Deena J. Tampi, MSN, MBA-HCA

Behavioral health care providers are needed now more than ever to help support frontline caregivers and to provide access to care. Deena Tampi, MSN, MBA-HCA, offers insights about caring for the caregiver as well as providing access to care.

, Richmond, VA, where she uses her evidence-based expertise to ensure accountable care in behavioral health, ethics, and 

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 neurodegenerative disorder in the US after Alzheimer disease (AD).

 It is estimated that in the US alone approximately 630,000 individuals have a diagnosis of PD. The prevalence of PD increases with age and it is estimated that the prevalence will double by 2040.

 The disorder is significantly more common among individuals aged 80 years or older compared with those aged 40 to 49 years (1903 per 100,000 population versus 41 per 100,000 population, respectively). The overall cost of caring for individuals with PD is approximately $52 billion per year.

Although not one of the cardinal features of PD, psychotic symptoms are seen in approximately 25% to 30% of individuals with PD.

 The risk factors for the development of psychotic symptoms in PD (ie, PD psychosis) include older age, greater severity of illness, longer duration of illness, the axial rigidity subtype of PD, idiopathic PD, underlying dementia, delirium or depression, the presence of sleep disturbance including REM behavior disorder, reduced vision, and the use of dopaminergic agents (

 PD psychosis is also associated with worsening quality of life, greater caregiver distress, higher rates of institutionalization, increased mortality, and greater health care costs.

Among individuals with PD, visual hallucinations are the most prevalent psychotic symptom (

 Visual hallucinations are seen in approximately one-quarter to one-third of individuals with PD, with a lifetime prevalence of about 50%.

 Auditory hallucinations occur in approximately 20% of individuals with PD. Certain minor phenomena such as the “sense of presence” and visual illusions can be seen among 17% to 72% of individuals with PD and these may progress to visual hallucinations as the illness progresses. Delusions are not very common with a prevalence of approximately 5%.

National Institute of Neurological Disorders and Stroke

 (NIMH) has proposed the following for the diagnosis of PD psychosis:

â¼ The presence of one or more of the following symptoms: illusions, false sense of presence, hallucinations, or delusion;

â¼ The UK brain bank criteria for the diagnosis of PD is met;

â¼ The symptoms occurred after the diagnosis of PD;

â¼ The symptoms are recurrent or continuous for 1 month;

â¼ The symptoms are not better accounted for by another cause of Parkinsonism (eg, dementia with Lewy bodies; psychiatric disorders such as schizophrenia, schizoaffective disorder; delusional disorder or mood disorder with psychotic features; a general medical condition including delirium);

â¼ PD psychosis could be associated with or without insight, with or without dementia, and with or without treatment for PD.

The exact pathophysiology of PD psychosis is unclear, but findings indicate that the cholecystokinin gene (CCK)-45C-T polymorphism is most often associated with PD psychosis.

 Moreover, alterations in the visual processing areas in the brain along with pathologies in the hippocampus and cholinergic brain structures are seen among individuals with PD psychosis. Frontal cognitive dysfunction, impaired visual processing, sleep-wake cycle dysregulation and brainstem dysfunction all contribute to the development of PD psychosis.

When assessing patients, a thorough history assists in identifying risk and precipitating factors for PD psychosis.

 Precipitating factors include medical conditions such as dehydration, infections, metabolic dysfunction; psychosocial factors include poor sleep and limited nutrition; psychological factors include stress and hospital admissions as well as the use of drugs like amantadine, anticholinergic drugs, dopaminergic drugs, and beta-blockers.

The Movement Disorder Society Task Force that evaluated the rating scales for assessing PD psychosis 

that none of the currently available scales adequately captured its entire phenomenology.

 They recommend that the following be used as primary scales in clinical trials evaluating new treatments for patients with PD psychosis: the Neuropsychiatric Inventory (NPI) for the cognitively impaired population or when a caregiver is required; Schedule for Assessment of Positive Symptoms (SAPS), Positive and Negative Syndrome Scale (PANSS) or the Brief Psychiatric Rating Scale (BPRS) for the cognitively intact population or when the patient is the sole informant. The Clinical Global Impression Scale (CGIS) was suggested as a secondary outcome scale to measure change and response to treatment over time (See 

The first step in the management of PD psychosis is to assess the severity of symptoms. For mild symptoms that are not bothersome, there is no need for specific intervention other than providing reassurance and close monitoring to evaluate the progression of symptoms. The next step is to identify and treat for secondary causes of PD psychosis including medical disorders.

Medications that are used to treat the motor symptoms of PD may cause or worsen psychosis.

 A reduction or discontinuation of anticholinergics, monoamine oxidase inhibitors, levo- dopa, or dopamine agonists may result in the improvement of symptoms.

 If discontinuation of these agents is ineffective, psychotropic medications, may be indicated.

A systematic review of placebo-controlled trials by Wilby and colleagues

 demonstrated benefit for clozapine and pimavanserin for the treatment of PD psychosis. There were no definitive benefits noted for either quetiapine or olanzapine. The comparative studies showed improvements in PD psychosis symptoms when clozapine or comparator drug were assessed alone, but the data did not suggest any superiority of one active drug over the other drugs.

Pimavanserin, a novel 5-HT2A inverse agonist is the first FDA-approved antipsychotic for the treatment of hallucinations and delusions associated with PD psychosis.

 Pimavanserin improves symptoms of PD psychosis when compared with placebo (P = .0014). The adverse effect profile of pimavanserin include urinary tract infections, falls, peripheral edema, hallucinations, confusion, nausea, and headaches. Electroconvulsive therapy (ECT) has also been found to be beneficial for refractory symptoms.

Psychotic symptoms are not uncommon among patients with PD, and psychosis is associated with worse outcomes. Risk factors for PD psychosis include advancing age, more severe disease stage, cognitive impairments, depression, and sleep disorders.

The pathogenesis of PD psychosis involves neuropathological, neurochemical, and genetic changes. Management of PD psychosis involves treatment of underlying medical disorders and discontinuing drugs that may precipitate or worsen symptoms. Findings also indicate efficacy for clozapine and pimavanserin for the treatment of symptoms of PD psychosis. Pimavanserin remains the only FDA-approved medication for the treatment of PD psychosis. ECT may be beneficial for refractory PD psychosis symptoms.

 is Chairman, Department of Psychiatry & Behavioral Sciences, Cleveland Clinic Akron General, Akron, OH, and Chief, Section of Geriatric Psychiatry, and Professor of Medicine, Cleveland Clinic Lerner College of Medicine, Case Western Reserve University, Cleveland, OH; 

 is Executive Vice President, Diamond Healthcare, Richmond, VA. The authors report no conflicts of interest concerning the subject matter of this article.

1. Kowal SL, Dall TM, Chakrabarti R, et al. The current and projected economic burden of Parkinson disease in the United States. 

2. Pringsheim T, Jette N, Frolkis A, et al. The prevalence of Parkinson’s disease: a systematic review and meta-analysis. 

3. Parkinson’s Foundation. Understanding Parkinsons: 

4. Ffytche DH, Creese B, Politis M, et al. The psychosis spectrum in Parkinson disease. 

5. Mack J, Rabins P, Anderson K, et al. Prevalence of psychotic symptoms in a community-based Parkinson disease sample. 

6. Friedman JH. Parkinson disease psychosis: update. 

7. Ojo OO, Fernandez HH. Current understanding of psychosis in Parkinson disease. 

8. Chang A, Fox SH. Psychosis in Parkinson disease: epidemiology, pathophysiology, and management. 

9. Fredericks D, Norton JC, Atchison C, et al. Parkinson disease and Parkinson disease psychosis: a perspective on the challenges, treatments, and economic burden. 

10. Lenka A, Herath P, Christopher R, et al. Psychosis in Parkinson disease: from the soft signs to the hard science. 

11. FÃ©nelon G, Alves G. Epidemiology of psychosis in Parkinson disease. 

12. Ravina B, Marder K, Fernandez HH, et al for the NIMH work group. Diagnostic criteria for psychosis in Parkinson disease: report of an NINDS. 

13. Gallagher DA, Parkkinen L, O’Sullivan SS, et al. Testing an aetiological model of visual hallucinations in Parkinson disease. 

14. Levin J, Hasan A, HÃ¶glinger GU. Psychosis in Parkinson’s disease: identification, prevention and treatment.

15. Fernandez HH, Aarsland D, FÃ©nelon G, et al. Scales to assess psychosis in Parkinson disease: critique and recommendations. 

16. Cooney JW, Stacy M. Neuropsychiatric issues in Parkinson disease. Curr Neurol Neurosci Rep. 2016;16:49.
	17. Patel T, Chang F, for the Parkinson Society Canada. Parkinson disease guidelines for pharmacists. 

18. Wilby KJ, Johnson EG, Johnson HE, Ensom MHH. Evidence-based review of pharmacotherapy used for Parkinson disease psychosis. 

19. Bozymski KM, Lowe DK, Pasternak KM, et al. Pimavanserin: a novel antipsychotic for Parkinson disease psychosis. 

20. Ueda S, Koyama K, Okubo Y. Marked improvement of psychotic symptoms after electroconvulsive therapy in Parkinson disease. 

Parkinson disease psychosis is associated with worsening quality of life, greater caregiver distress, higher rates of institutionalization, increased mortality, and greater health care costs. The authors explore medical, psychosocial, and psychological factors associated with PD psychosis.

Parkinson Disease Psychosis

Alzheimer disease and other dementias are a major and increasing global health challenge. In 2010 there were 35.6 million individuals living with dementia and their numbers are expected to double every 20 years and reach approximately 115.4 million by 2050.

Behavioral and psychological symptoms of dementia (BPSD) is used to describe a group of diverse non-cognitive symptoms and behaviors that are frequently seen among individuals with dementia. BPSD affects approximately 90% of individuals at some point during the course of the illness, with greater prevalence noted among individuals receiving skilled care.

Common BPSD include apathy, anxiety, depression, agitation, psychosis, sleep disturbances, dysphoria, aberrant motor activity, hallucinations and delusions. There is emerging evidence that specific symptom patterns can be identified in different types of dementias. One recent study found that hallucination, abnormal motor behavior, and anxiety were significantly more frequent in Alzheimer disease (AD) and mixed dementia (MD) compared with vascular dementia (VD).

 Hallucinations and delusions were significantly more severe in AD and MD . Disinhibition was significantly more frequent and severe and agitation was significantly more severe in patients with VD.

BPSD is associated with faster cognitive decline, greater functional impairment, reduced quality of life for patients and their caregivers. BPSD is also a risk factor for earlier institutionalization among individuals with dementia. Moreover, BPSD adds to the overall cost of caring for individuals with dementia.

This spectrum of symptoms is thought to occur due to the complex interaction between biological, psychological, social, and environmental factors. These factors include structural, functional, and neurochemical changes in the brain, underlying medical or psychiatric disorders, preexisting personality traits, caregiver distress/depression, and misleading or lack of stimuli from the environment.

When an individual is being assessed for BPSD, it is vitally important to collect information from the caregivers of these individuals. Collateral information will provide insight into the type and duration of symptoms, aggravating and mitigating factors, prognostic factors, and a history of interventions that have been beneficial in managing BPSD. Underlying medical and psychiatric conditions should be evaluated and appropriately managed as these might be precipitating and/or worsening the BPSD. A thorough medication review will help eliminate the effect of medications, which may cause and/or aggravate the BPSD. This is also true of any illicit substances.

An assessment of BPSD includes the use of standardized and validated assessment scales such as the Neuropsychiatry Inventory (NPI) or the Behavioral Pathology in Alzheimer Disease Rating Scale (BEHAVE-AD). These standardized tools can assist in qualifying and quantifying the BPSD. They can also assist with tracking the progression of BPSD and the efficacy of interventions.

Both nonpharmacological and pharmacological management strategies have been found to be beneficial among individuals with BPSD. Among the nonpharmacological strategies, music therapy and behavioral management techniques appear to be effective for reducing the BPSD.

 These interventions have been shown to reduce the frequency and severity of the BPSD and also decrease caregiver burden with effect sizes similar to those of associated with pharmacotherapy.

To be successful nonpharmacological interventions need to be individualized and delivered in a caring way in a caring environment.

 Nonpharmacological interventions that targets both the patient and the provider improves the lives of both partners in the dyad.

Nonpharmacological management strategies are often used prior to or in conjunction with pharmacotherapy. This is done to minimize the exposure of individuals with BPSD to pharmacotherapeutic agents, given their significant adverse effect profile.

Although there are no FDA-approved medication classes to manage BPSD, many medications have been tested.

 Common medication classes that have been used in the management of BPSD include antidepressants, antipsychotics, anticonvulsants ,and cholinesterase inhibitors.

Findings from a meta-analysis indicates that only two medications had statistically significant higher response rates than placebo in the management of BPSD: dextromethorphan/quinidine [odds ratio (OR) = 3.04] and risperidone (OR =1.88) respectively.

 Dextromethorphan/quinidine and risperidone were also found to be superior to haloperidol and quetiapine. Haloperidol failed to demonstrate higher efficacy than placebo (OR = 0.86), and it was less efficacious compared with nearly all medications in the network. No individual SSRI was found to have significantly greater efficacy than placebo. There were non-significant differences in treatment acceptability for nearly all medications when compared with placebo, except for oxcarbazepine (OR = 3.73). Oxcarbazepine also had inferior acceptability when compared with donepezil and haloperidol.

Data from a second meta-analysis show that compared with placebo, aripiprazole, quetiapine, and risperidone were associated with improvements in symptoms on different standardized rating scales (

 However, the differences between the atypical antipsychotics were not significant for effectiveness, death, or cerebrovascular events. Compared with placebo, risperidone (OR = 3.85) and olanzapine (OR = 4.28) were associated with increased risk for cerebrovascular events.

A multidisciplinary team from Canada created an evidence-based algorithm for the management of BPSD.

 After a baseline assessment and the discontinuation of potentially exacerbating medications they recommend sequential trials using risperidone, aripiprazole or quetiapine, carbamazepine, citalopram, gabapentin, and prazosin, if pharmacotherapy is indicated.

A recent expert panel consensus recommended a step-wise approach to the management of BPSD.

 The panel recommendation is that management commence with the identification of underlying causes for BPSD. This should be followed by the implementation of nonpharmacological management strategies including caregiver training, environmental adaptations, person-centered care, and tailored activities. If pharmacologic interventions are required, the use of citalopram and analgesia should be given priority before other medication classes especially antipsychotics. For the management of psychosis, risperidone could be used after the evaluation and management of underlying causes for the psychosis.

In addition, emerging data indicate the efficacy of cannabinoid and electroconvulsive therapy (ECT) for the management of BPSD.

 Other treatments that are being studied include pimavanserin, lithium, gabapentin, mirtazapine, escitalopram, carbamazepine, and methylphenidate.

BPSD is associated with worse outcomes for patients with dementia. The management of patients is not standardized, but protocols generally involve the treatment of underlying symptoms followed by the use of nonpharmacological management techniques and evidence-based pharmacotherapy for refractory BPSD. When using antipsychotic medications, caution is advised given their significant adverse effect profile. Treatment outcomes among individuals with BPSD can be improved by using a risk to benefit analysis and step-wise approach to management.

1. Prince M, Bryce R, Albanese E, et al. The global prevalence of dementia: a systematic review and metaanalysis. 

2. Kales HC, Lyketsos CG, Miller EM, Ballard C. Management of behavioral and psychological symptoms in people with Alzheimer disease: an international Delphi consensus. 

3. Majer R, Simon V, Csiba L, et al. Behavioural and psychological symptoms in neurocognitive disorders: specific patterns in dementia subtypes. 

4. Abraha I, Rimland JM, Trotta FM, et al. Systematic review of systematic reviews of non-pharmacological interventions to treat behavioural disturbances in older patients with dementia. 

5. Brodaty H, Arasaratnam C. Meta-analysis of nonpharmacological interventions for neuropsychiatric symptoms of dementia. 

6. Caspar S, Davis ED, Douziech A, Scott DR. Nonpharmacological management of behavioral and psychological symptoms of dementia: what works, in what circumstances, and why? 

7. Wang F, Feng TY, Yang S, et al. Drug therapy for behavioral and psychological symptoms of dementia. 

8. Kongpakwattana K, Sawangjit R, Tawankanjanachot I, et al. Pharmacological treatments for alleviating agitation in dementia: a systematic review and network meta-analysis. 

9. Yunusa I, Alsumali A, Garba AE, et al. Assessment of reported comparative effectiveness and safety of atypical antipsychotics in the treatment of behavioral and psychological symptoms of dementia: a network meta-analysis. 

10. Davies SJ, Burhan AM, Kim D, et al. Sequential drug treatment algorithm for agitation and aggression in Alzheimer and mixed dementia. 

11. Kales HC, Lyketsos CG, Miller EM, Ballard C. Management of behavioral and psychological symptoms in people with Alzheimes disease: an international Delphi consensus. 

12. Tampi RR, Young JJ, Tampi DJ. Cannabinoids for the treatment of behavioral and psychological symptoms of dementia. 

13. Tampi RR, Tampi DJ, Young J, et al. The place for electroconvulsive therapy in the management of behavioral and psychological symptoms of dementia. 

14. Cummings J, Ritter A, Rothenberg K. Advances in management of neuropsychiatric syndromes in neurodegenerative diseases. 

15. Reus VI, Fochtmann LJ, Eyler AE, et al. The American Psychiatric Association practice guideline on the use of antipsychotics to treat agitation or psychosis in patients with dementia. 

BPSD is associated with worse outcomes for patients with dementia. Management is not standardized, but protocols generally involve the treatment of underlying symptoms followed by the use of nonpharmacological management techniques and evidence-based pharmacotherapy for refractory BPSD.

Managing Behavioral and Psychological Symptoms of Dementia

Edited by Helen Lavretsky,
Martha Sajatovic, and Charles Reynolds III;
New York: Oxford University Press; 2016
592 pages • $125 (hardcover)

Books on complementary and integrative therapies are rare, especially those that pertain to mental health and aging. Thus, it was a pleasant surprise to see this volume published by 

 earlier this year. This book has been thoughtfully edited by 3 of the foremost experts in the treatment of geriatric mental health disorders: Drs. 

, and Charles Reynolds III. Together they bring to bear years of research and clinical and scholarly acumen into editing a resource for anyone who is interested in learning more about the evidence behind complementary, alternative, and integrative medicine for late-life mental health disorders.

The book is divided into 4 parts. The first 3 parts provide an overview of the biology of aging, disorders associated with aging, and various 

 therapies that can promote well-being and reduce stress. These sections include chapters on nutrition, herbal remedies, hormone therapy, massage therapy, chiropractic care, Ayurveda, homeopathy, yoga, and other approaches. In addition, there is a well-written chapter on resilience building and its benefits for successful and positive aging. The last section deals with integrative interventions of cognitive aging and mental disorders in late life.

All the chapters are written by experts who have stellar credentials. The well-referenced chapters are succinct, and the 2-column format of the pages makes them easy to read. In addition, excellent tables and figures highlight the data. Overall, the information is up to date and very user friendly.

The hardcover edition looks and feels like a real textbook. For those who prefer an electronic version, the publisher has made one available.

The only criticism we have is that the book is priced at $125. We think that at this price, some readers who might otherwise have bought the book would hesitate to purchase it. However, if you can look beyond the price, this book is a wonderful asset to anyone who cares for older individuals with mental health issues. It has something for everyone, including the lay reader, the expert researcher, and the seasoned clinician. This book is going to join our personal library, and we plan to use the information in it for improving the care of older adults with psychiatric illness and for educating patients, families, trainees, and clinicians on complementary, alternative, and integrative medicine topics.

This article was originally posted on 6/13/16 and has since been updated.

Dr Tampi is Professor of Psychiatry at Case Western Reserve University School of Medicine and the Vice Chairman for Education and Faculty Development in the department of psychiatry at Metrohealth in Cleveland, Ohio. Ms Deena Tampi is the Executive Director of Behavioral Health Services at Saint Francis Hospital and Medical Center in Hartford, Connecticut. 

There is a paucity of information on complementary and integrative therapies, especially when they pertain to the topic of mental health and aging. But that's all changed.

Complementary and Integrative Therapies for Mental Health and Aging

Dementia is the leading cause of dependence and disability among older adults worldwide, with a total cost of US $604 billion- equivalent to almost 1% of the world’s gross domestic product.

 Currently, 35.6 million people worldwide have dementia, and it is estimated that the number of individuals with dementia in the world will double every 20 years to reach 115.4 million by 2050.

Although it is likely that the incidence of dementia will increase significantly worldwide in the coming years, a recent study that evaluated temporal trends from the Framingham Heart Study found that the incidence of dementia had declined over the past 4 decades (

The declining trend was more rapid for the incidence of vascular dementia than for that of Alzheimer disease (P = .004 vs P = .052), although the analyses of the dementia subtypes were based on smaller numbers than those for overall dementia. Note, however, that the risk reduction was seen only in persons who had at least a high school diploma.

When adjusted for vascular risk factors present at baseline or during midlife or for preexisting and incident stroke and other cardiovascular diseases, there was no significant difference in the results. The researchers also found that most indicators of cardiovascular health (excluding diabetes and obesity) had improved over the 4 spans of time studied. In addition, the investigators found a decrease in cardiovascular events and benefit for the use of antihypertensive medications on the risk of dementia during successive spans. This benefit was also more pronounced among individuals who had a high school diploma.

evaluated data from studies done in Western Europe (Sweden, the Netherlands, the UK, and Spain). The investigators found a 22% reduction (

 = .003) in the overall incidence of dementia in the UK study. In the study done in Spain, a 43% reduction was seen in dementia incidence in men (

 = .0002). The studies done in Sweden and the Netherlands indicated a non-significant reduction.

 found that the incidence of dementia in France had declined significantly in women (hazard ratio [HR], 0.62) when they compared data between 1988 and 1989 and between 1999 and 2000. Differences in education, vascular factors, and depression accounted only to some extent for this reduction (HR, 0.73).

In contrast to the data from these studies, a study from Sweden found that the incidence of dementia among people aged 85 years or older increased from 26.5% in 2000 to 2002 to 37.2% in 2005 to 2007 (

 evaluated data from 8 large population-based studies in Japan. They found that there was a higher incidence of all-cause dementia in 2008 compared with 1992 after controlling for age groups and sex. Similarly, a review by Chan and colleagues

 showed that the incidence of dementia in China in 1990 was 1.8% for 65- to 69-year-olds and 42.1% for 95- to 99-year-olds. By 2010 the incidence of dementia had increased to 2.6% for 65- to 69-year-olds and 60.5% for 95- to 99-year-olds.

One concern with a majority of epidemiological studies in dementia is that they often do not take into account the effects of prevention strategies, lifestyle factors, or risk modification strategies. Norton and colleagues

 estimated the population-attributable risk of Alzheimer disease worldwide for 7 risk factors: diabetes, depression, smoking, physical inactivity, midlife hypertension, midlife obesity, and low educational attainment. They found that the combined worldwide risk was approximately 30%. This suggests that a little under one-third of Alzheimer disease cases might be attributable to these potentially modifiable risk factors. It is postulated that a 10% to 25% reduction in these risk factors could prevent almost 3 million cases of Alzheimer disease worldwide.

 Lifestyle (ie, social, physical, and mental leisure activities) has been found to be protective against dementia.

Based on available evidence, it appears that the incidence of dementia is declining in the US and some countries of Western Europe. Improvements in the level of education and a reduction in vascular risk factors seem to be partly responsible for this decline. Education and lifestyle modification may also play a role in reducing the occurrence of dementia. Given these emerging trends, it is appropriate to be cautiously optimistic regarding a decline in the occurrence of dementia in certain parts of the world. However, with complex diseases such as dementia, only time will tell whether these positive trends are transient or the benefits obtained from improved educational status, risk factor modification, and lifestyle changes will be maintained.

Dr Tampi is Professor of Psychiatry at Case Western Reserve University School of Medicine and the Vice Chairman for Education and Faculty Development in the department of psychiatry at MetroHealth in Cleveland, OH. Ms Tampi is the Executive Director of Behavioral Health Services at Saint Francis Hospital and Medical Center in Hartford, CT. The authors report no conflicts of interest concerning the subject matter of this article.

 Sousa RM, Ferri CP, Acosta D, et al. Contribution of chronic diseases to disability in elderly people in countries with low and middle incomes: a 10/66 Dementia Research Group population-based survey. 

 Sousa RM, Ferri CP, Acosta D, et al. The contribution of chronic diseases to the prevalence of dependence among older people in Latin America, China and India: a 10/66 Dementia Research Group population-based survey. 

 Wimo A, JÃ¶nsson L, Bond J, et al. The worldwide economic impact of dementia 2010. 

 Prince M, Bryce R, Albanese E, et al. The global prevalence of dementia: a systematic review and metaanalysis. 

 Satizabal CL, Beiser AS, Chouraki V, et al. Incidence of dementia over three decades in the Framingham Heart Study. 

 Wu YT, Fratiglioni L, Matthews FE, et al. Dementia in western Europe: epidemiological evidence and implications for policy making. 

 Grasset L, Brayne C, Joly P, et al. Trends in dementia incidence: evolution over a 10-year period in France. 

. December 13, 2015; E-pub ahead of print.

 Mathillas J, LÃ¶vheim H, Gustafson Y. Increasing prevalence of dementia among very old people. 

 Dodge HH, Buracchio TJ, Fisher GG, et al. Trends in the prevalence of dementia in Japan. 

 Chan KY, Wang W, Wu JJ, et al. Epidemiology of Alzheimer disease and other forms of dementia in China, 1990-2010: a systematic review and analysis. 

 Norton S, Matthews FE, Barnes DE, et al. Potential for primary prevention of Alzheimer’s disease: an analysis of population-based data. 

 Barnes DE, Yaffe K. The projected effect of risk factor reduction on Alzheimer disease prevalence. 

 Di Marco LY, Marzo A, MuÃ±oz-Ruiz M, et al. Modifiable lifestyle factors in dementia: a systematic review of longitudinal observational cohort studies. 

The latest research on the global risk of Alzheimer disease and other dementias.

Is the Incidence of Dementia Declining?

Behavioral and psychological symptoms of dementia (BPSD) are a heterogeneous range of psychological reactions, psychiatric symptoms, and behaviors that are unsafe and disruptive and impair the care of the individual. About one-third of community-dwelling individuals with dementia exhibit BPSD.

 The prevalence increases to approximately 80% in individuals residing in nursing facilities.

 found that behavioral symptoms were observed in 72% of individuals more than 2 years before the actual diagnosis of dementia. The prevalence of BPSD increased to 81% 10 months after the formal diagnosis of dementia. Unlike cognition, which declines over time in individuals with dementia, BPSD tends to fluctuate; agitation is the most persistent symptom.

Apathy is the most common problem in individuals with dementia; it tends to occur early in the course of illness and remains stable through the course of the illness. Delusions commonly seen in individuals with dementia include false beliefs (eg, of theft, infidelity, misidentification syndromes). Individuals with dementia who have a family history of depression appear to be at greater risk for a major depressive episode than those without a family history. Disinhibition occurs in approximately one-third of the patients. In patients with hallucination, the most common form is visual hallucination. Irritability and mood lability become more prevalent with the progression of dementia.

Findings indicate that BPSD occurs because of the complex interactions between anatomical, functional, and biochemical changes that occur in the brain. Certain genes can predispose individuals to BPSD, and premorbid personality may contribute to the emergence of certain types of behavioral symptoms. 

 details the various neurobiological changes that contribute to the development of BPSD.

BPSD is associated with greater overall burden of care for individuals with dementia.

 The emergence of BPSD often results in the referral of patients with dementia to a specialist’s care. Paranoia, aggression, and sleep-wake cycle disturbances are associated with greater caregiver burden, caregiver depression, and the risk of institutionalization. BPSD results in the worsening of activities of daily living, faster cognitive decline, and a poorer quality of life. It also adds to the overall direct and indirect cost of care for individuals with dementia after adjusting for the severity of cognitive impairment and other comorbidities.

Assessment includes collateral information from caregivers and/or family members. Collateral information aids in determining the onset, the course, and the differential diagnosis of BPSD. It also helps identify risk and prognostic factors. Environmental factors and psychosocial stressors may be triggers for the onset or the worsening of symptoms. Underlying medical conditions, including pain syndromes, urinary tract infection, and dehydration, can result in exacerbation of symptoms. An evaluation for and management of these disorders will reduce the frequency and severity of BPSD and may mitigate the use of psychotropic medications.

Assessment tools such as the Neuropsychiatric Inventory, the Behavioral Pathology in Alzheimer Disease rating scale, the Consortium to Establish a Registry for Alzheimer Disease Behavior Rating Scale for Dementia, Dementia Behavior Disturbance scale, and the Neurobehavioral Rating Scale can be used to aid diagnosis of BPSD.

 These instruments help identify behaviors and rate their severity. They can also assist in tracking progression and in monitoring treatment response. An algorithm for the assessment of BPSD is presented in 

 provides an algorithm for the treatment of BPSD. Nonpharmacological strategies should be the primary intervention for patients with BPSD. If the symptoms of BPSD are not well managed with nonpharmacological strategies, judicious pharmacotherapeutic trials can be tried. A decline in cognition can result in the emergence or worsening of BPSD. A trial of cholinesterase inhibitors and/or memantine may be initiated to delay cognitive decline.

. Findings from a systematic review suggest that caregiver and residential care staff education and possibly cognitive stimulation therapy are effective in the management of BPSD.

 However, specialized dementia units were not consistently beneficial; changing the environment visually and unlocking doors reduced wandering.

Nonpharmacological interventions provided by caregivers can reduce the frequency and severity of symptoms and can reduce caregiver burden, with effect sizes similar to those associated with pharmacotherapy.

 Successful interventions included approximately 9 to 12 individual sessions designed to meet the needs of the patient and his or her caregivers and were delivered in the patient’s home using multiple components over 3 to 6 months with periodic follow-up.

One meta-analysis showed statistically significant results for nonpharmacological interventions on at least one measure of BPSD.

 These interventions included staff training in behavioral management strategies, mental health consultation and treatment planning, exercise, recreational activities, and music therapy or other forms of sensory stimulation. However, there were methodological limitations that suggest a possible risk of bias. Moreover, for many of the interventions, substantial resources from outside services were needed along with considerable time commitments from the nursing staff for the implementation of these strategies.

. If possible, behaviors should be grouped into different clusters (eg, psychotic, mood). These clusters act as psychobehavioral metaphors of primary psychiatric disorders. If these behaviors are not well managed by individual medication trials, a judicious combination of medications can be tried (eg, an antidepressant with an antipsychotic).

Caution must be exercised when prescribing medications, given their adverse-effect profile and the vulnerability of the population being treated. Medication combinations, such as 2 antipsychotics or 3 or 4 different medication classes, should be avoided to minimize serious adverse events. The duration of effective medication trials should be about 3 to 4 months of clinical stability, followed by a trial of medication taper and discontinuation.

A meta-analysis by Ballard and colleagues

 demonstrated that compared with placebo, risperidone and olanzapine reduced aggression. Individuals treated with risperidone also had significant improvements in psychosis. A meta-analysis by Schneider and colleagues

 also found evidence for the efficacy of aripiprazole and risperidone in the management of BPSD.

In a randomized, double-blind, placebo-controlled trial, outpatients with Alzheimer disease and psychosis, aggression, or agitation were randomly assigned to olanzapine, quetiapine, risperidone, or placebo. There were no significant differences among the active agents regarding the time to discontinuation of treatment for any reason.

 The median time to discontinuation of treatment because of a lack of efficacy favored olanzapine and risperidone over quetiapine and placebo. The time to the discontinuation of treatment because of adverse events or intolerability favored placebo compared with the active agents.

Sertraline and citalopram were associated with a reduction in symptoms of agitation.

 No differences in behavioral symptoms were seen when trazodone was compared with haloperidol. Both SSRIs and trazodone appear to be well tolerated compared with placebo, typical antipsychotics, and atypical antipsychotics. SSRIs and trazodone showed some benefit in the management of BPSD and were well tolerated.

Low-dose sodium valproate is ineffective in treating agitation in individuals with dementia, and high-dose divalproex sodium is associated with an unacceptable rate of adverse effects.

 In a literature review, Konovalov and colleagues

 found one study that showed statistically significant benefit of carbamazepine compared with placebo in the treatment of BPSD. However, most studies demonstrated no significant differences. In a majority of the studies, adverse effects were more frequent with the active medication.

Cholinesterase inhibitors provided modest improvements in neuropsychiatric and functional outcomes, with no differences in efficacy among the different drugs in this class.

 A meta-analysis showed modest improvements in symptoms with memantine.

 Moreover, it is well tolerated-the only adverse effects are confusion and sedation.

There is insufficient evidence to justify the use of benzodiazepines for managing BPSD.

 There have been only 5 controlled trials, which were of short duration and with a limited number of subjects. The efficacy data were limited and the adverse-effect profile was not benign.

The data for using pharmacotherapeutic agents in the management of BPSD are limited. There are no robust data on the efficacy of these drugs, but there are data on the adverse-effect profiles. Although limited, the best evidence for efficacy was found for antipsychotics, especially risperidone, olanzapine, and aripiprazole, and for SSRI antidepressants, namely sertraline and citalopram (

Antipsychotic use in elderly persons with dementia

Individuals at high risk for adverse effects of antipsychotics are those who are 85 years or older and who have vascular or mixed dementias or active cerebrovascular or cardiovascular diseases and significant impairments in activities of daily living. However, if the symptoms of BPSD are not sufficiently managed by other strategies, the use of antipsychotics may be justified.

When prescribing antipsychotic medications, it is sensible to use the lowest effective dose and for the shortest time to manage the symptoms. Close monitoring for adverse effects and their swift management in case they do arise will minimize serious adverse events.

 completed a post hoc analysis of pooled results from randomized controlled trials of persons with dementia who were treated with risperidone and olanzapine. Their results indicate an increased incidence of cerebrovascular adverse events. Some of the increased incidence could be accounted for by nonspecific events other than stroke. There were a greater number of persons with vascular and mixed dementias in the risperidone trials than in the olanzapine trials. In contrast to this post hoc analysis, other results show no increased risk of stroke in older individuals treated with risperidone and olanzapine compared with individuals treated with typical antipsychotics or untreated individuals with dementia.

FDA findings indicate that the use of atypical antipsychotics in individuals with BPSD is associated with increased mortality.

 The majority of placebo-controlled trials of olanzapine, aripiprazole, risperidone, and quetiapine showed 1.6- to 1.7-fold increases in mortality. Deaths were due to heart-related events (heart failure or sudden death) or infections (mainly pneumonia). The FDA asked the manufacturers of these drugs to include a black box warning in their labeling describing this risk and noting that these drugs are not approved for BPSD. Similar changes to the labeling for typical antipsychotics have also been added.

A meta-analysis by Schneider and colleagues

 found that the risk of death was greater among individuals who were treated with atypical antipsychotics. The sensitivity analyses did not show any evidence for differential risks for individual drugs, severity of dementia, sample selection, or the diagnosis. Wang and colleagues

 found that conventional antipsychotic medications were associated with a significantly higher adjusted risk of death than were atypical antipsychotic medications.

The risk of cerebrovascular adverse events was 1.3 to 2 times higher with active treatment compared with placebo; the risk of death was about 1.2 to 1.6 times higher.

 The risk is similar for typical and atypical antipsychotic agents. A higher than median dose of a drug, older age, a diagnosis of vascular dementia, and comorbid atrial fibrillation have been noted as risk factors for cerebrovascular adverse events. Older age, male sex, severe dementia, and functional impairment are associated with higher risk of death.

Common in individuals with dementia, BPSD is associated with poorer outcomes and greater burden of care. Data show that BPSD is caused by underlying neuroanatomical and neurochemical changes in the brain and a premorbid personality structure. Pharmacotherapy should be combined with nonpharmacological approaches for optimum results. The risk of prescribing medications for patients with BPSD (who are often elderly) should be carefully weighed with possible benefits. These medications should only be prescribed within the recommended dosage to reduce the risk of serious adverse events. Close monitoring of risk factors will also help mitigate serious adverse events.

Dr Tampi is Associate Clinical Professor of Psychiatry at the Yale University School of Medicine in New Haven, Conn. Ms Tampi is Executive Director of Behavioral Health Services at St Francis Care in Hartford, Conn. The authors report no conflicts of interest concerning the subject matter of this article.

 Lyketsos CG, Steinberg M, Tschanz JT, et al. Mental and behavioral disturbances in dementia: findings from the Cache County Study on Memory in Aging. 

An in-depth look into the behavioral and psychological symptoms of dementia.

Author | Deena J. Tampi, MSN, MBA-HCA