Migraine With Aura
Migraine with aura is a complex neurological disorder characterized by recurrent episodes of moderate to severe headache, often preceded by transient focal neurological symptoms known as aura[1]. Migraine, in general, affects a significant portion of the population, impacting approximately 8% of males and 17% of females [2]. It is recognized as one of the most disabling diseases globally and represents a considerable public health burden, ranking among the costliest neurological disorders for society [2].
Clinically, migraine is defined by diagnostic criteria established by the International Headache Society[1]. The International Classification of Headache Disorders (ICHD-II) distinguishes two main common forms: migraine with aura (MA) and migraine without aura (MO)[2]. While migraine without aura is characterized by headache associated with nausea or hypersensitivity to light and sound, migraine with aura is specifically marked by transient visual, sensory, or speech symptoms that typically precede the headache phase[1]. Individuals may experience attacks of only migraine with aura, only migraine without aura, or a combination of both[2]. There is ongoing debate within the scientific community regarding whether these two forms are distinct disorders or represent variations of a single disease entity with a common complex genetic background[2]. Diagnosing migraine with aura requires careful clinical assessment, as its neurological symptoms can sometimes be challenging to differentiate from those of other unrelated conditions[1].
The biological basis of migraine involves complex pathophysiology. Current theories suggest that migraine is primarily a result of neuronal dysfunction, with vascular changes considered downstream effects rather than primary causes [1]. Specifically, the headache phase is thought to involve the activation of the trigeminovascular system, while the aura symptoms are believed to be caused by cortical spreading depression (CSD), a slow-moving wave of neuronal and glial depolarization[2]. Migraine is viewed as a multi-factorial brain disorder with a significant genetic component, with heritability estimates for migraine reaching as high as 42-50% based on family and twin studies [1]. Despite this strong genetic influence, understanding of the molecular mechanisms contributing to its pathophysiology has been limited. Early genetic association studies identified relatively few genome-wide significant risk loci, but more recent meta-analyses of large cohorts have identified a greater number, such as 38 susceptibility loci for migraine [1].
Limitations
Section titled “Limitations”Understanding the genetic basis of migraine with aura is subject to several limitations inherent in current research methodologies and the complex nature of the condition. These limitations impact the interpretability and generalizability of findings, necessitating careful consideration when evaluating the identified susceptibility loci.
Challenges in Phenotypic Definition and Measurement
Section titled “Challenges in Phenotypic Definition and Measurement”Precise phenotypic definition and measurement pose significant challenges in genetic studies of migraine with aura. Diagnosing migraine aura accurately is difficult, as its transient visual, sensory, or speech symptoms can be confused with other neurological conditions[1]. This necessitates stricter diagnostic criteria for subtype analyses, often involving structured interviews by specialists in clinic-based settings, contrasting with the less extensive questionnaires used in population-based studies [1], [3]. Such variability in diagnostic rigor across studies can lead to reduced power to detect genuine genetic associations and introduces heterogeneity in clinical capture [1], [3].
Furthermore, there is ongoing debate regarding whether migraine with aura and migraine without aura are truly distinct entities or different manifestations of the same underlying disease[3], [4], [3], [5], [6], [6]. While some studies have suggested distinctness, others propose shared pathophysiology [7]. This phenotypic ambiguity complicates genetic analyses, as pooling or separating these subtypes may either dilute specific genetic signals or miss broader shared mechanisms, thereby affecting the interpretation of identified loci and hindering the elucidation of the specific pathophysiological mechanisms underpinning migraine aura [1].
Statistical Power and Study Design Constraints
Section titled “Statistical Power and Study Design Constraints”Genetic studies focusing specifically on migraine with aura are significantly constrained by statistical power due to considerably smaller sample sizes compared to analyses of migraine as a broader condition[1]. For instance, subtype analyses had only 6,332 cases, a fraction of the total sample size for general migraine studies, implying that two to three times larger sample sizes would be required to achieve comparable statistical power for subtypes[1]. This limitation directly impedes the ability to robustly identify susceptibility loci, potentially explaining why relatively few genetic associations have been revealed for the molecular mechanisms contributing to migraine pathophysiology despite its estimated heritability [1].
Differences in study design across cohorts also introduce constraints. Population-based studies, which often rely on questionnaires and include individuals with less severe migraine, may harbor a more genetically heterogeneous group with potentially lower genetic risk compared to clinic-based cohorts [3]. The inclusion of all non-migraine individuals as controls in population-based studies further means that effect sizes may not be directly comparable across different study designs, despite methods like pooled Z-score meta-analysis being used to address this [3]. These design variations and biases can obscure genuine associations and complicate the meta-analysis of findings, potentially leading to an underestimation of the genetic contribution specific to migraine with aura[3].
Incomplete Genetic Architecture and Generalizability
Section titled “Incomplete Genetic Architecture and Generalizability”Despite an estimated heritability of 42% for migraine, genetic association studies have only identified a limited number of genome-wide significant risk loci, indicating a substantial portion of the genetic architecture, or “missing heritability,” remains unexplained for migraine with aura[1]. This gap may be partly attributed to a potentially larger contribution to risk from low-frequency and rare genetic variations for this specific subtype, which are harder to detect with current genome-wide association study (GWAS) designs and sample sizes [1]. Consequently, understanding of the molecular mechanisms contributing to the pathophysiology of migraine aura remains incomplete, with genetic evidence still lacking to definitively favor theories of neuronal dysfunction over vascular changes [1].
Furthermore, the generalizability of current findings is limited by the ancestry composition of the study populations. Many large-scale genetic studies, including those for migraine, have predominantly focused on individuals of European ancestry [7]. This lack of diversity means that genetic variants identified may not be universally applicable or have the same effect sizes in other ancestral groups, hindering a comprehensive understanding of migraine with aura globally. The current research also largely omits the explicit consideration of environmental or gene-environment confounders, which are likely to play a significant role in a complex multifactorial disorder like migraine, further contributing to the remaining knowledge gaps in its etiology and progression.
Variants
Section titled “Variants”Genetic variations play a crucial role in an individual’s susceptibility to migraine, including the distinct subtype of migraine with aura. Research into these variants helps to unravel the complex interplay of neuronal, vascular, and inflammatory pathways that contribute to this debilitating neurological condition. Many identified variants affect genes involved in diverse cellular functions, from vascular regulation and neurotransmission to neuronal development and immune responses.
The FHL5 gene (Four And A Half LIM Domain Protein 5) is implicated in cell growth and differentiation, and its expression is particularly notable in vascular tissues. Variants such as rs2983896 and rs3798293 located in or near FHL5 have been identified as susceptibility loci for migraine. This episodic neurological disorder is understood to have a complex pathophysiology [2]. The “aura” specifically denotes these transient focal neurological symptoms [7]. While historically defined by diagnostic criteria, current conceptual frameworks increasingly view migraine as a multi-factorial brain disorder [7].
The operational definition of migraine generally involves recurrent attacks of moderate to severe headache, often accompanied by symptoms such as nausea or heightened sensitivity to light and sound[1]. For MA, these characteristic headache symptoms follow the distinct aura phase[1]. Notably, up to one-third of individuals experiencing migraine may encounter these aura symptoms [7]. The underlying pathophysiology is conceptualized as primarily neuronal dysfunction, with vascular changes considered secondary effects rather than primary causative factors [1].
Key Variants
Section titled “Key Variants”| RS ID | Gene | Related Traits |
|---|---|---|
| rs2983896 rs3798293 | FHL5 | migraine with aura migraine without aura, susceptibility to, 4, systolic blood pressure pulse pressure measurement, migraine without aura, susceptibility to, 4 migraine disorder, systolic blood pressure migraine disorder, pulse pressure measurement |
| rs2052692 | IRAG1 | migraine with aura migraine disorder, systolic blood pressure migraine disorder, diastolic blood pressure COVID-19 |
| rs77630941 | CUX1 | migraine with aura |
| rs11172113 | LRP1 | migraine disorder migraine without aura, susceptibility to, 4 FEV/FVC ratio, pulmonary function measurement, smoking behavior trait FEV/FVC ratio, pulmonary function measurement coronary artery disease |
| rs146778855 | CDH18 | migraine with aura |
| rs117608715 | NOL3 | migraine with aura |
| rs150592309 | ZNF511-PRAP1 | migraine with aura |
| rs112433120 | IGKV3OR2-268 - LINC01943 | migraine with aura |
| rs1364402 | CHRM2 | migraine with aura |
| rs2076054 | BPIFC | migraine with aura |
Classification and Nosology of Migraine Subtypes
Section titled “Classification and Nosology of Migraine Subtypes”The International Classification of Headache Disorders (ICHD), specifically its second edition (ICHD-II), formally recognizes two primary common forms of migraine: migraine with aura (MA) and migraine without aura (MO)[8] [2]. The fundamental distinction between these two forms lies in the presence or absence of the aura, which is a period characterized by diverse neurological symptoms that precede the headache phase[2]. Individuals may experience attacks of only MO, only MA, or a combination of both types in varying proportions throughout their lives [2].
A significant nosological debate persists regarding whether MA and MO should be considered distinct clinical entities or if they represent variations of a single disease entity sharing a common complex genetic background[2]. Some research studies have presented findings supporting the view that MA and MO are distinct disorders [9] [6], while other studies suggest they are not clearly separate entities [3] [5]. This ongoing discussion underscores the intricate nature of classifying migraine subtypes.
Diagnostic Criteria and Clinical Measurement
Section titled “Diagnostic Criteria and Clinical Measurement”The diagnosis of migraine, including its specific subtypes like MA, is based on standardized classification criteria established by the International Headache Society (IHS)[1]. In population-based research settings, diagnosis is frequently ascertained through the administration of detailed questionnaires [1]. Conversely, in clinic-based studies, diagnosis is typically assigned following structured interviews conducted either by telephone or in person [1]. A more stringent diagnostic process is often necessary for migraine subtypes, particularly MA, due to the challenge of differentiating aura symptoms from other neurological features that could arise from unrelated medical conditions [1].
The clinical criteria for MA specifically emphasize the transient nature of the visual, sensory, or speech symptoms that manifest prior to the headache. These symptoms are crucial for the operational definition of MA, as their presence or absence serves as the primary distinguishing factor from MO[2]. While these clinical criteria are widely applied in both clinical practice and research, the provided studies do not detail specific biomarkers, thresholds, or cut-off values used for the diagnostic differentiation of MA.
Pathophysiological Frameworks and Key Terminology
Section titled “Pathophysiological Frameworks and Key Terminology”The terminology associated with migraine with aura includes key abbreviations such as MA for migraine with aura and MO for migraine without aura[2]. The International Classification of Headache Disorders (ICHD) serves as the overarching nosological system, providing a standardized vocabulary for all headache diagnoses[8] [2]. From a conceptual standpoint, the headache phase of migraine is believed to be caused by the activation of the trigeminovascular system[10].
The aura itself is widely thought to be a manifestation of cortical spreading depression (CSD), described as a slowly propagating wave of neuronal and glial depolarization [11] [12]. This proposed distinction in the underlying mechanisms for the headache versus the aura further informs the specific terminology and comprehensive understanding of MA as a distinct migraine subtype[2]. Although genetic evidence points to a significant genetic component for migraine, the precise molecular mechanisms contributing to its pathophysiology remain a focus of ongoing research [1].
Signs and Symptoms
Section titled “Signs and Symptoms”Migraine with aura is a prevalent neurological disorder characterized by transient neurological symptoms that typically precede the headache phase[1]. These symptoms, collectively known as aura, are believed to stem from cortical spreading depression (CSD), a slow wave of neuronal and glial depolarization in the brain [2]. The subsequent headache phase is thought to involve activation of the trigeminovascular system[2].
Aura Phenomenology and Associated Headache
Section titled “Aura Phenomenology and Associated Headache”The clinical presentation of migraine with aura typically involves a range of transient neurological disturbances, most commonly visual, sensory, or speech symptoms[1]. Visual auras might include flickering lights, spots, or lines, while sensory auras could manifest as tingling or numbness, and speech auras as difficulty finding words or slurred speech. These aura symptoms usually precede the headache phase, which is described as moderate to severe and is often accompanied by nausea or heightened sensitivity to light and sound, mirroring the characteristics of migraine without aura[1]. Functional magnetic resonance imaging (fMRI) is a measurement approach that has been used to reveal the underlying mechanisms of migraine aura in the human visual cortex, providing objective insights into this complex neurological phenomenon [12].
Diagnostic Classification and Assessment
Section titled “Diagnostic Classification and Assessment”The diagnosis of migraine with aura is guided by the International Headache Society’s (IHS) diagnostic criteria, specifically the International Classification of Headache Disorders (ICHD-II)[1]. This standardized classification is crucial for distinguishing migraine with aura from other neurological conditions that may present with similar symptoms. Assessment methods for diagnosis typically involve structured interviews conducted in person or by telephone for clinic-based studies, or detailed questionnaires for population-based research, ensuring adherence to the IHS criteria[1]. The diagnostic significance of carefully evaluating aura symptoms is high, as they can be challenging to differentiate from other neurological features, necessitating a rigorous diagnostic process to avoid misdiagnosis and correctly identify this specific migraine subtype [1].
Clinical Spectrum and Heterogeneity
Section titled “Clinical Spectrum and Heterogeneity”Migraine with aura exhibits notable variability and heterogeneity in its clinical presentation among individuals. Patients may experience attacks solely with aura, solely without aura, or a combination of both types in varying proportions throughout their lifetime[2]. This phenotypic diversity fuels an ongoing debate regarding whether migraine with aura and migraine without aura are distinct disorders or merely represent different manifestations of a single underlying disease entity with a common complex genetic background[2]. Research suggests that migraine with aura may involve a higher degree of heterogeneity in its clinical capture and a more complex underlying biology, potentially due to a greater contribution from low-frequency and rare genetic variations[1].
Causes
Section titled “Causes”Migraine with aura is a complex neurological disorder influenced by a combination of genetic predispositions and various other biological and physiological factors. It is characterized by transient neurological symptoms, such as visual or sensory disturbances, that typically precede the headache phase[1]. Current research indicates that migraine is primarily a multifactorial brain disorder, with heritability estimates ranging from approximately 42% to 50% [13]. Understanding its causes involves examining the intricate interplay between inherited susceptibilities and the neurobiological mechanisms that drive its manifestation.
Genetic Architecture and Neurobiological Foundations
Section titled “Genetic Architecture and Neurobiological Foundations”Genetic factors play a substantial role in the susceptibility to migraine with aura, with family and twin studies consistently demonstrating a significant heritable component[13]. While rare monogenic forms of migraine exist, the common forms, including migraine with aura, are largely considered to be polygenic, involving multiple genetic variants that collectively increase risk[7]. Recent genome-wide association studies (GWAS) have identified at least 38 susceptibility loci for migraine, providing critical insights into the molecular pathways involved [1]. These genetic discoveries support existing theories of migraine pathophysiology and continue to uncover novel aspects of the disease.
The neurobiological basis of migraine with aura is closely linked to cortical spreading depression (CSD), a slow-moving wave of neuronal and glial depolarization across the cerebral cortex[11]. This phenomenon is widely believed to be the underlying mechanism responsible for the transient neurological symptoms of the aura phase [2]. Specific genetic variants, such as those in the dopamine beta-hydroxylase (DBH) gene, including a 19bp deletion polymorphism, have been associated with susceptibility to typical migraine and specifically migraine with aura, suggesting a role for neurotransmitter regulation in its pathology[2]. Additionally, polymorphisms in genes like estrogen receptor 1 (ESR1) have been investigated, although associations with migraine with aura have not always been consistently replicated across all studies[14].
Multifactorial Influences and Gene-Environment Interplay
Section titled “Multifactorial Influences and Gene-Environment Interplay”Migraine is fundamentally considered a multifactorial brain disorder, implying that its development and expression result from an intricate interplay between an individual’s genetic makeup and various external or internal factors [7]. While the provided research focuses predominantly on genetic aspects, the concept of multifactoriality inherently suggests that genetic predispositions interact with a range of environmental or physiological influences. The complex genetic background identified through studies indicates that these genetic susceptibilities likely modulate an individual’s response to various triggers, contributing to the episodic nature of migraine attacks. The precise mechanisms of these gene-environment interactions for migraine with aura require further elucidation.
Physiological and Age-Related Factors
Section titled “Physiological and Age-Related Factors”Beyond genetic and environmental interactions, certain physiological and age-related factors can influence the manifestation or profile of migraine. Clinical observations have shown that the characteristics of migraine can differ significantly based on an individual’s age and menopausal status [7]. For instance, differences in clinical profiles between migraineurs and non-migraineurs have been most notably observed concerning age and whether an individual is postmenopausal [7]. These shifts suggest that hormonal fluctuations and the aging process can modulate migraine susceptibility or its presentation, indicating a dynamic interaction between inherent biological processes and the complex underlying causes of the condition.
Biological Background of Migraine with Aura
Section titled “Biological Background of Migraine with Aura”Migraine with aura (MA) is an episodic neurological disorder characterized by a distinct sequence of symptoms, reflecting complex underlying biological mechanisms. It is one of the two prevalent forms of migraine, distinguished by transient neurological symptoms that precede the headache phase[2]. Understanding the biological underpinnings of MA involves exploring its genetic architecture, specific cellular events like cortical spreading depression, and the activation of neurovascular pathways.
Clinical Manifestations and Neurological Foundations
Section titled “Clinical Manifestations and Neurological Foundations”Migraine with aura is defined by recurrent attacks of moderate or severe headache, often associated with debilitating symptoms such as nausea and hypersensitivity to light and sound . This depolarization involves massive shifts in ion concentrations, particularly the efflux of potassium and influx of calcium, leading to a profound disruption of neuronal membrane potential and subsequent silencing of neuronal activity. The initial trigger for CSD often involves altered neuronal excitability, potentially through dysregulation of ion channels or neurotransmitter receptor activation, setting off a cascade of intracellular signaling events that propagate the wave. This wave of depolarization is the underlying mechanism for the transient visual, sensory, or speech symptoms experienced during the aura phase[2].
Genetic Underpinnings and Gene Regulatory Pathways
Section titled “Genetic Underpinnings and Gene Regulatory Pathways”The heritability of migraine, estimated at 42%, underscores a significant genetic component in its pathophysiology [1]. Recent genome-wide association studies (GWAS) have identified numerous susceptibility loci, with a meta-analysis of 375,000 individuals revealing 38 such loci [1]. These genetic variants likely influence gene regulation, impacting the expression levels of proteins critical for neuronal function, vascular control, or metabolic processes. Dysregulation in transcription factor activity or epigenetic modifications downstream of these genetic variations could alter the homeostatic balance of neuronal excitability, potentially lowering the threshold for cortical spreading depression or modulating the trigeminovascular system’s response.
Neurovascular Coupling and Regulatory Mechanisms
Section titled “Neurovascular Coupling and Regulatory Mechanisms”While migraine was historically viewed as a vascular disorder, current understanding posits neuronal dysfunction as primary, with vascular changes representing downstream effects [1]. The headache phase of migraine is believed to stem from activation of the trigeminovascular system[2]. This activation involves complex signaling pathways where neuropeptides released from trigeminal nerve endings interact with receptors on blood vessels, leading to vasodilation and plasma extravasation. Regulatory mechanisms such as post-translational modification of ion channels or G-protein coupled receptors in both neuronal and vascular cells could modulate the sensitivity and response of this system, contributing to the pain experience.
Systems-Level Dysregulation and Metabolic Homeostasis
Section titled “Systems-Level Dysregulation and Metabolic Homeostasis”The complex manifestation of migraine with aura arises from the intricate crosstalk and network interactions between various cellular and molecular pathways within the central nervous system and its vascular supply. Genetic predispositions interact with environmental factors to create a state of systems-level dysregulation, where the balance of neuronal excitability and inhibitory mechanisms is compromised. Furthermore, metabolic pathways, including energy metabolism and flux control within neurons and glia, are critical for maintaining cellular homeostasis and recovering from events like cortical spreading depression. Disturbances in these metabolic processes could exacerbate neuronal vulnerability, creating emergent properties that manifest as the episodic attacks characteristic of migraine with aura.
Pharmacogenetics for Migraine with Aura
Section titled “Pharmacogenetics for Migraine with Aura”Genetic Variants Affecting Neurotransmitter Pathways
Section titled “Genetic Variants Affecting Neurotransmitter Pathways”Polymorphisms within genes involved in neurotransmitter synthesis and metabolism can influence an individual’s susceptibility to migraine with aura, potentially impacting how they respond to treatments. For instance, variants in the dopamine beta-hydroxylase (DBH) gene have been associated with susceptibility to typical migraine, and specifically a 19bp deletion polymorphism at the DBH locus has been linked to migraine with aura.[15] The DBH enzyme is critical for converting dopamine to norepinephrine, suggesting that genetic variations could alter the balance of these neurotransmitters. While direct evidence on how these specific DBH variants affect the efficacy or adverse effects of migraine medications targeting dopaminergic or adrenergic systems is not explicitly detailed in the provided studies, understanding these genetic predispositions offers a foundation for future research into personalized therapeutic strategies.
Polymorphisms in Hormonal and Metabolic Pathways
Section titled “Polymorphisms in Hormonal and Metabolic Pathways”Genetic variations in genes related to hormonal regulation and metabolic processes have also been explored for their role in migraine. Polymorphisms in the Estrogen Receptor 1 (ESR1) gene, such as the G325C variant, have been investigated for associations with migraine, with one study reporting an association that suggests a role for estrogen signaling in migraine pathophysiology.[14]However, another study specifically examining migraine with aura in a Finnish population did not confirm an association for ESR1 variants, indicating the complex genetic landscape and the need for further replication studies.[16]
The MTHFR gene, which is involved in folate metabolism and can indirectly affect neurotransmitter synthesis, was also tested for association with migraine with aura in the same Finnish cohort. This investigation did not confirm an association between MTHFR variants and migraine with aura.[16]Although MTHFR is recognized as a phase II enzyme with broad metabolic implications, its direct pharmacogenetic relevance for migraine with aura treatment, based on the provided context, remains unestablished.
Clinical Relevance and Future Directions
Section titled “Clinical Relevance and Future Directions”The identification of genetic variants in genes such as DBH and ESR1, even when primarily linked to migraine susceptibility, provides valuable insights into potential biological pathways that could be targeted by therapeutic interventions. [15]While current research does not offer specific dosing recommendations or drug selection guidelines for migraine with aura treatments based on these pharmacogenetic findings, these genetic associations lay the groundwork for future pharmacogenomic studies. Such research could investigate how these and other genetic variants influence drug absorption, distribution, metabolism, and excretion, or modulate drug efficacy and adverse reactions, ultimately enabling more personalized prescribing approaches for individuals with migraine with aura.
Frequently Asked Questions About Migraine With Aura
Section titled “Frequently Asked Questions About Migraine With Aura”These questions address the most important and specific aspects of migraine with aura based on current genetic research.
1. My mom has migraine with aura. Will I definitely get it too?
Section titled “1. My mom has migraine with aura. Will I definitely get it too?”Not necessarily. While migraine with aura has a strong genetic component, estimated at 42-50% heritable, it’s not a guarantee. You inherit a predisposition from your family, but other factors also play a role. Many people with a family history never develop the condition, while others do.
2. Why do I get migraines with aura, but my sibling only gets regular migraines?
Section titled “2. Why do I get migraines with aura, but my sibling only gets regular migraines?”That’s a great question, and scientists are still figuring it out! While both forms share a significant genetic background, there’s a debate about whether they’re distinct or variations of the same disease. It’s possible you’ve inherited slightly different genetic susceptibilities that lead to the aura symptoms in your case.
3. Can my kids inherit my migraine with aura even if their other parent doesn’t have it?
Section titled “3. Can my kids inherit my migraine with aura even if their other parent doesn’t have it?”Yes, they can. Since migraine with aura is considered a multi-factorial condition with a strong genetic influence, they can inherit susceptibility from you. Even if only one parent has it, the genetic predisposition can be passed down, increasing their risk compared to the general population.
4. Why was it so hard for doctors to diagnose my migraine with aura?
Section titled “4. Why was it so hard for doctors to diagnose my migraine with aura?”Diagnosing migraine with aura can be tricky because its transient visual, sensory, or speech symptoms can be confused with other neurological conditions. Doctors need to be very thorough to differentiate it from unrelated issues. This complexity sometimes requires specialized clinical assessment to ensure an accurate diagnosis.
5. Does stress make my migraines worse because of my genes?
Section titled “5. Does stress make my migraines worse because of my genes?”Stress is a common migraine trigger, and your genetic makeup can influence how your brain responds to it. While the exact genetic links to stress response in migraine are complex, your inherent neuronal sensitivity, partly determined by your genes, might make you more prone to a stress-induced attack. It’s a classic gene-environment interaction.
6. Why do some foods trigger my aura, but my friend with migraine can eat anything?
Section titled “6. Why do some foods trigger my aura, but my friend with migraine can eat anything?”Your individual genetic profile likely influences how your body processes certain foods and chemicals, making you more susceptible to specific triggers. While researchers are still identifying all the genes involved, variations in your genetic makeup can lead to different sensitivities, causing specific foods to activate your trigeminal system.
7. Are my “bad” genes making my migraine attacks more severe than others?
Section titled “7. Are my “bad” genes making my migraine attacks more severe than others?”It’s possible. The severity and frequency of migraine attacks can be influenced by your genetic predisposition, among other factors. Researchers have identified 38 susceptibility loci for migraine, and variations in these or other as-yet-undiscovered genes could contribute to a more pronounced or severe presentation in you.
8. Can I overcome my genetic predisposition to migraine with aura by living a super healthy lifestyle?
Section titled “8. Can I overcome my genetic predisposition to migraine with aura by living a super healthy lifestyle?”A healthy lifestyle can definitely help manage and potentially reduce the frequency or severity of your migraines. While you can’t change your genes, lifestyle choices like managing stress, getting enough sleep, and avoiding known triggers can significantly impact how your genetic predisposition manifests. It’s about workingwith your genetics, not against them.
9. Why do some people never get migraine with aura, even if it runs in their family?
Section titled “9. Why do some people never get migraine with aura, even if it runs in their family?”Migraine with aura is a complex multi-factorial disorder, meaning it’s not solely determined by genetics. Even with a genetic predisposition, other factors like environmental triggers, lifestyle, and other protective genetic variations can influence whether someone develops the condition or not. It’s a combination of many influences.
10. Is there a genetic test that can tell me exactly what causes my aura migraines?
Section titled “10. Is there a genetic test that can tell me exactly what causes my aura migraines?”Currently, there isn’t a single genetic test that can pinpoint the exact cause of your individual migraine with aura. While researchers have identified many genetic susceptibility loci for migraine, the condition is complex, involving many genes and environmental factors. Genetic tests are not yet precise enough for personalized diagnostic or prognostic use in this way.
This FAQ was automatically generated based on current genetic research and may be updated as new information becomes available.
Disclaimer: This information is for educational purposes only and should not be used as a substitute for professional medical advice. Always consult with a healthcare provider for personalized medical guidance.
References
Section titled “References”[1] Gormley P, et al. “Meta-analysis of 375,000 individuals identifies 38 susceptibility loci for migraine.” Nat Genet, vol. 48, no. 8, 2016, pp. 886-892. PMID: 27322543.
[2] Anttila V, et al. “Genome-wide association study of migraine implicates a common susceptibility variant on 8q22.1.” Nat Genet, vol. 42, no. 10, 2010, pp. 869-873. PMID: 20802479.
[3] Ligthart L, Boomsma DI, Martin NG, Stubbe JH, Nyholt DR. “Migraine with aura and migraine without aura are not distinct entities: further evidence from a large Dutch population study.”Twin Res Hum Genet, vol. 9, 2006, pp. 54-63.
[4] Kallela, M., et al. “Familial migraine with and without aura: clinical characteristics and co-occurrence.” Eur J Neurol, vol. 8, no. 5, 2001, pp. 441-449.
[5] Nyholt DR, Gillespie NG, Heath AC, Merikangas KR, Duffy DL, Martin NG. “Latent class and genetic analysis does not support migraine with aura and migraine without aura as separate entities.”Genet Epidemiol, vol. 26, 2004, pp. 231-244.
[6] Russell MB, et al. “Migraine without aura and migraine with aura are distinct disorders. A population-based twin survey.”Headache, vol. 42, no. 4, 2002, pp. 332-336.
[7] Chasman DI, et al. “Genome-wide association study reveals three susceptibility loci for common migraine in the general population.” Nat Genet, vol. 43, no. 7, 2011, pp. 695-698. PMID: 21666692.
[8] International Headache Society. “The International Classification of Headache Disorders: 2nd edition.”Cephalalgia, vol. 24, no. Suppl 1, 2004, pp. 9-160.
[9] Russell MB, Rasmussen BK, Fenger K, Olesen J. “Migraine without aura and migraine with aura are distinct clinical entities: a study of four hundred and eighty-four male and female migraineurs from the general population.”Cephalalgia, vol. 16, 1996, pp. 239-245.
[10] Goadsby, P. J., et al. “Migraine—current understanding and treatment.” New England Journal of Medicine, vol. 346, no. 4, 2002, pp. 257-270.
[11] Lauritzen M. “Pathophysiology of the migraine aura. The spreading depression theory.” Brain, vol. 117, 1994, pp. 199-210. PMID: 7908596.
[12] Hadjikhani N, et al. “Mechanisms of migraine aura revealed by functional MRI in human visual cortex.” Proc Natl Acad Sci U S A, vol. 98, 2001, pp. 4687-4692. PMID: 11287655.
[13] Stam AH, et al. “Migraine with aura and migraine without aura: a genetic study.”Cephalalgia, vol. 30, no. 3, 2010, pp. 281-288.
[14] Oterino A, et al. “Association of migraine and ESR1 G325C polymorphism.” Neuroreport, vol. 17, no. 1, 2006, pp. 61-64.
[15] Lea RA, et al. “Evidence for allelic association of the dopamine beta-hydroxylase gene (DBH) with susceptibility to typical migraine.” Neurogenetics, vol. 3, no. 1, 2000, pp. 35-40.
[16] Kaunisto MA, et al. “Testing of variants of the MTHFR and ESR1 genes in 1798 Finnish individuals fails to confirm the association with migraine with aura.”Cephalalgia, vol. 26, no. 12, 2006, pp. 1462-1472.