Pain
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The threshold at which noxious stimulation with a pressure algometer gives rise to a complaint of pain has been studied in neurological and psychiatric patients with pain and in two patients with fluctuating pain of organic origin. A correlation of r = 0.69 (P less than 0.0025) was demonstrated between two observers using the pressure algometer independently. ⋯ The threshold was also raised, outside the affected areas, in the two patients with fluctuating pain when the latter was more severe. Some requirements for an improved technique of pressure algometry are discussed.
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An electrophysiological analysis has been made of 82 L7 dorsal horn neurons antidromically activated from the contralateral C1 anterolateral quadrant (ALQ) of unanesthetized rhesus monkeys (bilateral carotid ligation). This analysis was made to compare refractory periods and antidromic activation thresholds with these same parameters of ALQ stimulation required to produce pain in conscious humans. Refractory periods of laminae IV-VI cells that were optimally but not exclusively responsive to noxious skin stimulation ranged from 0.8 to 2.8 msec (m = 1.5) and were briefer than those of lamina I cells. ⋯ Unlike lamina I cells, refractory periods and electrical thresholds of laminae IV-VI nociceptive neurons closely parallel those of ALQ-evoked pain in man. However, both lamina I and laminae IV-VI neurons usually responded to nociceptive skin temperatures (greater than 43 degrees C). This analysis indicates that pain may be signaled by the combined output of dorsal horn laminae I and IV-VI but that activation of only laminae IV-VI wide dynamic range neurons is sufficient to produce pain.
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These studies have examined threshold, frequency, and refractory period characteristics of a neural population in the anterolateral quandrant (ALQ) of the spinal cord of man, stimulation of which produces pain. Subjects were 18 conscious humans undergoing percutaneous anterolateral cordotomy for relief of intractable pain. Pain could be produced by ALQ stimulation in all subjects. ⋯ In 2 of 3 subjects, increases in stimulation frequency up to 500/sec did not produce pain when stimulation intensity was below threshold at 50/sec. The neuronal refractory period for pain in these subjects ranged between 1.0 and 2.0 msec, but the majority of relative refractory periods fell between 1.0 and 1.5 msec. The threshold, frequency, and refractory period data obtained in this study are similar to those found for wide dynamic range cells in the ventral half of the dorsal horn in the monkey and suggest that activation of these cells is a sufficient condition to produce pain in man.