Pain
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Impulse frequency and number of recruited central neurons are relevant for pain encoding and temporal as well as spatial summation of pain (SSP). Whereas SSP of heat-induced pain is well characterized, mechanical SSP (MSSP) has been less studied. MSSP may be relevant for chronic pain conditions like fibromyalgia (FM) and play an important role in the pathogenesis of this chronic pain syndrome. ⋯ Furthermore, muscle stimuli elicited more MSSP when separated by 8 cm than 4 cm and this finding was not different between NC and FM subjects. Thus, mechanisms of MSSP were similar for both FM and NC subjects. The important role of MSSP for pain encoding suggests that decreasing pain in some muscle areas by local anesthetics or other means may improve overall clinical pain of FM patients.
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Changes in pain produced by psychological factors (e.g., placebo analgesia) are thought to result from the activity of specific cortical regions. However, subcortical nuclei, including the periaqueductal gray and the rostroventral medulla, also show selective activation when subjects expect pain relief. These brainstem regions send inhibitory projections to the spine and produce diffuse analgesic responses. ⋯ These findings provide direct evidence that the modulation of pain by expectations is mediated by endogenous pain modulatory systems affecting nociceptive signal processing at the earliest stage of the central nervous system. Expectation effects, therefore, depend as much about what takes place in the spine as they do about what takes place in the brain. Furthermore, complete suppression of the analgesic response normally produced by descending inhibition suggests that anti-analgesic expectations can block the efficacy of pharmacologically valid treatments which has important implications for clinical practice.
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Nociceptive impulse activity was recorded extracellularly from single A delta and C primary afferents of the guinea pig's medial articular nerve after induction of an experimental osteoarthritis in the knee joint by partial medial menisectomy and transection of the anterior cruciate ligament (PMM+TACL). Also, the analgesic effects of intra-articular hyaluronan solutions were evaluated. Healthy, PMM+TACL operated, sham-operated (opening of the joint capsule without PMM and TACL surgery) and acutely inflamed (intra-articular kaolin-carrageenan, K-C) animals were used. ⋯ Augmentation of movement-evoked discharges in K-C acutely inflamed knee joints was similar to that observed one week after PMM+TACL. Our results indicate that in the PMM+TACL model of osteoarthritis in guinea pigs, enhancement of nociceptive responses to joint movement was primarily associated to post-surgical inflammation. Intra-articular injection of an elastoviscous hyaluronan solution reduced the augmented nerve activity.
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Throughout the long history of opioid drug use by humans, it has been known that opioids are powerful analgesics, but they can cause addiction. It has also been observed, and is now substantiated by multiple reports and studies, that during opioid treatment of severe and short-term pain, addiction arises only rarely. ⋯ Since the potentially devastating effects of addiction can substantially offset the benefits of opioid pain relief, it seems timely to reexamine addiction mechanisms and their relevance to the practice of long-term opioid treatment for pain. This article reviews the neurobiological and genetic basis of addiction, its terminology and diagnosis, the evidence on addiction rates during opioid treatment of chronic pain and the implications of biological mechanisms in formulating rational opioid treatment regimes.