These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


PUBMED FOR HANDHELDS

Search MEDLINE/PubMed


  • Title: Stress and chronic headache: a psychophysiological analysis of mechanisms.
    Author: Feuerstein M, Bush C, Corbisiero R.
    Journal: J Psychosom Res; 1982; 26(2):167-82. PubMed ID: 7077548.
    Abstract:
    This study investigated the effects of three types of laboratory stressors (stressful imagery, mental arithmetic, pain) on temporal artery, skeletal muscle, general autonomic [digital blood volume pulse (DBVP), spontaneous resistance responses (SRR's)] and self-report measures of distress in chronic migraine, mixed, muscle contraction and non-headache controls. All subjects were female, free of medication at time of testing and equated for age. Headache subjects reported a 19 year history of headache. Results revealed a pattern of digital BVP (constriction), SSR's (increase) and frontal EMG (increase) indicative of a general autonomic-skeletal muscle arousal response to all three stressors in all groups, while the temporal artery response to the pain stimulus was vasodilation. Distress ratings were elevated during the stress periods for all four group. Pain threshold and tolerance and the tendency to utilize cognitive coping strategies during exposure to pain did not differ across the four groups. The results do not support the general autonomic dysfunction theory of migraine or the specificity hypothesis implicating an overreactive temporal artery or skeletal muscle response to stress in migraine and muscle contraction headache, respectively. Despite epidemiological research supporting the stress-headache relationship, the present results indicate that the psychophysiological mechanism underlying this relationship does not appear to involve abnormal tonic levels or phasic response to stress. It is argued that the temporal artery dilation response to pain questions the role of stress in triggering the two stage vasoconstriction-dilation mechanism of migraine and suggests the need to evaluate a four stage model as a potential psychophysiological mechanism underlying the stress-headache relationship.
    [Abstract] [Full Text] [Related] [New Search]