Unitary hypothesis for multiple triggers of the pain and strain of migraine
Article first published online: 27 OCT 2005
Copyright © 2005 Wiley-Liss, Inc.
Journal of Comparative Neurology
Special Issue: The Anatomy of the Soul
Volume 493, Issue 1, pages 9–14, 5 December 2005
How to Cite
Burstein, R. and Jakubowski, M. (2005), Unitary hypothesis for multiple triggers of the pain and strain of migraine. J. Comp. Neurol., 493: 9–14. doi: 10.1002/cne.20688
- Issue published online: 27 OCT 2005
- Article first published online: 27 OCT 2005
- Manuscript Accepted: 3 JUN 2005
- Manuscript Received: 27 APR 2005
- National Institutes of Health. Grant Numbers: DE13347, NS051484, NS35611
Migraine headache is triggered by and associated with a variety of hormonal, emotional, nutritional, and physiological changes. The perception of migraine headache is formed when nociceptive signals originating in the meninges are conveyed to the somatosensory cortex through the trigeminal ganglion, medullary dorsal horn, and thalamus. Is there a common descending pathway accounting for the activation of meningeal nociceptors by different migraine triggers? We propose that different migraine triggers activate a wide variety of brain areas that impinge on parasympathetic neurons innervating the meninges. According to this hypothesis, migraine triggers such as perfume, stress, or awakening activate multiple hypothalamic, limbic, and cortical areas, all of which contain neurons that project to the preganglionic parasympathetic neurons in the superior salivatory nucleus (SSN). The SSN, in turn, activates postganglionic parasympathetic neurons in the sphenopalatine ganglion, resulting in vasodilation and local release of inflammatory molecules that activate meningeal nociceptors. Are there ascending pathways through which the trigeminovascular system can induce the wide variety of migraine symptoms? We propose that trigeminovascular projections from the medullary dorsal horn to selective areas in the midbrain, hypothalamus, amygdala, and basal forebrain are functionally positioned to produce migraine symptoms such as irritability, loss of appetite, fatigue, depression, or the quest for solitude. Bidirectional trafficking by which the trigeminovascular system can activate the same brain areas that have triggered its own activity in the first place provides an attractive network of perpetual feedback that drives a migraine attack for many hours and even days. J. Comp. Neurol. 493:9–14, 2005. © 2005 Wiley-Liss, Inc.