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1. Quantitative 2-deoxyglucose (2-DG) experiments were undertaken to determine the spatial distribution of nociceptive responses in the rat spinal cord. Twenty unanesthetized, paralyzed rats with T2 transected spinal cords were divided into groups (n = 4) and stimulated with non-noxious (35 degrees C) or graded noxious temperatures (45 degrees, 47 degrees, 48 degrees, and 49 degrees C). Stimulation was delivered by cyclical immersion of one hind paw in a temperature-controlled water bath. 2. When stimulation began, 50 microCi of 2-DG was injected into the rat, and timed sequential blood samples were drawn to monitor plasma glucose and 2-DG levels. On termination of stimulation, spinal cords were removed, sectioned, and prepared for autoradiography. Local rates of spinal cord metabolism were obtained by microcomputer analysis of autoradiographs. 3. Nociceptive stimulation produced increases in glucose utilization in some of the grey matter laminae previously implicated in nociceptive processing. Within the nociceptive range, 49 degrees and 48 degrees C intensities elicited significantly greater responses than did 45 degrees C stimulation. 4. The rostrocaudal spatial distribution of nociceptive responses was most extensive within laminae V-VI with stimulus-evoked metabolic activity extending 9 mm from L2-L5. Similarly, metabolic increases occurred over 7 mm within lamina VII. In contrast, metabolic activity within the upper dorsal horn (laminae I-IV) extended only 3 mm and was limited to L4. Metabolic patterns within laminae VIII-IX sharply differed from those within other laminae in that no increases occurred within L4, although regions of L3 and L5 were responsive to stimulation.(ABSTRACT TRUNCATED AT 250 WORDS)

The direct depressive effect of opioids on the transmission of nociceptive processing at the spinal level is well documented (see refs in Le Bars and Besson, 1981; Duggan and North, 1984; Yaksh and Noueihed, 1985; Zieglgansberger, 1986; Besson and Chaouch, 1987). Both pre- and postsynaptic mechanisms have been proposed as an explanation of the depressive effects of opioids on the activity of nociceptive dorsal horn neurons. Despite the lack of morphological evidence for a direct presynaptic control by enkephalinergic axo-axonic synapses, there is evidence for a presynaptic action of opioid substances (Fields et al, 1980; Jessell and Iversen, 1977; Lamotte et al, 1976; MacDonald and Nelson, 1978; Mudge et al, 1979; Sastry, 1979). In addition both electrophysiological (Barker et al, 1978; Zieglgansberger and Tulloch, 1979; Yoshimura and North, 1983) and immunocytochemical (Aronin et al, 1981; Hunt et al, 1980; Ruda, 1982; Ruda et al, 1984) investigations support postsynaptic sites of action of opioids.

Responses induced by tooth pulp stimulation were studied in 27 gallamine immobilized adult cats. Single units were recorded from the amygdala using stainless steel microelectrodes. Of 57 amygdaloid neurons, 8 were responsive to only non-nociceptive (tap and/or hair bending) stimuli, 7 were responsive to both nociceptive (pinch) and non-nociceptive stimuli, 18 were responsive to nociceptive stimuli, non-nociceptive stimuli and tooth pulp stimulation, and the others did not respond to these stimuli. The neurons in the amygdala responsive to tooth pulp stimulation were localized in the nucleus amygdaloideus centralis (pars lateralis) [Acl], nucleus amygdaloideus centralis (pars medialis) [Acl] and nucleus amygdaloideus basalis (pars magnocellularis) [Abm]. The response induced by tooth pulp stimulation was depressed by morphine and reversed by naloxone. These results suggest that Acl, Acm and Abm in the amygdala may receive pain sensation evoked by tooth pulp stimulation. Moreover, there is a possibility that these nuclei may be related to the emotional component involved in nociceptive processing.

Hunger and pain are basic drives that compete for a behavioral response when experienced together. To investigate the cortical processes underlying hunger-pain interactions, we manipulated participants' hunger and presented photographs of appetizing food or inedible objects in combination with painful laser stimuli. Fourteen healthy participants completed two EEG sessions: one after an overnight fast, the other following a large breakfast. Spatio-temporal patterns of cortical activation underlying the hunger-pain competition were explored with 128-channel EEG recordings and source dipole analysis of laser-evoked potentials (LEPs). We found that initial pain ratings were temporarily reduced when participants were hungry compared with fed. Source activity in parahippocampal gyrus was weaker when participants were hungry, and activations of operculo-insular cortex, anterior cingulate cortex, parahippocampal gyrus, and cerebellum were smaller in the context of appetitive food photographs than in that of inedible object photographs. Cortical processing of noxious stimuli in pain-related brain structures is reduced and pain temporarily attenuated when people are hungry or passively viewing food photographs, suggesting a possible interaction between the opposing motivational forces of the eating drive and pain.

Inoculation is one of the first and most common experiences of procedural pain in infancy. However, little is known about how needle puncture pain is processed by the central nervous system in children. In this study, we describe for the first time the event-related activity in the infant brain during routine inoculation using electroencephalography. Fifteen healthy term-born infants aged 1 to 2 months (n = 12) or 12 months (n = 5) were studied in an outpatient clinic. Pain behavior was scored using the Modified Behavioral Pain Scale. A distinct inoculation event-related vertex potential, consisting of 2 late negative-positive complexes, was observable in single trials after needle contact with the skin. The amplitude of both negative-positive components was significantly greater in the 12-month group. Both inoculation event-related potential amplitude and behavioral pain scores increased with age but the 2 measures were not correlated with each other. These components are the first recordings of brain activity in response to real-life needle pain in infants up to a year old. They provide new evidence of postnatal nociceptive processing and, combined with more traditional behavioral pain scores, offer a potentially more sensitive measure for testing the efficacy of analgesic protocols in this age group.

There is a lack of objective outcome measures for monitoring key neural mechanisms underlying chronic pain, such as central sensitization. Recently, we combined psychophysical Multiple Threshold Tracking (MTT) with evoked potentials (EPs) to study neurophysiological activity related to processing of single- and double-pulse electronociceptive stimuli. Results from pain-free subjects measured at the Technical Medical Center of the University of Twente suggest that the MTT-EP method might be a promising step toward a diagnostic tool for chronic pain patients. A next step is exploration of its replicability in a hospital environment and its behavior in chronic pain patients. We explored the replicability of the MTT-EP method in twenty pain-free subjects (Central Sensitization Inventory (CSI)-score 14.6 ± 8.8) at St. Antonius Hospital. Secondly, we measured nociceptive detection thresholds (NDTs) and EPs from seven failed back surgery syndrome (FBSS) patients (CSI-score 49.0 ± 15.5). Preliminary results show values of NDTs and EPs, habituation and paired-pulse facilitation, which are in line with results from the University of Twente. Again, EPs are modulated by stimulus detection and amplitudes. Strikingly, we found higher NDTs in FBSS patients and EPs appeared modulated by stimulus detection, but not by amplitudes. Since similar phenomena in NDTs and EPs were observed during nociceptive stimulation in pain-free subjects at St. Antonius hospital, it can be concluded that results of MTT-EP method can be replicated. Secondly, the observed altered behavior of NDTs and EPs in FBSS patients showing signs of central sensitization allows further hypotheses regarding responsiveness to mechanisms underlying chronic pain.

We manipulated the sense of body ownership with the rubber hand illusion (RHI) to determine if perception of a potentially painful threat to the rubber hand can modify the mechanical pain threshold (MPT). Simultaneous tactile stimulation of the subject's concealed hand and the appropriately positioned visible rubber hand generated the illusion of false body ownership. The MPT was recorded on the left hand of the subjects before and after induction of the RHI, as well as during the phase in which the model hand was pricked with a sharp knife or touched by the blunt knife handle. The results indicate that the RHI could be successfully generated with our set-up. Mechanical stimuli were perceived as more painful in the condition where the rubber hand was simultaneously pricked with a knife. Our findings suggest that the illusion of body ownership gates nociceptive processing of potentially painful stimuli.