Although chronic pain and depression commonly co-occur, causal relationships have yet to be established. A reciprocal relationship, with depression increasing pain and vice versa, is most frequently suggested, but experimental evidence is needed to validate such a view. The most straightforward approach would be a demonstration that increasing or decreasing depressed mood predictably modifies pain responses. The current experiment tested whether experimentally induced depressed and happy mood have differential effects on pain ratings and tolerance in 55 patients suffering from chronic back pain. Participants were randomly assigned to depressed, neutral (control) or elated mood induction conditions. They completed a physically passive baseline task prior to receiving mood induction, then a clinically relevant physically active task (holding a heavy bag) to elicit pain responses and tolerance. Measures were taken immediately after the baseline task and immediately after the mood induction to assess the changes in mood, pain ratings and tolerance before and after the experimental manipulation. Results indicate that the induction of depressed mood resulted in significantly higher pain ratings at rest and lower pain tolerance, whilst induced happy mood resulted in significantly lower pain ratings at rest and greater pain tolerance. Correlations between changes in mood on the one hand and changes in pain response and pain tolerance on the other hand were consistent with these findings. It is concluded that, in chronic back pain patients, experimentally induced negative mood increases self-reported pain and decreases tolerance for a pain-relevant task, with positive mood having the opposite effect.

It is recognized that the World Health Organization (WHO) analgesic ladder, while providing relief of cancer pain towards the end of life for many sufferers worldwide, may have limitations in the context of longer survival and increasing disease complexity. To complement this, it is suggested that a more comprehensive model of managing cancer pain is needed that is mechanism-based and multimodal, using combination therapies including interventions where appropriate, tailored to the needs of an individual, with the aim to optimize pain relief with minimization of adverse effects.

Clinical guidelines are statements that have been systematically developed and which aim to assist clinicians in making decisions about treatment for specific conditions, and promote best practice. They are linked to evidence and are meant to facilitate good medical practice. We are not aware of any guidelines for the safe practice of acupuncture in a conventional healthcare setting, yet they are necessary as acupuncture may be performed in a variety of settings and by a variety of healthcare professionals: doctors, nurses, physiotherapists, midwives, and non medically trained practitioners. These guidelines were developed for use in cancer patients, mainly for pain but also for some non-pain indications such as hot flushes. They are presented here as a template for other acupuncturists who are requested to provide policies for acupuncture treatment for cancer patients.This article includes a general review of the evidence on mechanisms, effectiveness and safety of acupuncture that is intended to be used in conjunction with the guidelines; and the guidelines themselves. An appendix includes instructions for self acupuncture. The guidelines contain sections on roles and responsibilities, criteria for acupuncture practice, indications for acupuncture, contraindications and cautions, acupuncture treatment, and review and audit. These guidelines set basic, minimum standards of care, and need reassessment and ongoing validation as further data and evidence accumulate.

It is recognized that the World Health Organization (WHO) analgesic ladder, whilst providing relief of cancer pain towards the end of life for many sufferers world-wide, may have limitations in the context of longer survival and increasing disease complexity. To complement this, it is suggested that a more comprehensive model of managing cancer pain is needed that is mechanism-based and multimodal, using combination therapies including interventions where appropriate, tailored to the needs of an individual, with the aim to optimize pain relief with minimization of adverse effects.

Mental defeat is a psychological construct that has recently been applied to characterize the experience of chronic pain. Elevated levels of mental defeat have been identified in patients with chronic pain, and while its presence distinguishes treatment seeking from non-treatment seeking individuals, the link between mental defeat and disability in chronic pain is yet to be established. The current study investigated the extent to which mental defeat is associated with pain-related interference, distress and disability. A total of 133 participants completed the Pain Self Perception Scale that assessed mental defeat in relation to pain. Moreover, the participants were asked to complete a set of questionnaires that measured pain interference, distress, disability and other demographic (age, body mass index), clinical (pain intensity) and psychological (catastrophizing, worry, rumination and health anxiety) predictors of disability. Mental defeat was found to be strongly correlated with pain interference, sleep disturbance, anxiety, depression, functional disability and psychosocial disability. These correlations remained significant even when pain intensity and demographic variables were partialled out. Relative to chronic pain patients with lower levels of mental defeat, those with higher levels of mental defeat reported greater degree of pain interference, distress and disability. In a series of regression analyses, mental defeat emerged as the strongest predictor of pain interference, depression and psychosocial disability, whereas catastrophizing was the best predictor of sleep interference, anxiety and functional disability. These findings suggest that mental defeat may be an important mediator of distress and disability in chronic pain. Theoretical and clinical implications are discussed.

No abstract

The endocrine effects of opioids used for the management of persistent pain are poorly understood by clinicians and patients, and hormone levels are rarely measured. It is recognized that opioids exert this effect via the hypothalamic-pituitary-gonadal axis. Additional effects on adrenal hormones, weight, blood pressure and bone density may also occur. Symptoms and signs of sex hormone deficiency occur in both men and women but are under-reported and are often clinically unrecognized. The potential effects of long term opioid therapy on the endocrine system should be explained to patients before opioid therapy is commenced. Monitoring of sex hormones is recommended; if there are deficiencies opioids should be tapered and withdrawn, if this is clinically acceptable. If opioid therapy has to continue, hormone replacement therapy should be initiated and monitored by an endocrinologist.

Diabetic painful neuropathy (DPN) is one of the most common causes of neuropathic pain. The management of DPN consists of excluding other causes of painful peripheral neuropathy, maximising diabetic control and using medications to alleviate pain. The precise relationship between glycaemic control and the development and severity of DPN remains controversial. In this context, drugs such as aldose reductase inhibitors, ACE inhibitors, lipid-lowering agents and alpha-lipoic acid (thioctic acid) may have a useful role to play. There is also evidence that a successful pancreatic transplant may improve symptoms over time, but the mainstay of management continues to be symptomatic control of pain with drugs. Evidence from placebo-controlled studies has shown that opioids, antiepileptic and antidepressant drugs together with capsaicin are effective for alleviating DPN. Tramadol and oxycodone have been shown to be effective in studies of limited duration but their adverse effects, such as constipation and physical dependency, may limit their usefulness as a first-line treatment for DPN. Of the antidepressant drugs, the tricyclic antidepressants have been shown to be effective for alleviating DPN. These medications are widely used but their anticholinergic and sedative properties may not be well tolerated by patients. There is also good evidence that the serotonin-noradrenaline reuptake inhibitor antidepressant drugs venlafaxine and duloxetine are effective for treating DPN. However, venlafaxine may cause cardiac dysrhythmias, and patients using this medication require careful cardiac monitoring. Duloxetine appears to be less cardiotoxic and is licensed in the US and EU for alleviating DPN. The gabapentinoid group of drugs, gabapentin and pregabalin, appear to be the most evidence-based of the antiepileptic drugs for treating DPN. Large placebo-controlled studies have been performed with both of these agents. For many patients, it is still unclear what advantages pregabalin has over gabapentin for DPN. Until better evidence emerges, the potential availability of less expensive generic formulations of gabapentin, together with greater experience with its use, favour gabapentin as the main antiepileptic drug for alleviating DPN. Topiramate, lamotrigine, sodium valproate and oxcarbazepine have been shown to be effective in smaller studies but do not have the same evidence base as the gabapentinoid group of drugs. Of the newer antiepileptic drugs, lacosamide appears to be the most promising for alleviating DPN. Capsaicin has the best evidence base of all the topical agents, but local anaesthetic patches may also have a useful therapeutic role. It is not possible to nominate a single drug as the first-line treatment for DPN and there is evidence that a low-dose combination of two or more drugs rather than a single agent may provide better symptomatic relief with fewer adverse effects. Further studies are necessary to clarify the best combination(s) of treatment for DPN.