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Neuropsychology of Ageing > Lecture 10: Dementia with Lewy bodies > Flashcards

Lecture 10: Dementia with Lewy bodies Flashcards

1
Q

Dementia with Lewy bodies:

  • Progressive cognitive decline
  • Core features
  • DLB:
A
  • Progressive cognitive decline
  • Core features
    • Parkinsonism
    • Visual hallucinations
    • Fluctuations cognitive functioning and arousal
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2
Q

Dementia with Lewy bodies

  • epidemiology (prevalence)
  • typical age
  • mean survival time
A
  • most frequent neurodegenerative dementia after AD (VaD more common but its not neurodegenerative)
  • third most common form dementia, after AD and vascular dementia
    • 5 - 20% of dementia cases
  • first described in 1961
  • symptoms usually appear after 60.
    • Early onset rare
    • No increase prevalence with age
  • Mean survival time 8-10 years
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3
Q

Dementia with Lewy bodies

  • Neuropathology
A
  • Lewy bodies.
    • Discovered by Fritz Heinrich Lewy in 1910
  • abnormal aggregates of proteins inside nerve cells
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4
Q

Neuropathology

  • Main component Lewy bodies:
  • Lewy neurites:
  • DLB example class neurodegenerative diseases:
  • ¤Similarities DLB and PD:
A
  • Main component Lewy bodies: alpha-synuclein
    • protein abundant in brain
    • for reasons unclear, alpha-synuclein clumps together
  • Lewy neurites, common feature in DLB
    • neurites containing abnormal alpha-synuclein
    • neurite: any projection from cell body
  • DLB example class neurodegenerative diseases - synucleinopathies
    • other example Parkinson’s Disease (PD)
    • Lewy bodies and Lewy neuritis in nerve cells PD
  • Similarities DLB and PD
    • Symptoms DLB, PD and PD dementia overlap
    • Effects on cognition, movement and behaviour
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5
Q

Progression Lewy Body Pathology

  • Braak et al (2003) staging LB pathology:
  • LB pathology in DLB similar as PD:
A

Braak et al (2003) staging LB pathology:

  • I – VI peripheral NS - brainstem - cortex

LB pathology in DLB similar as PD:

  • Most autopsy cases: LB in cortical areas

advanced Braak stage

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6
Q

Neuropathology

  • DLB - LB (lewy Bodies) in
  • PD (Parkinson’s Disease) – LB in
A
  • DLB - LB in
    • cortex and limbic areas
    • subcortical (locus coerules, substantia nigra, nucleaus basalis of Meynert)
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7
Q

Neuropathology

  • LB can occur in:
  • AD pathology in DLB?
A
  • Lewy bodies in 20-35% older persons with dementia, not all DLB
    • Lewy bodies not common in healthy persons
  • Many DLB patients also AD pathology (amyloid plaques)
    • Up to 75-90% of patients with DLB
    • Tangles less common in DLB
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8
Q

Neuropathology

  • cholinergic neurons:
A
  • Loss of cholinergic neurons and depletion choline levels in brain
    • Cholinergic deficit more pronounced DLB than in AD
    • Cholinergic deficit early in disease
  • Cholinergic depletion factor in symptoms early DLB
    • Reduced alertness and attention, visual hallucinations
  • Increasing ACTh levels - acetylcholinesterase inhibitors (pharmacological treatment)
    • can have positive effects on symptoms
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9
Q

Neuropathology

  • Dopamine deficiency:
  • Genetics:
A
  • Dopamine deficiency
    • LB in substantia nigra
    • Loss of dopamine receptors
      • Available dopamine has less impact
      • Weak response to dopaminergic drugs
  • Genetics:
    • No specific genes identified
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10
Q

Neuroimaging (DLB):

  • Atrophy:
A
  • atrophy in dorsal midbrain, striatum and hypothalamus
  • little atrophy in hippocampus
    • (so different than early AD)
    • generally lower areas of the brain
  • overall less atrophy than in AD or FTD
    • Not different from HC (healthy older people)
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11
Q

Clinical features

  • In addition to progressive cognitive decline:
A
  1. Parkinsonism
  2. Visual hallucinations
  3. Fluctuations cognitive functioning and arousal
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12
Q

Parkinsonism in DLB patients:

A

Parkinsonism:

  • in 70 – 100% of patients with DLB
  • rigidity, bradykinesia, shuffling gait, stooped posture, masked face
  • tremor less common
  • severity varies
    • usually less severe in DLB than in PD
  • patients may report frequent unexplained falls
  • Parkinsonism must be spontaneous, i.e. not attributable to medication.
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13
Q

Dementia with Lewy bodies

  • Visual hallucinations (VH)
  • VH can occur in AD
  • relative onset of VH
A

Visual hallucinations

  • Fully formed detailed objects, people or animals.
  • Auditory, tactile, olfactory hallucinations less common
  • 22-89% of cases DLB
  • DLB with VH typically more severe cognitive and functional impairments
    • Visuospatial functions (Mosimann et al., 2004)
    • More LB in temporal lobe
  • VH can occur in AD
    • 11-28% of cases
  • VH onset from onset cognitive impairments
    • DLB: 1.5-2 years after onset (so quite early), sometimes even before onset cognitive impairments
    • AD: 5 – 7 years after onset
    • Distinction useful differential diagnosis AD en DLB
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14
Q

Dementia with Lewy bodies

  • Fluctuations in cognitive functioning and arousal
  • Ferman et al. (2004): fluctuation questionnaire completed by informants
A

Fluctuations in cognitive functioning and arousal

  • Fluctuations in attention, incoherent speech, impaired awareness of surroundings, staring into space, “switched off”
  • Reported prevalence: 10% to 80%

Ferman et al. (2004): fluctuation questionnaire completed by informants

  • Items best distinguished DLB from AD and HC:
    1. Daytime drowsiness and lethargy
    2. Daytime sleep 2 hrs or more.
    3. Staring into space for long periods
    4. Flow of ideas seems unclear, disorganised, not logical
  • 3 or 4 feature present 63% DLB patients (n=70), 12% AD patients (n=70), 0.5% normal elderly (n=200).
  • not all DLB patients had fluctuations
  • presence of fluctuations not associated with parkinsonism
  • different underlying causes

Picture: White columns: normal elderly; Grey Columns: AD; Black Columns: DLB. Numbers according to items previously mentioned.

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15
Q

Distribution clinical features in DLB

  • Clinical features overlap in DLB and AD
  • from: Ferman et al. (2006)
    • Percentage of patients with symptoms DLB N=89
A
  • hence these core features might be good indicators to differentiate between AD and DLB
  • 73% of AD’s had none of these core features, none had all three of them
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16
Q

Further clinical feature: core feature according to Smith & Bondi (2013)

  • Sleep disorders:
  • early indicator for DLB?
A
  • Sleep disorders
    • 70 to 75% of DLB cases
    • in particular REM Sleep Behavior Disorder – RBD
      • loss of muscle atonia during REM sleep
      • movements during REM sleep
      • Result: one might act out dreams
  • RBD can be early sign DLB, precede cognitive impairment by several years
    • Presence of RBD is risk factor:
      • 12-year risk 52% (Postuma et al., 2009)
      • case of confirmed DLB after 20 years of RBD.
  • Poor sleep quality also common
    • Can contribute to excessive daytime sleepiness
17
Q

Differential Diagnosis DLB:

A
  • Probable DLB: presence dementia plus at least 2 core features
  • Possible DLB: presence dementia plus 1 out of 3 core features
  • Suggestive features support diagnosis
  • Counter indicators: evidence CVD or other physical or brain disorder
18
Q

Central and core features of possible and probable DLB (diagnosis):

A
19
Q

Suggestive features for for possible and probable DLB (diagnosis)

A
20
Q

Counterindicators for DLB (Diagnosis):

A
21
Q

Diagnosis

  • Temporal sequence important for diagnosis:
A

Temporal sequence important for diagnosis:

  • DLB: dementia before or at same time as parkinsonism (e.g. motor-symptoms)
  • Parkinson dementia: dementia when Parkinson symptoms already obvious
  • Parkinson’s disease dementia (PDD): 3-5% dementia cases
22
Q

Neuropsychology of DLB:

A
  • Impairments in visual perceptual skills, attention, EF and fluency
  • Memory impairments less prominent than in AD
  • Overlap symptoms DLB and AD: misdiagnosis common.
  • Search neuropsychological profiles
23
Q

Neuropsychology of DLB:

  • Visuospatial abilities
    • Calderon et al., 2001
    • 9 probable AD patients, 10 probable DLB patients, 17 HC
    • Tests of visuospatial abilities/perception memory and attention/EF
A
  • Pronounced deficits in visuospatial abilities/perception compared to HC and AD
24
Q

Neuropsychology of DLB

  • Memory
A
  • Episodic memory less impaired in DLB than in AD
  • autopsy-confirmed DLB (n=24), autopsy-confirmed AD (n=24) and HC (n=24) (Hamilton et al. 2004)
    • Difference DLB – AD retention and recognition episodic memory
      • patients with DLB were less impaired compared with AD but worse than HC
    • No difference DLB and AD learning and immediate recall
  • Memory deficits early stage DLB usually mild (milder than AD)
    • little atrophy hippocampus
25
Q

Neuropsychology

  • Executive functions/attention
A

Executive functions/attention

  • DLB and AD (based on clinical diagnosis) and matched HC
  • Stroop (COWAT) and TMT B poorer in DLB than HC and AD
26
Q

Neuropsychology

  • Language
A

Language

  • Boston naming test
    • Ferman et al. (2006): DLB > AD, DLB < HC
    • Hamilton et al. (2004): no difference DLB - AD
    • Calderon et al (2001): no difference DLB - AD
27
Q

Neuropsychology

  • Meta-analysis neuropsychological differences DLB and AD (Gurnani & Gavett, 2017) –
    • 14 studies included autopsy confirmed DLB (n=155) or AD (n=431)
A
  • AD memory worse
  • DLB visuospatial worse
  • No differences attention, processing speed, EF, language
28
Q

Neuropsychology

  • Neuropsychological pattern similar in DLB and PDD
    • (Troster & Browner, 2013)
A

Neuropsychological pattern similar in DLB and PDD (parkinson’s disease dementia)

  • EF (e.g. Stroop, TMT WCST) and attention impaired
  • Memory - impairment similar severity
  • Language - naming relatively spared
  • Visuospatial abilities – impaired, more severe than in AD
29
Q

Neuropsychiatric symptoms (DLB)

A
  • Hallucinations and delusions
    • Similar prevalence in DLB and PDD
    • Can occur several times/day
    • More frequent in night or evening
    • Delusions of misidentification (Capgras), theft, infidelity
  • Depression
    • Common all forms dementia, possibly more common DLB than AD
  • Apathy
  • Anxiety
30
Q

Early symptoms/prodromal DLB:

A
  • aMCI or naMCI
    • latter more common
  • Transient disturbances consciousness
  • Visual hallucinations
  • RBD
    • ± 50% DLB cases prior cognitive decline
  • Parkinsonism
  • Hyposmia (reduced sense of smell)
    • one of the areas were LB are found is in the Olfactory Bulb
31
Q

Treatment DLB

  • Pharmacological
  • Non-pharmacological
A

Pharmacological

  • No cure, some symptoms treated with medication.
  • Levadopa/L-dopa for motor functions/parkinsonism
  • Acetylcholinesterase inhibitors - cognition
  • Oversensitivity neuroleptic medication
  • used to treat hallucinations or agitation
  • can severely worsen motor and cognitivempairments in DLB

Non-pharmacological

  • Often supporting the family caregiver
  • Educate family to cope with behaviour
    • e.g. “go along”, give reassurance, instead of trying to reason with the patient
  • if hallucinations are not distressing or harmful to the patient, why correct them
    • unsuccessful and distressing

Neuropsychology of Ageing (12 decks)

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