Pain
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Evoked potentials in response to painful stimuli have been studied as objective measures of pain. Bromm has advocated experimental conditions in which, (1) stimulus intensities are randomized, and (2) subjects rate each stimulus. However, a cognitive, i.e. information processing, 'late positive component' (LPC), e.g. the P300, may be elicited by these same conditions, whether or not the stimuli are painful. ⋯ The Incremental LPC (average amplitudes from 350 to 650 ms) had a more parietal topography (amplitude at electrode Pz greater than at Cz) than the Oddball Standards LPC (Cz > Pz; protocol x electrode interaction P<0.001). This implies that the Rating Protocol LPC included P300-like activity. The parietal Incremental activity began as early as 250-350 ms after the stimulus in the responses to the most painful stimuli and therefore can confound the measurement of pain activity in the evoked potential.
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Parietal, insular and anterior cingulate cortices are involved in the processing of noxious inputs and genesis of pain sensation. Parietal lesions may generate central pain by mechanisms generally assumed to involve the 'medial' pain system (i.e. medial thalamic nuclei and anterior cingulate cortex (ACC)). We report here PET and fMRI data in a patient who developed central pain and allodynia in her left side after a bifocal infarct involving both the right parietal cortex (SI and SII) and the right ACC (Brodmann areas 24 and 32), thus questioning the schematic representation of cortical pain processing. ⋯ Conversely, both PET and fMRI data argue in favour of plastic changes in the 'lateral discriminative' pain system. Particularly, allodynia was associated with increased activity anteriorly to the infarct in the right insula/SII cortex. This response is likely to be responsible for the strange and very unpleasant allodynic sensation elicited on the left side by a non-noxious stimulation.
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A number of studies have examined the effects of naloxone on nitrous oxide-induced analgesia with conflicting results. In the present study the effects of a relatively high dose of naloxone was examined to determine its effects on nitrous oxide-induced analgesia, as well as on the subjective and psychomotor effects of nitrous oxide. Fourteen subjects participated in a four-session crossover trial in which they received intravenous injections of either saline or 30mg/70kg naloxone 10min into a 35min period in which they were inhaling either 100% oxygen or 30% nitrous oxide in oxygen. ⋯ Subjects reported higher pain ratings after the naloxone injection than the saline injection, but there was no evidence of naloxone reversing the analgesic effects of nitrous oxide. Similarly while naloxone also affected mood and impaired psychomotor performance, there was no evidence of naloxone reversing the effect of nitrous oxide on these measures. The results of this study call into question the role of the opioidergic system in mediating various effects of nitrous oxide in humans.