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.


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.


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.


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.



I had the pleasure of being invited to observe a workshop by Teepa Snow (  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.


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

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.


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

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.


There are two types of risk factors that are associated with the development of dementing conditions as we age.  First, there are factors that we cannot control.  The strongest risk factor for becoming demented is not directly controllable, age.  If you live to be in your mid-80s or older, the risk is near 50%.  There are other associated risk factors that are correlated with cognitive decline with aging such as apolipoprotein gene carrier status (Apoe4 has the greatest risk whereas Apoe2 has the least), Mild Cognitive Impairment, cancer (there is an inverse association between cancer and cognitive decline), and sex (women are at greater risk than men).

Second, there are also factors over which you have at least some degree of control.  These include history of head injury (hence the desire to wear seatbelts and helmets), blood pressure at midlife and beyond, type II diabetes mellitus, stroke, exercise), smoking, drug and alcohol use. 

Many believe, despite no good empirical evidence that dietary supplements such as vitamins may be neuroprotective.   The latter is interesting as health problems are associated with either deficiency or excess concentrations, which is not a problem for most of us.  A case in point is Vitamin D,  there has been a recent surge in interest in vitamin D to promote brain health.  Two recent findings from the Atherosclerosis Risk in Communities Study suggest that it is premature to take vitamin D to promote brain health.

First, the cognition study was published in the European Journal of Neurology in May 2014 based on analysis of 1650 participants.  There was no association between lower levels of vitamin D and cognitive testing.  Second, the MRI study was published in JAMA Neurology in May 2014 involving 1622 participants.  Levels of vitamin D were not associated with white matter disease and did not prevent “subclinical” strokes.

It appears from past studies that there is an association of between low levels of vitamin D and hypertension, diabetes, heart attack, and stroke but this may just be a marker for poor health.  It’s too early to recommend supplementation with vitamin D for those with normal blood levels as a “neuroprotective” strategy.

The relative risk of hypertension and cognitive decline is complex.  An article in Neurology (2014, 82, 2187-2195) reports findings from the Age, Gene/Environment Susceptibility Reykjavik Study suggested that cognitive impairment in late life are dependent upon having a history of hypertension in midlife.  Those with normal blood pressure in midlife had increased risk of white matter lesions and cerebral microbleeds if they experienced hypertension in late life.  On the other hand, those with midlife hypertension had more brain atrophy and lower memory scores if they had lower late life diastolic blood pressure.

Finally, there is another recent study (Neurology, 2014) showing an inverse association between cancer and cognitive decline.   There is no clear explanation of possible mechanism behind such a correlation.

The relationships between medical/life style factors and cognitive decline appear to be quit complex.  The most proactive things we can do are to stay in shape, eat healthy, seek experiences, maintain health/wellness, and keep monitoring our short-term memory.



The “amyloid hypothesis” of Alzheimer’s disease postulates that Alzheimer’s is caused by the accumulation of a protein named beta-amyloid that produces the “gunky” deposits called plaques in the brain.  Despite the evidence that this is not the root cause (may be an effect of the brain changes in Alzheimer’s rather than a cause), the theory has become scientific orthodoxy, dogma and accepted on faith rather than evidence.  It has dominated research aimed at slowing or reversing Alzheimer’s disease leaving little funding for other approaches.

 But there is a kink in the armor.  There is accumulating evidence that treating amyloids is not the solution.  For example, six new drugs that decrease beta-amyloid reached phase II and III clinical trials in 2012.  Three of the studies were discontinued because concerns about safety or lack of efficacy.    Furthermore, we know that the brains of those who will develop Alzheimer’s disease is different from the brains of those who don’t.  However, it is also clear that having amyloid deposits does not guarantee that one will develop symptoms.  Even autopsy studies, heretofore the “definitive” proof, demonstrate that we can die with the pathology of Alzheimer’s disease but without clinically relevant symptoms.

To date the clinical trials of amyloid drugs have been conducted on those who already clearly have Alzheimer’s disease.  The assumption is that intervention is too late; the pathology has advanced too far to reverse or slow.  The next strategy in pursuit of the amyloid hypothesis is to intervene earlier, before the brain is so severely damaged.

Hence the ambitious attempt to recruit seniors who are willing to have their brains scanned for amyloids well before any memory symptoms and are willing to enter a clinical trial of an anti-amyloid drug, the Anti-Amyloid Treatment in Asymptomatic Alzheimer’s Study (“Study tests healthy seniors for silent signs of Alzheimer’s disease,” June 10, 2014, Naples Daily News).  The question is “can intervening early make a difference for those who do [develop Alzheimer’s disease]?  We won’t know the results for several years but this is the clearest test of the amyloid hypothesis to date. 

In the meantime, Alzheimer’s is a complex disease that has no simple neurobiology.  There is current research that focuses on biological processes other than amyloids.  For example, we need to pursue more rigorously the other major pathology, Tau proteins that form tangles in the brain of those with Alzheimer’s disease.  We need to pursue research into the hypothesis that Alzheimer’s disease is related to “Type III diabetes.”  We need to pursue the “mitochondria hypothesis” (Laura Spinney, “Genetic risk for Alzheimer’s Ignored for decades,” 2014, Scientific American). We need to broaden our gaze if we are to find better treatments than we have now.



Notwithstanding many technological advances, there is still no fool-proof method for diagnosing Alzheimer’s disease, (avoiding the fact that the brain changes occur decades before symptoms).  There is no blood test or imaging technique that is definitive.  Even autopsy diagnosis has its problems.  Diagnosis of Alzheimer’s disease remains a clinical diagnosis based on history, symptoms, patterns, and clinical judgment.

 The criteria for a diagnosis of possible Alzheimer’s disease:

  • The afflicted individual must be demented – disabled by the decline.
  • Symptoms appear gradually over months to years
  • There is progressive worsening of cognition
  • The initial and cardinal deficit is short-term memory (i.e., new learning)
  • Less commonly language deficits (e.g., word-finding) appear early
  • There are deficits in other skills such as planning, reasoning, judgment, sequencing

The diagnosis of possible Alzheimer’s disease:

  • There is sudden onset of symptoms
  • Progression is not gradual
  • There is concomitant cerebrovascular disease
  • Clinical features of Lewy body disease
  • There are other medical (e.g., thyroid disease, cancer) or neurologic diseases (e.g., head injury, stroke) present that may impair mental functions
  • There are medications or drugs present that may impair cognition

Mild Cognitive Impairment is diagnosed when:

  • Cognitive decline noted by self or informant or clinician
  • Objective evidence of cognitive decline – most typically in short-term memory
  •  Independence is not compromised


  • CT or MRI based images are prudent to rule out pathology such as cerebrovascular disease or tumors that would modify clinical management
  • Amyloid tests in isolation cannot reliably diagnose Alzheimer’s disease or Mild Cognitive Impairment
  • Measuring CSF and/or blood levels of amyloid or tau proteins are not clinically useful at this time.

Persons with rapid onset (onset within one year) cognitive decline should be referred to specialists who have experience and diagnostic capabilities to evaluate and manage these conditions.

Pharmacological treatment:

  • Cholinesterase inhibitors (CHIs) include Aricept (donepezil), Exelon (rivastigmine), and Razadyne (galantamine)
  • CHIs are recommended for treatment of Alzheimer’s disease or Alzheimer’s disease with a cerebrovascular component
  • CHIs are recommended for treatment of dementia associated with Parkinson’s or Lewy body disease
  • The findings for effectiveness of CHIs for treating vascular dementia is inconsistent
  • Evidence of effectiveness of CHIs indicate that they are comparable and selection should be made based on clinical criteria such as tolerability and ease of use
  • The combination of CHIs and Namenda (memantine), although rational and safe, lacks empirical support for increased efficacy
  • CHI use may increase risk of gastrointestinal bleeding, tachycardia, or heart block; worsen asthma or other pulmonary disease; cause urinary obstruction; increase risk of seizures, or prolong actions of muscle relaxants
  • There is no clear evidence for efficacy of CHIs in neuropsychiatric disease
  • Discontinuation of CHIs should be based on side effects, drug costs, or dementia progressing to end stage (stage 7).


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