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Abstract

This update aimed to assess whether recent studies offer confirmation or new insights into the debated relationship between alcoholic drinks (AD) and migraine. Reported discrepancies in alcohol consumption and its triggering role across primary headache types may reflect methodological differences and variations in headache classification by the International Headache Society. Recent prospective studies focusing on the triggering role of AD, vasodilation as a possible mechanism, alcohol consumption patterns, alcohol infusion, and alcohol-induced analgesia were evaluated and discussed. These studies largely confirm the limited role of AD as a triggering factor for migraine. In addition, recent evidence once again highlights the lower consumption of AD among migraine patients, raising the question of whether this finding reflects reverse causality, rather than a protective effect of avoidance. Although many substances have been tested for their ability to provoke migraine and induce cerebrovascular dilatation, ethanol—a natural vasodilator—has never been systematically tested in migraine patients. Some studies show that ethanol infusion does not provoke headache within 5 to 8 hours, but may induce a delayed hangover headache in certain individuals. Finally, despite evidence that moderate alcohol consumption may have analgesic effects and be associated with reduced chronic pain, it remains unclear why this does not occur in migraine patients.

Keywords

alcohol migraine migraine pathogenesis trigger factors alcohol consumption alcohol analgesia cerebral vasodilation trigeminovascular hypothesis

1 Introduction

Extensive literature concerns dietary triggers of migraine, with scarce evidence [1]. Among them, alcoholic drinks (AD) are the most commonly considered by patients and researchers. The topic was previously and extensively reviewed [2 –4 ]. A great variability in the percentage of migraine patients referring to AD as a trigger was underlined. Additionally, studies reporting AD as a trigger of migraine with and without aura, tension-type headache, and cluster headache were noted. Some studies suggesting AD triggers all primary headaches raise concerns about study methods or challenge the pathogenetic theory of primary headaches [4 –6 ]. However, a large study based on detailed anamnesis during patient consultation, showed that migraine with aura and tension-type headache patients do not refer to AD as a headache trigger, while only 5% of migraine without aura patients do [7].

Part of the discrepancies may be due to the headache classification by the International Headache Society (IHS). Alcohol-induced headache was not considered merely a migraine or headache trigger but was included in the secondary headaches chapter in ICHD-3 (Headache attributed to a substance or its withdrawal, code 8.1.4) [8], despite numerous issues previously discussed [3]. Only one of these phenotypic characteristics is required for alcohol-induced headache: bilateral localization, pulsating quality, or aggravation by physical activity, all shared by migraine and tension-type headaches. Any headache in close temporal relation to AD ingestion may be coded as secondary, distinguished only as immediate alcohol-induced headache (IAIH) if it develops within three hours, and delayed alcohol-induced headache (DAIH) if it develops within 5 to 12 hours (hangover headache). Also, it is important to question whether, when asked, the patient is referring to IAIH, DAIH, a migraine attack, or a tension-type headache attack.

Numerous factors may affect the reliability of survey data and contribute to inconsistent results. Considering the overlapping features and minimal differences between migraine and tension-type headache [9], the 25-35% of non-migraine attacks in migraine sufferers reported in Spectrum and Pamina studies [10, 11], the great diagnostic variability a few years later in the same subject [12, 13], the great variability of treated attacks in clinical trials [14], bias related to self-reported diagnoses, administered questionnaires and recall bias [15], we see the potential for error in studies of the alcohol/headache relationship. The risk is that many scientific results based on this classification may be unreliable and eventually discarded, with research focusing on marginal and frequently insignificant variations in an extremely variable pathology, rather than addressing the core issue. Perhaps research focused on very specific headache phenotypes, such as strictly unilateral migraine with nausea/vomiting, would yield less conflicting results.

If we accept that AD are triggering factors for most primary headaches, as reported in previous reviews and meta-analyses [2, 4, 5], we cannot ignore a single pathogenetic mechanism among various primary headaches, compatible with the continuum model, where headache attacks vary in severity from episodic tension-type headache to a full-blown migraine. Following this logic, it would be difficult to understand why botulinum toxin and calcitonin gene-related peptide (CGRP) monoclonal antibodies are substantially ineffective and not approved for treating tension-type headaches [16, 17]. Otherwise, if this is not the case, a multitude of studies suffer from biases and should not be considered, leaving the same questions about the alcohol/headache relationship.

Because retrospective studies have already been included in previous reviews and meta-analyses, and the factors influencing the assessment of the triggering role of alcoholic beverages have been extensively discussed, the present update focused primarily on more recent prospective studies. A systematic literature search was performed in MEDLINE from January 2015 onward using the keywords “migraine OR headache” AND “alcohol”. In addition, studies addressing alcohol consumption patterns in patients with headache, alcohol infusion, alcohol-induced vasodilation, and alcohol-induced analgesia were also identified, evaluated, and discussed.

2 Are AD, particularly alcohol, triggers of migraine or headache

The frequency estimate of trigger factors varies based on study approach and population, but prospective diary studies provide stronger evidence [15]. A review showed alcohol (AD) as a migraine trigger in a variable percentage (from zero to one-third of patients), while prospective studies showed negligible importance [2 –4 ]. Patients’ retrospective perception of triggers does not reliably mirror prospective diary recordings. In recent years, a growing number of prospective studies have been performed. Among the nutritional factors of the baseline assessment, only the consumption of wine correlated with the diary recording on day-1 (preceding headache day) [18].

Recently, digital platforms have been used. Applying the Curelator digital platform and individual N=1 analysis to the PAMINA study database identified a wider range of potential triggers, including AD in fewer than 10% of patients. This analysis showed high inter- individual heterogeneity, with 85% of patients having unique profiles [19].

Studies using smartphone headache diary apps report alcohol as a trigger in less than 5% of patients when asked to select triggers from a list, introducing judgment bias [20]. A more recent individual-level analysis using the Curelator Headache platform (now called N1-Headache) showed that same-day alcohol consumption increased the risk of an attack in less than 0.5% of drinkers [21]. In a larger cohort of over 1000 individuals with episodic migraine, alcohol was not associated with migraine attacks in 63% of subjects and was more often associated with a decreased (7%) rather than an increased (1%) risk, suggesting avoiding known triggers may no longer be justified [22]. Alcohol intake was less frequent among those who did not suspect alcohol as a trigger [23].

Analysis of data from the same platform in a large multicultural cohort consuming low doses of alcohol found no significant effect on migraine attacks within 24 hours [24]. Another study showed no association between consuming 1-2

servings of alcohol and the risk of a headache the following day, but a higher risk after consuming 3 or more servings, suggestive of a hangover headache [25].

Regarding hangover headache (DAIH), an increased risk has traditionally been reported in migraine patients [3]. However, the characteristics of the headache and the frequency of associated symptoms were not different between migraine and non-migraine patients [26]. Others report that migraine sufferers had a higher tendency to experience migraine-like symptoms such as headache and nausea after drinking than nonsufferers [27]. More recently, a study on DAIH showed that 40% of participants had a prior history of headache, especially migraine, and that symptoms typical of migraine occurred more frequently in this group. One-third of DAIH cases met the ICHD criteria for migraine, especially in those with a history of headache [28]. These studies highlight that hangover headaches with migraine-like features can also occur in healthy individuals.

In summary, assigning causal status to a probable headache trigger is difficult [29, 30]. The low consistency suggests alcoholic beverages alone are insufficient as a singular trigger, and their effects depend on a fluctuating trigger threshold [19]. Many prospective studies using digital platforms and individual level analysis do not show increases in migraine attacks after alcohol consumption, consistent with findings from headache centers [7]. It is true that studies using smartphone-based electronic diaries include only highly adherent, technologically engaged participants, and therefore their findings may not be generalizable to the entire population of individuals with migraine; however, demographic and baseline characteristics, such as the number of migraine days per month (6–7), were comparable to those reported in other prospective studies using paper diaries in similar populations [18, 19].

Additionally, hangover headaches can have migraine features even in individuals not suffering from migraine.

3 Reduced alcohol consumption in headache patients. What are the reasons

Some cross-sectional studies have reported a lower prevalence of migraine among alcohol users [3, 31]. The Hunt 3 follow-up study showed a lower risk of developing migraine (but not tension-type headache) among those who consumed alcohol at least once a month, and even more so among those who reported drinking alcohol eight times or more per month, compared to abstainers [32]. Another longitudinal study (Twin Omnibus) reported that subjects with weekly or more frequent alcohol consumption had a lower risk of developing migraine compared to subjects with less frequent or no consumption [33]. A risk reduction was also reported in a large European Health Interview Survey conducted in Spain, where migraine patients who drank 5 or 10 standard alcohol units per week had a lower risk compared to those who did not drink at all, as well as in a large longitudinal study on lifestyle conducted among participants who did not have migraine at baseline [34, 35]. Moreover, the frequency of migraine attacks was inversely correlated with alcohol consumption [3, 34]. A recent systematic review and meta-analysis confirmed that alcohol consumption and migraine are inversely correlated, but no relationship was found between TTH and drinking [36].

Some contradictory data on alcohol consumption in cluster headache (CH) patients have been reported [4]. Recent Scandinavian studies have not fully clarified this relationship. Steinberg et al. [37], confirming alcohol as a trigger in 55% of CH patients (similar to some previous studies), outlined that headache severity was inversely proportional to alcohol consumption. That is, higher severity was observed in the patient group reporting sporadic or no alcohol intake compared to those consuming 3–4 standard units per week or more. Conversely, another study showed that although fewer CH patients consumed alcohol compared to controls (61% vs. 90%), the average weekly alcohol intake was unexpectedly higher among CH patients. However, this seems to be due to a higher frequency of heavy drinkers in the CH population (especially in men and chronic CH patients), rather than alcohol being a less common trigger for those who do consume it during active disease periods, compared to those who report it as a trigger [38].

Although lower alcohol consumption in patients with migraine is strongly supported by cross- sectional and longitudinal studies, the direction of causality remains debated.

The lower risk of migraine among alcohol consumers compared to abstainers likely reflects the fact that alcohol is a commonly perceived trigger of headache and migraine, suggesting reverse causality, as several researchers believe. A limited body of literature supports this hypothesis, with some conflicting evidence:

(1) Confirming previous findings, a recent study in a Dutch population showed that individuals with migraine are less likely to drink alcohol compared to the general population [39]. The same group reported in a precedent cross- sectional web-based questionnaire study that a total of 16% of patients who stopped consuming alcohol did so because it triggered their attacks [6]. This percentage is higher than the 3% reported in a previous headache center study performed by face to face interview [7].

(2) Mendelian randomization studies are less prone to the biases inherent in observational studies, particularly reverse causation and confounding, and therefore provide more robust estimates of causal relationships between exposures and outcomes. Although a recent

Mendelian randomization study on genetic variants of alcohol-metabolizing enzymes supports the reverse causality hypothesis [40], some evidence contradicts the notion that the effect of alcohol consumption on migraine risk is entirely explained by reverse causality [41]. In fact, another Mendelian randomization study reported that alcohol consumption is not associated with migraine [42].

(3) Alcohol intake was found to be less frequent among migraine patients who did not suspect alcohol as a risk factor [23].

4 Migraine provocation studies. Why not ethanol

To study migraine pathophysiology, various substances, including calcitonin gene-related peptide (CGRP), pituitary adenylate cyclase- activating polypeptide (PACAP), vasoactive intestinal polypeptide (VIP), and cilostazol, have been tested for their ability to provoke migraine and their correlation with cerebrovascular dilation, recently assessed using magnetic resonance angiography [43]. Some previous discrepancies [44, 45] now seem partially resolved, such as the ability of VIP and adrenomedullin to provoke migraine and the ability of sildenafil to induce cerebral vasodilation [46 –48 ].

As summarized by Ashina in a recent review [49], the results of provocation studies with vasodilating drugs can be synthesized as follows:

(1) Healthy volunteers generally develop no more than a mild headache, whereas individuals with migraine are more likely to experience a migraine attack.

(2) People with migraine report that the provoked attack closely mimics their usual spontaneous attacks.

(3) Prolonged arterial dilation can induce a delayed migraine-like headache, even in individuals with no history of headaches, as observed in some subjects tested with PACAP30, nitroglycerin, and VIP [50 –52 ].

(4) Evidence suggests that certain migraine- inducing signaling substances may increase susceptibility to migraine attacks by directly affecting structures within the central nervous system, such as ATP-sensitive potassium channel openers.

Regarding the correlation between vasodilation and migraine features, findings have not been uniform [43]. Notably, no correlation has been found between vasodilation and initial headache onset [44]. During spontaneous migraine attacks, slight ipsilateral intracranial but not extracranial vasodilation has been observed, while CGRP- induced delayed migraine-like attacks were associated with dilation of the middle meningeal artery (MMA) and middle cerebral artery (MCA) on the headache side in 75% of patients [53, 54]. However, no difference in arterial circumference between the pain and non-pain side was reported during PACAP38-induced migraine-like attacks [55]. In cilostazol-induced unilateral migraine, an increase in MMA artery circumference was observed at migraine onset specifically on the headache side, but no differences were noted during the late migraine attack [43].

Experimental provocation using self-reported natural trigger factors induces migraine with aura only in a very small subset of patients, suggesting that further research should focus on chemical triggers [56]. Aura has been induced by CGRP infusion and nitroglycerin administration in some individuals with migraine with aura. However, in these subjects, these substances also provoked migraine without aura, even in those who had never experienced spontaneous attacks without aura. This suggests that these drugs exert their migraine-provoking effects “downstream” of the aura pathophysiological process, making them ineffective for experimental aura induction [57]. However, when a previous study was extended to a larger sample, 13 (38%) of 34 participants developed migraine aura following intravenous CGRP infusion. Importantly, all reported aura attacks closely resembled the participants’ usual spontaneous migraine auras [58]. Recently, levcromakalim infusion, an ATP-sensitive potassium channel opener, was reported as a potent inducer of both aura and headache, likely through distinct mechanisms [59], though preliminary subsequent findings have not fully supported this hypothesis [60].

The exact role of vascular involvement in migraine has been a topic of much debate. An important study concluded that migraine pain is not accompanied by extracranial arterial dilation and only slight intracranial dilation, suggesting that vasodilation itself is not a principal component of migraine pain. Instead, future research should focus on peripheral and central pain pathways rather than simple arterial dilation [54]. This perspective has contributed to a shift in emphasis from the mechanical distension of vascular smooth muscle cells to the activation and sensitization of perivascular sensory afferents as key mechanisms in migraine pain [61]. Recently, a study demonstrated that cAMP-evoked migraine attacks and cranial arterial dilation do not require CGRP receptor activation [62].

A key limitation of human provocation studies is that they cannot determine what triggers the initial endogenous release of signaling molecules. In this regard, investigating natural triggers, such as ethanol, would have been equally or even more informative. Ethanol could provide critical insights into many of the inconsistencies and uncertainties surrounding the alcohol-migraine relationship. In fact, observational studies of alcoholic beverages are limited by the difficulty of accurately assessing both the quantity and type of alcohol consumed.

5 Alcohol infusion: a mine to exploit

One of the main challenges with alcohol ingestion in experimental studies is the substantial and uncontrollable pharmacokinetic variability in brain alcohol exposure, even when dosing is carefully calculated and controlled. While infusion methodologies offer precise exposure control, they are technically complex [63].

Studies using the “alcohol clamp”, a technique that infuses alcohol to maintain a target breath/ blood alcohol concentration for an extended period (typically 3 hours), have not reported migraine attacks within the 8-hour timeframe of typical session studies conducted on several hundred healthy subjects and surprisingly no other hangover symptoms were noted either [3, 4]. Additionally, in a recent study examining the acute effects of intravenous alcohol and its metabolite acetaldehyde on cognitive function in approximately 300 Japanese participants, headache was not mentioned as an observed effect during the 4-hour experimental session, although this was not the study’s primary focus [64].

A preliminary non-placebo-controlled study in social drinkers found that intravenous alcohol administration provoked mild to moderate hangover symptoms in 79% of participants, with headache being one of the most frequently reported symptoms, especially among females. This study aligns with other reports suggesting that individuals with heightened sensitivity to acute alcohol effects are also more prone to experiencing hangover symptoms [65]. A subsequent, larger study reported a nearly identical proportion of participants experiencing hangovers (78%), with headache present in 32% of the total sample, as assessed by the Alcohol Hangover Scale administered the following morning. Notably, this study measured hangover symptoms from hospital discharge (at least 5 hours after the infusion began) until 10 a.m. the next morning. However, similar to the previous studies, headache was not reported during the approximately 3-hour infusion period or the subsequent 2-hour post-infusion observation period while participants remained in the hospital. Furthermore, no significant relationship was found between alcohol consumption measures and hangover severity [66].

More than a decade ago, it was suggested that studies using this technique in individuals with migraine could provide valuable insights into the alcohol-headache relationship [3, 4]. Specifically, such experiments could help clarify several aspects:

(1) Whether IAIH occurs in both migraine and non-headache subjects.

(2) Whether migraine patients experience their typical migraine attack or DAIH following alcohol infusion.

(3) The correlation between alcohol-induced headache and vascular changes in cranial arteries.

(4) Whether aura can be provoked by alcohol.

(5) Whether alcohol itself is sufficient to trigger headaches, or if other components (e.g., sulfites, biogemic amines, congeners) play a necessary role in AD-induced headaches.

It is notable that, despite this longstanding suggestion, alcohol, one of the most widely recognized natural triggers with vasodilating properties, has yet to be systematically investigated in studies evaluating the effects of vasodilating drugs.

6 Role of alcohol vasodilation

Numerous studies have attempted to distinguish the behavioral and pharmacological effects of alcohol from those of its metabolites. Ethanol does not act through specific receptors but instead exerts its effects directly or via its metabolites, which interact with various neurotransmitter systems.

Most ethanol consumed is metabolized in the liver into acetaldehyde and acetate. While both metabolites enter the circulation, only acetate freely diffuses into the brain, similar to ethanol itself. In the brain, acetate is almost exclusively metabolized by astrocytes, where it contributes to energy production, acetylcholine synthesis, and the recycling of gamma-aminobutyric acid (GABA) and glutamate [67]. Some ethanol is also metabolized directly in the brain by catalase and cytochrome P-4502E1, leading to the production of acetaldehyde. However, the extent to which alcohol’s effects, particularly those on cerebral vessels, are due to ethanol itself or its biologically active metabolites remains a subject of debate.

Acute exposure to toxicologically relevant concentrations of ethanol leads to widespread constriction of cerebral arteries, an effect observed across different species and vessel types. This response appears to be largely mediated by ethanol itself rather than by its vasoactive metabolites [68]. However, numerous studies using noninvasive imaging techniques have established that low to moderate doses of alcohol, whether administered orally or intravenously (via the alcohol clamp technique), result in increased cerebral blood flow (CBF) [4].

Small to moderate doses of ethanol provoke global and regional increases in CBF, either through localized neural activity or mechanisms involving acetate and its metabolite adenosine, a potent vasodilator [69]. A single dose of alcohol sufficient to cause mild intoxication has been associated with increased CBF in multiple cortical and subcortical brain regions, as detected by magnetic resonance imaging. In contrast, direct acetate infusion, at concentrations comparable to those observed during alcohol consumption, increased CBF only in the bilateral thalami, without inducing a sensation of intoxication. These findings suggest that most of the cortical CBF response to alcohol is not mediated by acetate [70].

In the context of migraine pain, animal studies have shown that alcohol provokes neurogenic inflammation in the trigeminovascular system, mimicking the effects of capsaicin. This process involves vasodilation of meningeal vessels via CGRP release from perivascular sensory nerve terminals [71].

A recent study further demonstrated that adenosine infusion (a metabolite of acetate) induces headache in migraine patients and is accompanied by short-lasting dilation of intracerebral and extracerebral arteries. However, these headaches did not develop into full migraine attacks [72].

7 Alcohol analgesia: what is the role in headache patients

An extensive review suggests that low-to- moderate alcohol consumption may be associated with a reduced likelihood of developing chronic pain and improved pain outcomes in conditions such as chronic widespread pain, back pain, fibromyalgia, and rheumatoid arthritis [73]. Evidence from both animal and human studies indicates that acute alcohol administration confers short-term pain-inhibitory effects [73 –75 ]. In an animal model of migraine, ethanol initially produced analgesic effects within the first two hours after ingestion. However, 4–6 hours later, pain sensitivity increased, resembling hangover- related hypersensitivity and headache. This delayed hyperalgesia was attributed to acetate accumulation rather than acetaldehyde [76].

In humans, alcohol is frequently used as self-medication for pain relief. A meta-analysis of 18 studies investigating alcohol’s impact on acute pain in healthy participants found strong evidence supporting its analgesic effects. Pain reduction correlated with blood alcohol concentration (BAC), with the greatest relief occurring at 0.08% BAC, equivalent to consuming about three standard drinks [77]. Another meta-analysis confirmed that any level of alcohol consumption was associated with lower odds of chronic pain [78]. However, fibromyalgia patients appeared to derive less benefit from alcohol, suggesting that individuals with less centralized forms of pain might experience greater relief from moderate alcohol consumption [79]. In contrast, migraine patients do not commonly use alcohol as a self-medication, which aligns with their lower risk of developing alcohol use disorder (AUD) [80].

Approximately 540 million people worldwide carry a genetic variant of aldehyde dehydrogenase 2 (ALDH2), known as ALDH2*2, which leads to facial flushing and tachycardia upon alcohol consumption. This variant is particularly common in Asian populations, who also demonstrate greater pain sensitivity compared to other ethnic groups. ALDH2 deficiency results in elevated blood acetaldehyde levels and reduced acetate production, and studies in both humans and rodents have linked this condition to increased pain sensitivity to various stimuli [81, 82]. In ALDH2-deficient individuals, even one or two AD cause significantly higher blood acetaldehyde levels [83].

A recent study in mice suggests that ethanol induces delayed and prolonged periorbital mechanical allodynia, which the authors linked to DAIH in migraine patients. This effect was mediated by acetaldehyde-induced CGRP release, which activated CGRP receptors in Schwann cells of dorsal root ganglion neurons. However, even at the highest intragastric ethanol dose (4 mL/kg), mice did not exhibit acute spontaneous nociceptive behaviors. The authors proposed that the high ethanol concentrations required to trigger TRPV1-mediated acute pain were not reached with the doses used [84]. Notably, these ethanol doses correspond to consuming 3–5 alcoholic units in humans, supporting the idea that acute alcohol and acetaldehyde do not produce immediate nociceptive effects.

Alcohol may exert both hypoalgesic (pain- reducing) and hyperalgesic (pain-enhancing) effects at multiple levels of the pain-processing system and through diverse neurotransmitter pathways [75]. This complex interaction highlights the need for further research to fully elucidate alcohol’s effects on pain perception and migraine pathophysiology.

8 Conclusions

(1) Alcohol consumption in sufficient amounts (though typically lesser in headache patients) can provoke hangover headache (DAIH). Low doses of alcohol may act as a migraine trigger in a small subset of patients, but not consistently. This inconsistency is likely due to the presence of other triggers, variations in individual alcohol sensitivity, or the involvement of certain AD components.

(2) If alcohol consumption indeed triggers all types of principal idiopathic headaches (such as migraine with and without aura, tension-type headache, and cluster headache), it suggests a central or neuronal mechanism of alcohol action, rather than localized vasodilation of the meningeal arteries. Initial vasodilation, induced by various substances, may provoke headaches in both healthy subjects and migraine patients. However, full migraine attacks are predominantly, though not exclusively, seen in migraine patients.

(3) If alcohol consumption can provoke DAIH, often with migraine features, it is likely that once alcohol is metabolized, migraine provocation depends on changes in neurotransmitter activity within pain circuits. In this context, alcohol could trigger aura (via cortical spreading depression) and migraine headache through distinct subcortical pathways, as previously suggested. Studies with levcromakalim, a drug that opens ATP-sensitive potassium channels, support this idea.

(4) The vasodilation mechanism would require facilitation of central antinociceptive pathways in headache-prone subjects, as localized peripheral vascular hypersensitivity or defects in basal vascular tone are not clinically sustainable. Vasodilation may be just one of many potential migraine triggers, with the primary mechanism likely occurring in the brain. The inconsistencies in studies correlating cranial vasodilation with headache suggest that vasodilation is not the main driver of migraine pain. Furthermore, alcohol infusion does not provoke an immediate headache. Thus, experiments involving alcohol infusion in headache pathogenesis studies can be extremely useful.

(5) The inverse relationship between alcohol consumption and migraine frequency may be explained by reverse causality, although some studies offer different interpretations. Factors such as sociality, the anti-stress effects of alcohol, and mild unpleasant sensations (but not necessarily headache) may also play a role. It is commonly believed that a threshold of trigger exposure must be reached to initiate a migraine attack, which could potentially be reached by combining several suspected triggers. Similarly, anyone can experience a migraine attack, experimentally induced, if exposed to a sufficiently strong stimulus, including alcohol-induced headache. Hangover headaches, even those with migraine-like features, can occur in anyone, though migraine patients are considered more susceptible.

Footnotes

Acknowledgements

The authors thank all contributors to this work for their support and discussions and acknowledge the use of AI–based tools for English language editing and grammar correction; all scientific content and interpretations remain the responsibility of the authors.

Funding Information

No funding was received for this study

Author Contribution

Alessandro Panconesi and Maria Letizia Bartolozzi contributed substantially to the conception and design of the study, analysis and interpretation of data, revising the article critically and final approval of the version to be submitted.

Declaration of Conflicting Interests

The authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article. The authors received no financial support for the research, authorship, and/or publication of this article.

Data Availability Statement

Data sharing not applicable to this article as no datasets were generated or analysed during the current study

Ethics Statement

Not applicable.

Informed Consent

Not applicable.

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Alcohol and Headache: an Update

Abstract

Keywords

1 Introduction

2 Are AD, particularly alcohol, triggers of migraine or headache

3 Reduced alcohol consumption in headache patients. What are the reasons

4 Migraine provocation studies. Why not ethanol

5 Alcohol infusion: a mine to exploit

6 Role of alcohol vasodilation

7 Alcohol analgesia: what is the role in headache patients

8 Conclusions

Footnotes

Acknowledgements

Funding Information

Author Contribution

Declaration of Conflicting Interests

Data Availability Statement

Ethics Statement

Informed Consent

References