Pressure pain thresholds: Subject factors and the meaning of peak pressures.

BACKGROUND: The assessment of pressure pain has become an integral part in pain research. The distribution of pressure under a plunger can be uneven. However, measurements based on conventional devices show the applied force or mean pressure, failing to take local pressure peaks into account. Our main question was whether peak pressures under the probe are responsible for pain onset. METHODS: A force-controlled algometer was fitted with a newly developed pressure-indicating film. Pressure pain thresholds (PPTs) of 100 healthy subjects (57 men, age 18-66 years) were assessed at 29 sites across the body. Each site was measured three times, nonconsecutively and presented in randomized order. Forty subjects were manual labourers. RESULTS: Pressure distributions on hard tissue (bone) were more heterogeneous and showed more prominent peaks beneath the probe when reaching the PPT. Soft tissue (e.g. muscle) created a distinct distribution, with higher pressure especially around the corners of the probe. A high variability of PPTs between subjects and different measurement sites was observed. Men as well as manual labourers had comparatively higher adjusted pressure pain thresholds (force and pressure). CONCLUSIONS: Peak pressures could be relevant for pain onset and should be accounted for in mechanical pain studies. The probe, indentation depth and tissue properties have a major impact on pressure distributions and may therefore affect the perception of pressure pain. Due to higher intra-individual differences regarding peak pressures at the spinous processes, breastbone, forehead and abdomen caution are needed when interpreting those sites. SIGNIFICANCE: This study adds some important considerations for the use of pressure algometers. It was found that during pressure pain thresholds readings distinct peak pressure profiles could arise, which may influence the perception of pain. Peak pressure could be another contributing factor, which may explain some of the high variability in pressure pain readings.

Determination of haemoglobin adducts of acrylamide and glycidamide in smoking and non-smoking persons of the general population.

Acrylamide (AA) is a food-borne toxicant suspected to be carcinogenic to humans. It is formed in the heating process of starch-containing food. Currently, there is a great discussion about the possible human health risks connected with the dietary uptake of acrylamide. Haemoglobin adducts of acrylamide and its oxidative metabolite glycidamide are both markers of biochemical effect. However, because glycidamide has a higher carcinogenic potency than acrylamide itself, the glycidamide adduct might mirror the genotoxicity better than acrylamide adducts. In order to gain more information about the human metabolism of acrylamide, we investigated a small group of persons for the effective internal doses of acrylamide and glycidamide using haemoglobin adducts as parameters of biochemical effect. The collective was subdivided into non-smokers (n=13) and smokers (n=16) by determining the smoking-specific acrylonitrile haemoglobin adduct (N-cyanoethylvaline, CEV). The mean values for the adducts of acrylamide (N-2-carbamoylethylvaline, AAVal) and glycidamide (N-(R,S)-2-hydroxy-2-carbamoylethylvaline, GAVal) in nonsmokers was 19 pmol/g globin AAVal (range 7-31 pmol/g globin) and 17 pmol/g globin GAVal (range 9-23 pmol/g globin). For smokers mean levels of AAVal were 80 pmol/g globin (range: 25-199 pmol/g globin) and those of GAVal were 53 pmol/g globin (range: 22-119 pmol/g globin). Metabolism to glycidamide turned out to be significantly more effective in non-smokers than in the higher exposed smokers. Compared with studies in rats, the metabolic conversion of acrylamide to glycidamide as measured by haemoglobin adducts seems to occur to a similar extent in humans as in rats. Risk estimations on acrylamide based on experimental data obtained in rats obviously did not overestimate the cancer risk for the general population. Furthermore, our results might indicate that the dose-response curve for acrylamide is not linear. This would be in line with the results of animal experiments on rodents.