Dementia, by Dr Kamal Kejriwal MD AAFP, CMD Geriatric Fellowship Program Director, Kaiser Fontana
Dementia, by Dr Sherif Iskander Geriatric Fellows Dr Marian Assal, Geriatrician, Kaiser Fontana, as presented within the 2018 January GWEP conference
1. 1
DEMENTIA
Dr Kamal Kejriwal MD AAFP,CMD
Geriatric Fellowship Program
Director, Kaiser Fontana
Dr Sherif Iskander Geriatric Fellows
Dr Marian Assal, Geriatrician,
Kaiser Fontana
2. 2
OBJECTIVES
Know and understand:
• The risks for and causes of dementia
• The evaluation of patients with dementia
• How to plan behavioral and pharmacologic
treatment strategies to minimize the personal,
social, & financial impacts of dementia
• How to refer patients and caregivers to
available community resources
3. 3
TOPICS COVERED
• Epidemiology and Societal Impact
• Risk Factors and Prevention
• Assessment Methods
• Differential Diagnosis
• Treatment and Management
• Resources
7. 4
WHAT IS DEMENTIA?
• An acquired syndrome of decline in memory
and other cognitive functions sufficient to
affect daily life in an alert patient
• Progressive and disabling
• iNnohtearenntaspect of aging
• Different from normal cognitive lapses
8.
9.
10.
11. 5
THE EPIDEMIOLOGY OF
DEMENTIA
• 6%‒8% of people 65 yr have Alzheimer dementia (AD)
Prevalence doubles every 5 yr
Nearly 45% of those aged 85+ have AD
• Vascular dementia co-occurs with an estimated 15%–
20% of AD cases ― “mixed dementia”
• Lewy body dementia (LBD) ― second most common
cause of dementia
12.
13. 7
ETIOLOGY
• Alzheimer disease
Amyloid plaques/oligomers
Tau neurofibrillary tangles
• Lewy body and Parkinson dementia
Cytoplasmic α-synuclein inclusion bodies
• Frontotemporal dementia
Tau or ubiquitin proteins
14. 9
THE GENETICS OF DEMENTIA
Early onset (<60 years old)
• Amyloid precursor protein (APP)
• Presenilin proteins (PS1 and PS2)
Late onset
• Apolipoprotein E gene (APOE 2/3/4) ― chromosome 19
APOE4 ― two alleles confers greatest risk in dose-related fashion
ApProOteEc2tiv―e
• Sleiontgidlee-npuoclymorphisms
Clusterin (CLU-C), complement component receptor 1 (CR1),and
phosphatidylinositol binding clathrin assembly protein (PICALM)
15. 8
RISK FACTORS FOR DEMENTIA
Protective Factors
Definite: unknown
Possible
• NSAIDs
• Antioxidants
• Intellectual activity
• Physical activity
• Statin
Possible
Risk Factors
Definite
• Age
• Family history
• AllePleOE4a
• Down syndrome
• Hraeuamdat
• Fewer years of formal education
• Late-onset major depressive
disorder
• Cardiovascular risk factors
(hypertension, diabetes,
hypercholesterolemia, obesity)
16. 10
ASSESSMEN T: HISTORY
Ask both the patient and a reliable informant
about the patient’s:
history
• Date of onset of current condition and nature
of symptoms
• Medical history
• eCduircraetniotnms& medication
• Paalcttoehrnosluosfeor abuse
• Living arrangements
17. 11
ASSESSMEN T: PHYSICAL
Examine:
• Neurologic status
• Mental status
• Functional status
Include:
• Quantified screens for cognition
For example, Folstein’s MMSE, Mini-Cog,
SLUMS, MoCA
• Neuropsychologic testing
21. 14
ASSESSMEN T: BRAIN IMAGING
Consider imaging when:
• Onset occurs at age <65 years
• Neurologic signs are asymmetric or focal
• Clinical picture suggests normal-pressure hydrocephalus
• Patient has had recent fall or other head trauma
Consider:
• Noncontrast computed topography head scan
• Magnetic resonance imaging
• Positron emission tomography
23. 16
NORMAL AGING
• No consistent, progressive deviations on testing
of memory
• Some decline in processing and recall of new
information: slower, harder
• Reminders work—visual tips, notes
• Absence of significant effects on ADLs or IADLs
due to cognition
24. 17
MILD COGNITIVE IMPAIRMENT
• Subjective complaint of decline in at least one cognitive
domain: noticeable and measurable
• Nmopaiirment in independent living
• 9.4 to 14.3/1000 person-years convert to Alzheimer
disease
• ~50% with amnestic MCI maintain stable level of
impairment or return to normal cognitive status in 35 yr
25. 18
DELIRIUM VS. DEMENTIA
• Delirium and dementia often occur together in older
hospitalized patients
• Tsthinegduiishing signs of delirium are:
Acute onset
Cognitive fluctuations over hours or days
Impaired consciousness and attention
Altered sleep cycles
Search for underlying dementia once delirium cleared
26. 19
DEPRESSI ON VS. DEM ENTI A (1 of 2)
The symptoms of depression and dementia often
overlap:
• Impaired concentration
• Lack of motivation, loss of interest, apathy
• Psychomotor retardation
• Sleep disturbance
27. 20
DEPRESSI ON VS. DEM ENTI A (2 of 2)
• Patients with primary depression are generally
unlike those with dementia in that they:
Demonstrate motivation during cognitive testing
Express cognitive complaints that exceed
measured deficits
Maintain language and motor skills
• ~50% presenting with reversible dementia and
depression progress to dementia within 5 yr
28. 21
ALZHEIMER DISEASE
• aOdnusaelt: gr
• Cognitive symptoms: memory impairment core feature
with difficulty learning new information
• Motor symptoms: rare early, apraxia later
• Progression: gradual, over 8–10 yr on average
• Lab tests: normal
• Imaging: possible global atrophy, small hippocampal
volumes
29. 22
VASCULAR DEMENTIA
• aOynbse:sumdden/stepwise
• Cognitive symptoms: depend on anatomy of ischemia,
but dysexecutive syndrome common
• Motor symptoms: correlates with ischemia
• Progression: stepwise with further ischemia
• Lab tests: normal
• Iomrtaicgainlogr:scubcortical changes on MRI
30. 23
LEWY BODY DEMENTIA
• aOdnusaelt: gr
• Cognitive symptoms: memory, visuospatial,
hallucinations, fluctuations
• Motor symptoms: parkinsonism
• Progression: gradual, but usually faster than AD
• Lab tests: normal
• Imaging: possible global atrophy
31. 24
FRONTOTEMPORAL DEMENTIA
• aOdnusaelt,:ugsruallyage <60
• Cognitive symptoms: executive, language, and
behavioral dysfunction, including disinhibition and
hyperorality
• Motor symptoms: none; may be associated with ALS
in rare cases
• Progression: gradual but faster than AD
• Lab tests: normal
• Imaging: atrophy in frontal and temporal lobes
32. 27
PRIMARY GOAL OF TREATMENT
To enhance quality of life and
maximize functional performance by
improving cognition, mood, and behavior
34. 25
Stage 1: No cognitive impairment
Unimpaired individuals experience no memory problems, and none is evident to a
health care professional during a medical interview.
Stage 2: Very mild cognitive decline
Individuals at this stage feel as if they have memory lapses, especially in forgetting
familiar words or names or the location of keys, eyeglasses, or other everyday
objects. However, these problems are not evident during a medical examination or
apparent to friends, family, or coworkers.
Stage 3: Mild cognitive decline
Early-stage Alzheimer disease can be diagnosed in some, but not all, individuals.
Friends, family, or coworkers begin to notice deficiencies. Problems with memory or
concentration may be measurable in clinical testing or discernible during a detailed
medical interview.
Stage 4: Moderate cognitive decline (mild or early-stage Alzheimer disease)
At this stage, a careful medical interview detects clear-cut deficiencies. The affected
individual may seem subdued and withdrawn, especially in socially or mentally
challenging situations.
THE GENERAL PROGRESSION OF
DEMENTIA (1 of 2)
35. 26
Stage 5: Moderately severe cognitive decline (moderate or mid-stage Alzheimer
disease)
Major gaps in memory and deficits in cognitive function emerge. Some assistance with
day-to-day activities becomes essential.
Stage 6: Severe cognitive decline (moderately severe or mid-stage Alzheimer disease)
Memory difficulties continue to worsen, significant personality changes may emerge,
and affected individuals need extensive help with customary daily activities.
Stage 7: Very severe cognitive decline (severe or late-stage Alzheimer disease)
This is the final stage of the disease when individuals lose the ability to respond to their
environment, to speak, and ultimately to control movement.
THE GENERAL PROGRESSION OF
DEMENTIA (2 of 2)
39. Typical Hospice Eligibility Criteria
(Local Coverage Determinations)
Functional AssessmentStaging
1. No difficulties
2. Subjective forgetfulness
3. Decreased executivefunction
4. Difficulty with complextasks
5. Requires supervision with ADLs
6. Impaired ADLs withincontinence
7. Stage Seven
A. Ability to speak limited to 6
words
B. Ability to speak limited to a
single word
C. Loss of ambulation
D. Inability to sit
E. Inability to smile
F. Inability to hold head up
40. Feeding Tubes inAdvance
Dementia
Studies show no impact of feedingtubes in
advanced dementia on:
Survival(Median survival 56 days)
Pressure ulcer healing
Aspiration pneumonia
Likely increase inburdens
Loss of experience/connection of feeding
Restraints
Complications are common
Dehydration isnot painful
Use associated with decreased satisfaction
with endof life care
Sampson EL, Candy B, Jones L, “Enteral tube feeding or older people with
advanced dementia. Cochrane Database Syst. Rev. 2009;(2):CD007209
41. End of Life DecisionMaking:
Feeding Tubes inDementia
Telephone survey of 450 relatives of SNF
patients
with advanced dementia who had feeding tubes
85%of decisions were made in hospital
47%reported discussion lasted <15minutes
1/3 family members recalled that no risks of tube
feeding presented
50%felt hospital physician was “strongly in
favor of tube insertion”
13%“felt pressured to put in a feeding tube”
Approx. 25%regretted the feeding tube
decision
Kuo, Sylvia, Poster Presentation, American Geriatrics
Society Annual Meeting, May 12, 2010, Orlando,FL
42. Non-pharmacologic Interventions for
Behavioral Problems
Many programs have worked, but difficult to
generalize as to what can be dispensed or
spread
Pain and symptom control
Exercise
Music/Recordings
Optimal level of activity
Environmental changes: light, reassuring
picture
Treating each patient with personalized
care
Resources: A Systematic Evidence Review of Non-pharmacological Interventions for Behavioral Symptoms of Dementia
(VA’s Health Services Research & Development Service’s (HSR&D’s) Evidence-based Synthesis Program (2011)
http://www.hsrd.research.va.gov/publications/esp/Dementia-Nonpharm.pdf
See also extensive materials below from IA Adapt, Interact, Hand in Hand
44. ABCDs Examples
Antecedents
Diagnoses (What is the
cause of dementia? )
What other diagnoses
exist?
Fatigue, hunger,pain
Levels of stimulation
Restraint
Staff or resident
approaches
Gender & Cultural
Lack of exercise
Behaviors
What exactly is the
behavior?
Crying
Yelling
Biting
Hitting
Grabbing
Fecal play
Time of day
Exact setting and details
as possible
Consequences
Attention
Isolation
Abuse
Injury
Medication response
Other positive
reinforcement
B
E=Emotional
Engagement
45. Common ReasonsforDifficult Behaviors
inPatientswith Dementia
Response toTrigger
Other Medical
Pain
Personality
Iatrogenic: othermeds
Sleep Deficit
Social/
Caregiver
Enjoys the behavior
Delirium
Discomfort
Psychosis
Fear/Boredom/Anxiety
Adjustment
Problems
Behaviors
J
46. Approach to Medicationsfor
Behavioral Problems in SNFIV
First try:
Behavioral interventions (at least2 trials)
Medication toxicities minimized
(e.g. anticholinergic medications)
Require (As per Title 22 and CMS)
Behavior causes significant impairment of
quality of life or danger to self or others
Informed consent for seriousrisks(including
death) obtained
Avoid prn antipsychotics in dementia
47. Advancecare planning for
patients with dementia
1. Educate physicians, families and staff about
trajectory of illness ofdementia
2. Elicit patient’s goals of care based on
advance directives and prior values
3. Educate families and physicians about
burdens and benefits of interventions,
including lack of benefit for tube feeding.
4. Complete POLST documents: assess notonly
completion but quality of the conversations
5. Consider hospice ifappropriate
48. 28
NONPHARMACOLOGIC
MANAGEMENT (1 of 2)
• Cognitive rehabilitation
• Supportive individual and group therapy
• Physical and mental activity
• Regular appointments every 3–6 months
• Family and caregiver education and support
• Attention to safety
Need for supervision, wandering, driving etc.
49.
50.
51.
52.
53. 29
NONPHARMACOLOGIC
MANAGEMENT (2 of 2)
• Environmental modification
Orientation and memory measures such as
clocks, calendars, to-do list, visual clues, simple
and compassionate communication style
54.
55. 30
PHARMACOLOGIC MANAGEMENT
• Treatment should be individualized
• Cholinesterase inhibitors: donepezil, rivastigmine,
galantamine
• Memantine
• Other cognitive enhancers
• Antidepressants
• Psychoactive medications
56. 31
CHOLINESTERASE INHIBITORS
(1 of 2)
• Slow breakdown of acetylcholine
• Clinical trials demonstrate modest delay in cognitive
decline compared with placebo in AD
• GI side effects common
Mitigated by slow titration curve
Maximum dosing of donepezil 23 mg/day creates significant
side effects without evidence of improving global function
• No evidence of difference in efficacy among drugs
57. 32
CHOLINESTERASE INHIBITORS
(2 of 2)
• Use in other dementias
Widespread use in vascular dementia not
recommended
Behavioral disturbances in Lewy body dementia can
benefit from treatment
Rivastigmine is FDA-approved for mild to moderate
dementia in Parkinson dementia
Treatment in frontotemporal dementia may worsen
agitation
58. 33
MEMANTINE
• Neuroprotective effect is to reduce glutamate-mediated
excitotoxicity
• Modest benefit on cognition, ADLs, and behavior in AD
• Limited effect on cognition and no evidence to support
widespread use in vascular dementia
• FovDeAd-afoprpmroderate to severe AD
• Common adverse events: constipation, dizziness,
headache
59. 34
OTHER COGNITIVE
ENHANCERS
• Vitamin E (α–tocopherol) may lower rate of decline, but
no evidence of cognitive improvement in AD
No longer recommended due to evidence of increased
mortality with high-dose supplementation
• Selegiline may low rate of decline, but no evidence of
cognitive improvement in AD
• Ginkgo biloba offers no benefit in slowing cognitive
decline in MCI
60. 35
SYMPTOM MANAGEMENT (1 of 2)
• Psychoactive medications
Behavioral disturbances best managed nonpharmacologically,
eg, reducing overstimulation, environmental modification
• Antidepressants
Depressed mood, low appetite, insomnia, fatigue, irritability,
agitation
fPeocstisvieblfyorefdisinhibitionand compulsive behaviors
Caution: falls and anticholinergic effects that may worsen
confusion (ie, paroxetine)
61. 36
SYMPTOM MANAGEMENT (2 of 2)
• 1st/2nd-generation antipsychotics
Limited evidence of efficacy and increased risk of all-cause
mortality in dementia
Should be used with caution in targeting delusions, hallucinations,
and paranoia ― frequently attempt to taper off
• Valproic acid and carbamazepine
Possible options, but with limited evidence and increased risk of
mortality
• Benzodiazepines and anticholinergic medications should
be avoided
62. 37
RESOURCES FOR
MANAGING DEMENTIA (1 of 2)
• Specialist referral to:
Geriatric psychiatrist
Neurologist
Neuropsychologist
• Social worker
• Physical therapist
• Nurse
63. 38
RESOURCES FOR
MANAGING DEMENTIA (2 of 2)
• oArttworilnl,ecyofnservatorship,estate planning
• Community: neighbors & friends, aging & mental health
networks, adult day care, respite care, home-health
agency
• Organizations: Alzheimer’s Association, AreaAgencies
on Aging, Councils onAging
• Services: Meals-on-Wheels, senior citizen centers
64. 39
SUMMARY (1 of 2)
• Dementia is common in older adults but is not
an inherent part of aging
• AsDthei most common type of dementia,
followed by vascular dementia and dementia
with Lewy bodies
• Evaluation includes history with informant,
physical & functional assessment, focused
labs, & possibly brain imaging
65. 40
SUMMARY (2 of 2)
• Primary treatment goals: enhance quality of life
and maximize function by improving cognition,
mood, behavior
• Treatment may involve both medications and
nonpharmacologic interventions
• Community resources should be used to
support patient, family, caregivers
66.
67. 41
CASE 1 (1 of 4)
• An 80-year-old woman is brought to the office because
she has hallucinations of children and small animals
when she is alone in a room. The hallucinations
sometimes disturb and agitate her.
• Hamerilyf also notes that she is having more difficulty
walking and has hand tremors when she sits quietly.
• Sah9e-has month history of short-term memory loss;
problems with orientation that sometimes worsen
dramatically; and difficulty managing her finances,
preparing complex meals, and following TV shows.
68. 42
CASE 1 (2 of 4)
–Mental State Examination is• Hcoerresonthe Mini
23 of 30.
• On physical examination, there are signs of cogwheel
rigidity and resting tremors, which have been noted
for the past year.
69. 43
CASE 1 (3 of 4)
Which of the following is the most likely diagnosis?
A. Dementia with Lewy bodies
B. Alzheimer disease
C. Parkinson disease with dementia
D. Huntington disease
70. 44
CASE 1 (4 of 4)
Which of the following is the most likely diagnosis?
A. Dementia with Lewy bodies
B. Alzheimer disease
C. Parkinson disease with dementia
D. Huntington disease
71. 45
CASE 2 (1 of 4)
• A 67-year-old man comes to the office to establish care.
• History includes mild hypertension.
• The patient is married and maintains an active
professional and social life. He is physically active,
does not smoke, and drinks 1–2 glasses of wine daily.
• Medications include hydrochlorothiazide 12.5 mg/day,
aspirin 81 mg/day, and a daily multivitamin.
72. 46
CASE 2 (2 of 4)
• Fstaomryilyishniotablefor an 84- year-old maternal
aunt who recently died after 6 years in the memory-
disorders unit of a nursing home.
• H’sisdeaautnhthas caused the patient to worry about
his own risk of dementia. He requests a referral for
genetic testing for Alzheimer disease.
• Physical examination is unremarkable.
73. 47
CASE 2 (3 of 4)
Which of the following is true about risk of Alzheimer
disease?
A. Mutations in 4 known deterministic (causative) genes
are associated with autosomal-dominant AD.
B. The lifetime risk of developing AD in the general
population is approximately 20%, assuming a life span
of 75 to 80 years.
C. AD is sporadic in approximately 75% of all cases.
D. Genetic risk for AD varies by race and ethnicity.
74. 48
CASE 2 (4 of 4)
Which of the following is true about risk of Alzheimer
disease?
A. Mutations in 4 known deterministic (causative) genes
are associated with autosomal-dominant AD.
B. The lifetime risk of developing AD in the general
population is approximately 20%, assuming a life span
of 75 to 80 years.
C. AD is sporadic in approximately 75% of all cases.
D. Genetic risk for AD varies by race and ethnicity.
75. 50
CASE 3 (2 of 4)
• Tiehnet’spawtifeexpresses concern about his ability
to drive safely. She sometimes feels nervous riding
with him. She notes that he has stopped driving at
night or when it rains, that he drives shorter distances
and less often since he retired 5 years ago, and that he
received a traffic citation about 4 years ago. He has
had no accidents or additional citations since then.
• Wkehdeinfhaesthinks he is a safe driver, the patient
says, “I’m probably a little bit slower than I used to be,
but overall I’d say yes, I’m still a perfectly safe driver.”
76. 51
CASE 3 (3 of 4)
Which of the following is the strongest evidence of the
patient’s risk for unsafe driving?
A. Patient’s self-restriction and situational avoidance
B. History of a traffic citation in the past 5 years
C. Spouse’s concern
D. Score ≤24 on MMSE
E. Patient’s self-rating of driving ability
77. 52
CASE 3 (4 of 4)
Which of the following is the strongest evidence of the
patient’s risk for unsafe driving?
A. Patient’s self-restriction and situational avoidance
B. History of a traffic citation in the past 5 years
C. Spouse’s concern
D. Score ≤24 on MMSE
E. Patient’s self-rating of driving ability