Pain experiences cause increased plasma cortisol levels with significant elevation of the daily average. Whereas in cases of acute pain, a direct but unspecific stress reaction not connected with the pain seems to be likely, the underlying cause in cases of chronic and episodic pain appears to be a complex and enduring activation of the hypothalamic-pituitary-adrenal axis, likewise independent from pain, probably associated with concomitant depressive symptoms and disruption of the circadian rhythm of release controlled by the hypothalamus.

The pathological decrease of NE and 5-HIAA in the CSF points to the crucial role of noradrenergic and serotonergic transmitter systems in the generation, modulation, and perpetuation of chronic and episodic pain syndromes. It indicates that antidepressants are effective drugs in these diseases. However, a discriminative neurochemical pattern between pain and depression could not be established. The demonstration of polyvalent correlations between different neurotransmitters is indicative of complex neurobiological coupling between cortical, limbic, and hypothalamic neuronal networks on the one hand and the nociceptive descending system on the other hand in the genesis of pain and depression.

No abstract

These results suggest a sympathetic dysfunction in both headache-syndromes and suggest that the ANS plays an important role on the pathophysiology and the maintenance of the headaches.

No abstract