Tarek K. Rajji, MD

 was characterized as a pandemic, it was clear that older adults in general, and those with 

 (ADRD) in particular, would be severely impacted both directly by the virus and indirectly by the social consequences and responses.

 Now, approaching 2 years since SARS-CoV-2 emerged, we are starting to measure the impact of COVID-19 on older patients with cognitive impairment and ADRD. Further, we can begin to review neurobiological issues associated with COVID-19 in older adults, and consider how COVID-19 may contribute to cognitive impairment and future cases of dementia.

Caring for Older Adults With Mental Health Disorders During the Pandemic

PTSD in Late Life: An Update on Clinical Issues

Joan M. Cook, PhD; Bret R. Rutherford, MD; and Ron Acierno, PhD

Recognizing and Addressing Psychiatric Implications of Sleep Disorders

Christine Juang, PhD; Colleen Mills-Finnerty, PhD; Erin Cassidy-Eagle, PhD, DBSM; Makoto Kawai, MD; Christine Gould, PhD

The demographics of COVID-19 cases have shifted over time, with older adults being most impacted early in the pandemic, and later waves involving younger individuals.

 Similarly, risk varied by setting, with an early wave of COVID-19 cases in congregate settings including nursing homes, retirement homes, and hospitals. These frequent and widespread outbreaks were associated with significant morbidity and mortality. Despite campaigns to vaccinate nursing home residents, they still account for a large proportion of the total deaths due to COVID-19.

The severity of COVID-19 spans the spectrum from asymptomatic carrier state to severe illness and death, with age being the strongest demographic risk factor for a more severe illness: Age has an exponential relationship with infection fatality rate, reaching 15% at age 85.

 Older adults with cognitive impairment are doubly at risk, with age and cognitive impairment independently contributing to illness severity.

 Cognitive impairment has been associated with double the risk of COVID-19 mortality in nursing homes.

 Even when controlling for residence in a nursing home, those with dementia had twice the risk of acquiring COVID-19.

We had anticipated that rates of behavioral and psychologic symptoms associated with dementia (BPSD) would increase as a result of indirect factors such as disruption to care, social isolation, and disruption to routine.

 Unfortunately, this has been borne out, with studies reporting increases in BPSD including anxiety, depression, insomnia, wandering, and agitation.

Alongside the risk of mortality, the pandemic is also affecting mental health negatively, both via the direct effect of the virus and indirectly via the massive disruption to society in response to the pandemic. Early and ongoing mental health consequences of the pandemic include increased rates of symptoms of depression, anxiety, substance use, and suicidal ideation. However, paradoxically, younger individuals may be more impacted than older ones.

 Similarly, while the pandemic may have increased BPSD in some individuals with dementia, this has not been universally true. For example, in New Brunswick, Canada, despite a marked reduction in family visits and periods of lockdown (mitigated by virtual visits and volunteer services), there was no change in rates of agitation, and a reduction in rates of depression among nursing home residents, with more than half of them having dementia.

The availability of safe and effective COVID-19 vaccines is thought to be a key element to ending the pandemic. Early on, in the context of limited supply, governments prioritized vaccination for high-risk groups such as the elderly and those living in long-term care (LTC) facilities. Thus, most individuals with dementia were prioritized for vaccination. For example, in Ontario, Canada, despite only 0.5% of the population living in LTC facilities, vaccination initially was reserved for LTC residents and health professionals when vaccines first became available in December 2019.

 By March 2020, more than 92% of LTC residents had received at least 1 dose of a COVID-19 vaccine, which was estimated to have reduced mortality by 96%.

 The recent approval by the US Food and Drug Administration of booster shots for older persons (ie, a third dose) may offer them further protection and also deepen current inequities when vaccination remains unavailable due to supply constraints in some jurisdictions.

COVID-19 is transmitted person to person via inhalation of respiratory droplets and their deposition on mucous membranes, and to a lesser extent by contaminated hands contacting mucous membranes.

 The virus enters cells via the angiotensin-converting enzyme 2 receptor, present not only in the respiratory and gastrointestinal tract but also in other organs, including the brain and blood vessels.

 Thus, COVID-19 can potentially lead to neuropathology via systemic and inflammatory indirect effects and by its direct action on the nervous system.

Although most cases of COVID-19 are classified as mild, severe cases occur in individuals of all ages, most commonly in older adults. Common acute symptoms include cough, fever, fatigue, headache, myalgias, and diarrhea.

 Symptoms can progress and involve hypoxemia and acute respiratory distress syndrome.

 In addition, injury to all organ systems due to severe inflammation, thromboembolic events, and neurologic complications can occur.

The neurologic consequences of severe COVID-19 are common and involve both the central nervous system (CNS) and peripheral nervous system (PNS) (

 Dizziness and headache are the most common CNS manifestations, which can also include cerebrovascular disease (eg, ischemic stroke, hemorrhage), ataxia, and seizure. Delirium is a common presentation of older adults with COVID-19; it has a very poor prognosis and is associated with permanent cognitive impairment.

 Anosmia and ageusia are the most common PNS manifestations.

 Common CNS and PNS Manifestations of COVID-19

Neurologic manifestations can occur within the first days of illness and persist months after hospital discharge.

 Isolating the virus in cerebrospinal fluid is rare.

 Cognitive impairment is a commonly reported symptom in survivors of severe COVID-19 at 60 days post discharge.

 Although research is needed to confirm the neuropsychiatric sequelae of COVID-19, a broad spectrum of neuropsychiatric symptoms have been reported, including headaches, sleep disorders, encephalopathy, myalgia, and ageusia.

 The term long COVID refers to the persistence of symptoms after the resolution of the acute infection, and a broad range of symptoms have been reported, including neuropsychiatric symptoms such as cognitive impairment, insomnia, impaired concentration, posttraumatic symptoms, and headache.

 Long COVID is not always associated with the severity of acute COVID-19 or risk factors for severe COVID-19, and it may involve multiple organ damage by other direct mechanisms.

 Long COVID is thought to be relatively common, but estimates of its prevalence vary widely depending on definition and time since infection. It may also depend on the SARS-CoV-2 genetic variant.

There is evidence for both structural and functional brain changes following COVID-19, and these changes may be associated with the neurologic symptoms of long COVID. Various studies have reported heterogenous findings. A recent systematic review summarizing the neuroimaging findings associated with COVID-19 in older adults reported widespread neuropathological issues typically associated with cerebrovascular damage, most consistently in white matter, brainstem, and frontotemporal cortical areas.

 A case-control study of patients who recovered from COVID-19 found hypometabolism in frontotemporal regions, which was associated with neurological symptoms.

 A study of United Kingdom Biobank participants by Douaud et al found changes in 394 individuals who had brain imaging before and after a COVID-19 infection, compared with 388 matched controls without a history of COVID-19. Among those who had survived COVID-19, Douaud et al identified reductions in grey matter in the left parahippocampal gyrus, left lateral orbitofrontal cortex, and left insula.

Although it is staggering that approximately 1 in 500 Americans has died of COVID-19, mortality is the tip of the iceberg. The Centers for Disease Control and Prevention estimates that as of May 29, 2021, there had been more than 100 million individuals with symptomatic COVID-19 in the United States, 10 million of them 65 years or older.

 The sequelae from severe COVID-19 are risk factors for dementia, and they may increase the growing number of individuals living with dementia. Understanding the specific contribution of a past COVID-19 infection on future risks of dementia will require longitudinal studies. These risks may be substantial given the cerebrovascular changes associated with past infection. During the next few years, post-COVID-19 issues may occur mostly in older adults. However, COVID-19 may also increase the risk of future cognitive impairment and dementia in younger individuals, because early life experiences and exposures contribute to the risk of dementia, as is the case in other risk factors for dementia such as low level of education or depression early in life. The magnitude of the current and future human, financial, and societal cost of COVID-19 is unknown, but certainly worrisome.

On the other hand, we expect that the pandemic will lead to numerous changes that benefit older adults. Specifically, the spotlight on nursing homes has revealed systemic flaws and inequities in many countries that now will be hard to ignore. The pivot to virtual care has spurred some innovation that may facilitate access to care going forward.

In our own experience, working at the Centre for Addiction in Mental Health in Toronto, we have had to pivot to providing care to older individuals despite multiple waves of COVID-19 cases in the community. Some of the changes in our practice and our environment will have long-lasting benefits. The heterogeneity of real-world experience, compared with averages often reported in research, is humbling. Some of our older patients have shown remarkable resilience through the pandemic and have adjusted their lifestyle to thrive during this time. Others have had their usual coping mechanisms totally disrupted and are suffering, needing additional mental health and social resources. In our geriatric mental health inpatient unit, technology (eg, internet-connected tablets) has been helpful to connect patients to family, activities, and entertainment. We have also noticed an improved access to specialist consultations with virtual care and additional physician-to-physician consultation options. In our outpatient setting, virtual care options introduced to reduce risk of COVID-19 have also reduced barriers for certain patients who prefer it or may have mobility issues.

The impact of the pandemic on older adults and those with dementia has been immense. Vaccination can dramatically reduce severe outcomes from COVID-19 in older adults. The indirect impact of the pandemic on individuals with dementia, such as isolation and disruption of care, can be pronounced, but they can also be mitigated. COVID-19 causes neurological damage that is not restricted to severe cases or older adults. A significant proportion of individuals infected by COVID-19 will experience long-term negative impact, including an increased risk of dementia. Research to better understand the neurobiology and the long-term neuropsychiatric impacts of COVID-19 is critical, as it will shift the understanding of the risk-benefit of population-level interventions to prevent COVID-19. The pandemic is not over. Efforts to protect everyone, including older adults, from COVID-19 are essential.

 is an assistant professor of psychiatry at the University of Toronto and a clinician scientist at the Campbell Family Mental Health Research Institute, Centre for Addiction and Mental Health, in Toronto, Canada. 

 is an associate professor of psychiatry at the University of Toronto and chief of geriatric psychiatry at the Centre for Addiction and Mental Health. 

 is the Labatt Family Chair of the Department of Psychiatry in the Faculty of Medicine at the University of Toronto and a clinician scientist in the Campbell Family Mental Health Research Institute, Centre for Addiction and Mental Health.

Anticipating and mitigating the impact of the COVID-19 pandemic on Alzheimer’s disease and related dementias

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Changing age distribution of the COVID-19 pandemic – United States, May-August 2020

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Risk factors associated with all-cause 30-day mortality in nursing home residents with COVID-19

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Assessing the age specificity of infection fatality rates for COVID-19: systematic review, meta-analysis, and public policy implications

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Evaluating the effect of COVID-19 pandemic lockdown on long-term care residents’ mental health: a data-driven approach in New Brunswick

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Articles

How does COVID-19 contribute to cognitive impairment in older adults and future cases of dementia?

COVID-19, Cognition, and Dementias: What Role Has the Pandemic Played?

A global health crisis is emerging because of the changing demographics and care of older adults with schizophrenia. Individuals aged 55 years and older will soon account for 25% or more of the total population of patients with schizophrenia worldwide.

 Among persons aged 60 years and older with mental and substance-use disorders, schizophrenia ranks third in causes of disability-adjusted life-years.

 Older adults with schizophrenia also have a substantial impact on health care costs, with an estimated greater expenditure per person compared with most other medical and psychiatric disorders.

Research on older patients with schizophrenia has been neglected; roughly 1% of the schizophrenia literature focuses on this population.

 With the prevalence of schizophrenia in older adults set to double and reach 1.1 million people in the US by 2025 and 10 million worldwide by 2050, greater attention to research and policy regarding this population is needed.

Older patients with schizophrenia include individuals with an early-onset that persists into later life and those with a late onset of this condition. There are currently two generations of older adults with schizophrenia: the “old-old” (those 75 years and older) and “young-old” (aged 55 to 74 years).

 Although more adults with schizophrenia are living longer, their life expectancy is still shorter than that of unaffected individuals. The risk of mortality is two to three times greater in patients with schizophrenia than in the general population, and this gap has been increasing over the past decades.

 In older adults with schizophrenia, the mortality rate and deaths caused by suicide and accidents are higher than in healthy peers.

Older persons with schizophrenia also have higher rates of congestive heart failure, chronic obstructive pulmonary disease, and hypothyroidism than unaffected peers. This is partially due to lifestyle factors such as poor diet, smoking, and physical inactivity as well as antipsychotic drug effects. Given the limited knowledge of the mechanisms underlying the increased morbidity and mortality in elderly patients with schizophrenia, further research is needed to identify modifiable clinical and social risk factors.

It has been commonly understood that positive symptoms of schizophrenia decline in later life, while negative symptoms dominate the presentation in older age. However, findings from several studies have invalidated this notion. The International Study of Schizophrenia (ISoS) assessed 18 global cohorts over 15- and 25-year periods and found 77% of patients had no evidence of significant negative symptoms over the course of their illness.

 Similarly, a longitudinal study of institutionalized geriatric patients with schizophrenia showed no significant changes in negative symptoms over time.

 From a clinical perspective, negative symptoms do not dominate in older adults with schizophrenia and are often expressed in a similar magnitude seen in younger patients.

Cognitive deficits are a fundamental feature of schizophrenia; they are observed across the life span of affected individuals and are among the strongest predictors of functional disability. Functional disability accounts for roughly half of schizophrenia treatment costs, which increase substantially later in life. Older adults with schizophrenia have significant cognitive deficits in executive functioning, speed of processing, attention/vigilance, working memory, verbal learning, visual learning, reasoning, and problem-solving.

Research has shown a heterogeneity in the trajectory of cognitive function in older patients with schizophrenia based on residential status.

 Cognitive decline in community-dwelling patients with schizophrenia is similar to that in unaffected individuals until the age of 65 to 70 years. After 70 years of age, an accelerated cognitive decline in older adults with schizophrenia cannot be ruled out. Cognitive decline is also greater in older adults with schizophrenia who had long periods of institutionalization, especially those over 65 years of age.

In a longitudinal study, three cognitive function trajectories in patients with schizophrenia were identified. They included stable cognition observed in 50% of the cohort, a slight decline in 40%, and a rapid decline in 10%. The course of cognitive decline for healthy peers is similar to the stable schizophrenia group.

Because most studies found no significant decline in cognitive function in older patients with schizophrenia compared with their healthy peers, it is believed that schizophrenia is a syndrome of premature aging. Preserving and improving cognitive function in older adults with schizophrenia are thus important objectives with significant individual and public health benefits.

Differentiating between schizophrenia and Alzheimer disease with psychosis in older adults can be difficult, but there are distinguishing features (

). The prevalence of dementia in older adults with schizophrenia is expected to increase significantly. Older individuals with schizophrenia have a two-fold increased risk of developing dementia before the age of 80 years when compared with the general population. Several factors associated with the increased risk of dementia include age, low educational attainment, premorbid cognitive dysfunction, cardiovascular disease, polypharmacy, and a history of alcohol and/or substance abuse.

The etiology of dementia in older adults with schizophrenia remains unknown. However, long-term exposure to a high anticholinergic burden is associated with cognitive deficits in individuals with and without schizophrenia. It is interesting to note that older adults with schizophrenia and a high anticholinergic burden have a cognitive impairment profile consistent with that observed in Alzheimer dementia.

The Anticholinergic Cognitive Burden scale is a useful tool to identify patients at risk for anticholinergic-related cognitive impairment.8 In older adults with schizophrenia, the anticholinergic burden should be assessed before additional medication is prescribed.

A common feature in schizophrenia is impaired insight-more than 50% of individuals have moderate to severe deficits.9 Impaired insight significantly affects health outcomes by reducing patients’ awareness of their mental disorder, its symptoms and implications, and treatment adherence. In a review that examined the effects of aging on insight into illness in adults with schizophrenia, impaired insight followed a U-shaped trajectory.

 More specifically, insight is severely impaired during the first episode of psychosis, modestly improves during midlife, and declines again in later life. The association between impaired insight and illness severity, as well as cognition, is stronger in older adults with schizophrenia than in younger patients. Noninvasive neurostimulation techniques, cognitive-enhancing medications, and early intervention to improve insight into illness should be considered for older individuals with schizophrenia.

Older adults are more susceptible than younger individuals to the adverse effects of antipsychotics. This is because of age-related pharmacokinetic changes that increase the distributed volume and elimination half-life of antipsychotic drugs, changes in the permeability of the blood-brain barrier that increase drug availability in the brain, and pharmacodynamic changes that decrease the absolute number of dopaminergic neurons and D2 receptor density in the brain. In older adults with schizophrenia, extrapyramidal symptoms occur at lower D2 receptor occupancies than in younger patients. Older age is also a risk factor for antipsychotic adverse effects such as parkinsonism, tardive dyskinesia, falls, and metabolic syndrome. These drug effects can further impair cognitive and functional capacity in older patients with schizophrenia.

Despite the limited research and challenges in using antipsychotics to treat older adults with schizophrenia, these drugs are effective in controlling psychotic symptoms. Olanzapine and risperidone are efficacious in treating older patients with non-resistant schizophrenia. We recommend risperidone as the first-line treatment in this population because olanzapine has a high anticholinergic burden. Other second-generation antipsychotics with a low anticholinergic burden should also be considered, such as aripiprazole and ziprasidone.

Because of the risk of agranulocytosis, few studies have examined the efficacy of clozapine in older patients with treatment-resistant schizophrenia. Nevertheless, we believe it is worth considering over other anti- psychotic medications that have an equally high anticholinergic burden, such as olanzapine.

In view of their adverse effects, antipsychotic drugs should be prescribed with care and at the lowest therapeutic dose. 

 lists anti- psychotic dosing regimens for older adults with schizophrenia. A helpful method to determine the appropriate dosage and minimize adverse effects is to measure a patient’s serum prolactin levels.

A longitudinal positron emission tomography study found the antipsychotic dosage can be successfully reduced in over 80% of patients with stable late-life schizophrenia.

 Moreover, a lower dosage led to fewer adverse effects and extrapyramidal symptoms, less hyperprolactinemia, and improved clinical symptoms through reduced D2/3 receptor occupancy.

A follow-up study found that reducing antipsychotic dosages by up to 40% increased D2 receptor availability in the striatum.

 This increase allows the striatum D2 receptors to contribute more significantly to cognitive function, and it can be targeted by interventions that promote cognitive enhancement in late-life schizophrenia.

The decision to start a second-generation antipsychotic in an elderly patient with dementia is not to be taken lightly. In April 2005, the FDA asked manufacturers of second-generation antipsychotics to include a “black box” warning in their label. Using clinical data, the FDA determined that elderly patients with dementia who were treated with second-generation antipsychotics for behavioral disorders had an increased risk of mortality. In June 2008, the FDA extended this warning to include first-generation antipsychotics.

Nonpharmacologic psychosocial interventions

Nonpharmacologic interventions help reduce psychotic symptoms and augment pharmacotherapy. Cognitive remediation is a behavioral intervention developed to improve cognitive deficits by repeated task practice and/or strategy acquisition. Although patients with early-stage and early-chronic schizophrenia have greater improvement in their working memory after receiving cognitive remediation than older patients, adaptations in existing programs can address the cognitive needs of older individuals.

Cognitive-behavioral therapy is another nonpharmacologic intervention widely used to resolve problems with social relatedness, positive and negative symptoms, and mood in older adults with schizophrenia. Social skills therapy has also been used in this population to treat difficulties with social interaction, while exercise programs help reduce declines in cognition and activities of daily living. The use of mobile devices to facilitate these psychosocial interventions can improve the dissemination of psychosocial interventions in the community setting.

Given the adverse effects of antipsychotic drugs in older adults with schizophrenia, alternative treatments are needed. Brain stimulation in the form of electroconvulsive therapy, transcranial magnetic stimulation, and deep brain stimulation offer viable solutions, especially in the context of medication resistance. Bilateral electroconvulsive therapy has been effective for both acute and maintenance treatment of older adults with early-onset schizophrenia, but not for older patients with late-onset schizophrenia. A pilot study of magnetic seizure therapy in patients with treatment-resistant schizophrenia showed significant clinical and quality-of-life improvement, but more trials with larger cohorts are needed.

 Unfortunately, transcranial magnetic stimulation and deep brain stimulation have not been evaluated in older adults with schizophrenia.

The current knowledge of schizophrenia in older adults reveals a different state of health compared with younger affected individuals. More research to understand the neurology underlying its clinical features, along with the development of novel age-appropriate services and treatments to improve impairments in older adults with schizophrenia, should be prioritized.

Dr Khan is Research Fellow, Centre for Addiction and Mental Health (CAMH), and Campbell Family Research Institute, and Department of Psychiatry, University of Toronto, Ontario, Canada; Dr Rajji is Deputy Physician-in-Chief, Clinical Research, and Chief, Adult Neurodevelopment and Geriatric Psychiatry, CAMH, and Campbell Family Research Institute. He is also Canada Research Chair, Neurostimulation for Cognitive Disorders, and Associate Professor of Psychiatry, University of Toronto. 

The authors report no conflicts of interest concerning the subject matter of this article.

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With the prevalence of schizophrenia in older adults set to double and reach 1.1 million people in the US by 2025, greater attention to research and policy regarding this population is needed.

Tarek K. Rajji, MD

Articles

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