Clinical Outcomes in Patients with Parkinson's Disease Treated with a Monoamine Oxidase Type‐B inhibitor: A Cross‐Sectional, Cohort Study

Abstract

Study ObjectiveTo evaluate the long‐term risk of developing cognitive symptoms (e.g., dementia, hallucinations), dyskinesia, falls, and freezing of gait (FoG) in patients with Parkinson's disease (PD) who received monoamine oxidase type B inhibitors (MAOB‐Is) compared with patients who had never received MAOB‐Is.DesignRetrospective, cross‐sectional, cohort study.SettingAcademic movement disorders clinic.PatientsOne hundred eighty‐one patients with idiopathic PD who were receiving MAOB‐I therapy on a long‐term basis for a minimum of 1 year (MAOB‐I current‐user cohort) and 121 patients with idiopathic PD who had never received MAOB‐I therapy (MAOB‐I never‐user cohort [control group]) between January 1, 1996, and November 30, 2011.Measurements and Main ResultsThe five study outcome variables were dementia, dyskinesia, falls, FoG, and hallucinations. Baseline and outcome data were collected from medical records. Patients in the MAOB‐I current‐user group were included only if absence of the specified outcomes was documented at baseline. Adjusted multiple logistic regression analyses were performed to calculate the odds ratios (ORs) for MAOB‐I use versus never use on clinical outcomes. MAOB‐I treatment was associated with a 44.7% reduced risk of dyskinesia (adjusted OR 0.553, 95% confidence interval 0.314–0.976, p=0.041), with the greatest risk reduction observed after 2 years of treatment. No significant association was noted with MAOB‐I use and development of dementia, falls, FoG, or hallucinations.ConclusionLong‐term use of MAOB‐I therapy was associated with reduced risk of dyskinesia in patients with PD.

Pharmacological treatment in Parkinson's disease: Effects on gait

“…These findings were in line with earlier work showing marginally faster gait speed in PD subjects on MAOB-I compared to placebo [82]. However, a more recent, retrospective study could not replicate a beneficial long-term effect of MAOB-I on FoG or fall risk [83]. In addition, clinical lore suggests that addition of a MAOB-I to a patient developing FoG does not reduce the symptom.…”

Biological and Clinical Implications of Comorbidities in Parkinson’s Disease

“…For example, monoamine oxidase inhibitors (MAOI), which enhance dopamine function, have shown positive effects in patients with treatment-resistant depression (Fawcett et al, 2016 ). Monoamine oxidase type B (MAOB) inhibitors have elicited neuroprotective effects in preclinical models of PD and longer exposure to these inhibitors have been associated with less clinical decline in PD patients (Hauser et al, 2017 ) and reduced risk of dyskinesia (Dashtipour et al, 2015 ). Early treatment with rasagline, another MAOB inhibitor, resulted in improvement in UPDRS scores thus showing promise as a neuroprotective agent in PD patients (Olanow et al, 2009 ).…”

Monoamine Oxidase Inhibitors—Revisiting a Therapeutic Principle

“…In 2009, the FDA expanded the indication for rasagiline from monotherapy and adjunct to levodopa to include adjunct to dopamine agonists. A recent cross-sectional cohort study reviewed the outcome of clinical MAO-B inhibitor investigation and demonstrated that MAO-B inhibitor therapy was associated with reduced risk of dyskinesia in patients with PD (Dashtipour et al, 2015). Currently, safinamide, approved in the EU, is waiting for regulatory approval as an add-on therapy to stable-dose levodopa, alone or in combination with other PD therapies in mid-to late-stage fluctuating PD patients (Deeks, 2015).…”