Obstructive sleep apnea syndrome (OSAS) is associated with cognitive and functional deficits, most of which are corrected after positive airway pressure (PAP) treatment. Previous studies investigating the neural underpinnings of OSAS failed to provide consistent results both on the cerebral substrates underlying cognitive deficits and on the effect of treatment on these anomalies. The aims of the study were a) to investigate whether never-treated OSA patients demonstrated differences in brain activation compared to healthy controls during a cognitive task; and b) to investigate whether any improvements in cognitive functioning found in OSA patients after treatment reflected a change in the underlying cerebral activity. OSA patients and healthy controls underwent functional magnetic resonance imaging (fMRI) scanning. They were compared on performance and brain activation during a 2-back working-memory task. Patients were also re-evaluated after 3 months treatment with PAP. Cognitive functions were evaluated using neurocognitive tests. Sleepiness (ESS), mood (Beck Depression Inventory) and, quality-of-life (SF-36) were also assessed. The Sleep Disorders Center and CERMAC at the Vita-Salute San Raffaele University. 17 OSA patients and 15 age- and education-matched healthy controls. PAP treatment for 3 months. Compared to controls, never-treated OSA patients showed increased activations in the left frontal cortex, medial precuneus, and hippocampus, and decreased activations in the caudal pons. OSA patients showed decreases in activation with treatment in the left inferior frontal gyrus and anterior cingulate cortex, and bilaterally in the hippocampus. Most neurocognitive domains, impaired at baseline, showed significant improvement after treatment. OSA patients showed an overrecruitment of brain regions compared to controls, in the presence of the same level of performance on a working-memory task. Decreases of activation in prefrontal and hippocampal structures were observed after treatment in comparison to baseline. These findings may reflect a neural compensation mechanism in never-treated patients, which is reduced by effective treatment.
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.
Sleep State Misperception (SSM) is described as the tendency of Insomnia Disorder (ID) patients to overestimate Sleep Latency (SL) and underestimate Total Sleep Time (TST). Literature exploring topographical components in ID with SSM is scarce and does not allow us to fully understand the potential mechanisms underlying this phenomenon. This study aims to evaluate the existence of sleep EEG topography alterations in ID patients associated with SSM compared to Healthy Controls (HC), focusing on two distinct periods: the Sleep Onset (SO) and the whole night. Twenty ID patients (mean age: 43.5±12.7; 7M/13F) and 18 HCs (mean age: 41.6±11.9; 8M/10F) underwent a night of Polysomnography (PSG) and completed sleep diaries the following morning upon awakening. Two SSM indices, referring to the misperception of SL (SLm) and TST (TSTm), were calculated by comparing objective and subjective sleep indices extracted by PSG and sleep diary. According to these indices, the entire sample was split into 4 sub-groups: ID +SLm vs HC -SLm; ID +TSTm vs HC -TSTm. Considering the SO, the two-way mixed-design ANOVA showed a significant main effect of Groups pointing to a decreased delta/beta ratio in the whole scalp topography. Moreover, we found a significant interaction effect for the sigma and beta bands. Post Hoc tests showed higher sigma and beta power in anterior and temporo-parietal sites during the SO period in IDs +SLm compared to HC -SLm. Considering the whole night, the unpaired t-test revealed in IDs +TSTm significantly lower delta power during NREM, and lower delta/beta ratio index during NREM and REM sleep compared to HCs -TSTm. Finally, we found diffuse significant negative correlations between SSM indices and the delta/beta ratio during SO, NREM, and REM sleep. The main finding of the present study suggests that higher SL overestimation and TST underestimation are both phenomena related to diffuse cortical hyperarousal interpreted as a sleep state-independent electrophysiological correlate of the SSM, both during the SO and the whole night.