Here are some of my favorite myths regarding the brain and how memory works.

  1. - Listening to Mozart or classical music improves intelligence.  This belief is based on  the “Mozart Effect” from a 1993 study suggesting that listening to Mozart may improve intelligence.  However, subsequent research demonstrated that the effect was restricted to spatial intelligence and is temporary.  The effect is not restricted to classical music and is probably has to do with improved mood and enjoyment.

  2. - The right brain is creative whereas the left brain is logical.  This long-standing belief stems from the fact that the brain has two hemispheres that have different functions.  The right  brain controls left sided motor/sensory function whereas the left brain controls right side motor/sensory function.  Furthermore, there is a long standing debate about localized versus distributed brain functions based on injuries (e.g., a left brain stroke produces language deficits) and the effects of “split brain” surgery that cuts the corpus collosum (the communication channel between the hemispheres).  Clearly the intact brain uses both hemispheres in a collaborative manner.  Creativity involves integrity of both hemispheres.

  3. - You only use 10% of your brain capacity.  This makes for interesting science fiction such as the movie Lucy but we use all parts of our brain even for simple tasks.  This belief probably is based on trying to motivate students to give more effort in school.

  4. - Adults do not make new brain cells.  This myth arises from many early studies and theories that we are fixed in abilities either in childhood or early adulthood.  The definitive study was completed in 1998 and demonstrated that adult’s brains are capable of “neural plasticity.”  You can teach an old dog new tricks.  As long as we retain awareness our brains are programed to elaborate circuits based on experience and practice.

  5. - Memories are accurate and we store all details of experience.  This myth arose from early neurosurgery findings that stimulating specific places in the brain produced what appeared to be recollections of specific events and facts as well as our attempts to use computers to model how the brain works.  Indeed,  the accuracy of these memories is very unreliable when facts were checked.  For most of us memory is full of errors, gaps, approximations, and susceptible to suggestion.  There are very few who have “photographic memory.”  Memory is a reconstructive process based on storing the “”gist” of events and filling in gaps.

  6. - Playing games, doing mentally challenging tasks, and mental exercise improves short-term memory.  Doing challenging or stimulating activities improves brain function due to increasing alertness or arousal and taking advantage of neuroplasticity also known as learning to learn.  We build knowledge, expertise, and skills by practice and repetition.   However, this is long-term memory and problem solving.  Short-term memory does not respond to practice but rather is like the “save” button on a computer.  Short-term memory relies on planning strategies to remember.  It takes effort and time.  We remember best what we spend the time to truly understand.  Short-term memory works by the One Minute Rule – anything given less than one minute of thought will fade from memory.

 

 

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The cholinesterase inhibitors like Aricept (i.e., donepezil) have been available for treatment of dementias such as Alzheimer’s disease since the mid 1990s. It is clear that long term use of these medications slows the progression of Alzheimer’s disease (in those who tolerate them) and that discontinuing the medication after extended use produces a more rapid decline even in those so impaired that they are in skilled nursing facilities. Despite these findings, the cholinesterase inhibitors are often maligned, not used, or discontinued too soon because they do not produce dramatic effects and do not stop or reverse decline.

One way to determine the efficacy of these medications is to determine if treatment reduces the burden that caregivers express (“Effects on caregiver burden of donepezil hydrochloride dosage increase to 10 mg in patients with Alzheimer’s disease,” Nakamura et al. Patient Preference and Adherence, 2014, 8, 1223-1228, PMID: 25258516). Normally, Aricept is initially given at a dose of 5 mg and increased to 10 mg after about 4 weeks. This study followed 27 Japanese patients (who tolerated treatment) (average age = 86.5) with moderate to severe Alzheimer’s disease. Participants were assessed before and after being switched to 10 mg donepezil and observed for 16 weeks. Assessments were made of severity of disease (i.e., orientation, speech, bathing, toileting, and dressing), caregiver burden, and swallowing at week 4, 8 12, &16. All study participants were still cared for at home.

The increase in dose from 5 to 10 mg. had no statistically significant effect on severity of the disease. However, the higher dose significantly reduced self-report of caregiver strain. The increased dose also produced small improvements in dressing, bathing, and toileting. Finally, the higher dose of donepezil improved swallowing in those participants that had swallowing problems at the beginning of the study.

Of course, this was a small study that did not include a placebo treatment and was only carried out over the course of 6 weeks. However it makes clear that rather than relying on impressionistic feelings, we need simple objective rating scales other than just the Mini Mental State Exam to gather data to inform clinical decision-making. A small increase in dose of Aricept improved both caregiver distress and self-care/swallowing in patients. Although cholinesterase inhibitors do not have dramatic actions or cure dementia, they do have a positive effect for many who tolerate them.

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We often get so focused on Alzheimer’s disease that we neglect other causes of memory loss and cognitive dysfunction.  Stroke is the second most likely cause of cognitive dysfunction after Alzheimer’s disease in the elderly.  Furthermore, there is a complex interaction between cerebrovascular health and Alzheimer’s disease.

 Post-stroke cognitive impairment may affect several domains of cognitive abilities such as attention (tracking the moment), memory (recalling new information and/or details of personal history), language (expressive and/or receptive speech), orientation (for time, place, and/or person), and executive functions (planning. judgment, reasoning, and/or social graces).  The effects of stroke may be temporary (e.g., TIA) or persisting depending on the size of the lesion and timing of treatment.  The effects may be severe (e.g., cause dementia) or mild (e.g., cause mild cognitive impairment) and may affect single skills or multiple skills.

There are three basic types of stroke.  Ischemic stroke caused by blood clots (i.e., embolic) or by fat deposits (i.e., thrombotic).  Stroke may also be caused by ruptured blood vessels (i.e., hemorrhagic).  This distinction is critical in that treatment for the former is via blood thinners whereas the later are made worse by blood thinners.  TIAs are “transient” or temporary events that may resolve within minutes to hours.  Strokes may be single events or recurrent and cumulative.  Stroke is evaluated and diagnosed by means of symptoms and signs such as one-sided weakness along with a physical exam, blood work, and imaging such as MRI.

There are a number of risk factors for stroke that are fixed and cannot be modified such as age, genetics, ethnicity, and sex. However, there are also a number of factors that are modifiable or manageable to reduce risk.  These factors include cerebrovascular disease (e.g., hypertension), heart disease (e.g., infarcts, atrial fibrillation), diabetes mellitus, hyperlipidemia, cigarette smoking, and alcohol abuse.

Not all stokes cause severe enough damage to produce dementia.  Some cause minor damage.  Vascular dementia is a permanent and irreversible condition where stroke causes disability as a result of impaired cognition that interferes with long-term independence.  The exact clinical manifestation depends upon the size, location, and type of damage caused by the stroke.  Early impairment is more typically manifested as alterations of attention and executive functions rather than memory.  There are often greater deficits proximal in time to the stroke with recovery over the course of months if there is no new event.

Stroke is very pervasive and may either be the source of cognitive decline or contribute added disability to conditions like Alzheimer’s disease, head injury, Parkinson’s disease, or Lewy body disease.  Signs of stroke include sudden weakness or numbness of face, arm or leg especially on one side of the body; sudden confusion, trouble talking, or understanding; sudden trouble seeing; or sudden trouble walking, dizziness, or sudden loss of balance.  Women sometimes have unique symptoms stoke not found in men such as sudden onset of face and limb pain, hiccups, nausea, general weakness, chest pain, shortness of breath, or palpitations.  If you have any of these sudden symptoms or signs, call 911 and act quickly as early diagnosis and treatment are essential for better outcome.

 

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Benzodiazepines are widely used to treat anxiety and/or insomnia. They include medications like Valium (diazepam), Xanax (alprazolam), Ativan (lorazepam), and Klonopin (clonazepam) that are used for anxiety and Restoril (temazepam) and Halcion (triazolam) that are used to help induce sleep.

Benzodiazepines may also be separated into those that are long acting (e.g., Valium and Klonopin) and those that are short acting (e.g., Xanax and Halcion). Long acting medications tend to remain in the body for extended periods of time (e.g., days) whereas short acting medications remain in the body for hours – hence you need to take the medication more than once a day to maintain effects.

Benzodiazepines are probably most effectively used as short-term management of anxiety and insomnia. As with any medication, there are trade offs that must be considered by both prescribers and consumers. First, there are withdrawal effects such as rebound anxiety after chronic use that makes discontinuation a problem. Second, these medications may have a deleterious effect on memory, cognition, and balance. Finally, the long-term efficacy of these medications is unproven for insomnia and questioned for anxiety.

The results of a recent study suggest a correlation between use of benzodiazepines and Alzheimer’s disease (Benzodiazepines may be linked to Alzheimer’s disease, Z. Kimietowicz, 2014, British Medical Journal, 349, g5555, PMID: 25208536). The findings were based on a retrospective population study of about 39,000 insured residents of Quebec over 66 years of age based on claims between 2000-2009.

Any use of benzodiazepines was associated with a greater risk of Alzheimer’s disease. Long-term use of benzodiazepines was more common in those with a diagnosis Alzheimer’s disease (32.9%) than for those without this diagnosis (21.8%) regardless of whether the medication was short or long acting. The association was stronger for long acting medications – possibly because of cumulative actions. The risk appeared to be associated with use for greater than three months. There was no association between Alzheimer’s disease and anxiety, depression, or insomnia.

Of course these findings do not suggest that benzodiazepine use causes Alzheimer’s disease. Unlike chronic use of drugs like alcohol or cocaine, there is no pathophysiologic mechanism for these medications to cause a decline in memory or degeneration of the brain. Instead these findings remind us that benzodiazepines are still commonly used to try to manage difficult behaviors in demented elderly despite warnings of adverse effects with chronic use and no clear demonstration of efficacy.

Benzodiazepines are best utilized as targeted medications for short-term management of anxiety. They may be effective for getting through a particularly bad day or a stressful event like going to the dentist or flying. They are not long-tem solutions for behavioral disturbances.

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Alzheimer’s disease was first described as a case study of Auguste Deter, 51 year old, in a paper by Dr. Alois Alzheimer in 1907. He visually inspected her brain after her death and described “tangled bundles of fibrils” in her cortex that we now identify as plaques and tangles. Despite having over 100 years of study, we still have more questions than answers regarding etiology and biological processes underlying this progressive neurological disease (“Alzheimer’s disease: still a perplexing problem, Krishma Chinthapelli, British Medical Journal, 2014, 349, Q4433, PMID: 25005430).

Prime Minister David Cameron announced support for the world’s most extensive population study in saying “dementia now stands alongside cancer as one of the greatest enemies of humanity.” Despite launching a study with quadruple the funding of previous work, there are huge challenges to be overcome. For example he stated that we still don’t know how the brain becomes diseased and only 3 of 101 dementia drugs developed since 1998 have made it to market.

There are three major hypotheses directing most of the medical research. The most popular hypothesis is that Alzheimer’s disease is the result of dense accumulation of amyloids (a brain protein responsible for plaques). The major problem with this theory is that amyloids do not correlate well with atrophy (brain shrinkage) and are not always present in persons with the symptoms of Alzheimer’s disease.

The second hypothesis is technically named hyperphorylated tau (the brain protein responsible for tangles). Tangles correlate better with both neuronal loss and cognitive symptoms than amyloids. However, this is a much more difficult to measure with current technology and therefore less well studied.

Last is the acetylcholine hypothesis (a neurotransmitter believed by some to be necessary to form memories). Indeed, reduced levels of acetylcholine have been found in the brains of those with Alzheimer’s disease. This has lead to the development of medications like Aricept and Exelon that are modestly helpful in some but clearly do not cure or stop the progression of the disease.

One obstacle to advancement is the fact that not all with dementia have Alzheimer’s disease (the most prevalent diagnosis of dementia). Also, not everyone with Alzheimer’s pathology as currently defined becomes demented. Therefore, accurate diagnosis is difficult. Early identification of Alzheimer’s disease remains uncertain as up to 25% of those in a recent clinical trail were misdiagnosed. Even tissue analysis is not accurate. For example, more than 50% of those with probable Alzheimer’s disease also have brain infarcts and 25% or more of those with a heavy burden of amyloids have normal cognition. So it appears that the current definition used for diagnosis of Alzheimer’s disease is arbitrary.
Finally, plaques and tangles are common in the aged but do not correlate well with clinical symptoms. There are no biomarkers that reliably identify Alzheimer’s disease. And, imaging by means of PET and MRI has poor sensitivity and specificity.

We clearly have a long way to go. Dementia including Alzheimer’s disease is not a part of normal aging. My hope is that these enhanced initiatives do not myopically stay focused on amyloids. Maybe it is time to give up the concept of Alzheimer’s disease in favor of understanding better the concept of dementia and the multiple pathways leading to functional decline that is associated with aging for some.

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There are many stressors that confront us such as divorce, dementia, death, illnesses, caregiving, injury, retirement, addictions, and/or neurological disease.  Managing the emotions and behavioral changes required to move forward requires effort, persistence, emotional support, and saying the “right” things to yourself.  This is the foundation of resilience.

Self talk  (“psyching oneself up”) as psychotherapy and self-help was popularized by Albert Ellis as “rational emotive therapy” and is broadly discussed today as “cognitive behavioral therapy.”  The underlying assumption is that the dialogues you engage in with yourself are the foundation for behavioral change and managing difficult emotions.

Consider the statement “I can’t do it.”  Or sometimes others will try to help by pointing to someone who made the change you are seeking but you say to yourself “He/she can do it but that doesn’t apply to me.”  For example, “I can’t handle being a caregiver,”  “I can’t place my spouse/parent in a memory care unit,” or “I can’t change this destructive behavior that is interfering with my life.”  What this statement actually means is that managing stressful situations and behavioral change is hard.  Change usually involves creating discomfort and giving up some elements of security for a period of time needed to calm emotions and build new habits.   It may help to say to yourself that yes, this situation is difficult but that “I can make the change if I put the right structure in place and get through the discomfort.”

Another self-defeating statement we tell ourselves is that “I need my ______.”  Fill in the blank with car, coffee sugar, cigarettes, drink ….  We actually only need air, water, shelter, and food to survive.  It is also helpful to have love and connectedness.   There are many destructive behaviors and substances that we feel we need but can do without if we endure the period of discomfort in making a change.

Whether needing to make changes or managing a difficult situation the “I can’t do it” may mean that “I don’t know how” or “I don’t know where to start.”  As long as your memory holds, you can learn new things and build new habits and behaviors.  Today’s world is full of opportunity to learn.  We have access to massive information via computers.  There are many support groups.  There are courses to take.  There are many self-help books.  There are many talk therapists who can help support and direct you.

Don’t give in to setbacks, mistakes, fear, procrastination, feeling that something is “too” hard, being tired or the myriad of other excuses we use to defeat our own best interests.  Set realistic goals for making the changes you want.  Break the changes into “baby” steps that keep moving you toward your goal.  Reward your self along the way as you make progress.   Get support, don’t go it alone.

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When do you move a person with memory loss from their home to a greater level of care?  This is a very complicated and subjective decision. 

Let’s start by assuming the person is living at home with a family member and memory loss is still mild to moderate.  Furthermore, assume they have lived in the same house and neighborhood for at least 5-10 years.  All of their friends and routines are well established and over learned.  In short, there are few surprises and little need to learn much that is new.  Life runs mostly on long-term memory.  The best place to be is at home and in familiar locations with lock-step routines.  Minimum care is needed.   As the memory loss and confusion builds the decision will become more and more the role of the primary caregiver and family.

This is the time the family to evaluate possible future needs and resources, should memory decline and other skills deteriorate.  What are the options for outside care?  Either one can bring the care into the home or move to another location where care is available.   Which route one chooses depends on personal preference and financial resources. Home care has the advantage of being in a familiar environment and established routines.  There is nothing new to learn other than familiarity and comfort with new caregivers/companions.

Alternatively one can move to a community with multiple levels of care that may include independent living, assisted living, memory care, and skilled nursing.   These may be on one campus or separate locations.  The campus concept may be either “a la carte” or a continuing care retirement community CCRC).  The former has set prices, either to rent or own, for all different levels of care.  You pay and move as you need services.  It often helps to have long-term care insurance to afford advanced levels of care.  Of course this must be purchased before you need it as insurance companies screen for memory loss to qualify.

A CCRC offers admission and the promise of a more-or-less fixed price, either to own or rent, plus variable entry fees.  In effect, you are paying for long-term care insurance in a lump sum up front.  Of course, as with long-term care insurance, you must choose before there are noticeable changes in memory.

In short, choices depend upon taste, whether you want to be close to family, comfort, level of memory loss, and financial resources.  This is very complex decision making which is often made when you are stressed and with great resistance to the loss of independence.  There are a number of useful resources with persons quite knowledgeable and who will spend the time to help you understand the choices and trade-offs.  For example, you may wish to work with independent case managers, organizations such as the Alzheimer’s Support Network, your financial advisors, and/or an elder care attorney.

Of course it is always better to make these decisions proactively rather than reactive to crises.  This is where good memory assessment by a memory expert helps you better know what stage of memory loss you are dealing with. Thorough feedback from the assessment takes time and repeated assessments are required to monitor and track changes that may require implementation of plans.

 

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I had the pleasure of being invited to observe a workshop by Teepa Snow (http://www.TeepaSnow.com).  The event was hosted by the Alzheimer’s Support Network and, to my great pleasure, was attended by staff from diverse facilities and organizations that provide dementia care. 

Teepa is a very skillful and talented presenter/trainer.  Her focus was on doing.  She presented conceptual training in the form of role-plays of many challenges we face when trying to get into the world of someone who is demented.  Her teaching style focused on doing rather than saying.  She challenged but always coached participants into a success by offering specific prompts and modeling.  Caregiving is not an intellectual exercise but is a hands on, participatory activity.

Teepa’s message is clear.  You must provide person-centered care to be effective in caring for those with severe cognitive decline.  We often give lip service to the concept of person-centered care but the actual practice takes intention, time, and effort.

There are several points that she drove home to me.  I am only sorry that I must say rather than show you how her strategies work.

First, caregivers must often approach someone who is confused, fearful, or in distress.  Teepa shows how to approach a person with dementia to about 6 feet, smile greet, move slowly, and get to eye-to-eye level.  Despite the fact that many of us know this, we try to “save time” by direct, quick contact.

Second, words often get in the way.  We are so accustomed to telling and asking that we forget that in working with infants, toddlers and pets they do not process our words.  Rather we must use prompts, gestures, and demonstrations to show what we want done.  We talk as patter to relax and comfort.  It’s not the words but rather the tones, cadence, and calmness that we use words to convey safety and contact.  Finally, touch is an important component of caregiving.  It is so much more natural to do these acts with children or pets than adults.

Third, caregiving requires that you override your natural tendencies to react to the behavior emitted rather than work to understand and manage the communication with someone who is likely unable to express their needs in words.  We must resist talking louder or using a condescending tone to our voice.  We must avoid scolding.  We must not blame the victim for what they can no longer do or understand.  We need to realize that we are often the problem, not the person who is demented.

Finally, dementia care takes enormous energy, presence, and focus.  The skills of care are natural to some but many of us need to work hard to master them and practice often.  Caregiving takes time and cannot be approached as a task to get done.  Caregiving is a human interaction where we assist someone who is confused to feel safe, supported, and understood.  We must facilitate engagement in those who cannot initiate on their own.  We must be with them in the moment.

I am sure that I have not done justice to Teepa’s message.  However, I hope that she gains a much larger audience of those who care for demented adults when she is invited to Naples again.

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Stress is a pervasive condition that affects our mental and physical functioning.  The term covers both situations that we may call “stressful” such as being told we have cancer or Alzheimer’s disease, caregiving for someone with dementia, or having to give a speech or our reaction to the stressful event such as racing heart, dry mouth, or worry.  Stress can be “negative,” as in being sued, having a car accident, or getting divorced, or “positive,” as in taking a vacation, getting married, or winning the lottery. 

Stressors vary in terms of duration, intensity, novelty, and type.  The ranges of stressors includes threat of death, threat of bodily injury, illness, grief, divorce, grief, moving, night shift work, commuting, and noise.

The formal study of stress started with the seminal book The Stress of Life by Hans Selye that was published about 70 years ago.  He is credited as the first to describe the impact of mental events on body tissues.  There are two major biological systems that are engaged by stressors.  The sympatho-adreno-medullary axis that releases adrenaline and the Hypothalamic-Pituitary-Axis that releases CRF, ACTH, and cortisol.  These systems have a profound and pervasive effect on the body during engagement of the “flight-or-fight response.”

People vary greatly in their ability to handle stress.  Some are more resilient than others depending on such factors as cognitive abilities, physical makeup, mental health, social support, and proneness to substance abuse.    More contemporary research on stress addresses possible neurotoxic effects.  We may ask does stress does contribute to or cause dementia?   Greenberg, Tanev, Marin, and Pitman provide a recent review of this topic (Stress, PTSD, and dementia, Alzheimer’s and Dementia, 2014, 10, S155-S165 http://www.ncbi.nlm.nih.gov/pubmed/24924667).

Greenberg et al. reviewed 8 studies that focused on the correlation between life stress and cognitive impairment.  Two longitudinal studies focused on a cohort of Catholic  nuns – the longest being 5 years.  The results indicated that those high in neuroticism (assume higher stress) showed greater cognitive decline than those low in neuroticism.   There was no association with Alzheimer’s disease.  Another study measured the correlation between stressful life events and cognitive decline in participants with and without Mild Cognitive Impairment.  High stress in normals was not associated with cognitive decline but high stress was associated with faster decline in those with Mild Cognitive Impairment.

A longitudinal (35 years) Swedish study of women found  that those with the most stress had great white matter disease on MRIs as well as a higher rate of Alzheimer’s disease whereas a second Swedish study showed that high job strain with low social support was associated with higher rates of vascular dementia..  A Chinese longitudinal study (5 years) found an association between death of a spouse or financial crises but not death of an offspring, serious illness, accident, or law suit with cognitive impairment.  Finally, a British study found an association between perceived stress, low education and lowered MMSE scores.

In conclusion, it appears that stress does not cause dementia or more specifically Alzheimer’s disease.  Stress may contribute to cognitive impairment in some but dementia.  Even for those with Post Traumatic Stress Disorder (those experiencing profound stressors), most (90%) did not develop dementia.  It appears that chronic stress is neither necessary nor sufficient to cause dementia.

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There is increasing empirical evidence that a life style that includes at least moderate, consistent exercise improves cognitive and health outcomes as we age.   It seems logical that exercise would be helpful to improve outcomes of those with neurodegenerative diseases such as Parkinson’s disease where there is progressive loss of neuromuscular abilities.  Fortunately there is an encouraging review that serves as the basis for this article: “An evidence based exercise regimen for patients with mild to moderate Parkinson’s disease” (Brain Sciences, 2013, 3, 87-100 http://qxmd.com/r/24961308)

Parkinson’s disease is, by some accounts, the second most common neurodegenerative disorder and affects 4-5 million of those over 50.  The primary symptoms involve motor control: resting tremor, slow response initiation (called bradykinesia), muscular rigidity, and postural instability.  It is now clear that exercise improves physical function, self-reported quality of life, strength, and gait speed as well as prolongs life in Parkinson’s disease.

Prospective studies have demonstrated neuroprotective effects of exercise in Parkinson’s disease.  Moderate to strenuous but not light exercise reduces the incidence of Parkinson’s disease in population studies.  The exercises that were beneficial included swimming, running, tennis, basketball, and cycling.   It appears that exercising patterns of those between 35-39 are especially helpful in the long run.

Three general types of exercises should be included: cardiovascular/aerobic training, balance training, and strength training.  Increasing amounts/intensity of cardiovascular exercise produces better results.  High intensity treadmill or cycling improved gait, balance, and quality of life more than conventional therapy in mild to moderate Parkinson’s disease.  Intense cardiovascular exercise also improved brain plasticity, language, and cognitive functioning in Parkinson’s disease.

Balance training is also an essential component of exercise in Parkinson’s disease.  Dopamine replacement medications are insufficient to control postural instability and balance.  Balance and strength training improve gait, ambulation, and equilibrium.  Motor controlled video games may also be helpful.  Finally, there is clear evidence that Tai Chi is more effective in preventing falls than conventional physical therapy for balance in mild to moderate Parkinson’s disease.

The third component of exercise is strength training.   Parkinson’s disease not only induces motor dysfunction but also affects strength.  Indeed, the benefits of resistance  training include improved strength, endurance, and response initiation.  It is also clear that there are greater gains from three sets of each exercise when compared to only one set.

In summary, the prescription for exercise in mild to moderate Parkinson’s disease should include:

  1. Cardiovascular exercise such as treadmill, cycling, running, tennis at high intensity for up to 30 minutes three times per week.
  2. Strength training with 3 sets of each exercise with high load 2-3 times per week.
  3. Balance training such as Tai Chi for an hour 1-2 times each week.

 

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