Movement Disorders
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Movement Disorders AgeingandComplexhealth Lucy Osborne, Kriisan ManoharasundaramMovement Disorders AgeingandComplexhealth Lucy Osborne, Kriisan ManoharasundaramDifferentials for tremor- put in the chat ● Parkinsonʼs ● Multiple system atrophy ● Huntingtonʼs chorea ● Benign essential tremor ● Spinal trauma ● CO2 retention ● Hyperthyroidism ● SLE ● MS ● Liver cirrhosis ● Smoking ● Ataxia ● Salbutamol ● Cerebellar infarct ● SSRIs ● Lewy Body Dementia ● Lithium ● Motor neurone disease ● Caffeine ● Polymyalgia rheumatica ● Alcohol withdrawalParkinson’s vs Benign EssentialTremor Parkinson’s Benign Essential Tremor Asymmetrical Symmetrical 4-6 Hz- ‘pill rolling tremor’ 5-8 Hz Worse at rest, improved on movement Worse on movement- ‘intention tremor’ Worse with alcohol Improved with alcohol Micrographia Voice tremor Reduced during sleep Absent during sleep Other Parkinson’s features No other Parkinson’s features Benign EssentialTremor NeurodegenerativeGABAergic Does not present with Affects voluntary muscles- dysfunction ofthe cerebellar other neuro signs dentate nucleus commonly hands, head, Can worsen jaw with time Associatedwith certaingene- autosomal dominant Voice tremor Worsewithcaffeine, alcohol, fatigue,hot Associated with age >40 or cold Does not need treatment Treatmentissymptommanagementwith if not affecting pt Clinicaldiagnosis propanolol or primidone physicallyor mentallyParkinson’s signs and symptoms Cogwheel Rigidity ● Pill-rolling tremor ● Anosmia ● Hypomimia ● Micrographia ● Difficultyinitiating movement ● Difficultyturning ● Small steps- shuffling gait ● Postural instability- falls ● Insomnia Resting tremor Bradykinesia ● Depression ● Cognitive impairment ● Memory lossParkinson’s Progressive decline in dopaminein thebasal ganglia Diagnosed by a specialist using UK Parkinsonʼs disease Society Brain Bank Typicallyelderly males ClinicalDiagnostic Criteria Combination of genetic and Linked with pesticide environmental exposure factorsParkinson’s management- 2023 CCA station (explaining) Holistic Medical Supportgroups- Parkinsons UK Levodopa Care planning Peripheraldecarboxylaseinhibitors Tell DVLA COMTinhibitors Exercise Dopamineagonists Therapy MAO-B inhibitors Occupational therapy Physiotherapy Speechandlanguage therapyTreatment Examples Mechanism of action Indication Side effects Levodopa + Co-benyldopa Levodopa increases levels of Most effective Dyskinesias- decarboxylase Co-careldopa dopamine in basal ganglia treatment but dystonia, chorea, inhibitor (+ stops working athetosis COMT Levodopa Decarboxylase inhibitors prevent over time so used inhibitor) breakdown peripherally before as last resort Decarboxylase levodopa reaches the brain LEVODOPA inhibitors- IS TIMED Benserazide or COMT inhibitors inhibit MEDICATION Carbidopa Catechol-O-methyltransferase enzyme that breaks down COMT inhibitors- levodopa Entacapone Dopamine Bromocryptine Stimulate dopamine receptors Parkinson’s Pulmonary agonists Cabergoline symptoms- fibrosis before levodopa, Hallucinations or with levodopa Delusions MAO-B Selegiline Monoamine oxidase enzymes Parkinson’s Orthostatic inhibitors Rasagiline break down neurotransmitters- symptoms- hypotension dopamine, adrenaline, serotonin, before levodopa, Dizziness MAO-B inhibitors stop this or with levodopa Drowsiness InsomniaParkinson’s examinationParkinson’s examination Adapted neuro exam Split into: ● General inspection-obvioustremor-pill-rolling,hypomimia ● Tremor-resting, postural,action, bradykinesia ● Tone-cogwheel rigidity ● Power,reflexes, sensation ● Gait ● Eyemovements (union jack) ● Speech- ʻbaby hippopotamusʼ ● Extras- lying and standingBP, assesswriting, formaltestofcognition- 4ATVascular ParkinsonismDrug-induced ParkinsonismNormal pressure hydrocephalusLewy Body Dementia- redone in psychMultiple System AtrophyProgressive supranuclear palsyCortico-basal degenerationComprehensive Geriatric AssessmentDifferentials for tremor- put in the chat ● Parkinsonʼs ● Multiple system atrophy ● Huntingtonʼs chorea ● Benign essential tremor ● Spinal trauma ● CO2 retention ● Hyperthyroidism ● SLE ● MS ● Liver cirrhosis ● Smoking ● Ataxia ● Salbutamol ● Cerebellar infarct ● SSRIs ● Lewy Body Dementia ● Lithium ● Motor neurone disease ● Caffeine ● Polymyalgia rheumatica ● Alcohol withdrawalParkinson’s vs Benign EssentialTremor Parkinson’s Benign Essential Tremor Asymmetrical Symmetrical 4-6 Hz- ‘pill rolling tremor’ 5-8 Hz Worse at rest, improved on movement Worse on movement- ‘intention tremor’ Worse with alcohol Improved with alcohol Micrographia Voice tremor Reduced during sleep Absent during sleep Other Parkinson’s features No other Parkinson’s features Benign EssentialTremor NeurodegenerativeGABAergic Does not present with Affects voluntary muscles- dysfunction ofthe cerebellar other neuro signs dentate nucleus commonly hands, head, Can worsen jaw with time Associatedwith certaingene- autosomal dominant Voice tremor Worsewithcaffeine, alcohol, fatigue,hot Associated with age >40 or cold Does not need treatment Treatmentissymptommanagementwith if not affecting pt Clinicaldiagnosis propanolol or primidone physicallyor mentallyParkinson’s signs and symptoms Cogwheel Rigidity ● Pill-rolling tremor ● Anosmia ● Hypomimia ● Micrographia ● Difficultyinitiating movement ● Difficultyturning ● Small steps- shuffling gait ● Postural instability- falls ● Insomnia Resting tremor Bradykinesia ● Depression ● Cognitive impairment ● Memory lossParkinson’s Progressive decline in dopaminein thebasal ganglia Diagnosed by a specialist using UK Parkinsonʼs disease Society Brain Bank Typicallyelderly males ClinicalDiagnostic Criteria Combination of genetic and Linked with pesticide environmental exposure factorsParkinson’s management- 2023 CCA station (explaining) Holistic Medical Supportgroups- Parkinsons UK Levodopa Care planning Peripheraldecarboxylaseinhibitors Tell DVLA COMTinhibitors Exercise Dopamineagonists Therapy MAO-B inhibitors Occupational therapy Physiotherapy Speechandlanguage therapyTreatment Examples Mechanism of action Indication Side effects Levodopa + Co-benyldopa Levodopa increases levels of Most effective Dyskinesias- decarboxylase Co-careldopa dopamine in basal ganglia treatment but dystonia, chorea, inhibitor (+ stops working athetosis COMT Levodopa Decarboxylase inhibitors prevent over time so used inhibitor) breakdown peripherally before as last resort Decarboxylase levodopa reaches the brain LEVODOPA inhibitors- IS TIMED Benserazide or COMT inhibitors inhibit MEDICATION Carbidopa Catechol-O-methyltransferase enzyme that breaks down COMT inhibitors- levodopa Entacapone Dopamine Bromocryptine Stimulate dopamine receptors Parkinson’s Pulmonary agonists Cabergoline symptoms- fibrosis before levodopa, Hallucinations or with levodopa Delusions MAO-B Selegiline Monoamine oxidase enzymes Parkinson’s Orthostatic inhibitors Rasagiline break down neurotransmitters- symptoms- hypotension dopamine, adrenaline, serotonin, before levodopa, Dizziness MAO-B inhibitors stop this or with levodopa Drowsiness InsomniaParkinson’s examinationParkinson’s examination Adapted neuro exam Split into: ● General inspection-obvioustremor-pill-rolling,hypomimia ● Tremor-resting, postural,action, bradykinesia ● Tone-cogwheel rigidity ● Power,reflexes, sensation ● Gait ● Eyemovements (union jack) ● Speech- ʻbaby hippopotamusʼ ● Extras- lying and standingBP, assesswriting, formaltestofcognition- 4ATVascular ParkinsonismDrug-induced ParkinsonismNormal pressure hydrocephalusLewy Body Dementia- redone in psychMultiple System AtrophyProgressive supranuclear palsyCortico-basal degenerationComprehensive Geriatric Assessment