A Critical View on the Role of Migraine Triggers in the Genesis of Migraine Pain

@article{Levy2009ACV,
  title={A Critical View on the Role of Migraine Triggers in the Genesis of Migraine Pain},
  author={Dan Levy and Andrew M. Strassman and Rami Burstein},
  journal={Headache: The Journal of Head and Face Pain},
  year={2009},
  volume={49}
}
A number of distinct endogenous and exogenous factors have been implicated in migraine precipitation but the exact nature of the triggering process itself and its relationship to the genesis of the headache remains largely speculative. In this article, we examine the potential sites and downstream cascades through which migraine triggers might exert their action to promote the activation of the migraine pain pathway. We further look at the laterality of the headache as a potential indicator for… 

Where does a migraine attack originate? In the brainstem

TLDR
It is concluded that the initialization of a migraine attack can be explained as an altered function of the neuronal elements of the brainstem nuclei.

Cerebellar involvement in migraine

TLDR
It is hoped that future studies can provide an answer as to how the cerebellum may be involved and whether treatment options specifically targeting the cere bellum could provide alleviation of this disorder.

Endogenous Mechanisms Underlying the Activation and Sensitization of Meningeal Nociceptors: The Role of Immuno-Vascular Interactions and Cortical Spreading Depression

  • D. Levy
  • Biology, Medicine
    Current Pain and Headache Reports
  • 2012
TLDR
Electrophysiological data provided the first direct evidence that CSD is indeed a powerful endogenous process that can lead to persistent activation of meningeal nociceptors and the migraine pain pathway.

Alcohol-induced headaches: Evidence for a central mechanism?

  • A. Panconesi
  • Medicine, Psychology
    Journal of neurosciences in rural practice
  • 2016
TLDR
The conclusion was that vasodilatation is hardly compatible with ADs trigger activity of all primary headaches and a common pathogenetic mechanism at cortical, or more likely at subcortical/brainstem, level is more plausible.

8 Lifestyle Contributors to Headache

TLDR
Patients with migraine, tension-type headache, and perhaps some other headache types may benefit from an organized plan to address lifestyle issues and triggers, as well as behavioral interventions such as relaxation training, stress-management training, and the acquisition of pacing and self-monitoring skills.

The Multitarget Drug Approach in Migraine Treatment: The New Challenge to Conquer

TLDR
The design, discovery, and development of new drugs that reach several (instead of unique) specific targets (functional selectivity) involved in the migraine pathophysiology is essential to progress in the migraines treatment and open a new field of study about the main pathways and targets that could synergistically improve the migraine management.

Migraine in childhood: an organic, biobehavioral, or psychosomatic disorder?

TLDR
The most recent findings on neurological, psychological, and environmental factors that may potentially cause migraine are analyzed and any alteration in genetics or in cerebral areas or networks that can explain migraine vulnerability are analyzed.

The biological basis of headache

  • L. Kelman
  • Psychology
    Expert review of neurotherapeutics
  • 2011
TLDR
The dynamic imaging of pain and headache is rapidly evolving and providing new insights and directions of research, and the components are analyzed in this article.

Genetics of Migraine: Insights into the Molecular Basis of Migraine Disorders

TLDR
With respect to common polygenic migraine, genome‐wide association studies have now identified single nucleotide polymorphisms at 38 loci significantly associated with migraine risk, suggesting that both neuronal and vascular pathways also contribute to the pathophysiology of common migraine.
...

References

SHOWING 1-10 OF 54 REFERENCES

Unitary hypothesis for multiple triggers of the pain and strain of migraine

TLDR
It is proposed 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.

Different patterns of parasympathetic activation in uni- and bilateral migraineurs.

TLDR
It is concluded that Cranial parasympathetic function does differ among patients with various migraine types at rest, and a model of within-brainstem interaction between the two locus coeruleus nuclei, which are involved in control of pain and cranial parASYmpathetic outflow is suggested.

Intrinsic brain activity triggers trigeminal meningeal afferents in a migraine model

TLDR
This work establishes a link between migraine aura and headache by demonstrating that cortical spreading depression activates trigeminovascular afferents and evokes a series of cortical meningeal and brainstem events consistent with the development of headache.

Brain Hyperexcitability: The Basis for Antiepileptic Drugs in Migraine Prevention

TLDR
Functional magnetic resonance imaging of the brain and magnetoencephalography provide the most consistent evidence for the role of brain hyperexcitability in migraine and confirm that triggering an abnormal electric and metabolic event consistent with the cortical spreading depression of Leao is anatomically and functionally linked with migraine aura symptoms.

A PET study exploring the laterality of brainstem activation in migraine using glyceryl trinitrate.

TLDR
Results suggest that lateralization of pain in migraine is due to lateralized brain dysfunction, and the activation persisted after pain was controlled by sumatriptan.

Chronic pain and medullary descending facilitation

The Triggers or Precipitants of the Acute Migraine Attack

  • L. Kelman
  • Medicine, Psychology
    Cephalalgia : an international journal of headache
  • 2007
TLDR
Tiggers were more likely to be associated with a more florid acute migraine attack and differences were seen between women and men, aura and no aura, episodic and chronic migraine, and between migraine and probable migraine.

Calcitonin gene–related peptide does not excite or sensitize meningeal nociceptors: Implications for the pathophysiology of migraine

TLDR
The results of this study suggest that CGRP effects in the meninges, including meningeal vasodilatation, are not sufficient to activate or sensitizeMeningeal nociceptors.

Sensitization of meningeal sensory neurons and the origin of headaches

TLDR
The activity of primary afferent neurons in the rat trigeminal ganglion that innervate the dural venous sinuses are recorded, showing properties of meningeal afferents that may contribute to the intracranial mechanical hypersensitivity that is characteristic of some types of clinically occurring headaches, and to the throbbing pain of migraine.
...