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Neuropsychology of Ageing > Lecture 8: Vascular dementia > Flashcards

Lecture 8: Vascular dementia Flashcards

1
Q

Criteria dementia/major neurocognitive disorders (DSM V):

A
  1. Evidence significant cognitive decline based on report patient or informant AND objective deficits (>2 SD below appropriate norms)
  2. Cognitive deficits sufficient to interfere with independence
  3. Cognitive deficits not exclusively in context delirium
  4. Cognitive deficits not attributed to Axis 1 disorder (e.g. depression or schizophrenia)
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2
Q

¨Vascular dementia (VaD) – dementia caused by cerebrovascular disease

A
  • Cerebrovascular disease (CVD) – diseases of blood vessels in brain affect blood supply
    • Cerebrovascular pathology associated with reduction in blood flow
    • Until 1960s cerebrovascular disease regarded main cause dementia in older adults
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3
Q

Prevalence

  • Vascular dementia:
A

Vascular dementia:

  • second most common form of dementia, after AD
    • Netherlands: 16% of dementia cases are vascular dementia (Alzheimer Nederland)
    • UK: 17% vascular (Alzheimer Society)
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4
Q

Vascular cognitive impairment (VCI):

  • all forms cognitive impairment caused by cerebrovascular disease (Gorelick et al., 2011)
A
  • Ranging from Very mild to severe
  • Milder forms: VCI no dementia (VCIND) or vascular MCI (VaMCI)
  • More severe forms: consequences for daily functioning, vascular dementia (VaD)
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5
Q

VaD result from 2 main forms cerebrovascular disease:

A
  1. white matter lesions, lacunar infarcts, small vessel stroke
  2. cerebral arteries stroke/large vessel stroke
  • or combination of 1 and 2
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6
Q

white matter lesions, lacunar infarcts, small vessel stroke:

A
  • problem with blood supply, hence not enough oxygen
  • vessel disease - hypoperfusion brain tissue - degeneration white matter (white matter lesions)
  • vessel disease - microbleeds in brain tissue - tissue death
  • diffuse

Picture: White matter lesions visible as hyperintensities on MRI scans: minor (L) and extensive (R)

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7
Q

VaD result 2 main forms cerebrovascular disease

  1. white matter lesions, lacunar infarcts, small vessel stroke
    * Atherosclerosis:

Lacunar refers to small blood vessels deep inside the brain.

A

Atherosclerosis:

  • build up plaque inside arteries
  • hardens and narrows the arteries
  • limits flow blood to tissues
  • risk rupture
  • Narrowed arteries or high blood pressure increase risk lacunar infarct/lacunar stroke.
  • Lacunar infarct/lacunar stroke most common type of ischaemic stroke
    • Lacunar infarct: narrowed arteries blocked more easily.
    • Leads to lack of oxygen and blood in the area.
  • Microbleeds: occurs when small bloos vessels rupture, hence, damage.
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8
Q

VaD result 2 main forms cerebrovascular disease

  1. cerebral arteries stroke/large vessel stroke:
    * Picture: Likelihood of stroke for particullar areas*
A
  • Ischemic (meaning occlusion/blockage) or hemorrhagic (rupture)
  • More localised
  • Strategic location or volume
  • VaD and large vessel disease. Areas medial cerebral artery & carotid artery
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9
Q

Clinical features

Clinical presentation VaD diverse:

(Vascular dementia)

A
  • Clinical presentation VaD diverse – “heterogeneity is the rule”
    • variety cerebrovascular events can lead to symptoms
    • damage can occur in variety locations
    • criteria for diagnosis revised number of times
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10
Q

VaD result 2 main forms cerebrovascular disease (percentages/relative frequencies):

  1. white matter lesions, lacunar infarcts, small vessel stroke
  2. cerebral arteries stroke/large vessel stroke
A
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11
Q

Clinical features

  • Earlier criteria (e.g. DSM 4)

Vascular dementia

A
  • Memory prominent impairment.
    • Memory critical impairment (from AD)
    • memory not always most prominent impairment in VaD
    • pathology may not include medial temporal areas (as AD)
  • stepwise deterioration (abrupt deterioration and stable intervals)
    • Cognitive decline in steps: rapid decline and stable periods
    • Further stroke - rapid decline
    • Unlike gradual decline AD
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12
Q

Clinical features (nowadays)

Vascular dementia

A

Diagnosis VCI/VaD based on 2 factors

  • Presence cognitive impairment (dementia/MCI) on neuropsychological tests
  • Presence cerebrovascular disorder (CVD) on neuroimaging
    • Regardless of cause, e.g. atherosclerosis, ischemic, hemorrhagic.

Plus a third and most difficult condition:

  • Establish relationship cognitive impairment and CVD.
    • Location of lesions in line cognitive impairments observed
    • Cognitive impairments appear shortly after onset CVD
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13
Q

VCI

Clinical features

  • Most recent criteria for diagnosis (Gorelick et al., 2011)
A
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14
Q

Most recent criteria for diagnosis (Gorelick et al., 2011)

  • Vasular dementia:

Clinical features

A
  • see picture: so a single isolated cognitive impairment (as sometimes occurs due to strok) is not sufficient
  • if there is hemianopia (which is usually caused by a stroke) that would disqualify for dementia….

Original table: https://www.ahajournals.org/doi/full/10.1161/STR.0b013e3182299496

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15
Q

Most recent criteria for diagnosis (Gorelick et al., 2011)

  • Probable Dementia
A
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16
Q

Most recent criteria for diagnosis (Gorelick et al., 2011)

  • “possible dementia”
A

Possible VaD

  • cognitive impairment and CVD
  • no clear relationship
  • Insufficient evidence, information missing
  • Aphasia too severe to assess cognition
  • Indications neurodegenerative or other diseases
17
Q

Clinical features

Most recent criteria for diagnosis (Gorelick et al., 2011)

  • VaMCI
A

VaMCI

  • cognitive impairment at least 1 domain
  • Instrumental activities daily living intact/only mildly impaired.
  • Relationship moment and severity cerebrovascular event and onset cognitive deficit
18
Q

Clinical features

  • VCIND/VaMCI:
A
  • Functions affected vary, can include memory, executive function, attention, visuospatial functions
  • can be precursor/prodromal stage VaD
    • Conversion rates vary (up to 50%)
  • Persons with VCIND may revert back normal performance
19
Q

Clinical features

  • Definitive diagnosis VaD confirmed post-mortem:
A

Definitive diagnosis VaD confirmed post-mortem:

  • Evidence cerebrovascular disease in brain
  • Absence of AD pathology or other disease that can cause dementia
20
Q

Risk factors VCI same as for stroke:

A
  • Age biggest risk factor.
  • Other unmodifiable risk factors:
    • male sex
    • low birth weight
    • genetic factors
      • Notch 3 gene – causative gene for cerebral autosomal dominant arteriopathy with subcortical infarcts and leucoencephalopathy (CADASIL) – hereditary form of VaD.
  • Modifiable risk factors include: hypertension, smoking, diabetes, obesity (same as for stroke)
21
Q

Difficulties diagnosis VaD:

A
  • common occurrence mixed dementia: cerebrovascular pathology and AD pathology
    • mixed dementia at least as common as pure VaD or pure AD
      • Schneider et al . (2009): mixed pathology nearly as common as pure AD.
    • large proportion AD cases also CVD (up to 80%)
  • overlap in clinical features VaD and AD
22
Q

Difficulties diagnosis VaD

  • Stepwise course uncommon in VaD (Gorelick et al., 2011) -> believed to be defining feature decades ago
  • Demonstration link CVD and cognitive deficits
A
  • Stepwise course uncommon in VaD (Gorelick et al., 2011)
    • Insidious onset and gradual decline more common in VaD
    • so it can’t be used as a distinguising factor anymore
  • Demonstration link CVD and cognitive deficits
    • No stepwise decline
    • “silent” or asymptomatic infarcts
23
Q

Cognitive impairments present in Vascular dementia:

  • stepwise vs gradual decline
  • subcortical vs cortical
A
  • VaD often consequence additive effect of cerebrovascular disorders
    • progressive decline in cognitive functions
  • Brain areas affected influence pattern of cognitive decline
    • Lacunar infarcts and white matter lesions often in subcortical (“deep”) areas
  • VaD referred to as “subcortical” or “frontal-subcortical” dementia
    • AD referred to as “cortical” dementia
  • Not all VaD caused by subcortical pathology
    • Neuropathology cortical or subcortical.
    • Emphasis research on subcortical VaD
      • includes infarcts white matter, subcortical grey matter (e.g. basal ganglia)
24
Q

Cognitive impairments

  • subcortical VaD (Binswanger’s disease)
A
  • subcortical VaD (Binswanger’s disease)
    • EF relatively more impaired than in AD
    • interruption frontal subcortical circuits
    • episodic memory relatively less impaired than in AD
25
Q

Cognitive imairments:

  • Subcortical – cortical dementia (table 6.2 Smith and Bondi, 2013):
A
  • cortical dementia referred to AD
  • subcortical dementia referred to VaD
26
Q

Cognitive impairments VaD

  • Amount white matter abnormalities (WMA) in persons with VaD associated with EF (Price et al., 2005)
A

Amount white matter abnormalities (WMA) in persons with VaD associated with EF (Price et al., 2005)

  • more WMA, poorer performance EF task (WMS – mental control subtest ± WM task)
  • No association WMA severity and memory performance
27
Q

Cognitive impairments

  • Limitation studies comparing VaD and AD cognitive profile: diagnosis not confirmed in autopsy
A

Limitation studies comparing VaD and AD cognitive profile: diagnosis not confirmed in autopsy

  • Clinical diagnosis – possibility of misclassifications
  • Difficult to compare neuropsychological profiles, if uncertain who has AD and who has VaD
28
Q

Cognitive impairments

  • Reed et al. (2007) autopsy diagnosis confirmed:
  • neuropsychological profiles in autopsy confirmed AD (n=23) and CVD (n=11)
  • AD - plaques and tangles
  • CVD - infarcts: subcortical (including hippocampus, internal capsule, white matter, subcortical grey matter (e.g. basal ganglia), brain stem and cerebellum) and cortical (cortical grey matter)
    • only small lesions - lacunar infarct, microinfarct

Classification (profiles):

  • Cases substantial ischemic pathology and little AD pathology - VaD
  • Cases substantial AD pathology, little vascular pathology - AD
  • Mixed cases
A

Cognitive impairments

Reed et al. (2007) autopsy diagnosis confirmed

  • AD: memory poorer than EF
  • CVD/VaD: EF poorer than memory

In cases with cognitive impairments:

  • Low Memory score: 79% AD, 0% CVD
  • Low EF score: 5% AD, 67% CVD
  • 45% CVD cases and 4% AD cases no cognitive impairments during life
29
Q

Differential diagnosis VaD and AD

  • How does diagnosis based on neuropsychological profiles compare to autopsy-confirmed diagnosis?
  • ¨Reed et al. (2004), from same sample as Reed et al. (2007):*
  • diagnosis on based neuropsychological test:
    • AD – prominent episodic memory impairment (rapid forgetting), no prominent impairments EF
    • Ischemic vascular dementia (ILVD) – impaired EF (poor initiation, poor switching, poor WM, perseverations), impaired memory (poor learning, but relatively good recognition)
  • Mixed – features of both AD and IVD
A

¨Reed et al. (2004), from same sample as Reed et al. (2007)

  • Diagnosis AD mostly correct.
  • Diagnosis IVD and mixed less likely to be correct, but correctly distinguished form AD
    • no IVD/ Mixed incorrectly diagnosed as AD
  • Episodic memory impairment useful key cognitive impairments to distinguish AD from VaD
  • impairment EF less useful as clinical feature to identify VaD

McGuiness et al. (2010). No difference EF in VaD (46) & AD (76)

30
Q

Differential diagnosis VaD and AD

  • How does diagnosis based on neuropsychological profiles compare to autopsy-confirmed diagnosis?
  • Naming:
A
  • BNT: VaD better than AD, worse than matched HC
    • Overall VaD group less impaired than AD group (Lukatela et al 1998)
    • Fewer semantic errors suggests semantic memory relatively intact
31
Q

Differential diagnosis VaD and AD

  • How does diagnosis based on neuropsychological profiles compare to autopsy-confirmed diagnosis?
  • Language:
A
  • Similar pattern language impairments in VaD and AD (Vuorinen et al. 2000).
    • Naming, comprehension, production narrative
    • Preserved word repetition, reading out words – require no semantic processing
32
Q

How does diagnosis based on neuropsychological profiles compare to autopsy-confirmed diagnosis?

Other cognitive impairments

  • Visuospatial deficits
    • IVD – white matter abnormalities probable IVD
    • AD – without cortical or subcortical infarction on MRI
A

Rey complex figure test (Freeman et al., 2000)

  • Copying: AD more accurate than IVD, HC more accurate than AD and IVD.

Recognition after 20 min delay

  • IVD higher scores than AD, IVD worse score than HC
  • Visuospatial abilities more impaired in VaD than AD,
  • Visual memory less impaired in VaD than AD

Clock drawing:

  • Patients diagnosed VaD and severe WMA, more errors on CDT than those with mild WMA (Price et al. 2005)
33
Q

Cognitive impairments VaD versus AD

  • Meta-analysis (Mathias & Burke, 2009)
  • 81 studies comparing cognitive performance in persons diagnosed with AD and VaD
A
  • Episodic memory more impaired in AD than VaD: confirmed
  • EF more impaired in VaD than AD: not confirmed
  • NB. no distinction between different subgroups, e.g. subcortical or cortical VaD
  • Very few tests discriminated between 2 groups, exceptions were
    • Emotional recognition test: VaD worse than AD
    • Delayed Story Recall: VaD better than AD
34
Q

Neuropsychiatric symptoms (NPS)/behavioural disturbances:

  • Common in VaD and mixed AD/VaD
A
  • Overall prevalence NPS similar in AD and VaD groups (69.7% vs. 69.4%). AD (n=166) higher frequency agitation/aggression and irritability/lability than VaD (n=136) (D’Onofrio et al., 2012)
  • Postmorten confirmed AD (n = 40) or VaD (n = 40). Most prevalent agitation (57.0%), depression (41.2%) , anxiety (35.4%). No difference AD and VaD (Echavarri et al., 2013)
  • VaD patients (n=34) significantly more agitation (40 vs. 14%) and sleep disturbances (57 vs. 32%) than AD patients (n=92) (Anor et al., 2017). (-> contrary to the study above by D’Onofrio et al., 2012)
  • overall it seems that there are no large differences in NPS
35
Q

Assessment

  • (differential) diagnosis of VaD
    • Interview and history
    • Neuropsychological assessment
    • Neuroimaging, corroborating MRI essential
A

Interview and history:

  • patient and informant, (early) signs and symptoms
  • stepwise course not critical sign VaD

Neuropsychological assessment

  • sufficient breadth: memory, language, speed, attention, visuospatial, EF
  • include learning across trials, delayed retention and recognition
    • AD poor all indices, VaD better recognition

Neuroimaging, corroborating MRI essential

  • Lacunar infarcts and white matter hyperintensities
  • Amount of CVD sufficient to account for the cognitive difficulties
36
Q

¨Vascular dementia

  • pharmacological intervention
  • Current treatments aimed at (modifiable) risk factors VaD
A
  • ¨No pharmacological intervention specifically for VaD
    • Acetylcholinesterase inhibitors, glutamate antagonists
      • mixed reports effect on cognition (Tuokko & Smart, 2018)
      • Frequent severe side-effects
  • hypertension, diabetes, obesity - medication or life style changes
  • Reducing risk factors could prevent VaD
  • Importance diagnosis - different interventions VaD and AD
37
Q

Intervention VaD:

  • Non-pharmacological interventions
A

Non-pharmacological interventions

  • Same approaches as used in AD (very little differences)
  • Similar effects

Neuropsychology of Ageing (12 decks)

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