Pain
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Nearly all amputees continue to feel their missing limb as if it still existed, and many experience chronic phantom limb pain (PLP). What is the origin of these sensations? There is currently a broad consensus among investigators that PLP is a top-down phenomenon, triggered by loss of sensory input and caused by maladaptive cortical plasticity. We tested the alternative hypothesis that PLP is primarily a bottom-up process, due not to the loss of input but rather to exaggerated input, generated ectopically in axotomized primary afferent neurons in the dorsal root ganglia (DRGs) that used to innervate the limb. ⋯ The suppression of PLP and npPLS could also be demonstrated using dilute lidocaine concentrations that are sufficient to suppress DRG ectopia but not to block the propagation of impulses generated further distally in the nerve. PLP is driven primarily by activity generated within the DRG. We recommend the DRG as a target for treatment of PLP and perhaps also other types of regional neuropathic pain.
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Patient ratings of satisfaction with their postoperative pain treatment tend to be high even in those with substantial pain. Determinants are poorly understood and have not previously been studied in large-scale, international datasets. PAIN OUT, a European Union-funded acute pain registry and research project, collects patient-reported outcome data on postoperative day 1 using the self-reported International Pain Outcome Questionnaire (IPO), and patient, clinical, and treatment characteristics. ⋯ Effects were highly consistent across centres and countries. We conclude that satisfaction with postoperative pain treatment is associated with the patients' actual pain experience, but more strongly with impressions of improvement and appropriateness of care. To the degree they desire, patients should be provided with information and involved in pain treatment decisions.
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Vulvodynia is a prevalent vulvovaginal pain condition that interferes with women's psychological health. Given the central role of sexuality and relationships in vulvodynia, relationship satisfaction may be an important moderator of daily partner responses to this pain and associated negative sequelae, such as depression. ⋯ Relationship satisfaction on the preceding day moderated the associations between partner responses and women's depressive symptoms in several significant ways: (1) On days after women reported higher relationship satisfaction than usual, their perception of greater facilitative male partner responses was associated with their decreased depression; (2) on days after women reported lower relationship satisfaction than usual, their perception of greater negative male partner responses was associated with their increased depression; (3) on days after men reported higher relationship satisfaction than usual, their self-reported higher negative responses were associated with decreased women's depression, and higher solicitous responses were associated with increased women's depression, whereas (4) on days after men reported lower relationship satisfaction than usual, their self-reported higher negative responses were related to increased women's depression, and higher solicitous responses were associated with decreased women's depression. Targeting partner responses and relationship satisfaction may enhance the quality of interventions aimed at reducing depression in women with vulvodynia.
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Urinary bladder pain is a primary symptom associated with interstitial cystitis/painful bladder syndrome. We used systemic injections of cyclophosphamide (CYP), an alkylating antineoplastic agent, to induce cystitis and examine the roles of 2 channels previously demonstrated to be required for inflammatory visceral hyperalgesia: transient receptor potential vanilloid-1 (TRPV1) and ankyrin-1 (TRPA1). Injection of CYP (100 mg/kg, i.p.) every other day for 5 days was accompanied by bladder edema and urothelial ulceration, but without significant plasma extravasation or infiltration of neutrophils. ⋯ Moreover, bladder hyperalgesia was reversed by acute treatment with the TRPA1 antagonist HC-030031 (300 mg/kg, i.p.). Our results indicate that CYP-induced bladder hyperalgesia can be induced without robust inflammation or changes in primary afferent TRPV1. However, significant changes were observed in TRPA1 expression, and blockade of TRPA1 alleviated CYP-induced bladder hyperalgesia.