week 13- dementia Flashcards
1
Q
is memory loss need to be present in dementia
A
no affects many cognitive domains and not necessarily memory
2
Q
6 key neurocognitive domains in dementia
A
- perceptual-motor function
- language
- executive function
- learning and memory
- complex attention
- social cognition
3
Q
types of cognitive decline
A
-psuedodementia (depression or other psyhiatric disorder)
-delirium
-MCI
-dementia (AD, vascular, Lewy body, frontotemporal)
4
Q
dementia definition in DSM 4
A
Dementia is often associated with memory loss, but definitions have evolved to think beyond memory impairment and describe a diverse group of disorders that affects multiple cognitive domains.
DSM-IV (1994) characterized dementia as a chronically progressive brain disease that impairs intellect and behaviour to the point where customary activities of daily living become compromised.1
5
Q
dementia definition in DSM 5
A
replaced the term ‘dementia’ to major neurocognitive disorder characterized by:
- evidence of significant cognitive decline in one or more cognitive domains compared to a previous level of performance
- persistent and progressive decline over time
- cognitive deficits interfere with independence in everyday activities
- not associated with delirium or another psychiatric/mental disorder
6
Q
prevalence of dementia
A
increasing/// 2022 was 600k Canadians
7
Q
age of onset in dementia
A
Dementia typically begins after age 60, and the prevalence doubles approximately every 5 years thereafter; in persons aged 85 and older, around half have dementia.4
8
Q
women or men in dementia more
A
More prevalent among women, likely due to longer life expectancy
9
Q
most common form of dementia
A
Alzheimer disease is the most common cause of dementia (70-80% of all cases)
Other causes include:
* Vascular dementia (15%)
* Lewy body dementia (5%)
* Frontotemporal dementia (25% in patients with dementia >65 y/o)
* Mixed dementia (most common: Alzheimer disease with vascular dementia)
10
Q
strongest risk factor for dementia
A
age
The lifetime risk of dementia is approximately 17%,
with the incidence doubling each decade after 60 years of age.5
11
Q
things that increase risk of dementia
A
- family history of dementia
- apolipoprotein E4 genotype
- personal history of cardiovascular, cerebrovascular disease,
diabetes mellitus, hypertension, obesity (midlife) - history of significant head injury
- hearing loss
- vitamin D deficiency
- chronic sleep deprivation
- cigarette smoking
- lower education level
12
Q
protective factors against dementia
A
- physical activity
- higher education level
- ongoing intellectual stimulation
- social engagement
13
Q
dementia definition? what is affected?
A
Cognitive decline from a previous level of performance in one or more cognitive domains that interferes with independence in activities of daily living. ADL
14
Q
most common symptom in dementia
A
memory impairment
15
Q
symptoms in dementia- agnosia
A
Agnosia: inability to recognize and name familiar objects when visual perception is adequate.1
16
Q
symptoms in dementia- aphasia
A
Aphasia: language disturbance which can be motor or sensory aphasia.
17
Q
symptoms in dementia- apraxia
A
Apraxia: inability to perform a motor task despite intact motor function.
18
Q
symptoms in dementia- executive dysfunction
A
Executive dysfunction: inability to think abstractly and to plan and carry out complex behaviors including initiating the steps necessary to do a task, monitoring progress, and stopping the task.
19
Q
symptoms in dementia- neuro and social deficits
A
Neuropsychiatric and social deficits presenting as depression, apathy, anxiety, hallucinations, delusions, agitation, insomnia, sleep disturbances, compulsions, or disinhibition
20
Q
examples in the complex attention cognitive domain effected by dementia
A
Normal, routine tasks take longer; difficulty in completing tasks when multiple stimuli are present; difficulty in maintaining information while completing task (e.g., completing mental math calculations, remembering a phone number to dial); work requires more overview/rechecking than before.
21
Q
examples in the executive function cognitive domain effected by dementia
A
Difficulty in completing previously familiar multistep tasks, such as preparing a meal; no longer wanting to participate in activities of the home; difficulty in completing activities or tasks because of easy distractibility; social outings become more taxing and less enjoyable.
22
Q
examples in the language cognitive domain effected by dementia
A
Difficulty finding the correct words; using general pronouns regularly instead of names; mispronunciation of words; problems with understanding verbal and written communication.
23
Q
examples in the learning and memory cognitive domain effected by dementia
A
Forgetting to buy items or buying the same items multiple times at the store; repetition in conversations; difficulty in recalling recent events; relying on lists of tasks to complete; forgetting to pay bills.
24
Q
examples in the perceptiual-motor cognitive domain effected by dementia
A
Difficulty in using familiar technology, tools, or kitchen appliances; getting lost in familiar environments.
25
examples in the social cognition cognitive domain effected by dementia
Apathy, increase in inappropriate behaviors, loss of empathy, impaired judgment.
26
symptoms differing in dementia depending on what area of the brain effected
* Short term memory loss: hippocampus
* Word finding difficulty: temporoparietal junction of the left hemisphere
* Problems with articulation, fluency, comprehension, or word meaning are anatomically distinct
and less common
* Visuospatial dysfunction: right parietal lobe is one of the brain areas affected
* Executive dysfunction: varies and could include the frontal lobes or subcortical areas like the
basal ganglia or cerebral white matter.
* Apathy or indifference (separate from depression): may have a similar anatomy as executive
dysfunction.
* Apraxia, (loss of learned motor behaviors), may result from dysfunction of the frontal or parietal
lobes, especially the left parietal lobe.
27
physical exams to see neurological findings in dementia
* Eye movement abnormalities
* Parkinsonism or other motor abnormalities
* Focal neurological deficits
28
time course of dementia
Insidious onset and gradual progression of symptoms
29
if dementia develops quickly what is usually the cause
When dementia develops quickly (over a few weeks to a few months) suspect rapidly progressive dementia. This could be caused by fatal and potentially transmissible conditions, such as prion disease, or manageable causes, such as infections, toxins, neoplasms, and autoimmune and inflammatory diseases.
30
median survival for demtnai
The median survival time after diagnosis of dementia is 4.5 years, but this varies based on age at diagnosis, ranging from 10.7 years for patients diagnosed in their 60s to 3.8 years for patients diagnosed in their 90s
31
dementia symptoms
* Behavioral problems, depression, and psychotic symptoms are common in all types of dementia.
* Eventually, most individuals with dementia struggle to perform simple tasks without assistance
32
1st step if think patient has memory loss of dementia
brief initial screening (i.e. mini cog)
if positive then do MMSE, MOCA
if positive screen for depression, CBC, b12, MRI, viral testing , thyroid
33
obtain history in dementia
* Characterize the nature, magnitude, and course of cognitive changes
* Nature: cognitive domains affected.
* Magnitude: severity as it relates to current functional abilities - does the cognitive loss affect
activities of daily living (ADL) and/or instrumental ADL?
* Course: insidious onset and a slow progression? rapid onset and fluctuating and stepwise
progression?
* Past medical history: vascular disease risk factors (hypertension and diabetes), existing brain conditions (such as stroke, Parkinson’s Disease, head trauma),
* Medication review: medications that impair cognition (e.g. anticholinergics, sleep aids and anxiolytics, analgesics such as codeine containing agents)
34
what can impair cognition
medications
(e.g. anticholinergics, sleep aids and anxiolytics, analgesics such as codeine containing agents)
35
medical history important for dementia
Past medical history: vascular disease risk factors (hypertension and diabetes), existing brain conditions (such as stroke, Parkinson’s Disease, head trauma),
36
history taking in dementia
Family history of dementia, especially young-onset dementia in first-degree relatives (inherited form of dementia)
* Social history: alcohol or other substance use, smoking history, risk for social isolation?
* Safety concerns: driving ability, episodes of wandering, vulnerability to financial or physical abuse
37
physical exam in dementia
* Neurological exam: evaluate objective evidence of neurocognitive problems, focal neurologic signs, parkinsonism
* Gait analysis
38
cognitive tests in dementia
who does them
what can effect results
* Conducted to screen for cognitive impairment (if dementia is suspected) and quantify severity of impairment.
* Can be completed by the patient or a reliable informant.
* Factors that can affect results include the patient’s educational level, age and language.
39
which cognitive test covers all 6 domains of dementia
cambridge cognitive examination
40
whats more important when diagnosing dementia; sensitivity of specificity
specificity
* When diagnosing dementia, valuing the specificity of the test over sensitivity can help avoid misdiagnosis and unnecessary tests.
41
early diagnosis of dementia via high sensitivity or specificity
* However, early diagnosis of dementia is important for effective interventions and education, and in some cases tests with high sensitivity to avoid mislabeling dementia as normal aging is preferable.
42
high LR+ in dementia
positive test indicates high probability of dementia
43
best LR- in dementia
less likely to mislabel a patient with dementia as experiencing normal aging.
44
USPSTF on current evidences of screening for cognitive impairment in adults
current evidence is insufficient to assess the benefits vs. harms of screening for cognitive impairment in older adults.
45
If dementia is suspected, physicians can use brief screening tests such as
Mini-Cog or General Practitioner Assessment of Cognition
If the results are abnormal, further evaluation is warranted using more in-depth screening tools such as the Montreal Cognitive Assessment, Saint Louis University Mental Status Examination, or Mini-Mental State Examination
46
3 brief initial screening tests for cognitive impairment
1. mini-cog
2. general practitioner assessment of cognition (GPCOG)
3. ascertain dementia 8-item informant questionnaire
47
highest sensitivity for brief initial screening test
mini-cog (less specificity)
48
mini cog includes
A brief cognitive assessment that involves repeating three unrelated words, performing a clock drawing test, and recalling the three words
49
General Practitioner Assessment of Cognition (GPCOG) includes
Validated in the primary care setting that includes a patient screen and an informant component. It evaluates recall, time orientation, clock drawing, and information components.
50
Ascertain Dementia 8-Item Informant Questionnaire includes
Informant-based test that screens for major and minor neurocognitive disorders. It can also be administered to the patient but is less sensitive in that format.
51
if the brief screening test is positive or negative do what next
* Positive brief screening test→further cognitive test to quantify degree of impairment.
* If findings are normal on the cognitive test, consider referring for neuropsychiatric evaluation
especially if cognitive impairment is strongly suspected.
52
what tests to do after positive brief screening test for dementia
MMSE, MoCA, SLUM
53
MMSE
good specificity and sensitivity
54
alternative to MMSE
Montreal Cognitive Assessment (MoCA) and Saint Louis University Mental Status Examination (SLUM)
55
MMSE is bad because
copyrighted
56
what is pseudodementia
* Psychiatric disease can lead to impaired cognition (pseudodementia).
* Clinical presentation: poor focus and concentration may primary complaint
* The symptoms should improve with appropriate psychiatric treatment.
57
geriatric depression scale
5-item validated screening tool for depression in older patients
58
dementia and depression
Untreated mood disorders may increase the risk of developing age-related dementia, and psychiatric symptoms can worsen cognitive impairment in patients with dementia.
* It is important to not overlook the possibility of depression when screening for and treating dementia
59
lab tests for dementia
* Standard laboratory evaluation for patients with cognitive impairment (AAFP)5: CBC, comprehensive metabolic panel, TSH, and B12
* Other tests to consider based on specific concerns: HIV testing, rapid plasma regain (RPR) testing (neurosyphilis), inflammatory markers (vasculitis), CSF analysis (lumbar puncture) in patients with rapidly progressive symptoms to rule out prion disease or other infections.
60
best neuroimaging fro dementia
MRI without contrast, but CT scan if MRI contraindicated
61
routine neuroimaging in suspected dementia ebcause
to rule out intracranial abnormalities and may be helpful in determining dementia subtype.
62
is genetic testing recommended in routine testing for dementia
* Genetic testing for apolipoprotein E4 allele is not recommended as part of the routine evaluation for cognitive impairment. (doest change manamgent and freaks patient out)
* Referral for genetic testing should be considered in patients with positive family history (Alzheimer disease at a young age in an autosomal dominant pattern)
63
12 actions for healthier brain (dementia prevention)
1. physical activity
2. protect heart
3. socialize
4. manage medical conditions
5. challenge thinking, learn new things
6. good sleep
7. treat depression
8. avoid excess alcohol
9. maintain your hearing
10. find meaning in life
11. avoid head injury
12. adopt healthy behaviours
64
ddx for dementia
* Delirium
* Psychiatric Disorder (Pseudodementia)
* Mild Cognitive Impairment
* NormalAging
65
what is delirium
Acute confusional state that often occurs in response to an identifiable trigger
66
who is delirium common in
Delirium is a common and preventable condition that affects a significant portion of hospitalized older patients (as many as half of all people age 65 and older who are hospitalized).
67
delirium outcomes
unctional and cognitive decline, loss of independence, institutionalization, and death.
68
ethology of delirium
* Multifactorial and complex interrelationship between patient vulnerability (predisposing factors) and noxious insults (precipitating factors).
* Removing or treating one risk factor alone may not resolve delirium, as addressing multiple factors is often necessary for symptom improvement.
69
predisposing factors for delirium
* Dementia or cognitive impairment
* Comorbidity/severity of illness
* Depression
* Vision and/or hearing
impairment
* Functional impairment
* History of transient
ischemia or stroke
* History of alcohol abuse
* History of hypertension
* Carotid artery disease
* History of delirium
* Age>70
70
precipitating factors for delirium
* Drugs (polypharmacy, psychoactive medications, sedatives, hypnotics)
* Alcohol intoxication/withdrawal
* Use of physical restraints
* Indwelling bladder catheter
* Physiologic (sleep deprivation)
* Metabolic disturbance
* Infection
* Iatrogenic complications
* Major surgical procedure
* Trauma admission
* Urgent admission
* Coma
* ICU stay > 10 days
71
symptoms of delirium
* Inattention: difficulty focusing, maintaining, and shifting attention or concentration.
* Reduced orientation to their environment, and at times to oneself.
* Appears easily distracted, have difficulty with multistep commands, and struggle to follow the flow of a conversation.
* Disorganized thoughts, disjointed speech, and an unclear or illogical flow of ideas
* Additional presenting signs and symptoms based on precipitating factor/etiology (i.e. if have pneumonia that precipitated it will have respiratory symptoms too)
72
hyperactive and hypoactive delirium
* Hyperactive: restlessness, agitation, hallucinations, delusions
* Hypoactive: lethargic, slow to respond
73
time course in delirium
* Acute (mental status changes typically occur over hours to days)
* The disturbance of awareness tends to develop over hours to days
* Fluctuating course, with symptoms waxing and waning in severity over a 24-hour period.
* Lucid intervals are characteristic, and the symptoms of delirium can be reversible within a short time.
74
common mechanisms in delirium and dementia
ssociated with decreased cerebral metabolism, cholinergic deficiency, inflammation, and abnormal glucose metabolism
75
can delirium and dementia coexist
yes- Dementia being a major risk factor for delirium and delirium leading to worsened cognitive functioning.
76
delirium vs dementia
* Both presents with altered mental status
* Delirium is acute and likely reversible while dementia is chronic and seldom reversible
77
diagnose dementia if have delirium?
The diagnosis of dementia cannot be made until delirium resolves.
78
types of deleicirum examples
* Substance intoxication delirium
* Substance withdrawal delirium
* Medication‐induced delirium
* Delirium due to another medical condition
79
clinical evaluation of delirium
* Establish diagnosis of delirium (clinical diagnosis)
* Determine the potential cause(s)
* Rule out life-threatening contributors
History and physical examination, including medication review, to evaluate cognitive change and identify potential causes.
80
brief cognitive screening test for delirium
Confusion Assessment Method (CAM)
* Standardized, validated diagnostic 4-item algorithm for delirium
* Presence of acute onset and fluctuating course, inattention, and either disorganized thinking or
altered level of consciousness
* Sensitivity of 94-100%, specificity of 90-95%, and high inter-rater reliability.
81
lab work for delirium
Based on clinical judgement and patient presentation
* CBC, chemistries, glucose, renal and liver function tests, urinalysis, test for occult infection should
help identify majority of possible causes
82
MILD COGNITIVE IMPAIRMENT (MCI)/
MILD NEUROCOGNITIVE DISORDER (MILD NCD) defimition
* A decline from a previous state of mental functioning that causes no or minimal interference with daily activities.
* Symptomatic predementia syndrome
83
MCI DSMV changes
* The DSM-V introduced the term "mild neurocognitive disorder" as a new framework for the diagnosis of mild cognitive impairment (MCI), replacing the previous non-specific category of "cognitive disorder not otherwise specified.”6
84
how to classify MCI
amnestic (memory loss) or non-amnestic
85
how many people with MCI get AD
Approximately 12% to 15% of persons with MCI will progress each year to AD or other forms of dementia.
86
symptoms of MCI
* Presents with cognitive complaints (usually memory impairment) and describes compensatory methods to adapt (i.e. lists, reminders, alarms).
* ‘modest’ cognitive decline compared to ‘significant’ cognitive decline in dementia
* Maintains level of function and capacity for independence in everyday activities6
* KEY feature differentiating MCI from dementia
87
how to differentiate MCI from dementia
can still do ADL and the cognitive decline isn't as much
88
time course of MCI
* Insidious, gradual, progressive onset
* Transitional state between normal, age-associated memory impairment and dementia.
89
amnestic vs non-amnestic MCI progression to major neurocognitve disorder (dementia)
* Amnestic MCI more likely to progress to Alzheimer’s disease
* Older individuals with non-amnestic MCI likely to progress to other forms of dementia (FTD,
dementia with Lew bodies, vascular dementia
90
how often to assess people with MCI to see if progress for dementia
Persons with suspected MCI should be reassessed on an annually to evaluate for progression to dementia.
91
NIA-AA diagnostic criteria for mild cognitive impairment
* The patient, an informant who knows the patient well, or a clinician observing the patient notes a concern regarding a change in cognition in comparison to the patient’s previous level.
* There is evidence of lower performance in one or more cognitive domains (memory, executive function, attention, language, and/or visuospatial skills) that is greater than would be expected for the patient’s age and educational background.
* The patient maintains preserved independence in functional abilities, although they may take more time, be less efficient, and make more errors at performing such activities than in the past.
* The patient does not meet criteria for dementia.
92
subtypes of demntia
* Alzheimer’s Disease
* Vascular Dementia
* Lewy Body Dementia
* Frontotemporal Lobe Dementia
* Mixed Dementia
93
most common mixed dementia
(most commonly associated with AD neurodegeneration and cerebrovascular disease)
94
pathologic hallmark of AD
amyloid plaques and neurofibrillary tangles
95
definition of Alzheimers
Diffuse functional and structural abnormalities in the brain that lead to progressive cognitive and behavioral deficits and functional decline.
96
most common dementia in older
AD
97
late vs early onset AD
Late onset AD is the most common form of the disorder, accounting for greater than 95% of all AD cases
98
non modifiable risk factors in AD - age
* Age is the single most important and validated risk factor for AD.
* Incidence and prevalence both increase with age: 3% among adults between the ages of 65 to 74, 17% in persons aged 75 to 84, and 32% in individuals age 85 and older
99
non modifiable risk factors in AD - gender
* More common among women, although study results are conflicting.
* In population-based studies, more than half reported a greater risk of AD in women, while the others found no difference.
* Gender-related factors such as life expectancy, education, occupation, and lifestyle, which can directly impact the risk of Alzheimer's disease
100
non modifiable risk factors in AD - race and ethnicity
* Possible, but difficult to determine since due to other confounding factors like education, access to healthcare, cultural beliefs and environmental factors.
* Environmental factors may have a larger impact on AD development than race.
* While biological or genetic differences may contribute to AD risk, accounting for social, cultural, and environmental factors can diminish racial and ethnic group differences in AD risk.
101
non modifiable risk factors in AD - genetic factors
* Apolipoprotein E Genotype: major determinant of risk in families with late-onset AD
* Three allelic forms (ε2, ε3, and ε4): risk increased 4x with at least one ε4 allele and 12x with two copies of the ε4 allele. ε4 genotype by itself is neither necessary nor sufficient to develop AD.
* In the Framingham study, individuals with the APOE ε4 genotype had varying risks of developing Alzheimer's disease (AD) by age 85, with 55% of ε4 homozygote carriers, 27% of ε4 heterozygote carriers, and 9% of noncarriers developing AD
102
modifiable risk factors in AD - education
* Low educational attainment, poor educational quality, and illiteracy have been shown to be associated with increased risk for AD.
* Education may be a marker of cognitive reserve as it modifies the association between AD neuropathology and level of cognitive function.
* Low education relative risk (RR) estimate for AD of 1.80 (95% CI 1.45–2.27) compared to high education.
* Unclear to what extent low education contributes to AD or whether early educational interventions will protect against the development of dementia
103
modifiable risk factors in AD - depression
Depression may mimic dementia (pseudodementia), but it’s also a risk factor for AD.
* increased risk of AD in patients with a history of late life depression (OR 1.65 (95% CI)1.42-1.92)
104
modifiable risk factors in AD - traumatic brain injury (TBI)
Moderate or severe TBI is a risk factor for AD in late life and may precipitate earlier onset of the disease. ( → magnitude of AD risk increases with TBI severity
105
Vascular risk factors in alzheimers
* Hypercholesterolemia, hypertension, diabetes mellitus, metabolic syndrome, obesity, and physical inactivity, have all been associated with a greater risk of developing AD in later life.
* High midlife total cholesterol and blood pressure levels are associated with a 2-3x increased risk of developing AD decades later (potentially conveying a greater risk than that caused by APOE ε4 allele)
* In a community-based cohort study, higher glucose levels were associated with an increased risk of dementia in populations both with and without diabetes mellitus.
* Metabolic syndrome is also associated with an increased risk for AD, although it is more consistently related to a greater risk of vascular dementia.
* Midlife obesity and physical inactivity are interrelated risk factors that independently increase the risk for developing AD in late life. More than 35% of current US adults meeting criteria for obesity, raising concerns about its potential contribution to the projected increases in AD incidence rates.
* Vascular factors independently increase AD risk. Having multiple cardiovascular risk factors in midlife greatly raises the risk of dementia in later life. Around one-third of AD cases globally could be prevented by addressing modifiable vascular risk factors.
106
which allele is most genetic risk for AD
e4 allele
107
108
amnestic presentation in AD
most common (memory)
* Difficulty remembering conversations, dates, appointments, and may misplace items.
* Memory deficits are gradually progressive and interfere with daily activities.
109
nonamnestic presentation in AD
* Language impairment: word-finding problems and progress to paraphasic errors and
circumlocution.
* Visuospatial presentation: deficits in spatial cognition, poor object and face recognition, difficulty perceiving multiple visual elements, and trouble understanding written language.
* Executive dysfunction: impairments in reasoning, judgment, problem-solving, and completing complex tasks
110
time course in AD
indisidious osnet, slowly progressive
111
clinical presentation in AD
* Changes in personality: Seen in later stages of AD and may include increased passivity, lack of interest, agitation, restlessness, and overactivity.
* Symptoms of depression: More than 30% of persons with AD develop symptoms of depression, including irritability, changes in appetite or sleep, trouble concentrating or making decisions, low energy, social withdrawal, and decline in physical function.
* Late-stage symptoms: Increased confusion, dysphagia, impaired gait, repeated falls, aggression, agitation, physical or verbal hostility.
* Become increasingly frail and dependent for self-care and activities of daily living, with bowel and bladder incontinence.
* May become immobile and bed-bound, increasing the risk of pressure sores, malnutrition, dehydration, and pneumonia.
112
further testing in AD
Definitive workup requires neuropathological confirmation (autopsy or biopsy), however new and “less invasive” diagnostic approaches are being researched:
Functional neuroimaging:
* Positron emission tomography (PET) with fluorodeoxyglucose (FDG): changes suggestive of AD (sensitivity
of 91% and specificity of 85%); helps differentiate frontotemporal dementia from AD.12
* Amyloid PET: Used in evaluating cognitive impairment for AD or other causes of cognitive decline. Associated with changes in management plans in over 60% of patients in a recent study.12
* Functional neuroimaging with tau radioligands: Appropriate for research purposes.
Cerebrospinal fluid (CSF) testing:
* May be considered to obtain evidence of AD (low amyloid and high tau levels).
* Can also help diagnose other neurodegenerative diseases or other etiologies.
113
genetic testing in AD? who for and what not to do?
* Recommended for young patients with a history of first-degree relatives with young- onset dementia.12
* Rare autosomal dominant forms of dementia warrant genetic counseling.
* APOE genotype is not recommended for routine evaluation of AD: most do not have the associated alleles, and current medical management would not change by the test results.
114
NIAAA criteria for AD on slide 60 and DSM5 on slide 61
115
causative vs probable vs possible AD in DSM-V
causative/ probable = genetic testing
possible= no evidence of genes with3 symptoms of memory, cogntition etc
116
how to present an AD diagnosis to patients
* Diagnosing Alzheimer's disease (AD) is challenging due to emotional responses from patients and families.
* Factors like coping mechanisms, culture, family dynamics, and existing knowledge impact reactions. Clinicians should be empathetic, honest, and provide resources for education and support.
* Goals include protecting memory, delaying progression, and ensuring safety.
* Use "Alzheimer disease" for diagnosis communication.
* Encourage local support groups and resources for effective patient management.
117
non pharmacological treatment in AD
* Vascular risk factor modification has known cardiovascular benefits that are strongly linked to cognitive decline.
* Follow established cardiovascular prevention guidelines when treating patients with memory complaints, taking into account their comorbid illnesses, quality of life, treatment costs, and life expectancy.
* Nonpharmacologic interventions, such as physical activity, mentally stimulating activities, and social activities, may provide cognitive benefits.
* Tailor these interventions to the individual's physical abilities, comorbid illnesses, social situation, and interests.
118
pharmalogic therapy for AD
cholinesterase inhibitors, NMDA receptor antagonists, and potentially aducanumab and other monoclonal antibodies targeting amyloid.
119
future preventative strategies fro AD
ncluding antiamyloid therapies, vascular risk factor modification, anti-inflammatory medications, antioxidants, exercise, social engagement, and cognitive stimulation.
120
caregiver support in AD
* Caregivers of individuals with AD face increased depression, work absence, and health problems.
* Clinicians should provide educational resources, practical tips, and effective communication strategies to caregivers.
121
definition of vascular dementia
Stepwise or progressive accumulation of cognitive deficits in association with repeated strokes.
122
2nd most common cause of dementia in 65+ yrs
vascular dementia
123
risk factors for vascular dementia
hyperlipidemia, hypertension, diabetes mellitus, and smoking (tobacco)
124
symptoms of vascular dementia
* Depends on the location of clinical stroke(s) and/or subcortical cerebrovascular disease +/- focal neurologic signs on PE
* Prominent disturbance in processing speed and frontal–executive function
* Development or worsening of cognitive deficits following a cerebrovascular event increases the certainty of vascular dementia.
* Should have evidence of relevant cerebrovascular disease by brain imaging1
125
physical signs and vascular dementia
* Physical signs: hemiparesis, pseudobulbar palsy and visual field defects
126
time course of vascular dementia
* Acute onset (following cerebrovascular event) of cognitive impairment with some stabilization (if only one vascular event) and/or stepwise deterioration (if multiple infarcts)
* Unpredictable disease progression
127
probable vs possible vascular neurocogntive disorder
Probable vascular neurocognitive disorder is diagnosed if one of the following is present; otherwise possible vascular neurocognitive disorder should be diagnosed:
1. Clinicalcriteriaaresupportedbyneuroimagingevidenceofsignificantparenchymalinjuryattributedto
cerebrovascular disease (neuroimaging-supported)
2. The neurocognitive syndrome is temporally related to one or more documented cerebrovascular events
3. Both clinical and genetic (e.g. - cerebral autosomal dominant arteriopathy with subcortical infarcts and
leukoencephalopathy) evidence of cerebrovascular disease is present.
Possible vascular neurocognitive disorder is diagnosed if the clinical criteria are met but neuroimaging is not available and the temporal relationship of the neurocognitive syndrome with one or more cerebrovascular events is not established.
128
how to prevent vascular dementia
prevented by modifying risk factors such as diabetes, hypertension, smoking, and hyperlipidemia.
* Hypertension is a crucial risk factor that should be addressed, as antihypertensive medications can reduce the risk.
* Managing coronary artery disease, atrial fibrillation, and ischemic heart disease is also important.
* For patients with early cognitive impairment or evidence of stroke or carotid artery disease, secondary prevention with treatments like carotid endarterectomy, antiplatelet agents, warfarin, or physical exercise can slow down disease progression.
129
lewy body dementia definition
Lewy body dementia is a type of dementia characterized by the presence of Lewy bodies (abnormal intracellular inclusions consisting of α-synuclein) in the cortex.
130
WHATS PRESENT IN LEW BODY DEMEMNTIA
Lewy bodies with alpha synculein in the cortex
131
core features of Lewy body dementia
* Fluctuating cognition with pronounced variations in attention and alertness
* Recurrent visual hallucinations that are well formed and detailed
* Spontaneous features of parkinsonism (bradykinesia, rest tremor, or rigidity) subsequent to the development of cognitive decline.
132
suggestive features of Lewy body dementia
* Rapid eye movement (REM) sleep behaviour disorder
* Severe neuroleptic sensitivity: poor tolerance of neuroleptics and dopaminergics.
133
how many features to diagnose Lewy body dementia
2 core features or 1 suggestive and 1+ core feature
134
further testing in lewy body dementia
-sleep polysomnogrphay to see if have REM sleep behaviour disroder
-low stratal dopamine uptake on CT or PET scan
-CT or MRI for structural changes in temporal
135
frontotemporal dementia (picks disease) definition
Frontotemporal dementia (FTD) is a spectrum of clinical syndromes characterized by neuronal degeneration involving the frontal and anterior temporal lobes of the brain.
136
types of frontotemporal lobe dementia
* Behavior variant (bvFTD)
* Language variant:
* Non-fluent variant primary progressive aphasia (nfvPPA)
* Semantic variant primary progressive aphasia (svPPA)
137
mean age in frontotemporal dementia
58
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which type of frontotemporal lobe dementia more often occurs in men and women
bvFTD and svPPA are more prevalent in men,
while nfvPPA predominantly occurs in women.
* Behavior variant (bvFTD)
* Language variant:
* Non-fluent variant primary progressive aphasia (nfvPPA)
* Semantic variant primary progressive aphasia (svPPA)
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risk factors for frontotemporal dementia
-genetic
-headtrauma
-thyroid disease
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symptoms in frontotemporal dementia
* Wide range of presentations in relation to the areas involved.
* Associated with prominent decline in social cognition and/or executive abilities, but with relative sparing of learning and memory, and perceptual–motor function.
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timing of frontotemporal dememtian
* Insidious onset and gradually progressive impairment
* Memory, abstract thinking, and calculating abilities are spared earlier in the disease course.
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most common type of frontotemporal dementai
Behavior variant type FTD (bvFTD)
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Behavior variant type FTD (bvFTD) symptoms
* Presents with a cluster of altered behavior and personality changes earlier in the disease process:
* disinhibition (most common presentation)
* loss of emotional reactivity and disease insight
* Apathy
* impaired abstract thinking
* and executive function that gradually worsens over time.
May demonstrate a change in dietary behavior and loss of fundamental emotions and empathy
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most common symptom in Behavior variant type FTD (bvFTD)
disinhibition
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memory in Behavior variant type FTD (bvFTD)
Intact memory until late in the disease
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semantic variant FTD symptoms
* Presents with language difficulties characterized by: * Paraphasia
* Difficulty in understanding the meaning of words
* Impaired comprehension
* Difficulty in recognizing unfamiliar objects or faces.
* Speech is fluent but doe not make any sense.
* Memory is affected late in the disease.
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Non-fluent variant Primary Progressive Aphasia (nfvPPA) symptoms
* Presents with effortful halted speech and paraphasia (jumbled words)
* Difficulty in understanding complex sentences and naming objects.
* Memory, abstract thinking, and calculating abilities are spared earlier in the disease course.
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portable vs possible frontotemporal dementia
probable if have genetic and evidence of frontal or temporal lobe in neuroimagingin
possible if no evidence of genes and no neuroimaging done
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further testing in frontotemporal dementia
* Biomarker in blood and CSF: neurofilament light chain
* Neuroimaging: MRI, CT scan, PET demonstrates non-specific atrophy and hypoperfusion in the frontal and temporal lobes. May aid in diagnosis or rule out other causes
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BEHAVIORAL AND PSYCHOLOGICAL SYMPTOMS OF DEMENTIA (BPSD)
Behavioral and psychological symptoms of dementia (BPSD) include a range of neuropsychiatric disturbances such as agitation, aggression, depression, and apathy.
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behaviour in dementia
individuals with dementia have at least one symptom, commonly depression or apathy, while delusions, agitation, and abnormal motor behavior occur in about a third of patients
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causes of behavioural and psychological symptoms ind dementia (BPSD)
* Multi-factorial
* Interactions between biology, prior experiences, and the current environment contribute to neuropsychiatric symptoms.
* BPSD is associated with brain volume reductions, neurotransmitter alterations, and non-biological factors such as pre-morbid neuroticism and problematic caregiver communication styles.
* Environmental factors, unmet needs, behavioral/learning, and patient-environment mismatch also play a role in BPSD.
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BPSD includes
ncludes emotional, perceptual, and behavioral disturbances that are similar to those seen in psychiatric disorders.
* 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)
* vegetative (disturbances in sleep and appetite)
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sundown in BPSD
* Sundowning affects 2/3 of patients with dementia: behavioral disturbances often occur in the evening
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physical findings for delirium
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
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BPSD evaluation
* Standardized tools like the Neuropsychiatric Inventory (NPI) or the Behavioral Pathology in Alzheimer's Disease rating scale (BEHAVE-AD) to assess overall BPSD and establish a clear baseline to assess treatment effects.
* No need for laboratory or imaging tests for dementia patients with gradually worsening BPSD, unless there are indications from history or physical examination.
* For delirium cases with sudden or rapid onset of symptoms, basic studies should be conducted: CBC, electrolytes, liver and function tests, TSH, toxicology screen, urinalysis, CT scan (head).
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managment of BPSD
* 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.
* Effective management of BPSD requires a coordinated interprofessional health care team that partners with the patient's home caregiver.
