Pain
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In 144 healthy subjects tonic heat stimuli were applied with a contact thermode and systematically varied with respect to 3 parameters: temperature T, rate of temperature change RTC, and duration D. In addition, the stimulus temperature at which the first sensation of pain occurred was produced by some subjects. In both types of experiments, subjects compared heat intensity felt at the beginning and the end of the stimulus and then set stimulus temperature to correspond with their initial sensation. ⋯ The average skin temperature of the point of transition from adaptation to sensitization was equal to the average pain threshold temperature. The temperature change response maintained individual differences of thermal and pain sensitivity and was highly consistent for each subject. Potential applications of the procedure in clinical and experimental pain research are discussed.
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Comparative Study
The McGill Pain Questionnaire reconsidered: confirming the factor structure and examining appropriate uses.
A major problem in the understanding and psychological treatment of chronic pain patients is the inadequacy of available assessment procedures. Currently, the most frequently used instrument is the Pain Rating Index (PRI) of the McGill Pain Questionnaire, designed to assess 3 components of pain (i.e., sensory, affective, and evaluative) postulated by the Gate Control Theory. The PRI has been used in many studies to make differential diagnoses, to describe different groups of pain patients, and to identify the factor composition of the instrument itself. ⋯ Subsequent analyses revealed that the 3 components of the PRI do not display adequate discriminant validity. The current use of 3 subscales to establish differential diagnoses or patterns of different pain syndromes may lead to inappropriate classification and treatment decisions. The major conclusion of these findings is that use of only the total score of the PRI is appropriate for pain assessment.
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Recent evidence has underscored the importance of parental models and vicarious learning in the etiology of pain behavior. The present study investigated the relationships between the number of familial pain models to which an individual has been exposed, the individual's reports of current pain experiences, and the role of gender. ⋯ Additionally, pain models had a greater impact on females than on males. These findings are discussed in terms of vicarious learning and health locus of control processes.
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In a prospective study 58 patients undergoing limb amputation were interviewed the day before operation about their pre-amputation limb pain and 8 days, 6 months and 2 years after limb loss about their stump and phantom limb pain. All but one patient had experienced pain in the limb prior to amputation. Pre-amputation limb pain lasted less than 1 month in 25% of patients and more than 1 month in the remaining 75% of patients. ⋯ Both the localization and character of phantom pain changed within the first half year; no further change occurred later in the course. The incidence of stump pain 8 days, 6 months and 2 years after limb loss was 57, 22 and 21%, respectively. It is suggested that preoperative limb pain plays a role in phantom pain immediately after amputation, but probably not in late persistent phantom pain.
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Ketamine is an injectable anesthetic agent that has been shown to interact as an agonist at opiate receptors. In addition, its antinociceptive action in rats is antagonized by the narcotic receptor antagonist naloxone. Thus it was assumed that the anesthetic may activate the pain inhibitory pathway, originating in the periaqueductal gray (PAG) and descending into the spinal cord, in a manner similar to that of narcotics like morphine. ⋯ This action interfered with opiate actions in the PAG and made data from the microinjection studies difficult to interpret. The descending, pain inhibitory neuronal system originating in the PAG does not appear to participate in the antinociceptive action of ketamine measured by the tail-flick reflex. Perhaps the drug's effects are associated with alternative opiate mechanisms and/or opiate receptor subtypes not present on the cells of origin of the descending nerves within the PAG.