The journal of pain : official journal of the American Pain Society
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Recent data show that dry eye (DE) susceptibility and other chronic pain syndromes (CPS) such as chronic widespread pain, irritable bowel syndrome, and pelvic pain, might share common heritable factors. Previously, we showed that DE patients described more severe symptoms and tended to report features of neuropathic ocular pain (NOP). We hypothesized that patients with a greater number of CPS would have a different DE phenotype compared with those with fewer CPS. We recruited a cohort of 154 DE patients from the Miami Veterans Affairs Hospital and defined high and low CPS groups using cluster analysis. In addition to worse nonocular pain complaints and higher post-traumatic stress disorder and depression scores (P < .01), we found that the high CPS group reported more severe neuropathic type DE symptoms compared with the low CPS group, including worse ocular pain assessed via 3 different pain scales (P < .05), with similar objective corneal DE signs. To our knowledge, this was the first study to show that DE patients who manifest a greater number of comorbid CPS reported more severe DE symptoms and features of NOP. These findings provided further evidence that NOP might represent a central pain disorder, and that shared mechanistic factors might underlie vulnerability to some forms of DE and other comorbid CPS. ⋯ DE patients reported more frequent CPS (high CPS group) and reported worse DE symptoms and ocular and nonocular pain scores. The high CPS group reported symptoms of NOP that share causal genetic factors with comorbid CPS. These results imply that an NOP evaluation and treatment should be considered for DE patients.
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Diabetes mellitus (DM) has well known costly complications but we hypothesized that costs of care for chronic pain treated with opioid analgesic (OA) medications would also be substantial. In a statewide, privately insured cohort of 29,033 adults aged 18 to 64 years with DM and noncancer pain who filled OA prescription(s) from 2008 to 2012, our outcomes were costs for specific health care services and total costs per 6-month intervals after the first filled OA prescription. Average daily OA dose (4 categories) and total dose (quartiles) in morphine-equivalent milligrams were calculated per 6-month interval after the first OA prescription and combined into a novel OA dose measure. Associations of OA measures with costs of care (n = 126,854 6-month intervals) were examined using generalized estimating equations adjusted for clinical conditions, psychotherapeutic drugs, and DM treatment. Incremental costs for each type of health care service and total cost of care increased progressively with average daily and total OA dose versus no OAs. The combined OA measure identified the highest incremental total costs per 6-month interval that were increased by $8,389 for 50- to 99-mg average daily dose plus >900 mg total dose and, by $9,181 and $9,958 respectively, for ≥100 mg average daily dose plus 301- to 900-mg or >900 mg total dose. In this statewide DM cohort, total health care costs per 6-month interval increased progressively with higher average daily OA dose and with total OA dose but the greatest increases of >$8,000 were distinguished by combinations of higher average daily and total OA doses. ⋯ The higher costs of care for opioid-treated patients appeared for all types of services and likely reflects multiple factors including morbidity from the underlying cause of pain, care and complications related to opioid use, and poorer control of diabetes as found in other studies.
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Looking at one's own body might induce visual analgesia. However, the cognitive and physiological mechanisms underlying such visual analgesia are unknown. Because body and pain representations in the brain are multisensory, and have been reported to partially overlap, we herein investigated whether experimentally-induced changes in bodily self-consciousness (BSC) modulate pain. We measured physiological responses to pain (skin conductance response [SCR]) and the subjective experience of pain, under conditions of manipulated BSC. First we investigated whether looking at a virtual body that was associated with BSC (embodiment) reduced responses to pain, which revealed the effect of BSC on pain processing. Second, we manipulated the visual size of the virtual body during painful stimulation, a procedure known to modulate pain processing when used with biological bodies, but never studied with embodied avatars. We found reduced SCR in conditions of illusory embodiment, and a negative correlation between virtual body size and SCR, whereas subjective pain ratings were not affected by these manipulations. These results suggest that pain processing is modulated during illusory states of BSC and that these changes are greater for larger virtual bodies, which sustains that pain and its physiological mechanisms are associated with the bodily self, opening promising avenues for future pain treatments. ⋯ We show that BSC affects the processing of painful stimuli with induction of different levels of pain responses for embodied virtual bodies of different sizes. Our data reveal novel links between pain and self and suggest that embodied virtual bodies are a promising technique for future pain treatments.
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Osteoarthritis (OA) pain is most commonly characterized by movement-triggered joint pain. However, in advanced disease, OA pain becomes persistent, ongoing and resistant to treatment with nonsteroidal anti-inflammatory drugs (NSAIDs). The mechanisms underlying ongoing pain in advanced OA are poorly understood. We recently showed that intra-articular (i.a.) injection of monosodium iodoacetate (MIA) into the rat knee joint produces concentration-dependent outcomes. Thus, a low dose of i.a. MIA produces NSAID-sensitive weight asymmetry without evidence of ongoing pain and a high i.a. MIA dose produces weight asymmetry and NSAID-resistant ongoing pain. In the present study, palpation of the ipsilateral hind limb of rats treated 14 days previously with high, but not low, doses of i.a. MIA produced expression of the early oncogene, FOS, in the spinal dorsal horn. Inactivation of descending pain facilitatory pathways using a microinjection of lidocaine within the rostral ventromedial medulla induced conditioned place preference selectively in rats treated with the high dose of MIA. Conditioned place preference to intra-articular lidocaine was blocked by pretreatment with duloxetine (30 mg/kg, intraperitoneally at -30 minutes). These observations are consistent with the likelihood of a neuropathic component of OA that elicits ongoing, NSAID-resistant pain and central sensitization that is mediated, in part, by descending modulatory mechanisms. This model provides a basis for exploration of underlying mechanisms promoting neuropathic components of OA pain and for the identification of mechanisms that might guide drug discovery for treatment of advanced OA pain without the need for joint replacement. ⋯ Difficulty in managing advanced OA pain often results in joint replacement therapy in these patients. Improved understanding of mechanisms driving NSAID-resistant ongoing OA pain might facilitate development of alternatives to joint replacement therapy. Our findings suggest that central sensitization and neuropathic features contribute to NSAID-resistant ongoing OA joint pain.
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Catastrophizing is associated with negative outcomes in chronic pain and illness. The communal coping model (CCM) and cognitive behavioral (CB) formulations provide differing accounts of the function of catastrophizing in these contexts. In the present study we examined predictions from CCM and CB theoretical models in a sample of 116 patients with chronic fatigue to test (1) whether patient-reported solicitous responses from significant others mediate the relationship of catastrophizing with patient-reported pain and fatigue behaviors, as predicted by the CCM; and (2) whether pain and fatigue behaviors mediate the relationship of catastrophizing with solicitous responses, consistent with a CB model. This work is a secondary data analysis in which the strength of the indirect (i.e., mediating) effects among study variables was examined. Consistent with CB models, pain and fatigue behaviors were associated with catastrophizing and solicitous responses, and there was a significant indirect effect of catastrophizing on solicitous responses through pain and fatigue behaviors. Results were inconsistent with the CCM; catastrophizing was not significantly associated with solicitous responses, nor did solicitous responses mediate the relationship between catastrophizing and pain or fatigue behaviors. These findings highlight the importance of behavioral expressions of pain and fatigue in understanding the relationship of catastrophizing to solicitous responses in chronic fatigue. ⋯ This study of chronic fatigue patients tested CB and CCMs of catastrophizing, pain, and fatigue behaviors, and solicitous responses by significant others. Results were more consistent with CB formulations, which highlighted the importance of behavioral expressions of pain and fatigue in understanding the relationship of catastrophizing to solicitous responses.