M. Tech. / Insomnia is defined as inadequate sleep due to difficulty falling asleep, difficulty staying asleep, waking up too early, and not being able to get back to sleep. In Western industrialised nations, between 30% and 40% of individuals suffer from at least occasional periods of sleep disturbance. The significance of sleep lies in its impact on the Central Nervous System as extended periods without sleep will result in disturbances in mental function. The remedy used in this study was Coffea cruda 200cH. This homoeopathic remedy is used clinically for its sedative and calming effect on the nervous system, in the homoeopathic treatment of insomnia. Although there is some research evidence that Coffea cruda has an effect on sleep in animals, there is no research on its effect on human subjects. The aim of this study was to determine the efficacy of a homoeopathic remedy Coffea cruda 200cH in the treatment of insomnia that is characterised with a difficulty in falling asleep. The quality of sleep was assessed in terms of duration of sleep, changes in sleep pattern, and satisfaction with sleep. This was a double blind placebo controlled study. The duration of the clinical trial lasted for four weeks. A total of thirty participants, meeting the inclusion criteria (Appendix B) were recruited via advertisements (Appendix E) in local newspapers, pamphlets and emails, sent in and around the University of Johannesburg Health Clinic, the University of Witwatersrand Sleep Unit, campuses, shopping malls and residential areas. Participants were also recruited via advertisements on a local radio station. At the initial consultation the participants were requested to sign a consent form (Appendix A). The researcher then completed the questionnaire (Appendix B) to assess suitability for the study. Participants were given a 50ml bottle of medication in liquid form, and were requested to shake the bottle and then take ten iv drops under the tongue just before going to bed, for four weeks. A homoeopathic pharmaceutical company blinded the medication. By selecting a medication, the participant automatically allocated themselves to either the experimental or control group. Participants were also given a sleep diary to be completed every morning (Appendix C). There were follow up visits with participants on the second and fourth week where the sleep diary was checked to improve compliance and a case history was taken (Appendix D). All results were compared to the initial assessment and changes were recorded. Data were analysed according to the General Linear Model: Repeated Measures, Mann-Whitney test (non-parametric test), Cross-tabulation, Fisher’s exact test and Regression Analysis. Statistical data proved that both the experimental and control groups had statistically significant results. It is unclear why the control group behaved in the same way as the experimental group. A longer trial is required to distinguish if this was purely due to the placebo effect.

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Insomnia disorder is a debilitating sleep disorder that impacts nearly 10% of Canadian adults. Cognitive Behavioural Therapy for insomnia (CBT-I) is a psychological treatment that targets cognitions and behaviours to improve sleep outcomes. CBT-I has been shown to be an effective treatment for insomnia symptoms; however, little is known about the cognitive and physiological underpinnings of the treatment response. This thesis examines correlates of cognitive, clinical, and biological markers of change across group CBT-I treatment. Specifically, we evaluated: (1) objective and subjective cognitive and psychosocial functioning, (2) discrepancies between objective and subjective measures of sleep, and (3) the relationship between a biological marker of stress and sleep parameters. The first study in this thesis investigated how objective and self-report measures of cognitive functioning, and psychosocial functioning changed across CBT-I. Findings illustrated that changes in self-report cognitive ability and psychosocial functioning were related to the improvements in insomnia symptom severity across treatment. The second study investigated the discrepancy between objectively measured sleep with actigraphy and self-reported sleep variables. Findings showed that the mismatch between objective and subjective sleep parameters decreased early on during the implementation of CBT-I. Additionally, improvement of clinical symptoms was related to a decrease in sleep discrepancies across treatment. In the third study, we examined if there was a relationship between a biological marker of oxidative stress across CBT-I. Results showed that following CBT-I, the biological marker was related to both objective sleep parameters and self-reported symptom improvement. Overall, this thesis demonstrates that in our well-characterized sample of adults with insomnia disorder, group CBT-I was associated with significant post-group changes in cognitive, clinical, and biological factors. This has important implications for the factors that may influence an individual’s treatment response to CBT-I, and thus lead to improvements in tailoring treatments to optimize outcomes for treatment of insomnia disorder. / Dissertation / Doctor of Philosophy (PhD) / Insomnia disorder is a sleep disorder that negatively affects day-to-day-functioning and is associated with poorer mental and health outcomes. Cognitive Behavioural Therapy for insomnia (CBT-I) is an established psychological treatment that focuses on changing sleep behaviours and thinking patterns for improving sleep. This thesis aimed to examine factors that may be related to how CBT-I works to improve sleep with both self-reported and objective measures. We investigated whether cognition (e.g., memory and attention), different measures of sleep, clinical symptoms, and biological factors associated with sleep changed across treatment with CBT-I. Results indicated that several self-reported measures of cognition and sleep improved across CBT-I. Our findings suggest that these variables were related to improvements in sleep following CBT-I. By understanding what factors may be contributing to sleep difficulties and change across CBT-I, we can improve treatment outcomes and better adapt treatment strategies to those struggling with insomnia disorder.

Previous research supports the efficacy of cognitive-behavioral therapy for insomnia (CBT-I) in patients with comorbid psychiatric diagnoses; however, questions remain about the effectiveness of CBT-I due to the fact that previous studies excluded patients with significant psychiatric symptoms and comorbid diagnoses. This study begins to address this gap in the insomnia literature by testing a five-session CBT-I intervention in a diverse sample of patients receiving mental health treatment in an outpatient psychiatry clinic (N=23) who continue to experience chronic insomnia despite receiving pharmacological treatment for sleep. Participants were randomized to CBT-I (n=13) or a treatment as usual control group (n=10). Following one week of baseline sleep diary assessment, those in the CBT-I group completed five sessions of individual treatment; three in-person and two by phone. Those in the treatment as usual group continued with medication treatment as prescribed by their psychiatrist for a five-week period and were then given the opportunity to cross over to receive CBT-I. Study results show that adding a brief CBT-I intervention to usual care led to significant improvements in sleep compared to treatment as usual. Effect sizes were generally large, illustrating the potency of CBT-I in a psychiatric sample. Sleep gains were largely maintained at two-month follow-up. No significant changes in depression or anxiety severity were seen in the CBT-I group, suggesting that sleep interventions alone may not have the same impact in a psychiatric population with more severe and chronic mental health symptoms. Quality of life in the area of social functioning was improved following CBT-I compared to treatment as usual; however, this gain was not maintained at two-month follow-up. Finally, CBT-I was not associated with a reduction in use of sleep medication. This may reflect this sample's high level of chronicity of insomnia or a propensity towards medication dependency. In sum, the findings of this study suggest that selected patients with complex and chronic psychiatric conditions can obtain sleep improvements with CBT-I beyond those obtained with pharmacotherapy alone. Future research should focus on identifying factors that predict which “real-world” psychiatric patients are most likely to undergo and benefit from CBT-I.

A double-blind comparison was conducted using typical doses of soporific agents from three drug classes and a placebo. Drugs which were used in the study included secobarbital, flurazepam hydrochloride, and thioridazine. Subjects were 40 outpatient volunteers whose primary complaint was difficulty in falling to sleep. Subjects were randomly assigned to one of the three drug groups or the placebo group. One of the drugs or the placebo was administered to each subject for 3 nights. Half of the subjects in each of the four groups were told the drug had caused any observed changes in their sleep behavior and were in this way led to attribute any changed sleep behavior externally to the drug. The other half were told the drugs were not typically used to treat insomnia and changes in their sleep were due to changes made in their own behavior, thus attributing any changes in sleep behavior internally. The implication for clinicians was that a short course of drug therapy using a placebo or one of several soporific drugs might be used equally effectively to treat primary latency insomnia. Additionally, the results demonstrated that clinicians might expect the effectiveness of treatment to be maintained following treatment. Recommendations included a suggestion for future research with soporific drugs in other classes.

Daytime cognitive performance and sleep/wake cycles are strongly interrelated, and cognitive dysfunction has been extensively investigated in relation to insomnia. However, methods and outcomes vary widely by study, making comparison difficult without more systematic evaluation. Review of the literature reveals discrepant findings for the relationship between both subjective and objective measures of cognitive performance and insomnia. The current meta-analysis included 42 studies investigating the relationship between insomnia and cognitive performance. Results confirmed the discrepant nature of previous findings and suggest that type of cognitive performance (e.g., simple attention, procedural memory, verbal functions) is important to consider when discussing the impact of insomnia. Mixed-effect meta-analysis of aggregate effect sizes suggest impairments in working memory, complex attention, and episodic memory are significantly associated with insomnia. Analysis of the grouped subjective cognitive performance effect size revealed no significant impact of insomnia. Average age and gender makeup of the sample, study quality, and type of insomnia measure (i.e., clinical or diagnostic criteria, validated scale, or single unvalidated item) did not consistently moderate findings. These results confirm the equivocal nature of the relationship between insomnia and cognitive performance. Overall, about 44% of the studies included in the analysis failed to use DSM or ICSD criteria when categorizing insomnia. Additionally, the cognitive measures used varied widely and certain measures may not be sensitive enough to detect the degree of cognitive deficit that may be present for individuals with insomnia. This indicates a need for the standardization of methods used when assessing both insomnia and cognitive performance to elucidate these relationships.

Accurate assessment of sleep-wake patterns is important for sleep researchers and clinicians. Actigraphs are low-cost, non-intrusive, wrist-worn activity detectors used to estimate sleep-wake patterns in a natural environment for several nights. Although actigraphy shows good sensitivity (sleep detection), it has consistently demonstrated poor specificity (wakefulness detection while lying in bed relatively motionless). Because insomnia is characterized by wakefulness in bed, actigraphy may not be a valid objective measure of wakefulness for this group. It is possible that refinement of actigraphy software settings for sleep/wake algorithms might improve specificity. The current studies investigated this hypothesis by comparing wake parameters from 48 combinations of actigraphy settings to determine which sleep/wake algorithms best inform insomnia diagnosis and treatment. In the first study, none of the 48 actigraphy setting combinations consistently discriminated between adults with insomnia (n = 69) and non-insomnia (n = 80) on all three wake parameters, and no setting clearly discriminated between groups for the composite variable, total wake time. Similarly, in the second study, no setting combinations consistently discriminated between adults treated for insomnia (n = 18) and controls with untreated insomnia (n = 26) on all three wake parameters. Although two setting combinations discriminated between groups for the composite variable, total wake time, the values were extreme which raises validity concerns. Therefore, no actigraphy setting recommendations can be made based on the current findings. This research offers insights about the effects of actigraphy software settings on actigraphy specificity as it pertains to the diagnosis and treatment of insomnia.

Thesis (M.Tech.: Homoeopathy)-Dept. of Homoeopathy, Durban Institute of Technology, 2005 xli, 193 p. : ill. ; 30 cm / The purpose of this double-blind placebo controlled study was to evaluate the efficacy of homoeopathic simillimum in the treatment of chronic primary insomnia.

Systematic Review: Chronic pain and insomnia are highly comorbid, and evidence suggests a reciprocal relationship between these. CBT-I has been shown to improve sleep in those with chronic pain, therefore the potential of improved sleep leading to improvements in pain symptoms is a possibility. This led to the question: Does CBT-I improve pain symptoms in those with chronic pain and insomnia? A systematic review of the literature was conducted resulting in eight papers regarding six studies. Evidence was moderate that CBT-I improved sleep and pain related disability, but did not improve self reported pain levels. This discrepancy between improvements in pain related disability and no changes in self-reported pain levels led to the research question for the empirical element of the current thesis. Empirical Element of Thesis Objective: Chronic low back pain (CLBP) is a common form of chronic pain that affects a large population each year. Chronic pain and insomnia are highly comorbid conditions, yet knowledge about how patients perceive their interaction is limited. This qualitative study aims to inform our understanding of the patient experience with particular reference to beliefs and attributions surrounding pain, poor sleep and their interaction. Methods: 11 outpatients from a chronic pain clinic were recruited who suffered CLBP as their main symptom, and who had subsequently developed insomnia as a result. Data were analysed using Interpretative Phenomenological Analysis (IPA). Results: Qualitative analysis produced five super-ordinate themes: 1) the privacy of pain and solitude of sleep; 2) sleep/pain interaction; 3) night-time thinking; 4) adjustment and acceptance; and 5) self-management. Discussion: The first three themes combine to create the individual experience of CLBP: the visceral, emotional experience; the pre-existing and shifting beliefs; and the thought content. Once this is in place, the individual can reflect on what this means to them, and through acceptance, move through to adjustment. The individual accepts elements of their current experience, but where they see the opportunity to take control, these adjustments are translated into actions relating to self-management. These themes suggest CBT-I should be adapted to include pain specific beliefs to form a CBT for Insomnia and Chronic Pain (‘CBT-CPI’).

Chronic neuropathic pain, epilepsy, depression and anxiety disorders have been treated successfully with pregabalin. Normal subjects, epileptics and patients with neuropathic pain to whom pregabalin was prescribed showed an improvement in objective and subjective sleep parameters. To determine if pregabalin’s sleep enhancing effect is an independent process, it is necessary to test pregabalin in primary insomniacs who do not have conditions that could be treated by pregabalin. My study was designed as a double blind, randomised, crossover, placebo controlled trial, with 50 milligrams of pregabalin or placebo was administered for eight consecutive nights. I performed polysomnographic recordings on eight female chronic primary insomniacs on five nights. Sleep recordings were performed prior to the intervention, and on the first night and eighth night of each treatment. Subjects filled out subjective scales at baseline and night eight of every treatment. While polysomnography and subjective scales showed that my subjects were insomniac, sleep variables during the pregabalin or placebo period were unchanged when compared to baseline. A daily dose of 50 mg pregabalin did not have any significant effects on either sleep architecture or subjective sleep variables in female chronic primary insomniacs.