Pain
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An experimental arthritis induced by injection of kaolin and carrageenan into the knee joint resulted in a temporal relationship between glutamate dorsal horn content and paw withdrawal latency (PWL) which was positively correlated. Limping, guarding, increased response to heat stimuli (hyperalgesia) and altered staining patterns for glutamate (GLU), substance P (SP), and calcitonin gene-related peptide (CGRP) were monitored in the awake behaving arthritic rat over a 1 week time course. A decrease in PWL occurred on the side ipsilateral to the inflamed knee as early as 4 h after the induction of arthritis indicating the animals are hyperalgesic. ⋯ Rather, there was an increase in CGRP content in the middle portion of the superficial dorsal horn which is the termination site of knee joint afferents. These data indicate that the development of heat hyperalgesia is dependent on GLU and possibly SP. Since inflammation of the knee joint does not involve the foot pad, the heat hyperalgesia observed during the first 24 h following induction of arthritis represents a central neuronal sensitization.
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In this open, uncontrolled trial, 20 patients with upper trapezius muscle trigger point pain and ipsilateral masseter muscle pain received a single trigger point injection of 2% lidocaine solution (without epinephrine) in the upper trapezius muscle. Following the trapezius injection, there was a significant (P < 0.001) reduction in pain intensity ratings for pain in the masseter region. ⋯ Overall, however, a significant relationship between EMG activity in the masseter and the self-report of pain was not found with the present data set. These clinical findings support the contention that sources of deep pain can produce heterotopic sensory and motor changes in distant anatomical regions.
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Nociceptive flexion reflexes (RIII response) of the lower limbs were recorded after unilateral cervico-thoracic anterolateral cordotomy (ALC) in 7 patients. Pre-operative recordings were also obtained in 1 patient and follow-up observations in 3 patients. Flexion reflexes ipsilateral to cordotomy remained normal after surgery. ⋯ We conclude that the dissociation between flexion reflexes and pain sensation, which was evidenced even in case of depressed RIII responses, should be attributable to the surgical lesion of spinothalamic fibers. Dissociation between RIII and subjective pain is a landmark indicating a lesion of the spinothalamic fibers, and may be used for the clinical assessment of spinothalamic dysfunction. Conversely, RIII depression after ALC does not depend upon the surgical lesion to the spinothalamic axons, but may be secondary to interruption of ascending spinoreticular fibers in the anterolateral quadrant, and/or of descending excitatory axons in the ventral cord.
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The Beck Depression Inventory (BDI) has been widely used to document the prevalence of depressive symptomatology in samples of chronic pain patients and as an outcome measure in studies of the psychological management of chronic pain. Several BDI items have a somatic content (sleep disturbance, fatigue, etc). Since chronic pain may have similar somatic effects, the significance of the total BDI score in this population is unclear. ⋯ Among the most frequently endorsed items were those loading on the somatic factor. The pattern of relationships between individual factor scores and measures of pain, mood, cognition, and physical functioning indicated that the use of the total BDI score may give a misleading impression of the nature and degree of affective disturbance in this group of patients. The implications of these findings for our understanding of BDI scores obtained by chronic pain patients are discussed.
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An experimental arthritis of the knee joint resulted in limping, guarding, and an increased response to heat stimuli (heat hyperalgesia). Spinal administration of the non-N-methyl-D-aspartate (non-NMDA) antagonist, 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), significantly reduced the degree of peripheral inflammation, thermal and behavioral manifestations of arthritis. NMDA antagonists had no effect on the inflammation but did prevent the development of the heat hyperalgesia. Thus, central non-NMDA receptors play a major role in the development of peripheral inflammation while both non-NMDA and NMDA receptors are involved in the development of heat hyperalgesia.