Cognitive behavioral therapy for insomnia helps to reverse cognitive impairment in insomnia patients.

Introduction: Insomnia is the most common of sleep disorders, it induces a wide variety of organic symptoms, including somatic and cognitive impairments. There are pharmacological drugs nowadays that help diminish sleep impairments due to insomnia. However, most of them seem to be worsening cognitive impairments, benzodiazepine receptor agonists, in particular, seem to induce an even worst deterioration of cognitive function. On the other hand, cognitive behavioral therapy for insomnia (CBT-I) has shown to be a reliable tool to improve the whole picture of insomnia. Objectives: To analyze the effect of CBT-I on insomnia symptoms and cognitive performance in patients suffering from chronic insomnia. Material and Methods: Ten subjects with a diagnosis of insomnia and no pharmacological treatment were evaluated pre- and post-six biweekly sessions of CBT-I with two neuropsychological batteries, BANFE and NEUROPSI attention and memory. Results: CBT-I significantly improves both the symptoms of insomnia, measured subjectively with a sleep diary and the Athens insomnia scale, and the cognitive performance measured with the neuropsychological batteries. Discussion: CBT-I is not only an effective tool for the treatment of insomnia but also helps to ameliorate cognitive performance.

GABAA receptor agonist at the caudo-lateral peribrachial area suppresses ponto-geniculo-occipital waves and its related states.

PURPOSE: In order to explore the potential role of GABA, acetylcholine and glutamate in the caudo-lateral peribrachial area (C-PBL) over Rapid-Eye-Movement sleep (REM) onset and maintenance as well as on synchronized sleep with ponto-geniculo-occipital (PGO) waves (SP) in cats, a muscimol, carbachol and L-glutamate local application was performed and behavioral states were assessed. METHODS: Fourteen chronically implanted, adult, male cats underwent a 23 hour polysomnographic recording after 3 pharmacological manipulations: carbachol, muscimol and L-glutamate. Each cat received all three drugs randomly with a seven day interval. RESULTS: 1) Carbachol increases waking, SP and REM sleep while decreases slow wave sleep (SWS). 2) Muscimol decreases SP percentage and number while increases REM sleep onset. 3) Carbachol facilitates PGO activity and increases the latency to both SWS1 and REM sleep but enhances PGO activity while muscimol decreases it. CONCLUSIONS: Acetylcholine promotes PGO related states (SP as well as REM sleep), while GABA reduces only SP and specifically PGOs.

Update of sleep alterations in depression.

Sleep disturbances in depression are up to 70%. Patients frequently have difficulty in falling asleep, frequent awakenings during the night and non-restorative sleep. Sleep abnormalities in depression are mainly characterized by increased rapid eye movement (REM) sleep and reduced slow wave sleep. Among the mechanisms of sleep disturbances in depression are hyperactivation of the hypothalamic-pituitary-adrenal axis, CLOCK gene polymorphism and primary sleep disorders. The habenula is a structure regulating the activities of monoaminergic neurons in the brain. The hyperactivation of the habenula has also been implicated, together with sleep disturbances, in depression. The presence of depression in primary sleep disorders is common. Sleep disturbances treatment include pharmacotherapy or Cognitive Behavioral Therapy.