Pain
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In a group of 30 subjects suffering from sympathetic reflex dystrophies of the limbs, the sympathetic ganglia of the affected side were blocked with a local anesthetic. Using an original method, we measured the cutaneous pain threshold before the block and at prefixed intervals after the block during a period of 2 days. In all subjects the cutaneous pain threshold showed damped oscillations both in the limb ipsilateral to the block and in the contralateral one. The analysis of these oscillations showed: (a) that the sympathetic control of the cutaneous pain threshold may be exerted through a negative feedback loop (skin-afferent input-CNS-sympathetic output-skin); (b) that the afferent discharge of a limb controls the contralateral sympathetic output through central mechanisms.
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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.