Self-observation as a source of pain perception.
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The present study was designed to investigate the pain relief mechanism of electrical stimulation to the pituitary and the relationship between hypothalamic and pituitary analgesic mechanism through the observation of monkey behavior and characteristics of tooth pulp-evoked potentials. The results suggest that pituitary-stimulating analgesia should be differentiated from hypothalamic-stimulating effect. In view of the facts, the theory of the Pituitary Inhibitory System is proposed.
Pain sensitivity and tolerance were studied using the cold-pressor technique. A 3 independent groups design was employed using rumination as the independent variable. Group 1 was given a situation in which anger-related self-rumination was introduced. Group 2 was given a self-related rumination task in which anger was not induced. Group 3 received a rumination task not related to the self. In addition, the State-Trait Anger Expression Inventory was given prior to the experiment to test the hypothesis that ratings on the Anger-In subtest would correlate with pain sensitivity. In each group were 6 men and 6 women. Each participant took the anger and another inventory not relevant to the present study before the experiment. An anger measure was taken before and after the experiment for each group to see if the anger induction in Group 1 actually increased anger. There were no differences among the 3 groups on the second anger measure, so differences between Groups 1 and 2 could not be attributed to anger. A 1-way analysis of variance for 3 groups showed a strong main effect on pain tolerance but not pain sensitivity. Groups 1 and 2 were significantly more tolerant of pain than Group 3. The correlation of ratings on the Anger-In (internalized anger) subtest fell short of statistical significance with pain sensitivity and also was not significant for pain tolerance. Results were discussed in terms of the possibility that self-rumination may increase pain tolerance by requiring a greater cognitive load than nonself rumination.
Starting from a case of marked pain insensitivity in a patient suffering from catatonic schizophrenia we state in this paper that analgesia seems to be an ubiquitous phenomenon which is not only caused by physical disorders of the central nervous system. Different models of interpretation as to be found in scientific literature are reviewed. On the basis of today's physiological knowledge, five hypotheses on causal explanation of pain insensitivity in schizophrenics are discussed: Hypalgesia and analgesia are an expression of motorial inability to react; a consequence of a disorder of consciousness; an analgetic effect of neuroleptic drugs; a basic deficit in schizophrenia and; a result of a disturbed psycho-physiological development.
The most important studies on weather-related pain have been analysed and their results compared. Since different medicometeorological classifications were used, and individual reactions to the weather vary considerably, it is possible to recognize unequivocal, universally valid relationships only with difficulty. Rheumatic pain arises mainly in a cold front area, in unstable polar air, and in thunderstorms. Amputation- and scar-related pain is similarly dependent upon changes in the weather. Headaches and migraine are typical signs of an imminent change in the weather. The question as to whether or not the endorphin concentration is of significance for meteorogenic pain is discussed, and possible influences of atmospherics activity noted.
Much evidence indicates that women experience painful stimuli as more intense than men do. Nevertheless, some data suggest that sustained low-level pain may be more disturbing to men than to women. The current experiment evaluated the hypothesis that pain is more disturbing for men than for women by comparing across genders sensory and emotional aspects of pain evoked by capsaicin. Ten men and 10 women (aged 20-46 years) received topical capsaicin for 30 min on the face in one session and on the ankle in another. The subjects rated on visual analog scales pain intensity, unpleasantness and anxiety each minute during capsaicin application and for 30 min after its removal. During capsaicin application, females rated both pain intensity (P = 0.04) and unpleasantness (P = 0.05) higher than did males. Further, subjects rated pain intensity and unpleasantness higher on the face than on the ankle, although the physical stimulus was the same. Despite their lower pain ratings, men reported more pain-related anxiety than women (P = 0.02) Moreover, men showed a significant positive correlation between anxiety and pain intensity and unpleasantness, whereas women did not. After removing the capsaicin, there was no overall effect of sex on either intensity (P = 0.18) or unpleasantness (P = 0.37) of the residual sensation. However, men still showed a positive correlation between anxiety and the intensity and unpleasantness of the sensation. Our data confirm with the topical capsaicin model that women rate pain higher than men, but despite their lower pain ratings, males have more anxiety related to pain.
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The lipid mediator prostaglandin E2 (PGE2) has diverse biological activity in a variety of tissues. Four different receptor subtypes (EP1-4) mediate these wide-ranging effects. The EP-receptor subtypes differ in tissue distribution, ligand-binding affinity, and coupling to intracellular signaling pathways. To identify the physiological roles for one of these receptors, the EP1 receptor, we generated EP1-deficient (EP1-/-) mice using homologous recombination in embryonic stem cells derived from the DBA/1lacJ strain of mice. The EP1-/- mice are healthy and fertile, without any overt physical defects. However, their pain-sensitivity responses, tested in two acute prostaglandin-dependent models, were reduced by approximately 50%. This reduction in the perception of pain was virtually identical to that achieved through pharmacological inhibition of prostaglandin synthesis in wild-type mice using a cyclooxygenase inhibitor. In addition, systolic blood pressure is significantly reduced in EP1 receptor-deficient mice and accompanied by increased renin-angiotensin activity, especially in males, suggesting a role for this receptor in cardiovascular homeostasis. Thus, the EP1 receptor for PGE2 plays a direct role in mediating algesia and in regulation of blood pressure.
We investigated the relation between the subjective sensation of pain and two different components of the laser evoked potential, namely the vertex response (N220-P350) and an earlier lateralized response (middle-latency NP160). Brain responses to laser stimuli were obtained in 15 subjects under attentive and distractive conditions. Although stimulus intensity was kept constant, it was perceived as significantly higher when subjects attended the stimulation. There was a positive correlation between subjective intensity perception and the amplitude of the vertex potential, but no correlation existed with the middle-latency component. While laser vertex potentials may reflect attentional/perceptual mechanisms that determine subjective experience, the NP160 behaves as a pre-perceptual sensory response that should be advantageous in the assessment of early cortical pain processing.
Complete loss of parietal peritoneal sensitivity observed in a patient with long-standing ascites secondary to cirrhosis of the liver prompted an investigation of peritoneal sensitivity in 22 patients with the same condition. In all of them a decrease of the peritoneal sensitivity to needle perforation was found. All perceived peritoneal perforation as less painful than perforation of the abdominal skin by the same needle. In 8 control patients perforation of the peritoneum caused more discomfort than the perforation of the skin. In 7 cirrhotic patients where a histologic examination of the parietal peritoneum was available a chronic fibrotic peritonitis was present. Peritoneal insensitivity may partly account for mild abdominal symptoms in cirrhotics developing bacterial peritonitis.
Results from laboratory and naturalistic studies have demonstrated decreased subjective pain ratings in hypertensives and individuals at risk for hypertension. Based on previous evidence that the nociceptive withdrawal reflex may provide an objective index of pain threshold in humans, the present study examined the intensity of sural nerve stimulation required to elicit nociceptive withdrawal in offspring of hypertensives and normotensives. Participants included 60 men and 56 women who were normotensive, 18-23 years of age, and predominately Caucasian. To assess the nociceptive withdrawal reflex, ascending and descending intensities of electrical stimulation were applied over the sural nerve while electromyographic activity was recorded from the ipsilateral biceps femoris muscle. Analyses of the intensity of electrical stimulation required to reach the thresholds for nociceptive withdrawal and subjective pain revealed a pattern of hypoalgesia in individuals at risk for hypertension. First, significantly higher intensities were required to elicit nociceptive withdrawal in offspring of hypertensives versus normotensives. Second, offspring of hypertensives endured significantly more intense stimulation before reporting pain. Third, both parental history of hypertension and resting systolic blood pressure were significant independent predictors of stimulation intensity at nociceptive withdrawal reflex and subjective pain thresholds. These results confirm and extend previous observations of an association between risk for hypertension and hypoalgesia, and suggest that hypoalgesia should be examined as a potential predictor of progressive blood pressure increases in individuals at risk for hypertension.
The purpose of this study was to determine the effect of conventional low-intensity transcutaneous electrical nerve stimulation (TENS) waveform and frequency characteristics on experimentally induced acute pain. Each of 28 male subjects received six forms of TENS and one control treatment during a single testing session. Treatments used one of two waveforms (monophasic or biphasic) and one of three frequencies (30, 60, or 85 Hz) administered to the forearm. Treatment effects were ascertained from alterations in pain-threshold and pain-tolerance responses induced by noxious electrical stimulation of the ipsilateral fifth digit. The TENS waveform and frequency had a negligible effect on pain threshold. The results indicated that waveform did not influence pain tolerance significantly. Pain tolerance, however, increased significantly at the frequency of 60 Hz but decreased significantly at both 30 and 85 Hz (p less than .05). We concluded that TENS frequency is an important factor in altering the subjects' perception of experimentally induced pain.