Pain
-
Comparative Study
Maintenance of windup of second pain requires less frequent stimulation in fibromyalgia patients compared to normal controls.
Many chronic pain syndromes, including fibromyalgia (FM), show evidence of central nervous system hyperexcitability related to central sensitization. Windup (WU) of second pain reflects increased excitability of spinal cord neurons that is related to central sensitization. Psychophysical testing can help characterize this important central nervous system phenomenon because of the parallels between electrophysiological WU and WU of second pain. ⋯ Thus, unlike NC subjects, FM subjects showed enhanced second pain during WU-M stimuli at very low stimulus frequencies, indicating central sensitization. Increased WU sensitivity, enhanced WU-M, and increased WU-related aftersensations help account for persistent pain conditions in FM subjects. In addition to WU, WU-M appears to be a useful tool to study mechanisms of pain in patients with characteristics of central sensitization.
-
To investigate neglect, extinction, and body-perception in patients suffering from complex regional pain syndrome (CRPS). So-called 'neglect-like' symptoms have been reported in CRPS, however no studies have yet analyzed this phenomenon which might substantiate the theory of the central nervous system involvement in the pathophysiology of CRPS. A total of 114 patients with CRPS of the upper limb underwent bedside neurological examination. 'Neglect-like' symptoms were determined by asking all patients what kind of feeling they had toward the affected hand (feeling of foreignness). ⋯ A large proportion of CRPS patients have disturbances of the self-perception of the hand, indicating an alteration of higher central nervous system processing. There are no indicators that classic neglect or extinction contribute to these findings. Physical therapy of such patients should take this observation into consideration.
-
Comparative Study
Role of TNF-alpha in sensitization of nociceptive dorsal horn neurons induced by application of nucleus pulposus to L5 dorsal root ganglion in rats.
Herniation of the nucleus pulposus (NP) from lumbar intervertebral discs commonly results in radiculopathic pain and paresthesia (sciatica). While traditionally considered the result of mechanical compression of the dorsal root ganglion (DRG) and/or spinal nerve root, recent studies implicate pro-inflammatory mediators released from or evoked by NP, a possibility that was presently investigated. Single-unit recordings were made from L5 wide dynamic range dorsal horn neurons in pentobarbital-anesthetized rats. ⋯ Thermally and mechanically evoked responses were not significantly affected in control rats or those treated with NP + soluble TNF-alpha receptor type 1. These results indicate that sensitization of nociceptive spinal neuronal responses develops quickly following exposure of the DRG to NP, and that TNF-alpha is involved. This electrophysiological model of herniated NP may prove useful in further characterizing the role of inflammatory mediators in hyperalgesia and allodynia resulting from lumbar disc herniation.
-
Comparative Study
Rapid deterioration of pain sensory-discriminative information in short-term memory.
The assessment of pain and analgesic efficacy sometimes relies on the retrospective evaluation of pain felt in the immediate, recent or distant past, yet we have a very limited understanding of the processes involved in the encoding, maintenance and intentional retrieval of pain. We examine the properties of the short-term memory of thermal and pain sensation intensity with a delayed-discrimination task using pairs of heat pain, warm and cool stimulation in healthy volunteers. Performance decreased as a function of the inter-stimulus interval (ISI), indicating a robust deterioration of sensory information over the test period of 4-14 s. ⋯ Importantly, performance declined steadily with increasing ISI (from 6 to 14 s)--but only for pairs of heat pain stimuli that were relatively difficult to discriminate (Delta-T < or = 1.0 degree C; perceptual difference < or = 32/100 pain rating units) while no deterioration in performance was observed for the largest temperature difference tested (Delta T = 1.5 degrees C; perceptual difference of 50 units). These results are consistent with the possibility that short-term memory for pain and temperature sensation intensity relies on a transient analog representation that is quickly degraded and transformed into a more resistant but less precise categorical format. This implies that retrospective pain ratings obtained even after very short delays may be rather inaccurate but relatively reliable.
-
Comparative Study
HIV-1 gp120 stimulates proinflammatory cytokine-mediated pain facilitation via activation of nitric oxide synthase-I (nNOS).
It has become clear that spinal cord glia (microglia and astrocytes) importantly contribute to the creation of exaggerated pain responses. One model used to study this is peri-spinal (intrathecal, i.t.) administration of gp120, an envelope protein of HIV-1 known to activate glia. Previous studies demonstrated that i.t. gp120 produces pain facilitation via the release of glial proinflammatory cytokines. ⋯ Both abolished gp120-induced mechanical allodynia. While the literature pre-dominantly documents that proinflammatory cytokines stimulate the production of NO rather than the reverse, here we show that gp120-induced NO increases proinflammatory cytokine mRNA levels (RT-PCR) and both protein expression and protein release (serial ELISA). Furthermore, gp120 increases mRNA for IL1 converting enzyme and matrix metalloproteinase-9, enzymes responsible for activation and release of proinflammatory cytokines.