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Sub-Acute (Theory) > W13: Parkinson's > Flashcards

W13: Parkinson's Flashcards

1
Q

What is the basal ganglia? What does it control

A

The basal ganglia is a collection of neurons
Controls:
- Regulates voluntary movement –> controls initiation, speed and amplitude of movement
- Inhibits unwanted movement

NOTE: it is a modulator of movement, it does not directly produce movement.

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2
Q

What does the basal ganglia have strong connections with?

A

Cerebral cortex, brainstem & thalamus

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3
Q

Other than motor modulation, what else does the basal ganglia control?

A
  • Procedural & habitual learning
  • Eye movements
  • Cognition
  • Emotional regulation
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4
Q

What is the thalamus?

A
  • Has excitatory connections to the motor cortex
    (ie it tells the motor cortex to send a signal to move the muscle)
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5
Q

At rest the thalamus is inhibited by? Why?

A

The basal ganglia

At rest excitatory connections need to be inhibited otherwise a person will have a lot of wanted movements

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6
Q

What are the three main pathways in the basal ganglia?

A

Nigrostriatal pathway
Indirect pathway
Direct pathway

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7
Q

Explain the difference between receptors and what pathway they are involved with?

How does this affect movement

A

D1: Synapse with the direct pathway and are excitatory (difficulty initiating movement)
D2: Synapse with the indirect pathway and are inhibitory (difficulty increasing movement)

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8
Q

What is the pre-motor/premodal period?

A

Symptoms that occur before diagnosis
- Constipation
- REM sleep behavior disorder (RBD)
- Excessive daytime sleepiness (EDS)
- Hyposmia (reduced sense of smell)
- Depression
- Fatigue.

This can be up to 20 years!

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9
Q

What are some early Parknson’s disease symptoms? Motor vs non-motor symptoms?

A

Motor: bradykinesia, rigidity and tremor
Non-motor: Pain, fatigue and mild cognitive impairment

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10
Q

What are some late/advanced Parkinson’s symptoms?

A

Motor:
- Postural instability
- Falls
- Freezing of gait
- Dysphagia (difficulty swallowing)

Non-motor:
- Urinary symptoms
- Orthostatic hypotension
- Dementia

Additional complications
- Dyskinesia
- Psychosis

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11
Q

Distinguish between early and progressed Parkinson’s symptoms

A

Early symptoms
* Vague and non-specific
* Inexplicable tiredness
* unwarranted fatigability
* Mild muscular aches and cramps
* Cognitive impairment affecting executive function and memory
* Depression

Progressed symptoms
* Tremor results in spills of drinks and food
* Speech difficulties
* Reduced facial expression
* Possible drooling
* Difficulty initiating movement
* Freezing on a social outing

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12
Q

List the primary motor and non-motor Parkinson’s impairments

A

Motor:
- Bradykinesia
- Hypokinesia
- Akinesia
- Decreased postural instability
- Tremor
- Rigidity

Non-motor:
- Decreased autonomic function
- Sensory function

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13
Q

List the secondary and non-motor impairments

A

Motor:
- Dyskinesia
- Dystonia

Non-motor
- Neuropsychiatric features
- Sleep problems
- Pain
- Fatigue

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14
Q

Define bradykinesia

A

Slowness in initiating and performing movement.

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15
Q

Define hypokinesia

A

Reduced amplitude or size of movement

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16
Q

Define akinesia

A

Absence or difficulty in initiating movement (or maintaining movement) aka freezing eg speech, handwriting or gait

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17
Q

Define rigidity

A

Increased muscle tone causing stiffness and resistance to movement in the limbs or trunk, present in both directions of movement (flexion and extension). In Parkinson’s disease, this can lead to a sensation of muscle tightness and can impact posture and mobility.

18
Q

Define tremor

A

An involuntary, rhythmic shaking, usually starting in the hands and occurring at rest, characteristic of Parkinson’s disease

19
Q

What can increase the chance of freezing in Parkinson’s patients?

A

Walking in small space, turning, cluttered environments, when distracted

20
Q

In terms of freezing (ie akinesia) what is festination?

A

Progressive shortening of stride length and increasing cadence (often prior to freezing)

21
Q

What is most commonly affected by a tremor? How is it suppressed?

A
  • Hands, feet, lips and chin are most commonly affected
  • Suppressed by voluntary activity, sleep and complete relaxation
21
Q

What is dyskinesia? How does it present differently to a tremor?

A

Dyskinesia: Can occur in the head or trunk. Irregular (Writhing/Wriggling/twitching/jerks) movements

Tremor: Involuntary, uncontrolled, often smooth, flowing, or writhing movements.

22
Q

Distinguish between tremor and dyskinesia

A

Tremor = primary impairment. Direct cause of PD, due to loss of dopamine in BG. Often first sign of PD. Regular in direction. Regular in amplitude.

Note: resting (4-6hz) & action/postural (6-15Hz)

Dyskinesia = secondary impairment. Indirect cause of PD. Due to medications. Takes a long time to develop. Irregular in direction. Irregular in amplitude.

Note: 1-4Hz

23
Q

Outline disease severity of Parkinson’s based off the Hoehn and Yahr scale

A

Stage 1: symptoms of PD are mild and only seen on one side of the body (unilateral)

Stage 2: Symptoms of PD on both sides of the body (bilateral involvement) or at the midline

Stage 3: Symptoms of PD are characterised by a loss of balance and slowness of movement

Stage 4: Symptoms of PD are severely disabling

Stage 5: Symptoms of PD are severe and are characterised by an inability to rise

Note: stage 1 & 2 = early. Stage 3 = mid-stage. Stage 4 & 5 = advanced.

24
Q

Is there a cure for Parkinson’s? What is the aim of current therapies?

A

No cure
Aim is to treat symptoms of the disease (MDT approach is needed)

25
Q

How does LevaDopa work?

A

Levadopa passes the blood brain barrier and once in the brain it is converted into dopamine through the action of an enzyme.

This helps control symptoms eg tremor, rigidity and bradykinesia

26
Q

How do dopamine agonists work?

A

Mimics dopamine by directly stimulating dopamine receptors in the brain.

Note: this is different to Levadopa which converts into dopamine in the brain, replenishing dopamine levels.

27
Q

What are monoamine oxidase type B inhibitors?

A

Cause dopamine to accumulate in surviving nerve cells & reduce the symptoms of PD.

By inhibiting the COMT enzyme, these drugs reduce the breakdown of levodopa outside the brain, allowing higher and more consistent levels of levodopa to reach the brain.

28
Q

What are anticholinergics

A

Used to treat tremor

29
Q

What is amantadine?

A

Reduces symptoms and dyskinesia. Often used alone in Parkinson’s early stages

30
Q

What is the concern with levadopa?

How long will patients experience symptom relief after levadopa?

A

Concerns
- After 5–10 years it starts ‘wearing off’
- Dyskinesia
- Depression (is it due to the disease or medication?)

On period = 3-5 hrs

31
Q

What is the most common surgical treatment for PD? What other surgeries are there?

A

Deep brain cell stimulation
- Most common surgical treatment
- Used in people who respond to medication but have side effects (Motor fluctuations/off periods & Dyskinesia?)
- Ease symptoms/reduce medication needs
- Used for motor problems

Other treatments: targeted gene therapy & stem cell transplantation

32
Q

How does deep brain stimulation work?

A

involves implanting electrodes in the brain (usually in the subthalamic nucleus or globus pallidus internus) that deliver electrical pulses to regulate abnormal brain activity, improving motor symptoms like tremors, rigidity, and bradykinesia.

It can reduce medication needs and is typically used in patients with advanced PD who don’t respond well to drugs.

33
Q

What does physiotherapy management of PD involve?

A
  • Cueing and attentional/cognitive strategies
  • Task-specific training
  • Part-, whole- and dual- task training
  • Falls prevention
  • Balance training
  • Home modifications
  • Multifactorial interventions
  • Prescription of aids and equipment
  • General exercise
  • Treadmill training, dance, martial arts
34
Q

When is falls prevention training used

A
  • Balance training: Typically for patients with mild PD/mild risk of falls
  • Other strategies (prescription of aids): Typically provided for patients with mod-severe PD/mod-high probability of falling
35
Q

What criteria helps identify patients at risk of falls?

A
  • Previous falls in the past 12/12?
  • Previous freezing of gait in the past 1/12?
  • > 3.6s to walk 4m
35
Q

Summarise the treatment and findings from Canning and Morris

A

Canning: Home exercise
Progressive balance and LL strengthening exercises + cueing strategies (if freezing occurred). 40-60 min, 3x/wk, 6 months

Morris: Progressive resistance strength training or movement strategy training (mobility, balance during functional tasks) + education focussed on falls risk and prevention

Findings:
* Morris et al indicates Rx is effective
* Canning et al indicates it is not effectively significantly
* More individualised and supervised for Morris et al compared to Canning et al which was performed mainly at home (maybe individualised programs play a role in preventing falls

Conclusion: supervision seems to play a more critical role than dose in determining the effectiveness of home-based exercise.

35
Q

What does the LSVT program focus on? Is it restorative or compensative? What level intensity/effort is it?

A

Focuses on amplitude of movement rather than speed.

Restorative: aims to restore normal movement amplitude by recalibrating a patients sensory perception of movement. High intensive and high effort.

36
Q

What is the theory behind LSVT?

A
  • Awareness of amplitude
  • Improves self-cueing to action
  • Increase amplitude of motor output
  • Produce louder voice/movements
36
Q

Discuss the evidence of physiotherapy for managing signs and symptoms of PD

A

Benefits for physio were found in most outcomes over the short terms (< 3 months) –> most observed differences between treatments were small.

For some outcomes speed , berg balance and the unified Parksinsons disease rating scale the observed differences were at or approaching what was considered minimal clinically important changes

37
Q
A

Sub-Acute (Theory) (10 decks)

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