Introduction to Parkinson's Disease Lecture 1 PDF

INTRODUCTION TO PARKINSON’S DISEASE LECTURE 1 NP4 - NEUROLOGY QUICK GLANCE OF PD https://www.youtube.com/watch?v=Ztwkwqgvoso (1.48 secs) https://www.youtube.com/watch?v=IHDFQfmkKlg (6.48) DEFINING IPD Named after James Parkinson who published 'An Essay on the Shaking Palsy'...

INTRODUCTION TO PARKINSON’S DISEASE LECTURE 1 NP4 - NEUROLOGY QUICK GLANCE OF PD https://www.youtube.com/watch?v=Ztwkwqgvoso (1.48 secs) https://www.youtube.com/watch?v=IHDFQfmkKlg (6.48) DEFINING IPD Named after James Parkinson who published 'An Essay on the Shaking Palsy' in 1817, which established Parkinson’s as a recognised medical condition. He studied at the London Hospital Medical College, qualifying as a surgeon in 1784 when he was 29. DEFINING IPD Multiple systems atrophy Progressive IPD supranuclear palsy Parkinsonism Drug-induced Lewy body parkinsonism dementia Vascular parkinsonism AETIOLOGY Unknown aetiology. Several theories: Nicotine- IPD is less prevalent in smokers than lifelong abstainers. MPTP- caused severe parkinsonism in young drug abusers. Genetic factors- clustering of early-onset PD in some families.  PATHOLOGY Basal ganglia: Group of nuclei in the brain situated at the base of the forebrain (striatum, globus pallidus, substantia nigra [SN], nucleus accumbens, subthalamic nucleus). Associated with voluntary motor control, procedural learning, eye movements, cognitive and emotional functions. PATHOLOGY Depletion of pigmented dopaminergic neurons in SN Reduced Inclusion bodies (Lewy Degeneration in dopaminergic output bodies) develop in other basal from SN nigral cells ganglia nuclei Neurons in subthalamic nucleus become more active than usual in inhibiting activation of the cortex Bradykinesia CLINICAL FEATURES Bradykinesia Postural IPD Rigidity instability Resting Tremor PATHOLOGY CLINICAL FEATURES Cogwheel rigidity (upper limbs) Increased tone Flexed when opposite posture Rigidity arm moves actively Lead pipe rigidity (legs) CLINICAL FEATURES Difficulty initiating movement Poor rapid Reduced fine spontaneous Bradykinesia blinking movements (fingers) Facial immobility (hypomimia) CLINICAL FEATURES Basal ganglia Cerebellum PARKINSONISM COMPRISES FOUR CARDINAL MOTOR FEATURES Bradykinesia (slow and small movements). Reduced blink, face expression, and gesturing. Soft voice. Difficulty getting out of chair, shuffling steps, reduced arm swing, freezing Tremor (usually resting) “pill rolling”, often involves thumb Rigidity (different from spasticity) Postural changes. Imbalance, falls; stooped flexed posture  STAGES OF PD Stage 0 No signs of disease Stage 1 Unilateral disease Stage Unilateral disease plus axial involvement 1.5 Stage 2 Bilateral disease, without impaired balance Stage Bilateral disease, with impaired balance 2.5 Stage 3 Mild to moderate bilateral disease, some postural instability; physically dependent Stage 4 Severe disability; still able to walk or stand unassisted Stage 5 Wheelchair-bound or bedridden DIFFERENTIAL DIAGNOSIS OF PARKINSONISM Parkinson disease (idiopathic or genetic) Parkinson-plus degenerations (dementia with Lewy bodies, progressive supranuclear palsy, corticobasal degeneration, multiple system atrophy) Drug-induced parkinsonism (anti-dopaminergics) Rare but treatable in young people: Wilson disease and Dopa-responsive dystonia Other: “vascular” parkinsonism, brain trauma, CNS infection  DRUG-INDUCED PARKINSONISM Drugs that reduce dopamine transmission Antipsychotics / antiemetics: Risperidone, haloperidol, metoclopramide, promethazine, prochlorperazine, etc. Can be indistinguishable from PD Clozapine does not seem to cause it; quetiapine appears to have low rates Management: reduce or discontinue offending agent. Can take months to resolve! PARKINSON DISEASE (PD) Usually, idiopathic Substantia nigra degeneration causes dopamine deficiency in striatum  motor symptoms Dopaminergic therapy relieves motor symptoms PD TO CONTINUE… 2.2 ASSESSMENT AND TREATMENT OF PARKINSON’S DISEASE