Brain-derived neurotrophic factor in primary headaches.

Marlene Fischer,Dagny Holle,Charly Gaul,Stephanie Klien,Gregor Broessner,Hind Shanib,Georg Wille

doi:10.1007/s10194-012-0454-5

Marlene Fischer, Dagny Holle + Show 5 more

Open Access

https://doi.org/10.1007/s10194-012-0454-5

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Abstract

Brain derived neurotrophic factor (BDNF) is associated with pain modulation and central sensitization. Recently, a role of BDNF in migraine and cluster headache pathophysiology has been suspected due to its known interaction with calcitonin gene-related peptide. Bi-center prospective study was done enrolling four diagnostic groups: episodic migraine with and without aura, episodic cluster headache, frequent episodic tension-type headache, and healthy individuals. In migraineurs, venous blood samples were collected twice: outside and during migraine attacks prior to pain medication. In cluster headache patients serum samples were collected in and outside cluster bout. Analysis of BDNF was performed using enzyme-linked immunosorbent assay technique. Migraine patients revealed significantly higher BDNF serum levels during migraine attacks (n = 25) compared with headache-free intervals (n = 53, P < 0.01), patients with tension-type headache (n = 6, P < 0.05), and healthy controls (n = 22, P < 0.001). There was no significant difference between patients with migraine with aura compared with those without aura, neither during migraine attacks nor during headache-free periods. Cluster headache patients showed significantly higher BDNF concentrations inside (n = 42) and outside cluster bouts (n = 24) compared with healthy controls (P < 0.01, P < 0.05). BDNF is increased during migraine attacks, and in cluster headache, further supporting the involvement of BDNF in the pathophysiology of these primary headaches.

Highlights

Migraine is a neurologic disorder affecting about 11 % of the population [1]
Our main findings were (1) Brain derived neurotrophic factor (BDNF) is significantly elevated in patients with migraine and cluster headache compared with patients with tension-type headache and healthy controls
(2) During migraine attacks BDNF serum levels are significantly higher compared with headache-free periods and controls

Summary

Introduction

Migraine is a neurologic disorder affecting about 11 % of the population [1]. The mechanisms that have been implicated in the pathophysiology of migraine include neurogenic inflammation, cortical spreading depression, central sensitization, and vascular involvement [2]. Various peptides like calcitonin-gene related peptide (CGRP), vasoactive intestinal peptide, and substance P have been shown to mediate nociceptive effects during headache pain generation and central sensitization. In addition to effects on neuronal development and differentiation it has been shown to exert a pivotal role in the modulation of pain signaling [6]. It affects plasticity of synapses in trigeminal nociceptive pathways and is expressed in trigeminal ganglion neurons [7,8,9]. Trigeminal release of BDNF is induced by inflammatory stimuli such as tumor necrosis factor-alpha and vasoactive mediators of neurogenic inflammation including CGRP [8, 10].

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