The present study explored the associations of actigraphy-derived rest-activity patterns and circadian phase parameters with clinical symptoms and level 1 PSG results in 75 patients with chronic insomnia at a sleep clinic. Exploratory correlation analyses revealed significant associations of actigraphy-derived circadian phase parameters (L5 and M10 onset times) with insomnia severity and level 1 PSG parameters such as AHI or REM latency. The 75 subjects were further categorized into two groups based on rest-activity patterns or circadian phase using data-driven hierarchical clustering analysis. The analysis revealed that participants with poorer rest-activity patterns (low IS and high IV) exhibited higher insomnia severity scores compared to participants with better rest-activity patterns (high IS and low IV). In addition, late-phase participants (late L5 and M10 onset times) exhibited higher insomnia severity scores, longer sleep latency, longer REM latency, and lower AHI compared to early-phase participants (early L5 and M10 onset times). These associations remained significant even after adjusting for potential covariates including age, sex, BMI, and lights-off time.
There are several implications that arise from the present study. We did not identify strong relationships between actigraphy-derived rest-activity pattern parameters (IS and IV) and level 1 PSG results in patients with chronic insomnia. IS and IV are the most well-described rest-activity pattern parameters that measure the similarity of one 24-hour period to the next and the strength of consolidation of the rest-activity rhythm within a 24-hour period, respectively. Several studies have reported possible associations of IS and IV with the differential diagnosis, severity, and pathophysiology of diseases such as Alzheimer’s disease, Parkinson’s disease, bipolar disorder, and posttraumatic stress disorder.8,9 Changes in rest-activity patterns and circadian rhythm disruptions have been suggested to play pathophysiological roles in these conditions11,22 as well as in the initiation and progression of insomnia disorder.12,22−24 In the present study, we only identified a weak nonparametric positive association between IV and REM latency. However, following categorization of participants into two groups based on IS and IV (Group 1 and Group 2), no significant difference in REM latency was observed between the two groups (data not shown, P = 0.07, Mann-Whitney U test). In addition, other major level 1 PSG parameters such as TST, SL, WASO, N1/N2/N3/REM proportion, and AHI were not significantly associated with IS or IV. These findings are not entirely unexpected given the multifactorial pathophysiology of insomnia disorder.25,26 Although there is currently no consensus on the proportion of insomnia patients with circadian rhythm disruptions, the normal distribution of IS and IV parameters in our study suggests that only a subset of patients with chronic insomnia have abnormal rest-activity patterns and circadian rhythms. Another possibility is that actigraphy-derived rest-activity pattern parameters (IS and IV) are factors independent of insomnia severity, regardless of PSG parameters. Indeed, there is a discrepancy between objective measurements of sleep and subjective insomnia.27 This common misperception of sleep in patients with insomnia is problematic because patients perceive that they are getting insufficient sleep. Therefore, patients with insomnia that have sleep misperception might tend to spend more time on sleep than necessary, even during the daytime, which could result in inappropriate and irregular rest-activity patterns.
Participants with late circadian phase on actigraphy (Group L) presented with more complaints regarding insomnia symptoms and longer sleep and REM latency in PSG. Although this association may seem obvious, our findings have important clinical implications for the performance and interpretation of PSG in sleep clinics. The ecological validity of PSG has been questioned due to the disparity between the specialized environment required for level 1 PSG and patients’ home setting. For example, longer sleep or REM latency on PSG is typically considered to indicate difficulties with sleep initiation in the daily lives of patients. However, it could also be due to delayed circadian phase or discomfort induced by the numerous devices required for level 1 PSG on the day of assessment. Differentiating these factors in clinical practice is critical, but may be challenging due to limited information about the patients’ circadian phase or degree of discomfort in PSG. In the present study, actigraphy-derived circadian phase was calculated, revealing that patients with delayed circadian phase had more abnormal sleep and REM latency based on conventional cut-off scores. Thus, our findings imply a possible adjunctive role of actigraphy-derived circadian phase information for the performance and interpretation of PSG. For instance, patients with early circadian phase on actigraphy but abnormal sleep and REM latency on PSG may have more severe sleep initiation difficulties in daily life or feel more uncomfortable during PSG. In contrast, for patients with delayed circadian phase on actigraphy, our findings suggest that sleep physicians should assess patients’ PSG lights-off time based on patients’ routine sleep schedule reports and actigraphy-measured circadian phase before PSG. Theoretically, PSG lights-off time should be consistent with patients’ routine sleep schedule. However, in clinical practice, there may be discrepancies between PSG lights-off time and patients’ routine sleep schedule or circadian phase due to limited and imprecise information reported by patients. We conjecture that actigraphy-measured circadian phase may provide additional adjunctive information to sleep physicians for deriving plans for PSG lights-off time. In addition, sleep difficulties of patients with delayed circadian phase on actigraphy and abnormal sleep and REM latency on PSG may be due to initiation of sleep that is too early for patients’ circadian phase. Indeed, Flynn-Evans et al. analyzed dim light melatonin onset (DLMO) with sleep logs in 79 patients with insomnia and reported that a substantial proportion (10–22%) of patients with insomnia initiated sleep too early for their circadian phase.28 For these cases, reassessing circadian rest-activity phase in daily life and applying chronotherapy, melatonin, and/or timed light exposure are potential options for addressing sleep difficulties.29–31
Finally, participants with early circadian phase on actigraphy (Group E) exhibited a slightly higher AHI on PSG. This group difference could be caused by confounding factors. Indeed, participants in Group E were older than subjects in Group L (mean age of 60.6 and 53.7 years in Groups E and L, respectively), but no differences in sex or BMI were noted. However, after adjusting for possible covariates including age, subjects in Group E were still significantly more prone to have abnormal AHI on PSG. One large epidemiologic sleep study reported increased AHI values in morning- and evening-type individuals after stratifying the sample by BMI and age.32 The association between higher AHI values and early circadian phase observed in our study may reflect the protective role of a normal circadian phase in obstructive sleep apnea severity.
This study has several limitations. This study was conducted using a relatively small sample size. In addition, it should be noted that participants in our study were predominantly middle-aged to older adults. These points may limit the generalizability of our results at a population level. Furthermore, our study was cross-sectional; hence, causal relationships could not be conclusively demonstrated.
In conclusion, this study investigated the associations of actigraphy-derived rest-activity patterns and circadian phase with level 1 PSG results in patients with chronic insomnia. Our analysis revealed that participants with poorer rest-activity patterns (low IS and high IV) on actigraphy assessment exhibited higher insomnia severity scores compared to subjects with better rest-activity patterns (high IS and low IV). In addition, late-phase participants (late L5 and M10 onset times) exhibited higher insomnia severity scores, longer sleep latency, longer REM latency, and lower AHI compared to early-phase participants. Notably, these associations remained significant even after adjusting for covariates. We highlight the clinical implications and the possible adjunctive role of actigraphy-derived rest-activity patterns and circadian phase parameters for the performance and interpretation of PSG in patients with insomnia. Future studies using a larger sample size and repeated assessments of actigraphy and PSG are warranted.