The immediate cardiovascular response to joint mobilization of the neck- A randomized, placebo-controlled trial in pain-free adults

Some normotensive patients can have a spike in resting systolic blood pressure (SBP) in response to acute neck pain. Applying the typical dosage of mobilization may potentially result in a sympatho-excitatory response, further increasing resting SBP. Therefore, there is a need to explore other dosage regimens that could result in a decrease in SBP.

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Giving patients useful information about their illnesses

Tapp describes her experience of being the subject of bedside teaching.1 My mother was admitted to hospital for investigation of abdominal pain and a rising sensory level. She was examined by the...

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The analgesic and anti-inflammatory effects of Salvinorin A analogue β-tetrahydropyran Salvinorin B in mice

Abstract

Background

Drugs activating the mu opioid receptor are routinely used to treat severe acute and chronic pain. Unfortunately, side effects including nausea, constipation, respiratory depression, addiction and tolerance can limit clinical utility. In contrast, kappa opioid receptor (KOPr) agonists, such as Salvinorin A (SalA), have analgesic properties with little potential for abuse.

Methods

We evaluated SalA and the novel analogue β-tetrahydropyran Salvinorin B (β-THP SalB) for the ability to modulate pain and inflammation in vivo. The hot water tail-withdrawal assay, intradermal formalin-induced inflammatory pain and paclitaxel-induced neuropathic pain models were used to evaluate analgesic properties in mice. Tissue infiltration of inflammatory cells was measured by histology and flow cytometry.

Results

β-tetrahydropyran Salvinorin B produced a longer duration of action in the tail-withdrawal assay compared to the parent compound SalA, and, like SalA and U50,488, β-THP SalB is a full agonist at the KOPr. In the formalin-induced inflammatory pain model, β-THP SalB and SalA significantly reduced pain score, paw oedema and limited the infiltration of neutrophils into the inflamed tissue. β-THP SalB and SalA supressed both mechanical and cold allodynia in the paclitaxel-induced neuropathic pain model, in a dose-dependent manner.

Conclusions

Structural modification of SalA at the C-2 position alters its analgesic potency and efficacy in vivo. Substitution with a tetrahydropyran group at C-2 produced potent analgesic and anti-inflammatory effects, including a reduction in paclitaxel-induced neuropathic pain. This study highlights the potential for KOPr agonists as analgesics with anti-inflammatory action and little risk of abuse.

Significance

Salvinorin A and the novel analogue β-THP Salvinorin B show analgesic effects in the tail-withdrawal and formalin assays. They reduce oedema and decrease neutrophil infiltration into inflamed tissue, and suppress mechanical and cold allodynia in paclitaxel-induced neuropathic pain.

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Effects of Daily Physical Activity Level on Manual Wheelchair Propulsion Technique in Full-Time Manual Wheelchair Users during Steady State Treadmill Propulsion

What’s in a Name? The Case of Emotional Disclosure of Pain-Related Distress

Pain behavior plays a key role in many theoretical models of pain, with many of these models conceptualizing pain behaviors as potentially detrimental to patient functioning. We propose that a certain class of behaviors—talking to others about one’s pain-related distress (i.e., emotional disclosures of pain-related distress)—can be distinguished from other behaviors traditionally conceptualized as pain behaviors. Emotional disclosures of pain-related distress include verbally disclosing one’s anger, sadness, or worry about the pain and its impact to another person.

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The impact of parental modeling on child pain responses: The role of parent and child sex

Social modeling is a process by which pain behaviours are learned, and research has found parents act as models for their children’s behaviour. Despite social learning theory predicting that same-sex models have greater impact, no experimental investigation to date has examined the role of sex of the model or observer in social learning of pediatric pain. The present study recruited 168 parent-child dyads (equal father-son, father-daughter, mother-son, and mother-daughter dyads) where children were generally healthy 6- to 8-year-olds.

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The Role of Chronic Psychosocial Stress in Explaining Racial Differences in Stress Reactivity and Pain Sensitivity

Objective: To examine the role of psychosocial factors in mediating the relationship between African American (AA) race and both increased pain sensitivity and blunted stress reactivity. Methods: Participants included 133 AA and non-Hispanic white (nHW) individuals (mean [SD] age, 37 [9]) matched for age, sex, and socioeconomic status. Participants underwent mental stress testing (Trier Social Stress Test) while cardiovascular, hemodynamic, and neuroendocrine reactivity were measured. Participants completed questionnaires assessing potential sources of psychosocial stress and were tested for pain responses to cold pain and the temporal summation of heat pulses. Mediation analyses were used to determine the extent to which exposure to psychosocial stress accounted for the observed racial differences in stress reactivity and pain. Results: Chronic stress exposure and reactivity to mental stress was largely similar among AAs and nHWs; however, AAs exhibited heightened pain to both cold (p = .012) and heat (p = .004). Racial differences in the relationship between stress reactivity and pain were also observed: while greater stress reactivity was associated with decreased pain among nHWs, reactivity was either unrelated to or even positively associated with pain among AAs (e.g., r = −.21 among nHWs and r = .41 among AAs for stroke volume reactivity and cold pressor intensity). Adjusting for minor racial differences in chronic psychosocial stress did not change these findings. Conclusions: Accounting for psychosocial factors eliminated racial differences in stress reactivity but not racial differences in sensitivity to experimental pain tasks. Increased exposure to chronic stress may not explain AAs' increased pain sensitivity in laboratory settings.

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