Pain
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This study examined the extent to which measures of anxiety could predict pain and the length of hospitalization following surgery in 111 patients with gallstones over and above what could be predicted on the basis of biographical and medical status variables. Self-reported pain on the third day postoperative could hardly be explained by the variables measured. ⋯ Over and above these variables. A-state on the third postoperative day and also A-state and specific anxiety measured 1 day before surgery exerted a significant increase on the values of prediction of the length of postoperative hospitalization.
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Comparative Study
Comparison of human pain sensation and flexion withdrawal evoked by noxious radiant heat.
The purpose of this study was to determine the reliability of flexion withdrawal magnitude as an indicator of pain sensation. In 10 healthy human volunteers, we compared the magnitude and latency of integrated biceps EMG with the subjects' rating of pain, using a visual analog scale, elicited by noxious radiant heat stimuli applied to the dorsal forearm. ⋯ The pain intensity and withdrawal magnitude for each stimulus were poorly correlated. Under the conditions of this experiment, mean pain intensity and mean withdrawal magnitude were both well correlated with stimulus temperature, but the magnitude of withdrawal did not reliably reflect the intensity of pain sensation.
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The objective of this work was to simultaneously measure pain-related spinal and supraspinal physiological responses in humans. The sural nerve compound action potential (CAP), the spinal withdrawal reflex (RIII), the somatosensory evoked potential (SEP) and subjective magnitude ratings were elicited by electrical stimulation of the sural nerve in 10 healthy subjects. The sural nerve CAP was used to normalize the evoking stimulus current and to help identify the peripheral nerve afferent types contributing to the physiological and psychophysical responses. ⋯ Although the amplitudes of the P200 and P300 peaks of the SEP were significantly related to stimulation at noxious levels, both were also affected by stimulation at innocuous levels. This result implies that these peaks receive contributions from both noxious and innocuous somatosensory processes. Clearly, the non-pain-related components of these SEP peaks must be identified and isolated before their potential in measuring supraspinal nociceptive processes can be fully realized.
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In a previous report we presented a novel behavioral model of neuropathic pain disorders, produced in rat by a unilateral ligation of about half of the sciatic nerve. The model is characterized by rapid onset of behaviors suggesting spontaneous pain and disordered responses to non-noxious and noxious stimuli. These include reduced withdrawal thresholds to repetitive touch in the partially deafferented skin ('touched-evoked hyperesthesia'), touch-evoked allodynia, reduced withdrawal thresholds to noxious thermal stimuli and exaggerated responses to noxious heat and mechanical stimuli ('thermal hyperalgesia'). ⋯ Reversible sympathectomy was carried out using guanethidine injected intraperitoneally in 3 experiments, each at a different time in relation to the partial nerve injury. We found that: (1) sympathectomy performed several months postoperatively alleviated the sensory disorders bilaterally; (2) sympathectomy prior to nerve injury partially prevented the appearance of thermal hyperalgesia but did not affect hyperesthesia to repetitive touch; and (3) sympathectomy at the time of nerve injury aggravated the sensory disorders during the first few days. As maintenance and production of the sensory disorders in this animal model depended on sympathetic nervous outflow, we conclude that the rats were suffering from a syndrome analogous to sympathetically maintained causalgia in man.
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Fibromyalgia syndrome (FS) is a chronic pain disorder characterized by diffuse musculoskeletal soreness, stiffness, non-restorative sleep and psychological disturbance. At present, much about the etiology, pathological mechanisms and course of FS are unknown. Indeed, standardized diagnostic criteria have only been recently agreed upon. ⋯ The present paper describes the clinical presentation of FS and historical conceptualizations of the disorder. Available research on pathophysiological mechanisms in FS is then presented. In this section we have included literature concerning histology of muscle, sleep architecture, neurotransmitter anomalies and neuropeptide involvement in FS symptomatology.