We investigated the analgesic effects of escalating doses (0.214, 0.286, 0.357, and 0.429 mg/kg) of oral morphine on tolerance to painful cold pressor in a double-blind, active placebo-controlled (diphenhydramine) study in 45 normal volunteers. The highest dose of morphine administered is equivalent to the starting dose recommended by the Agency for Health Care Policy and Research for the management of cancer pain and acute postoperative pain. We assessed analgesia in terms of cold pressor tolerance time and self-reported ratings of pain intensity and unpleasantness. Subjects receiving the highest dose of oral morphine showed significantly higher tolerance time than subjects receiving diphenhydramine. Neither morphine or diphenhydramine significantly reduced ratings of pain intensity and unpleasantness. Neuropsychological testing revealed that the two highest doses of morphine impaired the episodic retrieval of a word list, but the same doses did not affect motor, perceptual, or attentional tasks.

Painful intracutaneous electric finger shock was delivered to the fifth digit of the non-dominant hand of five healthy volunteers. Whole head evoked magnetic field maps were collected and cortical localizations were calculated using local sphere equivalent current dipole fits. MRI scans were used to identify the anatomical structures where magnetic field sources were located. Anatomically, sources were identified bilaterally in the primary somatosensory region and SII-Insula regions. Additionally, frontal operculum sources were observed contralaterally in two subjects. Temporally, an initial contralateral SI activation at 40-60 ms was followed by several SII-Insula responses over the next several hundred milliseconds (ms). These SII-Insula responses were often interspersed with additional activations of the SI region. These later responses were observed in both hemispheres.

Sixty-five subjects experienced 2 cold pressor immersions. Following the initial immersion, subjects participated in the Velten mood induction procedure by reading either depressive, neutral or elative statements. The sensory discriminative response to pain was measured by ratings of pain, and the affective-reactive response to pain was measured by pain tolerance. Pain tolerance, but not pain ratings, were affected by mood inductions with subjects in the depression condition shortening their tolerance times more than the subjects in the neutral condition and the subjects in the elative condition increasing their tolerance times.

Phasic event-related desynchronization (ERD) of alpha activity briefly follows many types of stimulation. In order to define EEG changes resulting from longer stimulation. EEG records were made before and during hand immersion into cool and painfully cold water (cold pressor). Five minutes of 13-lead EEG records were obtained from 14 subjects for each condition. EEG frequency analysis was performed on artifact-free epochs from 60 to 240 sec following immersion. Following an initial phasic decrease in alpha power during cold water immersion, there was an augmentation of alpha power (8-12 Hz) in bilateral frontal and posterior electrodes. This augmentation was largely the result of an increase in the low alpha band (8-10 Hz). Alpha power at both central electrodes C3 and C4 changed little during cold water immersion. Cool water immersion produced less alpha power augmentation than cold water immersion. These observed changes were primarily in the high alpha band (10-12 Hz) and were larger in electrodes ipsilateral rather than contralateral to the stimulation. There was also an increase of beta bilaterally in frontal and posterior regions with cold water immersion. Our data demonstrate sustained topographic EEG responses during tonic stimulation from hand immersion in painfully cold water. These changes differ from those produced by stimulation with cool water immersion.

Surface magnetic and electric recordings were used to localize the sources of late pain-related magnetic fields and electric potentials, evoked by painful intracutaneous electric finger stimulation. We find that the source of the P90m component of the evoked magnetic field lies in the finger area of the primary somatosensory cortex; the sources of the N150m and P250m are found to reside in the frontal operculum. These findings are unexpected from the evoked electric potential data, which suggest a central location for these sources. We also note that the interpretation of the electric data was confounded by the presence of an alpha-like oscillation, which overlapped many components of the evoked potential.