European journal of pain : EJP
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Although many types of nerve damage can cause neuropathic pain, there are substantial commonalities in neuropathic pain symptoms, and patients can be divided into sub-groups based on their symptom profile rather than etiology. Mechanism-based treatment suggests that pharmacotherapy should be chosen be based shared commonalities of symptoms rather than etiology. The aim of the present study was to determine whether type of injury (etiology) or behavioral endpoint (symptom) is a better predictor of pharmacological responsivity in the most commonly used rodent models of neuropathic pain. ⋯ Hypersensitivity to heat and pressure were highly responsive to oxycodone, gabapentin, and amitriptyline; whereas cold and mechanical allodynia were more difficult to reverse. Moreover, CCI- and SNL-induced mechanical allodynia was completely insensitive to amitriptyline treatment. We conclude that regardless of model and time course of presentation, different symptoms of peripheral neuropathy have unique pharmacological responses.
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Randomized Controlled Trial
Effects of low-dose intranasal (S)-ketamine in patients with neuropathic pain.
NMDA receptors are involved in the development and maintenance of neuropathic pain. We evaluated the efficacy and safety of intranasal (S)-ketamine, one of the most potent clinically available NMDA receptor antagonists. ⋯ Intranasal administration of low dose (S)-ketamine rapidly induces adequate plasma concentrations of (S)-ketamine and subsequently of its metabolite (S)-norketamine. The time course of analgesia correlated with plasma concentrations.
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Comparative Study
A comparison of anatomical pain sites from a tertiary care sample: evidence of disconnect between functional and perceived disability specific to lower back pain.
Heterogeneity has been identified within chronic musculoskeletal pain (CMP) patient samples; however, investigations have typically focused on psychological constructs or coping (e.g., pain-related anxiety, catastrophizing) in this regard. Furthermore, studies to date have included either samples presenting with a specific anatomical site (e.g., only lower back pain) or a mix of anatomical sites (e.g., lower back, shoulder, or leg pain) as the primary pain complaint, without making comparisons based on the anatomical site of reported pain. For example, patients with chronic lower back pain (CLBP) may differ from those with chronic upper or lower extremity pain (ULEP) in presentation, recovery trajectory, and psychological variables. ⋯ Specifically, CLBP patients reported increasing perceived disability despite improvements in functional deficit, whereas ULEP patients did not. These findings suggest a disconnect between perceived disability and function that may be specific to lower back pain. Implications and directions for future research are discussed.
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Bortezomib is a proteasome inhibitor showing strong antitumor activity against many tumors, primarily multiple myeloma. Bortezomib-induced neuropathic pain is the main side effect and the dose-limiting factor of the drug in clinical practice. In order to obtain a pre-clinical model to reproduce the characteristic pain symptoms in bortezomib-treated patients, we developed an animal model of bortezomib-induced nociceptive sensory neuropathy. ⋯ The pathological examination revealed a dose-dependent axonopathy of the unmyelinated fibers in nerves of treated animals. No pathological alteration in most of DRG satellite cells and neurons was observed. Therefore, this animal model may be useful for studying the neurotoxicity and pain onset mechanisms related to bortezomib treatment.
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Chronic pain and PTSD are known to hold substantial comorbidity following traumatic injury. Although pharmacological agents have been examined in the treatment of pain and PTSD individually, little is known regarding the relationship of medication use with functioning in patients with comorbid conditions. This research examined the relationships of pain, PTSD, and medication use across physical and psychosocial functioning in patients with chronic pain following motor vehicle injury (N=234). ⋯ Opioids also were related to greater psychosocial impairment in patients without PTSD while PTSD was associated with greater impairment in patients not using opioids, (3) Opioid use evidenced a marginal interaction with pain on psychosocial functioning. Opioids were associated with greater psychosocial impairment among patients with high-pain, and high-pain was associated with greater impairment among opioid users, (4) SSRIs held a marginal interaction with PTSD such that PTSD was related to poorer psychosocial functioning only among individuals not using an SSRI, and (5) Anxiolytic use evidenced a marginal interaction with PTSD on physical functioning although no between-group differences were noted. These data suggest that PTSD symptomology may be an important consideration in determining treatment modality for patients experiencing pain subsequent to traumatic injury.