APS Press RoomNews Highlights from The Journal of Pain April 2007
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How your pain is assessed might depend on who is on the other end of the conversation, according to a study in The Journal of Pain, the peer-review publication of the American Pain Society.
Researchers from the University of Michigan observed pain and mood in 70 patients with low-back pain. At their two-week follow-up, they were asked to recall their post-procedural rating at the time they received epidural lumbar injections. Since there are no biomarkers for pain, subjective patient reports are used extensively in pain intensity evaluations. In this study, patients who were called by physicians gave pain ratings that closely matched the post-procedural ratings. However, those phoned by research assistants gave significantly worse pain ratings, showing a clear assessor bias in the pain ratings.
From a clinical perspective, the researchers noted that physicians depend on patient pain recall to assess trends and progression of therapy. From the study, it cannot be concluded that physicians or research assistant give inaccurate pain assessments. However, intensity ratings do differ based on the status of the reviewers. It was recommended that serial pain assessments should be by done individuals of similar status over time to minimize reporting biases.
Source: Assessor Status Influences Pain Recall, David A. Williams, Karen M. Park, Kristen R. Ambrose and Daniel J. Clauw, University of Michigan
Older, inexpensive antidepressant medications in the tricyclic classification often are prescribed to treat neuropathic pain. In various studies, several of these agents have been proven to block peripheral nerve sodium channels, which may be responsible for their analgesic action. Scientists from Merck Research Laboratories compared the sodium blocking abilities of several tricyclic antidepressants as well as some newer agents, known as selective serotonin reuptake inhibitors (SSRI).
Results showed that all drugs tested have some sodium channel blocking activity with the tricyclic amitriptyline, nortriptyline, imipramine, desipramine and maprotiline having therapeutic efficacy for treatment of neuropathic pain as well as depression. The SSRIs tested were fluoxetine, paroxetine, mianserine and zimelidine. They showed channel-blocking ability but were not as efficacious as tricyclics for treating post-herpectic neuralgia and diabetic neuropathy.
The researchers concluded: “Since neuropathic pain is a complex phenomenon that may involve a diversity of pain-signaling mechanisms, depending on patient population and underlying cause of the disease, it is likely that antidepressants derive their superior efficacy from the combination of several pharmacologic mechanisms. Our results suggest that one of these mechanisms is the blockade of peripheral nerve sodium channels.”
Source: Sodium Channel Blockers May Contribute to the Analgesic Efficacy of Antidepressants, Ivy E. Dick, Richard Brochu, Yamini Puorhit, Gregory Kaczorowski, William J. Martin and Birgit T. Priest, Department of Ion Channels, Merck Research Laboratories.
Brain imaging studies have identified a pain system that is activated in response to physically noxious stimuli. This neural network has been called the pain matrix. Researchers from the University of Liverpool investigated whether the pain matrix could be activated by the recall of pain memories in the absence of overt pain stimuli. Fourteen pain-free subjects were asked to recall painful episodes in response to hearing pain-related words.
The results showed that recall of pain memories did activate the pain matrix and suggest that pain-free individuals have a pain-processing network that can be activated by the cognitive reappraisal of a painful event triggered by pain-related words.
Source: Retrieving Autobiographical Memories of Painful Events Activates the Anterior Cingulate and Inferior Frontal Gyrus, Sioban Kelly, Donna Lloyd, Turo Nurmikko and Neil Roberts, Magnetic Resonance and Image Analysis Research Center, University of Liverpool, England
While it is well established that the cyclooxygenase enzyme plays an important role in the induction of pain and inflammation, researchers from National Institute of Dental and Craniofacial research evaluated the expression of COX-1 and COX-2 following extractions of impacted molars. Biopsies were performed on the extraction sites to assess levels of COX-1 and COX-2.
The results showed that that COX-1 is responsible for the immediate response to inflammatory stimuli and COX-2 becomes the primary contributor to prostaglandin production as inflammation progresses. The outcome of this study showed the peripheral elevation of COX-2 after tissue trauma. This may contribute to increased prostaglandin levels at the site of injury, the onset of pain, and the analgesic activity of nonselective and selective COX-2 inhibiting agents.
Source: Expression of COX-1 and COX-2 in a Clinical Model of Acute Inflammation, Asma A. Khan, Michael Iadarola, Hsiu-Ying T. Yang, and Raymond Dionne, National Institute of Dental and Craniofacial Research