[Peripheral stimulation of the trigeminal nerve by nasopharyngeal swabbing as a possible trigger of migraine attacks]. / Estimulación periférica del nervio trigémino mediante frotis nasofaríngeo como posible desencadenante de migraña.

INTRODUCTION: The role of the central and peripheral nervous system in the generation of migraine is not well understood. Our aim was to determine whether peripheral trigeminal nerve stimuli, such as nasopharyngeal swabs, could trigger migraine attacks. SUBJECTS AND METHODS: A survey was sent to 658 doctors, nurses and medical students, asking about the presence of headache suggestive of migraine after carrying out a SARS-CoV-2 swab test, their previous history of migraine, and demographic and headache-related characteristics. Those who tested positive or had associated clinical signs and symptoms of COVID were excluded. RESULTS: A total of 377 people were recruited, 309 of whom were included in the sample. Forty-seven (15.2%) reported headache suggestive of migraine after the swab test and 42 (89.4%) of them had a previous history of migraine. The risk of developing migraine was higher in the subgroup of patients with a history of headache suggestive of migraine - odds ratio: 22.6 (95% confidence interval: 8.597-59.397); p < 0.001. No differences were found between the main characteristics of attacks suggestive of migraine before and after the swab test, except for a lower percentage of associated aura afterwards (42.8% vs. 26.1%; p = 0.016). Individuals with previous attacks suggestive of migraine with a frequency of more than two episodes per month had a higher risk of developing a headache suggestive of migraine after the test - odds ratio = 2.353 (95% confidence interval: 1.077-5.145); p = 0.03. CONCLUSIONS: Nasopharyngeal swabbing may trigger migraine attacks, with a greater likelihood in individuals with a higher frequency of previous migraines. This would confirm the idea that peripheral stimuli on the trigeminal nerve can trigger migraine attacks in individuals with migraine, according to their degree of trigeminovascular sensitisation.

TITLE: Estimulación periférica del nervio trigémino mediante frotis nasofaríngeo como posible desencadenante de migraña.Introducción. La implicación del sistema nervioso central y periférico en la generación de la migraña no se conoce bien. Nuestro objetivo fue determinar si estímulos periféricos sobre el nervio trigémino, como el frotis nasofaríngeo, podrían desencadenar ataques de migraña. Sujetos y métodos. Se envió una encuesta a 658 médicos, enfermeras y estudiantes de medicina, preguntando por la presencia de cefalea sugestiva de migraña tras la realización de un frotis para la determinación del SARS-CoV-2, su historia previa de migraña, y sobre características demográficas y relacionadas con la cefalea. Los que tenían resultado positivo o que asociaban sintomatología de COVID fueron excluidos. Resultados. Se reclutó a 377 personas y se incluyó a 309. Cuarenta y siete (15,2%) refirieron cefalea sugestiva de migraña tras la realización del frotis, de las cuales 42 (89,4%) tenían historia previa de migraña. El riesgo de desarrollarla fue mayor en el subgrupo de pacientes con cefalea sugestiva de migraña previa ­razón de probabilidad: 22,6 (intervalo de confianza al 95%: 8,597-59,397); p < 0,001­. No hubo diferencias entre las características principales de los ataques sugestivos de migraña previos y los desencadenados tras la prueba, excepto un porcentaje menor de aura asociada tras el frotis (42,8% frente a 26,1%; p = 0,016). Los individuos con ataques sugestivos de migraña previos con frecuencia superior a dos episodios mensuales presentaron mayor riesgo de desarrollar una cefalea sugestiva de migraña tras el test ­razón de probabilidad = 2,353 (intervalo de confianza al 95%: 1,077-5,145); p = 0,03­. Conclusiones. El frotis nasofaríngeo podría desencadenar ataques de migraña, más probablemente en individuos con mayor frecuencia de migrañas previas. Esto confirmaría que estímulos periféricos sobre el nervio trigémino pueden desencadenar ataques de migraña en individuos con migraña, de acuerdo con su grado de sensibilización trigeminovascular.

Unraveling the role of calcitonin gene-related peptide b in gastrointestinal disorders: Implications for migraine

Introduction: Calcitonin gene-related peptide (CGRP) a is well-known to be implicated in migraine pathophysiology. Its b isoform, released mainly in the enteric nervous system, has not been as extensively studied. Previous research prompt CGRP has a role in gastrointestinal motility, as well as immune and intestinal blood flow regulation. It is postulated to help peptic ulcer healing, and immune cell migration and regulation in acute gastrointestinal infections. In COVID-19 between 2% and 50% of patients develop diarrhea, and its prevalence increases with the severity of the disease. The pathophysiology of the diarrhea in this infection is not completely clear but CGRP has been proposed to play a role in different aspects of the symptomatology. Inflammatory bowel disease (IBD), known to be associated with migraine, is a chronic gastrointestinal autoimmune disease. Neuropeptides like CGRP might play a role in the complex pathophysiology of the disease, but this has not been well established yet. On the other hand, the most frequent adverse event of new monoclonal antibodies against CGRP for migraine is constipation, which points out that the blockage may affect CGRPbeta release. Objective(s): To assess the role of CGRPbeta in two gastrointestinal disorders: COVID-19 with acute diarrhea;and IBD. Method(s): CGRPbeta were measured by ELISA (CUSABIO, China) in early morning serum samples in patients with IBD at diagnosis, as well as in COVID-19 inpatients experiencing diarrhea. We compared each group with a cohort of healthy controls matched by age and sex. Image: Results: Twenty-six COVID-19 inpatients with diarrhea were included (mean age=62+/-16 years, range 31-91 years;69.2% females) who were matched with 30 healthy controls (mean age=61+/-15 years, range 29-89 years, 66.6% women). Fifty-nine patients with early IBD (mean age 48.9+/-16.4 years, range 21-79 years;62,7% females were matched with 59 healthy controls (mean age 49.0+/-14.9 years, range 23-77 years;62,7% females). While CGRPbeta levels were significantly elevated in COVID-19 patients (6,3+/-2.6 pg/mL) vs controls (4.2+/-2.4 pg/mL) (+26.2%;p<0.01), CGRPbeta levels in patients with IBD were significantly decreased (3.1+/-1.8 pg/mL) as compared to controls (4.8+/-2.6 pg/mL) (-35.4%, p<0.001). Conclusion(s): CGRPbeta seems to exert different actions depending on the underlying conditions. While its increase with diarrhea in COVID-19 patients fits very well with the known acute effects of increase gastrointestinal motility in CGRP infusion in volunteers, the decrease in CGRPbeta levels in IBD confirm a protective role of this peptide in the homeostasis of the intestinal mucosa. These findings may help to explain the role of CGRPbeta in digestive manifestations of migraine and in the constipation seen in migraine patients on CGRP antibodies as well.