1. JP Parkinson’s Disease

2. Overview Idiopathic PD Clinically and pathologically distinct from other parkinsonian syndromes Degenerative disorder of the CNS Develops over months or several years Classification: movement disorder Combination of tremor, rigidity and akinesia

3. Causes Not well known Relatively uniform world-wide prevalence suggests that it is not environmental Possible factors: Nicotine Less prevalent in smokers Genetic factors Not usually familial Mutation in parkin gene may account for cases with an onset below the age of 40

4. Epidemiology Prevelence (per 100,000): Sweden 22.5 USA 20.5 Japan 16.9 England 12 Italy 10 Hair colour Black (least) Brown 40% more likely Blonde 60% more likely Red 100% more likely Melanin (pigment) is initally made the same way as dopamine

5. Epidemiology – cont. Age Very uncommon <30 Risk sharply increases at the age of 60 Gender More common in males

6. Pathophysiology Neurons from the substantia nigra (basal ganglia) extend into the putamen and caudate Release dopamine PD: Breakdown in connection between the substantia nigra and the putamen Symptoms occur when 20-50% levels of normal dopamine Usually around 60-80% of cells die in the substantia nigra Lewy Bodies when found in the substantia nigra is characteristic Dense protein core

8. Clinical Symptoms Initially tremor and slowness Limbs and joints feel stiff and ache Fine movements become difficult Difficulty “rising from a chair” or “getting in or out of bed” Writing becomes small (micrographia) and spidery Relatives notice slowness and an impassive face Nearly always more prominent on one side

9. Clinical Signs Tremor Rest tremor usually decreases with action Characteristic Rigidity Stiffness is equal in opposing muscle groups ‘Lead pipe’ Limbs, neck and axial muscles Akinesia & Bradykinesia Difficulty initiating movement Rapid fine finger movements are greatly affected Facial immobility Reduced blink rate Serpentine stare

10. Clinical Signs – cont. Postural changes Stoop Festinant gait (hurrying) and shuffling with poor arm swinging Balance deteriorates Speech Monotone Progresses to slurring dysarthria Other symptoms Heartburn, dribbling, dysphagia, constipation and weight loss Urinary difficulties Skin is greasy and sweating excessive

11. Course of the disease Worsens over 10-15 years Death results from bronchopneumonia

12. Differentials Alzheimer’s disease Multi-infarct dementia Repeated head injury Drug-induced Late effects of severe hypoxia or carbon monoxide poisoning Hypothyroidism Depression

13. Diagnosis No laboratory test Made by history and recognising physical signs

14. Treatment No drugs alter the course of disease Levodopa Effective in initial symptom treatment Issues: Fluctuates between effectiveness After several years levodopa becomes inefficient Side effects are severe: Initially: nausea and vomitting Later: episodes of immobility, dyskinesias Dopamine receptor agonists Generally less effective than levodopa but less side effects Usually primary treatment unless levodopa is absolutely necessary Used below the age of 70

15. Surgery Stereotactic neurosugery Provides effective, temporary improvement in tremor and dyskinesia Used before levodopa and in the past decade has become more popular

16. Physiotherapy Can improve gait Modifications at home Eg. Remove fiddly stuff from clothing Walking aids

17. Psychiatric Aspects Depression is common

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