Controls, and to a certain degree also migraineurs, responded to the stressor in the present study with a rapid increase followed by a relatively fast decrease in BP and HR, giving the curve a spike-like shape. However, in TTH patients, the SBP, DBP and HR profiles increased slowly and did not decrease during the stress test. A trend towards a different SBP profile was found when comparing the first and last 10-min interval in controls and TTH. The possible lack of HR-adaptation during stress reflects the lack of a HR-spike (followed by a decrease in HR) in TTH. A reduced early cardiovascular response to mental stress, with the heart rate response inversely correlated to the pain response, was found for fibromyalgia patients in a study with a similar design [48
]. Cardiac (HR) adaptation to mental stress has previously been reported in healthy students [49
], while deficient cardiac adaptation to calculative mental stress has been found in migraine patients [50
]. The migraine patients in our study did not show signs of deficient HR adaptation to stress. One may interpret the lack of an acute spike at the start of the cognitive task and the lack of HR adaptation as evidence of a deficient adaptive mechanism (or decreased autonomic excitability) to low-grade cognitive stress in TTH patients. It should be noted that due to a low sample size, especially in the TTH group, these results are tentative and are considered to be hypothesis-generating and not hypothesis-controlling.
HR in migraineurs recovered as much during the relaxation phase as controls. This is in accordance with another study [19
] which did not show a difference in HR recovery between students with migraine and controls after three minutes of mental arithmetic, although the authors reported faster recovery in peripheral resistance in migraine compared to controls. On the other hand, Holm et al
] found that migraineurs had delayed HR recovery after four minutes of stressful speech-preparation. Methodological differences make it difficult to compare short-lasting cognitive stress with the one-hour test we applied.
The observed skin blood flow reduction during test is probably related to a gradually increasing sympathetic vasoconstrictor tone to skin arterioles and AV-shunts during cognitive stress [51
]. However, we did not find any differences in finger BF development during the test between the three groups. This is in accordance with previous studies that have utilized finger temperature and pulse amplitude as indirect measures of finger blood flow during short-duration stress with generally negative results in TTH [25
] and migraine [19
We did find a delayed finger BF recovery profile after
stress in TTH compared to controls and migraineurs. Another study has previously reported prolonged skin vasoconstriction in TTH (earlobe pulse volume and finger temperature) [29
], which is in accordance with our findings. In addition, TTH patients had delayed pain recovery (Table ) and delayed EMG recovery in the trapezius area [34
]. Our findings in general fit well with the theoretical models of Eriksen & Ursin [1
] and McEwen [2
]. Our lack of HR adaptation in TTH is in accordance with McEwens concept of "allostatic load" which causes lack of adaptation to stress. Furthermore, the lack of skin BF recovery in TTH fits well both with the concept of "sustained arousal" in the model of Eriksen & Ursin, and with the concept of a prolonged response to a stressor in McEwens model.
The role of the autonomic nervous subsystems in TTH is not clear [25
]. Because muscular blood flow in tender points is decreased in TTH [52
], and because we observed increased skin vasoconstriction (reduced BF) during recovery after stress, which was correlated to low pain response during stress, it is possible that sympathetic dysregulation is involved, for instance as hyperactivity or hypersensitivity in the central autonomic network which again may be linked to increased central pain inhibition. It is also possible to explain this effect through pain-induced inhibition of sympathetic vasoconstriction in the skin however [53
Recently, decreased muscle blood flow during muscle exercise was found in fibromyalgia patients, suggesting that muscle ischemia contributes to pain in these patients [54
]. However, we were not able to measure intramuscular blood flow in the present study. Muscle blood flow is regulated differently from skin blood flow [55
] and the direct relevance of observed skin blood flow changes to the relationship between muscle blood flow and pain perceived as muscular is accordingly uncertain.
Also in migraine, there are still many uncertainties about the role of autonomic nervous subsystems [17
]. Some studies report autonomic dysfunction in migraineurs, such as orthostatic hypotension, noradrenergic or adrenergic hypofunction etc. [58
], but not all studies report such autonomic dysfunction [64
]. Many past studies have used procedures such as deep breathing tests, orthostatic tests, cold pressor tests and isometric work tests (sustained handgrip) and these responses are not directly comparable with autonomic response to cognitive stress of long duration used in the present study.
Cephalic and intracranial vessels may be regulated differently from peripheral vessels. Painful stimuli to tooth pulp induce a blood flow increase in orofacial areas [67
]. In chronic TTH patients, previously published data indicate cranial vasodilatation [68
]. In migraine, cephalic pulse amplitude may increase during a mental task in migraine [18
] but results are not consistent across studies [19
], and both deficient and normal vasoactivity has generally been reported in migraine [66
]. Our results support the view that dysfunctional peripheral blood flow regulation is not a substantial part of migraine pathophysiology.
Although we did not measure perceived stress in this study, we believe that the measured perceived tension is an indirect measure of the level of stress. The Norwegian word "anspenthet" describe a feeling of general psychological and muscular tension perceived in stressful situations [69
]. Tension responses did not differ, thus the level of stress seemed to be comparable between groups. However, TTH patients had a significantly less recovery from tension, indicating an inability to unwind after the stressor is removed [70
As to what is perceived as stressful, TTH-patients may be more likely to appraise daily situations as stressful, with a tendency towards passive coping, compared to non-headache controls [25
]. Because cognitive processing involving the prefrontal cortex can change the activity in the different parts of the periaqueductal grey matter (PAG), a difference in stress adaptive mechanisms may influence both the autonomic nervous system and pain control system in several ways, for instance by delaying sympathetic cardiovascular activation [71
]. PAG is also important in pain control and in central sensitization, possibly explaining allodynia and hyperalgesia to pressure stimuli [72
] and the increased stress-induced pain in TTH (Table , Figure ).