Headache and GLP-1 receptor agonists: when medications are therapeutic and when they contribute to the symptom

Abstract

Obesity is a complex metabolic disorder with significant implications for both individual and public health. It has been strongly linked to chronic headache conditions, including migraines and idiopathic intracranial hypertension (IIH). Individuals with obesity who suffer from migraine are at increased risk of chronification, while weight reduction has been associated with improvement in IIH-related headaches, likely due to a decrease in cerebrospinal fluid pressure. These observations underscore the importance of weight management strategies as a therapeutic consideration in patients with obesity and headache disorders. Glucagon-like peptide-1 receptor agonists (GLP-1 RAs) are pharmacological agents that mimic the hormone's endogenous activity. Analysis of selected studies highlights that these agents have emerged as a promising therapeutic option. The aim of this narrative review is to examine the role of GLP-1 RAs in the management of headaches, particularly in the context of IIH, migraine, and the gut–brain axis. Additionally, this review addresses the challenges associated with the use of this pharmaceutical class, including the potential for headaches as adverse effect, and identifies existing knowledge gaps that may guide future research.

Keywords

Glucagon-Like Peptide-1 Receptor Agonists - Headache Disorders - Obesity - Migraine Disorders

INTRODUCTION

Obesity is a condition associated with significant personal and social burden.[1] According to the World Health Organization (WHO), a body mass index ≥ 30 kg/m² defines obesity. Since the 1990s, the global prevalence of obesity has risen alarmingly, affecting both developed and developing countries.[2] In addition to being a major risk factor for cardiovascular disease, type-2 diabetes mellitus, and cancer, obesity also increases the risk of chronic pain syndromes, including headache disorders.[3] [4]

Glucagon-like peptide-1 (GLP-1) is an incretin hormone secreted by intestinal L-cells in response to nutrient intake.[5] Its primary role is to stimulate insulin secretion in a glucose-dependent manner and to suppress glucagon release, thereby contributing to glucose homeostasis.[6] Additionally, this hormone delays gastric emptying, enhances satiety, and reduces appetite, making it a key target in pharmacological strategies for weight management.[7] Glucagon-like peptide-1 receptor agonists (GLP-1 RAs) are synthetic agents that mimic the effects of the endogenous action of GLP-1 but offer enhanced stability due to resistance to enzymatic degradation by dipeptidyl-peptidase-4 (DPP-4).[8]

Over the past decade, GLP-1 RAs have emerged as a promising class of therapeutic agents, initially recognized for their role in glycemic control in type 2 diabetes mellitus.[2] Notably, agents such as liraglutide, semaglutide, exenatide, and tirzepatide have also been employed in the management of obesity, not only promoting weight loss but also offering beneficial metabolic effects on comorbid conditions such as hypertension and dyslipidemia.[2]

More recently, a growing body of evidence has indicated that therapeutic potential of GLP-1 RAs extends well beyond metabolic regulation, encompassing a range of actions within the central nervous system (CNS).[9] Studies have highlighted their capacity to modulate neuroinflammation and confer neuroprotective effects, raising intriguing possibilities for their use in related disorders.[7]

In particular, weight loss induced by GLP-1 RAs has been associated with significant improvement in debilitating headaches, especially in conditions such as idiopathic intracranial hypertension (IIH) and migraine, both of which are known to be exacerbated by obesity and its associated systemic inflammation.[10] Furthermore, the anti-inflammatory properties and cytokine-modulating effects of GLP-1 RAs appear to contribute to pain regulation, implying a supplementary therapeutic modality.[11]

The purpose of this paper is to provide a narrative review to explore the impact of GLP-1 RAs on headache management. We will examine their mechanisms of action within the CNS, their influence on inflammation and neuroprotection, and their potential to support weight reduction in the context of IIH and migraines. Additionally, we will consider their effects on the gut–brain axis, a growing area of interest in headache pathophysiology. Finally, this review will also address current challenges related to the use of GLP-1 RAs, such as the paradoxical occurrence of headaches as a side effect and highlight existing knowledge gaps to inform future research directions.

METHODS

A comprehensive literature review was conducted using peer-reviewed articles published in English with no restrictions on publications date. The databases searched included PubMed, Embase, OVID, CINAHL, and Cochrane. The search strategy employed the following descriptors: ((incretin mimetics) OR (glucagon-like peptide-1 receptor) OR (lose weight)) AND ((migraine) OR (headache syndromes) OR (intracranial idiopathic hypertension)).

Priority was given to original research articles, randomized controlled trials (RCTs), and systematic reviews. Case reports and expert opinion pieces were initially excluded, to maintain a higher level of evidence. A total of 770 articles were identified through the initial search. After screening and excluding studies that did not specifically address relationship between GLP-1 RAs and headache disorders, 178 were retained for further evaluation. Of these, 38 were selected and included in the final analysis presented in this manuscript (Supplementary Material Table S1–available at https://www.arquivosdeneuropsiquiatria.org/wp-content/uploads/2025/08/ANP-2025.0045-Supplementary-Material.docx) ([Figure 1]).

Figure 1 Preferred Reporting Items for Systematic reviews and Meta-Analyses (PRISMA) flow diagram for headache and GLP1 receptor: When medications are therapeutic and when they contribute to the symptom. Source: Page et al.

RESULTS

The analysis of the selected studies emphasized that GLP-1 RAs have an impact on headache management and other neurological conditions. Their metabolic and neurological effects synergistically contribute to neuroprotection.[7] While these drugs offer clear therapeutic benefits, they may also induce adverse effects in certain cases,[11] as shown in [Figure 2].

Note: License: Creative Commons Attribution-Noncommercial 3.0 Unported. Figure 2 The multisystem actions of glucagon-like peptide-1 (GLP-1) and its receptor agonists (GLP-1 Ras). (A) The molecular structure of human GLP-1. (B) The molecular structure of exenatide (gray colors indicate differences in structure from human GLP-1. (C) The molecular structure of liraglutide (gray colors indicate changes in structure from human GLP-1).

The activation of GLP-1 receptors (GLP-1 Rs) in the CNS plays a crucial role in modulating neuroinflammation and providing neuroprotection. In the hypothalamus and brainstem, receptor activation initiates signaling pathways that support cell growth and survival, enhance synaptogenesis, and stimulates autophagy, which is essential for clearing damaged proteins and maintaining cellular homeostasis.[12] Furthermore, GLP-1RAs reduce the secretion of proinflammatory cytokines, namely interleukin 6 (IL-6) and tumor necrosis factor alpha (TNF-α), which are often elevated in neuroinflammatory conditions like migraine.[1] By preventing apoptosis, fostering synaptic regeneration, and supporting neuronal recovery, GLP-1 RAs may contribute to clinical improvement across a range of neurological disorders.[3] [4]

Obesity is a major modifiable risk factor for chronic migraine, contributing to central sensitization and exacerbating the frequency and severity of attacks.[3] [4] Weight loss influences headache patterns in certain patients. During digestion, intestinal peptides such as GLP-1 and amylin are released and delay gastric emptying.[13] Concurrently, glucagon, secreted by the pancreas, and gastric leptin modulate appetite and reduce food intake by signaling satiety to the brain.[14]

The gut–brain axis is regulated by a dynamic balance between proinflammatory influences (such as sugar-rich diets that increase cell oxidative stress) and anti-inflammatory factors (such as a healthy diet, stress management, regular physical activity).[15] This equilibrium can be disrupted by factors that promote chronic low-grade inflammation, including sedentary behavior, exposure to xenobiotics, environmental pollution, inadequate nutrition, and sleep disturbances.[16] These factors collectively contribute to the development of neurodegenerative diseases, depression, cancer, and intestinal dysbiosis.[1] Over time, dysbiosis may aggravate conditions driven by neurogenic inflammation, such as migraines.[9]

The homeostasis of the gut–brain axis can be altered in other pathologies, including IIH.[5] In women, an increase of more than 20% in body weight increases the incidence of IIH from 0.9 to 19.3 cases per 100 thousand inhabitants.[15] Researchers have recently discovered the remarkable benefits of GLP-1 RAs in individuals with IIH.[17]

As a neurological disorder, IIH is characterized by elevated cerebrospinal fluid (CSF) pressure, which can lead to severe headaches, visual field disturbances due to papilledema, and ocular motor nerves palsy, among other features.[2] The condition has an incidence of 0.9 per 100 thousand people, exhibits a striking 8:1 female preponderance, and is frequently associated with obesity.[7] A reduction in body weight of just 5 to 10% has been shown to lower CSF pressure, which is directly correlated with headaches in IIH.[8] Consequently, pharmacologic agents such as liraglutide and semaglutide, which induce weight loss and reduce intracranial pressure, may provide substantial relief from IIH symptoms, significantly enhancing patients' quality of life.[18] However, long-term weight maintenance and adherence to treatment remain critical to achieving and sustaining clinical improvement.[5]

The link between obesity and IIH is well established, with weight loss resulting in measurable symptom relief.[19] Obesity is hypothesized to raise intracranial pressure via increased intra-abdominal pressure, which elevates venous pressure.[20] Additionally, estrogen-mediated pelvic adiposity in women leads to a prothrombotic state and further weight gain.[12] Adipose tissue expansion increases leptin levels, which regulate appetite, energy expenditure, and glucose and lipid metabolism via hypothalamic signaling.[19] In this context, reducing body mass helps mitigate the chronic low-grade inflammatory state that underpants IIH pathogenesis.[21] Notably, GLP-1 promotes weight loss through both neuronal and metabolic mechanisms.[11] It is present in the human choroid plexus, where GLP-1 RAs reduce CSF secretion and intracranial pressure by elevating intracellular cyclic adenosine monophosphate levels and inhibiting the Na +/K+ ATPase pump.[22]

Beyond their utility in IIH, GLP-1 RAs play a role in migraine management.[23] Preclinical studies have demonstrated that liraglutide stimulates IL-10 secretion, an anti-inflammatory cytokine, thereby alleviating migraine-like pain in rats.[24] Activated GLP-1 R also suppresses the production of pro-inflammatory cytokines such as interleukin 1 beta (IL-1β) and TNF-α, which are upregulated during migraine attacks.[7] Furthermore, these RAs modulate microglial activity, helping reduce chronic inflammation that contributes to central sensitization and symptom persistence.[12] The central mechanisms involved in migraine attenuation include restoration of immune cell balance and activation of neuroprotective pathways.[25]

Despite the benefits, some patients report increased headache frequency or intensity after initiating GLP-1 RA therapy.[11] This adverse effect may be related to GLP-1 R activation in the CNS, which can influence cerebrovascular tone and regional blood flow, potentially resulting in cerebral vasodilatation and headaches due to mechanical strain on pain-sensitive structures.[26] [27] Additionally, GLP-1-mediated modulation of pain pathways, particularly via microglial activation in the caudal trigeminal nucleus, may exacerbate central sensitization and worsen headache symptoms.[12] This phenomenon reflects the dynamic neurohormonal and metabolic shifts provoked by GLP-1 RAs therapy.[13] Headache is most often reported during the early stages of treatment and is usually transient.[13]

A meta-analysis by Filippatos et al. reported that, since 2009, headaches have been documented across several GLP-1 RAs trials.[26] They are generally mild, nondisabling, and most frequently occur within the first 26 weeks of treatment. They have been observed with liraglutide (1.8 mg daily), and semaglutide (1.5 mg weekly), exenatide (2 mg weekly), and dulaglutide (0.75 to 1.5 mg weekly).[28] [29] [30] Importantly, these events rarely lead to treatment discontinuation, unlike more severe adverse effects, such as pancreatitis, hypoglycemia, or dermatological reactions, which may necessitate withdrawal due a life-threatening risk.[31]

Ongoing research aims to identify biomarkers that may predict susceptibility to GLP-1 RA-induced headaches. Such predictive tools would support personalized therapy and optimize patient outcomes.[13] [17] It is essential to recognize that most individuals undergoing this treatment are obese, and that primary headaches are more prevalent and disabling in this population, with migraine being the most common diagnosis.[32] Obesity increases the risk of both episodic and chronic migraine through bidirectional central and peripheral mechanisms.[20] Nonetheless, headache occurring during GLP-1 RA therapy may not be directly drug-induced, as secondary factors like dehydration and hypoglycemia may contribute.[3] [4] Vomiting and nausea, common gastrointestinal side effects, can lead to dehydration, which is the predominant non-neurological contributor to headaches during treatment.[26]

Fasting-related headaches also merit consideration. These typically result from prolonged fasting, caloric restriction, dehydration, or hypoglycemia.[6] When this last one is the cause, the headache often arises after at least eight hours without food and is relieved by eating.[6] [33] Clinically, it presents as a widespread pain, mild-to-moderate and nonpulsatile, in the frontal region.[23] Although hypoglycemia is uncommon with GLP-1 RAs alone, the risk increases when used in combination with insulin or sulphonylureas. Therefore, patients should avoid extended fasting while on these medications.[26]

DISCUSSION

The use of weight loss medications, particularly GLP-1 RAs, is increasing steadily, both with and without medical supervision. Consequently, clinicians are more frequently confronted with the context of headache disorders.[17] These medications are often highly regarded by patients for their striking benefits, not only in terms of weight reduction but also of improving associated comorbidities such as hypertension, diabetes, depression, and anxiety.[11] This raises a timely clinical question: Could GLP-1 RAs represent a therapeutic strategy for obese patients with migraine or other headaches who also struggle with weight management?[22]

To make a well-informed, individualized decision, it is essential to recognize the variability in both therapeutic benefits and adverse effects among patients treated with GLP-1 RAs.[2] Factors such as a metabolic phenotype, presence of comorbidities, and individual sensitivity to hormonal fluctuations and weight loss play a critical role in treatment response.[11] Furthermore, treatment duration and dosage significantly influence both efficacy and tolerability. These variables underscore the importance of prescribing GLP-1 RAs under the guidance of experienced physicians, a message that must be clearly communicated to patients.[34]

While most headache exacerbations are observed in patients with a prior history of migraine, new onset (de novo) headaches have also been reported during GLP-1 RA therapy. A pharmacovigilance analysis using data from the FDA's Adverse Event Reporting System identified a statistically significant association between GLP-1 RAs and the onset of headache, with a reporting odds ratio (ROR) of 1.74, and migraine (ROR: 1.28), suggesting that these symptoms can develop regardless of pre-existing headache diagnoses.[17] [35] Therefore, careful clinical monitoring is warranted, especially during the early phases of treatment.

Another critical consideration is the role of obesity itself as a risk factor and disease modifier in migraine. It has been associated with increased migraine frequency, severity, and risk of chronification.[10] Weight loss reduces systemic inflammation and mitigates metabolic contributors, such as insulin resistance, oxidative stress, and cerebrovascular dysregulation.[27] Thus, the GLP-1 RAs directly exert dual benefits: through their anti-inflammatory and neuroprotective mechanisms, and by improving metabolic variables that worsen headache burden.[25]

Finally, emerging research is exploring how GLP-1 RAs may modulate central pain pathways, an area with significant therapeutic promise.[17] These findings may pave the way for novel interventions targeting chronic headache and migraine, particularly in patients with treatment-resistant forms of the disease. If substantiated by further clinical trials, such approaches could meaningfully improve the quality of life in this population, highlighting the need for continued, rigorous investigation.[24]

In conclusion, GLP-1 RAs have emerged as promising therapeutic agents for neurological conditions, with underlying metabolic and inflammatory components, including headache disorders in obese individuals.[25]

Given the notable interindividual variability in both efficacy and tolerability, a personalized prescription approach is essential to optimize outcomes and minimize adverse effects.[36] Future efforts to identify predictive biomarkers, which are more likely to benefit from GLP-1 RAs, will be key to stratifying patients based on likely therapeutic response or risk of side effects.[9]

As this field evolves, clinical observations and patient-reported outcomes should be more fully integrated into the research process. These perspectives are not anecdotal; rather, they offer valuable insight into the real-world impact of treatment and can help refine hypotheses about the pathophysiology of migraine.[17] A more collaborative interface between research and clinical practice will be essential in addressing the complex and multifactorial nature of headache disorders.

Emerging evidence also underscores the involvement of metabolic pathways in migraine pathogenesis, revealing novel therapeutic targets.[37] Through their anti-inflammatory and neuromodulatory actions, GLP-1 RAs may offer an additional mechanism for migraine control, particularly in cases with obesity, as it is a known risk factor for chronification. To date, however, no studies have specifically assessed this endpoint in migraine populations, highlighting a critical gap in the literature and an opportunity for future clinical trials.[7]

In combination with existing prophylactic treatments,[38] GLP-1 RAs may represent a valuable option for the subset of obese patients, especially those who are refractory to first- and second-line treatments, expanding the therapeutic armamentarium available to the neurologists managing these complex cases.

Conflict of Interest

The authors have no conflict of interest to declare.

Authors' Contributions

Conceptualization: RGL, ETF, LMPG; Data curation: RGL, ETF, LMPG; Formal analysis: RGL, ETF, LMPG; Project administration: RGL, ETF, LMPG; Resources: RGL, ETF, LMPG; Supervision: RGL; Validation: RGL, ETF, LMPG; Visualization: RGL, ETF, LMPG; Writing – original draft: ETF, LMPG; Writing–review & editing: RGL.

Data Availability Statement

The datasets generated and/or analyzed during the current study are available from the corresponding author upon reasonable request.

Editor-in-Chief: Hélio A. G. Teive (0000-0003-2305-1073).

Associate Editor: Pedro André Kowacs (0000-0001-7770-7475).

• References

• 1 Furman D, Campisi J, Verdin E, Carrera-Bastos P, Targ S, Franceschi C. et al. Chronic inflammation in the etiology of disease across the life span. Nat Med 2019; 25 (12) 1822-1832
• 2 Ryan D, Acosta A. GLP-1 receptor agonists: Nonglycemic clinical effects in weight loss and beyond. Obesity (Silver Spring) 2015; 23 (06) 1119-1129
• 3 Chai NC, Scher AI, Moghekar A, Bond DS, Peterlin BL. Obesity and headache: part I–a systematic review of the epidemiology of obesity and headache. Headache 2014; 54 (02) 219-234
• 4 Chai NC, Bond DS, Moghekar A, Scher AI, Peterlin BL. Obesity and headache: Part II–potential mechanism and treatment considerations. Headache 2014; 54 (03) 459-471
• 5 Moon MJ, Park S, Kim DK, Cho EB, Hwang JI, Vaudry H, Seong JY. Structural and molecular conservation of glucagon-like Peptide-1 and its receptor confers selective ligand-receptor interaction. Front Endocrinol (Lausanne) 2012; 3: 141
• 6 Rosenstock J, Fonseca VA, Gross JL, Ratner RE, Ahrén B, Chow FCC. et al; Harmony 6 Study Group. Advancing basal insulin replacement in type 2 diabetes inadequately controlled with insulin glargine plus oral agents: a comparison of adding albiglutide, a weekly GLP-1 receptor agonist, versus thrice-daily prandial insulin lispro. Diabetes Care 2014; 37 (08) 2317-2325
• 7 Kanoski SE, Hayes MR, Skibicka KP. GLP-1 and weight loss: unraveling the diverse neural circuitry. Am J Physiol Regul Integr Comp Physiol 2016; 310 (10) R885-R895
• 8 Shin SJ. Glucagon-like peptide-1 receptor agonists and their effects on weight reduction. J Diabetes Investig 2012; 3 (06) 490-491
• 9 Hölscher C. Protective properties of GLP-1 and associated peptide hormones in neurodegenerative disorders. Br J Pharmacol 2022; 179 (04) 695-714
• 10 Mollan SP, Tahrani AA, Sinclair AJ. The potentially modifiable risk factor in idiopathic intracranial hypertension: body weight. Neurol Clin Pract 2021; 11 (04) e504-e507
• 11 Zhao X, Wang M, Wen Z, Lu Z, Cui L, Fu C. et al. GLP-1 Receptor Agonists: Beyond Their Pancreatic Effects. Front Endocrinol (Lausanne) 2021; 12: 721135
• 12 Jing F, Zou Q, Wang Y, Cai Z, Tang Y. Activation of microglial GLP-1R in the trigeminal nucleus caudalis suppresses central sensitization of chronic migraine after recurrent nitroglycerin stimulation. J Headache Pain 2021; 22 (01) 86
• 13 Gao L, Yu S, Cipriani A, Wu S, Huang Y, Zhang Z. et al. Neurological Manifestation of Incretin-Based Therapies in Patients with Type 2 Diabetes: A Systematic Review and Network Meta-Analysis. Aging Dis 2019; 10 (06) 1311-1319
• 14 Karhunen LJ, Lappalainen RI, Haffner SM, Valve RH, Tuorila H, Miettinen H, Uusitupa MI. Serum leptin, food intake and preferences for sugar and fat in obese women. Int J Obes Relat Metab Disord 1998; 22 (08) 819-821
• 15 Walker RWH. Idiopathic intracranial hypertension: any light on the mechanism of the raised pressure?. J Neurol Neurosurg Psychiatry 2001; 71 (01) 1-5
• 16 Arai Y, Martin-Ruiz CM, Takayama M, Abe Y, Takebayashi T, Koyasu S. et al. Inflammation, But Not Telomere Length, Predicts Successful Ageing at Extreme Old Age: A Longitudinal Study of Semi-supercentenarians. EBioMedicine 2015; 2 (10) 1549-1558
• 17 Halloum W, Dughem YA, Beier D, Pellesi L. Glucagon-like peptide-1 (GLP-1) receptor agonists for headache and pain disorders: a systematic review. J Headache Pain 2024; 25 (01) 112
• 18 Hoffmann J. Clinical significance and therapeutic management of weight loss in patients with idiopathic intracranial hypertension. Neurology 2022; 99 (11) 451-452
• 19 Kesler A, Kliper E, Shenkerman G, Stern N. Idiopathic intracranial hypertension is associated with lower body adiposity. Ophthalmology 2010; 117 (01) 169-174
• 20 Jahromi SR, Martami F, Soltani KM, Togha M. Migraine and obesity: what is the real direction of their association?. Expert Rev Neurother 2023; 23 (01) 75-84
• 21 Ooi LY, Walker BR, Bodkin PA, Whittle IR. Idiopathic intracranial hypertension: can studies of obesity provide the key to understanding pathogenesis?. Br J Neurosurg 2008; 22 (02) 187-194
• 22 Botfield HF, Uldall MS, Westgate CSJ, Mitchell JL, Hagen SM, Gonzalez AM. et al. A glucagon-like peptide-1 receptor agonist reduces intracranial pressure in a rat model of hydrocephalus. Sci Transl Med 2017; 9 (404) eaan0972
• 23 Mitchell JL, Lyons HS, Walker JK, Yiangou A, Grech O, Alimajstorovic Z. et al. The effect of GLP-1RA exenatide on idiopathic intracranial hypertension: a randomized clinical trial. Brain 2023; 146 (05) 1821-1830
• 24 Jing F, Zou Q, Pu Y. GLP-1R agonist liraglutide attenuates pain hypersensitivity by stimulating IL-10 release in a nitroglycerin-induced chronic migraine mouse model. Neurosci Lett 2023; 812: 137397
• 25 Diz-Chaves Y, Maastor Z, Spuch C, Lamas JA, González-Matías LC, Mallo F. Glucagon-like peptide 1 receptor activation: anti-inflammatory effects in the brain. Neural Regen Res 2024; 19 (08) 1671-1677
• 26 Filippatos TD, Panagiotopoulou TV, Elisaf MS. Adverse Effects of GLP-1 Receptor Agonists. Rev Diabet Stud 2014; 11 (3-4): 202-230
• 27 Banerjee M, Pal R, Mukhopadhyay S, Nair K. GLP-1 Receptor Agonists and Risk of Adverse Cerebrovascular Outcomes in Type 2 Diabetes: A Systematic Review and Meta-Analysis of Randomized Controlled Trials. J Clin Endocrinol Metab 2023; 108 (07) 1806-1812
• 28 Dungan KM, Povedano ST, Forst T, González JG, Atisso C, Sealls W, Fahrbach JL. Once-weekly dulaglutide versus once-daily liraglutide in metformin-treated patients with type 2 diabetes (AWARD-6): a randomised, open-label, phase 3, non-inferiority trial. Lancet 2014; 384 (9951) 1349-1357
• 29 Diamant M, Van Gaal L, Guerci B, Stranks S, Han J, Malloy J. et al. Exenatide once weekly versus insulin glargine for type 2 diabetes (DURATION-3): 3-year results of an open-label randomised trial. Lancet Diabetes Endocrinol 2014; 2 (06) 464-473
• 30 Nauck M, Weinstock RS, Umpierrez GE, Guerci B, Skrivanek Z, Milicevic Z. Efficacy and safety of dulaglutide versus sitagliptin after 52 weeks in type 2 diabetes in a randomized controlled trial (AWARD-5). Diabetes Care 2014; 37 (08) 2149-2158
• 31 Alsuhibani A, Alrasheed M, Gari M, Hincapie AL, Guo JJ. Descriptive analysis of reported adverse events associated with anti-obesity medications using FDA Adverse Event Reporting System (FAERS) databases 2013-2020. Int J Clin Pharm 2022; 44 (01) 172-179
• 32 Peres MFP, Lerário DDG, Garrido AB, Zukerman E. Primary headaches in obese patients. Arq Neuro-Psiquiatria 2005; 63 (04) 931-933  × 2005000600005 PubMed
• 33 Headache Classification Committee of the International Headache Society (IHS). The International Classification of Headache Disorders, 3rd edition. Cephalalgia 2018; 38 (01) 1-211
• 34 Krajnc N, Itariu B, Macher S, Marik W, Harreiter J, Michl M. et al. Treatment with GLP-1 receptor agonists is associated with significant weight loss and favorable headache outcomes in idiopathic intracranial hypertension. J Headache Pain 2023; 24 (01) 89
• 35 Lu W, Wang S, Tang H, Yuan T, Zuo W, Liu Y. Neuropsychiatric adverse events associated with Glucagon-like peptide-1 receptor agonists: a pharmacovigilance analysis of the FDA Adverse Event Reporting System database. Eur Psychiatry 2025; 68 (01) e20
• 36 Liu L, Shi H, Shi Y, Wang A, Guo N, Tao H, Nahata MC. Comparative Efficacy and Safety of Glucagon-like Peptide-1 Receptor Agonists in Children and Adolescents with Obesity or Overweight: A Systematic Review and Network Meta-Analysis. Pharmaceuticals (Basel) 2024; 17 (07) 828
• 37 Pellesi L, Do TP, Hougaard A. Pharmacological management of migraine: current strategies and future directions. Expert Opin Pharmacother 2024; 25 (06) 673-683
• 38 Pellesi L, Garcia-Azorin D, Rubio-Beltrán E, Ha WS, Messina R, Ornello R. et al. Combining treatments for migraine prophylaxis: the state-of-the-art. J Headache Pain 2024; 25 (01) 214

Publikationsverlauf

Eingereicht: 07. Februar 2025

Angenommen: 02. August 2025

Artikel online veröffentlicht:
27. Oktober 2025