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New insights into pathophysiology of vestibular migraine.

Espinosa-Sanchez JM, Lopez-Escamez JA - Front Neurol (2015)

Bottom Line: Although cortical spreading depression can affect cortical areas involved in processing vestibular information, functional neuroimaging techniques suggest a dysmodulation in the multimodal sensory integration and processing of vestibular and nociceptive information, resulting from a vestibulo-thalamo-cortical dysfunction, as the pathogenic mechanism underlying VM.The elevated prevalence of VM suggests that multiple functional variants may confer a genetic susceptibility leading to a dysregulation of excitatory-inhibitory balance in brain structures involved in the processing of sensory information, vestibular inputs, and pain.The interactions among several functional and structural neural networks could explain the pathogenic mechanisms of VM.

View Article: PubMed Central - PubMed

Affiliation: Otology and Neurotology Group CTS495, Human DNA Variability Department, GENYO Centre for Genomics and Oncological Research Pfizer - University of Granada - Junta de Andalucia , Granada , Spain ; Department of Otolaryngology, Hospital San Agustin , Linares , Spain.

ABSTRACT
Vestibular migraine (VM) is a common disorder in which genetic, epigenetic, and environmental factors probably contribute to its development. The pathophysiology of VM is unknown; nevertheless in the last few years, several studies are contributing to understand the neurophysiological pathways involved in VM. The current hypotheses are mostly based on the knowledge of migraine itself. The evidence of trigeminal innervation of the labyrinth vessels and the localization of vasoactive neuropeptides in the perivascular afferent terminals of these trigeminal fibers support the involvement of the trigemino-vascular system. The neurogenic inflammation triggered by activation of the trigeminal-vestibulocochlear reflex, with the subsequent inner ear plasma protein extravasation and the release of inflammatory mediators, can contribute to a sustained activation and sensitization of the trigeminal primary afferent neurons explaining VM symptoms. The reciprocal connections between brainstem vestibular nuclei and the structures that modulate trigeminal nociceptive inputs (rostral ventromedial medulla, ventrolateral periaqueductal gray, locus coeruleus, and nucleus raphe magnus) are critical to understand the pathophysiology of VM. Although cortical spreading depression can affect cortical areas involved in processing vestibular information, functional neuroimaging techniques suggest a dysmodulation in the multimodal sensory integration and processing of vestibular and nociceptive information, resulting from a vestibulo-thalamo-cortical dysfunction, as the pathogenic mechanism underlying VM. The elevated prevalence of VM suggests that multiple functional variants may confer a genetic susceptibility leading to a dysregulation of excitatory-inhibitory balance in brain structures involved in the processing of sensory information, vestibular inputs, and pain. The interactions among several functional and structural neural networks could explain the pathogenic mechanisms of VM.

No MeSH data available.


Related in: MedlinePlus

Mechanisms involved in the pathophysiology of vestibular migraine. An abnormal brain sensitization leading to a dysmodulation of multimodal sensory integration in thalamo-cortical processing could interact with the trigemino-vascular reflex. The abnormal processing of vestibular and nociceptive information could determine a transient vestibular dysfunction associated with migraine features.
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Figure 1: Mechanisms involved in the pathophysiology of vestibular migraine. An abnormal brain sensitization leading to a dysmodulation of multimodal sensory integration in thalamo-cortical processing could interact with the trigemino-vascular reflex. The abnormal processing of vestibular and nociceptive information could determine a transient vestibular dysfunction associated with migraine features.

Mentions: We hypothesized that VM responds to an abnormal brain sensitization leading to a dysmodulation of multimodal sensory integration and processing at vestibulo-thalamo-cortical level (Figure 1). At the molecular level, this may result from functional variants affecting several ionic channels and receptors, and that can confer susceptibility to VM. Multiple brain networks are probably involved not only in the pain matrix and the vestibular pathways, but also in other structures such as the limbic system.


New insights into pathophysiology of vestibular migraine.

Espinosa-Sanchez JM, Lopez-Escamez JA - Front Neurol (2015)

Mechanisms involved in the pathophysiology of vestibular migraine. An abnormal brain sensitization leading to a dysmodulation of multimodal sensory integration in thalamo-cortical processing could interact with the trigemino-vascular reflex. The abnormal processing of vestibular and nociceptive information could determine a transient vestibular dysfunction associated with migraine features.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4319397&req=5

Figure 1: Mechanisms involved in the pathophysiology of vestibular migraine. An abnormal brain sensitization leading to a dysmodulation of multimodal sensory integration in thalamo-cortical processing could interact with the trigemino-vascular reflex. The abnormal processing of vestibular and nociceptive information could determine a transient vestibular dysfunction associated with migraine features.
Mentions: We hypothesized that VM responds to an abnormal brain sensitization leading to a dysmodulation of multimodal sensory integration and processing at vestibulo-thalamo-cortical level (Figure 1). At the molecular level, this may result from functional variants affecting several ionic channels and receptors, and that can confer susceptibility to VM. Multiple brain networks are probably involved not only in the pain matrix and the vestibular pathways, but also in other structures such as the limbic system.

Bottom Line: Although cortical spreading depression can affect cortical areas involved in processing vestibular information, functional neuroimaging techniques suggest a dysmodulation in the multimodal sensory integration and processing of vestibular and nociceptive information, resulting from a vestibulo-thalamo-cortical dysfunction, as the pathogenic mechanism underlying VM.The elevated prevalence of VM suggests that multiple functional variants may confer a genetic susceptibility leading to a dysregulation of excitatory-inhibitory balance in brain structures involved in the processing of sensory information, vestibular inputs, and pain.The interactions among several functional and structural neural networks could explain the pathogenic mechanisms of VM.

View Article: PubMed Central - PubMed

Affiliation: Otology and Neurotology Group CTS495, Human DNA Variability Department, GENYO Centre for Genomics and Oncological Research Pfizer - University of Granada - Junta de Andalucia , Granada , Spain ; Department of Otolaryngology, Hospital San Agustin , Linares , Spain.

ABSTRACT
Vestibular migraine (VM) is a common disorder in which genetic, epigenetic, and environmental factors probably contribute to its development. The pathophysiology of VM is unknown; nevertheless in the last few years, several studies are contributing to understand the neurophysiological pathways involved in VM. The current hypotheses are mostly based on the knowledge of migraine itself. The evidence of trigeminal innervation of the labyrinth vessels and the localization of vasoactive neuropeptides in the perivascular afferent terminals of these trigeminal fibers support the involvement of the trigemino-vascular system. The neurogenic inflammation triggered by activation of the trigeminal-vestibulocochlear reflex, with the subsequent inner ear plasma protein extravasation and the release of inflammatory mediators, can contribute to a sustained activation and sensitization of the trigeminal primary afferent neurons explaining VM symptoms. The reciprocal connections between brainstem vestibular nuclei and the structures that modulate trigeminal nociceptive inputs (rostral ventromedial medulla, ventrolateral periaqueductal gray, locus coeruleus, and nucleus raphe magnus) are critical to understand the pathophysiology of VM. Although cortical spreading depression can affect cortical areas involved in processing vestibular information, functional neuroimaging techniques suggest a dysmodulation in the multimodal sensory integration and processing of vestibular and nociceptive information, resulting from a vestibulo-thalamo-cortical dysfunction, as the pathogenic mechanism underlying VM. The elevated prevalence of VM suggests that multiple functional variants may confer a genetic susceptibility leading to a dysregulation of excitatory-inhibitory balance in brain structures involved in the processing of sensory information, vestibular inputs, and pain. The interactions among several functional and structural neural networks could explain the pathogenic mechanisms of VM.

No MeSH data available.


Related in: MedlinePlus