Parkinson's Flashcards

1
Q

explain the incidence of parkinsons

A

2nd most common
men 1.2-5x more likely

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2
Q

average age of onset of PD

A

50-60 years

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3
Q

what is parkinsonism

A

umbrella term used to describe bradykinetic syndromes that disturb the dopamine systems of basal ganglia

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4
Q

what exactly causes PD

A

don’t exactly know
genetic and environmental causes

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5
Q

what environmental factors can cause parkinsons

A

chemicals
- occupational exposure / pesticides

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6
Q

what produces dopamine

A

substantia nigra

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7
Q

what is the most common form of PD

A

idiopathic PD

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8
Q

what are the subtypes of idiopathic PD

A

postural instability gait disorder
tremor dominant

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9
Q

what can cause idiopathic PD

A

unknown things
gene mutation
substantia nigra degeneration

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10
Q

what can cause secondary PD

A

drug induced
hydrocephalus
infections
toxins
trauma
tumors

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11
Q

what toxins are listed specific to secondary PD

A

CO
pesticides
manganese

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12
Q

what are the forms of atypical parkinsons that cognitive dysfunction is seen in

A

alzheimers
fronto-temporal dementia
lewy body disease

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13
Q

what can be observed in an individual with cerebellar ataxia compared to PD

A

atax - wider base of support (drunk walking)

PD - small BOS and less mvmt

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14
Q

what is the main difference between idiopathic PD and atypical PD

A

bradykinetic mvmts are due to other neurodegenerative disease in atypical

– will have s/s that are not associated with idio PD

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15
Q

lack of dopamine production affects the

A

motor and non motor loops

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16
Q

what is dopamine responsible for

A

producing smooth purposeful movements

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17
Q

where does dopamine bind

A

caudate and putamen of striatum

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18
Q

when PD is diagnosed, explain the status of cells in the basal ganglia as well as dopamine receptors

A

50-60% cell death
70-80% loss of dopamine receptors

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19
Q

relation between symptoms and diagnosis of PD

A

symptoms typically precede diagnosis by 5-6 years

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20
Q

what non-motor loops can be damaged by PD

A

visual and emotional

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21
Q

what is the mean duration of PD and how does that affect life expectancy?

A

10-20 years

– people diagnosed typically live close to normal expectancy due to later age of diagnosis

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22
Q

what typically causes mortality in those with PD

A

CVD disease
pneumonia

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23
Q

how is the rate of progression in PD described

A

variability
– PIGD is seen to have faster progression as well as neurobehavioral disturbances/dementia

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24
Q

how is PD classified

A

hoehn - yahr classification

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25
Q

what does the hoehn yahr classification tell us

A

estimation of stage and severity via motor signs and elements of functional status

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26
Q

Hoehn-Yahr 1

A

minimal / absent disability
unilateral disability

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27
Q

Hoehn-Yahr 2

A

minimal bilateral/midline involvement
balance in tact

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28
Q

Hoehn-Yahr 3

A

impaired righting reflexes
unsteadiness turning/standing from seated
can live independently / continue forms of employment

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29
Q

Hoehn-Yahr 4

A

all symptoms present and severe
standing / walking only possible with assistance

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30
Q

Hoehn-Yahr 5

A

confined to bed/WC

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31
Q

what would intervention look like in Hoehn-Yahr 1

A

education with a possible maintenance exercise program

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32
Q

what could intervention look like in Hoehn-Yahr 2

A

may need DME
exercise plan

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33
Q

at what stage of the Hoehn-Yahr classifications does PT become absolutely necessary

A

3 and on

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34
Q

what is the gold standard of measuring PD progression

A

unified parkinson’s disease rating scale

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35
Q

how long does the UPDRS take to be administer? what can it be used for / what does it include

A

30 min

provide evidence of impairments outside of PT scope

Hoehn-Yahr stages

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36
Q

what are the motor signs associated with PD

A

weakness
apraxia
bradykinesia
akinesia
rigidity
postural instability
gait abnormalities

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37
Q

explain weakness seen in PD? is it motor neuron weakness?

A

not UMN weakness, instead weakness due to disuse and rigidity of muscle

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38
Q

what’s apraxia in PD due to

A

difficulty with automatic and voluntary movements directed through the pyramidal system

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39
Q

why is postural instability very important to address

A

those with PD are 2x more likely to fall

40
Q

what gait abnormalities are seen in PD

A

festination
trouble initiating/terminating
no arm swing
no trunk rotation
shortened step length

41
Q

what outcome measures can be used to assess PD patients

A

MCTSIB
Stand and Reach

42
Q

what is a typical presentation of akinesia in those with PD

A

mask-like facial expression

43
Q

what is the definition of rigidity

A

equal resistance in agonists / antagonists

44
Q

what is the symptom reported of rigidity

A

heaviness and stiffness in limb

45
Q

explain rigidity in relation to progression of PD

A

starts proximally in shoulders and neck and moves distally as progression occurs

46
Q

how is LOS affected by PD

A

reduced, more so forward than backward directions

47
Q

how do those with PD respond to perturbations

A

not well
– will not use postural control strategies due to abnormal coactivation of musculature / poor sensorimotor integration

48
Q

how does dual tasking affect postural control in those with PD

A

worsens

49
Q

why may a patient with PD experience dysphagia or dysarthria

A

rigidity in musculature leading to reduced ROM

  • can cause speech disorders
50
Q

what are non motor clinical signs of PD

A

depression anxiety apathy

_________ dysfunction
cognitive
autonomic
olfactory
visual / visuospatial perception
vestibular
auditory

51
Q

what is sialorrhea

A

excessive drooling

52
Q

what can lead to dementia in those with PD

A

depression

53
Q

what autonomic dysfunction can be seen in those with PD

A

hypotension
bowel/bladder
blurry vision
dyspnea
orthostatic hypotension

54
Q

how is visual and visuospatial perception dysfunction observed in those with PD

A

impaired postural control
abnormal vestibulospinal reflexes
impaired sensory integration

55
Q

what is the pharmacological agent that is used to treat PD

A

levadopa/carbidopa (sinemet)

56
Q

what is levodopa/carbidopa

A

gold standard for dopamine replacement

57
Q

what is something to keep in mind when working with those on levadopa/carbidopa

A

needs to be on a fixed schedule
&
on and off times when the drug is active

– want to do PT with patient when they are “on”

58
Q

how long after dosage does “on time” begin on levodopa/carbidopa

A

20-60 min

59
Q

side effects of levodopa/carbidopa

A

hypotension
nausea
dry mouth
dizziness
fluctuations
dyskinesia during “off times”

60
Q

what do dopamine agonists do

A

stimulate dopamine receptors in basal ganglia

61
Q

what is deep brain stimulation

A

multi-electrode leads implanted into thalamus

62
Q

where is deep brain stimulation implanted

A

subthalamic nucleus
globus palladis internus

63
Q

what is deep brain stimulation effective for? what are the side effects

A

advanced PD

depression, paresthesia, paresis, loss of balance, dystonia

64
Q

what are the cardinal signs of PD? what qualifies a diagnosis

A

rigidity
resting tremor
bradykinesia
postural instability

3 or more

65
Q

how would an exam look in those with PD

A

cognitive screen
msk screen
cardiopulm screen
movement analysis
postural control assessment

66
Q

what can be used to assess cognition

A

MMSE
MOCA
geriatric depression scale

67
Q

what posture is seen typically in those with PD? how could that affect MSK screen?

A

flexed / stooped
- kyphotic

limit shoulder, spine and hip ROM

68
Q

what is common pain wise in those with PD? why?

A

low back and neck pain

postural abnormalities

69
Q

what could indicate PD via cardiopulmonary screen

A

orthostatic hypotension

70
Q

what outcome measures can be used to test cardiopulmonary system

A

2/6 MWT

71
Q

what is looked at during movement analysis

A

if movements are bradykinetic
if the tremor affects ADLs
gait abnormalities
UE function

72
Q

what is used to test UE function

A

9 hold peg test

73
Q

what is the most recommended postural control assessment in PD populations

A

miniBEST test

74
Q

downward gaze palsy during neuro exam would indicate

A

progressive supranuclear palsy

75
Q

what condition may mimic PD but are instead atypical parkinsonism

A

freezing of gait and/or frequent falls early in the disease

76
Q

what would a patient present with that would cause one to think normal pressure hydrocephalus vs parkinson

A

urinary incontinence
freezing of gait
cognitive impairment

(wet wobbly wacky)

77
Q

what H&Y stage of PD is freezing of gait typically seen

A

3 into the late stages

78
Q

what typically causes normal hydrocephalus

A

older adults that have brain tissue atrophy and CSF is allowed to build up in the ventricles over time

79
Q

explain the difference between the current model of PD rehab and potential model

A

rehabilitation typically occurs once disability or acute events occur
– can be too late in the progression to really slow it down, more reactive than proactive

80
Q

when physical therapy is applied early in progression, what is each interval of care assessed by

A

progression of disease and its effect on mobility, ADLs and quality of life

81
Q

what H-Y classification is associated with early PD rehab? what is focused on intervention wise

A

1
restorative and preventative intervention strategies

82
Q

what H-Y classification is associated with middle PD rehab? what is focused on intervention wise

A

2-4

restorative and preventative intervention (may be some compensatory)

83
Q

what H-Y classification is associated with late PD rehab? what is focused on intervention wise

A

5

preventative and compensatory

84
Q

what is under the physical capacity umbrella in PD rehab

A

exercise tolerance
flexibility
strength (power)

85
Q

what manual activities are focused on in PD rehab

A

UE reach
dexterity

86
Q

what transfers are focused on during PD rehab

A

sit to/from stand
in/out bed
turning over

86
Q

additional areas to be focused on during PD rehab

A

pain management
respiratory function
education

87
Q

CPG guidelines suggest

A

aerobic exercise
resistance training
balance training
external cueing
community based exercise
gait training
task specific training

88
Q

what is the recommended level of aerobic exercise

A

moderate to high
60-75% max HR

89
Q

what is important to monitor during aerobic exercise?

A

vitals, RPE, exertional intolerance

90
Q

what can long term L-dopa administration produce

A

arrhythmias
orthostatic hypotension

91
Q

does the mode of resistance training make a significant difference in those with PD

A

no
- machines may be safer than free weights / may be easier to do body weight or bands

92
Q

recommended dosage of resistance training in PD patients

A

2 days per week

93
Q

what is recommended during gait training
- dosage
- cueing
- progressions

A

high repetition
block practice
external cues (visual and auditory)
varying directions/obstacle courses

94
Q

how is freezing gait solve

A

reset clock
weight shifts

95
Q

what is the focus on during gait training, in relation to automatic and intentional tasks

A

move from automatic tasks (cant do due to extrapyramidal system damage) and toward intentional tasks