The journal of pain : official journal of the American Pain Society
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A growing literature has reported significant reductions in pain sensitivity associated with increasing levels of blood pressure. However, most of this research has been limited to casual blood pressure assessments in white men. The present study examined associations between pain reports and ambulatory blood pressure in a sample of African American and white men and women. Possible response bias during pain assessment due to ethnicity and gender was evaluated with individualized pain rating scales. One hundred thirty-five (72 African American and 63 white) men and women underwent 24-hour blood pressure monitoring and arm ischemia pain sensitivity evaluation with both standard verbal rating scales and individually ordered verbal rating scales of intensity and unpleasantness. Lower individualized pain intensity and unpleasantness ratings were associated with higher levels of ambulatory blood pressure. African Americans and women reported higher levels of pain intensity when using the standard verbal rating scale but not when using the individually ordered rating scale. Collectively, these results support previous research relating reduced pain sensitivity with increased blood pressure among men and women. Furthermore, reported differences in pain sensitivity between ethnic groups and genders might in part be associated with variations in response styles to standard pain assessment tools. ⋯ The findings of the present study suggest that, in some instances, different ethnic groups and genders may use the same descriptors to report different levels of pain. In the context of clinical pain assessment, it may be important to consider the possibility that descriptions of painful sensations reflect, in part, demographic characteristics.
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Clinical Trial
Catastrophizing predicts changes in thermal pain responses after resolution of acute dental pain.
Substantial research suggests that coping strategies, especially catastrophizing, play an important role in shaping adjustment to chronic pain. Although laboratory and clinical studies both suggest that catastrophizing enhances pain, the interaction of catastrophizing and clinical pain on pain sensitivity has received little attention. The present study evaluated the extent to which catastrophizing influenced laboratory thermal pain responses during and after the resolution of acute dental pain. Thermal pain threshold and tolerance, as well as self-reported catastrophizing, were determined in 46 dental patients (15 men and 31 women) experiencing pain as a result of acute pulpitis. All subjects participated in 2 experimental sessions; the first took place immediately before endodontic treatment for relief of pulpal pain, and the second session occurred when patients were pain free, approximately 1 to 2 weeks later. Thermal pain thresholds increased on resolution of acute dental pain, whereas levels of catastrophizing did not change from pretreatment to post-treatment. Catastrophizing was unrelated to thermal pain responses in the presence of acute dental pain (ie, during the first session). Once patients were pain free, catastrophizing showed significant inverse associations with measures of thermal pain threshold and tolerance. In addition, catastrophizing was a robust predictor of changes in thermal pain responses across sessions, with higher baseline catastrophizing predicting reductions or relatively smaller increases in pain threshold and tolerance after successful treatment of acute pain. These data suggest that catastrophizing is prospectively associated with enhanced sensitivity to and reduced tolerance for thermal pain. The use of catastrophizing as a coping strategy might interfere with the resolution of sensitization after cessation of an acutely painful condition, or it might be associated with magnified experimental pain responses across time. ⋯ The findings of the present study suggest that, in some instances, different ethnic groups and genders may use the same descriptors to report different levels of pain. In the context of clinical pain assessment, it may be important to consider the possibility that descriptions of painful sensations reflect, in part, demographic characteristics.
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To examine the role of nerve growth factor (NGF) in postoperative pain, we administered the tyrosine kinase A (Trk A) immunoglobulin G (IgG) fusion (1 to 10 mg/kg) molecule before and after plantar incision. We also pretreated rats with a tumor necrosis factor receptor (TNFr) protein, p75 IgG fusion protein (5 to 10 mg/kg), to study the role of endogenous TNF in the development of pain behaviors after incision. Rats underwent a plantar incision, and responses to punctate and nonpunctate mechanical stimuli and withdrawal latency to radiant heat were measured. Rats were tested on the day of incision and daily for 4 days. Reduced withdrawal latency to radiant heat occurred after incision in the control group treated with IgG. Both pretreatment and treatment after incision with 5 mg/kg dose of Trk A IgG fusion protein increased the withdrawal latency to heat in incised rats (P <.05) through 4 days. A similar effect was observed after 10 mg/kg was administered after incision. Neither dose influenced the reduced withdrawal threshold and increased response to blunt mechanical stimulation caused by the incision. Pretreatment with 5 or 10 mg/kg of TNFr IgG fusion protein had no effect on any of the incision-induced pain-related behaviors. We conclude that sequestration of NGF affected responses to heat after incision but did not influence responses to mechanical stimuli. Thus, fibers sensitive to heat are influenced by NGF and probably do not contribute to exaggerated responses to mechanical stimuli. TNF does not appear to have a role in the pain behaviors. ⋯ To treat postoperative pain better, we should discover the factors that are causing incisional pain. One endogenous factor that contributes to pain after incision is NGF. Inhibition of NGF may provide a new way to treat pain after surgery with minimal side effects. This could improve outcome after surgery.
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Racial and ethnic minorities, older people, and women are differentially affected by chronic pain. This study aimed to identify the experiences of adult African Americans and whites with chronic pain while identifying patient clusters on the basis of clinical characteristics as well as race, age, and gender influences within and between clusters. Three clusters of patients with chronic pain were identified within race, age, and gender categories: chronic pain syndrome, good pain control, and disability with mild syndrome. African American and younger patients experiencing chronic pain were more likely to present with chronic pain syndrome. African American patients presenting with chronic pain syndrome or disability with mild pain syndrome reported a higher disability than their counterparts. Older patients and women within the good pain control cluster reported a lower level of (1) pain and depression and (2) depression, respectively. Older patients presenting with a disability with mild syndrome also reported lower pain and depression. Despite similar physical, emotional, and pain characteristics, this study confirmed that the chronic pain experience differs across racial and age groups. Further study is necessary to evaluate how these factors influence pain services among an ethnically diverse population across the age continuum. ⋯ This study found important racial and age-related variability in the symptom severity of patients with chronic pain presenting with similar physical, emotional, and pain characteristics to a tertiary care pain center. These findings have important clinical implications on chronic pain assessment and management.
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We present 2 patients with severe and intractable central poststroke pain (CPSP) after right posterolateral thalamic infarcts who were successfully treated with zonisamide. The mechanism of action was presumed to be the suppression of overacting thalamic relay neurons by blockade of low voltage-activated calcium channel or by increasing gamma-aminobutyric acid (GABA) release. Zonisamide can be one of the therapeutic options for severe CPSP and might provide an insight into the pathogenesis of CPSP. ⋯ The blockade of T-type VGCC or the increase in GABA release caused by zonisamide presumably suppresses abnormal activities of thalamic sensory neurons.