Posterior hypothalamic activation in paroxysmal hemicrania

Authors

  • Manjit S. Matharu MRCP,

    1. Headache Group, Queen Square, London, United Kingdom
    2. The National Hospital for Neurology and Neurosurgery, Queen Square, London, United Kingdom
    3. Department d'etudes Cognitives, Ecole Normale Supericure, Paris
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  • Anna S. Cohen MRCP,

    1. Headache Group, Queen Square, London, United Kingdom
    2. The National Hospital for Neurology and Neurosurgery, Queen Square, London, United Kingdom
    3. Department d'etudes Cognitives, Ecole Normale Supericure, Paris
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  • Richard S. J. Frackowiak MD, DSc,

    1. Wellcome Department of Imaging Neuroscience, Institute of Neurology, Queen Square, London, United Kingdom
    2. The National Hospital for Neurology and Neurosurgery, Queen Square, London, United Kingdom
    3. Istituto di Ricoverio e Cura a Carattere Scientifico (IRCCS) Santa Lucia, Rome, Italy
    4. Department d'etudes Cognitives, Ecole Normale Supericure, Paris
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  • Peter J. Goadsby MD, DSc

    Corresponding author
    1. Headache Group, Queen Square, London, United Kingdom
    2. The National Hospital for Neurology and Neurosurgery, Queen Square, London, United Kingdom
    3. Department d'etudes Cognitives, Ecole Normale Supericure, Paris
    • Institute of Neurology, Queen Square, London WC1N 3BG, United Kingdom
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Abstract

Objective

Paroxysmal hemicrania (PH) is a severe, strictly unilateral headache that lasts 2 to 30 minutes, occurs more than five times daily, is associated with trigeminal autonomic symptoms, and is exquisitely responsive to indomethacin. The purpose of the study was to determine the brain structures active in PH.

Methods

Seven PH patients were studied using positron emission tomography (PET). Each patient was scanned in three states: (1) acute PH attack–off indomethacin; (2) pain-free–off indomethacin; and (3) pain-free after administration of intramuscular indomethacin 100mg. The scan images were processed and analyzed using SPM99.

Results

The study showed no significant activations during state 1 compared with state 2, but there was relative activation of the pain neuromatrix in both states 1 and 2 compared with state 3. This suggests that there is persistent activation of the pain neuromatrix during acute PH attacks and during interictal pain-free states off indomethacin that is deactivated by the administration of indomethacin. In addition, the untreated PH state was associated with significant activation of the contralateral posterior hypothalamus and contralateral ventral midbrain, which extended over the red nucleus and the substantia nigra.

Interpretation

These activated subcortical structures may play a pivotal role in the pathophysiology of this syndrome. Ann Neurol 2006;59:535–545

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