one case of Alzheimer’s.”

When my dad was first diagnosed in 2003, my mother, four brothers and I all felt we were entering a world that was confusing, dark and depressing. People just didn’t talk about it when Alzheimer’s hit their families. They whispered about it, a diagnosis shrouded in shame. There was little information and even less hope.

We struggled to learn about medication and caregiving. We wrestled with handling our father’s diminishing independence. How would we explain to him he couldn’t drive anymore? How would we tell him he could no longer engage in one of his favorite pastimes, giving rousing speeches about the joys and rewards of public service? When the invitations came in, we’d just send his regrets.

I understand that when people look at Alzheimer families like ours from the outside, they often see dependent parents now cared for by their own offspring, and it seems like the parent-child roles are simply reversed. Not so. The truth is, you hardly feel like you’re the parent. You still feel like the helpless child. Even though your father or mother can’t work, can’t live alone and is as needy as a toddler, you don’t feel in control or in charge. No matter who you are, how old you are, what you’ve accomplished, what your financial situation is—when you’re dealing with a parent who has Alzheimer’s, you feel powerless. And as the disease unfolds, you feel ever more powerless, because you don’t know what to do or what to expect.

As one of my dad’s doctors told me, “Once you’ve seen one case of Alzheimer’s, you’ve seen…one case of Alzheimer’s.”

In fact, there was so little information back when my Dad was diagnosed that I wrote a book called What’s Happening to Grandpa? At the time, I said I did it to help my own and other children understand what was going on. In truth, I wrote it to explain Alzheimer’s to myself. After it came out, I noticed very few people came up to me to talk about it, because of the stigma still attached to the disease. And when I wanted to put on my broadcast journalist’s hat and shine a brighter light on it by turning the book into a TV special, no one was interested. I was told Alzheimer’s was a downer and would make for what they called “bad TV.” They said Alzheimer’s wasn’t big enough. It was just “an old person’s disease.”

Then almost out of nowhere came what I call The Alzheimer’s Turning Point. That was March 21, 2007, when The New York Times reported new Alzheimer’s Association statistics showing the number of people with Alzheimer’s was ballooning—rising by 10 percent in just the previous five years.2 They reported that fully 13 percent of Americans had Alzheimer’s—which meant one in eight people over the age of 65—and unless a cure was found, there would be more than 13 million people with Alzheimer’s by 2050, the best guess back then.3

That was the wakeup call the baby boomers heard. After all, we were the generation that believed ourselves to be so smart and savvy, that we were very sure our brainspan would match our lifespan. But now, just as the oldest boomers were entering their 60s, these new numbers meant we were at the leading edge of a tsunami—and it was happening not to some nameless old “them” out there. The surge was headed for us, too. And that, I believe, scared a lot of people right out of denial.

It seemed to me that all of a sudden, Alzheimer’s became frontpage news and people really started paying attention. That’s when HBO came to me and said, “We want to take an indepth look into Alzheimer’s disease, and we want you to be involved.”

So, starting on Mother’s Day last year, HBO aired the most comprehensive television event about the disease ever, “The Alzheimer’s Project.” There were four broadcasts and a companion book covering in great depth the cuttingedge science, the issue of caregiving, what it’s like to have the disease and the impact on the children and grandchildren of Alzheimer’s. Along with HBO’s legendary Sheila Nevins, I co-executive produced this massive project. All of a sudden, everywhere I went people approached me to voice their fears, share their experience and ask for advice. “The Alzheimer’s Project” won several Emmys. It attracted 11 million viewers when it aired, and people are still watching all four parts of it at

About the same time last year, I was working on the very first The Shriver Report: A Woman’s Nation Changes Everything. It was a landmark study—published in collaboration with the Center for American Progress—exploring a transformational moment in the United States. It arose from my work as First Lady of California, where I’ve helmed The Women’s Conference, the biggest forum for women in the nation.

The transformational moment was this: For the first time in our nation’s history, women were becoming the majority of the workforce—and also primary or co-breadwinners in almost two-thirds of American families.4 We were now what I called A Woman’s Nation. I knew this shift would impact every institution in our country: the family, the workplace, the healthcare system, government services, even the relationship between men and women themselves.

More than 40 percent of women said that they were the main caregivers for elderly parents.

What came out of that report—its studies, analyses, essays by cultural leaders and a huge, groundbreaking nationwide opinion survey—was the first comprehensive and accurate portrait of The Way Things Are Now in the American home and workplace. It was also the first accounting of exactly how out of step our institutions are with the needs of women today.

We learned that women aren’t just primary breadwinners. They’re still the primary caregivers in their families as well. Almost 70 percent of the women we surveyed for the first Shriver Report told us that despite working full-time, they’re still the ones most responsible for taking care of the children.5 More than 40 percent of them said that they were the main caregivers for elderly parents.6 And almost a third of them said they were primary caregivers of both their kids and their parents.

We wondered whether their employers were adjusting, offering help like child care and ?exible hours. You’d think so, because studies show that when “employees have greater access to ?exible work arrangements, they are more committed and loyal to their employers and are willing to work harder than required to help their employers be successful.”8 Yet we found that so many companies and institutions were simply out of touch with workers’ needs today.

We held roundtables around the country, where women who knew I was dealing with four kids, my own sick mother and a father with Alzheimer’s would come up to me and say, “Me, too! I’m in the same boat, and I need help!”

Bingo! That’s when I realized that Alzheimer’s was emerging as another huge transformational force exerting a powerful pressure on women, families and our institutions. Alzheimer’s was in the process of changing A Woman’s Nation forever.

Today, women are not only a dominant economic force in this country. They also make up 65 percent of the people with Alzheimer’s—and up to three-fifths of all Alzheimer caregivers are women as well.9

This perfect storm made me realize it was time for another Shriver Report, this time in partnership with the Alzheimer’s Association.

In addition to an indepth examination of the issues and trends by experts—and searingly honest personal essays by people from every walk of life affected by Alzheimer’s, including several women who have the disease—we have conducted an enormous nationwide survey of 3,118 adults, including more than 500 Alzheimer caregivers. Our findings show the huge impact of Alzheimer’s behind closed doors in this country:

Almost 90 percent of Americans who know someone with the disease are concerned that they or someone close to them will get Alzheimer’s.

Half of women caring for someone with Alzheimer’s are providing more than 40 hours a week of care. A third of women caregivers care for their loved one 24/7.

Nearly 41 percent of the women caregivers said they had no choice in taking care of their loved one with Alzheimer’s.

More than half of the family caregivers of people with Alzheimer’s we surveyed said it’s straining their family finances.

Nearly 65 percent of working caregivers of people with Alzheimer’s told us they need to come to work late, leave early or take time off from their jobs as a result of their caregiving responsibilities.

Nearly a third of women caregivers rate the physical stress level of caregiving a 5 out of 5.

The greatest fears women voice about getting Alzheimer’s is that they will forget their loved ones, become a burden to their families and not be able to care for themselves.

My hope is that this Shriver Report triggers another Alzheimer’s Turning Point and gets the national conversation focused on this disease and its ramifications. It’s time. We must face up to some big questions: With Americans living longer and with the incidence of Alzheimer’s growing, what’s going to happen to our women, our families, our workplaces, our attitudes, our society, as the Alzheimer wave hits over the next few decades? We’re talking crisis.

Doctors and researchers at the National Institute on Aging and the Alzheimer’s Association are now looking into the possibility of revising how and when they diagnose Alzheimer’s. They’ve begun the long process of reviewing what they call “the diagnostic criteria” for the disease.10

Why the review? Well, until now, Alzheimer’s has been diagnosed only when clinical symptoms are apparent. This means significant damage is already done in the brain, such as the telltale plaques and tangles so long considered the definitive sign of Alzheimer’s. But now, better diagnostic tools like MRIs and brain scans and spinal taps looking for specific biomarkers could mean that doctors might one day be able to detect changes in the living brain much earlier—years before there are even any signs of dementia.

But any possible revision of the way Alzheimer’s is diagnosed is still a long way off. And until then, some researchers are warning about using these very expensive high-tech tests for screening the general population, for two reasons. One, the tests sometimes find plaques in the brains of people who never even develop Alzheimer’s. And two, there’s no effective treatment or cure for Alzheimer’s anyway.11

So how many people do we think actually have or will get Alzheimer’s disease? Well, until there are new standards for diagnosis, it’s unclear. The estimates are all over the map. The actual number of Americans with Alzheimer’s disease today may be far more than the official 5.3 million number we all use.12 And what about the projection that by 2050, there’ll be up to 16 million people with Alzheimer’s disease in this country?13 I bet it could turn out to be a bigger number than that.

But whatever the number of cases is, this much we know for sure: Most of them are expected to be women. And most of the people who will end up taking care of them will be women, too.

The President’s Council of Economic Advisors reported this year that 43.5 million Americans—most of them women—are providing unpaid caregiving to relatives and friends over the age of 50.14

More specifically, our poll showed that today, the average unpaid Alzheimer caregivers are working women over the age of 50 providing care most commonly to their mothers (31 percent) and spouses (15 percent).

And that unpaid caregiving—which so often comes on top of a paying job and childrearing—is tough physical and emotional work.

The truth is it’s women who are the ones who generally do the hands-on grunt work of caregiving15—cleaning their parents or spouses and changing their diapers, feeding them, babysitting them, dispensing medication to them. While men do represent about a third of family caregivers16, they tend to arrange or supervise outside services.17

For decades, women have fought for respect for mothers and recognition that mothering is real work. Now we have to fight for respect for caregivers and recognition that caregiving is real work, too—billions of dollars worth of work.

AARP estimated that 34 million caregivers over the age of 18 in the United States provided $375 billion worth of unpaid services a year—more than the yearly state plus federal Medicaid spending—and that was three years ago!18 By the way, add this to the mix: Nearly 1.4 million kids aged 8 to 18 are helping take care of an adult relative19—250,000 of them caring for loved ones with Alzheimer’s or other dementias.20

This Woman’s Nation has truly become a Caregiver Nation as well, and Alzheimer’s is putting the pedal to the metal. To be specific:

This year it’s estimated there are 11.2 million Alzheimer and other dementia caregivers, and 6.7 million of them are—you guessed it—women.21

So with women shouldering the biggest brunt of the burden of all this caregiving, I find it ironic that we’re still seeing articles like, “Why Aren’t Women Happy?” They wonder why women aren’t satisfied with their advanced degrees and new corner offices. They ask, “What’s Happened to Her Sex Drive?” and “What’s Wrong With American Women?” Excuse me?

What’s right with American women is that they’re rearing and providing for the next generation of Americans, while at the same time caring and providing for the last generation of Americans. What’s right with American women is that they’re doing it, even though studies show that caregivers pay a steep price in terms of their own health—increased stress, depression, lost sleep, chronic anxiety, immunesystem deficiency.22 They’re paying a financial price as well, because full-time workers who are also caregiving at home have lower earning power.23

American women are stressedout and maxedout. There’s nothing wrong with them! They just need support. What has to get right is our institutions. They need to respond to the changing dynamic in the American home. People with Alzheimer’s cannot live alone, and the family members who live with them and take care of them need help.

Health and Human Services Secretary Kathleen Sebelius lays out for us in this report many provisions in the 2010 healthcare reform legislation, The Affordable Care Act, that provide relief for Alzheimer’s caregivers.

It’s a start. But we also need to have a national conversation about what else the growing millions of Alzheimer families need:

We have a Dependent Care Tax Credit for employment-related child care expenses. But what about a meaningful Elder Care Tax Credit?

How about incentivizing ?extime programs, so employers are really encouraged to offer ?exible work hours to their caregiving employees?

The federal government and some states provide for Maternity Leave and Family Leave. How about Elder Care Leave, including coverage for emergencies at home? Maybe more men would step up and help out at home if they knew taking time off was OK with their employers.

How about more access to high-quality Alzheimer training for both family members and paid home healthcare aides? How about actually teaching family members how to really stay on top of all the medications they have to dispense?

How about more elder daycare programs staffed with people actually accredited for Alzheimer care? Believe it or not, less than 1 percent of practicing nurses nationwide are credentialed in gerontology.24

And what about more government quality control of seniors’ programs, nursing homes and end-of-life facilities, before we have an epidemic of elder abuse accompanying the rise in Alzheimer’s?

How about more intergenerational daycare centers, like the one I visited in San Diego, where toddlers and people with Alzheimer’s spend the day together? They eat together, they dance together, go to storytime together. It’s quite moving to behold. And what about more intergenerational playgrounds? We built the first one in California, so Sandwich Generation people like me—taking care of both kids and parents—can go to one place with all of them.

And how about more governmental support for adult daycare and respite care programs in general, so we can give family caregivers a break now and then?

I know, I know. Let me say it before you do: “Who’s gonna pay for all these programs? We’re in a recession!” Many states, including my own, are struggling with staggering budget deficits. And many political leaders, including my own husband, are wrestling with cutting many of the same types of programs I’m advocating.

But that’s exactly why we need a new kind of national conversation about Alzheimer’s and growing old in America—just like the conversations heard around kitchen tables all over the country. Families are sitting down to figure out how to pay for their portion of the billions of dollars of unpaid care elders are receiving at home. American families are asking and answering the same questions we need to ask and answer on a state and national level:

“How can we afford this care? How can we pay for it?”

“Whose job is it—whose turn is it—to do the caregiving?”

We need more of us at that kitchen table. Not just the Alzheimer’s Association fighting the disease and providing support, but a partnership of families, businesses, faith-based institutions, unions, government leaders, insurance companies, healthcare institutions—everybody on the front lines, all of us accountable. And since personal and family responsibility will always be a huge piece of the Alzheimer’s care picture:

How about Elder Care Savings Plans like the 401K retirement savings plans and 529 college savings plans? Since our parents are living longer, many families could start socking away at least some money now.

If we wait until the crest of the Age Wave hits—and it’s coming—it will be too late. It’s just like Katrina. If the levees were built strong enough the first time, they would have held.

Of course, our biggest hope for Alzheimer’s lies in medical research. As you’ll read in this report, we’re getting closer, but our scientists are still chipping away at critical questions like these:

What causes Alzheimer’s? Is it inherited? What causes youngeronset Alzheimer’s? Is there any treatment that can delay the onset or slow down the course of the disease?

What about new tests that may be able to tell you if you’re going to get Alzheimer’s? Are the tests ready for use? Are they accurate? Who would be a candidate to take them? If there are no foolproof treatments yet, what’s the good of knowing?

What can we do to prevent Alzheimer’s? Do lifestyle changes really help? Should we all be hitting the treadmill, drinking tea, doing crossword puzzles, taking Omega-3 and Vitamin D?

Why do more women get Alzheimer’s than men? Is it just because women live longer? Does estrogen play a part in prevention? If so, how much and when?

What exactly is the natural course of the disease? Why does it play out in a few years for some patients, in a decade or more for others? Why do different people have different symptoms: some explosively angry, others hypersexual, still others mumbling or even silent? In other words, why is it that, “Once you’ve seen one case of Alzheimer’s, you’ve seen…one case of Alzheimer’s”?

And for God’s sake, when will there be a cure?

For HBO’s “The Alzheimer’s Project,” I visited labs where our brilliant scientists work around the clock, deeply immersed in research they hope will lead to a cure. But while the federal government will spend about $6 billion on cancer research and about $4 billion for research on cardiovascular diseases this coming year, we’re investing a fraction of that, less than $500 million a year, on Alzheimer research.25 The 2010 healthcare reform act could boost that effort some, but it won’t be enough.

I’ve come to believe that brain research is one of the most important investments our country can make, period. I believe the brain is for America today what the moon was for America in the 1960s: The Next Frontier. I’m convinced if we make a national commitment and launch more of our best doctors and scientists at the brain, they’ll one day produce treatments and prevention strategies and even cures—not just for Alzheimer’s but for a whole host of brain diseases, like Parkinson’s disease, Huntington’s disease, stroke, dementia, mental illness, Down syndrome, autism, addiction, depression. Unlocking the secrets of the brain will teach us more about who we are, how we work, how we learn, what makes us tick and what makes us sick and how to fix it—so that fewer families will have to go through what my family has gone through because of a devastating brain disease.

Which brings me back to my father.

Several months after my mother’s death last year, my four brothers and I wondered what to do with our dad. The house my parents had shared was way too big for him: too lonely, too isolated, too much. We wondered if we should we leave him in Washington or move him to Florida or California to live with one or another of his children?

We need a new kind of national conversation about Alzheimer’s and growing old in America.

After much discussion and debate and advice from doctors, we concluded the best thing for our dad would be to keep him in his neighborhood, down the street from two of my brothers, in a facility with lots of people and activities and full-time medical care. It was an excruciatingly painful decision, as it is for any Alzheimer family who makes it. We called it a “temporary decision,” and we’d see how it went.

We sold my parents’ home, packed everything up, moved it all out and put my dad into a beautiful assisted living home right down the street. When I went to check it out for the first time, I sat on the ?oor and burst into tears, unsure whether we were making the right decision. We made his room look exactly like his room at home. I don’t think he noticed, but it made us feel better.

I remember the first time I went there to visit him. It was seven years after his diagnosis, mind you, but it felt like I was dealing with his disease headon for the first time. Why? I realize now that while my mother was alive, I was more focused on her—talking to her every day, dealing her declining health, her strokes, her many emergency hospitalizations. Focusing on her distracted me from really feeling the impact of my dad’s disease. Call it what it was: denial. But since she’s gone, my dad’s Alzheimer’s has hit me in the face, and it’s cracked my denial wide open.

When I went to visit my father recently in Washington, I took him outside. There we were, three people sitting quietly on a park bench—his caregiver and me, with my dad in the middle. After a while, my father put his head down on the caregiver’s shoulder and nuzzled him, just like a little kid. It was a sweet moment, looking as he did like a child seeking and getting comfort. But not from me. It was as if I, his only daughter, weren’t there at all. I could have been a bystander. Actually, I was a bystander. That blew my mind and broke my heart.

Today, I visit him and call him, because I know I should. It’s the right thing to do. It’s the respectful thing to do. It’s what a good daughter does. I would want it done for me. But I still struggle. I struggle to find my place in his life and his care, and I struggle for a connection. I say, “Hello, Daddy.” He says, “God bless you!” I say, “How are you, Daddy?” He says, “You’re fantastic!” Sometimes he just mumbles. Sometimes I don’t get even that.

I watch my dad in the facility’s day room, playing with the same puzzles and alphabet blocks my kids had when they were 5 years old. Doing the same things we used to do in Mommy ‘n’ Me classes. I can’t even describe what I feel when I see that. If I want to remember Sargent Shriver, the smartest person I ever knew, the World War II naval hero, the editor of the Yale newspaper, the devoted husband and father, the brilliant and successful public servant with the dazzling intellect—that Sargent Shriver, my dad, is in the pictures on the wall in his room.

I’m so grateful to my brothers and their wives who have homes in Washington down the street from the facility, who step up in such a substantial way to take care of our dad. They have him over for dinner every night and take him to their kids’ basketball games and recitals and to church. They are fully present with him. They know how to deal with him and talk to him. When he refuses to get out of the car, my brothers say, “Fine!” When he growls at them, they growl back. When he mumbles, they mumble.

We talk about how women are doing the lion’s share of Alzheimer caregiving in this country. But all four of my brothers and men whose stories you’ll read in this report show us that men have been stepping up to the plate to care for ailing parents as well. And more men will have to, as more and more women, including their own wives, get the disease. As we investigate in this report, men are having to change their attitudes about what helping out at home means, about asking for ?exible work schedules, about how to run their own businesses, how to juggle doctors’ appointments, how to manage medications, how to take care of their aging inlaws when their wives can’t—how to sit and look into the face of a spouse or parent who doesn’t know who on earth they are and deal with it.

It’s a tough change for so many of them. We women inhabit caretaking roles easily, and men have said for so long, “I just don’t know how to do what you do, and I’m just not as good at it as you are.” Now women are asking the men in our lives to help us—and they are.

I watch my four brothers give their kids a new kind of role model to emulate: the strong, nurturing man. My brothers treat my father with such love—fixing his jacket, smoothing his hair, telling him, “Lookin’ sharp, Daddy!” One more time, he says, “That’s fantastic!” They take him to Orioles and Red Sox games and to Special Olympics and Best Buddies events, where former Peace Corps volunteers come up to see him. They know he has Alzheimer’s, but still they take his hand and tell him stories from the old days. It doesn’t matter that he doesn’t know who they are or that he doesn’t even remember the Peace Corps. What matters is that he’s comforted by the warmth of the human connection. These are the gifts my brothers bring to him.

And I’ve learned from my own children and my nieces and nephews. I watch how they talk and laugh with their grandpa, funny and free and easy. They love him, they laugh with him, they play with him, they’re fascinated by him. They don’t get bogged down in the sadness. My kids and my nieces and nephews all accept my father for who he is today—and that’s been a lesson in acceptance for me.

For the summer, we moved our dad out of the facility in Washington to our family home in Hyannisport. We all took turns living there with him. It felt good and right to be in the same house with him, being next to him at dinner, playing ball with him or just sitting in silence with him, staring out at the sea. I talked to him about my mother, and we looked at old pictures together. When I had to leave to go home to California, I felt guilty and con?icted.

I know that all in all, my family is so lucky. We’re truly blessed we have been able to keep our father at home for a long time. We are blessed to have the choices we have today. We’re especially blessed to have the resources to pay patient and loving caregivers who help us take care of our dad and make him feel loved.

But I know millions of others aren’t as lucky. Many are forced to quit jobs to stay home— or go through the wrenching process of sending a parent away to a facility, feeling judged and mortified and ashamed that they can’t care for their loved one themselves. That’s the double stigma of Alzheimer’s—ashamed that you have it in your family, ashamed that you can’t cope. For so many, the financial, emotional and spiritual costs are just way too much to bear.

My hope is that as the veil is lifted, as information and funds and support programs are made available, families will see that they’re not alone. As more people, like the ones you’ll meet in The Shriver Report, step out and speak out, sharing their personal journeys with Alzheimer’s, more families will see that there’s nothing to be ashamed of—that there’s hope out there because, together, we are finally making Alzheimer’s a national issue.

The truth is that we simply must put Alzheimer’s on the front burner because if we don’t, Alzheimer’s will not just devour our memories. It will also break our women, cripple our families, devastate our healthcare system and decimate the legacy of our generation.

But if we do, I’m convinced that this Woman’s Nation will be able to say that, believe it or not, there once was a time when there was no cure for Alzheimer’s.

Lithium: a medication for Alzheimer's disease?

According to scientists Alzheimer’s disease, a condition which leads to the size of the brain decreasing faster than ageing, could be treated by lithium, a naturally occurring element that is extremely inexpensive and already in use for other psychiatric disorders.

Lithium has been in use to treat bipolar affective disorders and now, researchers at Sao Paulo University in Brazil, led by Dr Orestes Forlenza have discovered that the pills slowed down memory loss in the elderly, reducing their cognitive decline. They also noted that there was a decrease in build-up of tangles of damaging proteins called phospho- tau in people’s cerebrospinal fluid which characterized Alzheimer’s disease.

For the study the team examined 41 people over the age of 60 with mild cognitive impairment, out of whom 21 took low doses of lithium every day for a year. All went through tests of memory and attention and a sample of their brain fluid was analyzed for tau concentrations. Although all the participants showed a decline in memory function over the year, those taking lithium showed less of a decline than those taking the placebo. Those taking lithium also had less of a form of the tau protein, pTau – a hallmark of Alzheimer’s disease – in their cerebrospinal fluid. The findings are published today in the British Journal of Psychiatry. The researchers now want to see larger studies to investigate whether lithium could have potential as a preventative treatment for Alzheimer’s.

Professor Allan Young, a psychiatrist from Imperial College London, described the study as “encouraging” – and particularly presents a value therapeutic opportunity, because no pharmaceutical company has a patent on lithium, meaning it is very cheap to prescribe. He added, “This trial adds to the increasing evidence that lithium may have beneficial effects on the brain and begs to be replicated in further randomised trials.”

Brain size clue in Alzheimer's disease

The brains of people diagnosed with Alzheimer’s disease start shrinking up to a decade before symptoms appear, a new study finds.

Researchers from Rush University Medical Center in Chicago and Massachusetts General Hospital in Boston performed brain neuroimaging scans on older adults with no signs of memory loss.

Of the 33 people in the Mass General group, eight developed Alzheimer’s didease over the course of 11 years. In the Rush group, only seven of 32 people followed for an average of seven years developed the disease.

About 55 percent of those whose brains were in the upper tertile (third) of atrophy developed Alzheimer’s disease, while none of those whose brains in the bottom tertile (little or no atrophy) developed Alzheimer’s disease.

Among those with moderate amounts of atrophy, about 20 percent developed the disease.

They could differentiate those who would decline from those who would remain healthy, according to the senior study author Leyla deToledo-Morrell, director of the graduate program in neuroscience at Rush University Medical Center. Based on the atrophy measurements, they claimed that they could even determine how quickly they were going to develop Alzheimer’s disease.

Doctors have long known that Alzheimer’s is an insidious disease, and that changes in the brain begin long before the first symptoms become evident, said Dr. Jeffrey Burns, director of the Alzheimer and Memory Program at University of Kansas Medical Center. This suggests, along with other studies, that Alzheimer’s disease neuropathology is likely present years, if not decades, before the emergence of symptoms.

What’s probably happening is that biochemical changes in the brain that are only partially understood cause degeneration of brain cells. Over time, the cells begin to die off, leading to structural changes in the brain tissue, or atrophy. Specifically, people in the study who would later be diagnosed with Alzheimer’s disease were more likely to show cortical thinning, or shrinkage, in several brain regions, including the medial temporal lobe, temporal pole and the superior frontal gyrus, which prior research has implicated in the early stages of Alzheimer’s disease. The amount of atrophy was much, much, much less than in a person with Alzheimer’s disease, but because each one who developed Alzheimer’s disease showed it, the results are extremely significant.

Eventually, the hope is that one day there will be drugs to slow the progression of the disease – there are none currently available – and being able to diagnosis Alzheimer’s early would mean people could start treatment before they have experienced significant declines.

If doctors can identify people at risk of the disease, they would be at much greater benefit from receiving treatment, rather than people who have already developed Alzheimer’s, who already have a certain amount of cell death and you can’t really rescue those cells. Though the number of participants in the study was small and the findings need to be repeated in larger populations, it is arguably remarkable they saw changes this clear with this small number of cases.

A a second study from the same journal may have practical applications immediately. The study found that vascular disease risk factors, such as hypertension, diabetes, cardiovascular disease and high cholesterol, may raise the risk of Alzheimer’s disease. The good news is that treating those conditions lowered the risk of Alzheimer’s disease. Chinese researchers followed 837 people over age 55 with mild cognitive impairment, which is often a precursor to Alzheimer’s, for five years. During that time, 298 developed Alzheimer’s, while the others still had mild cognitive impairment but had not progressed to Alzheimer’s. People who were treated for all of their vascular disease risk factors were less likely to progress to Alzheimer’s disease than those who weren’t treated or who only had some of their risk factors treated, according to the study. This study appears to imply that vascular disease has a real effect on the manifestation of Alzheimer’s disease. The vascular disease is damaging the brain and is probably causing the individual to have lowered resistance to the pathological effects of Alzheimer’s disease. Cholesterol-lowering medications, blood pressure medications and lifestyle changes such as losing weight and exercising can all help lower vascular disease risk factors.

Cognitive reserve and Alzheimer's disease biomarkers are independent determinants of cognition

Cognitive reserve and Alzheimer’s disease biomarkers are independent determinants of cognition Brain (2011) awr049 first published online April 7, 2011 doi:10.1093/brain/awr049

The link to this article in Brain is here.

The objective of the study above was to investigate how a measure of educational and occupational attainment, a component of cognitive reserve, modifies the relationship between biomarkers of pathology and cognition in Alzheimer’s disease. The biomarkers evaluated quantified neurodegeneration via atrophy on magnetic resonance images, neuronal injury via cerebral spinal fluid t-tau, brain amyloid-? load via cerebral spinal fluid amyloid-?1–42 and vascular disease via white matter hyperintensities on T2/proton density magnetic resonance images. They included very large samples – 109 cognitively normal subjects, 192 amnestic patients with mild cognitive impairment and 98 patients with Alzheimer’s disease, from the Alzheimer’s Disease Neuroimaging Initiative study, who had undergone baseline lumbar puncture and magnetic resonance imaging. We combined patients with mild cognitive impairment and Alzheimer’s disease in a group labelled ‘cognitively impaired’ subjects.

Their main conclusions included: (i) that in cognitively normal subjects, the variability in cognitive performance is explained partly by the American National Adult Reading Test and not by biomarkers of Alzheimer’s disease pathology; (ii) in cognitively impaired subjects, the American National Adult Reading Test, biomarkers of neuronal pathology (structural magnetic resonance imaging and cerebral spinal fluid t-tau) and amyloid load (cerebral spinal fluid amyloid-?1–42) all independently explain variability in general cognitive performance; and (iii) that the association between cognition and the American National Adult Reading Test was found to be additive rather than to interact with biomarkers of Alzheimer’s disease pathology.

The National Audit for Dementia

Many doctors find the term ‘clinical governance’ puzzling. It originated from the concept of governance, used in the commercial world for over a decade and introduced into the health sector by Nolan in 1994. ‘Corporate governance’ specifies arrangements that ensure that directors and senior managers of a company exercise their power responsibly (i.e. running the company in the interests of not only the shareholders, but also the broader community). The arrangements incorporate checks and balances upon the power of the chief executive, for example, by splitting the roles of the chairman and the managing director. The aim of corporate governance is to ensure that public service values are placed at the heart of the NHS. Clinical governance was introduced to ensure that each NHS organisation was made accountable for continuously improving the quality of its clinical services and for safeguarding high standards of care.

Clinical governance is:

  • ‘a system through which NHS organisations are accountable for continuously improving the quality of services’ (Professor Aidan Halligan)
  • a duty of quality’ (Health Act 1999).

The quality of service provided to pa tients is not confined to doctors’ clinical activity. Doctors cannot avoid responsibility for the use of resources or other aspects of patient care that impact on quality of care or the service provided, and they have a duty to highlight inadequate resources in this respect.

Clinical audit performed against relevant, definable and defendable standards is the process by which doctors can gather the evidence to improve patient care. Doctors have always had a duty to patients, but the Health Act (1999) now makes that duty a legal obligation.

A report into the care received by nearly 8,000 patients with dementia in 206 hospitals in England and Wales has revealed that few hospitals provide compulsotraining for their staff in awareness of dementia, that many patients with dementia are not having assessments of their mental health or state of nutrition and that there are serious delays for patients referred to in-hospital psychiatry liaison services.

Findings of the clinical audit – commissioned by the Healthcare Quality Improvement Partnership and conducted by a project team at The Royal College of Psychiatrists’ Centre for Quality Improvement - are also rather surprising in the current financial climate. The National Audit Office reported in 2007 that each hospital could save an average £6 million a year by correctly identifying dementia patients, providing more appropriate and timely care, thus reducing length of stay and improving health outcomes.

Selected Key Findings From The National Audit Of Dementia Interim Report:

  • 95% of hospitals do not have mandatory training in dementia awareness for all staff whose work is likely to bring them into contact with patients with dementia.
  • About one-third of patients did not have a nutritional assessment recorded during their admission.
  • Fewer than one-half of patients received a formal mental status test upon admission to hospital.
  • One-third of patients referred to in-hospital psychiatry liaison services not seen within 96 hours.

Management of behavioural variant frontotemporal dementia

I have been reading an extensive review of behavioural variant frontotemporal dementia which features in the January issue of the Lancet Neurology journal. The authors provide a comprehensive overview of the literature of this condition, as it currently stands, and I thought that the paper was interesting. Indeed, Piguet and colleagues are correct to discuss caregiver stress in the management of behavioural variant frontotemporal dementia. However, I would like to point out that it is the impulsivity and risk-taking behaviours of such patients which can be very distressing to the carers of such patients, particularly since the patients themselves tend not to have much insight into their behaviour and personality changes. It is precisely these types of symptoms which I showed could be treated using a psychostimulant, methylphenidate, in a placebo-controlled double-blind study, albeit with a small sample size. The full paper is visible HERE.

It is important to note however that methylphenidate has never been licensed routinely for this indication, and any individuals on pharmacological treatment for dementia should be entirely guided by their own physician.

Currently, no disease-specific treatment interventions for FTD exist. Consequently, treatment largely remains supportive and involves a combination of non-pharmacological and pharmacological measures aimed at reducing the effect of distressing symptoms.120 The role of pharmacological interventions in FTD remains uncertain, and only small and often conflicting treatment trials have been done so far; these studies have not considered the effect on carer stress as a major outcome variable. Selective serotonin reuptake inhibitors have been used to treat disinhibition and challenging behaviours, but evidence for their use remains contradictory.121122 Atypical antipsychotics such as olanzapine have been used for patients with prominent agitation, aggressive behaviour, or psychosis.123 Anticholinesterase inhibitors, the mainstay of AD therapy, do not have an established role in the treatment of FTD. One study reported improvement in measures of behavioural disturbance and carer stress with rivastigmine,124although deterioration in neuropsychiatric symptoms without cognitive improvement was shown with donepezil.125 Several drugs under development attempt to reduce aggregation of tau or TDP-43 and hence slow the fundamental pathological process in FTD.120126

Piguet OHornberger MMioshi EHodges JR.Behavioural-variant frontotemporal dementia: diagnosis, clinical staging, and management. Lancet Neurol. 2010 Dec 10. [Epub ahead of print] Neuroscience Research Australia, Randwick, NSW, Australia.

Abstract on MEDLINE here.

A new way of diagnosing the earliest stages of Alzheimer's Disease?

Alzheimer’s disease is the most common form of dementia in the UK, characterized by profound memory problems in affected individuals. Currently there is no single test or cure for dementia, a condition that affects over 800,000 people in the UK. The prospect of disease modification has intensified the need to diagnose very early Alzheimer’s Disease with high accuracy. The ultimate goal is possibly to identify and treat asymptomatic individuals with early stages of Alzheimer’s Disease, or those at high risk of developing the disease. By definition, such individuals will be asymptomatic, and disease biomarkers or high-risk traits will be require identification. For pre-symptomatic treatment trials, demonstration of disease modification will ultimately require evidence of delay to symptom-onset or conversion to Alzheimer’s Disease.

In a paper reported recently, UK experts say they may have found a way to check for Alzheimer’s years before symptoms appear. A lumbar puncture test (a test to get spinal fluid from an individual via his back) combined with a brain scan can identify patients with early tell-tale signs of dementia, they believe. Ultimately, doctors could use this to select patients to try out drugs that may slow or halt the disease. Although there are many candidate drugs and vaccines in the pipeline, it is hard for doctors to test how well these work because dementia is usually diagnosed only once the disease is moreadvanced. Researchers at the Institute of Neurology, University College of London, working with the National Hospital for Neurosurgery and Neurosurgery, Queen Square, London, believe they can now detect the most common form of dementia – Alzheimer’s disease – at its earliest stage, many years before symptoms appear.

Their approach checks for two things – shrinkage of the brain and lower than normal levels of a protein, called amyloid, in the cerebrospinal fluid (CSF) that bathes the brain and spinal cord. Experts already know that in Alzheimer’s there is loss of brain volume and an unusual build up of amyloid in the brain, meaning on the whole less amyloid in the CSF. There is, however, rather conflicting evidence for a relationship between measures of amyloid burden and brain volume in healthy controls, The research team reasoned that looking for these changes might offer a way of detecting the condition long before than is currently possible. To confirm this, they recruited 105 healthy volunteers to underwent a series of checks. All subjects were drawn from the Alzheimer’s Disease Neuroimaging Initiative (ADNI), a multi-centre publicly/privately-funded longitudinal study investigating adult subjects with Alzheimer’s Disease, ‘mild cognitive impairment’ of the memory variety, and normal cognition. Participants undergo baseline and periodic clinical and neuropsychometric assessments and serial MRI.

The volunteers had lumbar puncture tests to check their spinal cerebrospinal fluid (CSF) for levels of amyloid and MRI brain scans to calculate brain shrinkage. The results, published in Annals of Neurology (reference provided below), revealed that the brains of those normal individuals with low CSF levels of amyloid (38% of the group), shrank twice as quickly as the other group. They were also five times more likely to possess the APOE4 cholesterol risk gene and had higher levels of another culprit Alzheimer’s protein, tau. Crucially, the results may allow doctors to pursue avenues to test which drugs might be beneficial in delaying or preventing dementia.

Potential limitations of the study include the relatively high percentage of amyloid-positive normal controls, which may or may not reflect the true population prevalence of individuals with significant amyloid pathology in this age range. There are also a number of issues relating to the reproducibility, reliability, and reporting of biomarker levels in spinal fluid, which need to be standardized to allow for cross-study comparisons.

Notwithstanding that, the scope for further research is enormous. Whether excess rates of brain atrophy in apparently cognitively normal aged patients with CSF profiles suggestive of AD inevitably lead to cognitive impairment, and if so over what time frame, needs to be established. If this proves to be the case, the results we present have significant implications for very early intervention, demonstrating that biomarkers may be used not only to identify Alzheimer’s Disease pathology in asymptomatic individuals, but also to demonstrate and quantify pr-esymptomatic clinical dementia. This suggests that disease-modifying trials in asymptomatic individuals with the aim of preventing progression to cognitive impairment and dementia may be feasible one day.


Increased brain atrophy rates in cognitively normal older adults with low cerebrospinal fluid A?1-42. Jonathan M. Schott MD, Jonathan W. Bartlett PhD, Nick C. Fox MD, Josephine Barnes, for the Alzheimer’s Disease Neuroimaging Initiative Investigators Article first published online: 22 DEC 2010 DOI: 10.1002/ana.22315

You can view this paper here.

(c) Dr Shibley Rahman 2010

The enigma of the 'freezing-of-gait' in Parkinson's disease: variations on a theme?

This post is in the ‘Dementia’ part of my blog, but please note that not all patients with Parkinson’s disease have dementia. Some patients, however, do.

Parkinson’s disease is easily identifiable to the medical doctor in the UK, it is hoped, because the obvious ‘mask-life’ face of a patient, difficulties in walking (the shuffling gait), a tremor at rest, and stiffness of arms and legs. A particularly intriguing symptom of patients for decades undoubtedly in the research field has been the “freezing of gait” (FOG), which is typically a transient episode – lasting less than a minute, in which gait is halted and the patient complains that his/her feet are glued to the ground. When the patient overcomes the block, walking can be performed relatively smoothly. The most common form of FOG is ‘start hesitation’ (this is what happens when the patient wants to start walking) followed in frequency by ‘turning hesitation’. How or why this happens remains a mystery, but I bet during my lifetime some in-roads will be made into this by academic neurologists (not practising physicians). It is highly relevant as one-day a strategy involving offering cues in the environment may be of use in overcoming FOG problems. This video is for example a remarkable example of this.

As for my own interest in this incredibly interesting phenomenon, I once did at a questionnaire study as a post-doctoral research fellow with Prof Marjan Jahanshahi at Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology and the National Hospital for Neurology and Neurosurgery, University College London. This questionnaire at the factors which cause FOG, as perceived by patients attending the movement disorders clinic of the National. Hospital. This study examined the factors that induce FOG, and identified the cues and strategies that help overcome it through a postal survey of 130 PD patients. 72% reported FoG. The factors that commonly induced FOG, I found, were turning, fatigue, confined spaces and stressful situations, in addition to emotional factors. FOG was also ameliorated by various attentional and external cueing strategies. I feel that one day these results will be enormously useful in patients designing strategies for overcoming FOG, a very real and troublesome phenomenon for patients with Parkinson’s disease. I believe, personally, that it is these trigger factors which help us to understand the phenomenon of FOG, and it is these which my academic colleagues should invest their energies into discovering.

However, in many of the studies, there has been an emergent consensus to identify the factors which can cause patients to ‘unfreeze’ through the phenomenon known as ‘paradoxical kinesia‘. In an academic discussion on the subject, Dr. Friedrich Asmus and colleagues (2009) from the University of Tübingen, Germany, offered that, on the basis of the freezing study above, that, “in this context, visual cueing has a pivotal role, as shown by the report of a patient with PD during the war who was paradoxically able to run by following the footsteps of his wife in front of him. Smilar and reproducible effects of patterned movements like running stairs have been described in the context of paradoxical kinesis“. Another finding from the freezing study was that patients with Parkinson’s disease reported that turning difficulties appeared to be associated with freezing, but the problem was that only limited studies had been conducted to characterize these difficulties. In a formal analysis, the laboratory of Prof. Alice Nieuwboer at the University of Leuven in Belgium indeed this report to be borne out in formal gait analysis, and further found that, during turning, non-freezers and controls decreased their cadence whereas freezers increased it, which may be related to freezing-of-gait.

A major obstruction in this research is the observation that the underlying brain pathology underlying FOG remains largely unknown. Behavioural studies have helpfully identified several gait alterations in patients with Parkinson’s disease with FOG, even when the patient is not experiencing an actual FOG episode. These can be discovered when people with Parkinson’s disease are walking on a treadmill. Alterations include premature timing of muscle activations, increased variability of gait, increased temporal gait asymmetry and faulty generation of postural adjustments before step initiation. Recently, it was suggested that FOG may be caused by a failure to generate adequate amplitudes for the intended movement.

As an advance in the research from Snijders and colleagues published in Brain on 1st December 2010, a study was reported, which looked at gait planning in patients with freezing of gait, using motor imagery of walking in combination with brain scanning. They included 24 patients with Parkinson’s disease: 12 patients with freezing of gait, 12 matched patients without freezing of gait and 21 matched healthy controls. Subjects performed two previously validated tasks—motor imagery of gait and a visual imagery control task. During motor imagery of gait, patients with freezing of gait showed more activity than patients without freezing of gait in the mesencephalic locomotor region.

And what does this brain area do? Well, on deeper examination, it seems that – as usual – no-one precisely knows, and the situation is undoubtedly complicated by the fact that defining this region in the human brain has been troublesome, in relation to our non-human counterparts. Based on biologically hypothesized connections of the central pattern generator in the salamander, it is now a widely held belief that this part of the brain indeed represents some sort of a robotic system which acts as a generator of simple movements. For example, electrical measurement studies from Steeves and Jordan back in 1984 have shown that stimulation of the mesencephalic locomotor region (MLR) located in the brain of the salamander produce different gaits, swimming or walking, depending on intensity level.

So where is this part of the brain exactly? Well, they describe:

Ascending projections were observed to the subthalamic nucleus, caudal hypothalamic nuclei, the centrum medianum nucleus of the thalamus, the ventral tegmental area of Tsai, the superior colliculus, and the periaqueductal gray region. The ascending projections were also ipsilateral, with sparse contralateral labeling confined to areas which received ipsilateral projections. Projections to the contralateral cuneiform nucleus were also consistently observed. The results, when compared to those of another study, suggest that the classical MLR is anatomically distinct from the more medial sites in the mesencephalon which can also induce locomotion.

In all honesty, this leaves me pretty clueless, and I doubt whether a human neurosurgeon would feel particularly comfortable with this working definition, either. But that brings one onto a really interesting point – can knowing the abnormal part of the brain is help with precise neurosurgery into a part of the brain, called ‘stereotactic surgery’? Well – maybe no, if “patients with freezing of gait also tended to have decreased responses in mesial frontal and posterior parietal regions“.

Is what they’ve done useful then? Yeah, but it is also the case they’ve found brain areas which correlate with this abnormal behaviour, rather than necessarily causing it. I remember the classic Psychology finals question from Cambridge from the early 1980s which provided, “If we subtract the brain areas activated by Christian saying the Lord’s Prayer from those activated by atheists saying the same prayer, would we have found the neural substrate of Christianity?” The paper in my sense falls into this classic problem of brain scanning, but what choice did the investigators really have because they couldn’t have got them into a scanner, freeze, and then unfreeze? That would in a sense be the ideal experiment, and it indeed might be possible if there were a convincing animal model of FOG and freezing-of-gait, but this surely is a long-way off.

Interesting further reading

Anke H. Snijders, Inge Leunissen, Maaike Bakker, Sebastiaan Overeem, Rick C. Helmich, Bastiaan R. Bloem, and Ivan Toni. Gait-related cerebral alterations in patients with Parkinson’s disease with freezing of gait Brain first published online December 1, 2010 doi:10.1093/brain/awq324

Steeves JV, Jordan, LM.  Autoradiographic demonstration of the projections from the mesencephalic locomotor region. Brain Res. 1984 Jul 30;307(1-2):263-76.

Rahman, S, Griffin, HJ, Quinn, NP, Janahshahi, M.  The factors that induce or overcome freezing of gait in Parkinson’s disease. Behav Neurol 2008;19(3):127-36.

Terry Pratchett: "Shaking Hands With Death"

This is the BBC Dimbleby lecture given by Terry Pratchett in 2009: “Shaking Hands With Death“. Pratchett appealed to people to “keep things cheerful”, and proclaimed that “we are taking it fairly philosophically down here and possibly with a mild optimism.” Terry Pratchett has a rare form of dementia called posterior cortical atrophy. The location of this lecture is very poignant to me as it is where I took the MRCP(UK) part 1 examination, just off the Outer circle of Regents’s Park, London.

He has written passionately about the issue in ‘The Guardian’ (link here):

I got involved in the debate surrounding “assisted death” by accident after taking a long and informed look at my future as someone with Alzheimer’s and subsequently writing an article about my conclusions. As a result of my “coming out” about the disease I now have contacts in medical research industries all over the world, and I have no reason to believe that a “cure” is imminent. I do think, on their good advice, that there may be some very interesting developments in the next couple of years and I’m not the only one to hope for some kind of stepping stone – a treatment that will keep me going long enough for a better treatment to be developed.

Raising awareness of dementia with Lewy Bodies

Please note that this post is not about medical care of patients with dementia with Lewy Bodies. That specialist care should be given by an expert. This post is only intended to raise awareness in this type of dementia.

June Brown is better known as Dot Cotton in EastEnders. She gives a poignant description of her husband, Robert Arnold, who had dementia with Lewy Bodies; he sadly died. June Brown is devoted as the Patron of the Lewy Body Disease, and she in this video describes accurately the symptoms of this type of dementia. This video has been distributed by the Lewy Body Society. She explains about how the Society has been built from the aspiration to raise awareness of the disease, especially the fact that this disease is clearly different from other types of dementia. He describes how her husband had fluctuating levels of consciousness, typical of Lewy Body’s disease, ranging from complete lucidness to confusion and disorientation.

The President of the Lewy Body disease is Professor Ian McKeith, who is well known amongst experts in dementia to be world-renowned in the dementia with Lewy Bodies. He explains that it is the second-most common cause of dementia in elderly people, making up 1 in every 7 cases. Prof McKeith explains the prominent Parkinsonism, the visual hallucinations, and the problematic similarity with other types of dementia such as Alzheimer’s disease. Hallucinations might include seeing people in the house who weren’t in fact there. He resumes the theme from June Brown that the fluctuating levels of consciousness makes caring for a patient very unpredictable.

The Lewy Body Society can be found in this link. It is the only Charity devoted entirely to Lewy Body Society. Patients and carers will also find the Alzheimer’s Society helpful in their support of people involved in dementia care.

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