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Idiopathic parkinsons disease (IPD) PowerPoint Presentation

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Description : Check out this medical presentation on Neurology, which is titled "Idiopathic parkinson’s disease (IPD)", to know about the Definition, Aetiology, Pathology, Clinical features, Investigations, Differential diagnoses, and Management of Idiopathic parkinson’s disease (IPD).

Tags : Neurology, Idiopathic parkinson’s disease, IPD, Definition, Aetiology, Pathology, Clinical features, Investigations, Differential diagnoses, Management

Published on : Aug 18, 2021 | Views : 2003 | Downloads : 7

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Idiopathic parkinson’s disease (IPD) Dr Sabrina Akhtar
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Objectives Definition Aetiology Pathology Clinical features Investigations Differential diagnoses Management
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Objectives Definition Aetiology Pathology Clinical features Investigations Differential diagnoses Management
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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.
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Defining IPD -Degenerative, progressive disease affecting the basal ganglia. Movement disorders: 1) Akinetic-rigid syndromes - Slowed movement. - Increased tone. -> IPD, drug-induced parkinsonism, multiple systems atrophy, progressive supranuclear palsy. 2) Dyskinesias -Added, uncontrollable movements. -> Essential tremor, chorea, myoclonus, tics.
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Defining IPD
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Defining IPD Annual incidence- 0.2/1000. Prevalence- 1/500 (127 000 people in the UK). Tends to affect ≥50 years. 1/20 is under the age of 20 years. Incidence and prevalence increase with age. Equal sex incidence.
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Objectives Definition Aetiology Pathology Clinical features Investigations Differential diagnoses Management
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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.
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Objectives Definition Aetiology Pathology Clinical features Investigations Differential diagnoses Management
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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.
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Pathology
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Pathology
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Objectives Definition Aetiology Pathology Clinical features Investigations Differential diagnoses Management
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Clinical features
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Clinical features
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Clinical features
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Clinical features
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Clinical features
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Clinical features Gait: Stooping Slow to initiate walking Shortened stride Rapid small steps (shuffling) Tendency to run (festinating) Reduced arm swing Impaired balance on turning Falls common in later stages. Parkinson’s gait
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Clinical features Speech -Monotone tremulous, slurring dysarthria. -Soft, rapid, indistinct. Cognitive -Cognitive impairment in 1/3 of patients (loss of executive functions including planning/decision-making/controlling emotions). -Depression.
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Clinical features GI/others -Constipation/heartburn/dribbling/ dysphagia/weight loss. -Greasy skin. -Micrographia.
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Clinical features
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Objectives Definition Aetiology Pathology Clinical features Investigations Differential diagnoses Management
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Investigations Clinical diagnosis. <50 years: Test for Wilson’s disease. CT head scan if: - Pyramidal/cerebellar/autonomic involvement. - Diagnosis is in doubt.
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Objectives Definition Aetiology Pathology Clinical features Investigations Differential diagnoses Management
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Differential diagnoses Multiple systems atrophy Progressive supranuclear palsy Lewy body dementia Drug-induced parkinsonism Vascular parkinsonism
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Objectives Definition Aetiology Pathology Clinical features Investigations Differential diagnoses Management
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Management Medical: Levodopa + peripheral decarboxylase inhibitor (E.g. Carbidopa, Benserazide). -Levodopa: Precursor of dopamine stimulates remaining neurons to produce more dopamine. -Decarboxylase inhibitor: Prevents peripheral decarboxylation to dopamine and .:. peripheral SE’s.
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Management Side effects of levodopa: -N&V -Confusion -Visual hallucinations -Delusions -Chorea LT effects: -Levodopa-induced involuntary movements. -Gradually ineffective after several years. -Episodes of immobility (freezing). THEREFORE drugs are avoided until clinically necessary (significant disability) because of delayed unwanted effects.
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Management Other medical treatment options: -Dopamine receptor agonists (Bromocriptine/Cabergoline). -Amantadine. -Rivastigmine (cognitive changes). -Antioxidant compounds (Vitamins C & E- possible neuroprotective agents).
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Management Surgical -Stereotactic thalamotomy- temporary improvement of symptoms. Physiotherapy Reduces rigidity & corrects abnormal posture. Speech therapy -Dysarthria/dysphonia. Neuropsychiatric - SSRI’s for depression.
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Management Natural history: Slowly progressive (10-15 years). Bradykinesia & tremor worsen. Late deterioration despite Levodopa Rx occurs in 1/3-1/2 of patients after 3-5 years. This includes the ‘on-off’ phenomenon. Patient’s c/o limb & joint discomfort.
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Management Prognosis -Partly related to age of onset e.g. if symptoms start in middle life  disease likely to shorten lifespan (complications of immobility & tendency to fall). Onset >70 years of age unlikely to shorten life/become severe.
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Summary IPD is the most common cause of parkinsonism. Degenerative, progressive disease affecting the basal ganglia. Classical features include tremor, rigidity and bradykinesia. Mainstay of treatment is with levodopa & a PDI. Treatment is delayed until clinically necessary because of unwanted delayed effects of levodopa. Multi-disciplinary approach to management.
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Thank you!  Questions?