IM19.7-8 | Movement Disorder Investigation and Parkinson Therapy — Summary & Reflection

KEY TAKEAWAYS

Imaging in movement disorders — selection principles:
- Typical idiopathic PD: NO imaging needed for diagnosis (clinical)
- Atypical parkinsonism or uncertain tremor (ET vs PD): DAT-SPECT — abnormal (reduced) in PD/Parkinson-plus; normal in drug-induced parkinsonism and essential tremor
- Structural cause suspected, Parkinson-plus: MRI brain — hummingbird/penguin sign (PSP, sagittal T1), hot cross bun sign (MSA, axial T2 pons), basal ganglia T2 changes + face of panda (Wilson's), lacunar infarcts (vascular parkinsonism)
- DLB vs MSA: MIBG myocardial scintigraphy — reduced cardiac uptake in PD/DLB; preserved in MSA
- Wilson's confirmation: low ceruloplasmin + high 24-h urinary copper (>250 μg/24h) + liver biopsy copper >250 μg/g dry weight; KF rings on slit-lamp (virtually universal in neurological Wilson's)

Parkinson's pharmacotherapy:
- Levodopa/carbidopa: most effective; long-term complications: wearing-off (add COMT/MAO-B inhibitor), peak-dose dyskinesias (add amantadine), on-off (DBS). Interactions: non-selective MAOI (ABSOLUTE CI — hypertensive crisis); high-dose pyridoxine without DDI; protein meals (LNAA competition); AVOID D2-blocking antiemetics (metoclopramide)
- Dopamine agonists (pramipexole, ropinirole): direct D2/D3; monotherapy in young; watch impulse control disorders; sudden sleep attacks
- MAO-B inhibitors (selegiline, rasagiline): extend dopamine; pethidine = ABSOLUTE CI (serotonin syndrome); tramadol/SSRIs = caution
- COMT inhibitors (entacapone): adjunct to levodopa only; reduce wearing-off; diarrhoea; orange urine
- Anticholinergics (trihexyphenidyl): best for tremor; CONTRAINDICATED >70 years and in cognitive impairment — delirium/hallucinations
- Amantadine: NMDA antagonist; best evidence for reducing peak-dose dyskinesias; confusion, livedo reticularis; dose-reduce in CKD

REFLECT

Reflect on Mr Venkataraman's 5-year journey from diagnosis to wearing-off and peak-dose dyskinesias. His initial response to levodopa was excellent — this confirmed the diagnosis and was gratifying for both patient and physician. But the emergence of motor complications was an inevitable consequence of progressive nigrostriatal terminal degeneration combined with the short pharmacokinetic half-life of levodopa. How would you explain to Mr Venkataraman and his family that these fluctuations are not a sign of catastrophic disease worsening, but a predictable phenomenon that pharmacological strategies can substantially address? Now consider the drug interaction in Scenario C. The orthopaedic surgeon prescribing tramadol had no reason to flag the rasagiline interaction — but Mr Venkataraman's PD physician did. In a system where multiple specialists prescribe independently, whose responsibility is drug interaction checking — and what practical safeguards (medication reconciliation at each encounter, patient alert cards for dangerous interactions, pharmacist review) could have prevented this potentially fatal adverse event?