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Neuro 2 > Parkinson's Disease > Flashcards

Parkinson's Disease Flashcards

1
Q

What are the major functions of the basal ganglia?

A
  • motor control
  • eye movement loop
  • goal-directed behavior loop
  • social behavior loop
  • emotion loop
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2
Q

What are specific motor control functions of the basal ganglia?

A

o Initiation and execution of movement
o Prevention of unwanted movements through inhibitory control
o Direct and indirect pathways that work together to help create desired movement

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3
Q

What type of eye movements is the basal ganglia involved with?

A

saccadic eye movement

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4
Q

_________ elevates the effects of the basal ganglia and its modulation on movement

A

Dopamine

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5
Q

What inhibits dopamine?

A

ACh
- can quickly interrupt ongoing motor behavior in response to salient environmental stimuli

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6
Q

What are the primary neurotransmitters in direct and indirect pathways?

A

GABA and Glutamate

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7
Q

Dopamine has a _____ effect which leads to what?

A

dopamine has a dual effect which leads to a powerful decrease in suppression of thalamus by basal ganglia and leads to facilitation of movement

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8
Q

What are general signs and symptoms of basal ganglia dysfunction?

A
  • Difficulty initiating, continuing, or stopping movement
  • Muscle tone abnormalities
    o Rigidity – affects flexors more than extensors
  • Increased involuntary movements
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9
Q

What is hemiballismus?

A

hyperkinetic movement disorder characterized by violent involuntary limb movements on 1 side of body (affects proximal limbs)
- rotatory nature

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10
Q

What is chorea?

A

Chorea – jerky, involuntary movements (affects distal limbs)

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11
Q

What is athetosis?

A

involuntary muscle contractions cause writhing movements

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12
Q

What are some of the characteristics of the patient population we see Parkinson’s Disease (PD) in?

A
  • Older adults (> 60 y/o), mean age of onset – early 60s
  • Men > women
  • Decreased prevalence in black and Asian populations
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13
Q

What’s the difference between primary and secondary parkinsonism? Where does PD fall within these classifications?

A
  • Primary Parkinsonism (PD) = Parkinson’s disease
  • Secondary Parkinsonism – similarities in clinical impairments w/o perfectly fitting the molds for PD
    o PD as a result of something else: infectious/postencephalitic, atherosclerosis, toxic, drug-induced
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14
Q

Explain the pathophysiology behind PD.

A
  • Degeneration of dopaminergic neurons in the basal ganglia (loss of DA stores in substantia nigra)
  • As disease progresses, other regions of brains involved as well as impaired modulation of other neurotransmitters
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15
Q

How is PD diagnosed? What is the gold standard?

A
  • Diagnosis of exclusion
    o Only definitive way to diagnosis PD is post-mortem exam of the brain
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16
Q

When do we see motor symptoms develop in relation to when the disease process starts?

A
  • Motor symptoms do not appear until ~ 60% neurodegeneration has already occurred in basal ganglia
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17
Q

Describe bradykinesia, hypokinesia, and akinesia. How do they differ?

A
  • Bradykinesia – slow movements
  • Hypokinesia – small movements
  • Akinesia – absence of movements
  • Movements shrink down in amplitude and force with more complex tasks harder than simple commands
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18
Q

Define rigidity and describe the presentation commonly seen with PD.

A
  • Rigidity – passive resistance to stretch independent of velocity
    o Felt uniformly in all directions (asymmetrical early then eventually whole-body movement)
    o Seen proximal first
    o Leads to increased cognitive load, emotional stress, energy expenditure of movements
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19
Q

Long term effects of rigidity

A

o Long term effects: decreases ROM, contractures, postural deformities

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20
Q

Lead pipe vs cogwheel rigidity

A

lead pipe - sustained resistance

cogwheel - jerky, ratchet-like (lead pipe + tremor)

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21
Q

Define tremor and describe the presentation commonly seen with PD. What body parts are most common?

A
  • Tremor - involuntary, rhythmic muscle contraction leading to shaking movements in one or more parts of the body
    o Resting tremor early on
    o Hand and foot are most common
    o Tends to be mild, low frequency
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22
Q

What leads to postural instability in PD?

A
  • abnormal postural responses
  • small functional limits of stability
  • difficulties with self-initiated movements
  • reduced anticipatory postural adjustments and control
  • abnormal patterns of activation
  • midline disorientation
  • rigidity, weakness, loss of ROM, freezing, medication side effects
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23
Q

What are the 3 top risk factors for falls in PD patients?

A
  • Postural instability
  • Disease severity
  • Gait impairments (most notably Freezing of Gait)
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24
Q

What are additional risk factors for falls identified?

A
  • Dementia
  • Depression
  • Postural hypotension
  • Involuntary movements from long-term medication use
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25
Q

Explain the specific difficulties those with PD have with complex motor planning tasks.

A
  • Sequential movements – poor motor planning
  • Transitioning between movements
    o Motor preservation (fingers typing then continue when going to pick up glass of water)
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26
Q

What is the difference between a continuous and episodic gait characteristic?

A

Episodic changes, such as freezing of gait, can come on suddenly and randomly.
Continuous changes are changes in your gait that happen all the time while walking, such as walking more slowly than expected

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27
Q

What are the continuous gait impairments seen with PD

A

o Overall hypokinetic presentation (slow steps, reduction in arm swing, minimal trunk rotation, LE rigidity, axial rigidity)
o Increased variability and asymmetry
o Poor postural control
o Festinating gait
o Increase tendency for retropulsion and/or anteropulsion

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28
Q
  1. What are the episodic gait impairments seen with PD? What happens to these as the disease progresses?
A

o Festinating gait pattern
o Midline disorientation (anteropulsive or retropulsive)
o En Bloc turning (turn in a uniform, rigid presentation)
o Freezing of gait

Turn into continuous gait impairments as the disease progresses

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29
Q

List common non-motor symptoms seen with PD

A
  • Pain and paresthesias
  • Visual impairments
  • OH
  • Fatigue
  • Dementia
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30
Q

What types of pain patterns do we see with PD? What are common areas?

A
  • Musculoskeletal and neuropathic
    o Central pain thought to be due to abnormal modulation of pain caused by dopamine deficiency

Common areas:
- lower back
- legs
- shoulders
- face

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31
Q

What are the two subtypes of PD and how do they differ?

A
  • Postural Instability Gait Disorder phenotype
    o Postural instability and gait disturbances
    o More significant disease course
  • Tremor-Dominant phenotype
    o Demonstrate fewer problems with bradykinesia or postural instability
    o Lower prevalence of non-motor symptoms
    o Less likely to develop dementia and other cognitive deficits
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32
Q

Which subtype has the better prognosis overall?

A
  • Tremor-Dominant phenotype
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33
Q

How is PD staged and what are the different levels to this scale?

A

1 - unilateral involvement only
1.5 - unilateral and axial involvement
2 - bilateral involvement w/o impairment of balance
2.5 - mild bilateral disease with recovery on pull test
3 - mild to moderate bilateral disease; some postural instability; physically independent
4 - severe disability; still able to walk or stand unassisted
5 - wheelchair bound or bedridden unless aided

34
Q

H&Y 1 vs 1.5

A

1 - unilateral involvement only
1.5 - unilateral and axial involvement

35
Q

H&Y 2 vs 2.5

A

2 - bilateral involvement w/o impairment of balance
2.5 - mild bilateral disease with recovery on pull test

36
Q

H&Y 3-5

A

3 - mild to moderate bilateral disease; some postural instability; physically independent
4 - severe disability; still able to walk or stand unassisted
5 - wheelchair bound or bedridden unless aided

37
Q

What are the major medications used for PD symptom management?

A
  • Carbidopa & Levodopa (sinamet) - 1st line of defense
  • Dopamine agonists
  • COMT inhibitors
  • MAO-B inhibitors
  • Anticholinergics
38
Q

Carbidopa & Levodopa considerations

A

1st line of defense
o Levodopa converts into dopamine
o Carbidopa facilitates process and minimizes side effects

39
Q

Dopamine agonists considerations

A

o Mimic effect of dopamine by stimulating dopamine receptors
o Can be used to delay need for C&L, but often used in combo

40
Q

COMT inhibitors considerations

A

o Increase availability of dopamine by blocking disruptive enzymes
o Must be used with C&L to be effective

41
Q

MOA-B inhibitors considerations

A

o Mimics COMT inhibitors
o Often used as monotherapy in early stages or in combo with C&L later on

42
Q

Anticholinergics considerations

A

o Combat the reciprocal increase of Ach that is seen in response to dopamine depletion
o Primarily used to treat tremors in early stage of disease

43
Q

What are some specific considerations re: levodopa?

A
  • Does not improve ALL Parkinson’s symptoms
  • Typically worsens postural responses to external perturbations
  • Improves hypokinetic gait in early stages but tends to be less effective as disease progresses
  • Generally improves freezing of gait in the OFF state but not during the ON state
44
Q

Describe the prognosis for PD.

A
  • Does not lead to mortality
    o Common secondary sequelae that can lead to death: CHF and Pneumonia
  • Disease can progress quickly or can go several decades with only mild limitations
  • Increases chance of dementia – Lewy bodies dementia
45
Q

What are negative prognostic indicators for PD?

A
  • Degree of symmetry of symptoms
  • Postural Instability Gait Disorder (PIGD) phenotype
  • Higher baseline UPDRS motor score
    o Higher bradykinesia sub-scores
    o Higher baseline H&Y stage
  • Younger age at onset
  • Early cognitive decline or baseline cog impairment
  • Smoking Hx
  • Male
46
Q

What does the PDQ-39 measure? What has it been found to correlate with?

A
  • Evaluates PD specific health related QoL over the last month
  • Correlates w/ H&Y and has better construct validity than generic measures
47
Q

What is the MDS-UPDRS? Is it used clinically? If so, in what capacity?

A
  • Comprehensive assessment designed to monitor the burden and extent of PD across the disease course
  • Done more in research settings vs clinical settings
  • Parts 1 (non-motor experiences of daily living) and 3 (motor exam) done in clinical settings as they are commonly already done during exams
48
Q

What does the MoCA measure? What is its cut-off score?

A
  • Rapid screen of cog status designed to detect early dysfunction
  • > /= 26 points considered normal cog function for PD
49
Q

What does the Parkinson’s Fatigue Scale measure? What does it not measure?

A
  • Physical aspects of fatigue – measures presence of fatigue and impact on daily function
  • Does not measure:
    o Cognitive and emotional features of fatigue
    o Severity and frequency of fatigue symptoms
50
Q

What does the Freezing of Gait Questionnaire measure? What has it bene found to correlate with?

A
  • Assess freezing of gait severity unrelated to falls
  • Correlates well with H&Y stage
51
Q

What 2 outcome measures correlate well with H&Y stage?

A
  • PDQ-39
  • Freezing of Gait Questionnaire
52
Q

What are the major treatment strategies for the early stages of PD?

A
  • Promotion of active lifestyle
  • Encouragement of continued engagement in home, work, and leisure activities
  • Initiation and monitoring of exercise program
  • Dual-task activities, complex motor tasks
53
Q

What are the major treatment strategies for the middle stages of PD?

A
  • Promotion of active lifestyle
  • Continued engagement in home, work, and leisure activities
    o Modifications of task and/or environment when appropriate
  • Continued monitoring of exercise program
  • Encourage participation in activities and exercises during ON times
  • Initiate strategy training/cueing strategies with increased focus on cognitive movement strategies
  • Fall reduction interventions and education
54
Q

What are the major treatment strategies for the late stages of PD

A
  • Caregiver education and training (assistance and cueing)
  • Optimize sitting posture and tolerance
    o Skin breakdown prevention and education
    o Risk reduction for postural abnormalities and contractures
  • Implementations of exercise program w/ caregiver involvement (PROM and AAROM)
55
Q

What are the main and secondary focus for exercise programs for the late stages of PD?

A

main - prevent contractures

secondary - strengthening

56
Q

What are ways to remediate with PD?

A
  • motor learning
  • feedback strategies
  • principles of neuroplasticity
57
Q

What are ways to compensate with PD?

A
  • cueing strategies
  • AD
  • activity modifications
  • environmental modifications
58
Q

What are attentional cues? Why do we think they work for PD? What types do we use?

A
  • Internal and external cues
  • Try to backdoor the connection to get the motor system going
  • Use visual and auditory internal and external cues
59
Q

What are some of the functional implications of bradykinesia, and how do we treat it?

A

temporal (time)
- Gait speed
- Arm swing
- Step duration
- Double limb support duration
All treated with a focus on increasing speed

60
Q

What are some of the functional implications of hypokinesia, and how do we treat it?

A

Spatial (space)
- Arm swing
- Trunk rotation
- Step length
- Step height
- Weight shifting
- BoS
All treated with a focus on increasing amplitude

61
Q

What are some of the functional implications of rigidity, and how do we treat it?

A
  • Contractures, loss of ROM, skin breakdown
  • There is nothing PT can do to fix rigidity
  • Can work on secondary management
    o Contracture prevention and management
    o Joint integrity maintenance
    o Skin integrity considerations
62
Q

What are some of the functional implications of postural instability, and how do we treat it?

A
  • Leads to loss of balance and increased risk for falls
  • Teach them reactionary strategies and try to strengthening balance systems (visual, somatosensory, vestibular)
    o Restoring balance is the hardest because of the initiation of movement delays
63
Q

What are some remediation strategies to address retropulsion?

A

o Activities on wedges - heels on wedges
o Rocker board activities
o Reaching forward – forward displacement of CoG over BoS
o Encourage flexor moments at hips, knees, ankles

64
Q

What are some compensatory strategies to address retropulsion?

A

o Heel wedges
o Activity modifications – stand to side of kitchen appliance or “Power Stance” when opening a door
o AD

65
Q

What are some remediation strategies to address anteripulsion?

A
  • toes on wedges
  • rocker board
  • walking uphill
66
Q

How do we see a breakdown in complex motor tasks with these patients?

A
  • Sequential movements and transitioning between movements
67
Q

What are some treatment ideas for complex motor tasks?

A
  • Dual task
  • Multi-step activities
  • Obstacle courses
68
Q

Why do we see festinating gait?

A
  • Gait kinematics
  • Initiation problems
  • Disequilibrium problems
69
Q

What are the implications of this gait impairment?

A
  • CoG anterior to BoS leads to loss of balance
  • Freezing of gait
  • Significantly reduced economy of walking
70
Q

What is involved in the first step of addressing freezing of gait, identifying common triggers?

A
  • Competing stimuli in environment – small spaces, change in floor, doorways, furniture
  • Weight displacement on feet
  • Stress/anxiety/fear
  • Anticipatory freezing of gait
  • Turing around/changing direction
  • Cog tasks, attention-splitting tasks
  • crowds
71
Q

What is involved in the second step of addressing freezing of gait, internal strategies?

A
  • Never fight the freeze
  • Four S’s when Freezing
    o Stop
    o Stand tall
    o Shift weight
    o Step BIG
72
Q
  1. What are the general goals for gait training during the early stages of PD?
A
  • Primary focus – amplitude and symmetry
  • Neuroprotective strategies
  • Add dual-task (cog and motor)
  • Vary environment and task
73
Q
  1. What are the general goals for gait training during the middle stages of PD?
A
  • Primary focus – festination, retropulsion, loss of balance
  • Continue to address amplitude
  • Strategies for ON and OFF times
74
Q
  1. What are the general goals for gait training during the mid-late stages of PD?
A
  • Primary focus – Freezing of Gait, fall risk management
  • More involvement of family training/care partner assistance
  • Increase in OFF times, strategies crucial
75
Q

What are some strategies to improve turning performing in patients with PD?

A
  • Keep CoG over BoS – never pivot
  • Widen turn in open spaces
  • Clock turn
  • Small space – exaggerated marching turn
76
Q

Why should aerobic conditioning be a priority for PD? What has it been shown to improve?

A
  • Decreases economy of movement
  • Shown to improve VO2 max in PD
77
Q

What are the dosage guidelines for aerobic conditioning for PD? How can we measure progress?

A
  • 5x/week for at least 30 minutes (150 min/week)
  • Outcome measures
    o 2 and 6 min walk test
    o RPE/mRPE
78
Q

Why do we see weakness in PD and what are its implications?

A
  • Altered descending central drive, deconditioning, aging
    o Postural abnormalities and changes in muscle length tension (secondary)
  • Leads to balance deficits, falls, and overall functional decline
79
Q

What are the dosage guidelines for strengthening for PD? How can we measure progress?

A
  • 2-3x/week
  • 8-12 reps x 1-3 sets for general strengthening
  • Outcome measures
    o MDS-UPDRS
    o 5 times sit to stand
80
Q

What are the dosage guidelines for stretching for PD? What muscles should we focus on?

A
  • 3x/week (HEP)
  • Focus on spinal extension and rotation, Iliopsoas, hamstrings, gastroc, Pec Major
81
Q

What are some common secondary sequelae for PD?

A
  • Ortho - Forward head, rounded shoulders, kyphosis (shadow pillow supine position)
  • CV - Reduced CV function leads to reduction in activity tolerance
  • Pulmonary - Pulmonary considerations due to kyphotic posture, and lung capacity is often reduced

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