scholarly journals Migraine: Calcium Channels and Glia

2021 ◽  
Vol 22 (5) ◽  
pp. 2688
Author(s):  
Marta Kowalska ◽  
Michał Prendecki ◽  
Thomas Piekut ◽  
Wojciech Kozubski ◽  
Jolanta Dorszewska

Migraine is a common neurological disease that affects about 11% of the adult population. The disease is divided into two main clinical subtypes: migraine with aura and migraine without aura. According to the neurovascular theory of migraine, the activation of the trigeminovascular system (TGVS) and the release of numerous neuropeptides, including calcitonin gene-related peptide (CGRP) are involved in headache pathogenesis. TGVS can be activated by cortical spreading depression (CSD), a phenomenon responsible for the aura. The mechanism of CSD, stemming in part from aberrant interactions between neurons and glia have been studied in models of familial hemiplegic migraine (FHM), a rare monogenic form of migraine with aura. The present review focuses on those interactions, especially as seen in FHM type 1, a variant of the disease caused by a mutation in CACNA1A, which encodes the α1A subunit of the P/Q-type voltage-gated calcium channel.

Cephalalgia ◽  
2010 ◽  
Vol 30 (10) ◽  
pp. 1179-1186 ◽  
Author(s):  
Jakob Møller Hansen ◽  
Anne Werner Hauge ◽  
Jes Olesen ◽  
Messoud Ashina

Introduction: Calcitonin gene-related peptide (CGRP) is a key molecule in migraine pathogenesis. Intravenous CGRP infusion triggers delayed migraine-like attacks in patients with migraine without aura (MO). In contrast to patients with MO, in prior studies patients with familial hemiplegic migraine (FHM) did not report more migraine-like attacks compared to controls. Whether CGRP triggers migraine in patients with typical (non-hemiplegic) migraine with aura is (MA) unknown. In the present study we examined the migraine inducing effect of CGRP infusion in patients suffering from MA and healthy controls. Methods: Fourteen patients suffering exclusively from migraine with typical aura (MA) and 11 healthy volunteers received a continuous intravenous infusion of 1.5 µg/min CGRP over 20 minutes. Headache and other migraine symptoms were scored every 10 minutes for one hour and self recorded hourly thereafter and until 13 hours post-infusion. Results: CGRP infusion induced significantly more delayed headaches in MA patients (12 out of 14) than in controls (2 out of 11) ( p = 0.001). Furthermore, significantly more MA patients (57%; 8 out of 14) fulfilled criteria for an experimentally induced migraine attack after CGRP than controls (0%; 0 out of 11) ( P = 0.003). Four patients (28%) reported aura symptoms after CGRP infusion. Conclusion: CGRP triggered migraine-like attacks without aura in patients suffering exclusively from MA. It also triggered a typical aura in 28% of the patients. These data indicate similar neurobiological pathways responsible for triggering migraine headache in MA and MO patients, and suggest differences between MA/MO and FHM.


2011 ◽  
Vol 31 (15) ◽  
pp. 5755-5763 ◽  
Author(s):  
K. Eikermann-Haerter ◽  
I. Yuzawa ◽  
T. Qin ◽  
Y. Wang ◽  
K. Baek ◽  
...  

2015 ◽  
Vol 263 ◽  
pp. 214-220 ◽  
Author(s):  
Reinald Shyti ◽  
Katharina Eikermann-Haerter ◽  
Sandra H. van Heiningen ◽  
Onno C. Meijer ◽  
Cenk Ayata ◽  
...  

Cephalalgia ◽  
1993 ◽  
Vol 13 (4) ◽  
pp. 245-248 ◽  
Author(s):  
Michael Bjørn Russell ◽  
Jes Olesen

Studies of twins, spouses and familial aggregation strongly suggest that migraine without aura (MO) and migraine with aura (MA) are genetically determined. The mode of inheritance is most likely multifactorial in both MO and MA. However, autosomal dominant inheritance with reduced penetrance cannot be excluded in either MO or MA. At present the only evidence for genetic heterogeneity of MA is familial hemiplegic migraine with slowly progressive ataxia. This phenomenon can also be explained by linkage of different genes. All existing studies have been characterized by one or more of the following methodologic shortcomings: selection of probands from clinic populations, information obtained by questionnaire, family history obtained through probands, insufficient description of the attacks, lack of distinction between MO and MA. Useful strategies for future studies of migraine genetics are discussed.


2009 ◽  
Vol 66 (4) ◽  
pp. 564-568 ◽  
Author(s):  
Katharina Eikermann-Haerter ◽  
Michael J. Baum ◽  
Michel D. Ferrari ◽  
Arn M.J.M. van den Maagdenberg ◽  
Michael A. Moskowitz ◽  
...  

Cephalalgia ◽  
2003 ◽  
Vol 23 (9) ◽  
pp. 921-928 ◽  
Author(s):  
LL Thomsen ◽  
E Ostergaard ◽  
SF Romer ◽  
I Andersen ◽  
MK Eriksen ◽  
...  

In order to better understand sporadic hemiplegic migraine (SHM) and particularly its relation to familial hemiplegic migraine (FHM), migraine without aura (MO) and typical migraine with aura (typical MA), we investigated the occurrence of MO and typical MA among probands with SHM and their first-degree relatives. The pattern of familial aggregation of MO and typical MA was assessed by population relative risk calculations. A total of 105 SHM probands and 483 first-degree relatives were identified in the Danish population. Compared with the general population, SHM probands had no increased risk of MO, but a highly increased risk of typical MA. First-degree relatives of all SHM probands had an increased risk of both MO and typical MA, whereas first-degree relatives of probands with exclusively SHM had no increased risk of MO but an increased risk of typical MA. Our data suggest that SHM is a genetically heterogeneous disorder.


2019 ◽  
Vol 9 (7) ◽  
pp. 172 ◽  
Author(s):  
Salvo Lombardo ◽  
Emanuela Mazzon ◽  
Maria Basile ◽  
Eugenio Cavalli ◽  
Placido Bramanti ◽  
...  

Migraine is a disorder characterized by attacks of monolateral headaches, often accompanied by nausea, vomiting, and photophobia. Around 30% of patients also report aura symptoms. The cause of the aura is believed to be related to the cortical spreading depression (CSD), a wave of neuronal and glial depolarization originating in the occipital cortex, followed by temporary neuronal silencing. During a migraine attack, increased expression of inflammatory mediators, along with a decrease in the expression of anti-inflammatory genes, have been observed. The aim of this study was to evaluate the expression of inflammatory genes, in particular that of IL-1 receptor antagonist (IL-1RN), following CSD in a mouse model of familial hemiplegic migraine type 1 (FHM-1). We show here that the expression of IL-1RN was upregulated after the CSD, suggesting a possible attempt to modulate the inflammatory response. This study allows researchers to better understand the development of the disease and aids in the search for new therapeutic strategies in migraine.


2021 ◽  
pp. 105424
Author(s):  
Anisa Dehghani ◽  
Thas Phisonkunkasem ◽  
Sinem Yilmaz Ozcan ◽  
Turgay Dalkara ◽  
Arn M.J.M. van den Maagdenberg ◽  
...  

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