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The perception of pain in three groups of patients with angina pectoris has been studied. All patients went through a bicycle ergometer test with an increase of 10 wat each minute. Heart rates and ratings of pain were collected towards the end of each work load. Reliable results of diagnostic interest were obtained. The rating procedure is discussed and a new category rating scale with ratio properties is also presented.
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The hippocampus is an important structure for declarative, spatial, and contextual memory and is implicated in the perception of chronic pain. The hippocampal formation is vulnerable to damage from seizures, ischemia, and head trauma and is particularly sensitive to the effects of adrenal glucocorticoids secreted during the diurnal rhythm and chronic stress. Adrenal steroids typically have adaptive effects in the short run, but promote pathophysiology when there is either repeated stress or dysregulation of the HPA axis. The damaging actions of glucocorticoids under such conditions have been termed "allostatic load", referring to the cost to the body of adaptation to adverse conditions. Adrenal steroids display both protective and damaging effects in the hippocampus. They biphasically modulate excitability of hippocampal neurons, and high glucocorticoid levels and severe acute stress impair declarative memory in a reversible manner. The hippocampus also displays structural plasticity, involving ongoing neurogenesis of the dentate gyrus, synaptogenesis under control of estrogens in the CA1 region, and dendritic remodeling caused by repeated stress or elevated levels of exogenous glucocorticoids in the CA3 region. In all three forms of structural plasticity, excitatory amino acids participate along with circulating steroid hormones. Glucocorticoids and stressors suppress neurogenesis in the dentate gyrus. They also potentiate the damage produced by ischemia and seizures. Moreover, the aging rat hippocampus displays elevated and prolonged levels of excitatory amino acids released during acute stress. Our working hypothesis is that structural plasticity in response to repeated stress starts out as an adaptive and protective response, but ends up as damage if the imbalance in the regulation of the key mediators is not resolved. It is likely that morphological rearrangements in the hippocampus brought on by various types of allostatic load alter the manner in which the hippocampus participates in memory functions and it is conceivable that these may also have a role in chronic pain perception.
BACKGROUND: Experimental studies on humans have shown that recurrent pain is associated with altered pain perception. We measured the pressure pain threshold in regions of the body surface in a group of children who had recurrent abdominal pain and in a group of children with chronic or recurrent disease but with no pain. METHODS: Each group consisted of 45 boys and 55 girls ranging in age from 5 to 15.8 years. The regions of the body were the trapezius, deltoid, and supraspinous muscles, nine areas on the abdominal wall, and the median part of the tibias. Using an algometer, pressure was applied through a rubber disc with a surface area of 1 cm2 at a rate of 0.5 kg/cm2/s. The pressure values recorded with the algometer when the children communicated that they started to feel pain were considered as pressure pain thresholds. RESULTS: The pain thresholds were reduced in all regions investigated in children with recurrent pain. The median thresholds for all regions of the patients with and without pain were 1.60 and 2.2 kg/cm2, respectively. The diseases of children with pain did not influence the pain thresholds. CONCLUSION: There was an association between recurrent abdominal pain and a lower pressure pain threshold, with no influence of the type of disease, and there was a central nervous system alteration in the perception of pain in these patients.
Patients presenting to the emergency department have a common complaint of pain. Whether admitted to the hospital or discharged to home, patients are leaving the emergency department in a higher level of pain than would be considered tolerable or comfortable. Pain can be a major impediment to an adequate quality of life. Unrelieved or chronic pain causes anxiety, depression, sleep disturbances, decreased self-esteem and self-worth, inactivity, altered family dynamics, financial stress and an increase in the number of health-care visits. The purpose of this study was to evaluate patients' perception and report of pain in the ED from the time of arrival to the time of discharge. The sample consisted of 63 females and 62 males from an ED of an urban hospital in Trenton, New Jersey. The mean age for the males was 40 years, and the mean age for the females was 41 years. The pain level of the participants was measured by the use of a visual analogue scale at the time of arrival and at the time of discharge from the ED. A paired t-test for related samples revealed that the VAS scores decreased from 5.90 to 3.38 (p = .000).
We recorded magnetoencephalography (MEG) and functional magnetic resonance imaging (fMRI) following noxious laser stimulation in a Yoga Master who claims not to feel pain when meditating. As for background MEG activity, the power of alpha frequency bands peaking at around 10 Hz was much increased during meditation over occipital, parietal and temporal regions, when compared with the non-meditative state, which might mean the subject was very relaxed, though he did not fall asleep, during meditation. Primary pain-related cortical activities recorded from primary (SI) and secondary somatosensory cortices (SII) by MEG were very weak or absent during meditation. As for fMRI recording, there were remarkable changes in levels of activity in the thalamus, SII-insula (mainly the insula) and cingulate cortex between meditation and non-meditation. Activities in all three regions were increased during non-meditation, similar to results in normal subjects. In contrast, activities in all three regions were weaker during meditation, and the level was lower than the baseline in the thalamus. Recent neuroimaging and electrophysiological studies have clarified that the emotional aspect of pain perception mainly involves the insula and cingulate cortex. Though we cannot clearly explain this unusual condition in the Yoga Master, a change of multiple regions relating to pain perception could be responsible, since pain is a complex sensory and emotional experience.
During the last 2 decades, a vast amount of information has been obtained about the sensory system responsible for pain perception, with the result that there have been dramatic changes in the understanding of how pain is experienced and how pain can be modified. However, recent advances in the management of pain have been confined almost exclusively to adults. Consequently, our understanding about pain perception in infants, children and adolescents, our knowledge about the prevalence of different pain problems for children and data about the effectiveness of various pharmacological and nonpharmacological pain control methods are limited. This article explores the issue of the undertreatment of acute, recurrent, chronic and cancer pain in infants and children.
The study was performed to determine whether epidural fentanyl produced segmental sensory changes to electrical stimulation at different frequencies. Eight healthy volunteers received fentanyl 1 microgram/kg both intravenously and epidurally in a randomized, double-blind, cross-over fashion. Perception thresholds and amount of current required to elicit a predetermined level of moderate pain (Cmp) at 5,250, and 2000 Hz stimulation were measured at ipsilateral dermatomes C2 and L2 at 0, 5, 15, 30, 45, and 60 min after injection. Perceptions to 5,250, and 2000 Hz stimulation were unaffected by either intravenous or epidural fentanyl (P > 0.08). Intravenous fentanyl increased Cmp at both 5 and 250 Hz at both dermatomes (P < 0.004) and thus did not produce segmental analgesia. In contrast, epidural fentanyl increased Cmp only at the L2 dermatome and only at 5 Hz (P = 0.005). We conclude that an epidural bolus of fentanyl results in segmental spinal analgesia to transcutaneous electrical stimulation only at specific frequencies. Furthermore, pain produced by stimulation at 5 Hz may have a different pharmacology than pain produced by 250 Hz stimulation.
In 5 percent of adult patients with symptoms of acute abdominal illness ("Akutes Abdomen") several extraabdominal diseases can be responsible: pulmonary; cardiovascular; retroperitoneal, metabolic diseases; exogenous intoxications; varia. It often is difficult to look through the pathophysiological ways of abdominal pain perception. Besides direct stimulation of receptors by toxines and/or metabolic products, transmission of pain ("übertragener Schmerz") is as known for pain perception as emotional factors are. The decision not to operate is difficult and requires safe and immediate differential diagnosis, which mostly is achieved by a precise patient's history, clinical features like localisation and quality of pain as well as technical and laboratory studies.
The method by which the body detects, interprets, and responds to painful stimulation is tantamount to an orchestral concert, with each individual instrument contributing a subtle yet important element composing the finished product. The polymodal peripheral receptors initiate unpleasant sensations that can be modulated in the dorsal horn and the anterior columns of the spinal cord before reaching the cerebral cortex. Despite similar neurological "wiring," pain sensations from the skin are not the same in character as those from visceral organs. A reaction of pain is based upon interpretation in specific cerebral centers and the resultant motor function. With the advent of functional MRI and PET scanners, the understanding of the cerebral interpretation of pain is expanding. Remember as well that emotional and psychological factors are crucial in pain perception, and are the starting points for any individual's perception of a painful circumstance.
When the degree of genetic determination of a trait (i.e. its heritability) is high, one tends to presume that environmental factors will not modify its expression by much. Contrary to this expectation, we show here in rats that a psychosocial-behavioral variable, the identity of cagemates, can largely over-ride genetic predisposition to pain behavior. We used selection-line rats that consistently show high (HA) or low (LA) pain phenotype (autotomy) in the neuroma model of neuropathic pain. Normally, HA animals show autotomy after nerve injury while LA animals do not. However, when caged together with HA rats, LA rats showed high levels of autotomy. This occurred even when the individual HA cagemates were familiar preoperatively, and it did not depend on the actual performance of autotomy by the HA rats. Indeed, cage bedding soiled by HA rats was sufficient to induce a modest level of autotomy in LA animals. Chemical cues associated with HA rats, perhaps in combination with behavioral characteristics, are apparently able to induce pain phenotype despite the powerful protection otherwise rendered by the LA genotype. Social factors must be considered in behavior-related research on rodents that have undergone genetic modification. More generally, the overwhelming influence that psychosocial-behavioral variables have on pain perception, and on pain behavior, in humans may have evolutionary roots deeper than has previously been appreciated.
Congenital insensitivity to pain (hereditary sensory and autonomic neuropathy [HSAN] type V) is a rare disorder of pain perception in which pain sensation is absent from birth, with no other neurologic deficits. We report five Saudi patients (three male and two female) age 10 months to 23 years who lacked pain sensation from birth but have normal appreciation of other sensory modalities. They are from four related families who are descended from one grandfather. The patients had sustained many painless injuries resulting in fractures and disfigurement, but otherwise are completely normal.
Ketamine reduces nociception by binding noncompetitively to the N-methyl-D-aspartate (NMDA) receptor, activation of which increases spinal hypersensitivity. We studied 19 healthy, unmedicated male volunteers, aged 20-31 yr. Burn injuries were produced on the medial surface of the dominant calf with a 25 x 50 mm rectangular thermode. On 3 separate days, at least 1 week apart, subjects received a bolus of either ketamine 0.15 mg kg-1, ketamine 0.30 mg kg-1 or placebo, delivered by a mechanical infusion pump over 15 min. The bolus was followed by continuous infusion of ketamine 0.15 mg kg-1 h-1, ketamine 0.30 mg kg-1 h-1 or placebo, respectively, for 135 min. Ketamine reduced the magnitude of both primary and secondary hyperalgesia, and also pain evoked by prolonged noxious heat stimulation, in a dose-dependent manner. In contrast, ketamine did not alter phasic heat pain perception (perception of transient, painful, thermal stimuli) in undamaged skin. The analgesic effects of ketamine in the burn injury model are in agreement with results from experimental studies, and can be distinguished from those of local anaesthetics and opioids. Side effects caused by continuous infusion of ketamine 0.15 and 0.30 mg kg-1 h-1 were frequent but clinically acceptable.
UNLABELLED: The development of acute opioid tolerance in humans remains controversial. We tested the hypothesis that continuous remifentanil infusion leads to rapid development of opioid tolerance. Twenty healthy male volunteers were enrolled onto a randomized, placebo-controlled, double-blinded, cross-over design study to receive a 3 h continuous infusion of remifentanil (0.08 microg x kg(-1) x min(-1)) or saline. Test procedures included determination of pain perception thresholds and pain tolerance thresholds to heat and cold and neuroselective sine wave constant current at 5 Hz and 250 Hz. Test procedures were performed at baseline and then repeated at 25, 55, 85, 115, and 160 min (heat/cold) and at 35, 65, 95, 125, and 170 min (electrical current) during infusion. No significant decrease of the pain threshold devolutions between 55 and 180 min after the start of infusion of remifentanil could be detected. In conclusion, no development of acute opioid tolerance was observed during constant remifentanil infusion of 3 h in volunteers. IMPLICATIONS: The opioid remifentanil was applied to 20 volunteers at a constant concentration for 3 h while pain thresholds to temperature and current were repeatedly assessed. Our aim was to study whether thresholds decrease over time because of the rapid development of opioid tolerance. No development of rapid opioid tolerance was observed.
BACKGROUND: Several recent studies suggest that repetitive transcranial magnetic stimulation can temporarily reduce pain perception in neuropathic pain patients and in healthy adults using laboratory pain models. No studies have investigated the effects of prefrontal cortex stimulation using transcranial magnetic stimulation on postoperative pain. METHODS: Twenty gastric bypass surgery patients were randomly assigned to receive 20 min of either active or sham left prefrontal repetitive transcranial magnetic stimulation immediately after surgery. Patient-controlled analgesia pump use was tracked, and patients also rated pain and mood twice per day using visual analog scales. RESULTS: Groups were similar at baseline in terms of body mass index, age, mood ratings, pain ratings, surgery duration, time under anesthesia, and surgical anesthesia methods. Significant effects were observed for surgery type (open vs. laparoscopic) and condition (active vs. sham transcranial magnetic stimulation) on the cumulative amount of patient-delivered morphine during the 44 h after surgery. Active prefrontal repetitive transcranial magnetic stimulation was associated with a 40% reduction in total morphine use compared with sham during the 44 h after surgery. The effect seemed to be most prominent during the first 24 h after cortical stimulation delivery. No effects were observed for repetitive transcranial magnetic stimulation on mood ratings. CONCLUSIONS: A single session of postoperative prefrontal repetitive transcranial magnetic stimulation was associated with a reduction in patient-controlled analgesia pump use in gastric bypass surgery patients. This is important because the risks associated with postoperative morphine use are high, especially among obese patients who frequently have obstructive sleep apnea, right ventricular dysfunction, and pulmonary hypertension. These preliminary findings suggest a potential new noninvasive method for managing postoperative morphine use.
The efficacy, duration, and spread of epidural morphine hypoalgesia were assessed by an experimentally induced pricking pain evoked by laser stimulation. Four mg of plain morphine was injected epidurally in 7 volunteers at the L2-L3 interspace. Thresholds to warmth and pain perception, and pain-evoked potentials were measured. In the first experiment, hypoalgesia was monitored each hour for 7 h at various dermatomes. Hypoalgesia was detected at S1 dermatome after 2 h, but 3 h elapsed before hypoalgesia could be detected at the L1, T12, T10, T8, and T6 dermatomes. No effect was found at C7. No conduction delay was found along the pain pathway during hypoalgesia. Hypoalgesia lasted more than 7 h at S1, whereas hypoalgesia could not be detected after 5 h at other dermatomes. In the second experiment, naloxone (0.8 mg i.v.) was injected 230 min after injection of epidural morphine, and the subsequent recording 10 min later showed that hypoalgesia had been partly reversed. The onset and duration of hypoalgesia are different for experimentally induced pain and clinical pain. Experimentally laser-induced pain has the advantage of being quantitative, and is, as such, useful to assess hypoalgesia, and to test the potency of narcotics.
OBJECTIVE: Dermal inflammation from many causes may produce a reversible period of hyperalgesia (increased sensitivity to pain perception) or allodynia (pain from innocuous stimuli). Hyperalgesia and allodynia have received relatively little attention in clinical trials of acute pain. We sought to quantitate tactile allodynia and thermal hyperalgesia in outpatients presenting with acute dermal injuries. DESIGN: We performed a randomized clinical trial to compare standard methodology for the assessment of hyperalgesia with two novel simple quantitative techniques. PATIENTS: After Institutional Review Board approval, 40 patients presenting with acute chemical, thermal, mechanical, or infectious skin injury were subjected to a series of tests at the site of injury, an intact mirror site, and a noninjured ipsilateral control site. OUTCOME MEASURES: Quantitative thermal sensory testing (Medoc sensory analyzer) was followed by a 5-second application, in random order, of copper rods preheated in water to 40 degrees C, 43 degrees C, 46 degrees C, and 49 degrees C. Pressure testing was conducted with a 1.25-inch diameter commercially available pressure transducer gauge. RESULTS: The observed pattern of responses was remarkably consistent among testing methods. All challenges with the four different temperatures elicited pain scores on a visual analog scale markedly greater at the injured than at the mirror or control site (P < 0.001 vs control). Pressure discomfort thresholds followed a similar pattern. CONCLUSIONS: We conclude that hyperalgesia is a prominent contributor to discomfort in acute dermal injury and hence is a legitimate therapeutic target. Quantitation of the contribution of thermal hyperalgesia and tactile allodynia and assessment of their management is feasible using simple, rugged, low-cost methods. This inexpensive methodology may be useful in everyday clinical practice as well as in clinical research evaluating pharmacological agents to manage hyperalgesia.
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