Metacognition is defined as the ability to reflect on one’s mental state and to govern thoughts and beliefs. Metacognitive dysfunctions are typical of several psychopathologic conditions, and also a feature of insomnia disorder, possibly playing a crucial role in its genesis and maintenance. In the context of insomnia, metacognition describes how individuals react to their own sleep-related thoughts and beliefs, boosting the hyperarousal state experienced by these patients. Up to now, no studies evaluated the effect of cognitive behavioral therapy for insomnia (CBT-I) on metacognitive functioning. Therefore, the aim of our study was to evaluate the effect of CBT-I administered in group format in patients with insomnia disorder. As expected, all patients showed significant improvements in both insomnia and sleep diary parameters after treatment. Furthermore, an improvement was observed also in dysfunctional metacognitive levels, assessed by means of the Metacognitions Questionnaire-Insomnia (MCQ-I). However, 63% of patients still showed a MCQ-I score above the clinical cutoff after treatment. Dividing the sample on the basis of MCQ-I questionnaire scores after CBT-I, we found that patients, who still presented metacognitive impairment, received significant beneficial effects from CBT-I both on insomnia symptoms and on dysfunctional beliefs, but not on dysfunctional metacognitive functioning. These findings suggest that metacognition should be carefully evaluated in insomnia patients and further studies are needed to evaluate long-term implications of this remaining dysfunction.

Introduction Metacognition is defined as the ability to reflect on one’s mental state. Literature showed that dysfunctional metacognitive activity (such as worry and rumination) plays an important role in insomnia genesis and maintenance. The aim of this study is (i) to evaluate metacognition differences between insomnia disorders (ID) patients and good sleepers (GS)and (ii) to assess Cognitive-Behavioral Therapy for Insomnia (CBT-I) effectiveness on both insomnia and metacognitive abilities. Methods We compared 27 GS (Insomnia Severity Index, ISI<10) (63.0% female, mean age 33±13.7yrs) and 27 ID patients (51.9% female, mean age 46.4±13.7yrs) evaluated both by ISI and Metacognition Insomnia Questionnaire (MCQ-I). ID patients underwent 7-session of group CBT-I and were evaluated pre- (T0) and post- (T1) treatment. Results GS and ID patients differed in MCQ-I total score (GS=105.6±20.5 vs ID= 138.1±26.2). All ID patients’ scores were above the clinical cutoff of 110. ID patients showed significant improvements both at ISI (T0=14.67±4.67 vs T1=7.07±4.37, p<0.001) and Sleep Diary parameters (T0 vs T1, p<0.05) as sleep latency, wake after sleep onset and sleep efficiency at T1. ID patients also showed an improvement of MCQ-I scores at T1, nevertheless, maintaining MCQ-I the mean score above the clinical cutoff level (MCQ-I_T0=138.1±26.2 vs MCQ-I_T1=123.7±28.6; p<0.05). Indeed, 29.6% of ID patients maintained equal or worse MCQ-I score at T1 compared to T0; 63% of ID patients still had a MCQ-I score above the clinical cutoff at T1. Conclusion CBT-I results effective on insomnia symptoms. Metacognitive dysfunctions appears to be a core feature in ID patients compared to good sleepers. Although the score reduction was significant after CBT-I, metacognitive dysfunction did not show remission after treatment possibly indicating the need of a specific intervention on this aspect. Metacognitive dysfunction in ID needs to be further investigated and may represent a new treatment target, in order to improve CBT-I effectiveness. Support (if any) None

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Introduction Cognitive-Behavioral Therapy for Insomnia (CBT-I) is considered the first-choice treatment for Insomnia Disease (ID). The bi-directional causal relationship between insomnia and depression is recognized. Aim of our study is to investigate the role of depressive symptoms in predicting CBT-I outcomes, and the effectiveness of the treatment both on insomnia and depression. Methods 77 ID patients (mean age 38.2±10.4 years, 69.2% females) underwent 7-sessions group CBT-I and were assessed pre- (T0) post- (T1) and at long-term after CBT-I (T2=7.6±1.6 years after treatment). The primary outcomes are Insomnia Severity Index (ISI) and Sleep Diary parameters. The secondary outcome is Beck Depression Inventory-II (BDI). Patients were divided in two groups according to BDI baseline score (≥14): depressive (D) vs non-depressive (ND). Results All patients showed significant improvements at ISI score at T1 that were maintained at T2 (T0=16.2±4.8 vs T1=8.2±4.5 vs T2=10.0±6.1;p<0.001). Also Sleep Diary parameters (sleep latency, wake after sleep onset and sleep efficiency) showed significant improvement at T1 (p<0.001). Moreover all patients showed improvements of depressive symptoms at T1 that were maintained at T2 (T0=10.8±6.8 vs T1=6.2±5.5 vs T2=8.2±6.6; p<0.001). Indeed, if 29.3% if ID patients at T0 presented clinically significant depressive symptoms (BDI≥14), only 9.7% at T1 and 20.5% at T2. Nevertheless, we found an interaction between ISI along time (T0-T1-T2) and D vs ND group membership (ISI_TREAT*BDI_BL_GROUP Sig=p<0.05). In other words, group D patients at baseline showed a worsening of insomnia symptoms at the long-term evaluation (T2). Conclusion CBT-I showed improvements both in insomnia and in depressive symptoms at the end of treatment that are maintained at long-term (7.6yrs after treatment). Nevertheless, clinically significant depressive symptoms at the baseline predicted a worsening of insomnia at the long-term evaluation. This could suggest the need of a more frequent follow-up evaluation of CBT-I efficacy in those patients presenting depressive symptoms at the baseline. Support (if any) None