Selective depletion of CD8-positive leukocytes does not alter mercuric chloride induced acute renal failure in the rat

This study investigated the behaviour exhibited by 17 neuropathic pain patients (almost half of whom had documented neurological injury) with diffuse pain and extraterritorial sensory, sudomotor and vasomotor abnormalities, under the influence of intravenous administration of saline-controlled sodium amytal (SA), a medium action barbiturate. After SA (but not after normal saline) infusion, there was a dramatic and selective reduction of allodynia (touch-evoked pain) in all patients displaying this phenomenon, while pin prick and cold hypo- or hyperalgesia, as well as algometric pressure thresholds of the symptomatic limb (as a measurement of deep pain) were minimally changed in most patients. Spontaneous subjective pain was reduced substantially but not totally. The patients were able (once allodynia was eliminated) to recognize a deep-seated pain of which they were unaware before, evoked by firm but gentle palpation of the limb. Sympathetic blocks and A-fibre ischemic blocks in several patients and spinal stimulation in one patient produced effects identical to those observed during SA administration. The deep pain component was maintained despite elimination of allodynia even under stages of sleep induced by SA, at which time the patients would withdraw only the symptomatic limb upon firm but gentle palpation. We argue that neuropathic pain patients have two separate pain components, a cutaneous one (touch-evoked pain or allodynia) mediated by large fibres as a product of central sensitization, and a deep pain component mediated via nociceptors, which can be easily discriminated during systemic administration of SA.