Neuropsychological Aspects of Parkinson*s Disease
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Transcript Neuropsychological Aspects of Parkinson*s Disease
Parkinson’s Cognitive Problems
versus Other Neurological Diseases
14 February 2015
Carole A. Mazurowski, PhD
Health Psychology & Neuropsychology
6565 Americas Parkway NE, Suite 200,
Albuquerque, NM
505-620-2848
Main Parkinsonian Syndromes
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Primary (idiopathic) Parkinson's disease
– Tremor-predominant
– Bradykinetic primary
Secondary (acquired, symptomatic) parkinsonism
Pugilistic encephalopathy
Normal pressure hydrocephalus
Multiple system degenerations (parkinsonism plus)
Progressive supranuclear palsy
Shy-Drager syndrome
Striatonigral degeneration
Corticobasat ganglionic degeneration
Lewy body disease
Basic Neuropsychology
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Brain organization has areas for movement and
thinking spread in adjoining or overlapping
chunks all over.
Parkinson’s arises from loss of dopamine in the
substantia nigra of the brain.
Approximately 80% of substantia nigra cells are
usually destroyed before motor symptoms
appear.
PD often also involves losses in other
subcortical areas of the brain.
More Neuropsychology
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The substantia nigra is part of the basal
ganglia in the middle part of the brain
with neural tracts extending into frontal
lobes.
Changes do not show in
CT or MRIs
Diagnosis is through
Presenting symptoms
Dementia Rates in PD
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The percentage of PD patients to
experience a dementia ranges has been
estimated between 20% to 40%
Incidence rate increases with age. A
recent longitudinal study showed that by
85 years of age more than 65% of its PD
participants had dementia. Another study
found about 75% developed dementia 8
years into illness.
Movement, Mood & Thinking
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The basal ganglia has been best known as
the area where movement disorders
originated – originally it was thought PD
did not affect cognition
Current research shows the basal ganglia
governs starting and stopping thoughts
and actions as well as modulating mood
and cognition
Dementia in PD
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Dementia diagnosis requires memory
deficits plus at least one other cognitive
deficit that significantly interferes with
daily functioning
Most Parkinson’s patients eventually
experience some cognitive decline,
though it does not qualify as a dementia
syndrome
Alzheimer’s Brain
Note the rampant atrophy with particular
focus on memory & language areas
PD versus Alzheimer’s
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In Alzheimer’s Disease one of first signs is a
rapid decay of memory that does not respond
to cueing.
Although PD patients may experience memory
difficulties, there is a greater ability to recall
information with cues or multiple choices.
Like a house of cards collapsing, problems with
organizing and paying attention can impact
ability to remember.
FRONTOTEMPORAL DEMENTIA
Atrophy of frontal and temporal (near the
ears) brain areas
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Some lose language early in the illness
Others decline in social interpersonal conduct
Impairment in regulation of personal conduct
Emotional blunting
Loss of insight
Procedural Memory Problems
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As the corpus striatum, a part of the basal
ganglia, contributes to the procedural
memory system, PD patients whose
disease has affected that area may have
trouble with learning new skills and
response patterns to novel situations
By contrast, procedural memory is usually
spared in Alzheimer’s disease: playing
favorite piano tunes, for example.
Slowed Mental Processing
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This may be greater for individuals with
the more slowed type of PD, called
bradykinetic, versus tremor-predominant
Contributes to inability to start into action
and conversations
Executive Functioning Problems
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Difficulty developing successful problem-solving
strategies
Impaired set-shifting – getting stuck on one idea
when a new one is needed
Difficulty maintaining correct sequencing
Poor use of feedback from others
Poor use of internal cues to guide behavior
Difficulty holding back irrelevant responses
Poor initiation – starting an action or thought process
Impulsivity – starting into action quickly without
thinking
Inability to allocate attention where needed
Poor concept formation, particularly when the ideas
are abstract
Delirium
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Due to the PD brain’s greater struggles with
mental processing, risk is high for delirium for a
few days after general anesthesia
If there is a sudden decline in memory and
thinking, consult your physician to check current
medications or for an infectious process such as
urinary tract infection
Dehydration is a common cause of delirium
Kidney malfunction can cause Amantadine
buildup leading to delirium
Lewy Body Dementia
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A progressive dementia caused by abnormal
protein deposits (Lewy bodies) depleting
dopamine
PD also has Lewy bodies, but not as abundantly
as in LBD, where they also occur throughout the
brain
In LBD the cognitive decline begins at about the
same time as Parkinsonian symptoms start
occurring
Cognitive deficits are similar to PD, but
progressing faster and including more
visuospatial difficulties
Visual hallucinations early in illness
Confusion
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Patients without dementia sometimes mention
rare occurrences of sudden periods of
confusion
PD meds can make dreams more lifelike,
causing confusion with sudden awakening
Awakening away from home can cause
confusion before the patient reorients
Dementia patients often experience more
confusion towards the evening – known as
sundowning
Naps can be helpful to decrease confusion
Depression & Cognition
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There is a much higher rate of depression
in PD than most other neurological
disorders – multiple sclerosis, for
example.
In an older individual without neurological
disorders, depression itself can cause
what looks like a dementia.