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.
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Eighteen patients with chronic musculoskeletal pain completed a trial of EMG feedback where each subject was exposed to biofeedback, a control condition and a waiting list. Pain scores were determined pre- and posttrial, and the percentage change calculated for each subject. EMG activity and present pain measured during the trial gave an EMG/pain correlation for each patient. ⋯ In addition, patients with high EMG/pain correlations had a better outcome and this measure also correlated with pain scores. The relationship between self-concepts and EMG/pain correlations is discussed. The Illness Self-Concept Repertory Grid appears capable of predicting treatment outcome and shows promise as a prognostic tool.
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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.