Patients with magnesium, latent tetany and migraine head pain

reference

Cegielska J, Szmidt-Sałkowska E, Domitrz W, Gaweł M, Radzwoń-Zaleska M, Domitrz I. Migraine and their association with hyperactivity of cell membranes in the course of a latent magnesium deficiency-pre-study on the importance of latent tetany in the Migraine pathogenesis. nutrients . 2021; 13 (8): 2701.

Study goal

Determination of whether there is a connection between suspected latent magnesium deficiency and migraines by correlating the electrophysiological test to latent tetany

draft

quasi-experimental design

participant

The study took 35 consecutive patients from the headache clamp with diagnosed migraines (29 women and 6 men; at the age of 22–57). Eight patients had migraines with aura (i.e. classic migraines) and 27 had migraines without aura (ie ordinary migraines). All patients had normal serum levels from magnesium, potassium and parathyroid concentrations. For comparison, a control group of 24 healthy volunteers (17 women and 7 men; at the age of 23–61) was also examined.

patients with the following were excluded from the study:

• anamnesis of metabolic or hormone disorders, including thyroid and parathyroidal thyroid diseases
• cardiovascular diseases
• cancer or other serious diseases (dementia, depression)
• Participation in elimination diets
• Use of medication that influence the electrolyte concentration, or over -the -counter food supplements

study parameters evaluated

The investigators assessed the latent tetany for migraine patients and control patients by electrophysiological measurements using modified tests for the trousseau sign.

primary result measurements

The investigators calculated the correlation between spasmophilia (positive result of an electrophysiological latent tetany) and the migraine status.

important knowledge

Overall, no significant difference between the occurrence of spasmophilia was found in migraine and control groups ( p = 0.13). In the subgroup analysis, a statistical difference in patients with migraines with Aura was found in comparison to controls ( p = 0.04).

practice implications

This study offers the practitioner several insights that may not be obvious when reading it for the first time. Although there is an insight, there is no definitive answer to whether magnesium is a valuable intervention in migraine headache, nor is there an insight about the type of magnesium can best be tested as an intervention. However, it provides some provocative information on assessing latent magnesium failure, which can be useful for patient selection criteria in future studies on magnesium interventions in migraine patients.

It is important to recognize that this is not an intervention study and, as such, does not support or do not support the causality. Rather, the investigators were based on self -reports from migraine patients in diaries and correlated them with the reaction to a tetanie test. If this study had been expanded to add magnesium in patients with spasmophilia with primary endpoints of migraine frequency and intensity, more effects would be obvious.

The pathogenesis of migraine head pain has been examined for decades. Theories include neuronal disorders, ion channel disorders of receptors, including NMDA, AMPA, MGLUR, Cannabino, Vanilloid and Par. ^{1-3 However is. 4}

The simplification of the metabolic steps of pathophysiology results in the following:

It is known that magnesium blocks the calcium channel of the NMDA receptor. The NMDA receptor enables the release of glutamate. Without sufficient magnesium, the neuro -sexative glutamate is reinforced and increases oxidative stress. There is an increased blood circulation. Imaging methods (magnetic resonance spectroscopy) also show changes in the occipital cortex for migraines with aura. A moderate blood circulation, in particular the occipital cortex, can cause a phenomenon known as cortical spreading depression (CSD), which causes a self -spreading wave to other areas of the brain and the experience of headaches. It is noteworthy that a magnesium deficiency can lower the threshold for nociception and that an abnormal glutamate release is associated with migraines and other neurological diseases. ^{5-8 genetic and/or acquired mitochondrial dysfunction can also contribute to this cascade of events.}

With the lack of nutrients, this pathogenesis is relatively simple, but in the absence of a well -known insufficiency it can be more complex.