Migraine and Yawning

Güven, Bülent; Güven, Hayat; Çomoğlu, Selçuk

doi:10.1111/head.13195

Cited by 17 publications

(23 citation statements)

References 28 publications

(83 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Further, Jacome described 3 migraineurs with compulsive yawning as a prodromal symptom, independent of fatigue and drowsiness (154). In a recent cross-sectional study, 45.4% of 339 migraineurs reported repetitive yawning during migraine attacks (155). Sleepiness was significantly more often reported in patients with yawning compared to those who did not yawn during their migraine attacks.…”

Section: Resultsmentioning

confidence: 99%

Caffeine and Primary (Migraine) Headaches—Friend or Foe?

Alstadhaug

Andreou

2019

Front. Neurol.

View full text Add to dashboard Cite

Background: The actions of caffeine as an antagonist of adenosine receptors have been extensively studied, and there is no doubt that both daily and sporadic dietary consumption of caffeine has substantial biological effects on the nervous system. Caffeine influences headaches, the migraine syndrome in particular, but how is unclear.Materials and Methods: This is a narrative review based on selected articles from an extensive literature search. The aim of this study is to elucidate and discuss how caffeine may affect the migraine syndrome and discuss the potential pathophysiological pathways involved.Results: Whether caffeine has any significant analgesic and/or prophylactic effect in migraine remains elusive. Neither is it clear whether caffeine withdrawal is an important trigger for migraine. However, withdrawal after chronic exposure of caffeine may cause migraine-like headache and a syndrome similar to that experienced in the prodromal phase of migraine. Sensory hypersensitivity however, does not seem to be a part of the caffeine withdrawal syndrome. Whether it is among migraineurs is unknown. From a modern viewpoint, the traditional vascular explanation of the withdrawal headache is too simplistic and partly not conceivable. Peripheral mechanisms can hardly explain prodromal symptoms and non-headache withdrawal symptoms. Several lines of evidence point at the hypothalamus as a locus where pivotal actions take place.Conclusion: In general, chronic consumption of caffeine seems to increase the burden of migraine, but a protective effect as an acute treatment or in severely affected patients cannot be excluded. Future clinical trials should explore the relationship between caffeine withdrawal and migraine, and investigate the effects of long-term elimination.

show abstract

Section: Resultsmentioning

confidence: 99%

Caffeine and Primary (Migraine) Headaches—Friend or Foe?

Alstadhaug

Andreou

2019

Front. Neurol.

View full text Add to dashboard Cite

show abstract

“…Several clinical features point towards the limbic system and hypothalamus as prodrome/ attack-initiating brain structures. These include the well-described involvement of the hypothalamus in the regulation of yawning (24), tiredness and mood changes (17); the circadian rhythmicity of attacks (25); and the association of attacks with hormonal status and the menstrual cycle (26). Some of the typical premonitory symptoms (e.g.…”

Section: The Clinical Presentation Of Headache Pointing To Hypothalammentioning

confidence: 99%

Hypothalamic regulation of headache and migraine

May

Burstein

2019

Cephalalgia

View full text Add to dashboard Cite

Background The clinical picture, but also neuroimaging findings, suggested the brainstem and midbrain structures as possible driving or generating structures in migraine. Findings This has been intensely discussed in the last decades and the advent of modern imaging studies refined the involvement of rostral parts of the pons in acute migraine attacks, but more importantly suggested a predominant role of the hypothalamus and alterations in hypothalamic functional connectivity shortly before the beginning of migraine headaches. This was shown in the NO-triggered and also in the preictal stage of native human migraine attacks. Another headache type that is clinically even more suggestive of hypothalamic involvement is cluster headache, and indeed a structure in close proximity to the hypothalamus has been identified to play a crucial role in attack generation. Conclusion It is very likely that spontaneous oscillations of complex networks involving the hypothalamus, brainstem, and dopaminergic networks lead to changes in susceptibility thresholds that ultimately start but also terminate headache attacks. We will review clinical and neuroscience evidence that puts the hypothalamus in the center of scientific attention when attack generation is discussed.

show abstract

“…As well, the relationship between cortisol and migraine brings us to the Thompson Cortisol Hypothesis, which proposes yawning (a known premonitory migraine feature) and increased cortisol to be early indicators of neurological condition. [40][41][42] Our study shows that optimum CM management may lead to normalization of endogenous glucocorticoids level. Our findings demonstrate that emphasis on improving socio-cognitive skills of pain self-efficacy may be a key area of focus in CM management.…”

Section: Clinical Variablesmentioning

confidence: 63%

Section: Discussionmentioning

confidence: 99%

Endogenous glucocorticoids may serve as biomarkers for migraine chronification

Woldeamanuel

Sanjanwala

Cowan

2020

Therapeutic Advances in Chronic Disease

View full text Add to dashboard Cite

Aims: The aims of this study were to: (a) identify differences in serum and cerebrospinal fluid (CSF) glucocorticoids among episodic migraine (EM) and chronic migraine (CM) patients compared with controls; (b) determine longitudinal changes in serum glucocorticoids in CM patients; and (c) determine migraine-related clinical features contributing to glucocorticoid levels. Methods: Serum and CSF levels of cortisol and corticosterone were measured using liquid chromatography-mass spectrometry among adult patients with EM, CM, and controls. Serum and CSF samples were collected from 26 and four participants in each group, respectively. Serum glucocorticoids were measured at a second timepoint after 2 years among 10 of the CM patients, six of whom reverted to EM while four persisted as CM. Receiver operating characteristic (ROC) analysis was made to assess the migraine diagnostic performance of glucocorticoids. Regression analysis was conducted to determine the link between glucocorticoid levels and migraine-related clinical variables. Results: CM patients exhibited significantly elevated serum and CSF levels of cortisol and corticosterone compared with controls and EM patients (age, sex, body mass index adjusted; Kruskal–Wallis p < 0.05). ROC showed area-under-curve of 0.89 to differentiate CM from EM. CM patients with remission had their serum glucocorticoids return to control or near EM levels ( p < 0.05). Persistent CM showed unremitting serum glucocorticoids. Migraine frequency and disability contributed to increased cortisol, while pain self-efficacy predicted lower cortisol levels ( p < 0.005). Conclusion: Endogenous glucocorticoids may be biomarkers for migraine progression and for monitoring treatment response. Improving pain self-efficacy skills may help optimize endogenous glucocorticoid levels, which in turn may prevent migraine attacks.

show abstract

Migraine and Yawning

Cited by 17 publications

References 28 publications

Caffeine and Primary (Migraine) Headaches—Friend or Foe?

Caffeine and Primary (Migraine) Headaches—Friend or Foe?

Hypothalamic regulation of headache and migraine

Endogenous glucocorticoids may serve as biomarkers for migraine chronification

Contact Info

Product

Resources

About