Original articles

Abstract

Sleep disorders, such as insomnias, obstructive sleep apnoea, and central hypersomnias (narcolepsy, idiopathic hypersomnia), short sleep or sleep loss, and restless leg syndrome, are common disorders or complaints with a significant healthcare burden with consequences for healthcare contacts, medication use, education, employment and the risk of traffic accidents. There is now compelling evidence that the health-related (direct) and social (indirect) costs are significant, and comparable to those of other major disease areas. Thus, in order to care properly for patients presenting with sleep-related morbidity, and to reduce the consequential economic burden, accurate screening efforts and effective, cost-effective treatments need to be developed and employed. Disclosure: Nothing to disclose. Sleep disturbancies often precede the onset of psychiatric illnesses, and hence effects of risk genotypes on psychiatric disorders and mental health may be mediated by alterations in neurochemical systems that contribute to shaping the sleep patterns. This presentation will examine the associations of two psychiatric 'risk geno-types' with measures of sleep, relying in particular on data collected in a longitudinally observed population-representative sample, the Estonian Children Personality Behaviour and Health Study. The serotonin transporter promoter polymorphism (5-HTTLPR) that is associated with enhanced sensitivity of amygdala to stimuli with negative emotional valence and, in response to environmental adversities, with anxiety and affective disorders, had a complex relationship with sleep and psychiatric morbidity in this sample. We also studied the neuropeptide S receptor gene (NPSR1) A/T polymorphism (Asn 107 Ile), previously also associated with the development of anxiety and affective disorders in this sample (Laas et al., Int J Neuropsychopharmacol 2014, 17: 541-552). In animal experiments, higher NPS-ergic tone reduces sleep time. The human A/T exchange in NPSR1 affects receptor function so that the receptor encoded by the T-allele is more efficient in signal transduction. AA homozygotes, previously found to have higher prevalence of anxiety disorders, had higher frequency of sleep disturbances, especially if exposed to adverse family environment. No NPSR1 main effect on sleep duration was present; however, G 9 E interaction revealed that homozygotes (both AA and TT) slept less in adulthood if they had experienced adverse environment in adolescence. Conclusively, in this population-representative sample, genotype-related sleep problems precede genotype-related psychiatric disorders. Disclosure: Nothing to disclose. The mattress sensors provide unobtrusive means to diagnose sleep disorders. In Finland the big static charge sensitive bed (SCSB) has been replaced by smaller Emfit mattress in many laboratories. The Emfit sensor has been proven to produce similar signal as SCSB. Emfit sensor is suitable in detecting sleep apnea and periodic movements. In addition we have observed that increased negative intrathoracic pressure induces respiratory-related spikes to the Emfit signal. In some patients the respiratory induced spikes appear in sustained form, lasting up to several minutes, sometimes half an hour. In our sleep laboratory 10% of the patients were found to suffer from sustained Emfit spiking (increased respiratory resistance, IRR). We have shown that during IRR there is a sustained negative increase in the intrathoracic pressure and partial pressure of transcutaneus carbon dioxide presents a cumulative increase but arousals and apneas/hypopneas are sparse. However, the ESS scores between the OSA patients and the IRR patients did not differ and the GHQ-12 score of the IRR-patients was high as compared to OSA patients indicating more depressive mood. Previously IRR has been found to be more common among women than among men. We suggest that Emfit mattress provides an easy and patient friendly tool for diagnosing sleep apnea and some movement disorders. In addition it provides unobtrusive means to assess increased respiratory effort and thus adds information to full polysomnography, too. Disclosure: Nothing to disclose. Cognitive-behavioural treatment for insomnia should be approachable for large number of patients, considering the large prevalence of insomnia and the proven efficacy of CBT for insomnia in research settings. We developed a group training protocol in the footsteps of the Glasgow University manualized training program, consisting of 5 weekly 90 min sessions. Emotional state questionnaires, including Emotional State Questionnaire (EST-Q; Aluoja, Shlik) and sleep dysfunctional attitudes scales-Sleep Disturbance Questionnaire (SDQ) and Glasgow Content of Thoughts Inventory (GCTI), both by Glasgow University, and a locally developed sleep disorders questionnaire are filled on the 1st and 5th session. From January 2009 to 2014 29 training groups with 153 patients have finished training. The group therapy is applied by 2 mental health nurses, trained in sleep disorders, having preliminary CBT training, also performing independent outpatient visits, CPAP therapy, polysom-nography hookup and scoring, leading insomnia training courses for nurses. The centre also offers insomnia CBT courses for MD s and psychologists and teaches insomnia CBT for undergraduates. We shall review the results of the following study. Subjects: 94 consequtive participants from all groups, who have filled in the tests on both 1 and 5 th session. We aimed to evaluate if there is a significant change from 1st to 5th session in the parameters of the performed tests. Independent samples t-test was performed.