Parkinson's Disease

Question 1

Definition

Answer 1

Chronic progressive neurogenerative disorder - degeneration of dopamine producing neurones (substantia nigra of basal ganglia)

Question 2

Role of the Basal Ganglia

Answer 2

• Regulate movement (planning/initiation/termination + memory of movement)
• Regulate muscle tone (=required for movement)
• Control subconscious contraction of muscle
• act to inhibit antagonistic/unnecessary movements (rigidity + tremor)

Question 3

Position of the basal ganglia

Answer 3

Superior to thalamus 
- Caudate nucleus 
> Lateral to thalamus 
- Putamen (closer to cortex)
- Global Pallidus (closer to thalamus)
> Below the thalamus 
- Subthalamic Nuclei
> Midbrain
- Substantia Nigra

Question 4

Dopamine

Answer 4

> Excitatory Neurotransmitter
- used to send impulses to many brain regions (especially motor areas of cortex)
Produced by part of Substantia Nigra

Question 5

Pathophysiology of Parkinson’s

Answer 5

*2 pathways which both involve basal ganglia, thalamus + cortex
> Direct pathway
- promotes movement
- excited by dopamine (increased signals from thalamus to cortex)
> Indirect Pathway
- Inhibits movement
- inhibited by dopamine (decreased signals from thalamus to cortex)

> In parkinson’s; lack of dopamine due to degeneration of substantia nigra =
- lack of excitement of direct pathway
- lack of inhibition of indirect pathway
OVERALL LOSS OF MOVEMENT

Question 6

Primary Clinical features

Answer 6

> Diagnostic Tool (as well as persons response to dopamine replacement)

1. Bradykinesia/akinesia (lack of dopmaine = greater movement inhibition)
   > Bradykinesia = slower initiation of movement
   = progressive reduction in speed + amplitude of repetitive actions
   > Akinesia = no movement
2. Resting tremor (not every case of PD)
   > ‘Pill Rolling’ tremor
   - hands/arms/legs shake at rest (often in hands/fingers)
   - inhibited/reduced during movement
   *lack of inhibition of tremor (unwanted movement)
3. Rigidity
   > Stiff, inflexible muscles which resist passive movement
   - different to spasticity as rigidity is in both directions + not velocity dependent
   > ‘Lead pipe’ = throughout movement
   > ‘Cog Wheel’ = stop then give then stop motion

Question 7

Secondary Clinical features of Parkinson’s

Answer 7

> Difficulty initiating/terminating movement
Lack of spontaneous movement
‘Freezing’ when walking
Slow, shuffling gait (called ‘festinating gait’ + often struggle to stop)
Loss of stereotypical movement (e.g loss of arm swing when moving)
Difficulty with motor tasks (rolling/sit to stand/dressing/ shaving etc.)
Social difficulty due to:
- Loss of facial expressions + upwards gaze
- Monotone speech
Problems with swallowing/drooling (aspiration pneumonia risk)
Sleep disorders
Depression
Micrographia - writing gets smaller + smaller
*Cognitive difficulties in late stages

Question 8

Postural Instability - late stage Parkinson’s

Answer 8

> Flexed Posture 
- forward tilt of trunk
- slightly flexed hips + knees
- flexed elbows + wrists 
> Poor balance reactions = falls

Question 9

Assessment

Answer 9

> Hoehn + Yahr Scale
0 = no signs of disease
1 = unilateral involvement (minimal functional disability)
1.5 = unilateral involvement + neck and spine
2 = bilateral involvement with no impairment of balance
2.5 = mild bilateral symptoms +able to recover on pull test
- patient can keep balance when pulled backwards - initiation of trunk flexors + dorsiflexors is required
3 = Bilateral mild to moderate symptoms
- postural instability but still physically independent
4 = Severe disability but able to walk/stand unassisted
5 = Needing wheelchair or bedridden unless assisted

Question 10

Treatment - medication

Answer 10

> Dopamine replacements - Sinemet/Madopar
- dopamine requires a facilitator to cross the blood brain barrier
Dopamine copycats/agonists - Apomorphine
Dopamine protectors - stelegline (block enzymes that break down dopamine = Monoamine oxidase B (mao-B) + COMT)
Anticholinergics - arpicoline
- mainly younger patients
- dopamine is in a balance with acetylcholine - imbalance can cause increase in muscle tension, tremor, urgency and salivation
- these drugs reduce levels of acetylcholine to reduce effect of dopamine loss

• All drug effects reduce over time
• increasing dose will increase side effects e.g dyskinesias - strange movements
• problems with ‘on/off’ - motor fluctuations as medications wear off

Question 11

Treatments - Surgery

Answer 11

> Deep brain stimulation - treat tremor
Pallidotomy - electrical probe in global pallidus
- heated to destroy area of cells
Thalatomy - destroy thalamus

*All = v. invasive

+ stem cell research - use stem cells to replace lost dopamine producing cells

Question 12

Treatments - Physiotherapy

Answer 12

> Stretching - combat tone/rigidity
Strengthening - combat weakness from lack of movement
CV exercise - combat fatigue
Posture
Balance + Falls Prevention
Gait re-education
Transfers
functional activity practice + compensation strategies
education
Fatigue/pain management
cueing
- using visual/auditory/kinetic feedback to access motor pattern
- Parkinson’s affects the supplementary motor area + automatic movement which can be overridden by premotor area with sensory guided movement (requires focus + attention)

Question 13

Cause

Answer 13

> Unknown
possible genetic factors - 15% chance of inheritance
environmental factors - pollutants

Question 14

Prognosis

Answer 14

> Not a killer but immobility + mental disability will aid other killers
life expectancy is not significantly shorter
Quality of life is decreased for both patient + family

Question 15

Facts

Answer 15

> 1 in 500 have it in UK
- up to 1 in 50 over 80
1.5x more common in men
more common with increasing age