Hypothalamic Activation Greater in Chronic vs Episodic Migraine

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Greater activity was recorded in the right anterior hypothalamic region in people with chronic vs episodic migraine.
Greater activity was recorded in the right anterior hypothalamic region in people with chronic vs episodic migraine.

Examination of hypothalamic activity shows distinctly different patterns between episodic and chronic forms of migraine. Results of a recent study reported in Neurology demonstrate that activation of the hypothalamus increases in response to painful trigeminal stimulation in people with chronic migraine (CM) to a degree greater than for episodic migraine (EM) at the time of a headache, but not in healthy controls.1

The investigators recruited 63 participants from the headache outpatient department of the University Medical Center in Eppendorf, Hamburg, Germany, and via an online ad. Following exclusions for errors in data acquisition, 17 patients with CM, 18 with EM, and 19 healthy controls remained. Migraine attacks were stimulated in the CM and EM participants through repeated exposure to 4 types of sensory experiences: pain (ammonia), olfactory activation (rose), a control condition (air), and visual excitation (checkerboard).

The hypothalamic activity was well differentiated in the 2 different types of migraine. Using functional magnetic resonance imaging (fMRI), the investigators recorded greater activity in the right anterior hypothalamic region in people with CM not only compared with healthy controls but also with EMs who were scanned at the time of a headache. Conversely, the posterior part of the hypothalamus was more activated during the painful headache phase in both CM and EM compared with the headache-free phase.

The repeated initiation (chronicity) of migraine attacks was associated with anterior activation, while acute attacks, and specifically the pain component, were linked to posterior activation. The investigators hypothesized that the hypothalamus mediates the anterior activity that precipitates and initiates migraines and that posterior excitation of the descending pain pathway is involved in acute attacks.

These 2 patterns suggest possible separate roles for the different regions of the hypothalamus in migraine that may each be part of a progressive continuum from EM to CM. The investigators theorized that participants with CM were more likely than participants with EM to have a migraine at the time of fMRI scanning. This was confirmed when they compared all patients with headache to patients without headache and found greater posterior activation linked to the acute pain of the attack.

This study provides important clues to the mechanisms of migraine and the increasing trend in overall hypothalamic activity from healthy controls to EMs to CMs pointed strongly to a progression in migraine chronicity over time. The investigators observed that the frequency of attacks in CM and lack of headache-free days made it difficult to distinguish the interictal phase, suggesting that precursive anterior activation in EM may increasingly escalate toward CM, causing the threshold for future headaches to move lower by requiring less anterior stimulation for the re-initiation of chronic migraine attacks. Anterior hypothalamic activity, therefore, may provide a biomarker for future conversion to CM.

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Reference

  1. Schulte LH, Allers A, May A. Hypothalamus as a mediator of chronic migraine: evidence from high-resolution fMRI. Neurology. 2017;88:1-6.
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