We recorded deep pain and surface electromyographic (EMG) responses to stress in 22 migraineurs during headache-free periods, 18 patients with tension-type headache (TTH), and 44 healthy controls. Sixty minutes of cognitive stress was followed by 30 min relaxation. EMG and pain (visual analogue scale) in the trapezius, neck (splenius), temporalis and frontalis areas were recorded. TTH patients had higher pain responses in temporalis and frontalis (with similar trends for trapezius and splenius) and more potentiation of pain during the test than controls. Migraine patients developed more pain in the splenius and temporalis than controls. Muscle pain responses were more regional (more pain in the neck and trapezius compared with the temporalis and frontalis) in migraine than in TTH patients. TTH patients had delayed pain recovery in all muscle regions compared with controls, while migraine patients had delayed pain recovery in a more restricted area (trapezius and temporalis). EMG responses were not different from controls in headache patients, and EMG responses did not correlate with pain responses. TTH patients had delayed EMG recovery in the trapezius compared with controls and migraine patients. These results support the concept that (probably central) sensitization of pain pathways and the motor system is important in TTH. Less pronounced and more regional (either peripheral or central) trigeminocervical sensitization seems to be important in migraine. Surface-detectable muscular activation does not seem to be causal for pain during cognitive stress either in migraine or in TTH.
We found abnormal cardiovascular responses to a 60min long stressful task in fibromyalgia patients. Furthermore, we found a negative association between the heart rate response and the pain which developed during the stressful task in the fibromyalgia group, possibly a result of reduced stress-induced analgesia for fibromyalgia patients.
Background: Stress is a risk factor for musculoskeletal pain. We wanted to explore stress related physiology in healthy subjects in order to gain insight into mechanisms of pain development which may relate to the pathophysiology of musculoskeletal pain disorders.
The goal of this study was to explore the relationship between indicators of sympathoneural, sympathomedullar and hypothalamic-pituitary-adrenocortical (HPA) activity and stressinduced head and shoulder-neck pain in patients with migraine or tension-type headache (TTH). We measured noradrenaline, adrenaline and cortisol levels before and after low-grade cognitive stress in 21 migraineurs, 16 TTH patients and 34 controls. The stressor lasted for 60 min and was followed by 30 min of relaxation. Migraine patients had lower noradrenaline levels in blood platelets compared to controls. Pain responses correlated negatively with noradrenaline levels, and pain recovery correlated negatively with the cortisol change in migraineurs. TTH patients maintained cortisol secretion during the cognitive stress as opposed to the normal circadian decrease seen in controls and migraineurs. There may therefore be abnormal activation of the HPA axis in patients with TTH when coping with mental stress, but no association was found between pain and cortisol. A relationship between HPA activity and stress in TTH patients has to our knowledge not been reported before. In migraine, on the other hand, both sympathoneural activation and HPA activation seem to be linked to stress-induced muscle pain and recovery from pain respectively. The present study suggests that migraineurs and TTH patients cope differently with low-grade cognitive stress.
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