Migraine in Metabolic Syndrome

Güldiken, Babürhan; Güldiken, Sibel; Taskiran, Bengur; Koç, Gönül; Turgut, Nilda; Kabayel, Levent; Tuğrul, Armağan

doi:10.1097/nrl.0b013e31817781b6

Cited by 61 publications

(82 citation statements)

References 35 publications

(27 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The results of the study demonstrated that increased waist circumference, obesity, and impaired glucose metabolism, which are components of metabolic syndrome, were more frequent in patients with migraine. Insulin resistance was suggested to be responsible for high migraine prevalence because it is common in the pathogenesis of these disorders (32). A study evaluated 83 patients with episodic migraine patients, 83 patients with chronic migraine, and 83 healthy individuals, and BMI, waist circumference, and blood pressure measurements were performed.…”

Section: Migraine In the Presence Of Insulin Resistance And Obesitymentioning

confidence: 99%

The Relationship Between Migraine and Nutrition

Özturan¹,

Şanlıer²,

Coşkun³

2016

tnd

View full text Add to dashboard Cite

Section: Migraine In the Presence Of Insulin Resistance And Obesitymentioning

confidence: 99%

The Relationship Between Migraine and Nutrition

Özturan¹,

Şanlıer²,

Coşkun³

2016

tnd

View full text Add to dashboard Cite

“…Migraineurs are much more likely to have metabolic disorders than non-migraineurs [23][24][25][26][27][28][29] which we speculated is connected to carbohydrate disturbance of electrolytes [30]. Additionally, migraineurs have only nominal changes in voltage between states of action potential versus resting potential, indicating that a migraine brain is "always on," [31,32] supporting the theory that migraineurs have hyper sensitive sensory organs [33,34].…”

Section: Introductionmentioning

confidence: 56%

Migraine Cause And Treatment

Stanton¹

2015

Ment Health Fam Med

View full text Add to dashboard Cite

Background:Research shows that migraine brains have hyperactive sensory organs and multiple sensory receptor connections. Hyper activity of these organs needs extra supply of nutrition to support increased electrical activity. Today's medicines reduce or prevent the functioning of these neurons by blocking essential voltage dependent calcium or sodium channel instead of providing nutrients. We asked: if we provide support for extra electrical activity of migraineurs, would it prevent migraines without the use of medicines? Methods:We reviewed published literature and conducted research over 6 months studying 650 volunteer migraineurs in a migraine-research Facebook group. Participants were screened for migraine types, answered a questionnaire on medical conditions, medicines used, and lifestyle. They were provided instructions on the use of the migraine protocol and were evaluated weekly. Findings:Migraine frequency appears to be exacerbated by carbohydrate-rich and salt-and water-poor diets and may be worsened by medicines that block voltage gated calcium or sodium channels. Stopping these medicines, reducing carbohydrates and increasing saline in electrolytes appears to prevent and/or stop migraines.Conclusions: H 2 O and Na+ efflux from cells caused by glucose, electrolyte mineral (Na+, Cl-, K+) ratio may be disrupted in carbohydrate heavy diets causing migraines. Changes to diet that include increased salt intake along with reduced carbohydrate intake appears to prevent glucose induced electrolyte changes which then decreases migraine frequency. In the present study, all participants who made these dietary changes were able to eliminate migraine medications and remained migraine free.

show abstract

“…The extracranial terminal branches of the external carotid artery were suspected to be the reason of pain in the aura [11,12]. Newer data imply that migraine headache is caused by an inappropriate activation of trigeminovascular system, that is, pain sensitive innervation of dural, arachnoid, and pial vessels as well as large intracranial vessels by nociceptive fibers originating in trigeminal ganglion (TG) and travelling mainly through ophthalmic and to a much lesser extent through maxillary and mandibular divisions of trigeminal nerve [10,13,14]. Appropriately, "neurovascular disorder" definition has been used to address dysfunction of the cerebral nerves and blood vessels through cortical activation which is followed by brainstem activation with neurogenic inflammation and vasodilation [15][16][17].…”

Section: Pathophysiology Of Migrainementioning

confidence: 99%