Patho Exam 4 3/3 - Parkinson's Disease

Front 1

What are the two loops that influence or assist the cerebral cortex (direct motor pathways) in motor control?

Back 1

1. Basal ganglia-thalamic-cortical loop
2. Cerebellar-thalamic-cortical loop

Front 2

What type of walking movement is seen with damage to the cerebellum?

Back 2

Ataxic gait

**wide stance, side way jerking back and forth for balance, unability to walk on straight line

Front 3

What type of tremor is seen with damage to the cerebellum?

Back 3

Intention tremor

Front 4

What does intention tremor do?

Back 4

increases as an extremity approaches the endpoint of deliberate and visually guided movement (hence the name intention tremor).

(overshoot/undershoot; miss target)

Front 5

What are the two loops by which the basal ganglia controls movement?

Back 5

Direct Loop
Indirect Loop

Front 6

Which of the two basal ganglia loops involves recurrent excitation of cortical motor regions (via thalamus)?

Recepetors?
Neurotransmitter?

Back 6

Direct Loop
D1
Dopamine

Front 7

Which of the two basal ganglia loops involves recurrent inhibition of cortical motor regions (via thalamus)?

Recepetors?
Neurotransmitter?

Back 7

Indirect Loop
D2
Dopamine

Front 8

Which nucleus in the basal ganglia is directly involved in Parkinson’s disease?

Back 8

Substantia nigra compacta (SNc)

Front 9

What neurotransmitter is produced by the neurons of SNc (substantia nigra compacta) nucleus?

Back 9

Dopamine

Front 10

What determines whether the release of Dopamine neurotransmitter in other nuclei within the basal ganglia is excitatory or inhibitory?

Back 10

D1 receptor = excitation

D2 receptor = inhibition

Front 11

What are the two nuclei in the basal ganglia onto which Dopamine neurotransmitter is released?

Back 11

Putamen

Caudate Nuclei

Front 12

What receptor does dopaminergic input from the substantia nigra compacta (SNc) to the putamen and caudate nuclei stimulate in the direct loop?

What is the result?

Back 12

D1 receptor:
Increase in thalamocortical excitation

Front 13

What receptor does dopaminergic imput from the SNc to the putamen and caudate nuclei stimulate in the indirect pathway?

What is the effect?
What is the result?

Back 13

D2 receptor:
-Inhibiting indirect pathway
-Results in increasing excitation of the motor cortex

Front 14

What is the overall effect of dopaminergic imput from the SNc to the putamen and caudate nuclei?

Back 14

Increasing excitation of the motor cortex:
-exciting: direct loop
-inhibiting: indirect loop

Front 15

What are the neuropathological changes in Parkinson’s disease?

Back 15

Degeneration:
Substantia nigra compacta (SNc)

Front 16

What is degeneration (in terms on neurophysiology)?

Back 16

Neuronal loss
De-Pigmentation

Front 17

When considering the direct loop, what is the effect of the depletion of dopamine in the
SNc?

Back 17

Decreased cerebral cortical excitation over the thalmocortical projection fibers

Front 18

When considering the indirect loop, what is the effect of the depletion of dopamine in the
SNc?

Back 18

Increases:
-putamen / caudate inhibition of the thalamus

Results:
-inhibits cortex cortical motor regions

Front 19

Characteristics of Parkinson's Disease:
Lines of the patient’s face become smooth, the expression becomes fixed:
a. Bradykinesia
b. Rigidity
c. Postural instability
d. Resting tremor
e. Parkinsonian gait
f. Masked face

Back 19

f. Masked Force

Front 20

Characteristics of Parkinson's Disease:
Slowness of movement, difficulty to initiate and stop movement:
a. Bradykinesia
b. Rigidity
c. Postural instability
d. Resting tremor
e. Parkinsonian gait
f. Masked face

Back 20

a. Bradykinesia

Front 21

Characteristics of Parkinson's Disease:
Shuffling walk with a stooped position and a diminished or absent arm swing:
a. Bradykinesia
b. Rigidity
c. Postural instability
d. Resting tremor
e. Parkinsonian gait
f. Masked face

Back 21

e. Parkinsonian gait

Front 22

Characteristics of Parkinson's Disease:
Trembling in fingers, hands, arms, feet, legs, jaw, or head:
a. Bradykinesia
b. Rigidity
c. Postural instability
d. Resting tremor
e. Parkinsonian gait
f. Masked face

Back 22

d. Resting Tremor

Front 23

Characteristics of Parkinson's Disease:
Stiffness of limbs and trunk:
a. Bradykinesia
b. Rigidity
c. Postural instability
d. Resting tremor
e. Parkinsonian gait
f. Masked face

Back 23

b. Rigidity

Front 24

Characteristics of Parkinson's Disease:
Difficulty to adjust posture to maintain balance, leads to falls:
a. Bradykinesia
b. Rigidity
c. Postural instability
d. Resting tremor
e. Parkinsonian gait
f. Masked face

Back 24

c. Postural Instability

Front 25

When considering the neuropsychiatric disturbances, what is the Parkinsonian patient at risk for that is accompanied with behavior and mood alterations such as depression, apathy, and anxiety?

Back 25

Dementia

Front 26

Besides the deficits caused by depletion of dopamine in the SNc, what is the second major cause of behavioral alterations?

Back 26

Medication used to managed the disease

Front 27

Why is levodopa (L-DOPA) rather than dopamine used in the treatment of Parkinson’s disease?

Back 27

L-DOPA:
-cross the blood-brain barrier (unlike dopamine)
-enters neurons in SNc (substantia nigra compacta)

Front 28

Initially, why was large doses of L-DOPA needed to treat the disease?

Back 28

L-DOPA rapidly metabolized by DDC (dopadecarboxylase)

Front 29

What are the side-effects of large doses of L-DOPA?

Back 29

Nausea
Dyskinesias (motor conditions)
Joint Stiffness

Front 30

What role does a dopa-decarboxylase (DDC) inhibitors play in the treatment of Parkinson’s disease?

Back 30

DDC inhibitor:
-inhibiting DDC
-keeps Levodopa concentration higher
-allows 70 % reduction of Levodopa dose
-reduces severity of side-effects


Front 31

What role does a catechol-O-methyl transferase (COMT) Inhibitors play in the treatment of Parkinson’s disease?

Back 31

When DDC is inhibited another enzyme, catechol-O-methyl transferase (COMT), takes over the breakdown of Levodopa to 3-O-methyldopa (3-OMD. Consequently, COMT inhibitors were recently developed as a way of further improving the delivery of Levodopa to the brain

Front 32

What three drugs make up levodopa preparations?

Back 32

1. L-DOPA
2. DDC inhibitors
3. COMT inhibitors

Front 33

Define “on state” in terms of the patients response to Levodopa preparations.

Back 33

Time in which:
-good response to meds
-few symptoms

Front 34

Define “off state” in terms of the patients response to Levodopa preparations.

Back 34

Time in which:
-not responding to medication (significant motor defects)
-more symptoms

Front 35

What are the two approaches used to extend the time of either no doses or low doses of levodopa preparations?

Back 35

1. Use of Pharmaceutical Alternatives
2. Exercise

Front 36

What is the main reason pharmaceutical alternatives are used in the treatment of Parkinson’s Disease?

Back 36

delay use of levodopa preparations

lower dose of levodopa preparations

Front 37

Explain the action of Dopamine agonists

Back 37

Binds to dopaminergic post-synaptic receptors

(similar effects at L-DOPA)

Front 38

Explain the action of monoamine oxidase-B (MAO-B) inhibitor.

Back 38

Decreases the metabolism of dopamine:
-in basal ganglia cells
-increasing dopamine's availability

Front 39

In terms of Parkinson:

Physical functioning, health-related quality of life:
a. Evidence supporting the benefit
b. Insufficient evidence to support or refute the benefit
c. Need for future research

Back 39

a. Evidence supporting the benefit

Front 40

In terms of Parkinson:

Frequency of exercise in days per week:
a. Evidence supporting the benefit
b. Insufficient evidence to support or refute the benefit
c. Need for future research

Back 40

c. Need for future research

Front 41

In terms of Parkinson:

Reducing falls or depression:
a. Evidence supporting the benefit
b. Insufficient evidence to support or refute the benefit
c. Need for future research

Back 41

B. Insufficient evidence to support or refute the benefit

Front 42

In terms of Parkinson:

Intensity of exercise in terms of RP:
a. Evidence supporting the benefit
b. Insufficient evidence to support or refute the benefit
c. Need for future research

Back 42

c. Need for future research

Front 43

In terms of Parkinson:

Strength, balance and gait speed.
a. Evidence supporting the benefit
b. Insufficient evidence to support or refute the benefit
c. Need for future research

Back 43

a. Evidence supporting the benefit

Front 44

In terms of Parkinson:

Length of exercise bouts in minutes.
a. Evidence supporting the benefit
b. Insufficient evidence to support or refute the benefit
c. Need for future research

Back 44

c. Need for Future research

Front 45

In terms of Parkinson:

Type or mode (e,g, aerobic or resistant) of exercise
a. Evidence supporting the benefit
b. Insufficient evidence to support or refute the benefit
c. Need for future research

Back 45

C. Need for future research

Front 46

What has research demonstrated when comparing an exercise program under physiotherapist supervision vs self-supervised home program?

Back 46

physiotherapist supervision > a self-supervised home program

Front 47

With Parkinson's Disease:
Why is an exercise program under physiotherapist supervision better than self-supervised home program?

Back 47

Found to be more effective at improving:

ADL
Motor
Mental
Emotional Function
General Health

Front 48

In this stage levodopa preparations are usually first prescribed. Exercise prescription should be adjusted to the patient’s capabilities and capacities, but continued if the patient is willing.

Which stage of Parkinson’s disease is this?

Back 48

Parkinson's Disease: Stage III

Front 49

Most advanced Parkinson’s disease.

Which stage of Parkinson’s disease is this?

Back 49

Parkinson's Disease: Stage V

Front 50

Exercise should be continued as the primary treatment, with dopamine agonist and MAO-B inhibitors either initiated or continued.

Which stage of Parkinson’s disease is this?

Back 50

Parkinson's Disease: Stage II

Front 51

Physical movements become much slower and major impairments in walking straight and standing are present. Falling down is more common increasing the risk of injuries, especially in the elderly. Generalized dysfunction is moderately severe.

Which stage of Parkinson’s disease is this?

Back 51

Parkinson's Disease: Stage III

Front 52

Symptoms are severe and the individual is unable to complete day-to-day tasks and walking is little, if at all. For these reasons, patients are unable to live alone and are generally confined to a wheelchair. Surgery (e.g., deep brain stimulation therapy) is an option at this stage to alleviate some of the symptoms, but only in young and healthy individuals. A paucity of research exists to determine the feasibility, safety, and outcomes of exercise.

Which stage of Parkinson’s disease is this?

Back 52

Parkinson's Disease: Stage IV

Front 53

Early-Stage Parkinson’s disease

Which stage of Parkinson’s disease is this?

Back 53

Parkinson's Disease: Stage I

Front 54

In Dr. Pitetti’s opinion, exercise should be the primary treatment approach. However, medications may be started during this stage and typically involves the L-DOPA alternatives such as dopamine agonists and monamine oxidase-B (MAO-B) inhibitors.

Which stage of Parkinson’s disease is this?

Back 54

Parkinson's Disease: Stage I

Front 55

Moderate Parkinson’s Disease.

Which stage of Parkinson’s disease is this?

Back 55

Parkinson's Disease: Stage III

Front 56

Symptoms are generally mild and only cause minor inconveniences in day-to-day living. Minor tremors or shaking occurs, but is unilateral, affecting only one side of the body. Along with minor tremors, an individual's posture and balance become poorer and abnormal facial expressions become apparent. Overall, this stage causes no major problems and can last for several years.

Which stage of Parkinson’s disease is this?

Back 56

Parkinson's Disease: Stage I

Front 57

Symptoms are severe enough that individuals are unable to provide self-care and require around-the-clock care. Cachexia occurs in which unwanted loss of weight and muscle mass occurs. The overall quality of life of individuals in this stage declines due to multiple reasons such as speaking and movement difficulties, incontinence issues, frequent hospitalizations and recurrent infections. Therapies are the least effective in this stage of the disease.

Which stage of Parkinson’s disease is this?

Back 57

Parkinson's Disease: Stage V

Front 58

Bilateral symptoms develop in which both sides of the body are affected. Disability is minimal and daily tasks can still be performed, but are much harder to complete. Walking and balance problems become more severe with further declines in posture.

Which stage of Parkinson’s disease is this?

Back 58

Parkinson's Disease: Stage II