Vascular Cognitive Impairment

Stroke Strategies SLP NetworkSeptember 25, 2010

Angela SouthUniversity of Western Ontario Health and Rehabilitation

Sciences

DisclosuresFunding from Parkinson’s Society CanadaCIHR, 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)

ObjectivesReview the incidence and prevalence of dementia

and vascular cognitive impairmentDefine vascular cognitive impairment and

subtypesDefine the risk factors for vascular cognitive

impairmentDiscuss the impact of post-stroke cognitive

impairmentReview a historical perspective of VCIDiscuss deficits specific to VaD and VCIDiscuss potential assessment and treatment

implications

Historical Perspective – the pendulum swingsIn 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 13,9122016 16,805

Projected growth of 11.7%/yr yielding +300 new cases/yr

Prevalence of VaDConservatively 1-4% of individuals 65 and older

have VaDPrevalence doubling every 5-10 yearsIn 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 reasonsClear definition of the disorderOverlap with CVDOverlap with AD

Prevalence of VaDConservatively 1-4% of individuals 65 and older

have VaDPrevalence doubling every 5-10 yearsIn 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 reasonsClear definition of the disorderOverlap with CVDOverlap 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])

Dementia lacking distinctive histology (DLDH)

Binswanger disease

PPA

FTLD Pick Complex

Pick’s

Dementia with motor neurone diseases and movement disorders ALS, Parkinson’s, MS, HC, etc. Progressive supranuclear palsy (PSP)

and corticobasal degeneration (CBD)

AIDS dementia complex (ADC)

Creutzfeldt-Jakob disease (CJD)

Normal pressure hydrocephalus (NPH)

Syphilis

Wernicke-Korsakoff syndrome

Syndrome of acquired, progressive, persistentdecline in 3 of 5 spheres of mental activity(Cummings, Benson, & LoVerme, 1980)

  1. Memory2. Language and communication3. Personality4. Visuospatial skills5. Cognition (e.g., reasoning, abstraction, judgement,

etc.)

Dementia

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

gradual onset and continual decline including both:

A. Memory impairmentB. One (or more) of the following:

1. Language problems2. Movement programming

problems (apraxia)3. Perceptions stripped of

meaning (agnosia)4. Disturbance in executive

functioning (e.g., planning, organizing, sequencing ideas, etc.)

Cognitive deficits:1. Cause significant

impairment in social or 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/VaDHeterogenousOnset of cognitve impairment dementia should

have a temporal orientation to a CVD eventSeverity 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/yearIncidence of silent infarctions est. at 22 million in

11 million personsIn the Rotterdam study, those with silent infarction

had a two fold increased risk of dementiaPathology studies – small infarctions give a 5 fold

risk of developing dementia even after corrections for AD

Risk Factors for VCIHypertensionDiabetesHyperlipidemiaEstrogen replacement therapyTIA’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

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

Lacunar state 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

Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy

Binswanger’s disease 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

(Savundranayagam, Hummert, & Montgomery, 2005)

Impact of Communication Problems on Burdens

.48

.37

.57

.51CommunicationProblems

1.0*

Problem Behaviours

1.0*

DemandBurden

StressBurden

ObjectiveBurden

.51

.25

.46

1.0*

1.0*

1.0*

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

AttentionMemoryEFProcessing speedVisuospatial constructsMost predictive:

ALVT (verbal immediate memory), category VF, WAIS-RC digit symbol recall, block design

MemoryVCI/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 memoryFacial recognitionFigural memoryNo 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

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

Speech and Language Profile

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 VaDPsychomotor slowing is a definite characteristic of

VaDDepressionReduced verbal output/engagementEmotional withdrawalApathySomatic concernsanxiety

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-FACSFunctional 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 VCIPrimary 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 YouThe intuitive mind is a sacred gift, and the

rational mind its faithful servant. We have created a society that honours the servant and has forgotten the gift.Albert Einstein

Dementia – Risk Factors (Mendez & Cummings, 2003)

Fairly Definitive Age

Family history with 1st degree relative

Down’s syndrome

Frontal lobe signs

Presenilin mutations and abnormal APP

Apolipoprotein E 4 allele

Head trauma

Years of formal education

Small head size and brain volume

Supposed Inverse association with smoking

Alcohol and drug abuse

Exposure to metals such as aluminium, mercury, zinc

Industrial solvents and chemicals

Advanced maternal age

Electromagnetic fields

Family history of Down’s syndrome

Cerebro-and cardio-vascular diseases

Thyroid disease

Infectious diseases

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