• cytokine;
  • neurogenic inflammation;
  • comorbidity

Background and Objectives.—Migraine is characterized by the peripheral and central sensitization of pain perceptive neural systems, and neurogenic inflammation is a key step in the development of migraine headache. We focused on transforming growth factor-β1 (TGF-β1), which is a multifunctional proinflammatory cytokine. To address the possibility of TGF-β1 involvement in migraine, we investigated the plasma level of TGF-β1 in patients with migraine headache during headache-free periods.

Subjects and Methods.—Sixty-eight subjects with migraine participated: 23 with migraine with aura (MWA) and 45 without aura (MWoA). We recruited 58 healthy subjects without headache as controls. In addition, we examined 12 subjects with episodic tension-type headache. Platelet poor plasma (PPP) was obtained from subjects during headache free-periods. TGF-β1 levels in PPP were determined by enzyme-linked immunosorbent assay.

Results.—The TGF-β1 level in PPP was 2.62*± 0.23 (mean ± SE) ng/mL in migraine, 2.08 ± 0.20 ng/mL in tension-type headache, and 1.80 ± 0.09 ng/mL in controls (P= .007, ANOVA; *P < .01, post hoc tests vs. the controls).

Conclusion.—TGF-β1 in PPP was significantly increased in patients with migraine during headache-free periods. TGF-β1 may play some role in the development of migraine headache.