November 2010  << Back  

  Can't open the PDF? Click here for help.

 

 REVIEW ARTICLE

Primary prevention in geriatric psychiatry

Subramoniam Madhusoodanan, MD

St. John’s Episcopal Hospital, Far Rockaway, NY, USA
SUNY Downstate Medical Center, Brooklyn, NY, USA

Fayaz A. Ibrahim, MD

SUNY Downstate Medical Center, Brooklyn, NY, USA

Arsalan Malik, MD

SUNY Downstate Medical Center, Brooklyn, NY, USA

BACKGROUND: It is estimated that the number of older adults with mental illness will increase from 4 million in 1970 to 15 million by 2030. The cost of untreated mental illness in the United States is estimated to be >$100 billion annually and nearly half of that cost can be attributed to persons age ≥60. In this paper we present a comprehensive review of empiric data available on primary prevention for the most common psychiatric illnesses in this patient population.

METHODS: We did an English language literature review of published studies and selected only those with the strongest emphasis on primary prevention for the most common psychiatric illnesses in older adults.

RESULTS: Modifiable and nonmodifiable risk factors and several primary prevention strategies have been described, several of them with positive outcomes mainly for depressive disorders and suicide. In conditions such as bipolar disorder, dementias, and geriatric schizophrenia, there is either a paucity of studies or no robust primary prevention strategies identified.

CONCLUSIONS: Modification of risk factors, a healthy lifestyle that includes a healthy diet, exercise, socialization, and education are important aspects of primary prevention in elderly patients. Genetic engineering and vaccine therapies may open new and exciting opportunities for prevention of many psychiatric illnesses in the near future.

KEYWORDS: primary, prevention, geriatric, psychiatry

ANNALS OF CLINICAL PSYCHIATRY 2010;22(4):249-261

  INTRODUCTION

There has been interest in the phenomenon of aging since ancient times. Hippocrates observed certain conditions that commonly are seen in later life. Aristotle explained “aging” as the process of dissipation of heat and fluid from the body. The word “geriatric” was coined in 1909 by Ignatz L. Nascher, an immigrant from Vienna to the United States.1 Geriatric psychiatry is the branch of geriatric medicine concerned with the mental health of aging adults.

Mental health researchers and clinicians have focused most of their efforts on the treatment of disease rather than its prevention. For instance, the main focus in management of depressive disorders has been treatment with anti-depressants, psychotherapy, or both. Research indicates that even with optimal treatment, the burden of depression can be reduced by only one-third.2 It seems obvious that we need to channel more resources into prevention.3

Nearly one-half of the cost of untreated mental illness in the United States can be attributed to persons age ≥60.4 The average annual growth of national health care spending between 2008 and 2018 is projected to be 6.2%, which is 2.1% faster than the average annual growth in the gross domestic product.5 As the United States and the world pull themselves out of a major economic recession, older adults have been one of the hardest hit groups. The problem is going to worsen because the number of older adults with mental illness will likely quadruple from 4 million in 1970 to 15 million in 2030.6 Moving our health care system towards “health care” and away from “sick care” is critical to solving our long-term health care challenges.

In this paper, we present a comprehensive review of the available empiric data on primary prevention of the most common psychiatric illnesses in older adults. We did an English language literature review of published studies and selected only those with the strongest emphasis on primary prevention. By definition, primary prevention deals with the reduction in the incidence of a disorder.

The quality of the published literature is not uniform across various geriatric psychiatric disorders so we have attempted to suggest directions for future research. In general, we have tried to follow the Institute of Medicine’s model for prevention (IOM Model), which classifies prevention into 3 main categories: universal, selective, and indicated prevention.7 All these categories fall under primary prevention. However, the division of preventive strategies into these 3 subgroups is not very precise and the reader will find that some of the strategies suggested under a particular category also can be extended to other categories. For example, bolstering psychological resilience to prevent major depressive disorder (MDD) can be applied as a universal prevention strategy to all adults age >65 and also as a selective prevention strategy for persons under stress or who have a negative thinking process. In the following sections, we have tried to classify preventive strategies into their most appropriate subcategory of the IOM Model. The conceptual framework of universal, selective, and indicated prevention are described in Preventive psychiatry: We are getting closer to fulfilling the promise of reducing mental illness.

Depression

Historically, depression has been considered part of the normal aging process and was overlooked. Adequate attention has not been paid to identification, quantification of severity, or appropriate management of depression in elderly patients.8,9 Because until recently researchers have focused on secondary prevention, there are little empiric data on primary prevention.10 Alexopoulos and colleagues point out that the temporal and causal relationship between depression and its correlates is imprecise and is likely to be bidirectional at this time.11 Others have suggested that the risk factors for depression also may be the consequences of depression.12

The prevalence of depression varies widely depending on several factors, including definitions used (DSM vs the International Classification of Diseases), diagnostic scales, resident status, and comorbid medical conditions. The prevalence rate among community-dwelling older adults is estimated to be 1% to 2% but reaches as high as 6% to 10% among nursing home residents and 12% among medical inpatients.13

Universal prevention. There is strong evidence to suggest that primary care physicians (PCPs) often miss depression in older adults.14 Schulberg and colleagues proposed a comprehensive conceptual model for educating PCPs that includes improving psychiatric knowledge, interviewing skills, decision-making strategies, and attitude. There is evidence that geriatricians fail to recognize approximately one-half of depression cases among hospitalized older patients.15 The authors of this study advocate including a psycho-geriatrician on the geriatric team to improve diagnostic expertise. Studies demonstrate that early intervention screening methods increase detection of depression but their impact is not yet clearly documented.16 The most commonly used depression screening test is the Geriatric Depression Scale (GDS), which is sensitive and specific, quick to administer, and highly acceptable to patients.17 It can be used effectively in both the hospital and primary care setting.

Religiosity and spirituality have been shown to protect mental health. Blazer comments that religion and spirituality are intertwined with culture because cultural forces augment, shape, and perpetuate depression.18 Religiosity has been shown to protect against depression19-21 and scientists have noted the usefulness of spirituality and spiritual endeavors.22 Mental health professionals need to bolster such protective beliefs in patients. We also need to reach out to ethnic minorities because these individuals often seek religious leaders rather than mental health professionals when dealing with mental illness.23

For centuries, exercise has been known to improve general well-being regardless of age, gender, or physical ability. Older adults who exercise regularly report improved mood and self-satisfaction.24,25 The biological basis for this includes alterations in monoamine functioning, effects that are mediated by the hypothalamic-pituitary-adrenal axis or ß-endorphins.25 Regular exercise may prove to be one of the most beneficial and simple strategies to alleviate mental illness in elderly patients.

There are many barriers to therapy and access to care for the elderly. Stigma is 1 important factor that hinders delivery of quality care. Combating stigma requires an approach that targets the individual, community, and societal structure.26 Public stigma could be changed by protest, education, and media outreach. Self stigma could be diminished by cognitive reframing, acceptance, and disclosure of one’s psychiatric history, which enhances a sense of empowerment.

Discriminatory insurance and reimbursement policies affect delivery of quality care. Studies suggest that physicians are less likely to recognize depression when they see patients with prepaid insurance plans, compared with fee-for-service patients.27 There is evidence that minorities and Medicaid recipients are less likely to receive a MDD diagnosis.28 Evidence suggests that higher co-payments for mental health services also can restrict access to care.29,30 The bill passed in the US Senate in 2008 guaranteeing equal co-payment for medical and mental health services is a welcome step.31,32 We need to increase clinician recruitment, as the projected number of professionals in geriatric mental health falls short of demand.6,33 Changes in social policy are needed to overcome these barriers to quality care.34

Selective prevention. Reynolds and colleagues have suggested a few preventive strategies including better management of insomnia, problem-solving therapy for patients with medical comorbidities and disability, and social rhythm stabilizing therapy for patients with recent bereavement.10 There is evidence that stabilization of social rhythms may prevent bereavement-related depression.35,36 Simple day-to-day activities, such as leisure and group activities and interaction with people, predict better health, happiness, and longevity.37,38

There is some evidence of the benefits of brief interventions for preventing mood disorders, such as patient education39,40 and cognitive-behavioral therapy (CBT) to reduce negative thinking.41 Cuijpers demonstrated that their “coping with depression course” can serve as a useful form of bibliotherapy.42 The course is cognitive-behavioral in nature and based on the social learning theory that suggests depressed individuals have behavioral problems with cognitive patterns that can be unlearned.43 They add that this course can have a further reach in the community than other interventions because of its non-stigmatizing nature and active recruitment.

Resilience and optimism have been associated with greater psychological well being.44,45 Southwick and colleagues point out that stress-induced mood disorders can be prevented by bolstering stress resilience with aerobic exercise, meditation, enhancement of psychosocial, religious, and spiritual supports, re-education of patients to use more positive emotions, and cognitive reappraisal of negative emotions.25 Researchers noted the effective use of problem-solving skills to deal with life strain.46 Others suggest that problem-solving therapy47 may bolster psychological resilience.48

Social isolation is a major risk factor for developing a mood disorder.49 Increasing social support decreases the risk of depression.50 It has been hypothesized that a rich social network helps by reducing high-risk behaviors, fostering effective coping strategies, counteracting feelings of loneliness, and increasing feelings of autonomy.25

Indicated prevention. Sleep disturbance is an important risk factor for MDD51 and poor sleep quality is directly associated with subsequent life dissatisfaction.52 A study based on precursor attributable risk concluded that sleep problems would identify approximately one-half the new cases of MDD occurring the following year.53 Sleep pattern normalization has been shown to protect against depression after bereavement.35 Data show that CBT may be an excellent tool to manage chronic insomnia in later life.54 However, more controlled studies are required to further investigate the impact of CBT in decreasing the rates of mood disorders and to determine whether CBT would affect the number of hours, quality of sleep, or both.

Substantial evidence links low levels of bioavailable testosterone to depressive symptoms in older men55 and testosterone supplementation for depressed hypogonadal men has been shown to have a positive effect. Screening for free testosterone concentration and supplementation have been recommended for older men with depression.56 However a recent study that reviewed data from several androgen treatment trials and androgen replacement did not find testosterone treatment or replacement to be more efficacious than placebo for MDD. The authors stated “the clinical impression is that in some subthreshold depressive syndromes, testosterone may lead to antidepressant benefits.”57TABLE 1 lists the modifiable risk factors, possible interventions, and nonmodifiable risk factors for depression in the elderly.

Future research. Eaton and colleagues make a distinction among precursors, prodromes, and risk factors of an illness. They argue that precursor signs and symptoms will have greater predictive power than risk factors because they have some of the defining characteristics of the illness. They note that knowledge of precursor prevalence and attributable risk combined with environmental and host risk factors may facilitate development of better preventive/screening strategies. They caution, however, that progression of the disorder from risk factor to precursor to prodrome may not be linear and smooth.53

There is a growing consensus that early-onset depression persisting to late life should be distinguished from new-onset geriatric depression. Evidence suggests that new-onset geriatric depression has distinct neuropathogenic mechanisms that are quite different from recurrent depression.58 Patients with new-onset geriatric depression often have high-level premorbid psychosocial functioning, no family history of depression, less severe psychopathology, limited response to treatment, and overall worse prognosis.59

Cerebrovascular and neurodegenerative diseases and age-related hormonal changes have been implicated as causes of depression.55,60-62 “Vascular depression” is used to describe depression associated with atheromatous and microvascular injury in the brain.63 Better control of risk factors for coronary artery disease may decrease the incidence of depressive disorders.

There is evidence that persons with 5-HT transporter gene promoter polymorphism have a higher risk of developing depression in response to life stressors.64 However, it remains to be seen if genetic engineering can modify these defects and help prevent depression.


TABLE 1

Risk factors for depression in the elderly (modifiable and nonmodifiable) and possible interventions

Modifiable risk factors Possible interventions Nonmodifiable risk factors
Physical illness and associated handicap and disability Problem-solving therapy7 Sex
Genetic vulnerabilities eg, 5-HT transporter gene promoter polymorphism
Social isolation and institutionalization Increasing social support, social networks,22,48 caregiver assistance, respite programs  
Iatrogenic drug misuse/substance abuse Close monitoring of prescription and over-the-counter drugs by primary physicians and other health care staff and family  
Being a caregiver Support groups/respite  
Bereavement and other major loss events Psychotherapy, social rhythm stabilizing therapy33-36  
Socioeconomic deprivation Improving socioeconomic status and access to medical coverage25,28,32  
Availability of firearms Better gun control laws72,73,76,77 and limiting access; education83,84  
Sleep disturbance Sleep pattern normalization,33,51 cognitive-behavioral therapy  
Stress Aerobic exercise, meditation,22,40-44,46 enhancement of psychosocial, religious and spiritual supports, reeducation, cognitive reappraisal of negative emotions, and problem-solving therapy  
Vascular factors Proper control of hypertension, diabetes, hyperlipidemia; healthy diet, regular exercise  
Testosterone deficiency? Testosterone replacement?  
Mania and bipolar disorder

There is conflicting evidence regarding the incidence of mania among elderly persons. The prevalence ranges from 0.1% to 0.4% in patients age >65.65,66 The Epidemiologic Catchment Area study estimated a prevalence of approximately 9% among all nursing home residents and did not find mania among 923 community-dwelling elderly subjects.67 The data regarding the prevalence of bipolar disorder among community-dwelling older adults are limited. Overall, the rates of mania are considerably lower than the rates of depression in the elderly.68

Cutoff age for geriatric status has been a problem with studies of mania in the elderly.69 There are various studies done with different age cutoffs; many of these studies were conducted before the distinction of unipolar vs bipolar depression was made.70 Furthermore, mania in older adults can be caused by different etiological factors. It could be late-onset bipolar disorder, a manic episode in a patient with a previous depressive disorder, or a patient with a history of bipolar disorder earlier in life.69 Therefore, elderly persons presenting with mania are a heterogeneous group with wide variability in age of illness onset.68 Affective disorders can change polarity in late life, ie, new-onset mania in an elderly patient may be caused by a change in polarity of past depression.

Geriatric mania frequently is secondary and is associated with lower rates of family history of affective disorders and higher rates of organic or neurologic disorder.69 Substantial empiric data show a strong association between organic brain pathology and mania in geriatric patients. A recent study found that 20% of cases of first episode mania in older persons had a temporal association with cerebral organic disorders.71 There are several systemic medical conditions and medications associated with mania.69,72

We have not found any significant studies that address prevention of mania in the geriatric population. Some published studies suggest that excess disruptive life events are associated with mania.73,74 There are few studies regarding geriatric mania.69,75 Future studies should address preventive strategies based on correlates associated with bipolar disorders.69,72 Age of onset of first manic illness should be addressed specifically because age affects bipolar disorder in multiple ways.75 Shulman et al stress the importance of having a consensus between neurologists and psychiatrists to develop a clear understanding of etiology, pathogenesis, outcome, and management of geriatric bipolar disorder.65

Suicide

Suicide in the elderly is on the rise76 and as of 1994, the suicide rate among persons age >65 was the highest for all age groups at 18.1 per 100,000.77 It is a major public heath problem that is compounded by the projected doubling of the geriatric population in the next 2 decades.78 Furthermore, there is strong evidence that the suicide rate increases with age.79 Despite the magnitude of the problem, there are little empiric data focusing on prevention of suicide in the geriatric population. The “Agist bias” that depression and suicidal ideation are part of the normal aging process limits research and outreach efforts.80

Universal prevention. Twenty percent of older adults who committed suicide saw their PCP within the past 24 hours, 41% within the past week, and 75% within the past month.81 Physicians clearly are not well trained at recognizing depression and suicide risk. According to one study, approximately 42% of PCPs did not evaluate patients for access to firearms when treating the geriatric at-risk population.82 Price et al83 noted that family practice residency programs do not provide adequate training in firearm risks; another study demonstrated that patients usually are receptive to firearm risk counseling by physicians.84 Because geriatric patients with suicidal ideation visit PCPs more often than mental health professionals,85 health care professionals in primary care settings should receive training and education in this area. Studies have demonstrated that educating PCPs can reduce suicide rates.86,87 Because there is evidence that elderly persons utilize mental health services much less often than younger patients,85 PCPs should reach out to older individuals and provide continuity of care. A recent systematic review in a heterogeneous population concluded that physician education in recognizing and treating depression and restricted access to lethal methods reduce suicide rates.88

It is still unclear if the benefits of firearm ownership outweigh the risks of potential harm.89 Ready firearm availability is associated with an increased risk of suicide at home.90 Older persons are more likely to use a gun to commit suicide than younger adults.91 One study reported that 72% of suicides among persons age >65 were by firearms.92 This calls for media and public outreach to educate the community regarding the dangers of firearms at home. Studies indicate that legal purchase of handguns increases the risk of violent deaths over a follow-up period of >5 years.89 There is evidence supporting the concept of “check stops” in the purchase of firearms to prevent suicide. The implementation of the Brady Handgun Violence Prevention Act,93 which mandates background checks and waiting periods for the purchase of handguns, will help. Studies have shown a significant reduction in suicide rates for persons age ≥55 in states that had implemented both waiting periods and background checks.94

Evidence has linked the shortage of mental health professionals with increased suicide rates.95,96 Nevada and Montana, for instance, have the highest suicide rates and lowest number of mental health professionals. The suicide rate in some rural areas is 800% higher than the national average. Approximately three-quarters of rural counties in the United States lack a psychiatrist. Because the geriatric population will double in the next 2 decades, we should be recruiting more trained geriatric mental health professionals.

Selective prevention. There is a subtle type of suicidal behavior seen among nursing home residents who do not have an immediate way to commit suicide. Different types of indirect life-threatening behaviors have been documented among residents of long-term care facilities.97 For example, refusing to eat can be a manifestation of depression and an indirect form of suicide.98 Researchers reported that sub-intentional suicidal ideation and life-threatening behaviors largely go unnoticed in a medical inpatient setting. They found that 44% of men and 22% of women among institutionalized geriatric inpatients exhibited self-injurious behavior (SIB) in a 1-week period.99 Researchers suggested the following interventions could reduce the likelihood of premature death from “indirect” suicide: a) encourage continuity of care, b) discourage relocations, c) foster interpersonal mutuality, and d) reinforce comfort-giving behaviors. Researchers coined “sub-intentional suicide” for indirect self-destructive behaviors such as refusal to eat.100 The Scale for Suicide Ideation could help physicians identify SIB.101

The “Gatekeeper Model” also may be of value in preventing suicide in this population. It calls for general workers in the neighborhood, including clergy, postal or grocery delivery personnel, and pharmacists, to look out for older people who may be isolated or seemingly not well and refer them for mental health services.102 However, we need more controlled studies to demonstrate the potential benefits of this approach.

The Tele-Help/Tele-Check services evaluated by De Leo and colleagues found significantly fewer suicides among clients over 11 years of service delivery; however, the benefits were noticed only among women.103,104 Tele-Check is a system through which trained staff members contact each client twice a week with a short informal interview and to provide emotional support. Studies indicate that telephone outreach programs reduce psychological distress and suicidal ideation, if not completed suicide.105

Some studies recommend greater involvement of family members in reducing suicide rates. Richman proposed psychotherapeutic approaches that underscore the family’s crucial role.106 Researchers suggest that PCPs should take time to educate family members as they can be very helpful in assisting the patient to seek help.107,108

Indicated prevention. Several factors have been linked with suicide but none are more important than comorbid depressive disorders. MDD is the single most important factor associated with both attempted109 and completed suicides.110 Studies show significant reduction in suicide with early recognition and treatment of depression.86 Two major randomized control studies, PROSPECT (Prevention of Suicide in Primary Care Elderly: Collaborative Trial) and IMPACT (Improving Mood-Promoting Access to Collaborative Treatment) used a multidisciplinary approach to manage and prevent depressive disorders and showed a significant decrease in suicidal ideation and suicide risk in older primary care patients.111-113 A National Institutes of Health (NIH) consensus panel also concluded that recognizing and treating MDD can significantly prevent suicide.114

The other important factors associated with suicide include older age, male sex, white race, unmarried status,115 mental illness and substance abuse,116 interpersonal stressors and alcohol use,117 somatization disorders,118 hopelessness,119 and multiple medical comorbidities.120 A few studies have demonstrated the benefits of strategies aimed at these risk factors.

In a psychological autopsy study, elderly suicide victims were more likely to have experienced serious relationship and financial stressors in the previous year.121 This study also reported that suicide rates would drop by 27% if adequate social support were provided. Similarly other studies reported the benefits of interventions that foster connectedness to support services.122,123 Having a greater number of confidantes also is reported to be protective.124

Studies in adult cancer patients show that adequate pain management reduces requests to die.125 Whether this applies to older persons needs to be investigated. TABLE 2 lists the modifiable risk factors, possible interventions, and nonmodifiable risk factors for suicide in the elderly.


TABLE 2

Modifiable and nonmodifiable risk factors for suicide in the elderly and possible interventions

Modifiable Intervention Nonmodifiable
Inadequate training of PCPs regarding risk assessment/firearm risks Training of PCPs72,73,76,77,83,84 and firearm risk counseling by PCPs, community education regarding firearm risk Male sex
White race
Older age
Shortage of mental health professionals Increasing recruitment85,86 of trained geriatric mental health professionals  
Indirect self-destructive behavior Encourage continuity of care, discourage relocation, Gatekeeper Model, Tele-Help/Tele-Check, greater family involvement90-96  
Comorbid depressive disorders Early recognition and treatment76,99-111  
Unmarried status, mental illness, substance abuse, interpersonal stressors, alcohol use, somatization disorders, hopelessness Social support groups,105-115 psychiatric follow-up services  
Multiple medical comorbidities Medical monitoring and psychotherapy  
PCPs: primary care physicians.
Dementia

Dementia is a major public health challenge affecting the elderly. The prevalence and incidence of dementia increase with age, affecting 15% to 20% of persons age >75 and 25% to 50% age >85126 and imposing great economic burden on the health care system127 with worldwide costs estimated at well over $300 billion. Around the world, approximately 24 million people have dementia, with the number projected to double every 20 years.128 Dementia often is diagnosed or treated in community health care settings.129 Even when evaluated, it may be worked up incompletely. It is challenging to diagnose and inter-rater discordance in dementia and Alzheimer’s disease (AD) diagnosis has been documented.130 A thorough understanding of the etiopathogenesis, including risk factors of dementia, is important in preventing the disease.

Risk factors. Several biologic, psychosocial, and environmental risk factors have been implicated in dementia. The most established of the cytogenetic risk factors is the apolipoprotein E (APOE e4) genotype associated with increased risk of both late-onset sporadic familial AD and vascular dementia,131 the 2 most common forms of dementia. Dutch studies have estimated that eliminating APOE e4 could result in a 20% reduction in dementia.132 Presenilin genes are known contributors for early-onset AD, but these are far less common.133 Less than 1% of AD cases are associated with Down’s syndrome and trisomy 21, both of which produce a triple copy of the amyloid precursor protein. Other genetic factors, including traditional vascular risk factors such as male sex, increased age, obesity, lack of exercise,134 hypertension (at least in midlife),135 stroke,136,137 type 2 diabetes mellitus (more controversial),138 and high body mass index (BMI), have been clearly linked to vascular dementia and probably AD,139,140 further supporting a multifactorial etiology. The most important of these factors may be stroke. The prevalence of dementia in ischemic stroke patients is significantly higher than controls.141,142 Neurofibrillary tangles are the central event in both familial and sporadic AD and cerebral ischemia-induced tau hyperphosphorylation may be the final common pathway in tangle formation.143 Additionally mounting evidence supports the notion that oxidative stress144 also is implicated in dementia.

Several epidemiologic studies also have reported an increased risk of dementia in individuals with head trauma.145 Traumatic brain injury is a risk factor for dementia, mania, psychosis, and depression. Lifelong efforts to reduce brain trauma seem to be important in reducing geriatric mental illness. Likewise cigarette smoking has been linked to dementia146 although exercise147 and education148 appear to protect cognitive functioning and perhaps reduce the incidence of dementia.149 Focusing on diet, high intakes of total fat, saturated fat, and total cholesterol increase the risk for dementia and high fish intake may be protective.150,151 Another study found that vegetable fat and omega-6 fatty acids decreased the risk of AD, whereas saturated or trans unsaturated fats increased it.152

Universal prevention. Although some of the possible risk factors identified above are not modifiable at this time, such as the presence of APOE e4 allele, a substantial number could be modified that might prevent or delay dementia onset. The possible targets for intervention extend from the prenatal period to old age. Factors during early life such as nutrition, education, and parental socioeconomic status can influence development of dementia in later life.153 From mid to late life, a physically, socially, and intellectually active lifestyle may reduce the risk of dementia.154,155 Moreover, in light of the literature already reviewed, modification of cardiovascular risk factors such as hypertension, smoking, BMI, diabetes, dietary fat intake, dietary antioxidants, folate-vitamin B12-homocysteine metabolism, and physical exercise during this period all potentially can reduce the risk of dementia. The SystEur trial recently demonstrated that treatment of systolic high blood pressure could decrease the risk of dementia by one-half.156 This effort will have to involve large-scale public health interventions including education, early detection, and prevention of vascular disease through screening and control of hypertension and diabetes and prevention of obesity. Incorporating health-promoting changes into the daily lives of independently living older adults through occupational therapy also shows promise.157 Several studies have reported an inverse association between nonsteroidal anti-inflammatory drugs and the risk of dementia.158 The most recent Cochrane Database review concluded that statin use does not reduce the risk of dementia159 but this should be a priority for future research.

There is also need for adequately powered, randomized controlled trials (RCTs) to assess the preventive effect of omega-3 polyunsaturated fatty acids (PUFA) in dementia. A review of the Cochrane Database also shows no convincing evidence relating to the type or intensity of diabetes treatment in prevention or management of cognitive impairment in diabetic patients. Future research on treatments for diabetes should include standardized assessments of cognitive function as outcome measures. Ginkgolides found in biloba extract inhibit hippocampal neuron dysfunction and neuronal cell death caused by amyloid beta-protein 42 (Aβ42).160 They decrease Aβ42-induced pathological behaviors, enhance neurogenesis in animal models of AD, and inhibit Aβ aggregation, providing considerable rationale for ginkgo biloba extracts as a potential treatment for AD. However, according to the largest and longest clinical trial of its kind, ginkgo biloba extract as it is generally used does not prevent dementia in individuals with or without cognitive impairment and is not effective for AD.161

Selective prevention. Genetic screening in those with a family history of AD may help identify individuals at greater risk. Immunotherapy can attenuate amyloid neuropathology and improve cognitive function in transgenic models of AD.162 However, the first clinical trial was halted when 6% of AD patients developed aseptic meningoencephalitis. Currently >10 clinical trials of different types of Aβ immunotherapy are underway in patients with AD. The aim is to identify safe approaches for the efficacious antibody-mediated removal of brain beta-amyloid or its neurotoxic oligomeric precursors consisting of aggregated amyloid beta-peptide (Abeta).163 Recently, a group in Japan developed nonviral DNA vaccines and used them to obtain a substantial Abeta reduction in AD model mice without any side effects.164 DNA vaccination for AD may open up new avenues in vaccine therapy for safe and effective treatment and prevention.165 Finally therapies directed at preventing the early stages of apoptosis occurring with ischemia/reperfusion may prevent neuropathologic events seen in AD.143

Indicated prevention. Indicated prevention should include early detection and treatment of mild cognitive impairment (MCI) and pre-MCI stages (subjective cognitive impairment) of AD using effective cognitive screening instruments, such as the GDS and Functional Assessment Staging Test (FAST),166 and neuroimaging167 to predict future decline. In patients prone to developing dementia due to amyloid plaques, the Aβ vaccine and monoclonal antibody injections may prevent further deterioration of the illness or produce disease arrest in early stages. More research is needed in this area. Cholinesterase inhibitors and memantine as they are currently used only produce symptomatic benefit. They produce initial improvement and then a decline at the same rate as before treatment, delaying the final stage of AD by 6 to 12 months. They may have a role in prevention in the early subsyndromal stages of cognitive impairment. Further research is needed in this direction. TABLE 3 lists the modifiable and nonmodifiable risk factors for dementia and possible interventions.


TABLE 3

Modifiable and nonmodifiable risk factors for dementia and possible interventions

Modifiable Possible interventions Nonmodifiable
Hypertension124-132
Stroke
Type II diabetes mellitus
Early diagnosis and proper monitoring of medical conditions Genetic factors124 eg, apolipoprotein E genotype
Male sex
Older age
Obesity
High fat intake140,141
Healthy diet  
Lack of exercise Exercise  
Cigarette smoking136 Smoking cessation programs  
Head trauma135 Fall prevention strategies, helmets and protective devices for at-risk people  
Geriatric psychosis

Approximately 23% of the geriatric population experience late-life psychotic symptoms.168 Although psychotic disorders usually develop in early adulthood, in some cases initial onset can be in later life. Nearly 10% of geriatric patients admitted to an acute inpatient psychogeriatric unit had late-life onset psychotic symptoms.169 Psychosis has multiple causes in the elderly,170 including dementia, delirium, substance abuse, medical causes, depression, mania, both early- and late-onset schizophrenia, and delusional disorder.166-168 Approximately 50% of patients with AD may experience psychotic symptoms within 3 years of clinical diagnosis.171 The prevalence of schizophrenia in the elderly is the same as seen in the general population, approximately 1.5%.172 About 25% of elderly patients with schizophrenia have late-onset and 75% early-onset disease. Late-onset schizophrenia (LOS) is more frequent and more severe in women173-175 than in men. Very late-onset schizophrenia (after age 60) is less frequent with an estimated prevalence of 0.7%.176 The 6-month prevalence of major depression is estimated to be 0.1% to 0.5% in elderly men and 1% to 1.6% in elderly women. Psychotic depression is more common in depressed patients whose first depressive episode occurs later in life.177 Late-life delusional disorder usually occurs in the context of other psychiatric and medical conditions and may be precipitated by recent stressors or debilitating physical conditions.178 Thirty percent to 40% of hospitalized patients age ≥65 experience episodes of delirium.175 About three-fourths of elderly psychotic patients are female179 and the clinical manifestations consist mostly of delusions and hallucinations.174 Because the average lifespan is increasing, the prevalence of psychoses in older patients also is expected to increase. Psychosis in the elderly is a diagnostic and treatment challenge because it has multiple causes and antipsychotic treatment may cause serious side effects. The cost of LOS is at least as high as that seen in early-onset schizophrenia (EOS), at least $65 billion in the United States alone.180 Prevention is a priority.181

Historic trends. The historic tendency to view schizophrenia as having an onset restricted to adolescence or young adulthood was formalized in DSM-III, which did not permit a schizophrenia diagnosis if symptoms developed after age 45. However, several reports challenged that notion.182 DSM-III-R permitted diagnosis of schizophrenia late-onset type after age 45, and DSM-IV included no age-of-onset restriction for a schizophrenia diagnosis. The etiology and pathophysiology of late-onset and very late-onset schizophrenia are not well understood. It has been suggested that LOS is a neurodegenerative condition,183 resulting from acquired brain lesions,184 or secondary to sensory deficits and social isolation.173,185 When compared with patients with EOS, LOS patients were more likely to have had good premorbid functioning, been married, held a job, and had children.186 LOS is characterized by predominant bizarre delusions but formal thought disorder and inappropriateness of affect are much less common than has been seen in younger patients. Patients with onset of psychotic symptoms after age 40 usually lack predominant negative symptoms (particularly affective blunting)187 and a family history.188 They have less impairment in neurocognitive areas of learning and abstraction or cognitive flexibility, and they require lower dosages of neuroleptics to manage psychotic symptoms.189 Quantitative analyses of MRI scans in a sub-sample of patients showed larger thalami in the late-onset group than in the early-onset group.190 However even though EOS and LOS may not be phenotypically homogenous, several similarities have been observed. In investigations conducted at the Clinical Research Center for the Study of Late-Life Psychoses at the University of California, San Diego, patients with LOS (age of onset ≥45) were compared with patients of a similar age who had EOS.173 The 2 groups have similar apparent genetic risk, positive symptoms, treatment response, and disease course. On the other hand, the differences between these groups suggest that neurobiologic differences might mediate onset of schizophrenia symptoms.191 Elucidation of mediating factors may suggest novel intervention and preventive strategies.

Etiology. A number of medical illnesses (eg, delirium, thyroid disorders, infectious processes, blood glucose and electrolyte abnormalities, and CNS infections) can cause psychotic symptoms.192 Several medications can place older patients at risk for delirium, which may result in psychotic symptoms. The elderly are at risk for development of psychosis due to intentional or unintentional medication abuse.176 Medications with anticholinergic properties (eg, benztropine, promethazine, and tricyclic antidepressants) are particularly notable for producing delirium in older adults. Concomitant medications also place older patients at risk for delirium. In addition, withdrawal syndromes that sometimes occur after sudden cessation or a decrease in dosage of medications such as benzodiazepines may cause psychotic symptoms. Similarly, patients experiencing alcohol withdrawal may have psychotic symptoms. It has been reported that 11% to 13% of elderly patients with decreased visual acuity complain of elaborate and vivid visual hallucinations without other psychotic symptoms.193 Hallucinations also are a common consequence of vision loss, particularly age-related macular degeneration.

Universal prevention. Because LOS has such a varied etiopathogenesis, prevention, whether universal, selective, or indicated, is not easy. There is limited information on universal prevention of schizophrenia across all ages, but some insights may be learned from factors associated with delayed onset and remission of the illness in old age, including good premorbid adjustment, acute onset of symptoms, short duration of an ongoing episode, and the paucity of negative symptoms.194 Although effective preventive interventions are feasible, data on the safety and efficacy of primary preventive interventions are limited. Studies highlight the enrollment challenges facing efforts to identify the safest and most effective preventive interventions through clinical trials. The best primary prevention for schizophrenia-related psychosis in elderly patients would seemingly involve effective treatment and achieving remission of EOS. Other primary preventive measures for late-life psychosis include all the primary prevention strategies for dementia and depression, early recognition and treatment of medical conditions that could lead to delirium, and careful screening for substance abuse, which is often overlooked in all patients but especially in the elderly. As stated in the section on dementia, these universal precautions would include leading a physically, socially, and intellectually active lifestyle and early detection and modification of cardiovascular risk factors particularly hypertension, smoking, BMI, diabetes, dietary fat intake, dietary antioxidants, folate-vitamin B12-homocysteine metabolism, and obesity. Universal prevention could include regular hearing and vision assessments to help identify those at risk.

Selective prevention. Regular mental health screenings for first-degree relatives of patients with schizophrenia and bipolar disorder could be helpful. There is little research in this area and this needs to be addressed.

Indicated prevention. According to Wyatt,195 early or indicated intervention with antipsychotics during patients’ first psychotic episode, including treatment in the prodromal phase, may lead to a better long-term outcome. Several clinical trials suggest that antipsychotics have beneficial effects across the age spectrum in either preventing or postponing the first episode of psychosis in individuals at high risk.196 Evidence suggests that selective serotonin reuptake inhibitors, serotonin 5-HT2A and dopamine D3 receptor antagonists, mood-stabilizing medications as well as GABAergic, glutamatergic, and neuroprotective compounds also may help prevent first-episode psychosis. Although there are indications that effective preventive interventions are feasible, data on safety and efficacy of primary preventive interventions are limited.

  CONCLUSIONS

There are identifiable risk factors for many of the psychiatric disorders occurring in the geriatric population including depression, mania, suicide, dementias, and psychotic disorders. Modification of the risk factors, including a healthy lifestyle that emphasizes diet, exercise, socialization, and education are important aspects of primary prevention in the elderly. Genetic engineering and vaccine therapies may open new, exciting opportunities for prevention of many of the psychiatric illnesses in the near future.

DISCLOSURES: This study was not funded by any agency. The authors report no financial relationship with any company whose products are mentioned in this article, or with manufacturers of competing products.

    REFERENCES

  1. Clarfield MA. Dr. Ignatz Nascher and the birth of geriatrics. CMAJ. 1990;143:944–948.
  2. Andrews G, Issakidis C, Sanderson K, et al. Utilising survey data to inform public policy: comparison of the cost-effectiveness of treatment of ten mental disorders. Br J Psychiatry. 2004;184:526–533.
  3. Smit F, Ederveen A, Cuijpers P, et al. Opportunities for cost-effective prevention of late-life depression: an epidemiological approach. Arch Gen Psychiatry. 2006; 63:290–296.
  4.  National Governors Association. Mental health and aging fact sheet. Available at: http://www.nga.org/Files/pdf/0412FSAGING.pdf. Accessed November 16, 2010.
  5. Sisko A, Truffer C, Smith S, et al. Health spending projections through 2018: recession effects add uncertainty to the outlook. Health Affairs. 2009;28:w346–w357. Available at: http://content.healthaffairs.org/cgi/content/abstract/hlthaff.28.2.w346. Accessed November 16, 2010.
  6. Jeste DV, Alexopoulos GS, Bartels SJ, et al. Consensus statement on the upcoming crisis in geriatric mental health: research agenda for the next 2 decades. Arch Gen Psychiatry. 1999;56:848–853.
  7. Gordon RS Jr. An operational definition of disease prevention. Public Health Rep. 1983;98:107–109.
  8. Lebowitz BD, Pearson JL, Schneider LS, et al. Diagnosis and treatment of depression in late life: consensus statement update. JAMA. 1997;278:1186–1190.
  9. Cole MG, Bellavance F. The prognosis of depression in old age. Am J Geriatr Psychiatry. 1997;5:4–14.
  10. Reynolds CF III, Alexopoulos GS, Katz IR, et al. Chronic depression in the elderly: approaches for prevention. Drugs Aging. 2001;18:507–514.
  11. Alexopoulos GS, Borson S, Cuthbert BN, et al. Assessment of late life depression. Biol Psychiatry. 2002; 52:164–174.
  12. Charney DS, Reynolds CF, Lewis L, et al. Depression and Bipolar Support Alliance consensus statement on the unmet needs in diagnosis and treatment of mood disorders in late life. Arch Gen Psychiatry. 2003;60:664–672.
  13. Katz IR, Streim J, Parmelee P. Prevention of depression, recurrences, and complications in late life. Prev Med. 1994;23:743–750.
  14. Schulberg H, Saul M, McClelland M, et al. Assessing depression in primary medical and psychiatric practices. Arch Gen Psychiatry. 1985;42:1164–1170.
  15. Pepersack T, De Breucker S, Mekongo YN, et al. Correlates of unrecognized depression among hospitalized geriatric patients. J Psychiatr Pract. 2006;12: 160–167.
  16. Feightner JW, Worrall G. Early detection of depression by primary care physicians. CMAJ. 1990;142: 1215–1220.
  17. Brink TL, Yesavage JA, Lum O, et al. Screening tests for geriatric depression. Clin Gerontol. 1982;1:37–43.
  18. Blazer D. Spirituality, depression and suicide: a cross-cultural perspective. South Med J. 2007;100:735–736.
  19. Braam AW, Van den Eeden P, Prince MJ, et al. Religion as a cross-cultural determinant of depression in elderly Europeans: results from the EURODEP collaboration. Psychol Med. 2001;31:803–814.
  20. Koenig HG, George LK, Peterson BL. Religiosity and remission of depression in medically ill older patients. Am J Psychiatry. 1998;155:536–542.
  21. Moreira-Almeida A, Neto FL, Koenig HG. Religiousness and mental health: a review. Rev Bras Psiquiatr. 2006;28:242–250.
  22. Koenig HG, Weiner DK, Peterson BL, et al. Religious coping in the nursing home: a biopsychosocial model. Int J Psychiatry Med. 1997;27:365–376.
  23.  US Department of Health and Human Services. Mental health: a report of the Surgeon General—executive summary. Rockville, MD: US Department of Health and Human Services, Substance Abuse and Mental Health Services Administration, Center for Mental Health Services, National Institutes of Health, National Institute of Mental Health; 1999.
  24. Blumenthal JA, Schocken DD, Needels TL, et al. Psychological and physiological effects of physical conditioning on the elderly. J Psychosom Res. 1982;26:505–510.
  25. Southwick SM, Vythilingam M, Charney DS. The psychobiology of depression and resilience to stress: implications for prevention and treatment. Annu Rev Clin Psychol. 2005;1:255–291.
  26. Corrigan PW, Larson JE. Stigma. In: Mueser KT, Jeste DV, eds. Clinical handbook of schizophrenia. New York, NY: The Guilford Press; 2008:533–540.
  27. Wells KB, Hays RD, Burman A. Detection of depressive disorder for patients receiving prepaid or fee-for-service care. Results from the Medical Outcomes Study. JAMA. 1989;262:3298–3302.
  28. Harman JS, Schulberg HC, Mulsant BH, et al. The effect of patient and visit characteristics on diagnosis of depression in primary care. J Fam Pract. 2001;50:1068.
  29. Gottlieb GL. Barriers to care for older adults with depression. In: Schneider LS, Reynolds CF, Lebowitz BD, et al, eds. Diagnosis and treatment of depression in late life: results of the NIH Consensus Development Conference. Washington, DC: American Psychiatric Publishing, Inc.; 1994:375–396.
  30. Sirey JA, Bruce ML, Alexopoulos GS, et al. Stigma as a barrier to recovery: perceived stigma and patient-rated severity of illness as predictors of antidepressant drug adherence. Psychiatr Serv. 2001;52:1615–1620.
  31.  Medicare Improvements for Patients and Providers Act of 2008, Improvements for Patients and Providers Act of 2008, Pub L No 110-275, 122 Stat 2494 (2008).
  32. Trivedi AN, Swaminathan S, Mor V. Insurance parity and the use of outpatient mental health care following a psychiatric hospitalization. JAMA. 2008;300:2879–2885.
  33. Jeste DV. Psychiatry of old age is coming of age. Am J Psychiatry. 1997;154:1356–1358.
  34. Madhusoodanan S, Brenner R. Caring for the chronically mentally ill in nursing homes. Annals of Long-Term Care. 2007;15:29–31.
  35. Eaton WW, Badawi M, Melton B. Prodromes and precursors: epidemiologic data for primary prevention of disorders with slow onset. Am J Psychiatry. 1995;152:967–972.
  36. Brown LF, Reynolds CF III, Monk TH, et al. Social rhythm stability following late-life spousal bereavement: associations with depression and sleep impairment. Psychiatry Res. 1996;62:161–169.
  37. Palmore E. The relative importance of social factors in predicting longevity. In: Plamore EB, Jeffers FC, eds. Prediction of life span: recent findings. Lexington, MA: Heath Lexington Books; 1971:237–248.
  38. Palmore E, Luikart C. Health and social factors in life satisfaction. J Health Soc Behav. 1972;13:68–80.
  39. Gilden JL, Hendryx MS, Clar S, et al. Diabetes support groups improve health care of older diabetic patients. J Am Geriatr Soc. 1992;40:147–150.
  40. Phillips RSC. Preventing depression: a program for African American elders with chronic pain. Fam Community Health. 2000;22:57–65.
  41. Cole MG, Dendukuri N. The feasibility and effectiveness of brief interventions to prevent depression in older subjects: a systematic review. Int J Geriatr Psychiatry. 2004;19:1019–1025.
  42. Cuijpers P. A psychoeducational approach to the treatment of depression: a meta-analysis of Lewinsohn’s “coping with depression” course. Behav Ther. 1998; 29:521–533.
  43. Breckenridge JS, Zeiss AM, Thompson LW. The life satisfaction course: an intervention for the elderly. In: Munoz RF, ed. Depression prevention: research directions. Washington, DC: Hemisphere Publishing; 1987:185–196.
  44. Block J, Kremen AM. IQ and ego-resiliency: conceptual and empirical connections and separateness. J Personal Soc Psychol. 1996;70:349–361.
  45. Klohnen EC. Conceptual analysis and measurement of the construct of ego-resiliency. J Personal Soc Psychol. 1996;70:1067–1079.
  46. Denney NW. Critical thinking during the adult years: has the developmental function changed over the last four decades? Exp Aging Res. 1995;21:191–207.
  47. Hegel MT, Arean PA. Problem-Solving Treatment for Primary Care (PST-PC): a treatment manual for depression. Hanover, NH: Dartmouth University; 2003.
  48. Reynolds CF, Dew MA, Lenze EJ, et al. Preventing depression in medical illness: a new lead? Arch Gen Psychiatry. 2007;64:884–885.
  49. Resick PA. Stress and trauma. Philadelphia, PA: Psychology Press; 2001.
  50. Travis LA, Lyness JM, Shields CG, et al. Social support, depression, and functional disability in older adult primary-care patients. Am J Geriatr Psychiatry. 2004;12:265–271.
  51. Ford DE, Kamerow DB. Epidemiologic study of sleep disturbances and psychiatric disorders. An opportunity for prevention? JAMA. 1989;262:1479–1484.
  52. Paunio T, Korhonen T, Hublin C, et al. Longitudinal study on poor sleep and life dissatisfaction in a nationwide cohort of twins. Am J Epidemiol. 2009;169:206–213.
  53. Eaton WW, Badawi M, Melton B. Prodromes and precursors: epidemiologic data for primary prevention of disorders with slow onset. Am J Psychiatry. 1995;152:967–972.
  54. Morin CM, Hauri PJ, Espie CA, et al. Nonpharmacologic treatment of chronic insomnia. An American Academy of Sleep Medicine review. Sleep. 1999;22:1134–1156.
  55. Barrett-Connor E, Von Mühlen DG, Kritz-Silverstein D. Bioavailable testosterone and depressed mood in older men: the Rancho Bernardo Study. J Clin Endocrinol Metab. 1999;84:573–577.
  56. Almeida OP, Yeap BB, Hankey GJ, et al. Low free testosterone concentration as a potentially treatable cause of depressive symptoms in older men. Arch Gen Psychiatry. 2008;65:283–289.
  57. Amore M, Scarlatti F, Quarta AL, et al. Partial androgen deficiency, depression and testosterone treatment in aging men. Aging Clin Exp Res. 2009;21:1–8.
  58. Rapp MA, Dahlman K, Sano M, et al. Neuropsychological differences between late-onset and recurrent geriatric major depression. Am J Psychiatry. 2005;162:691–698.
  59. Depp CA, Jeste DV. Bipolar disorder in older adults: a critical review. Bipolar Disord. 2004;6:343–367.
  60. Butters MA, Young JB, Lopez O, et al. Pathways linking late-life depression to persistent cognitive impairment and dementia. Dialogues Clin Neurosci. 2008;10:345–357.
  61. Alexander GE, DeLong MR, Strick PL. Parallel organization of functionally segregated circuits linking basal ganglia and cortex. Annu Rev Neurosci. 1986;9:357–381.
  62. Cummings JL. Frontal-subcortical circuits and human behavior. Arch Neurol. 1993;50:873–880.
  63. Alexopoulos GS, Meyers BS, Young RC, et al. ‘Vascular depression’ hypothesis. Arch Gen Psychiatry. 1997;54:915–922.
  64. Caspi A, Sugden K, Moffitt TE, et al. Influence of life stress on depression: moderation by a polymorphism in the 5-HTT gene. Science. 2003;301:386–389.
  65. Shulman KI, Tohen M, Satlin A, et al. Mania compared with unipolar depression in old age. Am J Psychiatry. 1992;149:341–345.
  66. Snowdon J. A retrospective case-note study of bipolar disorder in old age. Br J Psychiatry. 1991;158:485–490.
  67. Kramer M, German PS, Anthony JC, et al. Patterns of mental disorders among the elderly residents of eastern Baltimore. J Am Geriatr Soc. 1985;33:236–245.
  68. Young RC, Klerman GL. Mania in late life: focus on age at onset. Am J Psychiatry. 1992;149:867–876.
  69. Van Gerpen MW, Johnson JE, Winstead DK. Mania in geriatric patient population: a review of the literature. Am J Geriatr Psychiatry. 1999;7:188–202.
  70. Yassa R, Nair NP, Iskandar H. Late-onset bipolar disorder. Psychiatr Clin North Am. 1988;11:117–131.
  71. Broadhead J, Jacoby R. Mania in old age: a first prospective study. Int J Geriatr Psychiatry. 1990;5:215–222.
  72. Krauthammer C, Klerman GL. Secondary mania: manic syndromes associated with antecedent physical illness or drugs. Arch Gen Psychiatry. 1978;35:1333–1339.
  73. Goodwin FK, Jamison KR. Manic-depressive illness. London, United Kingdom: Oxford University Press; 1990:142-146,151,416–502.
  74. Yassa R, Nair V, Nastase C, et al. Prevalence of bipolar disorder in a psychogeriatric population. J Affect Disord. 1998;14:197–201.
  75. Young RC. Bipolar mood disorders in the elderly. Psychiatry Clin North Am. 1997;20:121–136.
  76. Meehan PJ, Saltzman LE, Sattin RW. Suicides among older United States residents: epidemiologic characteristics and trends. Am J Public Health. 1991;81:1198–1200.
  77. Singh GK, Kochanek KD, MacDorman MF. Advance report of final mortality statistics, 1994. Month Vital Stat Rep. 1996;45(suppl 3):1–80.
  78.  Administration on Aging, US Department of Health and Human Services A. profile of older Americans: 2001. Available at: http://www.aoa.gov/aoaroot/aging_statistics/Profile/2009/docs/2009profile_508.pdf. Accessed November 16, 2010.
  79. Pearson JL, Conwell Y. Suicide in late-life: challenges and opportunities for research. Introduction. Int Psychogeriatr. 1995;7:131–136.
  80. Duberstein PR, Conwell Y, Cox C, et al. Attitudes toward self-determined death: a survey of primary care physicians. J Am Geriatr Soc. 1995;43:395–400.
  81. Conwell Y, Duberstein PR. Suicide in elders. Ann N Y Acad Sci. 2001;932:132–150.
  82. Kaplan MS, Adamek ME, Rhoades JA. Prevention of elderly suicide. Physicians’ assessment of firearm availability. Am J Prev Med. 1998;15:60–64.
  83. Price JH, Bedell AW, Everett SA, et al. Training in firearm safety counseling in family practice residency programs. J Community Health. 1997;22:91–99.
  84. Price JH, Clause M, Everett SA. Patients’ attitudes about the role of physicians in counseling about firearms. Patient Educ Couns. 1995;25:163–170.
  85. Goldstorm ID, Burns BJ, Kessler LG, et al. Mental health services use by elderly adults in a primary care setting. J Gerontol. 1987;42:147–153.
  86. Rihmer Z, Rutz W, Pihlgren H. Depression and suicide on Gotland. An intensive study of all suicides before and after a depression-training programme for general practitioners. J Affect Disord. 1995;35:147–152.
  87. Rutz W, von Knorring L, Wålinder J. Long-term effects of an educational program for general practitioners given by the Swedish Committee for the Prevention and Treatment of Depression. Acta Psychiatr Scand. 1992;85:83–88.
  88. Mann JJ, Apter A, Bertolote J, et al. Suicide prevention strategies: a systematic review. JAMA. 2005;295: 2064–2074.
  89. Cummings P, Koepsell TD, Grossman DC, et al. The association between the purchase of a handgun and homicide or suicide. Am J Public Health. 1997;87: 974–978.
  90. Kellermann AL, Rivara FP, Somes G, et al. Suicide in the home in relation to gun ownership. N Engl J Med. 1992;327:467–472.
  91. Conwell Y, Duberstein PR, Connor K, et al. Access to firearms and risk for suicide in middle-aged and older adults. Am J Geriatr Psychiatry. 2002;10:407–416.
  92.  Centers for Disease Control and Prevention. Injury prevention and control: data and statistics (WISQARSTM). Available at: http://www.cdc.gov/injury/wisqars/index.html. Accessed November 16, 2010.
  93.  Brady Handgun Violence Prevention Act. Pub L No. 103-159, 107 Stat 1536 (1993).
  94. Ludwig J, Cook PJ. Homicide and suicide rates associated with implementation of the Brady Handgun Violence Prevention Act. JAMA. 2000;284:585–591.
  95. Szanto K, Gildengers A, Mulsant BH, et al. Identification of suicidal ideation and prevention of suicidal behavior in the elderly. Drugs Aging. 2002;19:11–24.
  96.  PDV Foundation Inc. Dying by their own hand in rural America: suicide the second-leading cause of death in states with primarily rural populations. Available at: http://www.advancingsp.org/Press_Release_8_11_05.pdf. Accessed November 16, 2010.
  97. Osgood NJ, Brant BA. Suicidal behavior in long-term care facilities. Suicide Life Threat Behav. 1990;20:113–122.
  98. Conwell Y, Caine ED, Olsen K. Suicide and cancer in late life. Hosp Community Psychiatry. 1990;41: 1334–1339.
  99. Kastenbaum R, Mishra BL. Premature death and self-injurious behavior in old age. Geriatrics. 1971;26: 71–81.
  100. Farberow NL. Indirect self-destructive behavior: classification and characteristics. In: Farberow NL, ed. The many faces of suicide: indirect self-destructive behavior. New York, NY: McGraw-Hill; 1980:15–27.
  101. Beck AT, Kovacs M, Weissman A. Assessment of suicidal intention: the scale for suicide ideation. J Consult Clin Psychol. 1979;47:343–352.
  102. Florio ER, Hendryx MS, Jensen JE, et al. A comparison of suicidal and nonsuicidal elders referred to a community mental health center program. Suicide Life Threat Behav. 1997;27:182–193.
  103. De Leo D, Carollo G, Buono MD. Lower suicide rates associated with a Tele-Help/Tele-Check Service for the elderly at home. Am J Psychiatry. 1995;152:632–634.
  104. De Leo D, Dello Buono M, Dwyer J. Suicide among the elderly: the long-term impact of a telephone support and assessment intervention in northern Italy. Br J Psychiatry. 2002;181:226–229.
  105. McIntosh JL. Suicide prevention in the elderly (age 65-99). Suicide Life Threat Behav. 1995;25:180–192.
  106. Richman J. Preventing elderly suicide: overcoming personal despair, professional neglect, and social bias. New York, NY: Springer Publishing Company; 1993.
  107. Manthorpe J, Iliffe S. Suicide among older people. Nurs Older People. 2006;17:25–29.
  108. Waern M, Beskow J, Runeson B, et al. Suicidal feelings in the last year of life in elderly people who commit suicide. Lancet. 1999;354:917–918.
  109. Lyness JM, Conwell Y, Nelson JG. Suicide attempts in elderly psychiatric inpatients. J Am Geriatr Soc. 1992;40:320–324.
  110. Conwell T, Olsen K, Caine ED, et al. Suicide in later life: psychological autopsy findings. Int Psychogeriatr. 1991;3:59–66.
  111. Bruce ML, Ten Have TR, Reynolds CF III, et al. Reducing suicidal and depressive symptoms in depressed older primary care patients: a randomized controlled trial. JAMA. 2004;291:1081–1091.
  112. Unützer J, Katon W, Callahan CM, et al. Collaborative care management of late-life depression in the primary care setting: a randomized controlled trial. JAMA. 2002;288:2836–2845.
  113. Unützer J, Tang L, Oishi S, et al. Reducing suicidal ideation in depressed older primary care patients. J Am Geriatr Soc. 2006;54:1550–1556.
  114. Friedhoff AJ, Ballenger J, Bellack AS, et al, for the NIH Consensus Development Panel on Depression in Late Life. Diagnosis and treatment of depression in late life. JAMA. 1992;268:1018–1024.
  115. Peters KD, Kochanek KD, Murphy SL. Deaths: final data for 1996. Natl Vital Stat Rep. 1998;47:1–100.
  116. Conwell Y, Brent D. Suicide and aging. I: Patterns of psychiatric diagnosis. Int Psychogeriatr. 1995;7:149–164.
  117. Duberstein PR, Conwell Y, Caine ED. Interpersonal stressors, substance abuse, and suicide. J Nerv Mental Dis. 1993;181:80–85.
  118. Takahashi Y, Hirasawa H, Koyama K, et al. Suicide and aging in Japan: an examination of treated elderly attempters. Int Psychogeriatr. 1995;7:239–251.
  119. Beck AT, Brown G, Berchick RJ, et al. Relationship between hopelessness and ultimate suicide: a replication with psychiatric outpatients. Am J Psychiatry. 1990; 147:190–195.
  120. Harris EC, Barraclough BM. Suicide as an outcome for medical disorders. Medicine (Baltimore). 1994;73:281–296.
  121. Beautrais AL. A case control study of suicide and attempted suicide in older adults. Suicide Life Threat Behav. 2002;32:1–9.
  122. Morgan HG, Jones EM, Owen JH. Secondary prevention of non-fatal deliberate self-harm. The green card study. Br J Psychiatry. 1993;163:111–112.
  123. Motto JA, Heilbron D, Juster R. Communication as a suicide prevention program. In: Spoubrier JP, Vedrinne RJ, and the International Association for Suicide Prevention Congress, eds. Dépression et suicide: aspects médicaux, psychologiques et socio-culturels: comptes rendus. Paris, France: Pergamon Press; 1983:148–154.
  124. Miller M. Geriatric suicide: the Arizona study. Gerontologist. 1978;18:488–495.
  125. Foley KM. The relationship of pain and symptom management to patient requests for physician-assisted suicide. J Pain Symptom Manage. 1991;6:289–297.
  126. Kukull WA, Bowen JD. Dementia epidemiology. Med Clin North Am. 2002;86:573–590.
  127. Rice DP, Fillit HM, Max W, et al. Prevalence, costs, and treatment of Alzheimer’s disease and related dementia: a managed care perspective. Am J Manag Care. 2001; 7:809–818.
  128. Qui C, De Ronchi D, Fratiglioni L. The epidemiology of dementias: an update. Curr Opin Psychiatry. 2007;20:380–385.
  129. Fillit HM. The pharmacoeconomics of Alzheimer’s disease. Am J Manag Care. 2000;6:S1139–S1144.
  130. Hogervorst E, Barnetson L, Jobst KA, et al. Diagnosing dementia: interrater reliability assessment and accuracy of the NINCDS/ADRDA criteria versus CERAD histopathological criteria for Alzheimer’s disease. Dement Geriatr Cogn Disord. 2000;11:107–113.
  131. Hoenicka J. Genes in Alzheimer’s disease. Rev Neurol. 2006;42:302–305.
  132. Evans DA, Beckett LA, Field TS, et al. Apolipo-protein E epsilon4 and incidence of Alzheimer disease in a community population of older persons. JAMA. 1997;277:822–824.
  133. Lendon CL, Ashall F, Goate AM. Exploring the etiology of Alzheimer disease using molecular genetics. JAMA. 1997;277:825–831.
  134. Barnes DE, Yaffe K, Satariano WA, et al. A longitudinal study of cardiorespiratory fitness and cognitive function in healthy older adults. J Am Geriatr. 2003;51: 459–465.
  135. Petrovitch H, White LR, Izmirilian G, et al. Midlife blood pressure and neuritic plaques, neurofibrillary tangles, and brain weight at death: the HAAS. Honolulu-Asia Aging Study. Neurobiol Aging. 2000;21:57–62.
  136. Crawford JG. Alzheimer’s disease risk factors as related to cerebral blood flow. Med Hypotheses. 1996; 46:367–377.
  137. Hébert R, Lindsay J, Verreault R, et al. Vascular dementia: incidence and risk factors in the Canadian study of health and aging. Stroke. 2000;31:1487–1493.
  138. Breteler MM. Vascular involvement in cognitive decline and dementia. Epidemiologic evidence from the Rotterdam Study and the Rotterdam Scan Study. Ann NY Acad Sci. 2000;903:457–465.
  139. de la Torre JC. Alzheimer disease as a vascular disorder: nosological evidence. Stroke. 2002;33:1152–1162.
  140. de la Torre JC. Vascular basis of Alzheimer’s pathogenesis. Ann NY Acad Sci. 2002;977:196–215.
  141. Tatemichi TK, Desmond DW, Mayeux R, et al. Dementia after stroke: baseline frequency, risks and clinical features in a hospitalized cohort. Neurology. 1992;42:1185–1193.
  142. Loeb C, Gandolfo C, Croce R, et al. Dementia associated with lacunar infarction. Stroke. 1992;23:1225–1229.
  143. Wen Y, Yang SH, Liu R, et al. Cdk5 is involved in NFT-like tautopathy induced by transient cerebral ischemia in female rats. Biochim Biophys Acta. 2007;1772:473–483.
  144. Floyd RA, Hensley K. Oxidative stress in brain aging. Implications for therapeutics of neurodegenerative diseases. Neurobiol Aging. 2002;23:795–807.
  145. Plassman BL, Havlik RJ, Steffens DC, et al. Documented head injury in early adulthood and risk of Alzheimer’s disease and other dementias. Neurology. 2000;55:1158–1166.
  146. Juan D, Zhou DH, Li J, et al. A 2-year follow-up study of cigarette smoking and dementia. Eur J Neurology. 2004;11:277–282.
  147. Kramer AF, Colcombe SJ, McAuley E, et al. Fitness, aging and neurocognitive function. Neurobiol Aging. 2005;26:124–127.
  148. Perneczky R, Haussermann P, Diehl-Schmid J, et al. Metabolic correlates of brain reserve in dementia with Lewy bodies: an FDG PET study. Dementia Geriatr Cogn Disord. 2007;23:416–422.
  149. Langa KM, Larson EB, Karlawish JH, et al. Trends in the prevalence and mortality of cognitive impairment in the United States: is there evidence of a compression of cognitive morbidity? Alzheimers Dement. 2008;4:134–144.
  150. Engelhart MJ, Geerlings MI, Ruitenberg A, et al. Dietary intake of antioxidants and risk of Alzheimer disease. JAMA. 2002;287:3223–3229.
  151. Engelhart MJ, Geerlings MI, Ruitenberg A, et al. Diet and risk of dementia: does fat matter? The Rotterdam Study. Neurology. 2002;59:1915–1921.
  152. Morris MC, Evans DA, Bienias JL, et al. Dietary fats and the risk of incident Alzheimer disease. Arch Neurol. 2002;60:194–200.
  153. Moceri VM, Kukull WA, Emanuel I, et al. Early-life risk factors and the development of Alzheimer’s disease. Neurology. 2000;54:415–420.
  154. Solfrizzi V, Capurso C, D’Introno A, et al. Lifestyle-related factors in predementia and dementia syndromes. Expert Rev Neurother. 2008;8:133–158.
  155. Fratiglioni L, Qiu C. Prevention of common neurodegenerative disorders in the elderly. Exp Gerontol. 2009;44:46–50.
  156. Hannon O, Forrette F. Prevention of dementia: lessons from SYST-EUR and PROGRESS. J Neurol Sci. 2004;226:71–74.
  157. Clark F, Azen SP, Carlson M, et al. Embedding health-promoting changes into the lives of independent-living older adults: long-term follow-up of occupational therapy intervention. J Gerontol B Psychol Sci Soc Sci. 2001;56:P60–P63.
  158. Rich JB, Rasmusson DX, Folstein MF, et al. Nonsteroidal anti-inflammatory drugs in Alzheimer’s disease. Neurology. 1995;45:51–55.
  159. Scott HD, Laake K. Statins for the prevention of Alzheimer’s disease. Cochrane Database Syst Rev. 2001;(4):CD003160.
  160. Bastianetto S, Ramassamy C, Doré S, et al. The Ginkgo biloba extract (EGb 761) protects hippocampal neurons against cell death induced by beta-amyloid. Eur J Neurosci. 2000;12:1882–1890.
  161. DeKosky ST, Williamson JD, Fitzpatrick AL, et al. Ginkgo biloba for prevention of dementia: a randomized controlled trial. JAMA. 2008;300:2253–2262.
  162. Schenk D, Barbour R, Dunn W, et al. Immunization with amyloid-beta attenuates Alzheimer-disease-like pathology in the PDAPP mouse. Nature. 1999;400: 173–177.
  163. Nitsch RM, Hock C. Targeting beta-amyloid pathology in Alzheimer’s disease with Abeta immunotherapy. Neurotherapeutics. 2008;5:415–420.
  164. Okura Y, Matsumoto Y. Novel vaccine therapy for Alzheimer’s Disease—recent progress and our approach. Brain Nerve. 2008;60:931–940.
  165. Okura Y, Miyakoshi A, Kohyama K, et al. Non-viral Abeta DNA vaccine therapy against Alzheimer’s disease: long-term effects and safety. Proc Natl Acad Sci U S A. 2006;103:9619–9624.
  166. Reisberg B, Ferris SH, Anand R, et al. Clinical assessment of cognitive decline in normal aging and primary degenerative dementia: concordant ordinal measures. In: Psychiatry. New York, NY: Plenum Press; 1985:333–338.
  167. DeCarli C. The role of neuroimaging in dementia. Clin Geriatr Med. 2001;17:255–279.
  168. Jeste DV, Alexopoulos GS, Bartels SJ, et al. Consensus statement on the upcoming crisis in geriatric mental health: research agenda for the next 2 decades. Arch Gen Psychiatry. 1999;56:848–853.
  169. Reeves RR, Brister JC. Psychosis in late life: emerging issues. J Psychosoc Nurs Ment Health Serv. 2008;46:45–52.
  170. Pearlson GD, Petty RG. Late-life onset psychoses. In: Coffey CE, Cummins JL, eds. Textbook of geriatric neuropsychiatry. Washington, DC: American Psychiatric Publishing, Inc.; 1994:262–279.
  171. Ropacki SA, Jeste DV. Epidemiology of and risk factors for psychosis of Alzheimer’s disease: a review of 55 studies published from 1990 to 2003. Am J Psychiatry. 2005;162:2022–2030.
  172. Aleman A, Kahn RS, Selten JP. Sex differences in the risk for schizophrenia. Arch Gen Psychiatry. 2003;60:565–571.
  173. Hafner H. Epidemiology of schizophrenia. Can J Psychiatry. 1997;42:139–151.
  174. Jeste DV, Symonds LL, Harris MJ, et al. Nondementia nonpraecox dementia praecox? Late-onset schizophrenia. Am J Ger Psychiatry. 1997;5:302–317.
  175. Sajatovic M, Madhusoodanan S, Buckley T. Schizophrenia in elderly: guidelines for its recognition and treatment. CNS Drugs. 2000;13:103–115.
  176. Girard C, Simard M. Clinical characterization of late and very late onset first psychotic episode in psychiatric inpatients. Amer J Ger Psychiatry. 2008;16:478–487.
  177. Jorgensen P, Bennedsen B, Christensen J, et al. Acute and transient psychotic disorder: a 1 year follow up study. Acta Psychiatr Scand. 1997;96:150–154.
  178. Khouzam HR, Emez R. Late life psychosis: assessment and general treatment strategies. Compr Ther. 2007;33:127–143.
  179. Webster J, Grossberg GT. Late onset of psychotic symptoms. Am J Ger Psychiatry. 1998;6:196–202.
  180. Wyatt RJ, Henter L, Leary MC, et al. An economic evaluation of schizophrenia. Soc Psychiatry Psychiatr Epidemiol. 1995;30:196–205.
  181. Cuffel BJ, Jeste DV, Halpain M, et al. Treatment costs and use of community mental health services for schizophrenia by age-cohorts. Am J Psychiatry. 1996; 153:870–876.
  182. Fish F. Senile schizophrenia. Journal of Mental Science. 1960;106:938–946.
  183. Murray RM, O’Callaghan E, Castle DJ, et al. A neurodevelopmental approach to the classification of schizophrenia. Schizophr Bull. 1992;18:319–332.
  184. Miller BL, Lesser IM, Boone KB, et al. Brain lesions and cognitive function in late-life psychosis. Br J Psychiatry. 1991;158:76–82.
  185. Varner RV, Gaitz CM. Schizophrenic and paranoid disorders in the aged. Psychiatr Clin North Am. 1982;5:107–118.
  186. Jeste DV, Harris MJ, Krull A. Clinical and neuro-psychological characteristics of patients with late-onset schizophrenia. Am J Psychiatry. 1995;152:722–730.
  187. Howard R, Castle D, Wessely S, et al. A comparative study of 470 cases of early-onset and late-onset schizophrenia. Br J Psychiatry. 1993;163:352–357.
  188. Harris MJ. Psychosis in late life. Spotting new-onset disorders in your elderly patients. Postgrad Med. 1997;102:139–142.
  189. Palmer BW, McClure FS, Jeste DV. Schizophrenia in late life. Findings challenge traditional concepts. Harv Rev Psychiatry. 2001;9:51–58.
  190. Corey-Bloom J, Jernigan T, Archibald S, et al. Quantitative magnetic resonance imaging in late-life schizophrenia. Am J Psychiatry 1995;152:447–449.
  191. Jeste DV, Palmer BW, Harris MJ. Response to Almeida’s “Early- versus late-onset schizophrenia: is it time to define the difference?” (ltr). Am J Ger Psychiatry. 1998;6:346–347.
  192. Webster J, Grossberg GT. Late life onset of psychotic symptoms. Am J Geriatr Psychiatry. 1998;6:196–202.
  193. Tenisse RJ, Zitman FG, Raes DC. Clinical evaluation of 14 patients with Charles Bonnet syndrome (isolated visual hallucinations). Compr Psychiatry. 1994;35:70–75.
  194. Ram R, Bromet EJ, Eaton WW, et al. The natural course of schizophrenia: a review of first-admission studies. Schizophr Bull. 1992;18:185–207.
  195. Wyatt RJ. Neuroleptics and the natural course of schizophrenia. Schizophr Bull. 1991;17:325–351.
  196. McNamara R, Richtand N. Serotonin and dopamine interactions in psychosis prevention. Prog Brain Res. 2008;172:141–153.

CORRESPONDENCE: Subramoniam Madhusoodanan, MD, Department of Psychiatry, St. John’s Episcopal Hospital, 327 Beach 19th Street, Far Rockaway, NY 11691 USA, E-MAIL: sdanan@ehs.org