Pain
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Cold stimuli of varying intensities were randomly applied to upper middle incisors of 12 healthy young subjects for a mean duration of 2 min by individually adapted thermodes the temperatures of which ranged from +30 degrees C to -30 degrees C. The subjects were asked to rate the magnitude of their pain sensations during application of the stimuli by means of a linear potentiometer according to a category scale. After each stimulus, they were asked to describe the quality of their pain sensations. ⋯ This was described as a dull, burning pain which was difficult to localize. The human pain ratings are compared to recordings of intradental nerve fibres in the cat and, under the assumption that the response behaviour of human pulpal nerve fibres is comparable to that of the cat, we hypothesize that the first pain component is evoked by intradental A delta fibres exhibiting their typical phasic response behaviour and firing during the initial steep temperature decrease. After some seconds, intradental temperature reached values sufficient to evoke C-fibre activity associated with the second pain component.
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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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This study examined the effects of increasing the number of assessments on the reliability and validity of measures of average pain intensity. Two hundred chronic pain patients completed 2 weeks of hourly pain ratings. ⋯ Also, and as expected, the results indicate that a single rating of pain intensity is not adequately reliable or valid as a measure of average pain. However, a composite pain intensity score calculated from an average of 12 ratings across 4 days demonstrated adequate reliability and excellent validity as a measure of the average pain in this sample of chronic pain patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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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.