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UM - Neuro Conditions > Parkinson's Disease > Flashcards

Parkinson's Disease Flashcards

1
Q

What is PD

A

UMN Progressive disease

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2
Q

Define Parkinsonism

A

Clinical syndrome characterized by a variable combo of motor signs

  • Tremor
  • Bradykinesia
  • Rigidity
  • Decreased postural control
  • Gait difficulties
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3
Q

Define syndrome

A

A group of symptoms that occur together

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4
Q

Define Idiopathic Parkinson’s Disease

A

Chronic, progressive neurodegenerative condition characterized by degenration of dopaminergic neurons, leading to both motor and non-motor impairments

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5
Q

What is the 2nd most common neurodegenerative disorder

A

Idiopathic Parkinson’s Disease

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6
Q

By 2040, how many people will have PD (estimate)

A

13 million people

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7
Q

How many people each year are diagnosed with PD in the US

A

60,000

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8
Q

What percent of US pop over 65 has PD

A

1.6%

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9
Q

T or F: More females have PD

A

F - more men

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10
Q

What decade of life does a diagnosis usually occur?

A

5th and 6th decade of life

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11
Q

What percent of people show symptoms < 45 yo

A

5-10% of people

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12
Q

What does dopamine depletion in PD lead to

A

Abnormal habitual learning and loss of motor control

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13
Q

What is loss of automaticity

A

Inability to perform movements without attention directed towards the movement

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14
Q

What occurs with loss of automaticity

A

Habitual behaviour decrease/problems
Flexibility of motor behaviour is reduced
Dual tasking decreased
Exaggerated dependence on external motor drive

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15
Q

What does loss of automaticity contribute to

A 
Micrographia
Decreased:
- arm swing
- stride length
- facial expression
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16
Q

What gets damaged in PD

A

Sensorimotor striatum of the BG - SNc

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17
Q

What is the etiology of PD?

A 
- Unknown but combo of:
genetic
toxic
infectious
other/unkown
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18
Q

How is a diagnosis Made

A

ABSENSE of a specific marker or diagnostic test (It’s a diagnosis of exclusion)

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19
Q

What is a DaTSCAN

A
  • Specialized imaging technique captures detailed pictures of the dopamine neurons that is able to determine whether there is a REDUCTION OF DOPAMINE CELLS, which usually occurs w/PD
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20
Q

How is a clinical Dx made

A

Med Hx, presentation of symptoms (unilat onset, resting termor, levodopa response, LT comp. of levadopa treatment), exam findings, response to meds, and disease course

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21
Q

What is a method used to classify the degree of pathology in PD?

A

Braak Stages of PD

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22
Q

Presentation of Braak Stages 1 & 2

A

Impaired olfaction and constipation, possible presence of lewy bodies

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23
Q

When in the Braak stages are ___ displayed?

a) Sleep
b) Motor
c) Emotional
d) Cognitive

A

a) Mid-stage (3&4)
b) Mid-stage (3&4)
c) Later braak stages (5&6)
d) Later braak stages (5&6)

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24
Q

What occurs in the brain in Braak 3&4

A

Lewy bodies move to midbrain and frontal cortex

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25
Q

What occurs in the brain in Braak 5&6

A

Lewy bodies move to frontal cortex and sensorimotor cortex

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26
Q

What is a method used to measure the degree of disease in PD?

A

Modified Hoehn and Yahr Staging

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27
Q

What is Stage 0 of Modified Hoehn and Yahr Staging

A

No signs of disease

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28
Q

What is Stage 1 of Modified Hoehn and Yahr Staging

A

Unilateral disease

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29
Q

What is Stage 1.5 of Modified Hoehn and Yahr Staging

A

Unilat + axial

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30
Q

What is Stage 2 of Modified Hoehn and Yahr Staging

A

Bil disease w/o impairment of balance

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31
Q

What is Stage 2.5 of Modified Hoehn and Yahr Staging

A

Mild bil disease with recovery on pull test

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32
Q

What is Stage 3 of Modified Hoehn and Yahr Staging

A

Mild to moderate bil disease; some postural instability; physically independent

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33
Q

What is Stage 4 of Modified Hoehn and Yahr Staging

A

Severe disability; still able to walk or stand unassisted

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34
Q

What is Stage 5 of Modified Hoehn and Yahr Staging

A

WC bound or bedridden unless aided

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35
Q

What are some premanifest symptoms of PD

A 
Hyposmia (decreased olfaction)
Constipation
Depression & Anxiety
REM sleep behaviour disorder
Dec. Arm swing
Mild motor fun. changes
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36
Q

What are some early symptoms of PD

A 
Unilat tremor
Rigidity
Mild gait hypokinesia
Micrographia
Reduced speech volume
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37
Q

What are some middle symptoms of PD

A

Bil bradykinesia, axial and limb rigidty
Bal and gait dficits/falls
Speech impairments
May need ass toward end

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38
Q

What are some late symptoms of PD

A

Severe voluntary mvmt impairments
Pulm fun & swallowing
Dependence in mobility, self-care, and ADLs

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39
Q

What are the clinical features of PD

A

Tremor
Rigidity
Bradykinesia
Loss of postural control

40
Q

What is the first sign in 70% of people w/PD

A

Tremor

41
Q

T or F: Tremor is a fast frequency

A

False, it is slow, low (4-6 Hz)

42
Q

List and define the two types of rigidity

A

Cogwheel: Jerky resistance to passive mvmt
Leadpipe: Sustained resistance to passive movement

43
Q

What mm group is more affected w/Rigidity

A

Flexors –> stooped posture

Proximal earlier

44
Q

What is rigidity characterized by

A

Characterized by increased resistance to passive movement that affects proximal mm early

45
Q

What is the most disabling of the early PD symptoms?

A

Bradykinesia

46
Q

Define bradykinesia

A

Slowness of voluntary mvmt

47
Q

Define Hypokinesia

A

Reduction in mvmt amplitude - primary cause of dec gait speed and step length

48
Q

Define akinesia

A

Freezing episodes

49
Q

T or F: Individuals w/PD have perfect kinesthetic perception

A

False - it is impaired

50
Q

What is true of postural control

A

It worsens with disease progression and:

  • Dec. limits of stability, mag. of postural responses
  • Impaired postural adaptations
  • Altered anticipatory postural adjustments
51
Q

What % of PD Pts have fallen in the previous year

A

70% of PD Pts

52
Q

What are some secondary motor symptoms

A

Motor performance
Gait
Dual Tasking

53
Q

What gait disturbances are present w/PD

A

Slower, shorter step lengths w/Inc. variability and dec. trunk rot.

54
Q

What is true of dual tasking in PD

A

It will lead to dec. gait speed and inc. gait variability and manifests as difficulties prioritizing attention in complex environments

55
Q

What is hypokinetic dysarthria

A

Reduced speech volume, monotone speech, mumbled and imprecise articulation, variable speaking rates

56
Q

What is Hypomimia

A

Reduced facial mvmts/expression, slowed eye mvmts/blinking,

57
Q

What is micrographia a form of

A

Hypokinesia

58
Q

List some nonmotor symptom categories of PD

A

Autonomic dysfunction
Cognitive and emotional dysfunction
Sensory
Sleep disorders

59
Q

What is important about nonmotor symptoms

A

THEY ARE TREATABLE

60
Q

What is postprandial hypotension

A

BP drops after meals

61
Q

What are some Autonomic Dysfunctions that can occur w/PD

A 
CV Dysfunction
Thermoregulatory Dysfunction (hyperhydrosis)
Fatigue
Respiratory Dysfunction
62
Q

What are some examples of CV Dysfunction

A

Orthostatic hypotension and post prandial hypotension

63
Q

What are some respiratory dysfunctions w/PD

A

Difficulty with getting air out

64
Q

What are some Cog/Emo/Behav. Changes

A

Apathy and OC Behaviour

65
Q

What sensory changes w/PD

A

Olfactory - 70-90% Pts

Visual - “tired eyes”

66
Q

What can be a treatment of OH

A

Immediately: Drink 12-16 oz of ice water
Chronic: Inc. fluid and salt, elevate head of bed, abd binder, pressure stockings

67
Q

What is a good treatment for fatigue in PD

A

EXERCISE !!!

68
Q

What is a good treatment of Respiratory Dysfunction

A

Inspiratory and expiratory mm strength training

69
Q

What percept of PD Pts develop:
Major depression
Anxiety

A

30-45 dep

25-49 anx.

70
Q

What are the goals of medicine

A

1) Provide symptomatic relief for motor and non symptoms
2) Min. motor fluctuations and max “ON” Periods
3) Increase amount of dopamine available in BG

71
Q

List the medications for motor symptoms

A
  • L-Dopa
  • Dopamine agonist
  • COMT Inhibitors
  • MAO-B Inhibitors
  • Antiviral
  • Anticholinergics
72
Q

When was L-dopa first introduced

A

Late 60s

73
Q

What is the most effective treatment of motor symptoms of PD

A

Carbidopa + Levodopa to prevent L-DOPA being converted into dopamine in the bloodstream and reduce risk of side effects

74
Q

When should L-dopa be taken for max absorption

A

1/2 hour prior to mean and 1 hr after a meal

75
Q

What is a myth about L-dopa and what is the truth regarding it

A

Over time L-dopa stops working - False, overt the therapeutic window narrows as the efficacy threshold rises, and the dyskinesia threshold lowers

76
Q

What are the L-dopa risk factors for motor compications

A

Younger age at onsent of PD
Disease severity
Higher daily L-dopa dosage
Longer disease duration

77
Q

What is a dopamine agonist

A

A drug that mimics dopamine by stimulating postsynaptic dopamine receptors directly that works to treat the 4 primary clinical PD symptoms

78
Q

What is COMT

A

An enzyme involved in the peripheral degradation of L-dopa/dopamine

79
Q

What is a COMT inhibitor

A

Blocks the COMT enzyme to increase the availability of dopamine and effectively allow more time for L-dopa to be absorbed in the brain

80
Q

What is MAO

A

An enzyme in the cells of the body that breaks down neurotransmitters, w/B being mainly in the brain

81
Q

What is a MAO-B inhibitor

A

A drug that blocks the action of MAO-B to provide the brain more time to absorb and potentially boost the effectiveness of levadopa

82
Q

What antiviral drugs are used for PD and why

A

Amantadine to increase release of DA and then blocks ACh receptors -> can decrease dyskinesia

83
Q

What is the role of Anticholinergics in the treatment of PD?

A

To treat tremors by blocking ACh receptors to inhibit dopamine reuptake

84
Q

List the 2 types of Sx Procedures that can be done for PD

A

Lesioning procedures

DBS

85
Q

What are some types of lesioning

A

Both rarely performed today
Pallidotomy (GP destroyed)
Subthalamotomy (subthalamic nuc. destroyed)

86
Q

What is done in DBS

A

Electrode into brain and attaching it to computerized pulse generator which is implanted under the skin in the chest

87
Q

What are the 3 DBS targets for PD

A

STN (Subthalamic nucleus)
GPi (Globus Pallidus Interna)
Thalamus

88
Q

T or F: DBS increases the amount of dopamine in the brain

A

FALSE!! It paces the nuclei (STN and GPi) w/a constant steady-frequency to compensate for the excessive and abnormally patterned electrical dc in the GPI or STN

89
Q

1) DBS candidate

2) DBS non-candidate

A

1) Pt w/PD that is dopamine responsive, age 20-75
2) Non PD Parkinson symptoms, severe cognitive/depressive symptoms, inability to have sx, poor compliance or poor social support systems

90
Q

Which are some benefits of DBS

A

dec.: dyskinesia, dystonia, tremor, brady/hypokinesia, stiffness
Improve sleep

91
Q

What are some risks of DBS

A

2-3% risk of stroke, dec. in verbal fluency, changes in modd/apathy

92
Q

Define capacity

A

What you measure in the clinic

93
Q

Define performance

A

Measured in real life

94
Q

What is true about people w/PD and exercise?

A

Although Pts know the importance of exercise, they are not meeting the recommendations

95
Q

T or F: Once Pts reach moderate PD, it is too late for them to start exercising

A

FALSE!!! Exercise will make improvements in dopamine loss at any point in the disease

96
Q

What are the key elements of PT Intervention?

A
  • Early referral
  • Promote an active lifestyle
  • Rx of exercise [aerobic, strength, flexibility, and balance]
  • task specific training

UM - Neuro Conditions (12 decks)

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