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The pathophysiology of cluster headache. The vasoconstrictor secretion from the dura is thought to play an important role in the pathophysiology, although conclusive evidence is lacking. Multiple brain regions are involved in the manifestations of cluster headache. The paraventricular nucleus (PVN) in the hypothalamus, which is most likely activated by input from the subcortical structures, regulates the secretion of corticotropic hormone (ACTH), which in turn stimulates the adrenocortical glands to secrete cortisol and epinephrine. Once secreted, these hormones exert influence over the function of both the cerebral cortex and also the sympathetic system, which is essential in the presentation of the danger signal. Respiratory changes may occur during the parasympathetic activation and adrenergic changes, which are concurrent with the activation of the sympathetic system. The respiratory changes seem to be mediated by the brain stem, possibly by activation of the sympathetic system from the central nervous system.
Some aspects of the pathophysiology of cluster headache remain unknown. This may be due to complex interactions of the primary afferent inputs, secondary afferents, and trigeminal efferents. Research into this area could provide further insight into the pathophysiology of this complex intractable head pain.
An interesting observation is that vasoconstrictors are only released during the acute phase of the attack and not during the few hours between attacks. This has led some investigators to suggest that the hypoperfusion seen in cluster headache may be a result of a systemic release of vasopressors from the hypothalamus, and that the symptom relief that clinicians can provide with a vasoconstrictor is a result of restoring normal brain perfusion. This may be due to central release of vasodilators, acting through the diencephalic-hypothalamic system, or possibly through the sensory areas and cortical motor areas.
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