Safinamid Levodopa Terapisine Eklem, Orta Vadeli Parkinson Hastalığında Levodopa İndüklenmiş Diskinezilerin Tamamen Kaybolmasına Yol Açıyor: Bir Olgu Raporu

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Safinamide is a reversible monoamine oxidase-B inhibitor approved as add-on to levodopa for the management of motor fluctuations in Parkinson’s disease (PD). Beyond dopaminergic modulation, it also inhibits abnormal glutamate release, a mechanism implicated in the pathophysiology of levodopa-induced dyskinesias (LID). Clinical evidence of this potential, however, remains scarce.A 65-year-old woman with a 7-year history of PD complicated by truncal LID and end-of-dose motor fluctuations underwent comprehensive baseline assessment. Hourly MDS-UPDRS-III and UDysRS-III–IV scores were collected over a 12-hour observation period during stable levodopa/benserazide (200/50 mg q4h) therapy. Safinamide was subsequently initiated at 100 mg/day, and the same protocol was repeated after three months. At baseline, motor scores improved two hours post-dose during each interval (mean MDS-UPDRS-III: 24.3) but were consistently accompanied by troublesome trunk dyskinesias (mean UDysRS-III: 16.3; UDysRS-IV: 13.5). At four hours post-dose, dyskinesias lessened (mean UDysRS-III: 7; UDysRS-IV: 8) while parkinsonism worsened (mean MDS-UPDRS-III: 33.6). After three months of safinamide, two-hour post-dose motor scores were maintained (mean: 21.6), four-hour scores improved (mean: 24), and dyskinesias resolved across all intervals (mean UDysRS-III: 2.3; UDysRS-IV: 0). These findings support safinamide’s role in motor fluctuation control and suggest that glutamatergic modulation may underlie a clinically relevant antidyskinetic effect.

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