Pain
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Approximately 20% of patients suffering from stroke with pure or predominant sensory symptoms (referred to as sensory stroke patients) develop central poststroke pain (CPSP). It is largely unknown what distinguishes these patients from those who remain pain free. Using quantitative sensory testing (QST), we analyzed the somatosensory profiles of 50 patients with chronic sensory stroke, of which 25 suffered from CPSP. ⋯ In summary, our analysis reveals that CPSP is associated with impaired temperature perception and positive sensory signs, but differences between patients with CPSP and NPSS are subtle. Both patients with CPSP and NPSS show considerable QST changes on the ipsilesional body side. These results are in part paralleled by recent findings of bilaterally spread cortical atrophy in CPSP and might reflect chronic maladaptive cortical plasticity, particularly in patients with CPSP.
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Number-based assessment tools are used to evaluate pain perception in patients and determine the effect of pain management. The aim of this study was to determine the ability of chronic and acute pain patients to score their response to randomly applied noxious stimuli and assess the effect of opioid treatment. Thirty-seven healthy controls, 30 fibromyalgia patients, and 62 postoperative patients with acute pain received random heat pain (Hp) and electrical pain (Ep) stimuli. ⋯ The data were analyzed using a penalty score system, based on the assumption that stimuli of higher intensity are scored with a greater NRS, and stratified into cohorts corresponding to "good," "mediocre," and "poor" scoring. Healthy controls were well able to score pain with 73% (Hp) and 81% (Ep) of subjects classified into cohort "good." Fibromyalgia had a negative effect on scoring with 45% (Hp, P = 0.03 vs controls) and 67% (Ep) of patients in cohort "good." In controls, scoring deteriorated during opioid administration leaving just 40% (Hp, P = 0.015 vs baseline) and 70% (Ep) of subjects in the cohort "good." Similar observations were made in fibromyalgia patients (P = 0.02) but not in surgical patients with postoperative pain. Consistency to grade pain using an NRS is high in healthy volunteers but deteriorates in chronic pain and during opioid administration to volunteers and chronic pain patients but not to acute pain patients.
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The rostral ventromedial medulla (RVM) exerts both inhibitory and excitatory controls over nociceptive neurons in the spinal cord and medullary dorsal horn. Selective ablation of mu-opioid receptor (MOR)-expressing neurons in the RVM using saporin conjugated to the MOR agonist dermorphin-saporin (derm-sap) attenuates stress and injury-induced behavioral hypersensitivity, yet the effect of RVM derm-sap on the functional integrity of the descending inhibitory system and the properties of RVM neurons remain unknown. Three classes of RVM neurons (on-cells, off-cells, and neutral cells) have been described with distinct responses to noxious stimuli and MOR agonists. ⋯ Furthermore, electrical stimulation of the periaqueductal gray produced analgesia in both derm-sap and saporin controls with similar thresholds. Microinjection of kynurenic acid, a glutamate receptor antagonist, into the RVM disrupted periaqueductal gray stimulation-produced analgesia in both saporin-treated and derm-sap-treated rats. These results indicate that MOR-expressing neurons in the RVM are not required for analgesia produced by either direct or indirect activation of neurons in the RVM.
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Oscillations are fundamental to communication between neuronal ensembles. We previously reported that pain in awake rats enhances synchrony in primary somatosensory cortex (S1) and attenuates coherence between S1 and ventral posterolateral (VPL) thalamus. Here, we asked whether similar changes occur in anesthetized rats and whether pain modulates phase-amplitude coupling between VPL and S1. ⋯ Systemic or intrathalamic delivery of Z944 to rats with CCI normalized these changes. Systemic Z944 also reversed thermal hyperalgesia and conditioned place preference. These data suggest that pain-induced cortical synchrony and thalamocortical disconnectivity are directly related to burst firing in VPL.