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Parkinson’s Disease

Parkinson’s Disease. Harald Bjorndalen Adapted from lecture by Dr Zoe Campbell (Medical SpR ). Learning Outcomes. 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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Parkinson’s Disease

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  1. Parkinson’s Disease HaraldBjorndalen Adapted from lecture by Dr Zoe Campbell (Medical SpR)

  2. Learning Outcomes • Understand difference between Parkinson’s Disease and Parkinsonism • Describe clinical features of Parkinson’s disease • Describe basic management of parkinson’s disease

  3. Outline • Case • Pathophysiology • Definition • Clinical features • Investigations • Management • Prognosis

  4. 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.

  5. 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?

  6. Parkinson’s Disease

  7. Parkinson’s - Pathophysiology • Loss of dopaminergic neurones in the substantia nigra and appearance of eosiniphilic inclusion bodies (Lewy bodies)

  8. Parkinson’s - History • Classic TRIAD: • BRADYKINESIA / slowness • RIGIDITY / stiffness / increased tone • TREMOR / pill rolling / 4-6 Hz /resting • Postural instability

  9. Definition • Neurodegenerative disease of the dopamine generating neurones in the substantianigra, characterized by bradykinesia, rigidity, tremor, and postural instability

  10. Parkinson’s • What is PARKINSONISM? • What are the causes?

  11. Parkinsonism • 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

  12. Parkinson's - History • 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

  13. Parkinson’s - History • Anxiety/depression • Sleep disturbance • Postural hypotension • Sweating • Constipation • Drooling • Incontinence • Sexual dysfunction

  14. Parkinson's – Red Flags • 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

  15. Parkinson's - Examination • Cranial nerves • Upper limb • Lower limb • Gait • Function

  16. Parkinson's - Examination • Face – expressionless / mask like / reduced blinking

  17. Parkinson’s - Examination • Speech • Monotonous • Tremulous slurring dysarthria (due to akinesia, tremor and rigidity of bulbar area) • Dribbling and drooling

  18. Parkinson’s - Examination • Tremor • Worse at rest • Asymmetrical

  19. Increased tone / cogwheeling • Power normal • Reflexes normal • Sensation normal • Coordination normal (but might be slow)

  20. Parkinson’s - Examination • Gait • Stooped posture • Gunslinger/Hands over hernias • Shuffling • Reduced arm swing • Difficulty turning (axial rigidity)

  21. Parkinson’s - Examination • Rapidly open and close hands • Functional tasks • Get the patient to write a sentence • Draw a spiral • AMT • Lying / standing BP

  22. Parkinson’s - Investigation • 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.

  23. Parkinson’s - Management • MDT: • Physios • OT • Neurologist • GP • PD nurse • Support societies • Palliative care in the late stages

  24. Parkinson’s- Management • 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

  25. Non-motor symptoms in PD Citalopram Quetiapine, clozapine • 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 Acetylcholinesterase inhibitors clonazepam Oxybutynin, tolterodine movicol

  26. Dopamine agonist Disease progression Guidelines for drug management of PD Significant functional disability MAO-B inhibitor Levodopa (max 600mg/day) Add levodopa (max 600mg/day) Motor complications develop 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

  27. 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

  28. Parkinson’s - Management

  29. Case History 2 • 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?

  30. 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?

  31. 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

  32. 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

  33. Parkinson’s - Management • MDT: • Physio • OT • Neurologist • GP • Support societies • Palliative care in the late stages

  34. Parkinson’s - Prognosis • Progression variable • Usually the course is over 10-15 years • Death from pneumonia

  35. References/Further reading • - 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 NaghmeAdab, Management and treatment of Parkinson’s Disease, 2012

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