Pressure Pain Threshold Measurements Research Articles

Tension Headache: Botulinum Toxin Paralysis of Temporal Muscles

The pathogenetic mechanism of tension headache (TH) is still unknown. The role of pericranial muscle tension in TH is also enigmatic. To evaluate this factor in chronic TH, pericranial muscles were paralysed in 6 chronic TH patients, using botulinum toxin. All patients fulfilled the IHS criteria of chronic TH associated with involvement of the pericranial muscles, but not the current criteria for cervicogenic headache. The patients were followed-up regularly with evaluation of the paralysis, changes in pain intensity, and pressure pain threshold measurements. We primarily only injected the temporal muscle on the one side, using the other side as a control. Contralateral muscles were in some cases injected at a later stage. In our study, we did not find any significant reduction in pain intensity, as measured by the visual analogue scale, nor any changes in pressure pain threshold, as measured by an algometer. On the basis of our observations, we conclude that muscle tension in these muscles possibly plays a minor role in the genesis of chronic TH. In our study, however, we have only treated a limited number of patients, and only one pericranial muscle has been injected systematically. Further studies of various neck/posterior head muscles ought to be performed in order to further evaluate a possible effect of tension in the pericranial musculature in producing this type of pain.

Self-injur, pain, and the endorphin theory

Naltrexone doses of 0.5, 1.0, 1.5, and 2.0 mg/kg were administered in randomized orders to four participants with developmental disabilities and severe chronic self-injurious behavior (SIB) in a double-blind, placebo-controlled repeated reversal procedure. A nonspecific generalized attenuation of SIB was found, with different dosages in different individuals showing statistical, but not clinical, reductive significance in some cases, and “paradoxical” increases in others. Independent measurement of pressure pain thresholds with an algometer procedure disclosed no parallel correlations in pain sensitivity with SIB changes. Biochemistry assays showed expected neuroendocrine stimulatory or inhibitory effects of naltrexone, including a reduction of beta-endorphins, although the latter was overal low in all subjects. Post-hoc analyses suggested that SIB and beta-endorphin levels tended to covary in the same direction, but not in causal relation to each other. The results do not confirm a pain-system mediation of SIB, but do suggest that non-opiate mechanisms of naltrexone action merit clinical research.

Measurements of human pressure-pain thresholds on fingers and toes

Pressure-pain thresholds (PPT) were measured on fingers and toes with a hand-held electronic pressure algometer in 15 males and 15 females. The pressure algometer offered easy control of pressure application rate. The intra-individual coefficient of variation, based on repeated PPT measurements with a 1 week interval was 14%. The inter-individual coefficient of variation was 28% for females and 33% for males. In the course of 10 consecutive PPT measurements with short intervals (10 and 20 sec), no significant change in PPT was observed. PPT was found to be 50% higher in males than in females ( P < 0.0001). Slightly but significantly higher PPT values were found on the dominant compared to the non-dominant side ( P < 0.005).