Experimental data on age-related changes in pain perception have so far been contradictory. It has appeared that the type of pain induction method is critical in this context, with sensitivity to heat pain being decreased whereas sensitivity to pressure pain may be even enhanced in the elderly. Furthermore, it has been shown that temporal summation of heat pain is more pronounced in the elderly but it has remained unclear whether age differences in temporal summation are also evident when using other pain induction methods. No studies on age-related changes in spatial summation of pain have so far been conducted. The aim of the present study was to provide a comprehensive survey on age-related changes in pain perception, i.e. in somatosensory thresholds (warmth, cold, vibration), pain thresholds (heat, pressure) and spatial and temporal summation of heat and pressure pain. We investigated 20 young (mean age 27.1 years) and 20 elderly (mean age 71.6 years) subjects. Our results confirmed and extended previous findings by showing that somatosensory thresholds for non-noxious stimuli increase with age whereas pressure pain thresholds decrease and heat pain thresholds show no age-related changes. Apart from an enhanced temporal summation of heat pain, pain summation was not found to be critically affected by age. The results of the present study provide evidence for stimulus-specific changes in pain perception in the elderly, with deep tissue (muscle) nociception being affected differently by age than superficial tissue (skin) nociception. Summation mechanisms contribute only moderately to age changes in pain perception.

This study examined the sensory abnormalities in an unselected, consecutive group of patients with central post-stroke pain (CPSP) surviving more than 1 year after stroke. The sensory examination included clinical examination and quantitative measures with detection and pain thresholds to heat and cold stimuli, argon laser, von Frey hair and determination of stimulus-response function in the 10-45 degrees C range. Sensory examination was in 11 identified CPSP patients (5 female, 6 male; aged 43-80 years) carried out in the painful area using the contralateral homologue area as reference. Pain rating was performed using the McGill Pain Questionnaire and a VAS scale. All patients had ischemic (MRI verified) infarction. Of the 11 patients with supratentorial lesions, 5 had thalamic lesions; in addition, 7 patients had lesions in the brain stem/cerebellum. Median present spontaneous pain intensity on the VAS scale was 3.3 (range: 0-7.7). All patients had pain in the body part with sensory abnormalities, which in 8 patients extended the area with pain. Warm detection threshold was higher in the pain area in all patients, and all except 1 patient had increased cold detection threshold. Cold and heat pain thresholds were raised as well, but to a lesser degree. Sensibility to touch (von Frey hairs) and pain (argon laser) were changed in only 4 and 3 patients, respectively. A stimulus-response curve in the 10-45 degrees C range showed different patterns compared to the non-affected side. A cold allodynia in the 10-45 degrees C range was present in the painful area in 6 (56%) of the patients. The results support the theory that damage to the spino-thalamo-cortical pathway is a necessary condition in CPSP. It is proposed that the spontaneous pain in CPSP is linked to hyperexitability or spontaneous discharges in thalamic or cortical neurons that have lost part of their normal input.

Hyperactivity of N-methyl D-aspartate (NMDA) receptors may be one of the factors in the maintenance of persistent stump and phantom limb pain. Ketamine (bolus at 0.1 mg/kg/5 min followed by an infusion of 7 micrograms/kg/min) was administered intravenously to 11 patients with established stump and phantom limb pain in a double-blind saline-controlled study. All 11 patients responded with a decrease in the rating of stump and phantom limb pain assessed by visual analogue scale (VAS) and McGill Pain Questionnaire (MPQ). Ketamine increased pressure-pain thresholds significantly. Wind-up like pain (pain evoked by repeatedly tapping the dysaesthetic skin area) was reduced significantly by ketamine. In contrast, no effect was seen on pain evoked by repeated thermal stimuli. Side effects were observed in nine patients. The results support the notion that stump and phantom pain are generated by activity in afferent fibres activated by mechanical but not by thermal stimuli and that the NMDA receptor is involved in the maintenance of postamputation pain states. NMDA receptor antagonists may have a potential in the treatment of stump and phantom limb pain.

Ten patients (4 female, 6 male) aged 34-67 years suffering from peripheral neuropathic pain participated in a double-blind placebo-controlled study where ketamine or magnesium chloride were administered by a 10 min bolus infusion (ketamine: 0.84 mumol/kg = 0.2 mg/kg, magnesium: 0.16 mmol/kg) followed by a continuous infusion (ketamine: 1.3 mumol/kg/h = 0.3 mg/kg/h, magnesium: 0.16 mmol/kg/h). Ongoing pain determined by VAS score, area of touch-evoked allodynia, detection and pain thresholds to mechanical and thermal stimuli were measured before and during drug infusion. Ketamine produced a significant reduction of spontaneous pain (57%) and of the area of allodynia (33%). Magnesium chloride reduced pain (29%) and area of allodynia (18%) insignificantly. Following ketamine there was a significant correlation between the reduction in ongoing pain and reduction in area of touch-evoked allodynia. Detection and pain thresholds to mechanical and thermal stimuli were not significantly changed by the drugs. These findings suggest that both ongoing pain and touch-evoked pain (allodynia) in neuropathic pain are inter-related phenomena, which may be mediated by the same mechanism and involving a N-methyl-D-aspartate receptor.