Parkinson's & movement disorders flashcards
19 high-yield MRCP Part 1 cards from the Intellect Medicos Neurology course. Try to answer each question before you open it — then study them properly with spaced repetition, which brings each card back just before you would forget it.
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What is first-line treatment for early Parkinson's disease when motor symptoms affect quality of life?
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Levodopa (with a peripheral dopa-decarboxylase inhibitor, e.g. carbidopa or benserazide).
Why? Levodopa gives the best motor benefit. The decarboxylase inhibitor reduces peripheral conversion and nausea.
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Which adverse effect must patients starting a dopamine agonist (e.g. ropinirole, pramipexole) be warned about?
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Impulse control disorders (e.g. pathological gambling, hypersexuality, compulsive shopping).
Why? Agonists also cause excessive daytime sleepiness and hallucinations, which affects driving.
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Name a drug used to treat levodopa-induced peak-dose dyskinesia.
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Amantadine.
Why? Dyskinesia is the choreiform movement seen at peak levodopa levels. Options are lowering the levodopa dose or adding amantadine.
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How is end-of-dose 'wearing-off' managed in Parkinson's disease?
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Increase the dosing frequency, switch to modified-release levodopa, or add a COMT inhibitor (entacapone/opicapone) or MAO-B inhibitor.
Why? As the disease progresses, each levodopa dose lasts a shorter time. Spreading or prolonging the effect smooths the response.
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What is the first-line antiemetic in Parkinson's disease?
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Domperidone.
Why? Domperidone is a peripheral D2 antagonist that does not cross the blood-brain barrier, so it does not worsen parkinsonism.
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What is the first-line drug for hallucinations or psychosis in Parkinson's disease (without dementia) after reducing contributing drugs?
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Quetiapine.
Why? Quetiapine has weak D2 blockade, so it worsens motor symptoms less. Clozapine is second-line, with blood monitoring for agranulocytosis.
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When is a DaTscan (dopamine transporter SPECT) used in suspected Parkinson's disease?
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When the diagnosis is uncertain, e.g. to distinguish PD from essential tremor or drug-induced parkinsonism.
Why? PD shows reduced uptake in the posterior putamen. DaTscan is normal in drug-induced parkinsonism and essential tremor. PD is otherwise a clinical diagnosis.
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A 66-year-old has early unexplained backward falls, symmetrical bradykinesia and rigidity, and difficulty looking down when reading or using stairs. Levodopa gives little benefit. What is the most likely diagnosis?
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Progressive supranuclear palsy (Steele-Richardson-Olszewski syndrome).
Why? PSP is a tauopathy. Vertical (downgaze first) supranuclear gaze palsy and early falls are hallmarks. MRI may show midbrain atrophy (the "hummingbird" sign).
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Name three drug classes or drugs that cause drug-induced parkinsonism.
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Antipsychotics, metoclopramide (and prochlorperazine), and sodium valproate.
Why? Dopamine blockade produces symmetrical parkinsonism with little tremor. DaTscan is normal. Treatment is to stop the drug.
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What is the first-line drug for essential tremor?
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Propranolol.
Why? Essential tremor is a bilateral postural or action tremor, often familial (autosomal dominant), that improves with alcohol.
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Which drug is used to treat chorea in Huntington's disease?
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Tetrabenazine (a dopamine-depleting drug, VMAT2 inhibitor).
Why? Depleting presynaptic dopamine reduces the hyperkinetic movements. Antipsychotics are an alternative.
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What specific drugs are used in neuroleptic malignant syndrome, after stopping the causative drug?
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Dantrolene (and bromocriptine), alongside IV fluids and supportive care.
Why? Dantrolene stops calcium release from the sarcoplasmic reticulum, which reduces rigidity. Bromocriptine replaces dopamine activity.
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What is the mechanism of selegiline and rasagiline?
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MAO-B inhibitors: they reduce the breakdown of dopamine in the brain.
Why? They give mild symptomatic benefit in early PD, or reduce wearing-off as add-ons.
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What is the mechanism of entacapone and opicapone, and when are they used?
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COMT inhibitors: they reduce peripheral breakdown of levodopa. Used as add-ons for end-of-dose wearing-off.
Why? More levodopa reaches the brain and each dose lasts longer.
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Parkinson's disease with sudden, unpredictable 'off' periods: what is the rescue therapy?
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Subcutaneous apomorphine (a dopamine agonist).
Why? It acts within minutes. It can be given as intermittent injections or as a continuous infusion.
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What is the first-line drug treatment for Parkinson's disease dementia?
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An acetylcholinesterase inhibitor such as rivastigmine; memantine if not tolerated.
Why? Dementia appearing more than a year after motor symptoms suggests PD dementia rather than dementia with Lewy bodies.
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Which drug is first-line for postural hypotension in Parkinson's disease, after reviewing medications?
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Midodrine.
Why? Midodrine is an alpha-1 agonist that raises vascular tone. NICE says consider it after reviewing drugs that lower BP (e.g. antihypertensives and diuretics; dopaminergic drugs can also lower BP). Fludrocortisone is sometimes used as an alternative.
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What happens if a dopamine agonist is stopped abruptly, and how is it avoided?
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Dopamine agonist withdrawal syndrome (anxiety, pain, depression, drug craving); avoid by tapering gradually.
Why? This often arises when an agonist is stopped because of impulse control disorders. Reinstate the drug if symptoms are intolerable.
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A man on sertraline is started on tramadol. Within hours he is agitated, sweaty and febrile, with dilated pupils, hyperreflexia and clonus in the legs. What is the diagnosis, and which drug is used in severe cases?
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Serotonin syndrome; cyproheptadine (a 5-HT2A antagonist).
Why? Stop the serotonergic drugs and give supportive care with benzodiazepines and IV fluids.