Traumatic Life Experience and Pain Sensitization: Meta-analysis of Laboratory Findings.

Objectives: Psychological trauma often co-occurs with pain. This relationship has been explored using laboratory pain measures; however, findings have been mixed. Previous studies have limited operationalization of trauma (eg, posttraumatic stress disorder) or pain (eg, pain thresholds), which may contribute to conflicting results.

Emotion regulation strategies moderate the impact of negative affect induction on alcohol craving in college drinkers: an experimental paradigm.

: Observational studies suggest emotion regulation (ER) as a potential treatment target for problematic college drinking. The primary aim of this laboratory study was to determine whether trait ER strategies would moderate the impact of negative affect induction on alcohol craving in college drinkers. : Participants were randomly assigned to a neutral ( = 74) or a negative affect induction ( = 76) and reported their craving after the affect inductions.

Greater mechanical temporal summation of pain in Latinx-Americans and the role of adverse life experiences.

Introduction: Adverse life experiences disproportionately impact Latinx-Americans and are related to greater chronic pain rates. However, little is known about how adversities interact with central pain mechanisms for the development of later pain among Latinx-Americans.

Objectives: The current study examined the relationship between adverse life experiences (eg, trauma and ethnic discrimination) and correlates (eg, social status) with mechanical temporal summation of pain (a proxy measure of central sensitization) between pain-free U.

Hyperalgesia after a Drinking Episode in Young Adult Binge Drinkers: A Cross-Sectional Study.

Aims: Rodent studies propose potential mechanisms linking excessive drinking and pain hypersensitivity (hyperalgesia), such that stress hormones (i.e. epinephrine and cortisol) mediate induction and maintenance of alcohol withdrawal-induced hyperalgesia.

Divergent effects of conditioned pain modulation on subjective pain and nociceptive-related brain activity.

Background And Objectives: Pain is a complex experience involving both nociceptive and affective-cognitive mechanisms. The present study evaluated whether modulation of pain perception, employing a conditioned pain modulation (CPM) paradigm, is paralleled by changes in contact heat-evoked potentials (CHEPs), a brain response to nociceptive stimuli.

Methods: Participants were 25 healthy, pain-free, college students (12 males, 13 females, mean age 19.

Childhood Adversity and Pain Facilitation.

Objective: This study investigated whether childhood adversity would be associated with hypersensitivity on two measures of central pain facilitation: area of secondary allodynia and temporal summation of second pain (TSSP), and whether pain facilitation would be explained by adult posttraumatic stress disorder (PTSD) symptoms.

Method: Participants endorsing high (n = 31) and low (n = 31) childhood adversity underwent capsaicin-induced secondary allodynia and TSSP testing. The tests were conducted a week apart with test order counterbalanced.

Cumulative Childhood Adversity as a Risk Factor for Common Chronic Pain Conditions in Young Adults.

Objective: Multiple and specific types of childhood adverse events are risk factors for chronic pain conditions. Although both can covary, no study has evaluated one aspect while controlling for the other. Therefore, the current study examined whether more adverse events would be a risk factor for common chronic pain conditions and pain medication use in young adults after controlling for different adversity types such as physical, emotional, and sexual traumatic events or vice versa.

Does Pain Affect Preference? The Effect of Tonic Laboratory Pain on Discounting of Delayed Rewards.

Unlabelled: Chronic pain patients show elevated risk behavior on decision-making tasks, as well as increased health risk behaviors (eg, smoking, prescription opioid abuse). Determining pain's effect on underlying cognitive processes that are associated with risk behavior is confounded by comorbidities linked with chronic pain, including depression, anxiety, and substance abuse. Therefore, to understand pain's effect on delay discounting, a behavioral process assessing the extent to which outcomes are devalued as a function of their delay, the present study evaluated the effect of laboratory pain on delay discounting in healthy young adults (N = 85).

Generalized Pain Sensitization and Endogenous Oxytocin in Individuals With Symptoms of Migraine: A Cross-Sectional Study.

Objective: The current study examined pain and neurogenic inflammation responses to topical capsaicin during the interictal period (between headache) and their relationship with plasma oxytocin in individuals with migraine.

Background: Individuals with migraine can experience generalized (extracephalic) hyperalgesia, which can persist even between headache attacks. Elevated levels of plasma and cerebrospinal fluid oxytocin have been observed during migraine attacks, oxytocin levels being positively associated with the intensity of migraine symptoms.

Association Between Borderline Personality Features and Temporal Summation of Second Pain: A Cross-Sectional Study.

Individuals with greater borderline personality features may be vulnerable to chronic pain. Because pain is an unpleasant sensory and emotional experience, affect dysregulation as the core personality feature may be linked to pain hypersensitivity. Studies have found that greater borderline features are associated with increased intensity in clinical and experimental pain, and that depression mediates this increase.

Childhood Adversity and Pain Sensitization.

Objective: Childhood adversity is a vulnerability factor for chronic pain. However, the underlying pain mechanisms influenced by childhood adversity remain unknown. The aim of the current study was to evaluate the impact of childhood adversity on dynamic pain sensitivity in young adults.

Expectation of nocebo hyperalgesia affects EEG alpha-activity.

Changes in EEG activity have been related to clinical and experimental pain. Expectation of a negative outcome can lead to pain enhancement (nocebo hyperalgesia) and can alter the response to therapeutic interventions. The present study characterizes EEG alteration related to pain facilitation by nocebo.

Enhanced Area of Secondary Hyperalgesia in Women with Multiple Stressful Life Events: A Pilot Study.

Objective: Stressful life events are associated with increased pain severity and chronicity. However, the mechanism underlying this association remains disputed. Recent animal studies suggest that chronic stress increases pain sensitivity and persistence by enhancing peripheral and central sensitization mechanisms.

Molecular and preclinical basis to inhibit PGE2 receptors EP2 and EP4 as a novel nonsteroidal therapy for endometriosis.

Endometriosis is a debilitating, estrogen-dependent, progesterone-resistant, inflammatory gynecological disease of reproductive age women. Two major clinical symptoms of endometriosis are chronic intolerable pelvic pain and subfertility or infertility, which profoundly affect the quality of life in women. Current hormonal therapies to induce a hypoestrogenic state are unsuccessful because of undesirable side effects, reproductive health concerns, and failure to prevent recurrence of disease.

Effect of written emotional disclosure on secondary hyperalgesia in women with trauma history.

Objective: This study investigated the effects of written emotional disclosure on a model of chronic pain in healthy women with and without trauma history.

Method: Participants were prescreened for their trauma history (N = 78) and randomized to a disclosure or a control writing condition. Pain testing occurred either 1 day or 1 month after disclosure.

Consequences of perinatal bisphenol A exposure in a mouse model of multiple sclerosis.

Multiple sclerosis (MS) is a complex disease influenced by genetic and environmental contributing factors. Endocrine disrupting compounds (EDCs) such as bisphenol A (BPA) affect gene expression and hormone-regulated systems throughout the body. We investigated the effects of BPA on Theiler's-virus induced demyelination (TVID), a mouse model of MS.

Chronic social stress impairs virus specific adaptive immunity during acute Theiler's virus infection.

Prior exposure to social disruption (SDR) stress exacerbates Theiler's murine encephalomyelitis virus (TMEV) infection, a model of multiple sclerosis. Here we examined the impact of SDR on T cell responses to TMEV infection in SJL mice. SDR impaired viral clearance and exacerbated acute disease.

Translational approaches to treatment-induced symptoms in cancer patients.

Cancer therapy makes patients sick. The therapies that are available to clinicians allow them to successfully control nausea, emesis and pain. However, this is not the case for a number of other symptoms that include fatigue, distractibility, poor memory, and diminished interest in previously pleasurable activities.

Negative affect heightens opiate withdrawal-induced hyperalgesia in heroin dependent individuals.

This study examined the effect of emotion on opiate withdrawal induced hyperalgesia to determine whether emotional states modulate the magnitude of hyperalgesia. One hundred Hispanic men were recruited into one of three groups: heroin withdrawal, long-term heroin abstinence, and control. Participants were presented with pictures to induce neutral, positive, and negative emotional states.

Written emotional disclosure of trauma and trauma history alter pain sensitivity.

Unlabelled: The present study investigated whether written emotional disclosure of trauma and trauma history alters sensitivity to experimental pain in healthy women. We examined the immediate affective and physiological effects of written emotional disclosure and evaluated the pain modulatory effects of this personally relevant method of affect induction in women with and without trauma history. Participants wrote for 20 minutes about a traumatic or neutral topic prior to the thermal pain threshold and the ischemic pain tolerance tests.

Chronic restraint stress during early Theiler's virus infection exacerbates the subsequent demyelinating disease in SJL mice: II. CNS disease severity.

Theiler's murine encephalomyelitis virus (TMEV) infection is a well-characterized model of multiple sclerosis (MS). Previous research has shown that chronic restraint stress (RS) during early TMEV infection exacerbates behavioral signs of the disease. The present data suggest that RS-induced increases in CNS inflammation, demyelination, and axonal degeneration may underlie this exacerbation.

Effects of stress on the immune response to Theiler's virus--implications for virus-induced autoimmunity.

Psychological stress is an important factor in susceptibility to many diseases. Our laboratory has been investigating the impact of stress on the susceptibility to Theiler's virus-induced demyelination (TVID), a mouse model of multiple sclerosis. Using immunodominant viral peptides specific for identification of either CD4(+) or CD8(+) T cells, stress reduced IFN-gamma-producing virus-specific CD4(+) and CD8(+) T cells in the spleen and CD8(+) T cells in the CNS.

Restraint stress fails to render C57BL/6 mice susceptible to Theiler's virus-induced demyelination.

Objectives: Multiple sclerosis is a degenerative disease of the CNS with a pathology consistent with immunological mediation. Although its cause is unknown, multiple factors are thought to influence both the onset and exacerbation of the disease, including both genetic background as well as environmental factors.

Methods: We are interested in the effect of psychological stress on the onset and exacerbation of Theiler's virus-induced demyelinating disease (TVID), a murine model of MS in which viral persistence facilitates demyelination.

Spinal glia modulate both adaptive and pathological processes.

Recent research indicates that glial cells control complex functions within the nervous system. For example, it has been shown that glial cells contribute to the development of pathological pain, the process of long-term potentiation, and the formation of memories. These data suggest that glial cell activation exerts both adaptive and pathological effects within the CNS.

Restraint stress modulates virus specific adaptive immunity during acute Theiler's virus infection.

Multiple sclerosis (MS) is a devastating CNS disease of unknown origin. Multiple factors including genetic background, infection, and psychological stress affect the onset or progression of MS. Theiler's murine encephalomyelitis virus (TMEV) infection is an animal model of MS in which aberrant immunity leads to viral persistence and subsequently results in demyelination that resembles MS.