Parkinson's Disease Presentation PDF

Presentation by Lois Stevens Parkinson’s Disease Senior Lecturer  Analogy Thalamus – accelerator Basal Ganglia - brake  Basal Ganglia Impairment What happens when things go wrong? Too much inhibition – hypokinetic conditions – too little movement – PD...

Presentation by Lois Stevens Parkinson’s Disease Senior Lecturer  Analogy Thalamus – accelerator Basal Ganglia - brake  Basal Ganglia Impairment What happens when things go wrong? Too much inhibition – hypokinetic conditions – too little movement – PD Too little inhibition – hyperkinetic conditions – Huntington’s Disease, athetoid CP  Pathology Death of dopamine producing cells in the SN compacta – cause of cell death unknown About 80% of dopamine - producing cells die before clinical signs of disease become apparent Microscopic deposits known as Lewy bodies are formed within dopamine producing neurons Parkinson’s Disease  Effect on Movement Loss of dopamine → increased inhibition of thalamus by BG → reduced activity in motor cortex → decreased voluntary movement  Effect on Posture A second important BG motor circuit: GP → midbrain → reticulospinal and vestibulospinal tracts When this pathway is interrupted there is excessive contraction of postural muscles Rigidity  Parkinson’s Disease Most common BG motor disorder Main Motor Characteristics: - muscular rigidity – cog wheel/lead-pipe - bradykinesia – slowness of both voluntary and automatic movements e.g. reduced range of active motion, no arm swing – difficulty initiating movement, turning and stopping - resting tremor – pill rolling. Involuntary shaking, trembling or quivering of muscles - postural instability - balance problems  Additional Features shuffling gait kyphotic posture mask like facial expression – hypomimia speech – loss of expression, diction, volume – sometimes festination – monotonous, slurred postural instability fine motor impairment – e.g. difficulty with buttons freezing dyskinesia's  Gait Reduced stride and step length Slower, shuffling pattern with flexion of trunk and hips Reduced trunk rotation and arm swing Increased double stance Reduced heel strike Reduced toe clearance in swing phase Akinetic problems: initiation, freezing, termination - festination  Pharmacological Treatment Drug therapy that replaces dopamine – L-dopa – initially effective in reducing symptoms Effectiveness reduced by disease progression, intolerance and side – effects On/Off phenomenon: 'Off' time is when levodopa is no longer working well and symptoms such as tremor, rigidity and slow movement re-emerge.  On/Off https://youtu.be/sf1N0Zf5IqA  Surgical Treatment Transplantation of foetal brain tissue Deep Brain Stimulation Rehabilitation