Vascular Cognitive
Impairment
Stroke Strategies SLP Network
September 25, 2010
Angela South
University of Western Ontario Health and Rehabilitation
Sciences
Disclosures
Funding from Parkinson’s Society Canada
CIHR, NSERC, Parkinson’s Society Canada and Alzheimer’s
Society funded laboratories
A man does not consist of memory alone. He has
feeling, will, sensibilities, moral being --- matters of
which neuropsychology cannot speak. And it is here,
beyond the realm of an impersonal psychology, that
you may find ways to touch him, and change
him. Luria AR From a personal letter to Oliver
Sacks quoted in his 1985 book The Man Who Mistook
His Wife For a Hat London: Picador (p.32)
Objectives
 Review the incidence and prevalence of dementia and
vascular cognitive impairment
 Define vascular cognitive impairment and subtypes
 Define the risk factors for vascular cognitive impairment
 Discuss the impact of post-stroke cognitive impairment
 Review a historical perspective of VCI
 Discuss deficits specific to VaD and VCI
 Discuss potential assessment and treatment implications
Historical Perspective – the
pendulum swings
 In 1896 Kraepelin made the first distinction between
VaD and the tangles of AD on pathology examination
 Vascular etiologies were thought to account for almost
all dementia cases until the 1960’s and 70’s when focus
shifted to AD pathologies
 Now the pendulum is shifting back to a vascular etiology
with a focus on the overlap between AD-VCI
• Dr. Hachinski first to describe Multi-infarct dementia
(MID) and this was the center of the VaD discussion
• Today – the term VaD is used in a much wider context
than Hachinski, et al first described
• MID has lost popularity because VaD can be caused by
single infarcts. It is used more now as a subtype of VaD
• A struggle for a taxonomy
• Vascular cognitive impairment (VCI) vs Vascular dementia
(VaD) vs. VCI-ND
• Vascular cognitive disorder (VCD) including VaD and VCI
(equating more to MCI of vascular etiology) (Gustavo, et al,
2004)
Dementia Epidemiology – Worldwide*

35.6 million estimated 2010 (24.2M 2001; 4.6M new cases/yr)
 46% Asia
 30% Europe
 12% North America

Doubling ~ every 20 years
 65.7M 2030; 115.4M 2050

Majority (57.7%) live in low and middle income countries
 40% increase Europe over next 20 yrs
 63% ↑ North America
 77% ↑ southern Latin America; 134-146% rest of Latin America
 89% ↑ Asia Pacific; 117% East Asia; 107% South Asia
 125% ↑ North Africa and Middle East

$315 B (2005 US $) costs for dementia care/yr worldwide
* Alzheimer’s Disease International World Report, 2009 www.alz.co.uk/worldreport ; Ferri et al.,
2005; Wimo et al., 2003
Dementia Epidemiology – Selected
Countries
USA (http://www.alz.org/national/documents/report_alzfactsfigures2009.pdf)
 5.3 million
 ~ 500,000 < 65 yrs old (~ 200 K with AD)
 ~ $148 billion/yr for care
UK (http://www.alzheimers.org.uk/downloads/Dementia_UK_Full_Report.pdf)
 700,000
 ~15,000 < 65 yrs old
 > £17 billion/yr for care
 2/3 live in community
Epidemiology and Demographics:
Prevalence – Canada*
 ~ 500,000 (8% of 65+) (% distribution: community = institutions)
 103,000 new cases/yr (70,000 DAT) (CSHA, 2000)
 +71,000 < 65 yrs old
 ~1.5-2 ♀: 1 ♂
 2.4%
65-74 yrs
 34.5% 85+ yrs
 > 592,000 cases by 2021 (65 yrs + = 23-24% total pop)
 # cases will triple by 2031 (close to 1 million)
(http://www.alzheimer.ca/english/disease/stats-intro.htm; Alz. Soc. Canada,
2010; CSHA I Working Group, 1994, CMAJ)
Ontario and London Profiles
(courtesy Dr. M. Borrie)
Ontario (12,803,900 )
2007
160,624
2016
207,188
London (348,237) (LHIN 2)
2007
13,912
2016
16,805
 Projected growth of 11.7%/yr yielding +300 new cases/yr
Prevalence of VaD
 Conservatively 1-4% of individuals 65 and older have VaD
 Prevalence doubling every 5-10 years
 In pathologically confirmed cases of dementia VaD is
second only to AD and many cases have a mixed VaD/AD
pathology (Kirshner, 2010)
 Likely underestimated for a variety of reasons
 Clear definition of the disorder
 Overlap with CVD
 Overlap with AD
Prevalence of VaD
 Conservatively 1-4% of individuals 65 and older have VaD
 Prevalence doubling every 5-10 years
 In pathologically confirmed cases of dementia VaD is
second only to AD and many cases have a mixed VaD/AD
pathology (Kirshner, 2010)
 Likely underestimated for a variety of reasons
 Clear definition of the disorder
 Overlap with CVD
 Overlap with AD
Types of Dementia: Selected Examples

DAT/AD
 Familial-DAT
 Early onset-DAT
 Down’s syndrome-DAT

Mixed (DAT + VaD)

Vascular dementia (VaD)

Vascular cognitive impairment (VCI)

Dementia with Lewy bodies (DLB)

FTLD (FLD [Fv plus sub-variants] + PNFA
[Fv] + semantic dementia [Tv])

PPA

FTLD

Pick’s

Dementia with motor neurone
diseases and movement disorders
 ALS, Parkinson’s, MS, HC, etc.


Dementia lacking distinctive histology
(DLDH)

Binswanger disease
Pick Complex
Progressive supranuclear palsy (PSP)
and corticobasal degeneration (CBD)

AIDS dementia complex (ADC)

Creutzfeldt-Jakob disease (CJD)

Normal pressure hydrocephalus
(NPH)

Syphilis

Wernicke-Korsakoff syndrome
Dementia

Syndrome of acquired, progressive, persistent
decline in 3 of 5 spheres of mental activity
(Cummings, Benson, & LoVerme, 1980)
1. Memory
2. Language and communication
3. Personality
4. Visuospatial skills
5. Cognition (e.g., reasoning, abstraction, judgement, etc.)
Mild Cognitive Impairment (MCI)
(Ritchie & Touchon, 2000)

Not considered normal for age and education level

Defined clinically or neuropsychologically

Evolved from earlier concepts of cognitive decline in
aging without dementia:
 Benign senescent forgetfulness (Kral, 1962)
 Age-associated memory impairment (Crook et al., 1986)
 Age-associated cognitive decline (Levy et al., 1994)
 Mild cognitive decline (ICD-10, 1993)
 Cognitively impaired not demented (CSHA, 1994)
 Cognitively impaired not demented yet (CINDY) (CSHA, 1994)
Mild Cognitive Impairment (MCI)
(Petersen et al. 1999; Mendez & Cummings, 2003)
1.
Memory complaint, preferably corroborated by informant
2.
Objective memory impairment corrected for age and
education (i.e., scores 1.5 SDs or more below Mean for normals)
3.
Largely intact general cognitive function
4.
Essentially preserved activities of daily living (ADL)
5.
Not demented
6.
No specific medical, neurological or psychiatric causes
for memory difficulty
Dementia: DSM IV-TR (2000)
 Multiple cognitive deficits of  Cognitive deficits:
1. Cause significant
gradual onset and continual
impairment in social or
decline including both:
A.
B.
Memory impairment
One (or more) of the following:
1. Language problems
2. Movement programming
problems (apraxia)
3. Perceptions stripped of
meaning (agnosia)
4. Disturbance in executive
functioning (e.g., planning,
organizing, sequencing
ideas, etc.)
occupational functioning
2. Represent significant
decline from previous
functioning

Not due to other CNS
conditions, systemic conditions
known to cause dementia,
substance abuse induced
dementia, delirium, another
primary psychiatric disorder
Defining VaD (an enigma)
DSM – IV – TR (2000)
• Memory impairment
• Impairment in one other cognitive domain (language or
Visuospatial)
• Presence of cerebrovascular disease (focal clinical signs
or imaging)
• Cognitive deficits must be related to CVD and severe
enough to impair daily functional activities.
Defining VCI/VaD
 Heterogenous
 Onset of cognitve impairment dementia should have a
temporal orientation to a CVD event
 Severity depends on strategic location of infarcts and
volume of injury (tissue damage)
 Left carona radiata (Pohlasvaara, et al)
 Thalamus (RMDAS study)
Post-stroke cognitive impairment
(Vakhnina, et al 2009)
 Incidence of impaired cognitive function post stroke in
the elderly = 40-60% during first 6 months post TIA’s,
strokes with minimal impairments, minor strokes
 Severity reaches dementia criteria in 5-7% of cases in
the first 6 months post and in 20-25% of cases within 5
years of the stroke (non-severe ischemic strokes)
 Stroke can lead to recurrence or clinical manifestation
of underlying dementia or other neurodegenerative
processes
 The development of additional cerebrovascular disease
in the presence of at least 2 lacunar infarcts
significantly  probability of AD manifesting (Vakhnina,
et al 2009)
 Mild cognitive impairment (MCI or VaMCI is a major
determinant of post-stroke dementia: 8% conversion
per year from VaMCI to VaD (Sachdev, et al 2009)
 Those with greater executive function and language
impairment post stroke tended to progress to VaD.
Behavioural findings were more predictive than imaging
(Sachdev, et al 2009)
 Incidence of clinical stroke in US = 750,000/year
 Incidence of silent infarctions est. at 22 million in 11
million persons
 In the Rotterdam study, those with silent infarction had
a two fold increased risk of dementia
 Pathology studies – small infarctions give a 5 fold risk of
developing dementia even after corrections for AD
Risk Factors for VCI
 Hypertension
 Diabetes
 Hyperlipidemia
 Estrogen replacement therapy
 TIA’s
VCI/VaD Variations (Libon, et al)
 Extracranial
 More abrupt in onset with stepwise progression of dementia;
more characteristic of multi-infarct dementia
 Usually more disruption of cortical involvment
 Caused by blockage to one or more of the major cerebral
arteries
 Intracranial
 Slow, insidious progression
 Usually more subcortical in involvment
 Affects more of the smaller vessel systems (leukoariosis)
 Arteriopathies, leukoencephalopathy, amyloid angiopathy
 Also give a predominant subcortical feel deficits
VaD Subtypes (Kirshner, 2009)

Multiple large infarcts





Lacunar state




Cerebral autosomal dominant arteriopathy with subcortical infarcts and
leukoencephalopathy
Binswanger’s disease



Chronic HT patients
Small infarcts deep in the white matter, internal capsule, BG, brainstem
Increased reflexes, positive babinski, pseudobulbar affect, spastic tone, frontal release
signs
CADASIL


Classic MID
Can occur in single or multiple strokes
Location and extend of damage dependent
Insidious dementia, usually clinically obv. stroke but may be silent
Subcortical ateriosclerotic encephalopathy in elderly patients with chronic HT and hx of
acute strokes
CT/MRI extensive white matter disease or leukoaraiosis without obvious cortical infarcts
Misc. other vascular syndromes
Cognition

Mental processes where sensory information is transformed,
reduced, elaborated, stored, recovered and used

Processes of gaining knowledge, organizing information (new or
old), and using what has been learned

Includes, but is not limited to:







Memory systems and processes
Attention systems and processes
Judgment
Reasoning - decision making
Insightfulness
Language systems
Other systems and processes
Cognition

Mental processes where sensory information is transformed,
reduced, elaborated, stored, recovered and used

Processes of gaining knowledge, organizing information (new or
old), and using what has been learned

Includes, but is not limited to:






Memory systems and processes
Attention systems and processes
Judgment
Reasoning - decision making
Insightfulness
Other systems and processes
Impact of Communication
Problems on Burdens
1.0*
Demand
Burden
.51
1.0*
Communication
Problems
1.0*
.48
Problem
Behaviours
.37
.51
.57
1.0*
Stress
Burden
.25
1.0* .46
Objective
Burden
(Savundranayagam, Hummert, & Montgomery, 2005)
Caregivers’ Perspectives of Language
and Communication in Dementia

Caregivers identify problems early

Far reaching effects on their social and emotional well-being

Perceived to be a primary problem in caregiver coping and increased
risk for institutionalization
Cognitive Profiles
(Levy & Chelune, 2007)
 Executive Function/Attention
 Typical tasks requiring simple attention and tracking fail to
differentiate AD and VCI
 However as task complexity increases requiring mental
flexibility, set shifting, vigilance, sustained attention those
with VCI performed significantly worse than AD
 Multiple studies have reported that AD is superior to
VCI/VaD on tasks of new concept formation, freedom from
perseveration, initiation, planning, and self-regulation
 Difficulty assessing the demands of a task, adjusting
accordingly and then shifting to next task (Libon, et al)
 Show greater decrements in task to task trials suggesting
difficulty with set maintenance
 Subcortical – frontal circuits
Zhou and Jia (2009)
 Compared VCI-nd with controls (N=160)
 VIC-nd varied from controls on almost every task






Attention
Memory
EF
Processing speed
Visuospatial constructs
Most predictive:
 ALVT (verbal immediate memory), category VF, WAIS-RC digit
symbol recall, block design
 Memory
 VCI/VaD has more intact delayed and immediate recall for
verbal stimuli and story re-telling (recall) vs. AD
 Even when recall deficits are present they have better
cued and recognition recall. Not true in AD
 Declarative memory more preserved than procedural.
Opposite to AD
 Difficulty learning new motor tasks. Less carryover
between trials (thalamic – neostriatal – frontal circuits)
 Generally greater breakdown in semantic
memory/networks in AD than in VCI
 VCI patients with rapid rates of forgetting (greater
declarative memory deficits) are felt to have an overlap of
AD/VCI = Mixed Dementia or AD alone
Non-verbal visuospatial memory
 Facial recognition
 Figural memory
 No differences between AD and VaD
Contructional praxis and visuomotor problem solving
• No difference AD and VaD
• Clock drawing impaired for both
Verbal Fluency
 Mixed reports in the literature
 Studies have reported no difference between VaD and AD in
confrontation naming, phonemic fluency, or comprehension.
 Recent studies using newer methodologies have shown definitive
differences in behavioural and imaging results for phonemic
fluency with VaD being significantly worse than controls and AD.
Phonemic fluency is thought to reflect executive function
deficits in addition to language deficits. (Poore, 2006)
 AD tends to have more disruption of semantic knowledge will be
more impaired on category fluency such as naming animals. VD
outperforms AD here (Jones, Laukka, Backman, 2006)
 In sum, category fluency is likely more discriminative than letter
fluency. VaD will have category fluency deficits but not to the
degree of phonemic fluency; may or may not be equal to AD in
deficits
Speech and Language Profile
 Powell et al. (1988)
 VaD
 Narrative writing, writing to dictation, completion of nursery
rhymes, comprehension of complex auditory commands, and
grammatical complexity of spontaneous speech
 AD
 Information content of spontaneous speech, naming, auditory
comprehension, word discrimination, alphabet recitation and
comprehension of written material
 Speech melody and information content of spontaneous speech
clearly separated the two groups
 VaD is superior to AD in comprehension of single words
 AD is superior on simple measures of reading and writing
Levy and Chelune (2007)
Depression and Psychomotor in
VaD
 Psychomotor slowing is a definite characteristic of VaD
 Depression
 Reduced verbal output/engagement
 Emotional withdrawal
 Apathy
 Somatic concerns
 anxiety
SLP assessment considerations
 Comprehensive
 Cognitive communication measures
Arizona Battery of Communication Disorders of Dementia
Subtests of the PALPA
Cognitive Linguistic Quick Test
Phonemic/lexical fluency
Category fluency
Confrontation naming (BNT)
Discourse based assessment tasks (expression and comprehension
Semantic memory/knowledge – Pyramids and Palm Trees, PALPA
subtests
 Reading/Writing measures – BDAE subtests, PALPA subtests
 Visual perceptual measures (clock drawing, figure drawing, etc.)








 Assessments designed to assess general aphasia severity
or type of aphasia may not be useful (WAB or BDAE short
form) alone. Deficits in VaD not likely to manifest on
these types of tests.
 Caregiver profile and perspective of communication
through interview, profiles, scales
 Tests of functional communication
 Communication Abilities of Daily Living (CADL)
 ASHA-FACS
 Functional Communication Profile-R (FCP-R)
 May present with concomitant dysarthria or dysphagia
 May present with concomitant focal more cortical
language deficits if there was a large single/multi
infarct(s)
 Neuropsychiatry resources should be used as necessary
for in-depth cognitive testing
 Role of depression on communication should be
considered given high rate of depression in both
dementia and stroke
 Early testing of cognitive domains and identifying
presence of deficits may predict post-stroke VCI helping
to better prepare patients and families
Treatment considerations
 Given the elevated risk of VCI post stroke cognitive deficits should be
probed for their contributions to deficits and appropriate treatment
targets/prognosis
 To date – no study has looked at influence of VCI on aphasia recovery
 Generally deficits may require a more compensatory, supportive therapy
approach that focuses on the individual with VCI and communication
partners equally
 Presence of post-stroke VCI may impact both immediately after the
stroke and during chronic phases of treatment
 May not be initially evident and only manifest during chronic stages
therefore cognitive functions should be assessed/probed at every stage
of intervention for communication deficits post-stroke
 VCI may have a significant impact on communication
and on treatment outcomes
 Generally word retrieval deficits will be more mediated
by attention, executive function deficits vs. semantic
knowledge.
 Generally cued and recognition memory should be
maximized as strategies
 Reduce need for procedural learning
 Using functional communication therapies such as
narrative discourse based interventions may be valuable
given executive function and cognitive deficits
 Specific cognitive communication strategies should be
developed with patients and communication partners.
Medical management of VCI
 Primary intervention to reduce severity or slow
progression is management of vascular risk factors
particularly for those in at risk groups or those who have
already had a stroke/TIA.
 Traditional AD medications have been tried but without
much success. Memantine may be one possible option
Thank You
Dementia – Risk Factors
(Mendez & Cummings, 2003)
Fairly Definitive

Age

Supposed
Inverse association with smoking

Family history with 1st degree
relative

Alcohol and drug abuse

Exposure to metals such as
aluminium, mercury, zinc

Industrial solvents and chemicals

Advanced maternal age
Presenilin mutations and abnormal
APP

Electromagnetic fields

Apolipoprotein E 4 allele

Family history of Down’s syndrome

Head trauma

Cerebro-and cardio-vascular
diseases

Years of formal education

Thyroid disease

Small head size and brain volume

Infectious diseases



Down’s syndrome
Frontal lobe signs
Summary of Language and
Communication Changes in MCI
 Few studies
 Mostly screening/brief measures within larger test batteries of
cognition
 Decreasing verbal fluency scores (letter and semantic categories)
 Decreasing confrontation naming scores (Boston Naming Test –
BNT)
 Do not benefit from semantic cues