Tension-Type Headache (TH) is highly prevalent and associated with significant personal and social cost. The causes of TH are unclear, precluding optimal treatment or prevention at present. Stress is a well-documented correlate and trigger of TH activity, however the causal significance has not been experimentally demonstrated to date. Similarly, the mechanisms by which stress contributes to TH, if in fact it does, are not clearly understood. Findings of increased pain sensitivity in TH sufferers suggests TH pathophysiology may involve dysfunction in peripheral and/or central nervous system processing of pain. Studies on animals and healthy humans demonstrate that stress can increase pain sensitivity by affecting peripheral and central pain mechanisms proposed as dysfunctional in TH. It has therefore been proposed that stress may contribute to TH through aggravating already increased pain sensitivity in TH sufferers. However, this hypothesis has not been adequately examined in TH sufferers to date. Addressing the above issues, the present project conducted seven studies examining relationships between stress, pain sensitivity, and headache activity in TH sufferers. The aim was to test the hypothesis that stress contributes to TH by aggravating already increased pain sensitivity in TH sufferers. Studies 1 and 2 demonstrated increased general arousal and complex temporal relationships between general arousal and headache activity in the natural environment in Episodic TH (ETH) sufferers. In Study 3, experimentally induced stress of brief duration increased pressure pain sensitivity at the head in Chronic TH (CTH) sufferers more than in healthy controls. Study 4 found CTH sufferers to have increased levels of daily stress, increased pericranial muscle tenderness, and reduced pain thresholds, which were inter-related. Both daily stress and pain sensitivity were predictive of prospective daily headache activity. In Study 5, an experimental model demonstrated that stress-induced headache was associated with stress-induced increase in pericranial muscle tenderness and reduction in pressure pain thresholds at head and hand. Additionally, induced stress reduced pain tolerance and increased pain intensity ratings to cold pressor more in TH sufferers than in healthy controls (Study 7). Finally, TH sufferers were found to have abnormal temporal summation of pressure pain and impaired noxious inhibition of temporal summation compared to healthy controls, however neither temporal summation nor noxious inhibition of temporal summation were affected by induced stress (Study 6). Together, the results support the hypotheses: 1) Stress contributes to both ETH and CTH, and 2) Stress contributes to CTH through aggravating already increased pain sensitivity in CTH sufferers. Impaired pain inhibition and increased wind-up may be underlying abnormalities contributing to increased pain sensitivity in CTH sufferers.
| Identifer | oai:union.ndltd.org:ADTP/284094 |
| Date | January 2009 |
| Creators | Cathcart, Stuart |
| Source Sets | Australiasian Digital Theses Program |
| Language | EN-AUS |
| Detected Language | English |
| Rights | Copyright Stuart Cathcart 2009 |
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