Harald Bjorndalen
Adapted from lecture by Dr Zoe Campbell
(Medical SpR)
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Understand difference between Parkinson’s
Disease and Parkinsonism
Describe clinical features of Parkinson’s
disease
Describe basic management of parkinson’s
disease
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Case
Pathophysiology
Definition
Clinical features
Investigations
Management
Prognosis
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Clinical scenario
A 64 year old man attends his GP after his wife
persuaded him. For the last 6 months he has
noticed that he is slowing down. It takes him a
long time to do simple tasks like getting dressed.
His hands are shaking all the time, more so on
the right. His wife has noticed a change in his
gait saying he shuffles when he walks. He has no
past medical history of notes and is on no
regular medication and has no known allergies.
On examination he has a blank staring
expression and marked rigidity of his limbs,
more so on the right. He has resting pill rolling
tremor. His gait is shuffling and festinant.
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What are your differentials for this
gentleman?
How would you investigate this man?
How would you manage this gentleman?
What are the stages of managing Parkinson’s
Disease?
What are the Parkinson’s plus syndromes?
What drugs can cause Parkinsonism?
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Loss of dopaminergic
neurones in the
substantia nigra
and appearance of
eosiniphilic inclusion
bodies (Lewy bodies)
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Classic TRIAD:
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BRADYKINESIA / slowness
RIGIDITY / stiffness / increased tone
TREMOR / pill rolling / 4-6 Hz /resting
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Postural instability
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Neurodegenerative disease of the dopamine
generating neurones in the substantia nigra,
characterized by bradykinesia, rigidity,
tremor, and postural instability
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What is PARKINSONISM?
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What are the causes?
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Neurological syndrome characterised by
tremor, bradykinesia and rigidity.
Causes
DRUGS – Anti psychotics, metaclopramide,
TCA, MPTP
Vascular disease
Parkinson plus syndromes (multiple system
atrophy, progressive supranuclear palsy,
corticobasal degeneration, Lewy-body
dementia)
Trauma
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Onset - gradual
Tremor – at rest, usually first noticed in the
hands
Stiffness and slowness of movement.
Difficulty initiating movements (e.g. getting
out of chair, turning in bed)
Falls – Not usually frequent early on
Smaller hand writing
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Anxiety/depression
Sleep disturbance
Postural hypotension
Sweating
Constipation
Drooling
Incontinence
Sexual dysfunction
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Symmetry
Lower body involvement
Poor response to levodopa
Early falls / postural instability
Early autonomic disturbance (sexual, bladder,
postural hypotension)
Early eye movement disorders
Early dementia
Early dysarthria
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Cranial nerves
Upper limb
Lower limb
Gait
Function
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Face – expressionless / mask like / reduced
blinking
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Speech
Monotonous
Tremulous slurring dysarthria (due to
akinesia, tremor and rigidity of bulbar area)
Dribbling and drooling
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Tremor
Worse at rest
Asymmetrical
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Increased tone / cogwheeling
Power normal
Reflexes normal
Sensation normal
Coordination normal (but might be slow)
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Gait
Stooped posture
Gunslinger/Hands over hernias
Shuffling
Reduced arm swing
Difficulty turning (axial rigidity)
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Rapidly open and close hands
Functional tasks
Get the patient to write a sentence
Draw a spiral
AMT
Lying / standing BP
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Diagnosis is CLINICAL
Bedside tests: Levodopa trial.
Routine bloods
CT and MRI usually normal but may exclude
other causes of parkinsonism
PET / SPECT scans can be used to measure
dopaminergic function in basal ganglia.
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MDT:
Physios
OT
Neurologist
GP
PD nurse
Support societies
Palliative care in the late stages
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Medical:
Dopamine agonists e.g. ropinirole, bromocriptine
MAO inhibitors e.g. rasagiline
Levodopa + decarboxylase inhibitor
COMT e.g. Entacapone
Continuous dopamine therapy – Apomorphine
(syringe driver) or Duodopa (Intrajejunal infusion of
levodopa gel)
◦ Supportive medication e.g. Baclofen,
antidepressants
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Citalopram
Quetiapine, clozapine
Depression, psychosis
Dementia
Acetylcholinesterase inhibitors
Sleep disorders
◦ Restless legs syndrome
◦ Periodic limb movements of sleep
◦ REM sleep behaviour disorder
Falls
Autonomic disturbance
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urinary dysfunction
weight loss, dysphagia
constipation
erectile dysfunction
orthostatic hypotension
excessive sweating
sialorrhoea
clonazepam
Oxybutynin, tolterodine
movicol
Significant functional disability
Dopamine agonist
Disease progression
MAO-B inhibitor
Levodopa (max 600mg/day)
Add levodopa (max 600mg/day)
Motor complications develop
Guidelines for drug
management of PD
Add DA or entacapone
Add entacapone or DA
Switch to tolcapone if entacapone fails
Add MAO-B inhibitor if not already given
Add amantadine for dyskinesia
Severe motor complications
Consider apomorphine, Duodopa, DBS
Parkinson’s - Management
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Surgical:
Deep brain stimulation
A lead is implanted into the target area (brainstem)
This lead connects to a implantable pulse generator
Which connects to a device in the subclavian area of
the chest
• Device produces mono polar or bi polar electrical
stimulation to control symptoms
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74 year old
Diagnosed with PD, right sided tremor,
bradykinesia/rigidity-all mild
L-dopa started after 10 months as symptoms
worsened, problems with stairs
Started on sinemet 62.5mg od then incresed to
tds over 1 week.
No response after 2 weeks
What next?
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Dose incresed to 125mg tds with good response
Stable over 2 years then mobility worsened and
patient getting slow and stiff before next drug
dose
What next?
Increase sinemet to qds
(OR add entacapone)
Over next 3 years, dose increased to sinemet 250,
125, 250, 125 plus sinemet CR nocte
3 years after increase- fluctuations in responsedrugs not always helping him switch on, extra
movements an hour after taking his medications,
switched off prior to his next dose
What next?
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Sinemet decreased to 125 qds plus CR nocte
Entacapone added
No improvement, slightly worse over 6
months
What next?
Ropinirole added
Dose slowly increased over 8 months
(79 yrs old), hallucinations, mild cognitive
decline
Ropinirole decreased, symptoms worsened
Quetiapine added
Sinemet levels maintained
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Surgical:
Deep brain stimulation
A lead is implanted into the target area
(brainstem)
This lead connects to a implantable pulse
generator
Which connects to a device in the
subclavian area of the chest
Device produces mono-polar or bi-polar
electrical stimulation to control symptoms
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MDT:
Physio
OT
Neurologist
GP
Support societies
Palliative care in the late stages
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Progression variable
Usually the course is over 10-15 years
Death from pneumonia
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- Sam AH, Teo JTH, Rapid Medicine, WileyBlackwell 2010
- BMJ learning module: Parkinson's disease initial assessment and referral
- Lecture by Zoe Campell, Warwick Hospital,
2012
- SADH lecture by Naghme Adab,
Management and treatment of Parkinson’s
Disease, 2012