Iron Deposition in Pain‐Regulatory Nuclei in Episodic Migraine and Chronic Daily Headache by MRI

偏头痛 慢性偏头痛 光环 苍白球 医学 慢性疼痛 磁共振成像 先兆偏头痛 基底神经节 内科学 麻醉 物理疗法 放射科 中枢神经系统
作者
Stewart J. Tepper,Mark J. Lowe,Erik B. Beall,Micheal D. Phillips,Kecheng Liu,Mark J. Stillman,Mary Horvat,Stephen E. Jones
出处
期刊:Headache [Wiley]
卷期号:52 (2): 236-243 被引量:41
标识
DOI:10.1111/j.1526-4610.2011.02056.x
摘要

Background.— Progression of migraine toward a more disabling chronic form of at least 15 days/month is linked with frequency of attacks. Magnetic resonance imaging (MRI) findings of iron accumulation in the brain, especially in periaqueductal gray and red nucleus, have been correlated with both duration of illness and frequency of attacks. Methods.— This study therefore evaluated iron deposition as measured with MRI in basal ganglia and pain regulatory nuclei in neurologically healthy control volunteers and in patients with various migraine subtypes: episodic migraine (n = 10) with (n = 4) or without aura (n = 6), and chronic daily headache (n = 11), including medication overuse headache (MOH, n = 8), chronic tension‐type headache (n = 1), and primary chronic migraine (n = 2). The goal was to assess differences in iron deposition among migraine subtypes and controls in the hopes of linking the by‐products of frequent attacks or long duration of illness with these changes. Results.— The study sought to evaluate the tradeoff between sensitivity and specificity in T2 imaging of patients with migraine, and found that only T2 imaging in the globus pallidus was able to distinguish between episodic and chronic migraine, suggesting that this technique may be the most appropriate to assess migraine frequency. Patients with MOH did not demonstrate T2′ shortening. Conclusions.— Because iron accumulation should cause shortening of both T2 and T2′, although the lack of significance in observed T2′ difference could be due to increased variance in T2′ the measurement, these results suggest that a mechanism other than increased iron deposition may play a role in the genesis or pathophysiology of MOH.
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