Speaking about Taking Charge, Moving On and Enjoying Life

We had the honor of being invited to speak at Global Community Conference on Parkinson’s Disease: Beyond the Limits conference in Keystone, CO earlier this month. They had the usual keynote addresses and breakout sessions. The sessions fell under several headings. For example, Beyond Today was about research. Since the conference was being held in conjunction with a Keystone Dual Conference for Parkinson’s and Alzheimer’s, we had the benefit presentations from some of the world’s most renown researchers. In later blogs, we will discuss some of the research we learned about for it applies to LBD as well as PD.

Beyond the Pill was about non-medical treatment and Beyond the Worry was all about caregiving. In past blogs, we have already discussed non-medical treatment and I’m sure we’ll do more of that for it is the direction we see ourselves going in the next year. Sadly, the sessions about non-medical treatment we’d most like to have seen were at the same time as ours and so we didn’t learn a lot about that, at least not there.

We were in the series called Beyond the Tremors, i.e., non-motor symptoms. Besides ours, there were several other session on cognition, some taught by the above scientists. Addressing cognition so directly is a change for PD groups. They have traditionally avoided this subject or else, treated dementia as a symptom that PwPD occasionally developed towards the end of their lives.

However, we found that the old resistance of the PD community to see itself as a part of the Lewy body continuum was still there…a little less strong but still alive and well. Many had never heard of Lewy bodies, and if they had, were not aware that they caused PD as well as LBD. Of those who did know about Lewy bodies, fear was often present. One man who came to hear us put it this way, “I was afraid to attend your session. I was afraid you’d paint a dramatic picture of doom and gloom.” Another woman said, “When the doctor told me I had LBD, I felt I’d been given a life sentence.” We didn’t talk about doom and gloom or life sentences. We talked about hope and about taking charge, about a person’s power to slow down the disorder’s progress and increase one’s quality of life. The man who'd been afraid to come told us later, "I'm glad I came. It wasn't what I feared. Instead it was positive and helpful."

Yes, PD is a progressive disease that can and often does limit one’s thinking ability as well as one’s mobility. It is so easy to feel that the disorder has taken over and that neither the PwPD nor the caregiver is any longer in charge—to feel as though they are locked in a driverless train to death or worse, insanity. It’s scary, to say the least. We were there at that conference to tell families that they don’t have to feel so hopeless and helpless; that there are many things, from living a healthy, low-stress lifestyle to avoiding Lewy dangerous drugs, they can do. We talked about knowledge being power. The power, for instance to know which drugs are Lewy-safe and which may not be. You can’t stop that train, but you can slow it down so that you can enjoy the scenery and even the journey.

Our goal is to teach PD and LBD families not to let the disorder to take over but to “live until you die.” To take charge, move on and enjoy the life you have.

Find more about LBD in The Caregiver's Guide to Lewy Body Dementia available on LBDtools.com in the LBD Book Corner.
Parkinson’s disease

Part 6: LBD and PD Drugs

We could call this blog and the next one “The Balancing Act” because they are about two groups of drugs whose actions are polar opposites of each other. Today’s blog is about PD drugs. Next week’s will be about dementia drugs. Be sure to read both blogs—they go together but there was just too much information for a single blog.

No drug will cure PD or LBD—or any other neurological disorder for that matter. However, they do treat the symptoms and that adds to one’s quality of life. Both groups are well known to LBD families, especially those with PDD, where the dementia was preceded by the motor problems of Parkinson’s disease.

Lewy bodies attack brain cells and extract chemicals the brain cells use to transmit information (neurotransmitters).  In the mid-brain, they remove dopamine, needed for good motor functioning. In the cerebral cortex, they target acetylcholine, needed for good mental functioning. These two chemicals operate on a ratio system. If the level of acetylcholine is higher than that of dopamine, the body acts as though the dopamine level is too low—with poor motor functioning. Conversely, if the level of dopamine is higher, the body acts as though the acetylcholine level is too low—with poor cognitive functioning.

PD meds that are too strong will improve mobility but decrease cognition.







Dementia meds that are too strong will improve cognition but decrease mobility.


Drugs used to treat PD act to change the dopamine/acetylcholine ratio in four ways:

Dopamine replacement: Sinemet has been the most commonly used PD drug for years. It effectively controls motor symptoms with few short-term side effects. However, its long terms side effects such as muscle rigidity and confusion can be serious.

Dopamine copying or mimicking: Requip, Mirapex and Neupro are in a newer group called dopamine agonists.  They cause fewer long term problems and are now usually prescribed first with Sinemet added, if needed, for better control.  Short term side effects include increased confusion and hallucinations. These drugs are not recommended for anyone with dementia.

Dopamine preservation: The following drugs all act in various ways to preserve the level of dopamine in the cells.  Physicians usually prescribe these weaker drugs to boost the effectiveness of Sinemet.

Symmetrel has side effects include increased psychiatric symptoms and anxiety. It is not recommended for anyone with psychiatric symptoms (or LBD-related symptoms such as hallucinations or delusions.)

Eldepryl and Azilect are new, still controversial, drugs. They don’t appear to have any serious cognitive side effects.

Tasmar and Comtan are drugs that inhibit a chemical that helps to move dopamine out of the brain cells. They do not appear to have any serious cognitive side effects.

Acetylcholine blocking: Cogentin and Artane are anticholinergics that maintain the balance by blocking acetylcholine and preventing it from being effective. Motor functioning may improve, cognitive symptoms will likely increase.  These drugs are rarely used today.

The bottom line is that PD drugs strong enough to improve motor function tend to increase dementia symptoms. Next week’s blog will explain how dementia drugs strong enough to treat dementia may increase PD symptoms. Families and physicians usually have to look for a happy medium, giving up some mobility to maintain cognition or vice versa. Most families opt for more cognition.

The authors of this blog are not physicians. We report what we and other caregivers have learned by experience, from physicians and from the literature. This blog is informational only. You should always talk with a physician about individual issues.

More About the LBD Family

Last week’s blog discussed how Parkinson’s disease and two types of dementia are all members of the Lewy body family. This week expands on that with a more scientific view. Also, new research has suggested another member of the family, REM Sleep Behavior Disorder.

Damaged alpha-synuclein proteins clump together to form the microscopic round deposits called Lewy bodies. Unlike Alzheimer’s damaged proteins, found only in the cerebral cortex, Lewy bodies can be found in many areas of the brain. Besides dementia, these damaged proteins can cause motor problems, autonomic nervous system (ANS) dysfunctions, perceptual problems, mood disturbances and more, depending on where they are in the body.

At present, identifying the presence of Lewy bodies other than by their symptoms is difficult but that is changing. Brain scans are getting more accurate and researchers are actually finding Lewy bodies in other, more easily accessed areas of the body, like the gastro-intestinal (GI) tract.

Alzheimer’s damaged proteins are thug-like, attacking and killing whatever neurons (brain cells) they touch. Lewy bodies are more selective, choosing only those neurons that contain certain neurotransmitters—chemicals that the cells need to function properly. They extract the chemicals, leaving the cells weakened and eventually dead. The targeted neurotransmitters vary, depending on the area of the brain.

Parkinson’s Disease. In the mid-brain, Lewy bodies extract the chemical dopamine, instrumental in fine motor control. This results in the motor symptoms of Parkinson’s disease. Although PD starts out as a movement disorder, other symptoms appear the disease progresses. One of the most distressing is dementia. (See our 6/15/12 and 10/12/12 blogs.)

Lewy Body Dementia. While this term was once synonymous with Dementia with Lewy Bodies, it is now an umbrella term that defines both types of dementia caused by Lewy bodies: dementia with Lewy bodies (DLB) and Parkinson’s disease with dementia (PDD).

Dementia with Lewy Bodies (DLB). Dementia is defined as a loss of cognitive skills such as memory, thinking, or impulse control, severe enough to interfere with functional ability or activities of daily living. Such losses occur when Lewy bodies in the cerebral cortex target the chemical, acetylcholine. When no PD is involved, the resulting disorder is called Dementia with Lewy Bodies.

Parkinson’s Disease with Lewy Bodies (PDD). When someone with PD develops dementia, it means that the Lewy bodies have traveled from the midbrain to the cortex. Both dopamine and acetylcholine are targeted, which causes both motor and dementia symptoms.

People with PD (PwPD) are a ready-made group of people at risk for dementia. Therefore most of the subjects in the growing pool of research about early- and pre-Lewy body dementia are PwPD. However, it is important to remember that LBD doesn’t have to start with Parkinson’s. It can skip the PD and go right to dementia—and then of course, it’s called Dementia with Lewy bodies. Even so, since two types are so similar, almost everything researchers learn about PDD and its precursors, we can also apply to DLB, that is, to LBD in general.

 REM Sleep Behavior Disorder (RBD). Caregivers sometimes call RBD “Active Dreams” because the chemical switch that prevents movement during normal dreams is damaged. While RBD has been known to appear in childhood, it is more common after 50. A PwRBD can be very active, thrashing their limbs around, talking and even walking in their sleep. (See our 11/2/12 blog.)

Although RBD can occur alone, it is very common with PD and both types of Lewy body dementia. When researchers autopsied brains from people who died with RBD, they found Lewy bodies even when no other LB disorder was present.  Thus we include it here as a Lewy body disorder, usually the first one to appear.

Next week’s blog will be about disorders related to LBD and some lookalikes.

ADHD and Lewy Body Dementia

Both attention deficit, or inattention, and impulsive behaviors are common early LBD symptoms although until other symptoms show up, LBD is seldom suspected. Nevertheless, these symptoms may be stronger risk factors for LBD than previously thought.

Inattention and impulsivity are also symptoms of attention-deficit/hyperactivity disorder (ADHD), which starts in childhood, usually between age three to five, and can continue into adulthood. Unlike Lewy, it is often genetic, being passed on from parent to child. However, there are many similarities between ADHD and LBD. Like Lewy, it occurs most often in males. Inattention causes a child to have difficulty completing a task, following instructions, staying organized and processing information, similar to the way the same problem affects adults with LBD later in life.

Impulsivity leads to behavioral issues and a lack of emotional restraint. Again, this is similar to the behavioral and emotional issues of LBD. Tests of people with Parkinson’s also show higher than average levels of inattention. Researchers suggest that the reason for these similarities is that people with Lewy body disorders and ADHD all have low amounts of certain chemicals (neurotransmitters) that brain cells require for proper functioning, although the chemicals vary with the disorder.

Even more interesting, a recent study found that those with adult ADHD (AADHD), people whose attention deficit and hyperactivity continues past childhood, were three times more likely to develop LBD than someone without the disorder. Further, people with adult AADHD were no more likely than the general public to develop Alzheimer’s. If substantiated with further studies, this could make AADHD as strong and as specific an indicator of eventual LBD as Active Dreams. (November 2, Active Dreams, PD and LBD) Thus, we suggest that anyone with AADHD start planning ways to avoid or delay its advancement into dementia. If it turns out that the risk of LBD isn’t so great, what you’ve done won’t be wasted. After all, most of what you do to delay dementia makes you healthier anyway.

Association of Parkinson's disease with symptoms of attention deficit hyperactivity disorder in childhood.

Adult ADHD Linked to Increased Risk for Lewy Body Dementia.

Active Dreams, PD and LBD

REM Sleep Behavior Disorder (RBD) is sometimes called “Active Dreams” because people who have it physically act out their dreams in their sleep. There is a chemical switch in the brain that turns off mobility during dreams, allowing a more restful sleep. When the switch is damaged, a sleeping person may thrash their arms and legs around, talk out loud and become violent.

When the brains from people who had been diagnosed with RBD, or Active Dreams, were autopsied, researchers continually found Lewy bodies even when no other Lewy body disorder was present. Thus we consider the disorder a member of the Lewy body family, usually the first one to appear. Although RBD can occur alone, it can accompany Parkinson’s disease and both types of Lewy body dementia and may show up before any other Lewy body disorder. Active Dreams have long been considered a serious predictor of Dementia with Lewy Bodies (DLB). They are often the first precursor to appear, and can show up decades prior to dementia symptoms.

Recent studies have explored the relationships between RBD, PD and LBD further. They have found that there is at least a 65% chance that a person with Active Dreams will develop an alpha-synuclein-based disorder within an average of 11 years of an RBD diagnosis.  Alpha-synuclein is the protein that when damaged, can become Lewy bodies, which causes both PD and DLB. The other member of this group is Multiple System Atrophy (MSA) which affects the Autonomic Nervous System similar to the way LBD does. MSA does not belong to the Lewy Body family, but it is a close cousin, with its cause being another type of damaged alpha-synuclein protein. 

One of those studies found that Active Dreams developed prior to PD over half the time. Of this RBD first, then PD group, half also showed signs of Mild Cognitive Impairment (MCI) prior to their PD diagnosis. All of this RBD/MCI first, then PD group, all went on to develop dementia before the four year study ended. None of those with Active Dreams but no MCI at Parkinson’s diagnosis developed dementia before the end of the four years.

Thus, anyone who experienced Active Dreams prior to their PD diagnosis should be examined for MCI. If this is present, it is imperative for you to make plans for the future—while you still can. Dementia will likely follow soon. If MCI is not present, then dementia may wait many years to appear—if it ever does. However, be forewarned: you still need to plan ahead. People have been known to develop dementia 50 years after the onset of RBD. Therefore, this does not give you an “all clear.” It simply gives you hope of more years of dementia free living.

LBD: Parkinson's Dark Secret

Dr. Graham Lennox, of Cambridge’s Regent’s College, called dementia “the dark secret of Parkinson’s disease.” Nancy, a surviving LBD spouse, agrees. In 2006, Nancy’s husband, Del, was diagnosed with Parkinson’s with dementia (PDD). “We were shocked,” Nancy said. “We’d been dealing with his Parkinson’s for eight years—attending the support groups, listening to all those lectures—and yet, no one, not even Del’s doctor, had mentioned dementia until that day.” Nancy’s voice caught. “We thought we were coping, but this hit us hard. We weren't prepared.”

There were several reasons for Nancy and Del’s lack of information in 2006. Years later, these reasons still exist:

a)      PDD is a “new” disorder. Dementia was not even recognized as a Parkinson’s symptom until the early 1990s. Until then, it was considered to be two diseases: Parkinson’s and dementia, likely Alzheimer’s. In 1994, “Parkinson’s disease with dementia” was included in the DSM-IV, the basic diagnostic manual for mental disorders, and added to the insurance codes. It takes at least a couple of decades for awareness of a “new” disease to develop.

b)      PD doctors are movement, not dementia, specialists. Neurologists who specialize in treating Parkinson’s focus heavily on movement issues and are less likely to be trained to recognize early signs of PDD. Thus their patients’ dementia may go untreated until it is so severe that it can’t be ignored.

c)      Cross-sectional studies don’t tell the true story. Although dementia has finally become recognized as a symptom of PD, Parkinson’s websites often quote cross-sectional studies, which are a  single “snapshot” of a specified group of people—in this case, people with PD. These usually report a 10% to 30% rate of occurrence, numbers that make the possibility of impending dementia easy to ignore—or deny. Cumulative studies, which are of a group of people over time, show a different picture, with from 65% to 80% of Parkinson’s patients eventually developing dementia.

d)     Parkinson’s disease with dementia is often considered a symptom of late stage PD.  Although the possibility of PDD does increase with age, dementia can occur at any time, sometimes within months of a Parkinson’s diagnosis. Additionally, recent studies have found that mild cognitive impairment (MCI-LB), a major risk for eventual PDD, is often present in PD’s early stages—even at diagnosis.

 “Please spread the word,” Nancy begs. “Don’t leave other families in the dark as we were.” That’s our goal with this blog, our trainings, our book and our bookstore. You can help by telling others about these and about Parkinson’s and its connection to Lewy body dementia.

Mild Cognitive Impairment - Lewy Body (MCI-LB)

Until recently, a person had to be experiencing some sort of memory loss to be diagnosed with Mild Cognitive Impairment (MCI). However, in the last few years a new type of MCI has been identified—one that LBD families were quite familiar with. In MCI-LB, the basic definition remains the same: cognitive losses not severe enough to significantly interfere with functional ability or activities of daily living. However, the cognitive losses are “non-amnestic,” that is, they involve cognitive functions other than memory.

Dementia usually starts as mild cognitive impairment and increases very slowly. MCI-LB can occur by itself, or with other non-cognitive symptoms that also warn of eventual LBD.  Very little is known of how MCI precedes DLB, but much is being learned about how it occurs with PD. Here are some statistics:

• Mild cognitive impairment occurs in about 25% of newly diagnosed PD patient.
• The risk for dementia increases when MCI is present at or near PD diagnosis.
• The risk for dementia increases even more when other risk factors are also present at or near a PD diagnosis.

A person may have only one of the following symptoms (single domain) or several (multiple domain) or even all of them. However, to be defined as MCI, there must be some loss of executive function or memory. The John Hopkins Health Alerts listed these symptoms for non-amnestic MCI:

•    Executive function. These include difficulties with problem-solving, initiating and planning, multitasking, impulse control, following through and monitoring performance.

•    Memory. Memory retrieval may become difficult. This may include tasks learned long ago—playing the piano, using electrical equipment, driving or even brushing one’s teeth. Learning new information is still possible with adequate repetition.

•    Mental processing. Mental processes slow down the ability to process and respond to information. This has a domino effect that can impair other cognitive abilities, including problem-solving and memory retrieval.

•    Language. Finding the proper word to use becomes difficult (it’s on the tip of my tongue syndrome). 

•   Multitasking. Understanding and processing complex information becomes difficult. Being presented with more than one idea or choice at a time or needing to perform sequential tasks may become frustrating and stressful.

•    Attention. Maintaining focus or doing more than one thing at a time becomes difficult.

•    Visual-spatial abilities. Perceiving, processing and acting on visual information becomes difficult. This impairs driving, reaching or walking.

We are well aware that the most bothersome symptoms of MCI-LB are usually non-cognitive—things like hallucinations and even delusions. We plan to discuss them in a later blog.