Pain
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Chronic pain is often associated with changes in brain structure and function, and also cognitive deficits. It has been noted that these chronic pain-related alterations may resemble changes found in healthy aging, and thus may represent accelerated or premature aging of the brain. Here, we test the hypothesis that patients with chronic noncancer pain demonstrate accelerated brain aging compared with healthy control subjects. ⋯ A Bayesian independent-samples t test indicated moderate evidence in favor of the null hypothesis (BF01 = 4.875, ie, group means were equal). Our results provide indirect support for recent models of pain-related changes of brain structure, brain function, and cognitive functions. These models postulate network-specific maladaptive plasticity, rather than widespread or global neural degeneration.
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The amygdala is a key subcortical region believed to contribute to emotional components of pain. As opioid receptors are found in both the central (CeA) and basolateral (BLA) nuclei of the amygdala, we investigated the effects of morphine microinjection on evoked pain responses, pain-motivated behaviors, dopamine release in the nucleus accumbens (NAc), and descending modulation in rats with left-side spinal nerve ligation (SNL). Morphine administered into the right or left CeA had no effect on nerve injury-induced tactile allodynia or mechanical hyperalgesia. ⋯ Microinjection of morphine into the BLA had no effects on evoked behaviors and did not produce CPP in nerve-injured rats. These findings demonstrate that the amygdalar action of morphine is specific to the right CeA contralateral to the side of injury and results in enhancement of net descending inhibition. In addition, engagement of mu opioid receptors in the right CeA modulates affective qualities of ongoing pain through endogenous opioid neurotransmission within the rACC, revealing opioid-dependent functional connections from the CeA to the rACC.
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Altered pronociceptive and antinociceptive mechanisms are often implicated in painful conditions and have been increasingly studied over the past decade. For some painful conditions, alterations are well-established, but in populations with low back pain (LBP), there remains considerable debate whether these mechanisms are altered. The present systematic review aimed to address this issue by identifying studies assessing conditioned pain modulation (CPM) and/or temporal summation of pain (TSP) in patients with LBP, comparing with either a healthy control group or using a method with reference data available. ⋯ Nonetheless, CPM was impaired in patients with LBP compared with controls (standardized mean difference = -0.44 [-0.64 to -0.23], P < 0.001), and the magnitude of this impairment was related to pain chronicity (acute/recurrent vs chronic, P = 0.003), duration (RS = -0.62, P = 0.006), and severity (RS = -0.54, P = 0.02). Temporal summation of pain was facilitated in patients with LBP compared with controls (standardized mean difference = 0.50 [0.29-0.72], P < 0.001), and the magnitude of this facilitation was weakly related to pain severity (RS= 0.41, P = 0.04) and appeared to be influenced by test modality (P < 0.001). Impaired CPM and facilitated TSP were present in patients with LBP compared with controls, although the magnitude of differences was small which may direct future research on the clinical utility.
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Randomized Controlled Trial
Evaluating the Efficacy of an Attention Modification Program for Patients with Fibromyalgia: A Randomized Controlled Trial.
Persons with chronic musculoskeletal pain may be hypervigilant for pain-related cues which, paradoxically, may be maintaining their pain. Several randomized controlled trials have assessed whether a modified dot-probe protocol (ie, attention bias modification [ABM]) reduces chronic pain- and pain-related symptoms in persons with several diagnoses, including fibromyalgia. Scalability and economic efficiency potentiates the appeal of ABM protocols; however, research results have been mixed, with only some studies evidencing significant symptom gains from ABM and some evidencing gains for the control group. ⋯ Both groups had small significant (Ps < 0.05) improvements in pain experiences at posttreatment, but not at follow-up (Ps > 0.05). There were no significant changes for either group on measures of anxiety sensitivity, illness/injury sensitivity, pain-related fear, pain-related anxiety, or attentional biases (Ps > 0.05). The current findings add to the emerging and mixed literature regarding ABM for pain by demonstrating that ABM produces no substantive improvements in pain or pain-related constructs in a large sample of patients with fibromyalgia.