Pain
-
Radiographic knee osteoarthritis (OA) is a highly prevalent condition that has been the focus of a number of studies identifying factors that are prognostic of continued or worsening pain and function. Although prior prognostic studies have identified a number of demographic, physical, and psychological factors that are predictive of outcome, minimal focus has been placed on pain coping skills as prognostic factors, despite cross-sectional evidence suggesting that pain coping skills are associated with pain and function in knee OA. The present study reports on the use of pain coping skills as prognostic factors for changes in pain and/or function over a 1-year period. ⋯ Data from the Coping Strategies Questionnaire were compared against 1-year change in pain, function, or both, using established criteria for defining whether the patient got better, worse, or stayed the same over the 1-year period. Results revealed a significant effect for praying/hoping, increased behavioral activities, and pain catastrophizing as prognostic of pain outcomes; ignoring pain and praying/hoping were prognostic of function outcomes; and increased behavioral activities and pain catastrophizing were prognostic of a combined pain and function outcome. The findings provide important new evidence regarding the potential clinical relevance of a number of pain coping responses hypothesized to influence future pain and function in persons with arthritis.
-
Scientific evidence support the notion that migraine pathophysiology involves inherited alteration of brain excitability, intracranial arterial dilatation, recurrent activation and sensitization of the trigeminovascular pathway, and consequential structural and functional changes in genetically susceptible individuals. Evidence of altered brain excitability emerged from clinical and preclinical investigation of sensory auras, ictal and interictal hypersensitivity to visual, auditory and olfactory stimulation, and reduced activation of descending inhibitory pain pathways. ⋯ Also, structural and functional alterations include the presence of subcortical white mater lesions, thickening of cortical areas involved in processing sensory information, and cortical neuroplastic changes induced by cortical spreading depression. Here, we review recent anatomical data on the trigeminovascular pathway and its activation by cortical spreading depression, a novel understanding of the neural substrate of migraine-type photophobia, and modulation of the trigeminovascular pathway by the brainstem, hypothalamus and cortex.
-
There has been a tension between the needs of regulators and industry to demonstrate that interventions are effective and safe, and the needs of professionals to understand how well interventions will work for their patients, and patients to understand what might work for them as individuals. The custom has been to focus on statistical outcomes based on average results, but in-depth analysis based on outcomes obtained by individual patients demonstrates that few are average. ⋯ This changes how benefit and risk are seen; nonresponders should stop treatments that don't work and not, therefore, be exposed to risks, while responders have very large benefits to offset against rare but potentially serious harm. This alternative view, patient-centred and practice-orientated, has major implications for clinical practice, how and why we do clinical trials and how they are designed, how health economic evaluations are done, for decisions made by regulatory and other bodies, and for the theory and practice of evidence-based medicine.
-
The pain matrix is conceptualised here as a fluid system composed of several interacting networks. A nociceptive matrix receiving spinothalamic projections (mainly posterior operculoinsular areas) ensures the bodily specificity of pain and is the only one whose destruction entails selective pain deficits. Transition from cortical nociception to conscious pain relies on a second-order network, including posterior parietal, prefrontal and anterior insular areas. ⋯ Neuropathic allodynia has been associated with enhancement of ipsilateral over contralateral insular activation and lack of reactivity in orbitofrontal/perigenual areas. Although lack of response of perigenual cortices may be an epiphenomenon of chronic pain, the enhancement of ipsilateral activity may reflect disinhibition of ipsilateral spinothalamic pathways due to depression of their contralateral counterpart. This in turn may bias perceptual networks and contribute to the subjective painful experience.