# Post-stroke headache: a review of epidemiology, pathophysiology, and clinical management

**Authors:** Dabao Yao, Luwei Nie, Danyang Chen, Shiling Chen, Xuan Wu, Chao Pan, Yingxin Tang, Na Liu, Zhouping Tang

PMC · DOI: 10.3389/fnins.2026.1766866 · Frontiers in Neuroscience · 2026-03-18

## TL;DR

Post-stroke headaches are common but often ignored complications that affect recovery and quality of life, with limited evidence for effective treatments.

## Contribution

This review synthesizes current knowledge on post-stroke headache epidemiology, pathophysiology, and management, highlighting critical research gaps.

## Key findings

- Post-stroke headache prevalence ranges from 6–44% in ischemic stroke survivors.
- Risk factors include younger age, female sex, and posterior circulation lesions.
- Current treatment strategies lack strong evidence and rely on extrapolation from primary headache disorders.

## Abstract

Post-stroke headache (PSH) and its chronic counterpart, persistent post-stroke headache (PPSH), represent significant but frequently overlooked complications of cerebrovascular disease that adversely affect rehabilitation and quality of life. This review provides an updated synthesis of PSH, following its formal classification in the International Classification of Headache Disorders, 3rd edition (ICHD-3). We examine the epidemiology of PSH, noting a prevalence range of 6–44% in ischemic stroke survivors, with risk factors including younger age, female sex, and posterior circulation lesions. The pathophysiology is explored as a complex interplay involving the trigeminovascular system, neurogenic inflammation, and central sensitization, often exacerbated by structural factors such as edema and stroke topography. Clinical phenotypes vary, predominantly presenting as tension-type, though migraine-like features occur. Furthermore, this review highlights the critical role of headache as a sentinel symptom in the differential diagnosis of distinct stroke etiologies such as cervical artery dissection, reversible cerebral vasoconstriction syndrome, and cerebral venous thrombosis. A major finding is the significant gap in evidence-based management; current therapeutic strategies often rely on extrapolating data from primary headache disorders, with unverified safety profiles for newer agents such as triptans and calcitonin gene-related peptide (CGRP) antagonists in the post-stroke population. We conclude by emphasizing the urgent need for randomized controlled trials to establish safe, effective pharmacological and non-pharmacological interventions for this disabling condition.

## Linked entities

- **Diseases:** cerebrovascular disease (MONDO:0011057), ischemic stroke (MONDO:1060198), cervical artery dissection (MONDO:0006061), reversible cerebral vasoconstriction syndrome (MONDO:0017291)

## Full-text entities

- **Genes:** CALCA (calcitonin related polypeptide alpha) [NCBI Gene 796] {aka CALC1, CGRP, CGRP-I, CGRP-alpha, CGRP1, CT}
- **Diseases:** PPSH (MESH:D051298), cerebrovascular disease (MESH:D002561), cerebral vasoconstriction syndrome (MESH:D002547), Headache Disorders (MESH:D020773), neurogenic inflammation (MESH:D020078), tension (MESH:D018781), migraine (MESH:D008881), cervical artery dissection (MESH:D000094665), cerebral venous thrombosis (MESH:D020767), edema (MESH:D004487), post-stroke (MESH:D020521), posterior circulation lesions (MESH:D020520), ischemic stroke (MESH:D002544), headache (MESH:D006261)
- **Chemicals:** triptans (MESH:D014363)

## Full text

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## Figures

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## References

154 references — full list in the complete paper: https://tomesphere.com/paper/PMC13038870/full.md

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Source: https://tomesphere.com/paper/PMC13038870