The epidemiology of chronic pain in Libya: a cross-sectional telephone survey.

BACKGROUND: Chronic pain is a public health problem although there is a paucity of prevalence data from countries in the Middle East and North Africa. The aim of this study was to estimate the prevalence of chronic pain and neuropathic pain in a sample of the general adult population in Libya. METHODS: A cross-sectional telephone survey was conducted before the onset of the Libyan Civil War (February 2011) on a sample of self-declared Libyans who had a landline telephone and were at least 18 years of age. Random sampling of household telephone number dialling was undertaken in three major cities and interviews conducted using an Arabic version of the Structured Telephone Interviews Questionnaire on Chronic Pain previously used to collect data in Europe. In addition, an Arabic version of S-LANSS was used. 1212 individuals were interviewed (response rate = 95.1 %, mean age = 37.8 ± 13.9 years, female = 54.6 %). RESULTS: The prevalence of chronic pain ≥ 3 months was 19.6 % (95 % CI 14.6 % to 24.6 %) with a mean ± SD duration of pain of 6 · 5 ± 5 · 7 years and a higher prevalence for women. The prevalence of neuropathic pain in the respondents reporting chronic pain was 19 · 7 % (95 % CI 14 · 6-24 · 7), equivalent to 3 · 9 % (95 % CI 2 · 8 to 5 · 0 %) of the general adult population. Only, 71 (29 · 8 %) of respondents reported that their pain was being adequately controlled. CONCLUSIONS: The prevalence of chronic pain in the general adult population of Libya was approximately 20 % and comparable with Europe and North America. This suggests that chronic pain is a public health problem in Libya. Risk factors are being a woman, advanced age and unemployment. There is a need for improved health policies in Libya to ensure that patients with chronic pain receive effective management

Colocalized Structural and Functional Changes in the Cortex of Patients with Trigeminal Neuropathic Pain

Background: Recent data suggests that in chronic pain there are changes in gray matter consistent with decreased brain volume, indicating that the disease process may produce morphological changes in the brains of those affected. However, no study has evaluated cortical thickness in relation to specific functional changes in evoked pain. In this study we sought to investigate structural (gray matter thickness) and functional (blood oxygenation dependent level – BOLD) changes in cortical regions of precisely matched patients with chronic trigeminal neuropathic pain (TNP) affecting the right maxillary (V2) division of the trigeminal nerve. The model has a number of advantages including the evaluation of specific changes that can be mapped to known somatotopic anatomy. Methodology/Principal Findings: Cortical regions were chosen based on sensory (Somatosensory cortex (SI and SII), motor (MI) and posterior insula), or emotional (DLPFC, Frontal, Anterior Insula, Cingulate) processing of pain. Both structural and functional (to brush-induced allodynia) scans were obtained and averaged from two different imaging sessions separated by 2–6 months in all patients. Age and gender-matched healthy controls were also scanned twice for cortical thickness measurement. Changes in cortical thickness of TNP patients were frequently colocalized and correlated with functional allodynic activations, and included both cortical thickening and thinning in sensorimotor regions, and predominantly thinning in emotional regions. Conclusions: Overall, such patterns of cortical thickness suggest a dynamic functionally-driven plasticity of the brain. These structural changes, which correlated with the pain duration, age-at-onset, pain intensity and cortical activity, may be specific targets for evaluating therapeutic interventions

A new instrument for pain assessment in the immediate postoperative period

Perceptual-cognitive impairment after general anaesthesia may affect the ability to reliably report pain severity with the standard visual analog scale (VAS). To minimise these limitations, we developed 'PAULA the PAIN-METER' (PAULA): it has five coloured emoticon faces on the forefront, it is twice as long as a standard VAS scale, and patients use a slider to mark their pain experience. Forty-eight postoperative patients rated descriptive pain terms on PAULA and on a standard VAS immediately after admission and before discharge from the postanaesthesia care unit. Visual acuity was determined before both assessments. The values obtained with PAULA showed less variance than those obtained with the standard VAS, even at the first assessment, where only 23% of the patients had regained their visual acuity. Furthermore, the deviations of the absolute VAS values in individual patients for each descriptive pain term were significantly smaller with PAULA than with the standard VAS

Human psychophysics and rodent spinal neurones exhibit peripheral and central mechanisms of inflammatory pain in the UVB and UVB heat rekindling models

ABSTRACT: The predictive value of laboratory models for human pain processing is crucial for improving translational research. The discrepancy between peripheral and central mechanisms of pain is an important consideration for drug targets, and here we describe two models of inflammatory pain that involve ultraviolet B (UVB) irradiation, which can employ peripheral and central sensitisation to produce mechanical and thermal hyperalgesia in rats and humans. We use electrophysiology in rats to measure the mechanically- and thermally-evoked activity of rat spinal neurones and quantitative sensory testing to assess human psychophysical responses to mechanical and thermal stimulation in a model of UVB irradiation and in a model of UVB irradiation with heat rekindling. Our results demonstrate peripheral sensitisation in both species driven by UVB irradiation, with a clear mechanical and thermal hypersensitivity of rat dorsal horn neurones and enhanced perceptual responses of human subjects to both mechanical and thermal stimulation. Additional heat rekindling produces markers of central sensitisation in both species, including enhanced receptive field sizes. Importantly, we also showed a correlation in the evoked activity of rat spinal neurones to human thermal pain thresholds. The parallel results in rats and humans validate the translational use of both models and the potential for such models for preclinical assessment of prospective analgesics in inflammatory pain states. KEY POINTS: Translational research is key to bridging the gaps between preclinical findings and the patients, and a translational model of inflammatory pain will ideally induce both peripheral and central sensitisation, more effectively mimicking clinical pathophysiology in some chronic inflammatory conditions. . We conducted a parallel investigation of two models of inflammatory pain, using ultraviolet B (UVB) irradiation alone and UVB irradiation with heat rekindling. We used rodent electrophysiology and human quantitative sensory testing to characterise nociceptive processing in the peripheral and central nervous systems in both models. . In both species, UVB irradiation produces peripheral sensitisation measured as augmented evoked activity of rat dorsal horn neurones and increased perceptual responses of human subjects to mechanical and thermal stimuli. . In both species, UVB with heat rekindling produces central sensitisation. . UVB irradiation alone and UVB with heat rekindling are translational models of inflammation that produce peripheral and central sensitisation, respectively.

COX2 in CNS neural cells mediates mechanical inflammatory pain hypersensitivity in mice

A cardinal feature of peripheral inflammation is pain. The most common way of managing inflammatory pain is to use nonsteroidal antiinflammatory agents (NSAIDs) that reduce prostanoid production, for example, selective inhibitors of COX2. Prostaglandins produced after induction of COX2 in immune cells in inflamed tissue contribute both to the inflammation itself and to pain hypersensitivity, acting on peripheral terminals of nociceptors. COX2 is also induced after peripheral inflammation in neurons in the CNS, where it aids in developing a central component of inflammatory pain hypersensitivity by increasing neuronal excitation and reducing inhibition. We engineered mice with conditional deletion of Cox2 in neurons and glial cells to determine the relative contribution of peripheral and central COX2 to inflammatory pain hypersensitivity. In these mice, basal nociceptive pain was unchanged, as was the extent of peripheral inflammation, inflammatory thermal pain hypersensitivity, and fever induced by lipopolysaccharide. By contrast, peripheral inflammation–induced COX2 expression in the spinal cord was reduced, and mechanical hypersensitivity after both peripheral soft tissue and periarticular inflammation was abolished. Mechanical pain is a major symptom of most inflammatory conditions, such as postoperative pain and arthritis, and induction of COX2 in neural cells in the CNS seems to contribute to this