레보도파 요법 중인 파킨슨병 환자의 인지장애 위험 인자 연구
Risk Factors for Cognitive Impairment in Patient with Parkinson’s Disease Treated with Levodopa
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Background: Long-term levodopa therapy relieves the motor dysfunction associated with Parkinson’s disease (PD), but has variouseffects on non-motor symptoms, including cognitive dysfunction, hallucinations, and affective disorders, and can exacerbate certainaspects of dementia-like cognitive dysfunction. Here, we investigated the relationship between levodopa treatment anddevelopment of dementia in patients with PD. Methods: This retrospective study analyzed 76 consecutive patients with PD who hadtaken levodopa between 2011 and 2015. The participants were initially free of dementia and had initial daily levodopa doses of below600 mg. Patients who did and did not develop comorbid dementia were compared in terms of potential predictor variables, includingPD onset age, sex, levodopa doses, and non-dementia comorbidities. Results: Of the 76 patients, 21 (27.6%) developed dementia,which was followed by hallucinations and insomnia. The independent predictors of incident dementia were PD onset age andsecond-year and third-year average levodopa doses that were higher than the first-year average levodopa dose. Patients whodeveloped dementia had significantly higher average daily levodopa doses and levodopa dose increases over the 6-year treatmentperiod than those who did not develop dementia. In addition, patients with higher levodopa doses were more likely to experiencehallucinations. Conclusion: These results suggest that increases in levodopa doses may be associated with a greater risk ofcognitive impairment in patients with PD. Therefore, motor and cognitive functions and levodopa dose increases should beevaluated regularly during long-term levodopa therapy in patients with PD.
Abstract
Background: Long-term levodopa therapy relieves the motor dysfunction associated with Parkinson’s disease (PD), but has variouseffects on non-motor symptoms, including cognitive dysfunction, hallucinations, and affective disorders, and can exacerbate certainaspects of dementia-like cognitive dysfunction. Here, we investigated the relationship between levodopa treatment anddevelopment of dementia in patients with PD. Methods: This retrospective study analyzed 76 consecutive patients with PD who hadtaken levodopa between 2011 and 2015. The participants were initially free of dementia and had initial daily levodopa doses of below600 mg. Patients who did and did not develop comorbid dementia were compared in terms of potential predictor variables, includingPD onset age, sex, levodopa doses, and non-dementia comorbidities. Results: Of the 76 patients, 21 (27.6%) developed dementia,which was followed by hallucinations and insomnia. The independent predictors of incident dementia were PD onset age andsecond-year and third-year average levodopa doses that were higher than the first-year average levodopa dose. Patients whodeveloped dementia had significantly higher average daily levodopa doses and levodopa dose increases over the 6-year treatmentperiod than those who did not develop dementia. In addition, patients with higher levodopa doses were more likely to experiencehallucinations. Conclusion: These results suggest that increases in levodopa doses may be associated with a greater risk ofcognitive impairment in patients with PD. Therefore, motor and cognitive functions and levodopa dose increases should beevaluated regularly during long-term levodopa therapy in patients with PD.
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