Journal
NEUROLOGICAL SCIENCES
Volume 43, Issue 1, Pages 357-364Publisher
SPRINGER-VERLAG ITALIA SRL
DOI: 10.1007/s10072-021-05324-w
Keywords
Parkinson's disease; Safinamide; Fluctuations; Behavioral symptoms; Urinary dysfunction
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Funding
- Universita degli Studi della Campania Luigi Vanvitelli
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In a 6-month study of 20 fluctuating PD patients, safinamide 50 mg treatment showed significant improvements in interest, motivation, urinary disturbances, fatigue, apathy, and motor fluctuations. This suggests that safinamide may not only improve motor symptoms, but also significantly reduce non-motor symptom burden in PD patients through non-dopaminergic mechanisms.
Introduction Parkinson's disease (PD) patients in chronic levodopa treatment may experience motor and non-motor fluctuations, which may affect their quality of life. Safinamide is a new monoamine oxidase B inhibitor, also exerting a non-dopaminergic effect, recently approved as add-on therapy in fluctuating PD patients. Methods We performed a longitudinal prospective study in a cohort of 20 fluctuating PD patients, to test whether safinamide 50 mg may improve non-motor, cognitive, and behavioral symptoms over a 6-month treatment period. At each timepoint, clinical features were assessed by means of validated PD-specific scales. Neuropsychological assessment was performed by exploring all five cognitive domains. Results Compared to baseline, significant improvement was found in PD patients at 6-month follow-up in items investigating interest (p = 0.02), motivation (p = 0.02), and urinary disturbances (p = 0.03). Moreover, neuropsychiatric assessment showed a significant decrease in fatigue and apathy scores (p = 0.02 and p = 0.01, respectively). Motor assessment revealed a significant reduction in the total wake-up time spent in OFF state (p = 0.01). Follow-up neuropsychological evaluation did not reveal any change compared to baseline. Conclusions Our data reveal that, along with motor fluctuation improvement, treatment with safinamide 50 mg may significantly decrease non-motor symptom burden in PD patients. Interestingly, non-dopaminergic mechanisms, such as glutamatergic overdrive, have been demonstrated to play a role in many pathways underlying these symptoms. Thus, we hypothesize that the neurotransmitter receptor-binding profile of safinamide may explain our findings.
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