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A Rat Model of Central Fatigue Using a Modified Multiple Platform Method
Published on: August 14, 2018
Diffuse noxious inhibitory control is delayed in chronic fatigue syndrome: an experimental study
Mira Meeus1, Jo Nijs, Naomi Van de Wauwer
1Division of Musculoskeletal Physiotherapy, Department of Health Sciences, University College Antwerp (HA), Belgium Department of Human Physiology, Faculty of Physical Education and Physiotherapy, Vrije Universiteit Brussel (VUB), Belgium.
Pain
|July 12, 2008
Summary
Chronic Fatigue Syndrome (CFS) patients exhibit delayed pain inhibition, specifically in Diffuse Noxious Inhibitory Controls (DNIC), contributing to chronic widespread pain. Hypocortisolism was not evident in CFS patients.
Area of Science:
- Neuroscience
- Pain Research
- Endocrinology
Background:
- Chronic widespread pain in Chronic Fatigue Syndrome (CFS) may stem from deficient pain inhibition or hormonal issues.
- Diffuse noxious inhibitory controls (DNIC) and hypocortisolism are potential factors.
Purpose of the Study:
- To investigate endogenous pain inhibition and cortisol response to thermal noxious stimuli in CFS patients.
- To explore the role of DNIC and hypocortisolism in CFS-related chronic pain.
Main Methods:
- Thirty-one CFS patients and 31 controls underwent gradual immersion of the arm in 46°C water to assess thermal pain summation.
- Pain intensity was rated every 15 seconds during ascending and descending immersion.
- Salivary cortisol levels were measured before and after thermal stimuli.
Main Results:
- CFS patients reported higher overall pain but showed no difference in pain evolution compared to controls.
- Pain inhibition initiated slower in CFS patients during thermal stimuli.
- No significant differences in cortisol levels or response were observed between CFS patients and controls.
Conclusions:
- Delayed DNIC response to spatial summation of thermal stimuli may contribute to chronic widespread pain in CFS.
- Evidence for hypocortisolism in CFS was not found.
- Further research is needed to fully understand the role of delayed pain inhibition in CFS.
