The present study showed that the ESS score in our MSA patients was 6.2 ± 0.9. This ESS score was higher than the previously published score in Japanese healthy subjects (4.1 ± 0.3; n = 79; mean age, 67.0 ± 1.2)
. The prevalence of EDS in our MSA patients was 24%. This prevalence was similar to that reported in the SLEEMSA study
, which demonstrated that the prevalence of EDS in MSA patients (28%) was comparable to that in PD patients (29%), but the prevalence was higher than that in healthy subjects (2%). These findings raise the possibility that EDS is a common clinical feature in MSA patients despite the differences in ethnicity as well as in subtype
We also analyzed the effects of SDB and abnormal PLMS on EDS. Consistent with the results of previous studies
[6, 13], SDB was frequently observed in our study. A total of 24 patients (96%) met the criteria for SDB, and 56% of the patients met the criteria for severe SDB. The recent SLEEMSA study demonstrated the correlation between SDB, which was based on questionnaires, and EDS
. However, this study showed that there was no correlation between ESS scores and the parameters of SDB, which are AI, AHI, and mean SpO2 levels, in MSA patients, whereas SDB scores correlated with the EDS in patients with obstructive SAS in other studies
[14, 31]. These results suggest that SDB may not necessarily have a strong influence on EDS in MSA patients.
Although abnormal PLMS may be observed in MSA patients, there is no evidence that an increased prevalence of abnormal PLMS causes sleep disturbances and EDS in MSA patients. Vetrugno et al. reported that 15 of 18 patients with MSA (88%) presented with abnormal PLMS
. In the present study, the prevalence of abnormal PLMS was 44%, indicating that abnormal PLMS was frequently associated with MSA despite the differences in ethnicity, although it was less frequent than in the previous study
. We speculate that abnormal PLMS may not have a strong influence on EDS in MSA patients, because we did not find any significant correlations between the ESS scores and the indexes for PLM and PLM arousal. A lack of correlation between EDS and AHI or PLMS suggested an impairment of the normal sympathetic response to sleep apnea in MSA.
We showed that the disease duration and severity, impairments of cognitive or frontal function, as well as sleep quality that was evaluated by PSG, were not associated with EDS, while we identified a dose-dependent effect of antiparkinson drugs on EDS. Although this finding was not consistent with the SLEEMSA study, which showed a lack of correlation between the amount of dopaminergic treatment and EDS
, it suggests still another possibility that antiparkinson drugs may cause EDS, as is the case with PD
. However, because 84% of the patients in the present study had MSA-C, we were able to recruit only 11 patients who had been treated with antiparkinson drugs. In addition, it remains the possibility that there may be confounding factors that are correlated with EDS and LED, such as the disease severity and duration. Further studies should be performed in order to further investigate the effects of antiparkinson drugs on sleepiness in MSA patients.
As mentioned above, the major determinant of EDS in MSA patients remains unknown. It is possible that the involvement of the arousal system may be a determinant of EDS in patients with MSA. In addition, as has been reported for patients with Parkinson’s disease, several factors, such as depressive symptoms, hallucinations, psychosis, nocturia, and nocturnal motor symptoms, can be possible causes of the EDS in MSA patients
This study had several limitations. The first limitation of this study was that some of the subjects were administered a DA (3 patients) or an antidepressant (4 patients), and these medications can cause daytime sleepiness. The second limitation was the uncertainty over whether ESS is a suitable method for evaluating daytime sleepiness in MSA patients. This uncertainty may stem from the difficulty in ascertaining that MSA patients accurately rated their likelihood of falling asleep in some situations that they did not experience after disease progression. These limitations suggest the need for further investigations to determine objective sleep tests, such as a multiple sleep latency test, in MSA patients.