STROKE AND DEMENTIA

Dr. dr. Suherman, Sp.S (K)

INTRODUCTION

Stroke is associated with the risk of cognitive

impairment and dementia

Stroke is the leading cause of disability and the

second leading cause for dementia worldwide.

Current evidence suggests that 25-30% of

ischaemic stroke survivors develop

immediate or delayed vascular cognitive

impairment (VCI) or vascular dementia (VaD).

Raj N. Kalaria, Rufus Akinyemi, Masafumi Ihara, Stroke injury, cognitive impairment and vascular dementia, BBA -
Molecular Basis of Disease (2016), doi: 10.1016/j.bbadis.2016.01.015
WHAT IS A STROKE
• World Health Organization (WHO) defined
stroke as “rapidly developing clinical signs of
focal or global disturbance of cerebral
function, with symptoms lasting 24 h or
longer, or leading to death with no apparent
cause other than vascular origin
• An interruption of the supply of blood and
oxygen to an area of the brain.
• This causes the brain cells in an area to die, and
reduces the brain function in that area.
• The area of the body controlled by the damaged
area in unable to function properly.
• There are two types of stroke.

http://www.hc-sc.gc.ca/iyh-vsv/diseases-
maladies/stroke-vasculaire_e.html#ef
Slide 4
Dementia is a syndrome…that includes
loss of memory, judgment and
reasoning, and changes in mood,
behaviour and communication abilities.

Alzheimer’s Society of Canada

 WHAT IS DEMENTIA?

1.  in memory
2. And at least one of the following:
 Difficulty with language
 Difficulty with voluntarily moving despite having normal
muscle function
 Difficulty recognizing and identifying objects or persons
 Difficulty with planning, reasoning, problem solving and
judgment.

The Diagnostic and Statistical Manual published by the American Psychiatric

Association
DEMENTIA PREVALENCE AND INCIDENCE

• Overall dementia prevalence in affluent countries is 5 –

10% in individuals age 65 and older
• AD prevalence doubles every 4.3 years
• Vascular dementia (VaD) prevalence doubles every 5.3
years
• Age-adjusted dementia incidence rates (per 1000
person years) AD: 19.2; VaD: 14.6

©2011 AMERICAN HEART ASSOCIATION, INC.

ALL RIGHTS RESERVED. UNAUTHORIZED USE
PROHIBITED.
 Types of Dementia
Other
Dementia with Lewy bodies (3.1%)
(1.9%)

Frontotemporal dementia
(5.4%) Vascular
Dementia
8.7% Alzheimer’s
47.2%

Mixed Dementia
33.7%

Adapted from Feldman H, Levy A, Hsiung G, et al. A Canadian Cohort Study of Cognitive
Impairment and Related Dementias (ACCORD): Study Methods and Baseline Results.
Neuroepidemiology 2003;22: 265-274.
Vascular dementia is related to
stroke and can cause a loss in
memory, reasoning, thinking,
attention span and independence
with activities of daily living.

Alzheimer Society of Canada

Health and Quality of Life Outcomes 2004, 2:52
Vascular dementia results when a
critical part of the brain does not
receive enough oxygen.

http://www.emedicinehealth.com/stroke-related_dementia/article_em.htm
WHAT ARE THE SYMPTOM OF VASCULAR DEMENTIA

 Problems concentrating  Memory problems

and communicating (although this may not
be the first symptom)
 Depression accompanying
the dementia  A ‘stepped’
 Symptoms of stroke, such progression, with
as physical weakness symptoms remaining at
or paralysis a constant level and
then suddenly
 Seizures deteriorating
 Periods of acute
confusion
 OTHER SYMPTOMS MAY INCLUDE

 Hallucinations (seeing things that do not exist)

 Delusions (believing things that are not true)
 ‘Wandering’ and getting lost
 Physical or verbal aggression
 Restlessness

 Incontinence

http://www.alzheimers.org.uk/Facts_about_dementia/What_is_dementia/info_vascular.htm
STROKE AND DEMENTIA
• The results of our meta-analyses show that both prevalent and
incident strokes are strong independent risk factors for all-cause
dementia.
• six studies reporting that participants with a history of stroke had
59% increased risk of developing dementia compared with controls.
• The presence of multiple lesions, the volume of infarcts,and the
location of stroke (e.g., left hemisphere) have also been identified as
risk factors for poststroke dementia
 DEFINITION

The dementia that occurs after a

stroke, irrespective of the presumed
cause, and the final diagnosis of PSD
should be delaye to at least 6 months
after stroke according to American
Psychiatric Association's Diagnostic
and Statistical Manual of Mental
Disorder

PSD may impact all aspects of

cognitive functions, but attention and
executive function is the most affected
domains. A study suggested that the
presumed etiology of poststroke
dementia was vascular dementia in two-
thirds of patients and Alzheimer's
disease in one-third.
Hu GC, Chen YM. Post-stroke Dementia: Epidemiology, Mechanisms and Management.
International Journal of Gerontology. 2017; 11: 210-214.
 INCIDENCE AND PREVALENCE
A meta-analysis of 30 studies
established that dementia prevalence in
stroke patients increased from 10% before first stroke to 20%
soon after first stroke,

In the Rochester study, the RR of dementia after stroke was 8.8

after 1 year, then declined progressively to 4.2 after 3 years,
after 5 years, 2.5 after 10 years, and 2.0 after 25 years.

A study in Italy found that 21.5% patients developed dementia

after stroke during 4 years follow up

The prevalence of PSD ranges from 6 to 32% with the revalence

around 28% at 3 months point of time after stroke.

Hu GC, Chen YM. Post-stroke Dementia: Epidemiology, Mechanisms and Management.

International Journal of Gerontology. 2017; 11: 210-214.
The development of dementia after stroke depends on location and
volume of the stroke, degree of related neuronal damage, presence
of pre-existing cognitive impairment or other cerebral
Pathology

stroke survivors develop delayed dementia

beyond three months or only after recurrent
stroke

Stroke ischaemic usually have higher survival rates

developed dementia than do those with
hemorrhagic strokes,
RISK FACTORS OF DELAYED DEMENTIA AFTER STROKE INJURY
Demographic features Odds Ratios
(p=0.05-0.01)
Advanced age 6.6 for > 65 years; 1.05-1.2 per year
Genetics trait > 1.5
Low education 2.5
Stroke characteristics
Transient Ischaemic attack 1.83
Recurrent stroke 2.3
Multiple infarcts 2.5
strategically located infarct NA
Stroke severity 2.5
Neuroimaging markers of brain lession
Silent brain infarcts 1.8
White matter lession 2.5
Medial temporal lobe atrophy 2.69 – 5.2
Cerebral atrophy 2.6
Cerebral microbleeds NA
Stroke injury, cognitive impairment and vascular dementia Raj N. Kalaria, Rufus Akinyemi, Masafumi Ihara
 MODIFIABLE OR TREATABLE RISK FACTORS FOR DEMENTIA AFTER STROKE
INJURY
Risk Factor Clinical features and targets for modification

Hypertension Both systolic and diastolic pressures increase

risk; >140/90 mm Hg

Atrial fibrillation Both chronic and paroxysmal AF confer risk of stroke. AF involved in ~10% of
all strokes; in >80 year olds it is ~36%. Anticoagulants including aspirin
suggested but they are not without risk. Not recommended for those who
develop dementia.

Diabetes mellitus Risk of stroke can be independently increased by 1.8 to 6 fold. Strategies to
Type II reduce risk of stroke are focused in reducing co-morbidity with hypertension.

Dyslipidemia Elevated cholesterol and LDLs and lower HDLs increase stroke. Consistent
reduction of stroke risk by use of statins but only marginally effective in
dementia

Stroke injury, cognitive impairment and vascular dementia Raj N. Kalaria, Rufus Akinyemi, Masafumi Ihara
 MODIFIABLE OR TREATABLE RISK FACTORS FOR DEMENTIA
AFTER STROKE INJURY
Risk Factor Clinical features and targets for modification
Cardiac and Carotid Arterial stenosis or occlusion caused by
Arterial Diseases atherosclerotic plaques is well-known risks for
stroke and cerebral hypoperfusion. Both
asymptomatic and symptomatic arterial disease
are associated with cognitive impairment.
High Homocysteine Elevated homocysteine (>13 mg/ml) is considered risk for vascular
disease related cognitive impairment but not widely accepted. Diet
folate supplementation can lower homocysteine.

Obesity BMI of >25 and increased abdominal fat stroke

predictors of stroke risk. Body weight
reduction reduces risk of stroke.
Metabolic syndrome Cluster of modifiable subclinical and clinical conditions including
glucose tolerance, elevated blood pressure, low HDL and abdominal
obesity
increases risk of stroke. Aggressive strategy to reduce multiple
components would reduce risk.

Stroke injury, cognitive impairment and vascular dementia Raj N. Kalaria, Rufus Akinyemi, Masafumi Ihara
CHARACTERISTIC OF POST STROKE DEMENTIA
VCI DIAGNOSTIC CRITERIA: INTRODUCTION

1. The term VCI characterizes all forms of cognitive deficits

from VaD to MCI of vascular etiology.
2. These criteria cannot be used in subjects who have an
active diagnosis of drug or alcohol abuse/dependence.
Subjects must be free of any type of substance for at
least 3 months.
3. These criteria cannot be used in subjects with delirium.

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 VCI DIAGNOSTIC CRITERIA: DEMENTIA

1. The diagnosis of dementia should be based on a decline in

cognitive function from a prior baseline and a deficit in
performance in two or more cognitive domains that are of
sufficient severity to affect the subjects’ activities of daily living
2. The diagnosis of dementia must be based on cognitive testing,
and a minimum of 4 cognitive domains should be assessed:
executive/attention, memory, language, and visuospatial
functions.
3. The deficits in activities of daily living are independent of the
motor/sensory sequelae of the vascular event.

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 VCI DIAGNOSTIC CRITERIA: PROBABLE VAD

There is cognitive impairment and imaging evidence of CVD, and:

a) There is clear temporal relationship between a vascular event
(e.g., Clinical Stroke) and the onset of cognitive deficits; or
b) There is a clear relationship in the severity and pattern of
cognitive impairment, and the presence of diffuse, subcortical
CVD pathology (e.g., as in cerebral autosomal dominant
arteriopathy with subcortical infarcts and leukoencephalopathy,
CADASIL)
2) There is no history of gradually progressive cognitive deficits
before or after the stroke that suggests the presence of a non-
vascular neurodegenerative disorder.

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 VCI DIAGNOSTIC CRITERIA: POSSIBLE VAD
There is cognitive impairment and imaging evidence of CVD, but:
1) There is no clear relationship (temporal, severity, or cognitive pattern) between the
vascular disease (e.g., silent infarcts, subcortical small vessel disease) and the
cognitive impairment; or
2) There is insufficient information for the diagnosis of VaD (e.g., clinical symptoms suggest
the presence of vascular disease, but there are no CT/MRI studies available); or
3) Aphasia severity precludes proper cognitive assessment. However, patients with
documented evidence of normal cognitive function (e.g. annual cognitive evaluations)
before the clinical event that caused aphasia could be classified as Probable VaD; or
4) There is evidence of other neurodegenerative diseases or conditions in addition to CVD
that may affect cognition, such as: a. a history of other neurodegenerative disorders
(e.g., Parkinson’s disease, progressive supranuclear palsy, Dementia with Lewy bodies,
etc.); b. the presence of AD biology is confirmed by biomarkers (e.g., PET, CSF, amyloid
ligands) or genetic studies (e.g., PS1 mutation); or c. there is a history of active cancer,
or psychiatric or metabolic disorders that may affect cognitive function.

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 PATHOFISIOLOGY
• In clinical-pathologic studies, larger infarct volume and increased
number of macroscopic infarcts are associated with an increased
likelihood of dementia
• There is yet no reliable cut-point for infarct volume and dementia
• Infarct location is important: thalamus, angular gyrus and basal ganglia
may be more likely than other regions to result in cognitive impairment
• Still, regional factors have not been clearly defined and many other
regions have been related to dementia
• Microscopic infarcts have been related to dementia, even after
accounting for macroscopic infarcts
• Cognitive reserve and other co-existing pathologies may be additional
factors when relating cerebral infarctions to cognitive impairment and
dementia

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INFARCTIONS, ALZD PATHOLOGY AND DEMENTIA
• Most persons with dementia and almost half of those with clinically
probable AlzD have mixed (AlzD + CVD) pathology
• Infarcts appear additive with AlzD pathology in lowering cognitive
function, increasing the odds of dementia, and increasing the odds of
clinical AlzD
• The public health importance of infarcts and their role in dementia is
likely underestimated
• Prevention and therapies that decrease cerebral infarcts are likely to
lower the prevalence of dementia
• AlzD has been found to be the most common pathology associated
with MCI, though mixed pathologies are also common

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PROHIBITED.
WHITE MATTER DEGENERATION AND
CEREBRAL MICROBLEEDS
• White matter degeneration and cerebral microbleeds are
common in the brains of older persons, and may reflect
direct tissue damage
• A role for cognitive impairment associated with white matter
degeneration is suggested by neuroimaging studies, but it is
currently unclear whether white matter lesions represent
separate pathologic substrates of VCI
• Some studies have not shown clear associations between
neuropathologic measurements of white matter lesions and
cognitive function, unless they were part of a combined
vascular score that also included infarcts
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Localization of infarcts or tissue changes associated with
development of dementia after stroke
MANAGEMENT STRATEGY

Pharmacotherapy Strategy

Comunication strategy

ADL Strategy
PHARMACOTHERAPY
Blood pressure lowering agents

Lipid lowering agent

Cholinesterase inhibitors and

Memantine

Phosphodiesterase inhibitor (PDE)

 Summary of VCI Pharmacotherapy Recommendations
Treatment Recommendation, Comments
Class/Level of Evidence
Donepezil Level A, Class IIa for “pure” Study 307, 308 (N=1219): modest
VaD benefit for cognitive & global, less
robust for function; Study 319
(N=974): only cognitive benefit

Galantamine Level A, Class IIa for mixed Pure and mixed VaD
AlzD-CVD; Class IIb for Gal-Int-6 (N=592): benefit in all
“pure” VaD primary outcomes overall; only
cognitive benefit in pure disease;
“Pure” VaD (Gal-Int-26 – N=788):
modest benefit in cognitive/executive
measures

Rivastigmine Level C, Class IIb VCIND study (N=50): modest benefit

Memantine Level A, Class IIb in some executive functions
(N=900): modest cognitive benefit
only

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 COMMUNICATION STRATEGIES
• Eliminate distractions (e.g. TV, radio)
• Approach the person slowly and from the front; establish and maintain
eye contact
• Use short, simple sentences
• Speak slowly
• Give one instruction at a time
• Ask “yes/no” rather than “open-ended” questions
• Repeat messages using the same wording
• Paraphrase repeated messages
• Avoid interrupting the person; allow plenty of time to respond
• Encourage the person to “talk around” or describe the word he is
searching for.

Small et.al., (2003) Effectiveness of Communication Strategies Used by Caregivers of Persons With Alzheimer’s
Disease During Activities of Daily Living, Journal of Speech, Language and Hearing Research; 46, 2:353
Slide 34

ADL
Strategy
CONCLUSION
In conclusion, chronic brain changes related with advancing age
compromise the cognitive reserve and increase the risk of
poststroke dementia (PSD) when vascular attacks occur or recur.

After intervention for acute stroke, early and optimal intervention

should be directed to post-stroke dementia (PSD) in the window
before dementia sets in.

Detailed clinical and neuropsychological Assessment after

stroke is the crucial in order to estimate the prognosisand
program for secondary prev ention.

The current barriers for earlier identification of PSD is lack of

uniform diagnostic criteria,PSD-specific assessment tools and
precise biochemical marker.

Lastly, future researches might shed light on the

pathophysiologyand might come up with new diagnostic
neuroimaging techniques
 THANK YOU……

THANK YOU