Old Habits Die Hard: Dietary Habits of Migraine Patients Challenge our Understanding of Dietary Triggers.

peer reviewedIntroduction: Migraine is a multifactorial neurological disorder with a major metabolic facet. Dietary approaches represent a commonly implemented lifestyle modifying strategy in headache clinics, yet the precise relationship between diet and migraine is still a matter of debate. Materials and Methods: The study consisted of two parts: first, in a cross-sectional design, we compared alimentary habits of migraine subjects and a control group of healthy volunteers. For the second part, we prospectively evaluated patients' daily consumption of various potentially migraine-triggering foods over a two-month period in order to examine their possible association with the occurrence of a migraine attack. Results: Most migraine patients reported avoiding at least one potentially migraine-triggering food/drink from their diet. In spite of that, with the sole exemption of citrus fruits, there were no statistically significant differences with respect to consumption patterns between migraine patients and controls (including wine and chocolate). Consumption frequency over time was proportional to intake of potentially migraine-triggering foods the day before a migraine attack. Conclusion: Our results underline the need of performing trigger challenges in order to avoid falling into an association-causation fallacy when attempting to identify possible alimentary migraine triggers. Indeed, it is possible that intake of certain foods like chocolate before attacks is a consequence of pre-attack cravings or a simple coincidence facilitated by previously established dietary habits

Migraine triggers and habituation of visual evoked potentials

Background: Identifying specific subsets of patients within the clinical spectrum of migraine could help in personalizing migraine treatment. Profiling patients by combining clinical characteristics and neurophysiological biomarkers is largely unexplored. We studied the association between migraine attack triggers and habituation of visual evoked potentials. Methods: We personally interviewed 25 patients about their migraine triggers following a structured list, and measured the N1-P1 habituation slope over six blocks of 100 averaged pattern-reversal VEP afterwards. Results: The mean number of triggers per patient was 4.52 1.42. Habituation slopes differed significantly between subjects who reported stress as a migraine trigger (deficient VEP habituation) and subjects who did not (preserved VEP habituation). For the remaining categories, the mean amplitude slope was always positive, indicating deficient habituation, and was not significantly different between subgroups. Conclusions: Migraine patients not reporting perceived stress as a trigger for their attacks might constitute a distinct clinic-physiological subset within the migraine spectrum

Medication-overuse headache : a widely recognized entity amidst ongoing debate

Medication overuse in primary headache disorders is a worldwide phenomenon and has a role in the chronification of headache disorders. The burden of disease on individuals and societies is significant due to high costs and comorbidities. In the Third Edition of the International Classification of Headache Disorders, medication-overuse headache is recognized as a separate secondary entity next to mostly primary headache disorders, although many clinicians see the disease as a sole complication of primary headache disorders. In this review, we explore the historical background of medication-overuse headache, its epidemiology, phenomenology, pathophysiology and treatment options. The review explores relevant unanswered questions and summarizes the current debates in medication-overuse headache

Headache Related Alterations of Visual Processing in Migraine Patients.

peer reviewedMigraine is characterized by an increased sensitivity to visual stimuli that worsens during attacks. Recent evidence has shown that feedforward volleys carrying incoming visual information induce high-frequency (gamma) oscillations in the visual cortex, while feedback volleys arriving from higher order brain areas induce oscillatory activity at lower frequencies (theta/alpha/low beta). We investigated visually induced high (feedforward) and low (feedback) frequency activations in healthy subjects and various migraine patients. Visual evoked potentials from 20 healthy controls and 70 migraine patients (30 interictal and 20 ictal episodic migraineurs, 20 chronic migraineurs) were analyzed in the frequency domain. We compared power in the theta-alpha-low beta and gamma range between groups, and searched for correlations between the low-to-high frequency activity ratio and number of monthly headache and migraine days. Compared to healthy controls, interictal migraine patients had increased visually induced low frequency (feedback) activity. Conversely, ictal and chronic migraine patients showed an augmented gamma band (feedforward) power. The low-frequency-to-gamma (feedback/feedforward) activity ratio correlated negatively with monthly headache days and tended to do so with migraine days. Our findings show that visual processing is differentially altered depending on migraine cycle and type. Feedback control from higher order cortical areas predominates interictally in episodic migraine while migraine attacks and chronic migraine are associated with enhanced incoming afferent activity, confirming their similar electrophysiological profile. The presence of headache is associated with proportionally higher gamma (feedforward) activities. PERSPECTIVE: This study provides an insight into the pathophysiology of migraine headache from the perspective of cortical sensory processing dynamics. Patients with migraine present alterations in feedback and feedforward visual signaling that differ with the presence of headache

Determinants and consequences of abnormal visual cortex responsiveness in migraine without aura

La migraine est une maladie multifactorielle complexe, qui résulte de l'interaction entre une prédisposition génétique et un environnement facilitant. La majeure partie de l' information venant de notre entourage nous atteint via le système visuel, ce qui fait de la vision la modalité sensorielle la plus développée chez l'Homme et celle qui met en jeu les aires cérébrales les plus tendues. Un faisceau de données cliniques et expérimentales a montré que les patients migraineux sont hyper-réactifs à la stimulation visuelle, mais les déterminants de ce phénomène restent méconnus. De plus, bien qu'étroitement associée à la migraine, l‟hyper-réactivité visuelle n'est ni suffisante, ni nécessaire pour développer la, maladie ce qui suggère l'existence de mécanismes physiopathologiques additionnels. Dans cette thèse nous avons analysé des facteurs environnementaux, métaboliques, anatomo-fonctionnels, et neurochimiques liés à la réactivité visuelle chez les migraineux, et la possible implication de leur interaction dans la pathogénie de la maladie. Pour ce faire, nous avons réalisé une série d‟études neurophysiologiques et de neuroimagerie qui explorent des aspects distincts de la physiologie du cerveau. Les résultats montrent que (1) une part de la variabilité interindividuelle de la réactivité visuelle peut être expliquée par des influences environnementales; (2) l‟hyper-réactivité visuelle dans la migraine est le résultat d'un déséquilibre complexe entre les mécanismes qui favorisent une perception renforcée, et ceux qui protègent contre une surcharge sensorielle; (3) la réserve métabolique au niveau cortical est insuffisante face à la demande énergétique accrue due à l'hyper-réactivité visuelle. Ces résultats illustrent la complexité des mécanismes responsables de l'hyperréactivité visuelle dans la migraine, améliorent notre compréhension de la physiopathologie de cette maladie, et ouvrent la voie à des axes de recherche innovants

Métabolisme cérébral distinct en relation avec la sensibilité à la douleur entre sujets sains, migraine épisodique et migraine chronique

Introduction Allodynia, i.e. pain evoked by a non-painful stimulus, is prevalent in chronic pain and in migraine where it augments with disease severity and chronicity [1]. Central sensitization is thought to be the culprit [2]. It is not known, however, which central areas are involved. The aim of the present study was to evaluate whether brain metabolism in subjects that are more sensitive to pain is different between migraine patients and healthy controls. Subjects and methods Quantitative heat sensory testing on the forehead and 18FDG-PET were performed in 55 subjects: 20 healthy volunteers (HV, 21-59 years, 5M), 21 patients with episodic migraine in the interictal phase (MO, age range: 20-63 years, 5M) and 14 patients with chronic migraine (CM, age range: 22-62 years, 1M). The 3 cohorts were subdivided according to the median heat pain threshold into subgroups with low and high pain thresholds. PET results were compared between these subgroups in each cohort. Data analyses were restricted to areas of the pain/salience matrix. Results There was no significant difference in heat pain thresholds between HV (median: 43.7 °C), MO median: 44.2°C) and CM (median: 43.3°C) (p=0.64). In an SPM-ANOVA, a contrast modelling the potential gradual effect of increased differences in pain sensitivity in relation to disease severity showed significant metabolic changes in bilateral thalamus and midbrain (p < 0.001). Additional analyses revealed that hypometabolic areas in subgroups with a low heat pain threshold differed between HV (anterior cingulate and somatosensory cortices), MO (lower pons and somatosensory cortex) and CM (midbrain and thalamus) (Figure 1). Conclusion Overall migraine patients do not have reduced heat pain thresholds. However, hypometabolic areas related to high thermal pain sensitivity are strictly cortical in HV, but comprise the pons in episodic migraine and are restricted to midbrain and thalamus in chronic migraine. The distinct central correlates of heat pain sensitivity in migraine patients might therefore represent a biomarker of migraine and its chronification. Legend to figure Figure 1. Hypometabolic areas in low pain threshold subgroups in HV (green), MO (orange) and CM (red). p < 0.01 for display purpose.Les migraineux ont une sensibilité anormale à la douleur. Les mécanismes cérébraux en sont inconnus. Nous avons comparé le métabolisme cérébral chez des sujets sains et chez des migraineux épisodiques ou chroniques et correlé les résultats avec le seuil douloureux. Les aires cérébrales hypométaboliques liées à un seuil douloureux bas diffèrent entre groupes: régions corticales chez les sujets sains, aires corticales et sous-corticales dans la migraine épisodique, régions sous-corticales dans la migraine chronique .Le contrôle central de la douleur semble modifié distinctement dans les formes de migraine, ce qui pourrait en constituer un biomarqueur et avoir des implications thérapeutiques

Highlights in migraine electrophysiology: are controversies just reflecting disease heterogeneity?

PURPOSE OF REVIEW: In migraine, the brain is 'hyperresponsive', which refers to a deficit of habituation to repeated sensory stimuli between attacks. This deficit normalizes in peri-ictal and ictal phases. A decreased cortical preactivation of thalamo-cortical origin and an impaired intracortical inhibition are probably involved in its pathophysiology. RECENT FINDINGS: The reality of a habituation deficit of visual evoked potentials, a neurophysiological 'hallmark' of interictal migraine, has been questioned. Blinding may be an issue, but some genetic, environmental, or behavioural differences could also exist between populations. A habituation deficit is found interictally in other sensory modalities, and strongly depends on the time of the recordings within the migraine cycle. An impaired thalamocortical drive is demonstrated in interictal phase, and normalizes in ictal phase as well as in chronic migraine, where a strength enhancement of primary cortical activation is observed. An interictal dysexcitability, of subcortical or primary cortical origin, is suggested by magnetic stimulation. These phenomena could occur in varying degrees depending on patients and on the migraine cycle, and account for the heterogeneity of electrophysiological results. SUMMARY: Finding a reliable electrophysiological biomarker for such a multifaceted and cycling disease as migraine is still a challenge. A better standardization of protocols would be worthwhile

Brain correlates of single trial visual evoked potentials in migraine: more than meets the eye.

Background: Using conventional visual evoked potentials (VEPs), migraine patients were found to be hyperresponsive to visual stimulus. Considering that a significant portion of neuronal activity is lost for analysis in the averaging process of conventional VEPs, in this study we investigated visual evoked responses of migraine patients and healthy volunteers using a different approach: single trial analysis. This method permits to preserve all stimulus-induced neuronal activations, whether they are synchronized or not. In addition, we used MRI voxel-based morphometry to search for cortical regions where gray matter volume correlated with single trial (st) VEP amplitude. Finally, using resting-state functional MRI, we explored the connectivity between these regions. Results: stVEP amplitude was greater in episodic migraine patients than in healthy volunteers. Moreover, in migraine patients it correlated positively with gray matter volume of several brain areas likely involved in visual processing, mostly belonging to the ventral attention network. Finally, resting state functional connectivity corroborated the existence of functional interactions between these areas and helped delineating their directions. Conclusions: st-VEPs appear to be a reliable measure of cerebral responsiveness to visual stimuli. Mean st-VEP amplitude is higher in episodic migraine patients compared to controls. Visual hyper-responsiveness in migraine involves several functionally-interconnected brain regions, suggesting that it is the result of a complex multi-regional process coupled to stimulus driven attention systems rather than a localized alteration