Lecture 12: Parkinson Flashcards
(83 cards)
1
Q
course
A
chronic and progressive
2
Q
Prevalence
A
1% of >60 years population
- man>woman
- often between 55-65
- older -> higher risk
2
Q
most common symptom
A
tremor (2/3 parkinson patients experience)
3
Q
the prevalence is expected to___
A
increase:
1. aging population
2. increased life-expectancy
3. Industrialization/pollution
3
Q
2 nd most common neurodegen disorder
A
after AD
3
Q
how to differentiate between variants
A
course of disease (hard to differentiate by initial stage)
4
Q
2 subtypes of Parkinson
A
- Tremor-dominant
- Postural instability dominant
This subtype tends to have:
- Faster disease progression
- Worse cognitive decline
- More depressive symptoms
4
Q
clinical assessment to determine stage classification
A
HY scale (stage 1: oneside affected - stage 5: wheelchair)
5
Q
assessment to determine severity
A
Unified Parkinson disease rating scale (UPDRS)
5
Q
Unified Parkinson disease rating scale (UPDRS
A
4 parts: Part III Motor examination commonly used (also treatment effects)
6
Q
Neuropathology
A
Degeneration (thoai hoa) of dopamine (DA)-producing neurons in part
of substantia nigra (SN)
6
Q
+/- ___% of the DA neurons in SN are damaged
A
70%
7
Q
Cortico-basal ganglia motor loop controls
A
voluntary actions (also cognition and behavior processes)
7
Q
SN is part of
A
cortico-basal ganglia loops
8
Q
The disease does not affect the whole brain at once.
A
It spreads in stages through different brain regions — this is shown in the Braak model
8
Q
Why do dopamine (DA) neurons die
A
Lewy bodies=accumulation
of misfolded alpha-synuclein
9
Q
Braak staging
A
Starts in lower brainstem (stage 1–2): affects smell, sleep, autonomic function.
Spreads to midbrain (stage 3–4): affects substantia nigra, causes motor symptoms.
Later reaches cortex (stage 5–6): leads to cognitive, emotional, and psychiatric symptoms.
9
Q
Lewy bodies = alpha-
synuclein pathology can be seen in
A
Parkinson’s disease
atypical parkinsonism subtypes:
- MSA (Multiple System Atrophy)
- DLB (Dementia with Lewy Bodies)
9
Q
Tauopathies is cause of
A
Cortico-basal degeneration (CBD)
Progressive supranuclear paralysis (PSP)
10
Q
What are the 3 key components in diagnosing Parkinson’s disease?
A
- Required signs – Bradykinesia plus either rest tremor or rigidity
- Supportive criteria – e.g., good response to levodopa, rest tremor
- Red flags – e.g., early falls, early swallowing problems, symmetrical symptoms
11
Q
What is the main required symptom for diagnosing Parkinson’s disease?
A
Bradykinesia (slowness of movement), plus either rest tremor or rigidity
12
Q
Name two common supportive criteria that increase likelihood of PD.
A
- Good response to levodopa
- Presence of rest tremor
12
Q
What are some red flags that suggest atypical parkinsonism instead of PD?
A
- Early falls
- Early bulbar dysfunction (speech/swallowing issues)
- Bilateral symmetrical onset
- Ataxia (coordination problems)
13
Q
What is used to rule out tumors or strokes in parkinsonism diagnosis?
A
MRI brain scan
13
What is the importance of “order of symptom development” in diagnosis?
It helps distinguish PD from diseases like DLB or MSA, which may show cognitive or autonomic symptoms before motor signs
14
What is the difference between Parkinson’s disease and atypical parkinsonism in terms of medication response?
- PD usually responds well to dopaminergic medication (levodopa)
- Atypical parkinsonism often responds poorly
14
What does a SPECT DaTscan measure in Parkinson’s diagnosis?
Dopamine transporter activity in the caudate and putamen regions of the brain
15
Which atypical parkinsonism types are associated with tau pathology?
Corticobasal Degeneration (CBD)
Progressive Supranuclear Palsy (PSP
16
Which atypical parkinsonism types are linked to alpha-synuclein pathology?
Multiple System Atrophy (MSA)
Lewy Body Dementia (DLB)
17
Is there a cure for Parkinson’s disease?
No. Treatment focuses on symptom relief and supportive therapy.
17
What are the 3 main types of dopamine-based treatments?
1. Levodopa (L-Dopa)
2. Dopamine agonists
3. MAO-B inhibitors
17
What is the main goal of treatment in Parkinson’s disease?
To replace or increase dopamine in the brain and improve motor symptoms.
17
What are common side effects of dopamine treatments?
Narcolepsy (hypoactivity) to psychosis
Hyperkinetic movements
Dyskinesia (involuntary, jerky movements)
18
What side effects are especially associated with dopamine agonists?
Impulse control disorders, such as:
Gambling
Excessive shopping
Hypersexuality
19
What does “OFF-state” mean?
It’s when dopamine levels are too low, and symptoms return or worsen.
19
What does “ON-state” mean in Parkinson’s treatment?
It’s when dopamine levels are high enough, and the patient has good motor function.
19
What is the challenge of long-term dopamine therapy?
Maintaining stable dopamine levels becomes hard → leads to motor complications like ON/OFF fluctuations and dyskinesia.
20
What are response fluctuations in PD treatment?
Changes over time in how the body responds to dopamine meds, causing:
“Wearing-off” (meds lose effect too soon)
“Delayed ON” (meds take longer to work)
20
Side effects of DBS
affects non-motor functions
21
What percentage of people with Parkinson’s already have cognitive impairments at diagnosis?
About 24% already show impairments when diagnosed.
22
What percentage of Parkinson’s patients will develop cognitive impairments?
25–40% experience cognitive impairments at some point.
22
What are common executive dysfunctions in Parkinson’s?
- Difficulty starting actions
- Trouble shifting between tasks
- Problems stopping behavior (inhibition)
23
What kind of behavior is impaired in Parkinson’s patients?
Internally generated behavior (self-initiated actions), both automatic and controlled.
23
What are two attention-related cognitive issues in Parkinson’s disease?
Attention problems
Reduced processing speed
24
Why is cognitive control important in Parkinson’s?
Because even automatic actions (like walking) require more mental effort when dopamine is low.
25
What other cognitive domains are affected in Parkinson’s?
Visuospatial dysfunctions
Difficulty learning new skills
Trouble with social cognition (e.g., recognizing emotions)
26
Which brain areas are involved in Parkinson’s cognitive symptoms?
- Frontal cortex
- Striatum
- Substantia nigra
- Limbic circuits and associative circuits
26
What role does a clinical neuropsychologist play in PD?
They assess and help manage cognitive and emotional impairments, including attention, executive function, and learning difficulties.
27
What is the link between MCI and Parkinson’s dementia
Mild cognitive impairment (MCI) in Parkinson’s increases the risk of progressing to dementia
28
After how many years do most people with Parkinson’s develop dementia?
- After 10 years → ~50% develop dementia
- After 20 years → ~80% develop dementia
29
What behavioral symptom often comes before dementia in PD?
Apathy (lack of motivation)
29
What are the Movement Disorder Society’s diagnostic criteria for Parkinson’s dementia (2007)?
Parkinson’s diagnosis before dementia
MMSE < 26
Cognitive impairment in 2 or more domains that affect daily life
30
What cognitive domains must be impaired to diagnose PDD?
Attention
Executive function
Visuoconstruction
Memory
30
What neurotransmitter system is involved in PDD?
The cholinergic system (acetylcholine) is involved
30
How is PDD treated pharmacologically?
May use cholinesterase inhibitors
Avoid anticholinergic medications
31
How does PDD differ from other dementias (e.g., Alzheimer’s)?
In PDD: retrieval is impaired, but recognition is intact
Visuospatial problems are more severe
31
What percentage of people with Parkinson’s experience at least one neuropsychiatric symptom?
Up to 90% of Parkinson’s patients
32
What are common emotional symptoms in Parkinson’s disease?
Depression
Anxiety
Apathy
32
What sleep-related issue is common in Parkinson’s?
Sleep disorders (e.g., REM sleep behavior disorder, insomnia)
33
What are common behavioral and psychiatric symptoms in PD?
Psychosis (hallucinations, delusions)
Impulsivity (e.g., gambling, shopping)
33
What brain system is involved in both motor and neuropsychiatric symptoms in PD?
The dopamine system (especially in the frontal cortex, striatum, VTA, and nucleus accumbens)
34
What non-motor functions are affected by dopamine loss in Parkinson’s?
Motivation and reward, in addition to movement
34
What is the core symptom of depression according to DSM-5?
Depressed mood
Or loss of interest or pleasure (anhedonia)
(One of these must be present nearly every day for 2 weeks)
35
What percentage of people with Parkinson’s show depressive symptoms?
35–70%, or about 1 in 3 patients
35
What percentage of PD patients meet criteria for a formal mood disorder?
About 17% have a diagnosable depressive disorder
36
What neurotransmitters are involved in depression in PD?
Dopamine (disruption of motivation/reward pathway)
Also affected: serotonin and norepinephrine
36
What DSM-5 criteria (besides sad mood/loss of pleasure) are commonly seen in PD-related depression?
Loss of energy
Psychomotor retardation
Cognitive problems (difficulty concentrating, thinking)
36
What is a common timing pattern for depressive symptoms in PD?
Mood may drop during 'OFF' periods (when medication wears off)
37
What makes diagnosing depression in PD difficult?
Apathy
Mild Cognitive Impairment (MCI)
Parkinson’s dementia
38
What is the role of the clinical neuropsychologist in PD depression?
To differentiate depression from apathy, MCI, or dementia and guide treatment planning.
39
What types of anxiety disorders are common in Parkinson’s disease?
Generalized Anxiety Disorder (GAD)
Social anxiety disorder
Specific phobia
Panic disorder
40
What percentage of Parkinson’s patients show anxiety symptoms?
40–50%
41
What percentage of Parkinson’s patients have a formal anxiety disorder diagnosis?
30%
42
When can anxiety symptoms worsen in Parkinson’s patients?
During 'OFF' moments
During transitions between 'ON' and 'OFF' states
👉 These fluctuations are related to medication effects.
43
Can anxiety affect motor symptoms in PD?
Yes, anxiety can worsen motor symptoms (like tremors or stiffness).
44
What treatment may help with anxiety in PD patients?
Medication adjustments or specific anxiety treatments
45
What is the role of the clinical neuropsychologist in anxiety management?
To help identify, differentiate, and manage anxiety symptoms and their impact on motor and cognitive function.
46
What is apathy?
A decrease in motivation, interest, emotions, and goal-directed behavior
(tho o)
47
How is apathy related to cognitive symptoms in PD?
It may be linked to or predictive of cognitive decline
47
What brain system is thought to be involved in apathy?
The ventral dopamine (DA) circuit, especially the VTA–PFC pathway
(Ventral tegmental area to prefrontal cortex)
48
Why is apathy clinically important in Parkinson’s care
It increases caregiver burden (ganh nang)
Affects quality of life
Impacts treatment adherence
49
What makes diagnosing apathy in PD difficult?
It overlaps with:
Fatigue
Depression
Mild Cognitive Impairment (MCI)
Dementia
50
What is the role of the clinical neuropsychologist regarding apathy?
To help differentiate apathy from similar symptoms and support better management and care planning
