Pain
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The relationship between neuroticism and extraversion on the 4 major stages of pain processing, that of pain sensation intensity, pain unpleasantness, suffering, and pain behavior, were studied in 205 chronic pain patients (88 male and 117 female). Patients underwent psychological evaluation which included the Pain Experience visual analogue scales (VAS) (Price et al. 1983), NEO Personality Inventory (NEO-PI) (Costa and McCrae 1985), and the Psychosocial Pain Inventory (PPI) (Getto and Heaton 1980). Canonical correlation was used to control for pain sensation intensity in evaluating affective dimensions of pain and to control for neuroticism in assessing effects of extraversion on different stages and dimensions of pain. ⋯ Personality factors had their greatest impact on stages 3 (suffering) and 4 (illness behavior) of pain processing. The results of multiple regression analyses indicated that life-long vulnerability to anxiety and depression is paramount in understanding the relationship between personality and suffering in chronic pain. These findings provide support for the idea that personality traits influence the ways in which people cognitively process the meanings that chronic pain holds for their life, and hence the extent to which they suffer.
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The diagnostic value of greater occipital and supra-orbital nerve blockades in patients with cervicogenic headache, migraine without aura, and tension-type headache was investigated. The pain reduction after greater occipital nerve blockade was significantly more marked in the cervicogenic headache group than in the other categories. Moreover, pain reduction in the forehead was generally only found in the cervicogenic headache patients (77%). ⋯ This procedure did not result in distinct pain reduction. The effect obtained in cervicogenic headache is, accordingly, probably due to the local anaesthesia. The present results support the postulate that different pathogenetic factors probably are responsible for cervicogenic headache, tension-type headache, and migraine without aura.
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Thirty-four patients having chronic idiopathic headaches participated in a long-term study comparing autogenic relaxation training alone (REL) with combinations of relaxation and electromyographic biofeedback (REL + EMG) or relaxation and temperature biofeedback (REL + TEMP). Assignment to treatment conditions was balanced on demographics and clinical characteristics, as well as headache classification according to muscle contraction or vascular headache symptomatology. ⋯ Headache activity continued to improve over the follow-up period independent of treatment condition. These data indicate that EMG biofeedback augments long-term clinical improvements in headache patients who undergo autogenic relaxation training.
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The involvement of NMDA receptors in rats with peripheral inflammation and hyperalgesia was evaluated by administration of the non-competitive NMDA receptor antagonist, MK-801. Inflammation and hyperalgesia was induced by intradermal injection of complete Freund's adjuvant (CFA) or carrageenan into the left hind paw. The latency of paw withdrawal from a thermal stimulus was used as a measure of hyperalgesia in awake rats. ⋯ MK-801 had no significant effect on receptive field size of dorsal horn neurons in rats without CFA-induced inflammation but blocked a transient expansion of the receptive fields induced by 1 Hz, C-fiber intensity electrical stimulation of the sciatic nerve. The background activity and noxious heat-evoked response of dorsal horn neurons in rats with CFA-induced inflammation were primarily inhibited and noxious pinch-evoked activity was both facilitated and inhibited by the administration of MK-801. These results support the hypothesis that NMDA receptors are involved in the dorsal horn neuronal plasticity and behavioral hyperalgesia that follows peripheral tissue inflammation.
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The course of pain associated with temporomandibular disorders (TMD) and other chronic pain conditions is typically episodic. Its expression may influence when a person seeks treatment, for example, when the level of pain flares up or exceeds its characteristic severity. Improvement in pain status subsequent to entering treatment may be due to: (1) specific effects of treatment; (2) non-specific effects of treatment ('placebo effects'); or (3) regression to the mean. ⋯ A control group of TMD subjects not seeking treatment showed no mean reduction in pain intensity but reported lower pain intensity at baseline than the group seeking care. When both groups of subjects were stratified on baseline VAS pain values, the reduction in pain increased as the baseline pain level increased, but no differences between comparable treated and untreated cases in the extent of improvement were observed. The before-after differences in both groups may be attributed to regression to the mean.(ABSTRACT TRUNCATED AT 250 WORDS)