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Published on: June 2, 2014
Arterial hypertension in the chronic evolution of migraine: bystander or risk factor? An overview
Federico Mazzacane1,2, Gloria Vaghi3,4, Matteo Cotta Ramusino2
1Department of Brain and Behavioral Sciences, University of Pavia, 27100, Pavia, Italy.
Insights
Hypertension (HT) contributes to chronic migraine (CM) through shared mechanisms like endothelial dysfunction. While HT influences CM, more research is needed to confirm its direct causal role in migraine chronification.
Area of Science:
- Neurology
- Cardiovascular Medicine
Background:
- Migraine chronification is linked to various risk factors.
- Hypertension (HT) is a potential modifiable risk factor for chronic migraine (CM).
- This review examines shared mechanisms between HT and migraine evolution.
Purpose of the Study:
- To review clinical evidence on HT's role in the transition to CM.
- To explore biological mechanisms linking HT and migraine chronification.
- To assess the impact of antihypertensive drugs on migraine prophylaxis.
Main Methods:
- Narrative review of existing literature.
- Search for studies on HT and CM transition.
- Analysis of biological pathways and clinical observations.
Main Results:
- HT is implicated in mechanisms driving migraine and its chronicization.
- Endothelial dysfunction, BBB alterations, CGRP signaling, and RAAS are key pathways.
- Clinical data support HT's role in the transition to CM.
Conclusions:
- Shared pathophysiological mechanisms link HT to CM.
- A bidirectional relationship between HT and CM is suggested.
- Further research is required to establish a causal link between HT and CM.
Background:
Several risk factors are associated with the chronic evolution of migraine. Clinical and preclinical studies have provided data about the role of hypertension (HT) as one of the potential modifiable risk factors of chronic migraine (CM). This review is focused on the biological and clinical evidence supporting common mechanisms underlying HT and migraine and the potential role of HT in the transition from episodic to chronic migraine.
Methods:
We conducted a narrative review from a literature search covering the available evidence from studies investigating: i) the role of HT in the transition to CM in clinical practice; ii) the biological mechanisms potentially underpinning the association between HT and evolution to CM; iii) the role of antihypertensive medications in migraine prophylaxis.
Results:
HT proved to be at the base of multiple mechanisms underlying migraine and migraine chronicization. Endothelial dysfunction, blood-brain barrier alterations, calcitonin gene-related peptide signaling, and renin-angiotensin-aldosterone system dysregulation are involved in the worsening effect of HT on migraine frequency, and the role of HT in the transition to CM is supported by clinical observations.
Conclusions:
The observed evidence supports HT contribution to CM evolution due to shared pathophysiologic mechanisms. While a bidirectional influence appears to be ascertained, data are still lacking about the one-way role of HT as direct risk factor for CM transition. Further research is needed to confirm a causal role of HT in this process.
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