importance of tailored interventions to maintain exercise engagement, a priority for clinicians treating this rare headache disorder.

30.4% in adolescents [8–12]. This disparity reects a wide range of population stud­ied and exercise exposure as a key determinant, evident in our marathon-running patient. Peak prevalence occurs in the 20s–30s, with conicting data on sex predi­lection, though athletes (e.g., runners, weightlifters) predominate due to exertion exposure duration and intensity [8, 9, 12–14].

PEH’s pathophysiology is still poorly understood and mostly elusive. PEH’s mecha­nisms are likely to include musculoskeletal, cardiopulmonary, hemodynamic/cere­brovascular processes that directly or indirectly facilitate trigeminocervical activation through common biomarkers mediators (Fig.12.1). The migraine-like

features of PEH and higher occurrence in people with previous or family history of migraine may suggest overlapping pathways or common molecular mediators [2, 8,

Strenuous exercise induces the release of pro-inammatory, nociceptive media­tors from working muscles such as cytokines and prostaglandins, which are associ­ated with major primary headache disorders [17–19]. The increase in cardiac output and shear-stress in the vasculature stimulate nitric oxide (NO) formation and release, a classical headache-provoking molecule [17]. A recent report showed an increase in the circulating levels of calcitonin gene-related peptide (CGRP) in 48 runners after a half-marathon event [20]. Besides, the metabolic stress and related respira­tory decompensation (e.g., acidosis, hypoxia) are hallmark of intense exercise, and are also considered headache triggers [17, 21]. In susceptible individuals or in the context of Valsalva maneuvers, wherein incompetent venous vasculature is present, retrograde ow may result in a temporary rise in blood ow, elevating intracranial pressure and ultimately triggering head pain [22, 23]. Dysfunctional myogenic cere­brovascular autoregulation has been proposed [24]. In this scenario, the capacity to sustain stable tissue perfusion despite variations in pressure (i.e., increased cardiac output, blood pressure) and metabolic demands is disrupted, and the constriction of resistance cerebral blood vessels is not guaranteed, thus, resulting in vasodilation and head pain [2, 8, 24].

The patient reported no prior personal or familial history of migraine or aneu­rysm, no recent trauma, and no systemic symptoms. He denied any headache out­side the context of exercise. He had not changed his training routines signicantly, though he had recently increased the frequency of high-intensity interval sessions. There were no signs of dehydration or environmental triggers (e.g., heat, altitude) contributing to the symptoms.

Initial management focused on behavioral strategies including structured warm­ up protocols, diaphragmatic breathing training, hydration optimization, and posture correction. The patient was educated on avoiding Valsalva maneuvers and encour­aged to maintain physical activity with modications. Despite improvements, occa­sional headache recurrences prompted the addition of 25mg indomethacin, taken 30–60 min before runs exceeding 15 km, resulting in complete resolution of symptoms.

Emerging Therapies: CGRP antagonists (e.g., gepants) as an off-label pretreatment