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Neural substrate of depression during migraine.

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Title: Neural substrate of depression during migraine.
Authors: Burstein, Rami, Jakubowski, M.
Source: Neurological Sciences. May2009 Supplement 1, Vol. 30, p27-31. 5p.
Subjects: Migraine, Nutritional assessment, Trigeminal neuralgia, Meninges, Parasympathetic nervous system, Cell nuclei
Abstract: 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. 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 stress 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. 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 and the quest for solitude. The network of 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 mechanism of perpetual feedback that drives a migraine attack for many hours and even days. [ABSTRACT FROM AUTHOR]
Copyright of Neurological Sciences is the property of Springer Nature and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
Database: Psychology and Behavioral Sciences Collection
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  Data: <searchLink fieldCode="DE" term="%22Migraine%22">Migraine</searchLink><br /><searchLink fieldCode="DE" term="%22Nutritional+assessment%22">Nutritional assessment</searchLink><br /><searchLink fieldCode="DE" term="%22Trigeminal+neuralgia%22">Trigeminal neuralgia</searchLink><br /><searchLink fieldCode="DE" term="%22Meninges%22">Meninges</searchLink><br /><searchLink fieldCode="DE" term="%22Parasympathetic+nervous+system%22">Parasympathetic nervous system</searchLink><br /><searchLink fieldCode="DE" term="%22Cell+nuclei%22">Cell nuclei</searchLink>
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  Data: 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. 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 stress 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. 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 and the quest for solitude. The network of 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 mechanism of perpetual feedback that drives a migraine attack for many hours and even days. [ABSTRACT FROM AUTHOR]
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  Data: <i>Copyright of Neurological Sciences is the property of Springer Nature and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.</i> (Copyright applies to all Abstracts.)
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        Value: 10.1007/s10072-009-0061-7
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        Text: English
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      – SubjectFull: Migraine
        Type: general
      – SubjectFull: Nutritional assessment
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      – SubjectFull: Trigeminal neuralgia
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      – SubjectFull: Parasympathetic nervous system
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              Text: May2009 Supplement 1
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              Y: 2009
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