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TABLE 4 Demographic characteristics of patients as participants in phase 2 by randomisation group: PCAM vs doxepin 75mg sale anxiety xanax dosage. CAU Trial arm order doxepin 10mg mastercard anxiety level quiz, n (%) Demographic characteristics PCAM (maximum N = 43) CAU (maximum N = 34) Age (years) n = 43 n = 34 Mean (SD) 68 order 10mg doxepin with visa anxiety symptoms extensive list. CAU (continued) Trial arm buy cheap doxepin 75 mg anxiety yahoo, n (%) Demographic characteristics PCAM (maximum N = 43) CAU (maximum N = 34) Education n = 40 n = 33 HE/FE/higher school level 15 (37. Note Data completion rates were ≥ 83% and ≥ 78% for phases 1 and 2, respectively. Table 5 shows the self-reported health conditions of patients recruited to both phases. Although there are differences in the proportions having particular conditions, the overall levels of multimorbidity are similar across samples. Table 6 compares the same patient self-reported health conditions for patients in phase 2 by randomisation group (PCAM vs. There was a higher proportion of patients reporting higher levels of multimorbidity in the PCAM cohort. Additional data on the SIMD for the sample are included in additional tables (see Appendix 6, Tables 10 and 11). Patient-reported outcome data (Appendix 6, Tables 13–19) are also presented. This feasibility study was not powered to detect any significant changes in outcomes; its purpose was to estimate data completion rates, including completion rates for different outcome measures. However, if possible, some indication of whether or not an outcome measure was likely to be able to detect any change as a result of the PCAM intervention was also of interest. This issue may be freely reproduced for the purposes of private research and study and extracts (or indeed, the full report) may be included in professional journals 41 provided that suitable acknowledgement is made and the reproduction is not associated with any form of advertising. Applications for commercial reproduction should be addressed to: NIHR Journals Library, National Institute for Health Research, Evaluation, Trials and Studies Coordinating Centre, Alpha House, University of Southampton Science Park, Southampton SO16 7NS, UK. STUDY B: FEASIBILITY STUDY OF A CLUSTER RANDOMISED CONTROLLED TRIAL TABLE 5 Health-related characteristics of patients as participants in phases 1 and 2 Phase, n (%) Diagnosed with conditiona 1(N = 113) 2 (N = 77) High blood pressure 73 (64. Patients were asked to self-complete questions that were similar to, or reflected the main domains of, the PCAM tool, to see how they might assess themselves in relation to biopsychosocial concerns: these data are reported in Appendix 6, Tables 12 and 13. Table 7 shows the patient-reported biopsychosocial concerns (reflecting the PCAM domains) for participants in both phase 1 and phase 2, and Table 8 shows the same data for participants in phase 2 by randomisation group of PCAM or CAU. Data completion for these sets of questions was around 94%. Participants were most concerned about their health, followed by their lifestyle and their finances. Problems with daily activities and concerns about their social networks were also reported. Participants recruited by nurses in practices allocated to the PCAM arm had higher levels of concerns about daily activities, social networks and finances. CAU Trial arm, n (%) Diagnosed with conditiona PCAM (N = 43) CAU (N = 34) High blood pressure 30 (69. This issue may be freely reproduced for the purposes of private research and study and extracts (or indeed, the full report) may be included in professional journals 43 provided that suitable acknowledgement is made and the reproduction is not associated with any form of advertising. Applications for commercial reproduction should be addressed to: NIHR Journals Library, National Institute for Health Research, Evaluation, Trials and Studies Coordinating Centre, Alpha House, University of Southampton Science Park, Southampton SO16 7NS, UK. STUDY B: FEASIBILITY STUDY OF A CLUSTER RANDOMISED CONTROLLED TRIAL TABLE 8 Nurse demographic and clinical data by randomisation group: PCAM vs. CAU Trial arm Demographic and clinical data PCAM (N = 4) CAU (N = 3) Age (years) Mean (SD) 48. Note The completion rate was 100% for all seven nurses who participated in both the baseline and follow-up phases of the feasibility study. There were no apparent differences across phases or between PCAM and CAU cohorts. In Appendix 6, Tables 16 and 17 report on the WEMWBS, PEI and GHQ patient-reported outcomes. The percentages of participants completing follow-up outcome measures in phase 2 T1 are reduced because of the dropout rate of practice E. There was no apparent difference between measures on rates of completion. Although the study was not powered to observe any differences in outcomes, Table 17 in Appendix 6 presents an analysis of the outcome scores by randomised group. On the WEMWBS, the scores show a small reduction at follow-up (indicating worse mental well-being), but these are further reduced in the CAU arm. On the PEI, in which scores were also reduced in both trial arms, there was also a larger reduction observed in 44 NIHR Journals Library www. On the GHQ, in which reduced scores indicate an improvement in psychological morbidity, reductions were observed in both trial arms, with a larger reduction being observed in the PCAM arm. This might only very tentatively indicate that the PCAM tool might be likely to achieve more positive outcomes for patients than CAU, but this would require further testing on a larger sample. In Appendix 6, Tables 18 and 19 report on summary scores and subscales of the SF-12 for patient participants across phases and for phase 2 by randomised group. There were no differences observed between participants in phases 1 and 2, and no differences between PCAM and CAU cohorts from baseline to follow-up. Nurse participation information In total, 10 nurses provided data (Table 7), of whom seven participated from practices E, F, G and H in both phases, and had paired data available to summarise (Table 8). Practices E, G and J were randomised to the PCAM arm, and practices F and H were randomised to CAU. Practice K was enrolled but not randomised, and no phase 2 data were available. Practice J was enrolled, with two nurses recruited; however, no nurse data were provided. Nurse demographic and professional experience data were collected to indicate feasibility of data collection, and to test heterogeneity, which would affect a full trial. Table 8 shows the demographics of the nurse participants. Nurses in both arms were of a similar age group and sex (mostly female). The CAU nurses had been qualified for slightly longer, and those in the PCAM arm were more likely to have had some training in mental health in the past 5 years. Most nurses had used the Hospital Anxiety and Depression Scale (HADS) or the Patient Health Questionnaire – 9 (PHQ-9) depression screening tools. Additional nurse outcome data are presented Appendix 6, Tables 20–25, comparing nurses by randomisation group: PCAM versus CAU; however, numbers are too small to draw any conclusions from these data beyond completion rates. In these respects, the data show some slight improvements in nurses in the PCAM arm compared with the CAU nurses. This is the only discernible finding from these nurse outcome data. Table 24 in Appendix 6 presents nurse responses to questions about their perceptions of the care they deliver to patients and how patient centred they feel they are. Finally, Table 25 in Appendix 6, presents nurse responses to the DAQ. Conclusion The feasibility trial aimed to address the following questions: 1. Can we recruit and retain practices and nurses to take part in the study? This study has shown substantial difficulties in recruitment of practices (and, therefore, nurses) and significant retention problems for practices/nurses, which would indicate that any study would need to over-recruit the required number of practices and nurses by about one-third to account for potential practice/nurse attrition.

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It is less clear whether excess cognitive activity actu- crease at night purchase doxepin 10 mg visa anxiety 4th hereford cattle, decrease during the day buy doxepin 10 mg amex anxiety zantac, and are temporarily ally causes insomnia or is simply a byproduct of it generic 10mg doxepin with amex anxiety young child. Sleep apnea syndromes do not typically present with a for this type of arousal comes from electroencephalographic complaint of insomnia best doxepin 10mg anxiety 8 weeks postpartum. Several investigators have demonstrated that indi- within a syndrome of excessive daytime sleepiness, loud viduals with insomnia have reduced sleep propensity not snoring, breathing pauses during sleep, and obesity or crani- only at night, but also during the day. Conversely, individuals with advanced sleep phase positively with glucose metabolic rate in the medial orbito- syndrome complain of early morning awakening and sleepi- frontal cortex, a region implicated in both behavioral and ness in the evening hours. Jet lag and shift work sleep disor- electroencephalographic activation (29). Behavioral evi- ders are further examples of circadian sleep disorders that dence also supports the concept of increased cortical activity can present with insomnia problems. For in- Individuals who do not have other sleep disorders are stance, individuals with insomnia have better ability to recall diagnosed with primary insomnia. Such a model may involve rela- tive arousal in association with the insomnia complaint. One of the earliest and most enduring conceptualiza- tegrative neurobiological model of insomnia would involve tions of insomnia is that of psychophysiologic arousal. Overactivity together with other peripheral indicators of 'arousal. The ultimate goal of behavioral treatments for insomnia is to Caffeine is a stimulant and should be discontinued 4–6 hours help patients manage their sleep and sleep habits more effec- before bedtime. In addition to providing a safe alternative to pharma- Nicotine is a stimulant and should be avoided near bedtime and cotherapy, these nondrug treatments offer patients the po- on awakening. Alcohol is a depressant that can facilitate sleep onset, but can tential benefit of a greater sense of control over their sleep disrupt sleep later in the night. Most insomnia patients indicate that they would proximity to bedtime. A heavy meal too close to bedtime can interfere with sleep and Acomprehensive review of the efficacy of nonpharmaco- should be avoided. Data consistently indicated that approximately 70% to 80% of Adapted from Morin (1990). The magnitude of improvement was approximately 50%, with sleep latency reduced by about 30 minutes on average, from 60 to 30 minutes, and wake-time after sleep onset reduced from 70 to an individual has experienced the frustration of lying in bed 38 minutes. Subjective report of sleep quantity and quality being unable to sleep, anxiety develops about the ability to improved, based on sleep diary data. Relatively few studies sleep and the potential consequences of lack of sleep. This behavior and effort are incompatible with sleep, well maintained over at least 6 months (34). Good Sleep Practices (Sleep Hygiene The goal of stimulus control is to recondition cues such Education) as the bedroom and bedtime routine to elicit relaxation and sleep as opposed to anxiety, frustration, and wakefulness. Sleep hygiene education aims to promote environmental Stimulus control instructions are outlined in Table 133. Many of these behaviors are not intrinsically problem- Stimulus control requires effort and persistence, and often atic, but become detrimental to sleep if they are timed inap- leads to initial resistance and temporary worsening before propriately. For example, exercise too close to bedtime can improvement. Consistency and motivation are important cause physiologic arousal that can impair sleep onset, ingredients for a successful response. Quantitative reviews whereas exercise during the late afternoon or earlier evening of controlled intervention trials consistently support the ef- can have beneficial effects on sleep (35). Lifestyle factors ficacy of stimulus control therapy. There is no single stan- dard set of sleep hygiene recommendations; a sample of Lie down intending to go to bed only when you are sleepy. Do not watch commonly reported elements is included in Table 133. Get out of bed if you cannot fall asleep or go back to sleep within 10–15 minutes; return to bed only when you feel sleepy. Stimulus Control Therapy If you still cannot fall asleep, repeat the processing step as often Stimulus control techniques (36) are based on the premise as is necessary during the night. Set your alarm and maintain a regular arising time in the morning, that insomnia is exacerbated or maintained by a maladaptive irrespective of how much sleep you got during the night. Whatever the initial cause of the insomnia, when Adapted from refs. Chapter 133: Current and Experimental Therapeutics of Insomnia 1935 Sleep Restriction Therapy sense for some of the approaches to be combined, such as stimulus control and sleep restriction. The change in behav- Patients with insomnia often try to compensate for lost sleep ior advocated and the net result of each are similar, although by getting into bed early or remaining in bed after awaken- the rationales are different. Many individuals assume that bed rest can be accomplished with cognitive restructuring,can be may be restorative, even if no sleep is achieved. Unfortu- helpful for successful completion of any behavioral or cogni- nately, the excess time in bed results in increased wakeful- tive treatment. Effective, circumscribed, multicomponent ness in bed, which causes more frustration about difficulty therapies, such as that developed by Morin (39) combine sleeping and leads to even more pronounced insomnia. In- several different treatment approaches within a limited creased time awake in bed can thus contribute to condi- number of treatment sessions to treat insomnia. The treatments are integrated in a later session, and bed. Unlike stimulus control, sleep restriction addresses relapse prevention is addressed, promoting an overall focus only the amount of time one spends in bed, rather than how on self-efficacy. From the existing literature, it is not clear the time in or out of bed is spent. This approach involves an that such combined approaches are more effective than the initial curtailment of time in bed to the amount of time most effective of the individual techniques (e. Average sleep efficiency, which may have the added benefit of treating a broader range of represents the proportion of time in bed spent asleep, is patients without having to individualize treatment. After sleep efficiency reaches desired levels (typically 90%), time allowed in bed can be increased by increments of 15 minutes until desired total Other Nonpharmacologic Treatments sleep time at night is reached. If sleep efficiency remains Phototherapy low ( 80%), after the initial restriction, time in bed is further curtailed by 15-minute increments until sleep conti- As noted, insomnia associated with circadian rhythm sleep nuity improves sufficiently. Time in bed is not changed if disorders results from problems related to the timing of sleep efficiency is between 80% and 90%. Because light is the most potent zeitgeber, or time cue, for the circadian timing system, pho- totherapy can be used as part of a treatment regimen to Relaxation and Biofeedback Therapies adjust the timing of the sleep/wake cycle and address a corre- sponding complaint of insomnia and/or sleepiness. Relaxation techniques target the cognitive or physiologic Exposure to bright light shifts circadian phase in a time- arousal that interferes with sleep, as discussed. In general, bright light in the early relaxation therapies have been used for insomnia, including morning hours shifts sleep and circadian rhythms to an ear- progressive muscle relaxation and biofeedback to diminish lier time (i. Phototherapy can be deliv- ation treatments may be most useful for sleep onset insom- ered through artificial light, or by exposure to diffuse natural nia. In general, the magnitude of improvement seen with outdoor light. Artificial bright light has been shown to im- relaxation is smaller than for other behavioral approaches prove sleep maintenance insomnia in older adults (41) and (37).

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Serotonin transporter gene methylation is associated with hippocampal gray matter volume cheap doxepin 75 mg with amex anxiety poems. Dempster E doxepin 10mg visa anxiety symptoms over 100, Pidsley R buy doxepin 75 mg without a prescription anxiety and panic attacks, Schalkwyk L proven doxepin 75 mg anxiety symptoms 4-6, Owen S, Georgiades A, Kane F and Kalidini S. Disease- associated epigenetic changes in monozygotic twins discordant for schizophrenia and bipolar disorder. Nongeneomic transmission across generations of maternal behaiveor stress responses in the rat. DNA methylation signatures of mood stabilizers and antipsychotics in bipolar disorder. Stress and anxiety across the lifespan: structural plasticity and epigenetic regulation. Epigenetic regulation of gene expression: how the genome integrates intrinsic and environmental signals. Maternal plasma folate impacts differential methylation in an epigenome-wide meta-analysis of newborns. 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DNA methylation at the neonatal state and at the time of diagnosis etc. Perroud N, Salzmann A, Prada P, Nicastro R, Hoeppli M-E, Furrer S, Ardu S, Krejci I, Karange F and Malafosse A. Response to psychotherapy in borderline personality disorder and methylation status of the BDNF gene. The Tutsi genocide and transgenerational transmission of maternal stress: epigenetics and biology of the HPA axis. Non-coding RNAs as direct and indirect modulators of epigenetic regulation. Current Opinion in Clinical Nutritional and Metabolic Care 2012; 15: 330-335. Sex and diagnosis specific associations between DNA methylation of the oxytocin receptor gene etc. Biol Psychiatry Cogn Neurosci Neuroimaging 2016; 1: 141-151. Lasting epigenetic influence of early-life adversity on the BDNF gene. A role for histone acetylation mechanisms in adolescent alcohol exposure-induced deficits in hippocampal etc. Brain Struct Funct 2016 [Epub ahead of print] Schuch V, Utsumia D, Costa T, et al. Attention deficit hyperactivity disorder in the light of the epigenetic paradigm. Front Psychiatry 2015 [Epub ahead of print] Sun H, Maze I, Dietz D, et al. Morphine epigenomiclly regulates behaviour through alterations in histone H3 lysine 9 dimethylation in the nucleus accumbens. Abberant DNA methylation of rDNA and PRIMA 1 in borderline personality disorder. Tsankova N, Berton O, Rentha W, Kumar A, Neve R and Nestler E. Sustained hippocampal chromatin regulation in a mouse model of depression and antidepressant action. Weaver I, Champagne F, Brown S, Dymov S, sharma S, Meaney M, Szyf M. Reversal of maternal programming of stress response in adult offspring through methyl supplementation: altering epigenetic marking later in life. Genome-wide DNA methylation analysis of human brain tissue from schizophrenia patients. Yehuda R, Flory J, Bierer L, et al, Lower methylation of GR gene promoter 1F in peripheral blood of Veterans with PTSD. Holocaust exposure induced intergenerational effects on FKBP5 methylation. It promises to advance our understanding mankind in general and psychopathology in particular. Social functioning depends on managing social relationships. The necessary skills include ToM, recognition of social signals, social knowledge, emotion processing, attention, working memory and decision making (Green and Leitman, 2008). ToM refers to the ability to attribute mental states (such as thoughts, beliefs, desires and intentions) to people (yourself and others). In lay terms it roughly means “being able to tell” what other people are thinking and feeling. ToM has received attention, not only because it is fascinating, but also, because it is a new way of studying clinical conditions, particularly autism and schizophrenia, but also others (see below) The term, ToM, was first used by primatologists and psychologists Premack and Woodruff (1978) when they asked: “Does the chimpanzee have a theory of mind? Of greater importance at this point, is whether you have a ToM. It would be better if you had thought that Sally would think something which you knew to be wrong. ToM involves “thinking about people thinking about us”, and recognition/understanding, that others have minds like your own. In social situations, people with good ToM skills out manoeuvre those with poor ToM skills. And as mentioned, ToM dysfunction is a feature of some mental disorders. ToM is distinct from many cognitive functions, but how ToM and the executive functions are related is yet to be fully explained (Yeh, 2013; Mitchell R, Phillips, 2015). Various tests of ToM utilized different cognitive mechanisms (Ahmed & Miller, 2010). ToM can be viewed as having two components 1) cognitive ToM, which refers to the ability to make inferences about beliefs, thoughts, desires, motivations and intentions of others, and 2) empathetic/affective ToM, which refers to the ability to infer the feeling/emotions of others (Shamay-Tsoory et al, 2007). A recent fMRI study suggests that both cognitive and affective ToM are associated with activity in the superior temporal sulcus/temporo-parietal junction (STS/TPJ).

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