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Dementia is a term used to describe a group of symptoms affecting memory, thinking and social abilities. In people who have dementia, the symptoms interfere with their daily lives. Dementia isn't one specific disease. Several diseases can cause dementia.

Dementia generally involves memory loss. It's often one of the early symptoms of the condition. But having memory loss alone doesn't mean you have dementia. Memory loss can have different causes.

Alzheimer's disease is the most common cause of dementia in older adults, but there are other causes of dementia. Depending on the cause, some dementia symptoms might be reversible.

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Dementia symptoms vary depending on the cause. Common symptoms include:

Cognitive changes

• Memory loss, which is usually noticed by someone else.
• Problems communicating or finding words.
• Trouble with visual and spatial abilities, such as getting lost while driving.
• Problems with reasoning or problem-solving.
• Trouble performing complex tasks.
• Trouble with planning and organizing.
• Poor coordination and control of movements.
• Confusion and disorientation.

Psychological changes

• Personality changes.
• Depression.
• Inappropriate behavior.
• Being suspicious, known as paranoia.
• Seeing things that aren't there, known as hallucinations.

When to see a doctor

See a health care professional if you or a loved one has memory problems or other dementia symptoms. It's important to determine the cause. Some medical conditions that cause dementia symptoms can be treated.

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Dementia is caused by damage to or loss of nerve cells and their connections in the brain. The symptoms depend on the area of the brain that's damaged. Dementia can affect people differently.

Dementias are often grouped by what they have in common. They may be grouped by the protein or proteins deposited in the brain or by the part of the brain that's affected. Also, some diseases have symptoms like those of dementia. And some medicines can cause a reaction that includes dementia symptoms. Not getting enough of certain vitamins or minerals also can cause dementia symptoms. When this occurs, dementia symptoms may improve with treatment.

Progressive dementias

Dementias that are progressive get worse over time. Types of dementias that worsen and aren't reversible include:

Alzheimer's disease. This is the most common cause of dementia.

Although not all causes of Alzheimer's disease are known, experts do know that a small percentage are related to changes in three genes. These gene changes can be passed down from parent to child. While several genes are probably involved in Alzheimer's disease, one important gene that increases risk is apolipoprotein E4 ( APOE ).

People with Alzheimer's disease have plaques and tangles in their brains. Plaques are clumps of a protein called beta-amyloid. Tangles are fibrous masses made up of tau protein. It's thought that these clumps damage healthy brain cells and the fibers connecting them.

Vascular dementia. This type of dementia is caused by damage to the vessels that supply blood to the brain. Blood vessel problems can cause stroke or affect the brain in other ways, such as by damaging the fibers in the white matter of the brain.

The most common symptoms of vascular dementia include problems with problem-solving, slowed thinking, and loss of focus and organization. These tend to be more noticeable than memory loss.

Lewy body dementia. Lewy bodies are balloonlike clumps of protein. They have been found in the brains of people with Lewy body dementia, Alzheimer's disease and Parkinson's disease. Lewy body dementia is one of the more common types of dementia.

Common symptoms include acting out dreams in sleep and seeing things that aren't there, known as visual hallucinations. Symptoms also include problems with focus and attention. Other signs include uncoordinated or slow movement, tremors, and stiffness, known as parkinsonism.

• Frontotemporal dementia. This is a group of diseases characterized by the breakdown of nerve cells and their connections in the frontal and temporal lobes of the brain. These areas are associated with personality, behavior and language. Common symptoms affect behavior, personality, thinking, judgment, language and movement.
• Mixed dementia. Autopsy studies of the brains of people age 80 and older who had dementia indicate that many had a combination of several causes. People with mixed dementia can have Alzheimer's disease, vascular dementia and Lewy body dementia. Studies are ongoing to determine how having mixed dementia affects symptoms and treatments.

Other disorders linked to dementia

• Huntington's disease. Huntington's disease is caused by a genetic change. The disease causes certain nerve cells in the brain and spinal cord to waste away. Symptoms include a decline in thinking skills, known as cognitive skills. Symptoms usually appear around age 30 or 40.

Traumatic brain injury (TBI). This condition is most often caused by repetitive head trauma. Boxers, football players or soldiers might develop TBI .

Dementia symptoms depend on the part of the brain that's injured. TBI can cause depression, explosiveness, memory loss and impaired speech. TBI also may cause slow movement, tremors and stiffness. Symptoms might not appear until years after the trauma.

Creutzfeldt-Jakob disease. This rare brain disorder usually occurs in people without known risk factors. This condition might be due to deposits of infectious proteins called prions. Symptoms of this fatal condition usually appear after age 60.

Creutzfeldt-Jakob disease usually has no known cause but it can be passed down from a parent. It also may be caused by exposure to diseased brain or nervous system tissue, such as from a cornea transplant.

• Parkinson's disease. Many people with Parkinson's disease eventually develop dementia symptoms. When this happens, it's known as Parkinson's disease dementia.

Dementia-like conditions that can be reversed

Some causes of dementia-like symptoms can be reversed with treatment. They include:

• Infections and immune disorders. Dementia-like symptoms can result from a fever or other side effects of the body's attempt to fight off an infection. Multiple sclerosis and other conditions caused by the body's immune system attacking nerve cells also can cause dementia.
• Metabolic or endocrine problems. People with thyroid problems and low blood sugar can develop dementia-like symptoms or other personality changes. This also is true for people who have too little or too much sodium or calcium, or problems absorbing vitamin B-12.
• Low levels of certain nutrients. Not getting enough of certain vitamins or minerals in your diet can cause dementia symptoms. This includes not getting enough thiamin, also known as vitamin B-1, which is common in people with alcohol use disorder. It also includes not getting enough vitamin B-6, vitamin B-12, copper or vitamin E. Not drinking enough liquids, leading to dehydration, also can cause dementia symptoms.
• Medicine side effects. Side effects of medicines, a reaction to a medicine or an interaction of several medicines can cause dementia-like symptoms.
• Subdural bleeding. Bleeding between the surface of the brain and the covering over the brain can be common in older adults after a fall. Subdural bleeding can cause symptoms similar to those of dementia.
• Brain tumors. Rarely, dementia can result from damage caused by a brain tumor.
• Normal-pressure hydrocephalus. This condition is a buildup of fluid in the cavities in the brain known as ventricles. It can result in walking problems, loss of bladder control and memory loss.

Risk factors

Many factors can eventually contribute to dementia. Some factors, such as age, can't be changed. You can address other factors to reduce your risk.

Risk factors that can't be changed

• Age. The risk of dementia rises as you age, especially after age 65. However, dementia isn't a typical part of aging. Dementia also can occur in younger people.
• Family history. Having a family history of dementia puts you at greater risk of developing the condition. However, many people with a family history never develop symptoms, and many people without a family history do. There are tests to determine whether you have certain genetic changes that may increase your risk.
• Down syndrome. By middle age, many people with Down syndrome develop early-onset Alzheimer's disease.

Risk factors you can change

You might be able to control the following risk factors for dementia.

• Diet and exercise. Research has found that people at higher risk of dementia who followed a healthy lifestyle lowered their risk of cognitive decline. They ate a diet that included fish, fruits, vegetables and oils. They also exercised, had cognitive training and participated in social activities. While no specific diet is known to reduce dementia risk, research indicates that those who follow a Mediterranean style diet rich in produce, whole grains, nuts and seeds have better cognitive function.
• Drinking too much alcohol. Drinking large amounts of alcohol has long been known to cause brain changes. Several large studies and reviews found that alcohol use disorders were linked to an increased risk of dementia, particularly early-onset dementia.
• Cardiovascular risk factors. These include obesity, high blood pressure, high cholesterol, and the buildup of fats in the artery walls, known as atherosclerosis. Diabetes and smoking also are cardiovascular risk factors. Having diabetes can increase the risk of dementia, especially if it's poorly controlled. Smoking might increase the risk of developing dementia and blood vessel disease.
• Depression. Although not yet well understood, late-life depression might indicate the development of dementia.
• Air pollution. Studies in animals have indicated that air pollution particulates can speed degeneration of the nervous system. And human studies have found that air pollution exposure — particularly from traffic exhaust and burning wood — is associated with greater dementia risk.
• Head trauma. People who've had a severe head trauma have a greater risk of Alzheimer's disease. Several large studies found that in people age 50 years or older who had a traumatic brain injury (TBI), the risk of dementia and Alzheimer's disease increased. The risk increases in people with more-severe and multiple TBIs . Some studies indicate that the risk may be greatest within the first six months to two years after the TBI .
• Sleep problems. People who have sleep apnea and other sleep disturbances might be at higher risk of developing dementia.
• Low levels of certain vitamins and nutrients. Low levels of vitamin D, vitamin B-6, vitamin B-12 and folate can increase the risk of dementia.

Medicines that can worsen memory. These include sleep aids that contain diphenhydramine (Benadryl) and medicines to treat urinary urgency such as oxybutynin (Ditropan XL).

Also limit sedatives and sleeping tablets. Talk to a health care professional about whether any of the medicines you take might make your memory worse.

Complications

Dementia can affect many body systems and, therefore, the ability to function. Dementia can lead to:

• Poor nutrition. Many people with dementia eventually reduce or stop eating, affecting their nutrient intake. Ultimately, they may be unable to chew and swallow.
• Pneumonia. Trouble swallowing increases the risk of choking. And food or liquids can enter the lungs, known as aspiration. This can block breathing and cause pneumonia.
• Inability to perform self-care tasks. As dementia gets worse, people have a hard time bathing, dressing, and brushing their hair or teeth. They need help using the toilet and taking medicines as directed.
• Personal safety challenges. Some day-to-day situations can present safety issues for people with dementia. These include driving, cooking, and walking and living alone.
• Death. Coma and death can occur in late-stage dementia. This often happens because of an infection.

There's no sure way to prevent dementia, but there are steps you can take that might help. More research is needed, but it might be beneficial to do the following:

• Keep your mind active. Mentally stimulating activities might delay the onset of dementia and decrease its effects. Spend time reading, solving puzzles and playing word games.
• Be physically and socially active. Physical activity and social interaction might delay the onset of dementia and reduce its symptoms. Aim for 150 minutes of exercise a week.
• Quit smoking. Some studies have shown that smoking in middle age and beyond might increase the risk of dementia and blood vessel conditions. Quitting smoking might reduce the risk and improve health.

Get enough vitamins. Some research suggests that people with low levels of vitamin D in their blood are more likely to develop Alzheimer's disease and other forms of dementia. You can increase your vitamin D levels with certain foods, supplements and sun exposure.

More study is needed before an increase in vitamin D intake is recommended for preventing dementia. But it's a good idea to make sure you get adequate vitamin D. Taking a daily B-complex vitamin and vitamin C also might help.

Manage cardiovascular risk factors. Treat high blood pressure, high cholesterol and diabetes. Lose weight if you're overweight.

High blood pressure might lead to a higher risk of some types of dementia. More research is needed to determine whether treating high blood pressure may reduce the risk of dementia.

• Treat health conditions. See your doctor for treatment of depression or anxiety.
• Maintain a healthy diet. A diet such as the Mediterranean diet might promote health and lower the risk of developing dementia. A Mediterranean diet is rich in fruits, vegetables, whole grains and omega-3 fatty acids, which are commonly found in certain fish and nuts. This type of diet also improves cardiovascular health, which also may help lower dementia risk.
• Get good-quality sleep. Practice good sleep hygiene. Talk to a health care professional if you snore loudly or have periods where you stop breathing or gasp during sleep.
• Treat hearing problems. People with hearing loss have a greater chance of developing problems with thinking, known as cognitive decline. Early treatment of hearing loss, such as use of hearing aids, might help decrease the risk.

Dementia care at Mayo Clinic

• What is dementia? Alzheimer's Association. https://www.alz.org/alzheimers-dementia/what-is-dementia. Accessed April 24, 2023.
• Dementias. https://www.ninds.nih.gov/Disorders/Patient-Caregiver-Education/Hope-Through-Research/Dementia-Hope-Through-Research. Accessed April 24, 2023.
• Larson EB. Evaluation of cognitive impairment and dementia. https://www.uptodate.com/contents/search. Accessed April 24, 2023.
• Rao RV, et al. Rationale for multi-factorial approach for the reversal of cognitive decline in Alzheimer's disease and MCI: A review. International Journal of Molecular Sciences. 2023; doi:10.3390/ijms24021659.
• Press D, et al. Management of the patient with dementia. https://www.uptodate.com/contents/search. Accessed April 24, 2023.
• Livingston G, et al. Dementia prevention, intervention, and care: 2020 report of the Lancet Commission. The Lancet. 2020; doi:10.1016/S0140-6736(20)30367-6.
• Luo G, et al. Effectiveness of non-pharmacological therapies on cognitive function in patients with dementia — A network meta-analysis of randomized controlled trials. Frontiers in Aging: Neuroscience. 2023; doi:10.3389/fnagi.2023.1131744.
• Creutzfeldt-Jakob disease, classic (CJD): Occurrence and transmission. Centers for Disease Control and Prevention. https://www.cdc.gov/prions/cjd/occurrence-transmission.html?CDC_AA_refVal=https%3A%2F%2Fwww.cdc.gov%2Fprions%2Fcjd%2Foccurance-transmisison.html. Accessed April 24, 2023.
• Palimariciuc M, et al. The quest for neurodegenerative disease treatment — Focusing on Alzheimer's disease personalised diets. Current Issues in Molecular Biology. 2023; doi:10.3390/cimb45020098.
• Dementia. Merck Manual Professional Version. https://www.merckmanuals.com/professional/neurologic-disorders/delirium-and-dementia/dementia. Accessed April 24, 2023.
• Press D, et al. Prevention of dementia. https://www.uptodate.com/contents/search. Accessed April 24, 2023.
• Sleep issues and sundowning. Alzheimer's Association. https://www.alz.org/help-support/caregiving/stages-behaviors/sleep-issues-sundowning. Accessed May 2, 2023.
• Medications for memory. Alzheimer's Association. https://www.alz.org/alzheimers-dementia/treatments/medications-for-memory. Accessed April 24, 2023.
• How to communicate with a person with dementia. Alzheimer's Society. https://www.alzheimers.org.uk/about-dementia/symptoms-and-diagnosis/symptoms/tips-for-communicating-dementia. Accessed April 24, 2023.
• Press D, et al. Management of neuropsychiatric symptoms of dementia. https://www.uptodate.com/search/contents. Accessed May 2, 2023.
• Leqembi (approval letter). Biologic License Application 761269. U.S. Food and Drug Administration. https://www.accessdata.fda.gov/scripts/cder/daf/index.cfm?event=overview.process&ApplNo=761269. Accessed July 7, 2023.
• Lecanemab approved for treatment of early Alzheimer's disease. Alzheimer's Association. https://www.alz.org/alzheimers-dementia/treatments/lecanemab-leqembi. Accessed May 4, 2023.
• Van Dyck CH, et al. Lecanemab in early Alzheimer's disease. New England Journal of Medicine. 2023; doi:10.1056/NEJMoa2212948.
• Shi M, et al. Impact of anti-amyloid-β monoclonal antibodies on the pathology and clinical profile of Alzheimer's disease: A focus on aducanumab and lecanemab. Frontiers in Aging and Neuroscience. 2022; doi:10.3389/fnagi.2022.870517.
• Cummings J, et al. Alzheimer's disease drug development pipeline: 2022. Alzheimer's and Dementia. 2022; doi:10.1002/trc2.12295.
• Oxybutynin oral. Facts & Comparisons eAnswers. https://fco.factsandcomparisons.com. Accessed April 28, 2023.
• Diphenhydramine oral. Facts & Comparisons eAnswers. https://fco.factsandcomparisons.com. Accessed April 28, 2023.
• Rashad A, et al. Donanemab for Alzheimer's disease: A systematic review of clinical trials. Healthcare. 2022; doi:10.3390/healthcare11010032.
• Budson AE, et al. Cholinesterase inhibitors. In: Memory Loss, Alzheimer's Disease, and Dementia. 3rd ed. Elsevier; 2022. https://www.clinicalkey.com. Accessed May 4, 2023.
• Leqembi (prescribing information). Eisai; 2023. https://www.accessdata.fda.gov/scripts/cder/daf/index.cfm?event=overview.process&varApplNo=761269. Accessed July 10, 2023.
• Mintun MA, et al. Donanemab in early Alzheimer's disease. New England Journal of Medicine. 2021; doi:10.1056/NEJMoa2100708.
• Graff-Radford J (expert opinion). Mayo Clinic. May 15, 2023.
• Ami TR. Allscripts EPSi. Mayo Clinic. May 17, 2023.
• Limbic-predominant age-related TDP-43 encephalopathy (LATE)

Associated Procedures

• Complete blood count (CBC)
• EEG (electroencephalogram)

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The 7 Stages of Dementia: What to Expect

Sanjana is a health writer and editor. Her work spans various health-related topics, including mental health, fitness, nutrition, and wellness.

Shaheen Lakhan, MD, PhD, is an award-winning physician-scientist and clinical development specialist.

Catherine Falls Commercial / Getty Images

Dementia is marked by a severe decline in cognitive functions, such as thinking, reasoning, and remembering, to the extent that it interferes with the person's daily life.

Dementia typically affects older adults, but it is not a normal part of the aging process—while some amount of forgetfulness is normal with age, dementia is a severe disorder that can affect the person’s ability to function on a daily basis.

According to the National Institute on Aging, about one-third of all people above the age of 85 have some form of dementia. Dementia can stem from various causes, the most common being Alzheimer’s disease . Some of the other causes include Parkinson’s disease , Lewy body dementia , and frontotemporal dementia.

Dementia progresses in stages, ranging from mild to severe. In 1982, Dr. Barry Reisberg created the Global Deterioration Scale (GDS), consisting of seven stages, to help clinicians categorize the progression of dementia.

This article explores the seven stages of dementia, so you know what to expect if you or a loved one have been diagnosed with it.

The stages are as follows:

• No cognitive decline
• Very mild cognitive decline
• Mild cognitive decline
• Moderate cognitive decline
• Moderately severe cognitive decline
• Severe cognitive decline
• Very severe cognitive decline

Stages 1 to 3 are the pre-dementia stages; whereas Stages 4 to 7 are the dementia stages. Clinicians typically compare the person’s symptoms to the criteria listed for each stage and use their judgment to determine which stage the patient is at.

The 7 Stages of Dementia

The seven stages of dementia are outlined below.

Stage 1: No Cognitive Decline

At this stage, the person is able to function normally and doesn’t exhibit any signs of memory loss, confusion, or cognitive impairment.

However, the structure and functioning of their brain may have started to deteriorate, as the neurons (nerve cells) in their brain start to lose connection with other brain cells and die.

Stage 2: Very Mild Cognitive Decline

The person starts to experience occasional lapses of memory , such as:

• Forgetting where they keep familiar everyday objects
• Forgetting names they once knew very well

At this stage, the symptoms are unlikely to affect the person’s work or social interactions. 

In fact, the symptoms may even be too mild to detect in a clinical interview with a healthcare provider, as the person may be able to adequately perform memory tests during the interview. 

Stage 3: Mild Cognitive Decline

This is the stage where cognitive impairment starts to become more noticeable to the patient, as well as their friends, family members, and colleagues.

The person may start to show symptoms such as:

• Getting lost while walking or driving, particularly in unfamiliar places
• Reading something and retaining very little of it
• Forgetting the names of people they’ve just met
• Losing items of importance or value
• Having trouble concentrating and performing complex tasks
• Experiencing increasing difficulty in social settings
• Frequently forgetting words and the names of loved ones
• Performing poorly at work, to the extent that it becomes evident to colleagues

The person may start to feel anxious as their symptoms start to become apparent and interfere with their ability to function. 

Stage 4: Moderate Cognitive Decline

In this stage, the person will exhibit a definitive decline in cognitive ability in a clinical interview.

Some of the symptoms of this stage may include:

• Lack of knowledge of current and recent events
• Difficulty remembering parts of their own personal history
• Trouble with organizing, planning, traveling, and managing finances

At this stage, the person will likely still be able to recognize loved ones’ names and faces, and be able to navigate familiar places. However, they may start to avoid challenging situations in order to prevent anxiety and hide their distress from others.

Stage 5: Moderately Severe Cognitive Decline

From this stage onward, the person may no longer be able to function without some assistance. 

These are some of the symptoms of this stage:

• Difficulty recalling an important detail such as their address, phone number, or high school
• Disorientation in terms of place and time, such as confusion regarding the season, date, day of the week, or time of day
• Difficulty counting backward from 20 by 2s or from 40s by 4s (provided they are educated and were once able to do this calculation)
• Trouble with making decisions

In this stage, the person can likely still remember their own name and the names of their spouse and children, but they may struggle with recalling the names of their grandchildren. They may be able to eat and use the bathroom without assistance, but may need help with tasks such as deciding what to wear.

Stage 6: Severe Cognitive Decline

At this stage, the person may require a high degree of care , as they may have symptoms such as:

• Difficulty remembering the names of their spouse, children, or primary caregivers
• Lack of awareness regarding all the recent events and experiences in their life
• Patchy or skewed recollection of their early life
• Difficulty counting backward or forward to 10
• Lack of awareness regarding their surroundings as well as the time and place
• Inability to travel alone without assistance
• Tendency to wander

The person is also likely to experience emotional and personality changes, such as:

• Paranoia , hallucinations , and delusional behavior , such as talking to themselves or believing their caregivers are trying to harm them
• Obsessive symptoms, such as repeatedly performing cleaning activities
• Agitation, anxiety, and even violent behavior
• Loss of willpower, due to being unable to carry a thought long enough to complete the action

During this stage, the person is likely to still be able to remember their name, as well as distinguish between familiar and unfamiliar people in their environment. They will probably need assistance with daily living activities and may experience incontinence as well as sleep-related difficulties.

Stage 7: Very Severe Cognitive Decline

In the final stage, the brain appears to lose its connection to the body and becomes incapable of telling it what to do. 

The person is likely to progressively lose their motor skills as well as the ability to speak. They may only be able to utter unintelligible sounds or words, if at all. They will need assistance with all personal care tasks such as eating, walking, and using the bathroom.

A Word From Verywell

Dementia is a challenging condition to live with because it increasingly affects the person’s mental faculties and ability to function. Being aware of how the condition progresses can be useful because it can help you take steps to slow it down, in addition to helping you understand what to expect and how to prepare for it.

National Institute on Aging. What is dementia?

National Library of Medicine. Dementia . Medline Plus .

Centers for Disease Control and Prevention. About dementia .

Stanford Medicine Health Care. Dementia causes .

Reisberg B, Ferris SH, de Leon MJ, Crook T. The Global Deterioration Scale for assessment of primary degenerative dementia . Am J Psychiatry . 1982;139(9):1136-1139. doi:10.1176/ajp.139.9.1136

Florida Health Care Association. The Global Deterioration Scale for assessment of primary degenerative dementia .

American Physical Therapy Association. Global Deterioration Scale for assessment of primary degenerative dementia .

Beason-Held LL, Goh JO, An Y, et al. Changes in brain function occur years before the onset of cognitive impairment . J Neurosci . 2013;33(46):18008-18014. doi:10.1523/JNEUROSCI.1402-13.2013

By Sanjana Gupta Sanjana is a health writer and editor. Her work spans various health-related topics, including mental health, fitness, nutrition, and wellness.

• Last edited on October 3, 2022

Introduction to Dementia

Table of contents, normal aging and cognition, rapidly progressive dementias, common dementias, rare dementias, mixed presentations, behavioural and psychological symptoms of dementia, dementia, depression, or delirium, neuroimaging.

Dementia is a syndrome characterized by progressive neurocognitive decline of sufficient magnitude to interfere with normal social or occupational functions, or with usual daily activities. It is a broad diagnostic category that includes Alzheimer's disease , Lewy Body dementia , frontotemporal dementia , vascular dementia , Parkinson's disease , and Creutzfeldt–Jakob disease (among many others). It also includes rapidly progressive dementias that may be fully reversible if the etiology is correctly identified.

Epidemiology

• The incidence of dementia then doubles every 5 years after age 65. [2]
• By age 85, between 25% and 50% of people will exhibit signs of Alzheimer's disease.
• The percentage of all dementias due to Alzheimer's disease is at least 50% (with some estimates suggesting 60-90%).
• Females with dementia outnumber males by 2 to 1
• Alzheimer's Disease (AD) , average 11.7 years
• Frontotemporal Dementia (FTD) average 11 years
• Corticobasal Degeneration (CBD) average 11.8 years
• Progressive Supranuclear Palsy (PSP) average 5.6 years
• Dementia with Lewy Bodies (DLB) , average 3 years
• Decline in problem-solving, processing speed, and minor delays in word-finding can be common in normal ageing. Retrieval-type memory deficits are also commonly reported. In contrast to dementia, semantic memory and visuospatial functioning is generally preserved.

About 35%-40% of dementia cases are attributable to 9 modifiable factors across the lifespan. [4] These factors include: [5] More recently, the 2020 Lancet Commission on Dementia Prevention, Intervention and Care now include 12 potentially modifiable risk factors across the lifespan that can contribute to dementia: [6]

• Less education
• Hypertension
• Hearing loss
• Traumatic brain injury
• Alcohol misuse
• Physical inactivity
• Social isolation
• Air pollution

There remains debate as to how many cases of dementia with modifiable risk factors can truly be prevented even with risk factor modification. [7]

The World Health Organization (WHO) Dementia Prevention Guidelines

• Physical exercise (there is some conflicting data [9] )
• Tobacco cessation
• Reduce harmful drinking
• Lose excess weight in midlife
• Adhere to healthy diet (a Mediterranean-style diet may reduce dementia risk)
• Cognitive training can be tried for adults with normal cognition or mild impairment (but the quality of evidence to support this is low)
• Social participation and support are important throughout life (but limited evidence to support)
• Hypertension, diabetes, and depression should be managed according to existing guidelines (but it is not clear whether doing so will specifically lower dementia risk)

Dietary supplementation to prevent dementia has been a source of controversy due to a lack of convincing evidence from current studies, low quality studies, and multiple confounders in dietary research. [10] Vitamins B and E, polyunsaturated fatty acids, and multivitamins are not recommended for risk reduction of dementia. [11] [12]

Approach to Dementia

When seeing a patient with a non-rapidly progressive dementia (otherwise, see the rapidly progressive dementia approach below), it is good to have a systematic approach. The following is one approach: [13]

• Urinary tract infections are common in the elderly and can be causes of delirium! Additionally, a negative urine culture does not always mean there is no UTI, especially if the patient has classic symptoms of a UTI. [14] On the other hand, however, asymptomatic bacteriuria should not be treated with an antibiotic, due to adverse risks such as C. Diff infections and lack of evidence for changing outcomes. [15]
• Rule out depression (“pseudodementia”). Consider atypical presentations: anxiety, irritability, unexplained physical complaints, worsening cognition. Once the depression is treated, the dementia symptoms go away!
• Rule out any substance use disorders
• CBC (to rule out anaemia and some cancers that can may present with fatigue, weight loss, and other depressive symptoms)
• TSH (to rule out hypothyroidism that can cause a depressive syndrome)
• Creatinine (to rule out renal disease that can present with fatigue, weight loss, poor concentration, and other depressive symptoms, and to assess for overall renal function)
• Sodium, in particular for hyponatremia (which can present with fatigue, poor concentration, and other depressive symptoms)
• Calcium ( hypercalcemia may result in neuropsychiatric symptoms including psychosis and depression)
• Parathyroid hormone (PTH) and vitamin D (because increased PTH and decreased vitamin D may be associated with depressive symptoms)
• Glucose (to rule out diabetes that can present with fatigue, weight loss, and other depressive symptoms)
• Ferritin/iron (for fatigue and cognitive impairment)
• Vitamin B12 (to rule out low B12 that can cause a depressive syndrome)
• Folate level (to rule out low folates that can cause a depressive syndrome)
• Neuroimaging such as CT or MRI
• VDRL (screening for syphillis )
• HIV (for HIV-associated neuropsychiatric presentations or HIV-associated cognitive impairment)
• Serum albumin (to assess nutritional status and rule out diseases that can present with depressive symptoms)
• Medication-induced “dementia”
• Is there polypharmacy that could be contributing to the cognitive impairment?
• Is there the use of any anticholinergic medications (and anticholinergic toxicity ?)
• e.g. - steroid dementia syndrome related to glucocorticoid use.
• Do a neurological exam if appropriate
• Consider other neurological disorders including normal pressure hydrocephalus
• Major neurocognitive disorder (dementia): objective findings of cognitive loss with impairment of ADLs
• Mild cognitive impairment : objective findings of cognitive loss without impairment of ADLs
• Normal cognitive aging: no objective findings of cognitive loss

Rapidly Progressive Dementias (RPDs) are dementias that progress quickly – over the course of weeks to months (in rarer cases, may be over a period of 1-2 years). [16] Treatment of an RPD is dependent on the etiology of the dementia, some of which are fully treatable. This makes early recognition critical. Broadly, RPDs can be broken down into different etiologies:

• Prion disease (e.g. - Creutzfeldt-Jakob Disease (CJD) )
• Neurodegenerative diseases (e.g. - early onset Alzheimer's Disease (AD) )
• Psychiatric
• Toxic-Metabolic
• Leukoencephalopathies (e.g. - Multiple Sclerosis (MS) , Progressive Multifocal Leukoencephalopathy)
• V - Vascular
• I - Infectious
• T - Toxic-Metabolic
• A - Autoimmune
• M - Metastasis/Neoplastic
• I - Iatrogenic
• N - Neurodegenerative
• S - Systemic/Seizures

The most common dementia subtypes are below:

Common Dementia Subtypes and Presentation

Rarer dementia subtypes include the following:

Rare Dementia Subtypes and Presentation

Dementia is often due to more than one pathology. Some studies have shown that in a general population, 40% of patients have a combination of Alzheimer's Disease (AD) and vascular dementia , while only 30% had pure Alzheimer's and 12% had pure vascular dementia (VaD). About 12% had Alzheimer's combined with Parkinsons's Disease Dementia (PDD) (PD) or Dementia with Lewy Bodies (DLB) . [21]

Behavioural and Psychological Symptoms of Dementia (BPSD) will develop in more than 90% of individuals diagnosed with dementia. Symptoms include delusions, hallucinations, aggression, screaming, restlessness, wandering, depression, and anxiety.

• In the geriatric population, it is important to differentiate between delirium, dementia, and depression, which can be difficult to distinguish. [22] [23] [24] The prevalence of delirium superimposed on dementia ranges anywhere from 22% to 89% of hospitalized and community populations aged 65 and older with dementia.
• The negative outcomes of these co-occurring conditions include accelerated and long-term cognitive, functional decline, institutionalization, re-hospitalization, and increased mortality. [25]

A Comparison of Delirium, Dementia, and Depression

For older patients with cognitive symptoms, neuroimaging ( MRI preferred over CT ) is recommended if the following criteria is present: [26] [27]

• Onset of cognitive signs/symptoms within the past 2 years, regardless of the rate of progression
• Unexpected and unexplained decline in cognition and/or functional status in a patient already known to have dementia
• Recent and significant head trauma
• Unexplained neurological manifestations (new onset severe headache, seizures, Babinski sign, etc.), at onset or during evolution (this also includes gait disturbances)
• History of cancer, in particular if at risk for brain metastases
• Risk for intracranial bleeding
• Symptoms suggestive of normal pressure hydrocephalus
• Significant vascular risk factors
• Unusual or atypical cognitive symptoms or presentation (e.g. progressive aphasia)

Dementia Guidelines

For patients/family.

• UCSF: What is Dementia?
• iGeriCare - Online Resource For Patients/Family
• Regional Geriatric Progam of Toronto Resources
• YouTube: 1929 - Interviews With Elderly People Throughout The US

For Providers

• Continuum: Behavioral Neurology and Psychiatry June 2018, Volume 24, Issue 3
• Balogh, K., & Wong, R. Y. (2017). Twelve tips for assessing and managing mild cognitive impairment and major neurocognitive disorder in older people. British Columbia Medical Journal, 59(3), 158-164.
• Lee, L., Weston, W. W., Heckman, G., Gagnon, M., Lee, F. J., & Sloka, S. (2013). Structured approach to patients with memory difficulties in family practice. Canadian Family Physician, 59(3), 249-254.

Articles/News

• Toronto Star: The Fix - Dementia Butterfly Program

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RELATED TOPICS

INTRODUCTION

This topic reviews the clinical manifestations and diagnosis of AD. Other topics review the risk factors and treatment of AD:

● (See "Epidemiology, pathology, and pathogenesis of Alzheimer disease" .)

● (See "Treatment of Alzheimer disease" .)

Other topics review the approach to patients with cognitive impairment and dementia and the clinical features of other dementia syndromes:

What is Dementia? Presentation

Dementia is a syndrome that affects memory, thinking, behavior, and the ability to perform everyday tasks. It is often caused by progressive disorders and can be caused by a variety of factors, including age and genetics.

Diane Carbo

Discover the World of Dementia

Want to know more about dementia? It's a complex syndrome that affects memory, thinking, behavior, and everyday tasks. Join us as we explore the various types of dementia, including the most common one: Alzheimer's disease.

Unraveling the Causes of Dementia

What leads to dementia? While the exact cause is unknown, factors like age, family history, cardiovascular disease, and head trauma play a role in its development. Understanding the areas of the brain that are affected can help in planning future care.

The Most Common Types of Dementia

Alzheimer's disease, Lewy body dementia, vascular dementia, Fronto temporal lobe dementia, and mixed dementia are some of the most common types. Recognizing the early signs of multiple types of dementia is vital for early treatment, which can slow down cognitive decline.

Top Symptoms of Dementia

Forgetfulness, word-finding problems, changes in personality, difficulty with abstract thinking, trouble completing tasks, disorientation, poor judgment, and memory lapses are the key symptoms to look out for in dementia. Timely awareness and intervention are crucial.

Unveiling the Reality of Dementia

Living with dementia can be challenging, and some symptoms may go unnoticed or be concealed. It may take time for changes to become apparent. Your primary care doctor will guide you through medical history and diagnostic tests to ensure accurate diagnosis and care.

Word Finding or Word Confusion

Another symptom are word-finding problems or word confusion. It is normal for anyone to occasionally blank on a word. It is considered a red flag for all timers. If this happens with growing frequency, and if the words are simple or commonplace, Replacing the right word for another word is also a sign of dementia.

These are symptoms of dementia that occur early in the disease process.

Major changes in personality or mood.

The first sign of changes in personality, maybe withdrawal a person that is quiet, maybe more aggressive or vice versa, some develop uncharacteristic fears of new or unknown environment or situations. Others develop a distrust of others, whether strangers or familiar people.

Difficulty with abstract thinking

Another symptom of dementia is trouble with abstract thinking. Abstract thinking is the ability to think. And imagine in the terms of ideas, there is an increased difficulty in performing tasks that were once easy, such as shopping or balancing the checkbook. Another symptom of dementia.

Difficulty completing familiar tasks.

A common symptom of dementia is exhibited. When a person does not finish a task or an activity that is something they formerly enjoyed or used to engage in frequently. Some may become confused or distracted and do not return to finish.

Disorientation

Another symptom is disorientated. A person with dementia begins to be disoriented in new or unfamiliar environments.

They may wander off and get lost in public or get lost when driving or after parking the car. They may lose track of the time, day, month, or even the year. They may start to have trouble keeping appointments and remembering other reasons. Or commitments, another symptom is misplacing or losing items with our busy lifestyles.

We all have moments when we forgot where we place something. It is a problem when a person loses things often or misplaces them in unusual places, such as finding car keys in the refrigerator.

Poor or Impaired Judgement

Another symptom is poor or impaired judgment, poor or impaired judgment may exhibit as difficulty with decision making. This can also be related to other possible symptoms of dementia, such as lapses in memory, personality, changes and trouble with abstract thinking inappropriate choices are worrisome.

As unsound decisions affect personal safety, health, and finances. Many of these symptoms go in notice for a long period of time, especially in all timers disease. This is because the symptoms are often subtle or even well concealed by the person experiencing them. Many of them diagnosed with dementia symptoms, maybe aware of some of the changes that are occurring.

But denial and the ability to compensate to hide some of these symptoms may take some time for some patterns of behavior to make themselves obvious to others of gnosis and tests for dementia. Your primary care doctor will first do a complete medical history. There will also be questions about familial history to determine if there is a history of dementia in the family.

Accurate Diagnosis: Essential Tests for Memory Impairment

Discover the truth behind memory problems with specialized tests ordered by doctors. These tests rule out other medical conditions and determine the potential contributing factors. A brain scan may also be conducted. Find out if you're at risk for dementia with a variety of paper-and-pencil tests.

Enhanced Tests for Memory and Thinking

Uncover the full scope of your cognitive abilities with neuropsychological tests. These evaluations assess various brain functions, including memory, orientation, ability to follow instructions, and object recognition. The most commonly used tests are the Mini-Mental Status Exam (MMSE) and the St. Louis University Mental Status Exam (SLUMS).

Don't Jump to Conclusions

Memory problems don't automatically mean dementia. Various treatable medical conditions can cause similar symptoms, such as depression, drug interactions, thyroid problems, and excessive alcohol use. Even a urinary tract infection or certain vitamin deficiencies can lead to confusion. If diagnosed, these illnesses can be treated and the dementia-like symptoms reversed.

Treating the Symptoms

While there is currently no cure for dementia or Alzheimer's disease, treatments are available to manage symptoms, including memory problems. These treatments may also slow cognitive decline and address other symptoms as needed. With a cure for dementia still far off, it's time to focus on providing the best care possible to those suffering from this devastating condition.

A Person-Centered Approach

When it comes to dementia care, it's important to view the individual as more than just a disease or diagnosis. Person-centered care prioritizes the unique needs and preferences of the person with dementia, ensuring they receive personalized and respectful care. Family-centered care also recognizes the importance of supporting the caregiver along with the patient.

Person Centered Dementia Care explained

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Dementia Clinical Case

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Dementia is a word used to designate a set of symptoms that severely affect thinking, social skills, and memory. It is not a specific disease, but a consequence of other factors, such as aging (does not always cause dementia) or Alzheimer's disease (the most common cause of dementia). We are sure you already know all this information, and if you want to continue researching this topic or make a presentation on dementia, use the template we have specially designed to present a clinical case on this disease, which will serve to clarify facts or contribute to research.

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6.9 million Americans have Alzheimer's disease: How to reduce your risk

A new report estimates 6.9 million older Americans are living with Alzheimer’s disease in 2024, an increase of about 200,000 cases of the mind-robbing disease from 2023 and "a significant public health crisis," according to an expert.

Another 5 million to 7 million adults have mild cognitive impairment, a set of early changes to memory and thinking linked to Alzheimer's, according to an Alzheimer's Association's annual facts and figures report released Wednesday.

The report also highlights good news. Other studies indicate that dementia rates have declined over the past 25 years as more adults are achieving higher levels of education, staying active and exercising, reducing their blood pressure, avoiding cigarettes and staying socially engaged.

Adults face a higher risk of Alzheimer's and other types of dementia as they age, and the number of Americans 65 and older is projected to swell from 58 million in 2022 to 82 million in 2050. In just six years, the youngest baby boomers will be 65.

The nation's aging population will create profound economic and social challenges. The annual cost of caring for people with Alzheimer’s or other types of dementia will be $360 billion in 2024, up $15 billion from a year ago, the report said.

Medicare and Medicaid will cover the bulk of that, spending $231 billion this year to care for people with Alzheimer’s and dementia. Public and private spending to take care of Alzheimer's and dementia patients will skyrocket to nearly $1 trillion in 2050, the report projects.

"Our population is aging, so we really need to address these issues," said Sam Fazio, the Alzheimer Association's senior director of quality care and psychosocial research. "Alzheimer's disease remains a significant public health crisis."

Lifestyle changes reduce risk

Other Alzheimer's experts not involved with the report said more Americans are taking steps to reduce their risk for Alzheimer's or dementia.

Research suggests up to 40% of dementia cases can be prevented through lifestyle changes, said Dr. Keith Vossel, a neurologist and director of the Mary S. Easton Center for Alzheimer’s Research and Care at the University of California, Los Angeles.

Vossel said people who exercise regularly, do not smoke and achieve higher levels of education tend to have lower risk. Reducing blood pressure in midlife, in particular, is linked to lower risk, he said.

Paying close attention to elevated blood pressure is especially important, Vossel said. "We know that lowering blood pressure among people with elevated blood pressure in middle life can lower risk of dementia or (mild cognitive impairment) later on."

Caregivers spend 31 hours a week on Alzheimer's, dementia patients

Families and other caregivers take on an array of tasks, scheduling appointments and feeding and caring for people with Alzheimer's or dementia. The report said 11.5 million relatives and caregivers provided more than 18 million hours of unpaid care last year.

That amounted to a full-time job for caregivers who spent an average of nearly 31 hours a week caring for a person with Alzheimer's or dementia.

In July, the Centers for Medicare & Medicaid Services will launch an initiative to improve the quality of life for people with dementia, allowing them to remain at home and reduce the strain on unpaid caregivers. The model, called Guiding an Improved Dementia Experience , will coordinate care and provide a 24/7 support line. Families also can access care navigators who can connect patients and caregivers to services and support. Doctors and clinics who participate will receive a monthly per-patient fee from Medicare.

Fazio said access to navigators is crucial because the report showed that families live through a great deal of stress and that workers in the field believe the health care system is not equipped to help people living with dementia. President Joe Biden recently expanded a similar navigator plan for cancer patients in which private health insurers will cover such services.

Families "really want help and need help to navigate the system," Fazio said.

New drugs, old target

Of the eight drugs approved for Alzheimer's patients, only two attempt to attack the disease and slow memory and cognitive decline. Biogen has discontinued one of those drugs, aducanumab, sold under the brand Aduhelm. The Food and Drug Administration approved the drug despite mixed clinical trial results . Biogen also faced withering criticism when it launched Aduhelm, initially priced at $56,000 a year.

In January 2023, Eisai won FDA approval for its amyloid beta-busting drug , lecanemab. Sold under the brand name Leqembi, the drug is intended for patients in the early stages of the disease, the population studied in clinical trials.

The Alzheimer's Association report notes that the benefits of lecanemab "in the short term may be imperceptible" because it's designed to slow the disease, not reverse cognitive decline. The report said the long-term results of the drug are not clear.

Earlier this month, the FDA delayed action for Eli Lilly's drug  donanemab , the drug manufacturer said. The FDA expects to convene an advisory committee to discuss the treatment.

Clinical trials of all three amyloid-removing drugs have side effects visible on brain scans, such as brain swelling and bleeding. Some patients don't notice symptoms. Others have experienced headaches, dizziness, nausea, confusion and vision changes.

Though drugmakers largely have focused on drugs to target and clear amyloid from the brains of Alzheimer's patients, the report says, other studies are examining different methods of attacking the disease. Other potential drugs are being studied to limit the accumulation of tau protein, inflammation, altered cell metabolism and damage from toxic oxygen molecules, the report said.

Ken Alltucker is on Twitter at @kalltucker, or can be emailed at [email protected].

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Alzheimer’s association offers free presentations.

The Alzheimer’s Association, together with North Dakota State University Extension, will offer a free virtual presentation titled “Dementia Conversations: Driving, Doctor Visits, Legal and Financial Planning.”

The class will take place Monday, April 8, from noon-1 p.m. The presentation is free but registration is required.

The Alzheimer’s Association also will offer a free virtual presentation titled “Person-Centered Dementia Care: Recommendations for Professionals” on Monday, April 8, from 12:30-3:30 p.m. This presentation is free and open to healthcare and caregiving professionals. Registration is required.

Contact the Alzheimer’s Association of North Dakota for registration information.

These programs are supported by funding through the North Dakota Department of Health & Human Services, Adult & Aging Services Section.

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Spotlight Blog: Understanding Primary Progressive Aphasia, Bruce Willis and Wendy Williams’s Diagnoses

BU Center for Brain Recovery Researchers Discuss: Understanding Primary Progressive Aphasia, Bruce Willis’s and Wendy Williams’s Diagnoses

The recent diagnoses of Bruce Willis and Wendy Williams have brought a spotlight to a relatively lesser-known condition called primary progressive aphasia (PPA) and its broader category, frontotemporal dementia (FTD). Willis’s family revealed in 2022 that the beloved actor would be retiring due to frontotemporal dementia, following an initial diagnosis of aphasia. Similarly this past February, Wendy Williams’s medical team disclosed her diagnosis of primary progressive aphasia and frontotemporal dementia. Reports regarding these diagnoses have highlighted the impact these conditions have on the two public figures and their families.

At the Center for Brain Recovery, PhD students Nicole Carvalho and Marissa Russell are using their experience researching the two conditions, and working directly with patients to shed light on their complexities and nuances behind these diagnoses. Their work not only contributes to a greater understanding of these conditions but also aims to correct widespread misconceptions.

Defining PPA and FTD

Primary progressive aphasia is a nervous system syndrome that impairs the ability to communicate as a result of the degeneration of brain regions involved in language processing and behavior. It’s a form of neurodegenerative disease and subtype of frontotemporal dementia that specifically affects language comprehension and production ( ASHA ). In primary progressive aphasia, these areas are progressively damaged over time, leading to slow deterioration in the ability to use and understand language. Frontotemporal dementia, specifically, refers to a group of brain disorders affecting the frontal and temporal lobes, which are crucial for personality, behavior, and language. This umbrella term includes various forms of dementia, including primary progressive aphasia, which lead to nerve cell loss in critical brain areas ( MayoClinic ).

Misconceptions About PPA

Russell and Carvalho highlight several misconceptions about PPA that they aim to dispel through their research and outreach:

1) That primary progressive aphasia is the same as post-stroke aphasia. 

These disorders have different characteristics and prognosis, so it’s important that people understand the difference between them. Unlike post-stroke aphasia, PPA is not caused by a sudden cerebrovascular event (stroke) but rather by degeneration of brain regions involved in language processing. PPA often begins with subtle language difficulties and progresses to more severe impairments. On the other hand, post-stroke aphasia may improve over time with rehabilitation efforts.

2) That it’s just a normal part of aging. 

It’s not!  While deficits may start off mild (e.g., forgetting a word here and there), it is a neurodegenerative condition that impairs language abilities at an abnormally rapid pace. The development of PPA represents a distinct and pathological process separate from typical age-related changes. If someone experiences significant language difficulties that interfere with daily functioning, it is important to seek medical evaluation. 

3) That all people with primary progressive aphasia have the same symptoms. 

Apart from individual characteristics such as brain health and the age of onset, there are different subtypes of primary progressive aphasia that differ in initial manifestation of symptoms. The semantic variant is characterized by difficulty understanding or finding words. The nonfluent/agrammatic variant involves difficulty with sentence structure and grammar. The logopenic variant primarily involves problems with finding words and fluency.

4) That primary progressive aphasia only affects language skills. 

It primarily affects language skills, but its impact can extend beyond language abilities depending on the specific subtype and stage of the condition. Therefore, it ultimately leads to broader cognitive decline (e.g., difficulties with memory, attention, problem solving, etc).

Looking Ahead

The diagnoses of Bruce Willis and Wendy Williams have opened up conversations about primary progressive aphasia and frontotemporal dementia, conditions that impact many individuals yet aren’t generally well known by the general public. The work of researchers like Nicole Carvalho and Marissa Russell is essential in understanding these conditions, and making developments in the field of brain recovery.

At the Center for Brain Recovery, Marissa Russell is currently working under a grant that aims to use computational models to simulate language decline over time. This also helps to better understand translation and language control errors in Spanish-English bilinguals with semantic dementia (a frontotemporal dementia subtype). Additionally, the project aims to simulate recovery over time in bilinguals with post-stroke aphasia and normal language changes in older healthy bilingual adults.

We asked Nicole Carvalho, who is in the early phases of a new project that will investigate language skills in people with primary progressive aphasia, what are some things she would like people to understand about these disorders and diagnoses? She responded, “one of the common misconceptions about primary progressive aphasia is that it is the loss of intellect. That is not the case. The condition affects language skills, but other cognitive processes remain largely intact. What I would like people to know is that people with PPA are still people! They are just like everyone else, just with some communication difficulties. It is important to give them grace when communicating and to try to be helpful instead of speaking for them.”

Interested in learning more? Carvalho and Russell have provided the following resources:

Aphasia.org

Alzheimers.org

Mayo Clinic

Northwestern

Cleveland Clinic

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Behavioral and psychological symptoms in dementia.

Nancy Cloak ; Yasir Al Khalili .

Affiliations

Last Update: July 21, 2022 .

• Continuing Education Activity

Behavioral and psychological symptoms of dementia (BPSD) include a range of neuropsychiatric disturbances such as agitation, aggression, depression, and apathy. BPSD affects up to 97% of community-dwelling patients with dementia and has a significant impact on prognosis, institutionalization, and caregiver well-being. This activity reviews the evaluation and management of BPSD and highlights the role of the interprofessional team in improving care for patients with this condition.

• Review environmental, psychosocial, and medical factors that may contribute to behavioral and psychological symptoms of dementia.
• Identify evidence-based treatment interventions for behavioral and psychological symptoms of dementia.
• Outline a systematic strategy for evaluating and managing behavioral and psychological symptoms of dementia.
• Explain the importance of collaboration and communication among the interprofessional team in improving outcomes for patients affected by behavioral and psychological symptoms of dementia.
• Introduction

Dementia is the colloquial term that denotes the nosological distinction of major neurocognitive disorder in the Diagnostic and Statistical Manual 5 edition (DSM 5). Dementia refers to a collection of symptoms stemming from a broad array of etiologies precipitating in functionally impairing cognitive decline. While the presence of cognitive impairment is necessary and sufficient for a diagnosis of dementia, associated neuropsychiatric symptoms -known collectively as behavioral and psychological symptoms of dementia, or BPSD - are prevalent and can significantly impact the prognosis and management of dementia. For this reason, DSM 5 requires clinicians to specify whether BPSD is present and to specify the degree of severity; for example, a diagnosis of Alzheimer's dementia might be coded as “major neurocognitive disorder due to Alzheimer's disease, with behavioral disturbances, severe.” 

BPSD includes emotional, perceptual, and behavioral disturbances that are similar to those seen in psychiatric disorders. It may be clinically useful to classify them into five domains: cognitive/perceptual (delusions, hallucinations), motor (e.g., pacing, wandering, repetitive movements, physical aggression), verbal (e.g., yelling, calling out, repetitive speech, verbal aggression), emotional (e.g., euphoria, depression, apathy, anxiety, irritability), and vegetative (disturbances in sleep and appetite). 

There is no single etiology for BPSD. Instead, a biopsychosocial model has been proposed that attributes neuropsychiatric symptoms to interactions between an individual’s biology, prior experiences, and current environment. Dementia-related agitation, disinhibition, and psychosis are associated with volume reductions and decreased metabolism in the orbital and dorsolateral prefrontal cortex, anterior cingulate, insula, and temporal lobes – parts of the brain that mediate emotional regulation, self-awareness, and perception; and apathy is associated with small vessel white matter disease. [1]  BPSD has also correlated with alterations in cholinergic, noradrenergic, dopaminergic, serotonergic, and glutamatergic neurotransmission. [2]  This evidence is preliminary and primarily relates to Alzheimer’s disease, but supports some of the pharmacotherapies currently used to treat BPSD. 

A review addressing non-biological determinants of BPSD identified pre-morbid neuroticism (a personality trait characterized by a tendency to respond to challenges with exaggerated negative emotions such as anxiety, depression, and anger), pre-morbid post-traumatic stress disorder, problematic caregiver communication styles, and environmental factors (e.g., sensory over-or under-stimulation, or surroundings that are too hot, cold, or loud) also contribute to BPSD. [3]  From a theoretical perspective, three main categories of environmental contributions have been described: unmet needs (e.g., for food, fluid, companionship), behavioral/learning (e.g., when unwanted behavior is unwittingly reinforced, such as by providing attention when a patient calls out), and patient-environment mismatch (e.g., when a caregiver’s expectations exceed a patient’s capability).

• Epidemiology

In 2016, the worldwide prevalence of dementia was approximately 43.8 million, representing a 117% increase from 1990 and 28.8 million disability-adjusted life years, and it was the world’s fifth leading cause of mortality. [4]  The majority of patients with dementia experience BPSD at some point: when community-dwelling individuals with dementia have undergone assessment in longitudinal studies, up to 97% are affected by at least one symptom, most commonly depression or apathy, although delusions, agitation, and aberrant motor behavior (e.g., fidgeting, repetitive behaviors, wandering) occur in about a third of patients. Symptom severity increases with time and correlates with institutional placement. While few studies have characterized BPSD symptoms according to dementia etiology, delusions appear to be most common in Alzheimer's disease, depression, and apathy in vascular dementia, and disinhibition and eating disturbances in frontotemporal dementia. [5]

• History and Physical

The goal of the history for patients with BPSD is to establish priorities regarding the nature and urgency of interventions, characterize the symptoms, identify potentially reversible exacerbating factors, including environmental factors, medications, discomfort, substance use, and pre-morbid psychiatric disorders; and create a baseline for measuring the effectiveness of treatment. The goal of the physical examination is to confirm historical data and identify alternative or contributing psychiatric or general medical conditions. 

Behavioral disturbances often occur in the evening, a phenomenon is known as 'sundowning.' Some studies suggest that this phenomenon affects up to two-thirds of patients with dementia. [6]  One of the most common psychiatric sequelae observed in this demographic is delusions. Often the delusions consist of paranoid themes, as in Capgras syndrome and Othello syndrome. Hallucinations are not as prevalent as delusions with estimates as low as 7% at baseline. [7]  Furthermore, additional symptoms leading to subsequent hospital admissions include agitation, aggression, wandering, apathy, disinhibition, sleep disturbances, and depression. 

Physical Examination

The physical examination may document the problematic symptoms, although these are often intermittent. The primary role of the physical exam is to identify factors that may contribute to worsening BPSD, such as superimposed delirium or discomfort. For example, the exam may reveal an altered level of consciousness (somnolence or hyper-alertness), which is frequently a feature of delirium, or grimacing and guarding suggesting pain. Physical findings such as fever, hypoxia, abdominal tenderness, fluid overload, inflammation, or new localizing neurologic deficits may point to an acute medical condition that is causing delirium.

Unless there is evidence from the history or physical exam to suggest alternative causes, evaluation with laboratory or imaging is not necessary for patients with dementia who present with gradually worsening BPSD. Acute or subacute onset of symptoms should prompt basic studies (typically, complete blood count, electrolytes, evaluation of liver and kidney function, urinalysis, thyroid function tests, toxicology screen, and head CT) to evaluate for causes of delirium. Long term care staff members often attribute BPSD to urinary tract infections; however, the prevalence of bacteriuria is up to 50% in institutional settings, and routine testing may, therefore, lead to over-diagnosis, unnecessary antimicrobial treatment, and development of antibiotic resistance. According to the revised McGeer criteria, diagnostic evaluation and empiric therapy should be limited to patients who present with fever, dysuria, suprapubic pain, or new/increased urinary frequency, urgency, or incontinence, although other authors have suggested that culture and treatment could be initiated on the basis of an acute mental status change together with both change in the character of the urine and positive dipstick for either leukocyte esterase or nitrite. [8]

Establish Priorities

The first priority is characterizing the severity and nature of the symptoms – patients who are endangering themselves or others with aggressive behaviors or refusal of basic care will warrant more intensive management such as hospitalization. Therefore, the history should begin with an assessment of safety: has the patient been aggressive toward others, and if so, has this caused injury? Have they caused damage to property? Are they risking their health or safety by refusing basic hygiene, food, or fluids? Another priority is identifying delirium, which by definition is caused by a medical condition, medication, or non-prescribed CNS-active substance intoxication or withdrawal because this will require prompt medical evaluation and treatment (see Differential Diagnosis section). If delirium is identified, the patient will need a thorough medical evaluation, which is usually best accomplished in an inpatient setting.

Characterize Symptoms

Caregivers should be prompted to describe what they are seeing, rather than using generic terms such as “agitation” or “depression,” which can have different meanings to different observers. Other essential elements of the history include the onset (i.e., acute, sub-acute, or chronic/progressive), frequency, timing, and trajectory of the disturbances, and any relationship to environmental changes or medication changes. There may be a temporal relationship with events such as a change in environment (e.g., moving from home to nursing facility), or symptoms might worsen in the evenings, following family visits, or when providing personal care. 

Review Medications

Clinicians should ask caregivers about any changes in medications in the weeks preceding the onset or worsening of BPSD. Patients with dementia are susceptible to the CNS effects of medications, and not all culprit medications are easily recognized. In addition to the well-recognized adverse effects of bladder antispasmodics and histamine antagonists on cognition and behavior, antibiotics (especially trimethoprim-sulfamethoxazole and fluoroquinolones in the outpatient setting, and penicillins and most cephalosporins [excluding ceftriaxone] in the inpatient setting), antidepressants, benzodiazepines, digoxin, levetiracetam, and muscle relaxants can contribute to both agitation and apathy. Medication withdrawal, especially from antidepressants, benzodiazepines, or opioids, can also contribute to BPSD. Akathisia from antipsychotics, including second-generation antipsychotics, should be considered, especially in patients whose symptoms worsen despite increasing doses of these medications. 

Assess Comfort

The review of systems should address uncomfortable physical symptoms, including pain, constipation, and urinary retention. Because pain is present in 46 to 56% of patients with dementia and the presence of pain is associated with increased BPSD, the past medical history should have a review for painful conditions (e.g., neuropathy, osteoarthritis, peripheral vascular disease), and caregivers should be asked about both the patient’s self-report about pain and nonverbal signs of pain, because patients with dementia may demonstrate nonverbal signs of pain even though they do not report it. [9]  The Pain Assessment in Advanced Dementia (PAINAD) or Face, Legs, Activity, Cry, Consolability (FLACC) scales are both reliable and valid tools for objectively evaluating and tracking pain. Most hospitals and some nursing homes use one of these instruments, and family caregivers can also be trained to use them.

Review psychiatric history and substance use: Caregivers should be questioned about the past medical history of psychiatric disorders, especially psychotic, mood, anxiety, and post-traumatic stress disorders, and whether the patient could be using alcohol, cannabis, non-prescribed medications, or illicit drugs.

Create a Baseline

Since BPSD can fluctuate and their assessment is subjective, establishing a clear baseline for assessing the effects of treatment is critically important. For overall BPSD, clinicians can use a standardized instrument such as the Neuropsychiatric Inventory (NPI) or the Behavioral Pathology in Alzheimer’s Disease rating scale (BEHAVE-AD). Both are based on structured interviews with caregivers and have seen extensive use in research, with similar performance in detecting global changes. The NPI evaluates delusions, hallucinations, agitation/aggression, depression/dysphoria, anxiety, elation/euphoria, apathy/indifference, disinhibition, irritability/emotional lability, aberrant motor behavior, sleep disturbances, and disorders of appetite/eating; for each domain, caregivers are asked to rate frequency, severity, and the degree of distress it causes, over a time period specified by the interviewer. The BEHAVE-AD domains comprise delusions, hallucinations, activity disturbances, aggression, diurnal rhythm disturbances, tearfulness, depression, and anxiety; caregivers are asked to rate each symptom's severity over the past two weeks, provide a global rating of symptom severity, and identify the most troublesome symptom. The Cohen-Mansfield Agitation Inventory (CMAI) specifically evaluates agitated behaviors only, dividing them into four categories depending upon whether they are physical, verbal, aggressive, or non-aggressive.

While the NPI, BEHAVE-AD, and CMAI are gold standards for evaluating BPSD, they are time-consuming, and a reasonable alternative in clinical practice is to ask caregivers to very specifically describe a problematic symptom, quantify its frequency, and assess the degree of distress it causes. For example, a symptom might be described as "pushing me away when I try to give her a shower," and then quantified by the percentage of showering time that this occurs (e.g., 75% of the time) and the level of distress it causes for the caregiver (e.g., 7 on a scale of 0 to 10). Having caregivers use a calendar or notebook to keep a daily prospective diary is the best way to get accurate information; ideally, this should occur before any intervention for at least three days, and then be repeated after the intervention.

• Treatment / Management

Management of BPSD involves choosing an appropriate setting, treating discomfort, implementing non-pharmacological interventions, and then only, if needed, conducting systematic trials of evidence-based pharmacological therapies. Unless patients are endangering themselves or others, interventions should begin only after establishing a baseline by identifying and quantifying target symptoms, as described above.

Choose an appropriate setting: The first step in management is to decide on the proper setting for treatment and address safety issues. Patients with delirium are often best managed in a hospital to facilitate medical evaluation because parenteral medications may be required. Referral to a geropsychiatry unit is appropriate for medically stable patients who are endangering themselves or others (aggression with injury or capacity to cause injury, refusing fluids or basic hygiene, suicidal behavior), especially if pharmacotherapy has been refused or is ineffective. Pending transfer, patients who are dangerous to self or others require monitoring with one-on-one observation, and treatment with antipsychotic medications will usually be necessary, following a risk/benefit discussion with their surrogates or guardians. 

Treat discomfort: Before any BPSD-specific interventions, all patients should be assessed and treated for causes of discomfort (e.g., pain, constipation, urinary retention, is the environment too warm/cold/loud), as described above, and treated appropriately. 

Non-Pharmacological Interventions for BPSD

The next step in management is implementing non-pharmacological interventions, which may be sufficient alone for mild BPSD, and should always accompany any pharmacotherapy. Geriatrics organizations and experts advocate the use of non-pharmacological interventions for BPSD. However, a meta-analysis of 10 randomized controlled trials in patients with moderate to severe dementia found no benefit, except for music therapy in reducing overall BPSD and massage therapy in reducing depression. [10]

Caregiver training: However, this meta-analysis excluded interventions focused on caregiver training, which is effective in both reducing a range of BPSD as well as improving caregiver well-being. [11] Caregiver training typically focuses on understanding behavioral disturbances as responses to discomfort, unmet needs, or attempts to communicate; creating soothing environments with optimal levels of stimulation; and responding to patients in ways that de-escalate problematic behaviors (e.g., distraction, giving patients clear instructions and simple choices, not rewarding the behaviors). The Alzheimer's Association offers both online educational modules and in-person training classes, which also provide caregivers with professional and peer support. For patients whose BPSD occurs primarily during personal care, a randomized, multi-site crossover study showed that training caregivers to deliver a protocol called Bathing without a Battle (available online) reduced agitation, bathing time, and antipsychotic use. [12]

Other non-pharmacological approaches: While non-pharmacological interventions other than caregiver training and music therapy have not been consistently effective for overall BPSD in randomized, controlled trials, they may benefit individual patients, and unlike medications, rarely have adverse effects. Some of these include aromatherapy, bright light therapy to reduce circadian disturbances, massage, multisensory stimulation, and reminiscence therapy, in which patients are engaged in reviewing their past via conversation, photographs, or music. [13] Some interventions with anecdotal effectiveness for agitation include giving patients simple tasks to perform, such as folding laundry or using busy quilts (lap quilts with attached interesting objects such as zippers, Velcro, beads, ties, etc.) and weighted blankets (similar to those used to calm children with pervasive developmental disorders). A clinical trial (ClinicalTrials.gov ID NCT03643991 ) is currently underway to evaluate the latter. In general, non-pharmacological approaches are well-tolerated, but rare cases of worsening agitation have occurred with music therapy.

Pharmacologic Interventions for Agitation and Aggression

Psychotropic medications are frequently used to treat BPSD, although the side effect burden is high, and benefits are typically modest. Wandering and repetitive vocalizations rarely respond to pharmacotherapy and are best addressed with non-pharmacological measures. Pharmacological approaches will differ based on the nature and severity of the symptoms. The primary focus of clinical trials has been on symptoms of agitation, aggression, and psychosis since these are typically the most problematic and distressing manifestations of BPSD. 

Empiric treatment of pain: Painful conditions are present in at least 49% of patients with dementia, but only 20 to 40% of patients with dementia receive analgesics, compared to 60 to 80% of similar patients without dementia; this is believed to relate to both under-reporting by patients and under-recognition by clinicians. [9]  Since untreated pain has a strong relationship with BPSD, an 8-week multicenter cluster randomized controlled trial examined the effect of a stepwise protocol for empiric treatment of pain in patients with dementia-related agitation. Patients were started on routine acetaminophen (3 g daily) if they were not receiving analgesics. If this was insufficient, they were stepped up to low-dose morphine (up to 20 mg daily), buprenorphine transdermal patch (up to 10 mcg hourly), or pregabalin (up to 300 mg daily). The primary outcome measure was a change in scores on the Cohen-Mansfield Agitation Inventory; changes in cognitive and physical functioning were also assessed. After eight weeks, agitation was reduced by 17% in the intervention group (an effect comparable to that seen with risperidone, the antipsychotic most commonly used for BPSD), without any adverse effects on cognition or physical functioning, suggesting that treatment of pain did not achieve benefit for BPSD simply by sedating patients. [14]  This study supports the empiric treatment of known or potential pain as a first step in addressing BPSD. An excellent first step is initiating routine (not as-needed) acetaminophen, with a maximum recommended dose of 3 grams/day in the frail elderly. Topical therapies such as transdermal lidocaine, diclofenac gel, or methyl salicylate cream are safe. They can be effective if a localized source of pain is suspected. Duloxetine, gabapentin, or pregabalin can be helpful if there is a concern for neuropathic pain, although they are associated with an increase in falls. Clinicians should generally avoid using muscle relaxants, chronic NSAIDs, and tricyclic antidepressants. Although opioids can also contribute to falls and fractures, tramadol has a stronger association than most other opioids. Transdermal buprenorphine may be the safest alternative in this regard and also is relatively unaffected by renal insufficiency, which is common in older adults. [15]  

Antipsychotics: Second-generation antipsychotics (primarily risperidone, olanzapine, quetiapine, and aripiprazole) are the mainstay of treatment for agitation and aggression, although, in a systematic review of 16 meta-analyses of randomized, controlled trials of these agents, the effect sizes (differences between treatment and placebo) were typically quite small for risperidone, olanzapine, and aripiprazole, ranging between 0.15 to 0.30 in most studies, and quetiapine generally did not differ from placebo. Adverse effects including extrapyramidal symptoms, cerebrovascular events, somnolence, urinary tract symptoms, and death were higher in the antipsychotic group as a whole, and worsening confusion was common with quetiapine and olanzapine. [16]  In the United States, the Food and Drug Administration has issued a black box warning about the increased risk for death among elderly patients with dementia who receive treatment with antipsychotics for BPSD (3.5% vs. 2.3%, mainly due to cerebrovascular disease and infections). For this reason, antipsychotic medications should only be an option when non-pharmacological interventions and other pharmacological interventions, such as pain control and selective serotonin reuptake inhibitors (SSRIs), have been ineffective or in cases of behaviors that are dangerous to the patient or others. 

Starting and maximum doses of antipsychotics for BPSD are as follows: aripiprazole 2 mg daily and 15 mg daily, respectively; olanzapine 2.5 mg daily and 10 mg daily; quetiapine 12.5 mg twice daily and 100 mg twice daily; and risperidone 0.25 mg twice daily and 1 mg twice daily. Doses can be increased in small increments every two weeks if there is an insufficient improvement, based on prospective ratings from caregivers. Due to their potential to worsen motor symptoms, clinicians should avoid using antipsychotics other than quetiapine, pimavanserin, and clozapine in Lewy body dementia and dementia associated with Parkinson's disease. In the United States, pimavanserin is approved by the Food and Drug Association for the treatment of psychosis related to Parkinson's disease, although it carries the same black box warning as other antipsychotics. [17]  The starting and target dose is the same (34 mg). Like other antipsychotics, it prolongs the QT interval and carries a black box warning about the increased risk of death in geriatric patients with dementia. Patients receiving antipsychotic medications require monitoring for adverse motor effects, and periodic (every 3 to 6 months) attempts should be made to taper and discontinue the medication. Although the quality of evidence is low, antipsychotic discontinuation often does not result in worsening of BPSD, as evidenced by one longitudinal study in which about 80% of patients on long-term antipsychotics were successfully taken off their medication without increased BPSD or use of as-needed medication. [18]  Discontinuation may be less successful for patients who have had severe symptoms. 

Selective serotonin reuptake inhibitors (SSRIs): Due to the adverse effects associated with antipsychotics, other medications have undergone research for the treatment of agitation and aggression. A 2011 meta-analysis demonstrated that the SSRI antidepressants citalopram and sertraline were associated with improvement in these symptoms, with a rate of adverse effects similar to placebo, although trazodone was not effective. [19]  A subsequent multicenter randomized controlled trial of citalopram 30 mg daily versus placebo showed a number needed to treat for moderate to marked overall benefit in BPSD of 7, but there was no difference in agitation scores and patients had an average increase in corrected QT interval of 18 ms. [20]  Antidepressant dosing strategies used in the studies were the same as for depression, and researchers observed common SSRI adverse effects such as nausea and hyponatremia. It's wise to heed the geropsychiatry maxim "start low, go slow, but go as high as you need to go" when treating mild to moderate BPSD with SSRIs because too-rapid titration can worsen agitation. Citalopram should be started at 10 mg daily and sertraline at 25 mg daily. Target symptoms and their baseline frequency/severity should undergo an assessment before starting the medication, and patients should be followed up two to three weeks later for response and tolerability. If there is no benefit but also no adverse effects, citalopram dosing should increase to 20 mg and sertraline to 50 mg. Sertraline may be further increased to a maximum dose of 200 mg daily. The maximum recommended dose of citalopram is 20 mg daily due to QTc prolongation at higher doses. 

Other pharmacotherapies: The combination of dextromethorphan and quinidine, which has approval in the U.S. and Europe for pseudobulbar affect, was studied in a single randomized trial, with modest benefit for agitation but significant adverse effects, especially falls. [21] Prazosin (average dose of about 6 mg daily) was beneficial for BPSD without adverse effects on blood pressure in a single study with 22 participants. [22]  Medications that have no clinically meaningful efficacy for agitation or aggression include cholinesterase inhibitors, memantine, valproate, and benzodiazepines. [23] [24] [25] [26] [27]  An exception to the negative findings regarding cholinesterase inhibitors in the dementia population as a whole is the possible benefit for patients with Lewy body dementia and dementia associated with Parkinson's disease, in which a small effect size of 0.2 was found, albeit at the cost of an increase in motor symptoms. [28]  Both valproate and benzodiazepines have correlated with accelerating cognitive decline in patients with dementia. [26] [29]  Haloperidol is ineffective for BPSD in general but can be useful for aggression. [30]  Cannabinoids (dronabinol, purified delta-9-tetrahydrocannabinol, and nabilone) have been evaluated in a systematic review, in which the best randomized controlled trial evidence did not support benefit for a reduction in either symptoms or caregiver burden, although differences in adverse events were minimal. [31]  Among other complementary and alternative therapies; the only ginkgo at a dose of 240 mg/d has shown consistent benefit for BPSD in randomized, controlled trials, although these studies were of low to moderate quality. [32]

Pharmacologic Interventions for Depression and Apathy

While depression and apathy are the most common BPSD, fewer studies have examined outcomes of pharmacotherapy. 

Depression:  A meta-analysis of 10 studies of various antidepressants for treatment of depression in dementia showed no difference from placebo on the primary outcome measure (scores on depression rating scales) for antidepressants as a group or any individual agent; although there was a benefit for SSRIs (but not other antidepressants) regarding numbers of responders and remitters, the quality of this evidence was lower. Patients receiving antidepressants had higher rates of adverse events and study drop-out. [33]  In elderly patients without dementia, there was a greater response rate to a combination of citalopram (average dose 34 mg daily) and methylphenidate (average dose 16 mg daily) than to either medication alone, without an increase in adverse effects (25677354), but whether the combination would be effective in patients with dementia is unknown, and benefits of citalopram doses below the currently recommended maximum of 20 mg daily cannot be determined from this study. [34]  SSRIs are the antidepressant treatment of choice, with citalopram and sertraline favored due to fewer drug-drug interactions than paroxetine, fluoxetine, or fluoxetine, which inhibit cytochrome p450 enzymes.

Apathy: Methylphenidate may improve apathy, cognition, and functioning modestly, with minimal risk for adverse effects, but studies of cholinesterase inhibitors, memantine, and antidepressants have not demonstrated a benefit for apathy. [35] In the ADMET trial of methylphenidate, patients did not meet exclusion criteria if they had cardiovascular conditions but were excluded if they had agitation at baseline; there were no differences from placebo on any cardiac outcomes, but patients receiving methylphenidate did have greater weight loss, and two methylphenidate patients developed hallucinations or delusions, versus none on placebo (not statistically significant). [36]  The response to methylphenidate usually occurs within several days, so a good dosing strategy is to begin the immediate-release formulation at 2.5 or 5 mg twice daily (morning and early afternoon) and titrate up by 2.5 or 5 mg every week.

General Approach to Pharmacotherapy for BPSD

Given the limited overall benefits of pharmacotherapy, a systematic approach to implementing and evaluating BPSD is critical. Except for urgent situations involving safety, there should be an established, clear baseline regarding the frequency and severity of target behaviors. Medications should be given an adequate trial of at least four weeks at the maximum recommended dose before concluding they are ineffective. To avoid prematurely abandoning a potentially effective strategy, educating and supporting caregivers is a vital component of this process. Caregivers should understand that change is often so gradual that it may not be noticeable until comparing recent behavior diaries to those from 3 to 4 weeks prior. If an intervention (especially a medication) is truly ineffective after an adequate trial, it should be discontinued, and the lack of benefit documented.

For agitated behaviors, once uncomfortable symptoms have been treated, environmental triggers removed, and non-pharmacological interventions implemented, pharmacotherapy should start with citalopram or sertraline; if this is not effective, the next step would be adding risperidone or aripiprazole, unless the patient has Lewy body dementia or Parkinson's disease. For these cases, the clinician can add an acetylcholinesterase inhibitor if the patient is not already receiving one; if they are already taking an acetylcholinesterase inhibitor, pimavanserin or quetiapine can be options. Despite the lack of high-quality evidence for effectiveness, many clinicians will trial quetiapine in patients with Lewy body dementia or Parkinson's disease. A common error with quetiapine is inadequate dosing; doses up to 200 mg/d are useful in patients with re Parkinson disease without any adverse motor effects. Trials of antipsychotic tapering should take place every 3 to 6 months (sooner if adverse effects emerge). If an antipsychotic is insufficiently beneficial, an alternative antipsychotic can be tried using a cross-titration, but olanzapine should generally be avoided due to its anticholinergic effects and lower benefit overall. Finally, prazosin or dextromethorphan-quinidine are potential therapies. At each step, re-evaluation and attention to environmental factors and non-pharmacological interventions are necessary. Severe agitation or aggressive symptoms usually require immediate initiation of antipsychotic therapy to bring symptoms under control, but this should not obviate the need to implement other interventions concurrently or to attempt discontinuation when the patient stabilizes. For depression, pharmacotherapy should begin with citalopram or sertraline, with consideration of adding methylphenidate if there is a limited response after an adequate trial of the antidepressant. If symptoms do not respond, discontinue the medication. 

Treatment-Refractory Patients 

Neurostimulation therapies may have a role in refractory patients. While randomized, controlled trials have not found any benefit from transcranial direct current stimulation, repetitive transcranial magnetic stimulation was beneficial in a majority of studies, with minimal adverse effects. [37]  Electroconvulsive therapy is highly effective and safe for geriatric depression and has also shown effectiveness and tolerability for both depression and agitation/aggression in patients with dementia. [38]  The availability of these therapies is often a limiting factor.

• Differential Diagnosis

The differential diagnosis for BPSD includes:

• Schizophrenia
• Bipolar disorder
• Major depressive disorder
• Post-traumatic stress disorder
• Central nervous system (CNS) neoplasms

Delirium characteristically demonstrates acute onset, fluctuating course, and the presence of an underlying medical condition, medication or psychoactive substance, or medication/substance withdrawal. Patients with BPSD can also have superimposed delirium as a cause for an abrupt worsening of their usual symptoms. History is the key to differentiating BPSD from delirium: in delirium, the onset of symptoms occurs over days to 1 to 2 weeks, while in BPSD, symptoms gradually worsen over several weeks to months. Patients with delirium frequently have changes in the level of consciousness, such as periods of somnolence or extended periods of wakefulness, which are typically less prominent in BPSD. Visual hallucinations may be prominent in delirium, whereas delusions are more common in patients with BPSD. It can be challenging to distinguish Lewy body dementia from delirium since patients with Lewy body may have visual hallucinations and fluctuations in the level of consciousness, but these symptoms will have a more gradual onset than in patients with delirium. Patients with suspected delirium should have a thorough medical evaluation, beginning with history and physical and followed by targeted laboratory testing and imaging based on these findings; typically, comprehensive metabolic panel, CBC, urinalysis, cardiac enzymes, chest X-ray, and toxicology screens are performed routinely, with neuroimaging, lumbar puncture, blood gases, and EEG reserved for select cases. Unlike BPSD, symptoms related to delirium will resolve, albeit sometimes gradually, once the underlying cause is corrected.

Patients who have pain, urinary retention, constipation, or other causes of discomfort yet cannot communicate their experience may become agitated, but once the cause is corrected, the behavioral disturbances improve. 

Presentations of psychiatric conditions, such as schizophrenia, bipolar disorder, major depressive disorder, and post-traumatic stress disorder, may be quite similar to BPSD. Still, patients will have a history of these disorders before the onset of their dementia. In the case of psychotic or mood disorders, the presentation is generally episodic rather than continuous, which is typical for BPSD. 

Patients with primary CNS neoplasms have a high frequency of behavioral and psychological disturbance, most commonly apathy, anger, and disinhibition. Compared to BPSD, the emotional and behavioral symptoms that occur with CNS neoplasms are more prominent than the cognitive deficits that can also occur in patients with brain tumors, and there are usually other neurological findings. All patients with new BPSD should have a thorough neurological evaluation. Neuroimaging may be necessary, especially in patients with frontotemporal dementia, who frequently present with behavioral disturbances rather than memory impairment.

Dementia is associated with significant decreases in life expectancy compared to age-matched controls, with a median survival from diagnosis ranging from 4.5 years for men with Lewy body or Parkinsonian dementia to 12 years for women with Alzheimer’s disease. BPSD correlates with more rapid progression of dementia and earlier mortality; whether the treatment has any impact on these variables is unknown. [39]

• Complications

BPSD substantially contributes to the overall burden of dementia on patients, caregivers, and society. They predict more rapid cognitive decline and earlier mortality and are associated with increased hospital length of stay, hospital complications, earlier nursing home placement, and increased rates of psychiatric and cardiovascular disorders in family caregivers. [40]  Studies have not explicitly reported on injuries to patients and caregivers as a result of BPSD, but agitation and aggression would presumably increase the risk. Though whether the treatment has any impact on these variables is unknown, interventions that involve training and supporting family caregivers have been found to reduce or delay nursing home placement in the general population of patients with dementia.

• Deterrence and Patient Education

There are no studies specifically examining the prevention of BPSD, although some strategies have been shown to reduce the risk of cognitive decline and the development of dementia. Both a dietary intervention combining a Mediterranean diet with the Dietary Approach to Systolic Hypertension (DASH) and pharmacological treatment of hypertension results in a decreased risk for incident dementia and physical exercise improves cognitive function in patients with existing dementia. Although depression is associated with an increased risk of developing dementia, there is no consistent evidence that treating it reduces this risk, nor is there yet any good-quality evidence to support cognitive training exercises as a strategy for preventing dementia. [41]

• Enhancing Healthcare Team Outcomes

Effective management of BPSD requires a coordinated interprofessional health care team that partners with the patient's home caregiver. [40]  [Level 5]

• Nurses and nursing assistants are on the front lines of identifying, quantifying, and monitoring BPSD in hospitals and long-term care facilities, where they are usually the first to notice precipitants such as changes in the environment, medications, and physical symptoms. In addition to delivering direct nursing care, home health nurses provide education and guidance to family caregivers. 
• Physical, occupational, and recreational therapists can aid in identifying and removing sources of danger, assisting with family caregiver education, and providing non-pharmacological interventions such as busy quilts (or other forms of distracting activities) and weighted blankets. 
• Social workers can support family caregivers and connect them with resources such as caregiver education, respite, and permanent placement. 
• Clinical psychologists can create behavioral plans that integrate non-pharmacological interventions with measures to avoid inadvertently reinforcing undesirable behaviors.
• Pharmacists can assist in identifying medications or drug interactions that may contribute to BPSD, as well as checking for drug interactions and verifying dosing regimens.
• Physicians, nurse practitioners, and physician assistants perform medical evaluations, initiate and monitor pharmacotherapy, and oversee the interprofessional treatment plan.

All team members are responsible for maintaining clear communication with other team members, informing everyone regarding any concerns or new developments, and addressing safety risks. For in-home settings, a notebook that contains caregiver ratings of symptoms, medications, including date/time of any as-needed medications, and instructions given by each discipline can be immensely beneficial.

With open collaboration and communication among all members of the interprofessional healthcare team, the management of BPSD will be more effective and result in better patient outcomes. [Level 5]

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Disclosure: Nancy Cloak declares no relevant financial relationships with ineligible companies.

Disclosure: Yasir Al Khalili declares no relevant financial relationships with ineligible companies.

This book is distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) ( http://creativecommons.org/licenses/by-nc-nd/4.0/ ), which permits others to distribute the work, provided that the article is not altered or used commercially. You are not required to obtain permission to distribute this article, provided that you credit the author and journal.

• Cite this Page Cloak N, Al Khalili Y. Behavioral and Psychological Symptoms in Dementia. [Updated 2022 Jul 21]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-.

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Alzheimer’s ‘breakthrough’ stalls: why a much-hyped drug is facing approval delays

The benefits of drugs such as donanemab, aducanumab and lecanemab are proving harder to quantify than potential harms, experts say

I t was heralded in news articles as a “breakthrough”, a “turning point” and a “gamechanger” for Alzheimer’s disease. Some experts went so far as to call the drug, donanemab, the “beginning of the end” for the debilitating condition.

Pharmaceutical company Eli Lilly in May 2023 released data from a clinical trial they said showed donanemab slowed cognitive and functional decline in people with early symptomatic Alzheimer’s disease by 35% over 18 months.

The findings saw the head of Alzheimer’s Research UK and other experts call on drugs regulators to rapidly approve the treatment for use in patients.

But despite reports the US drugs regulator was set to approve donanemab “any day” , the Food and Drug Administration (FDA) instead announced on 8 March that it had delayed its decision.

The FDA said it wants an independent panel to further scrutinise data on the safety and efficacy of donanemab, with a decision now expected later in 2024. UK, European and Australian regulators are also still assessing the drug.

In a statement, the executive vice-president of Eli Lilly, Anne White, said: “We are confident in donanemab’s potential to offer very meaningful benefits to people with early symptomatic Alzheimer’s disease”.

“It was unexpected to learn the FDA will convene an advisory committee at this stage in the review process, but we look forward to the opportunity to further present the [trial] results and put donanemab’s strong efficacy in the context of safety,” she said. “We will work with the FDA and the stakeholders in the community to make that presentation and answer all questions.”

Dr Timothy Daly, a dementia researcher with Sorbonne University in Paris, says this delay comes as no surprise to him.

He says the benefits of donanemab, and similar, much-hyped drugs, including aducanumab and lecanemab, have proved harder to quantify than their potential harms.

“Under this narrative of drug success, there are some really strong side-effects,” Daly told Guardian Australia.

These are a type of drug known as novel monoclonal antibodies, and they target amyloid proteins in the brain. Many researchers believe the buildup of these proteins contributes to Alzheimer’s disease.

The drugs have been shown to reduce amyloid levels in the brain. But around three-in-10 people taking lecanemab or donanemab in clinical trials developed a condition known as amyloid-related imaging abnormalities, abbreviated to ARIA, a condition which can cause brain swelling or haemorrhaging.

“Mostly these seem to be minor, not come with any symptoms, and follow-up scans show they appear to have resolved,” Dr Sebastian Walsh, a public health doctor researching dementia risk reduction with the University of Cambridge in the UK, says.

“In a small percentage of participants it does seem to be much more serious, and there have been some deaths – particularly for those on blood-thinning-type medications.”

Some trial participants also experienced brain shrinkage – and the long-term effects of that are unknown.

‘It’s pure speculation’

In the donanemab trial, patients receiving the drug declined on average by 10 points on a 144-point scale that combined cognitive and functional scores. The placebo group who were not receiving the drug declined by 13 points.

This data was used by researchers to state that the drug slowed cognitive and functional decline by “more than one-third”, and offered people “extra months” or “up to one year of life” without further disease progression.

Walsh says efforts to translate clinical data into terms more meaningful for people to understand means the effects of the drug have been overblown in media reports.

“Whilst it is understandable that people want to think of other ways to present these numbers, it still needs to be scientifically valid,” he says.

“Those who have reported it being ‘an extra six months at higher function’ are on shaky ground scientifically I think. The trials didn’t measure recognition of a loved one, ability to drive, any of these things – extrapolating in this way is not really justified by the evidence we have. It’s pure speculation.”

A professor of neurology at Radboud University Medical Centre in the Netherlands, Edo Richard, told news channel Al Jazeera the drugs “clearly remove” amyloid proteins from the brain “very successfully”.

But a reduction in amyloid proteins does not necessarily lead to a slowing of cognitive decline, he said.

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Research into the disease dating back more than 25 years has found that amyloid proteins are present in the brains of people with dementia. But they are also found in people who don’t have dementia, and who never go on to develop it, Richard told Al Jazeera.

While many drugs trialled in the past have reduced amyloid levels, donanemab, aducanumab and lecanemab appear to be the first to have also led to a change in cognitive decline. But Richard claimed that change was “statistically significant, but clinically irrelevant”.

When the FDA approved aducanumab in 2021, three FDA advisory committee members who advised against its approval because of what they believed was a lack of efficacy data resigned. One of the people who resigned described it as “probably the worst drug approval decision in recent US history”.

When it came to implementation, the US health insurance program Medicare said it would not cover it, and clinicians have also been cautious, with little use of the drug.

The Australian regulator, the Therapeutic Goods Administration, in June found “there is no evidence of clinically meaningful efficacy” of aducanumab.

A ‘collective desperation’

As well as minimal meaningful clinical benefits from donanemab, patients also need to receive the drugs via an intravenous infusion at a medical clinic or hospital once every two to four weeks at a cost of about US$26,500, or A$40,500, a year plus undergo regular testing. It is a lot to ask of vulnerable people and their families.

Those who participate in clinical trials are also a highly selective group. In the donanemab trial, 1,320 participants with amyloid and early disease symptoms completed it. For every 10 people screened for eligibility for the trials, about eight were found to be ineligible.

In a commentary written for the Conversation , Walsh said if, when prescribed in the real world, “the drug eligibility is restricted to match the trial eligibility, then very few people will be eligible. If eligibility is broader, then already small effects are likely to be even smaller and side-effects more pronounced”.

The director of internal medicine and clinical epidemiology at the Princess Alexandra hospital in Queensland, Australia, Prof Ian Scott, published a paper in the February edition of the journal Age and Ageing with similar concerns. He wrote trials of amyloid-targeting monoclonal antibodies to date “do not provide high-quality evidence of clinically meaningful impacts at an affordable cost”.

Daly believes that significant focus on the potential of drugs that target amyloid buildup despite a lack of efficacy has been reductive , as it has seen less attention being paid to alternative hypotheses of what is causing the disease, and ways to tackle it.

A 2020 report from the Lancet commission on dementia estimated 40% of cases of age-related dementia are associated with 12 potentially modifiable risk factors across the lifetime, including air pollution, obesity, depression, and less education.

Daly says while such findings make it tempting to list lifestyle changes people can make to reduce dementia risk, this is also too simplistic, as it puts the onus on individuals rather than governments.

“Working conditions, forms of oppression and things that can’t as easily be seen as a dementia risk are just as important in preventing disease ,” Daly says.

“There is an iceberg here – don’t just look at the surface at drugs and lifestyle. There are living conditions and social structures that represent deeper contributions to risk in the population, and interventions targeting these are needed by governments to make our society fairer and more dementia-resilient.”

Walsh says there is understandably “a collective desperation” among scientists and patients for better treatments and preventive options for Alzheimer’s disease, which is the most common cause of dementia in western societies and which has no cure.

“But this cannot cloud objectiveness when we look at the evidence,” he says.

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