Band 5 Presentation Parkinson’s Disease Rónán Donohoe, 11 Mar ‘10

Parkinson’s Disease

Outline:
1. Overview
2. Pathophysiology
3. Medications QuickTimeª and a
4. Physiotherapy Management decompressor
are needed to see this picture.
5. Case Studies (discussed t/o)

1. Overview of Parkinson’s Disease (PD)

• first identified Dr James Parkinson: "The Shaking Palsy”, (1817)
• a degenerative movement disorder of CNS
• characterized by muscle rigidity, tremor, bradykinesia, postural
instability (“Parkinsonism”)
• result of decreased stimulation of the motor cortex by the basal
ganglia, due to insufficient formation of dopamine
• no cure, chronic & progressive

“Parkinsonism” / Parkinson-plus syndromes

• Drug induced
• Multiple infarction
• Degenerative conditions (Parkinson-plus)
o Progressive supranuclear palsy (PSP)
o Multiple system atrophy (MSA)
o Corticobasal degeneration (CBGD)
Diagnosis
• No diagnostic test
• Primarily clinical
• Depression and dementia often develop
• Rate of progression varies
Aetiology / Epidemiology
• Cause unknown
• No known social, economic or geographical variations
• Men slightly more likely to develop than women
• Prevalence - One in 500 people (around 120,000 individuals in the UK)
• Incidence – 4-20 per 100,000 (10,000 people in the UK are diagnosed each year)
• 1 per 100 over 75 yrs of age
• Average onset – 60 yrs
• 1 in 7 diagnosed < 50yrs

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Band 5 Presentation Parkinson’s Disease Rónán Donohoe, 11 Mar ‘10

2. Pathophysiology
Basal ganglia
The basal ganglia
are paired groups of
forebrain nuclei
found deep within
the cerebral
hemispheres that
help to control
movement

The overall function

of this loop (direct
pathway) is to select
a particular
movement or a
sequence of
movements while
suppressing others

Normal Movement

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Band 5 Presentation Parkinson’s Disease Rónán Donohoe, 11 Mar ‘10

Parkinson’s Disease
• Difficulty in initiating movements because of reduced dopaminergic input from
substantia nigra pars compacta
• Underactivity in direct pathway causes too much inhibition of thalamus and
prevents initiation of movements

Pathophysiology
• Death of Substantia Nigra cells (Dopamine producing nuclei)
• Loss of Dopamine production
• Lack of inhibition of cholinergic neurons
• Unopposed Excitation
• Normal balance of excitation and inhibition lost
• Smooth movement / Lack of movement control
• Lack of inhibition of reticular spinal + vestibulospinal tracts
• Excessive contraction of postural muscles

The deficits tend to fall into one of two categories:

• the presence of extraneous unwanted movements (Tremor)
• or an absence or difficulty with intended movements. (Rigidity,
Bradykinesia)

Tremor
• Head rotation • 5-6 Hz frequency
• Tongue in n out • Present at rest, absent in sleep, increased by
emotion, excitement or fatigue and on being
• Pill-rolling watched

Rigidity
• Uniform increase in tone in all muscle groups • Increases by mental concentration and active
of the area involved movements of other parts of the body
• Resistance throughout the whole range of • More in neck and forearm muscles
passive movement (lead pipe)
• Lead-pipe: smooth rigidity
• Exaggerated postural fixation
• Decreased by surgical incision in globus
• Cog-wheel: muscles yield in a seiries of jerks
pallidus and by administration of L-dopa
• Rigidity decreases on support and relaxation

Bradykinesia, hypokinesia
• Slowness and poverty of movement
• Voluntary and automatic movements are slow, reduced in amplitude and range
• Difficulty in modifying range and speed
• Micrographia
o Latent period between stimulus and response
o Fine movements are more affected
• Loss of normal trunk rotation as normal balanced activity between the flexors and
extensors is lost
• Rounded shoulders, head held forwards, Kyphosis
• Flexed posture
o Reduced thoracic expansion
o Lead to respiratory complications
• Posture can be voluntarily corrected but only temporarily
• Loss of arm swing during walking, lack of rotation component
o the characteristic shuffling gait

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Band 5 Presentation Parkinson’s Disease Rónán Donohoe, 11 Mar ‘10

o lean far forward, chase their CoG to avoid falling over - anteropulsion or
festination
• Inability to maintain repetitive movements or perform rapidly alternating movements
(Dysdiadochokinesia)
• Tends to sit still
• Mask face
• Mastication and swallowing affected
• Speech-slurred, monotonous
• Autonomic disturbances: Constipation, Orthostatic hypotension, Weight loss,
Excessive sweating, salivation
• Sleep disturbance
• Psychiatric problems
o Depression
o Dementia

Defective postural reflexes

• Typical flexed posture • Anti-gravity mechanisms – good
• Sticks to the position Weight shift is affected – shuffle,
• Postural fixation, protective Festinant gait
reactions, righting reflexes, tilting • Poor balance
reactions, locomotive reactions –
affected

Social problems
• Drool while eating • Impaired mobility
• Difficulty with voice production • Social isolation
• Lack of facial expression • Depression

Aims of management
• No cure
• Goals
o Improve function / safety
o Delay loss of independence
• Medical management
o Drugs / Surgery
o MDT approach

3. Medication
• To provide control of signs and symptoms for as long as possible while minimizing
adverse effects
• Medications usually provide good symptom management for 4-6 years, after this
disability progresses despite medical management
• Patients develop long term motor complications including fluctuations and dyskinesia
• As PD progresses fewer dopamine neurones are available to store and release the
derived dopamine so the patients clinical state begins to fluctuate more

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Band 5 Presentation Parkinson’s Disease Rónán Donohoe, 11 Mar ‘10

Levodopa (L-dopa) or Dopamine receptor agonists

• L-dopa is converted to dopamine in the brain to stimulate dopamine receptors
• L-dopa is given with a decarboxylase inhibitor (carbidopa) otherwise 90% would be
converted to dopamine in the body causing side effects
Most commonly prescribed: Madopar (co-beneldopa) & Sinemet (co-careldopa)
• usually started on a low dose and gradually increased satisfactory response
• Most people can tolerate & experience considerable long-term improvement, esp in
rigidity & bradykinesia.
• response can become less reliable longer term
o may experience effect wears off before the next one is due
o unwanted involuntary movements (dyskinesias) may appear,
o may be sudden switches from 'on' (being able to move) to 'off' (immobile)
• longer-term effects can sometimes be improved by altering the type or amount of
Sinemet or Madopar, or the frequency with which the drug is taken. If this is not
satisfactory, other types of drug can be combined with levodopa.

MAO-B inhibitors
• Blocks monoaomine oxidase type B (MAO-B), which breaks down dopamine in the
brain
• Selegiline - used to make the dose of Sinemet or Madopar last longer or reduce the
amount required. Examples: selegiline (Eldepryl/Zelapar) & rasagiline (Azilect).

Dopamine agonists
• work by stimulating the parts of the brain where dopamine acts
• unlike levodopa, do not require conversion by the brain cells first
• longer duration of action than levodopa and may suit some people better
• Dopamine agonists may be taken alone, but are usually used in conjunction
with levodopa to ‘smooth out’ control of symptoms in people whose response
to treatment is beginning to fluctuate
• + can act as a ‘rescue treatment’ when tablets fail to take effect
• - can only be given by injection or infusion
• Include bromocriptine (Parlodel®), lisuride (Revanil®), pergolide (Celance®),
ropinirole (ReQuip®), cabergoline (Cabaser®), pramipexole (Mirapexin®) and
Apomorphine (APO-go®) – pump (syringe driver) or pen for intermittent
injections
• Rotigotine (Neupro®) – 24 hour patches

Anticholinergics
• older drugs, less commonly prescribed nowadays
• inhibits acetylcholine receptors
• often prescribed alone, especially in the early stages before levodopa is necessary
• useful for younger people in the early stages of Parkinson's when symptoms are mild
• may also be used to reduce saliva production when drooling is a problem and to
damp down bladder contractions
Examples: trihexyphenidyl (Broflex, Artane, Agitane), benztropine (Cogentin),

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Band 5 Presentation Parkinson’s Disease Rónán Donohoe, 11 Mar ‘10

orphenadrine (Disipal), procyclidine (Kemadrin, Arpicolin)

Benzatropine (atropine was used before L-dopa)

Surgery - Deep brain stimulation, Lesioning (thalamotomy or pallidotomy)

4. Physiotherapy Management
• Early - Prevention / Education
• Middle - Compensation strategies
• Late - Respiratory status
- Function
- Aid and adaptations
- Palliative care

Treatment Approaches
• Normal movement re-education
• Biomechanical approach
• Relearning motor sequences
• General physiotherapy modalities
• Exercise – esp rotation
• Functional re-education
• Balance re-education

Principles of Treatment
• Assessment to identify treatment priorities & identify goals
• Early implementation of a preventative exercise programme
• Targeted intervention focusing on areas of deterioration
• Use of structured programmes based on the principles of psychometric learning to
address motor deficits

Physiotherapy
• Gait reeducation, improvement of balance and flexibility
• Enhancement of aerobic capacity
• Improvement of movement initiation - Mental rehearsal, Cueing strategies
• Improvement of functional independence, including mobility and ADL
• Provision of advice regarding safety in the home environment

Compensation strategies
• Breakdown complex movement sequences into simple component parts
• Arrange parts in a logical, sequential order
• Utilise prior mental rehearsal of the whole movement sequence
• Perform each part separately, ideally ending in a stable resting position from which
next step can be initiated
• Execute each part under conscious control
• Avoid simultaneous motor or cognitive tasks
• Use appropriate visual, auditory and somatosensory cues to initiate
• and maintain movement

Cues

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Band 5 Presentation Parkinson’s Disease Rónán Donohoe, 11 Mar ‘10

• Visual (spatial) practice walking -stripes on floor. Steeping over lines

• Auditory(Rhythm) listening to beats to initiate movement or maintain cadence
• Auditory/visual (spatial) verbal prompt/ to a visual cue to negotiate on steps
• Somatosensory (rhythm) steeping back to start walking, rocking side to side
• Mental rehearsal (spatial) visualisation of walking, Memorising parts of sequence

Physio Rx Web Reference:

GUIDELINES FOR PHYSIOTHERAPY PRACTICE IN PARKINSON'S DISEASE
http://hces.unn.ac.uk/guidelines/management.htm Northumbria University

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