The purposes of the study were to examine the psychosocial variables of hostility and social support, and their independent relationships with resting physiological levels and chronic pain symptoms, and to examine the independent relationships of chronic pain chronicity and social support with hostility.

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In this study, the use of hypnosis in the treatment of chronic low back pain is described in terms of Ecosystemic thinking, as opposed to traditional conceptualisations of hypnosis. Six case studies were used. Each is described in detail, as well as the therapeutic rationale behind each case, in order to present the reader with an understanding of the thinking behind using Ecosystemic hypnotherapy. / Psychology / M.A. (Psychology)

In this study, the use of hypnosis in the treatment of chronic low back pain is described in terms of Ecosystemic thinking, as opposed to traditional conceptualisations of hypnosis. Six case studies were used. Each is described in detail, as well as the therapeutic rationale behind each case, in order to present the reader with an understanding of the thinking behind using Ecosystemic hypnotherapy. / Psychology / M.A. (Psychology)

Nurses are at increased risk for job burnout, which can lead to psychological and physical problems, decreased quality of care, and premature exit from the profession. Studies have found common predictors of burnout in multiple service occupations, but there are important differences across settings. The current study used embedded mixed-method analyses to explore burnout in a sample of nurses that work with patients with chronic abdominal pain. Thirty-two nurses participated in focus groups and data analyses revealed the following six themes: negative pain beliefs, barriers to effective pain management, nurse empathy/compassion, moral distress, coping methods, and burnout. These themes were evaluated with proposed theoretical frameworks and the extant literature to build the Pediatric Chronic Pain Nurse Burnout model. The constructs in this model were then evaluated quantitatively via measures completed by 41 nurses. Analyses provided partial support for the model and highlighted areas for further evaluation of burnout in nursing.

Cancer-induced bone pain (CIBP), due to bony metastases, is a major clinical problem, significantly reducing quality of life in cancer patients. Current therapies often provide inadequate analgesia or unacceptable side effects. The aim of this thesis was to characterise behaviours of a preclinical model of CIBP and test novel analgesic interventions in this model. A secondary aim was to investigate the involvement of the N-methyl-D-Aspartate (NMDA) receptors and TRP channels (TRPM8, TRPV1 and TRPV4) in CIBP. Investigation of CIBP in a preclinical model may lead to better pain management in CIBP patients. The results presented here demonstrate that this model of CIBP develops behaviours that may be indicative of mechanical allodynia, thermal sensitivity, movement-evoked pain, ongoing pain and spontaneous pain. This suggests that this model reflects the clinical condition of CIBP, where patients suffer from constant background pain with spontaneous and movement-related breakthrough pain. In this study it was found that radiotherapy significantly attenuated movement-evoked pain and thermal sensitivity to 20°C and 40°C. XRT also significantly reduced anxiety and risk assessment behaviours (grooming behaviour and number of protected stretch attends) compared to untreated CIBP. Duloxetine attenuated CIBP-induced mechanical allodynia, thermal sensitivity to 40°C and movement-evoked pain, whereas S,S-reboxetine attenuated thermal sensitivity to 40°C but did not effect CIBP-induced mechanical allodynia or movement-evoked pain. In addition, CB 65 attenuated movement-evoked pain and thermal sensitivity to 40°C. A single dose of gabapentin did not attenuate CIBP-induced mechanical allodynia, thermal sensitivity to 40°C or movement-evoked pain. These studies confirm that the CIBP model shows characteristics and pharmacological sensitivities consistent with known and predicted mechanisms and validate it as a useful model for assessing potential new treatments proposed for use in patients. Behavioural results suggest that NMDA receptors containing the NR2A subunit are involved in CIBP-induced movement-evoked pain. This suggests that NR2A antagonists may be useful for treating CIBP-induced movement-evoked pain. Additionally, results show that there is increased expression of NR2A in the laminae I, II and III in the dorsal horn of the spinal cord. XRT treated animals also showed increased expression of NR2A in laminae I and II. The selective involvement of NR2A in CIBP is different to other chronic pain states, for example, neuropathic pain states that appear to involve the NR2B subunit. The TRPV1 antagonist AMG 9810 did not attenuate mechanical allodynia, thermal sensitivity to 40°C or movement-evoked pain. Interestingly, the TRPM8 agonist icilin attenuated movement-evoked pain, which suggests that icilin might be useful in the treatment of movement-evoked pain. The TRPV4 antagonist RN 1734 attenuated mechanical allodynia, thermal sensitivity to 40°C and movement-evoked pain in CIBP. This suggests RN 1734 may be useful in the treatment of mechanical allodynia, thermal sensitivity to 40°C and movement-evoked pain in CIBP. Results show that the expression of TRPV4 is increased in DRG ipsilateral to the cancerbearing tibia. In conclusion, these results show that the preclinical model of CIBP investigated in this thesis is suitable for testing novel analgesic interventions. This thesis identified some useful targets for the analgesic treatment of CIBP and results suggest that many different mechanisms contribute to CIBP. A point to consider is that any robust effective treatment may need to target all (or at least several) of these mechanisms.

Chronic non-specific low back pain (CNSLBP) is a widespread but poorly understood condition that places a substantial burden on the sufferer, health services and the wider economy. Existing approaches to management do not demonstrate impressive levels of effectiveness. There is growing evidence that CNSLBP is associated with significant alterations in central nervous system (CNS) structure and function, suggesting a possible role for the brain in the aetiology of the condition, and presenting a case for novel therapies which aim to treat CNSLBP by affecting brain function. One such potential therapeutic approach is non-invasive brain stimulation (NIBS). Following a literature review discussing the epidemiology and management of low back pain, the evidence for altered CNS function and the potential role of brain stimulation in CNSLBP and chronic pain generally this thesis includes 3 original scientific studies: (i) A Cochrane systematic review of the effectiveness of NIBS techniques for the treatment of chronic pain; (ii) A randomised double-blind exploratory study of transcranial direct current stimulation of the motor cortex in the treatment of CNSLBP; (iii) Is blinding to the stimulation condition maintained in trials comparing 2mA tDCS with sham stimulation? A randomised cross-over study. Results: There is limited existing evidence that some forms of NIBS may have a beneficial effect on chronic pain, though caution is warranted. Exploratory data from study 2 is not suggestive that tDCS to the motor cortex is effective for treating CNSLBP. Commonly used sham controls in trials of tDCS do not ensure adequate blinding, and so introduce a potential source of bias to the existing evidence base. Conclusion: Further research is required to establish the value of NIBS as a treatment for chronic pain and CNSLBP. Future research in tDCS will need to develop and employ fully validated sham controls to ensure adequate blinding. NIBS cannot currently be recommended for the treatment of CNSLBP.

As a major public health problem affecting more that 76.5 million Americans, chronic pain is one main reason why people seek medical attention. It is a pathological nervous system disorder that persists for months or years. Sensitization of nociceptive neurons in the dorsal horn of the spinal cord is crucial in the development of allodynia and hyperalgesia. The work presented in this thesis will focus on spinal protein kinase M zeta (PKMζ)-mediated plasticity and GABAergic disinhibition as spinal amplification mechanisms that orchestrate persistent changes in the dorsal horn of the spinal cord. As a result of central sensitization following peripheral nerve injruy, GABAergic disinhibition occurs due to an alteration in Cl- homeostasis via reduced KCC2 expression and function. Intrathecal administration of acetazolamide (ACT), a carbonic anhydrase inhibitor, attenuated neuropathic allodynia and spinal co-adminitation of ACT and midazolam (MZL), an allosteric modulator of the benzodiazepine class of GABAA receptors, synergistically inhibited neuropathic allodynia. Further studies concerning the impact of altered Cl-homeostasis via reduced KCC2-mediated Cl-extrusion capacity on the analgesic efficacy and potency of GABAA receptor agonist and allosteric modulators revealed that there is a differential regulation of the agonists and allosteric modulators at the GABAA receptor complex when Cl-homeostasis is altered. Another spinal amplification mechanism leading to central sensitization is PKMζ-mediated spinal LTP. In model of persistent nociceptive sensitization, allodynia induced by IL-6 injection or plantar incision was abolished by both the inhibition of protein translation machinery and PKMζ inhibitor, ZIP. However, only PKMζ inhibition prevented the enhanced pain hypersensitivity precipitated by a subsequent stimulus after the initial hypersensitivity had resolved, asserting that spinal PKMζ underlies the maintenance mechanisms of persistent nociceptive sensitization. Also, these results confirmed that the initiation mechanisms of persistent sensitization parallel LTP initiation mechanisms and the maintenance mechanisms of persistent sensitization parallel LTP maintenance mechanisms. Taken together, these results indicate that these amplification mechanisms drive a chronic persistent state in these models such that inhibition of these spinal amplication mechanisms will serve as an effective approach in the quenching chronic pain hypersensitivity in chronic pain models.