harald bjorndalen adapted from lecture by dr zoe campbell (medical spr)
TRANSCRIPT
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Parkinson’s DiseaseHarald 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
Learning Outcomes
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Case Pathophysiology Definition Clinical features Investigations Management Prognosis
Outline
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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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Parkinson’s Disease
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Loss of dopaminergic neurones in the substantia nigra and appearance of eosiniphilic inclusion bodies (Lewy bodies)
Parkinson’s - Pathophysiology
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Classic TRIAD:
BRADYKINESIA / slowness RIGIDITY / stiffness / increased tone TREMOR / pill rolling / 4-6 Hz /resting
Postural instability
Parkinson’s - History
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Neurodegenerative disease of the dopamine generating neurones in the substantia nigra, characterized by bradykinesia, rigidity, tremor, and postural instability
Definition
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What is PARKINSONISM?
What are the causes?
Parkinson’s
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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
Parkinsonism
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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
Parkinson's - History
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Anxiety/depression Sleep disturbance Postural hypotension Sweating Constipation Drooling Incontinence Sexual dysfunction
Parkinson’s - History
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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
Parkinson's – Red Flags
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Cranial nerves Upper limb Lower limb Gait Function
Parkinson's - Examination
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Face – expressionless / mask like / reduced blinking
Parkinson's - Examination
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Speech Monotonous Tremulous slurring dysarthria (due to
akinesia, tremor and rigidity of bulbar area) Dribbling and drooling
Parkinson’s - Examination
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Tremor Worse at rest Asymmetrical
Parkinson’s - Examination
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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)
Parkinson’s - Examination
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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
Parkinson’s - Examination
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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.
Parkinson’s - Investigation
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MDT: Physios OT Neurologist GP PD nurse Support societies Palliative care in the late stages
Parkinson’s - Management
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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
Parkinson’s- Management
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Depression, psychosis Dementia Sleep disorders
◦ Restless legs syndrome◦ Periodic limb movements of sleep◦ REM sleep behaviour disorder
Falls Autonomic disturbance
◦ urinary dysfunction◦ weight loss, dysphagia◦ constipation◦ erectile dysfunction◦ orthostatic hypotension◦ excessive sweating◦ sialorrhoea
Non-motor symptoms in PD
clonazepam
movicol
Citalopram Quetiapine, clozapine
Acetylcholinesterase inhibitors
Oxybutynin, tolterodine
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Guidelines for drug management of PD
Significant functional disability Disease progressionDopamine agonist
Add levodopa (max 600mg/day)
Motor complications develop
Add DA or entacapone
MAO-B inhibitor
Add entacapone or DA
Levodopa (max 600mg/day)
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
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Parkinson’s - Management
• 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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Parkinson’s - Management
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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?
Case History 2
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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 response-
drugs 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
Parkinson’s - Management
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MDT: Physio OT Neurologist GP Support societies Palliative care in the late stages
Parkinson’s - Management
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Progression variable Usually the course is over 10-15 years Death from pneumonia
Parkinson’s - Prognosis
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- Sam AH, Teo JTH, Rapid Medicine, Wiley-Blackwell 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
References/Further reading