PH3.7 | PH3.7 | Antiparkinsonian and Neurodegenerative Disorder Drugs — SDL Guide — Summary & Reflection

KEY TAKEAWAYS

Parkinson's disease results from nigrostriatal dopamine neuron degeneration → dopamine-ACh imbalance → tremor/rigidity/bradykinesia. Treatment restores this balance: dopaminergic (levodopa+carbidopa — gold standard; carbidopa blocks peripheral DDC; MAO-B inhibitors: selegiline/rasagiline — no tyramine reaction; DA agonists: pramipexole/ropinirole — impulse control disorder risk; amantadine — reduces dyskinesias) or anticholinergic (trihexyphenidyl — first-line for drug-induced parkinsonism and tremor). Drug-induced parkinsonism (haloperidol, metoclopramide → D2 block) → treat with anticholinergics, NOT levodopa (D2 receptor is blocked, not depleted; levodopa worsens psychosis if antipsychotic is cause). Alzheimer's: AChEIs (donepezil, rivastigmine — mild-moderate) + memantine (NMDA antagonist — moderate-severe).

REFLECT

A 70-year-old woman with moderately advanced Parkinson's disease on levodopa/carbidopa 25/100 mg three times daily reports that over the past 6 months she has 'good hours and bad hours' — in the morning she is mobile and can dress herself, but by early afternoon she 'freezes' for 1-2 hours before the evening dose. Review the pharmacological explanation for this 'wearing-off' phenomenon. What pharmacological strategies (not just one) could you add to her regimen to smooth out her motor control? Consider the mechanisms of each option (COMT inhibitor, MAO-B inhibitor, dopamine agonist) and what additional ADR monitoring each would require.