OBJECTIVE: To investigate the effect of L-dopa on the PLM/h index of spinal cord injured subjects. SETTING: São Paulo, Brazil. METHODS:Thirteen male volunteers with spinal cord section between T7 - T12, and mean age of 31.6+/-8.3 years participated in the study. L-dopa or placebo were administered for 30 days, 1 h before the volunteers went to sleep, in a double blind, crossover design. Polysomnographic recordings were performed on ten occasions: Phase 1: Basal night, following an adaptation night at the sleep laboratory; phase 2: after 1, 7, 21 and 30 days of L-dopa administration; phase 3: first night of L-dopa or placebo withdrawal; phase IV: 1, 7, 21 and 30 days after placebo ingestion. RESULTS: The index of PLM/h on the first night of L-dopa or placebo withdrawal (phase III) was lower than on both the basal night and the first night of L-dopa treatment. At the time of polysomnographic analysis, volunteers were divided into two groups: index of PLM/h below five and those whose index was above five. Comparison between L-dopa and placebo treatments revealed that only those volunteers with an index above five revealed a reduction in PLM in L-dopa. CONCLUSION: These results indicate that despite the spinal cord lesions, L-dopa treatment is capable of minimizing PLM during sleep.
RCT Entities:
OBJECTIVE: To investigate the effect of L-dopa on the PLM/h index of spinal cord injured subjects. SETTING: São Paulo, Brazil. METHODS: Thirteen male volunteers with spinal cord section between T7 - T12, and mean age of 31.6+/-8.3 years participated in the study. L-dopa or placebo were administered for 30 days, 1 h before the volunteers went to sleep, in a double blind, crossover design. Polysomnographic recordings were performed on ten occasions: Phase 1: Basal night, following an adaptation night at the sleep laboratory; phase 2: after 1, 7, 21 and 30 days of L-dopa administration; phase 3: first night of L-dopa or placebo withdrawal; phase IV: 1, 7, 21 and 30 days after placebo ingestion. RESULTS: The index of PLM/h on the first night of L-dopa or placebo withdrawal (phase III) was lower than on both the basal night and the first night of L-dopa treatment. At the time of polysomnographic analysis, volunteers were divided into two groups: index of PLM/h below five and those whose index was above five. Comparison between L-dopa and placebo treatments revealed that only those volunteers with an index above five revealed a reduction in PLM in L-dopa. CONCLUSION: These results indicate that despite the spinal cord lesions, L-dopa treatment is capable of minimizing PLM during sleep.