Parkinson's Disease Flashcards

1
Q

What does the cardinal signs ultimately lead to

A

Postural instability

1. Develops later in the disease
2. Characteristic flexed posture
3. Flexed hips and knees
4. Unable to access balance reactions

This leads to a high risk of falls in PD patients

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2
Q

Medical management of PD

A

people with Parkinson’s frequently have ‘on’ and ‘off’ times during the day where there symptoms are either less or more significantly impacting. This is due to medication they take either taking action or wearing off

Levodopa (with benserazide or carbidopa) e.g Sinemet or Madopar - side effects can be Dyskinesias, confusion, hallucinations and delusions, mood swings, psychological changes, sleepiness, fainting or dizziness

Anticholinergics - Block the action of Acetylcholine that has the opposite effect of dopamine. Can be used early on in the disease before the need for dopamine: side effects can be confusion, a dry mouth, constipation and blurred vision

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3
Q

Physiotherapy management for postural instability

A

Targeting flexed knees and hips - Specific stretches
Balance exercises to target balance
Cueing - improve movement pattern (gait)

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4
Q

Explain the striatum

A

Caudate nuclei and Putamen

An inhibitory system

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5
Q

What is cueing and what are the principles of cueing

A

Cueing is a type of treatment technique that uses visual, auditory or kinaesthetic feedback to allow a movement pattern to be accessed and used in a functional way.

Execution of movement - primary motor cortex. Executing and planning movement - Premotor area (PMA) and Supplementary motor area (SMA). In PD the Supplementary motor area (SMA) is affected which is involved in internally generated, automatic movement
BUT
The Premotor area (PMA) is intact which is involved in sensor-guided movement

THEREFORE –
‘ the automatic subconscious basis of posture and movement is lost (i.e. SMA) but abnormalities can often be overcome by voluntary effort (use of PMA) ’
Clinically this will mean that you can incorporate the use of external cues as a coping strategy in treatment

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6
Q

What are the early stages of the Hoehn & Yahr Scale

A

Stage 0 - no signs of disease
•Stage 1 – unilateral involvement with minimal functional disability
•Stage 1.5 –unilateral involvement also involving the neck and spine
•Stage 2 –bilateral) disease but no impairment of balance
•Stage 2.5 - mild bilateral symptoms with recovery when the ‘pull’ test is given (the doctor stands behind the person and asks them to maintain their balance when pulled backwards)

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7
Q

What are the 3 cardinal signs of PD

A
  1. Bradykinesia - Paucity or slowness of movement – with a slower and difficulty initiation of movement and a progressive reduction in the speed and amplitude of repetitive actions; Akinesia = no movement
  2. Resting Tremor (pill rolling) - Lack of dopamine leads to a release of inhibition of tremor. This tremor is normally inhibited during movement. One of the first signs of PD but may not always be present
  3. Rigidity - Lack of dopamine also results in rigidity:
    1. Stiff or inflexible muscles
    2. Resistance to passive movement
      Lead pipe rigidity (resistance throughout all of movement) or Cog wheel rigidity (gives little bit of way then provided resistance)
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8
Q

Symptoms of PD

A

Effects of Rigidity
•Feeling stiff and achy
•Moving is hard work
•Lack of movement results in weakness
•Facial expression (communicating with others)
•Sedentary lifestyle
•Flexed Trunk – can’t stand straight, COG is forward, difficulty walking, turning, reaching, standing from sitting positions (chair, toilet, bed)

Effects of Tremor
•Embarrassing
•Annoying
•Tiring
•Hand function
•Balance
Effects of Akinetic Syndrome
•Cant move
•Slow
•Get stuck / freeze
•Balance problems - Difficulty walking, getting out of a chair / off the toilet, Falls
•Depressing
•Can’t look after yourself
•Can’t cook meal
•Cant go out and about
•Reduced fitness levels
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9
Q

What are the output neurones of the basal ganglia

A

Globus pallidus (GPi) and substantia nigra (SNpr)

These are inhibitory neurones

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10
Q

State the stages of the scale that can be used to determine the progression of PD

A

Hoehn & Yahr Scale

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11
Q

Difference between rigidity and spasticity

A

Rigidity VS spasticity - spasticity is velocity dependent so quick PROM will kick in spasticity by feeling for resistance; spasticity is felt in Biceps, wrist and finger flexors for CVA, etc whereas rigidity in PD will feel resistance in both flexors and extensors throughout movement

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12
Q

What are the 5 nuclei of the basal ganglia

A
  1. Caudate nucleus
  2. Putamen
  3. Globus pallidus - internal and external
  4. Subthalamic nucleus (STN)
  5. Substanstia nigra (SN) - pors compacta, pors reticulat
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13
Q

What is the role of the basal ganglia

A

Believed to be storage of movement memory

1. Regulate planning, initiation & termination of movement
2. Regulate muscle tone required for specific body movements
3. Control subconscious or stereotyped contractions of skeletal muscles
4. Act to inhibit antagonistic or unnecessary movements - reciprocal inhibition

Basal ganglia part of a series of parallel loops involving the thalamus and cerebral cortex. Classic model proposes two pathways:

1. Direct pathway – promotes movement
2. Indirect pathway – inhibits movement.
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14
Q

Explain key features of the causes of PD

A

Neurodegeneration in the substantia nigra in the basal ganglia leading to a lack of dopamine

The basal ganglia contains parallel loop systems which usually produce movement – they are called the Direct Pathway and the Indirect Pathway.

Lack of dopamine leads to:

  1. Lack of excitement of the direct pathway leading to lack of movement
  2. Lack of inhibition of the indirect pathway leading to lack of movement

Therefore an overall lack of movement = bradykinesia or no movement =akinesia

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15
Q

Define PD

A

Parkinson’s Disease is a chronic, progressive neurodegenerative disorder resulting from the degeneration of dopamine producing neurones in the substantia nigra of the basal ganglia

Parkinson’s Disease and the ‘Parkinsonian syndrome’ comprise a group of disorders characterised by tremor and disturbance of voluntary movement, posture and balance

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16
Q

Explain role of dopamine in the direct pathway (go pathway) and indirect pathway (stop pathway) in normal brain function

A

SNpr main source of dopamine - an excitatory neurotransmitter

DOPAMINE EXCITES THE DIRECT AND INHIBITS THE INDIRECT PATHWAY ie. Inhibits inhibition of movement and promotes movement

17
Q

What are the secondary clinical features of PD

A

Overtime patients will develop these - activity, functional participation problems

  1. Difficulty initiating and terminating movement
  2. ‘Freezing’ when walking
  3. ‘Festinating’ gait pattern, shuffling gait - short stride length with rapid leg movement; usually cannot be stopped once begun
  4. Loss of stereotyped movements such as arm swing during gait
  5. Difficulty with motor tasks – turning over in bed, sit to stand, dressing, shaving
  6. Lack of spontaneous movement and initiating movement
  7. Loss of facial expressions, loss of upward gaze - therapist must be aware cognition, awareness and understanding is usually unaffected in PD but just require time to respond
  8. Monotone speech - difficulty communicate; can psychologically impact them as they can no longer socialise the way they used to
  9. Micrographia - writing becomes smaller with neurodegeneration
  10. Problems with swallow, drooling - can lead to aspirational pneumonia
  11. Sleep disorders - often due to rigidity causing difficulty and pain moving in bed
  12. Depression
18
Q

What are the later stages of the Hohenzollern & Yahr scale

A

Stage 3 – Bilateral mild to moderate disease, some postural instability; physically independent
•Stage 4 - Severe disability, but still able to walk or stand unassisted
•Stage 5 - Needing a wheelchair or bedridden unless assisted.