The main finding of the present study was an association of pain intensity perception with saliva cortisol responses and subjective helplessness after uncontrollable electrical stimuli in healthy young men. After uncontrollable stress exposure, significantly higher pain perception and helplessness ratings as well as a significantly more pronounced salivary cortisol response were found when compared to the controllable stress condition. Moreover, correlation analyses revealed significant positive associations between the three parameters in the total sample without significant differences of correlations between the controllable or uncontrollable condition. Thus, subjective helplessness seems to be a potent cognitive mediator of pain evaluation and HPA-axis activation.
Enhanced pain intensity experience after uncontrollable stress exposure and during states of helplessness is in line with previous findings in healthy subjects and patients with pain syndromes [8
]. On the other hand, cortisol elevation following uncontrollable aversive stress has also been a basic finding since the early studies of learned helplessness theory [2
]. However, the relationship between uncontrollable and potentially painful stress, subjective helplessness, and perceived pain intensity has not been sufficiently studied yet. Our results fit closely to very recent data from an interventional study with repetitive transcranial magnetic stimulation (rTMS) [17
]. The authors could show that fast left prefrontal rTMS acutely suppressed the analgesic effects of perceived controllability on the emotional dimension, but not on the sensory/discriminatory component of pain perception. After rTMS, perceived uncontrollability of a painful task was related to an emotionally more distressing pain perception; the findings were hypothetically linked to fast activation of left prefrontal cortical areas [17
The clinical studies in patients with often chronic pain syndromes seem, however, to be contradictory to the present findings. In several studies, lower mean diurnal cortisol levels were found in patients with chronic pain [28
], particularly with fibromyalgia [22
]. After metyrapone-induced hypocortisolism, an increase of mechanical pain sensitivity was found in healthy volunteers [21
]. Cortisol response after acute stress in patients with chronic pain seems to be either within the normal range (in patients with chronic pelvic pain) or reduced (in fibromyalgia) [32
]. In a recent study of this group [23
] diurnal salivary cortisol release was associated with depression in patients with fibromyalgia, but not with perceived pain. Another recent study investigated the impact of perceived control during a cold pressor test and the influence of active coping on salivary cortisol response and reported a weak interaction of high perceived control and active coping on higher cortisol responses which occurred only in women [33
]. In men, a reverse picture emerged. The authors claim that cortisol elevations after acute painful stress could be an adaptive neuroendocrine mechanism and interpreted their result as evidence that active coping and perceived control could potentiate adaptation [33
]. Although an adaptive function of cortisol responses after acute uncontrollable painful stress can not be ruled out, converging evidence shows, however, that negative cognitive and affective factors intensify both HPA axis activation and pain perception. Anticipatory and evaluative cognitions seem to be crucial for pain processing [8
] and cortisol response [28
]. Most likely blunted HPA axis reactivity and hypocortisolism as seen in post-traumatic stress disorder and fibromyalgia are consequences of chronic stress and a prolonged period of HPA axis hyperactivity [36
]. Our study suggests that acute painful stimulation is not followed by HPA axis activation under controllable conditions and when the perceived level of helplessness is low. Under such conditions pain was perceived less severe compared to uncontrollable stress exposure and states of induced helplessness.
However, generalization of our findings should be limited to healthy young men. Gender differences in stress response and pain perception should be taken into account [31
]. An influencing factor which has not been ruled in the present study was tobacco smoking. Smoking can activate the HPA axis, but non-smokers and smokers were equally distributed in both experimental groups.
Salivary cortisol responses were relatively small due to the mild stimulation compared to other stressors [37
]; the pain stimulation procedure used in the present study was quite artificial and might have led to a stimulation of both non-nociceptive and nociceptive fibers. Additionally, stress induction and measurement of altered pain intensity were implemented concurrently. Stressor modality, intensity and the temporal pattern of stress exposure seem all to have influence on pain processing [38
] and cortisol responses. The present findings are, therefore, in need for replication.