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Posterior hypothalamic activation in paroxysmal hemicrania.
Manjit S Matharu1, Anna S Cohen, Richard S J Frackowiak
1Headache Group, Institute of Neurology, Queen Square, London, UK.
Annals of Neurology
|February 21, 2006
Summary
Paroxysmal hemicrania (PH) involves persistent brain pain pathway activation, particularly the posterior hypothalamus and ventral midbrain, which is reversed by indomethacin treatment.
Area of Science:
- Neuroscience
- Headache Medicine
Background:
- Paroxysmal hemicrania (PH) is a severe, strictly unilateral headache.
- PH attacks are brief, frequent, and accompanied by autonomic symptoms.
- Indomethacin is a highly effective treatment for PH.
Purpose of the Study:
- To identify the specific brain structures activated during paroxysmal hemicrania attacks.
- To understand the neural mechanisms underlying PH pathophysiology.
Main Methods:
- Seven PH patients underwent positron emission tomography (PET) scans.
- Scans were performed during acute attacks, pain-free periods off medication, and after indomethacin administration.
- Image analysis utilized SPM99 software.
Main Results:
- Persistent activation of the pain neuromatrix was observed in both symptomatic and interictal states off indomethacin.
- Indomethacin administration deactivated this pain neuromatrix.
- Significant activation of the contralateral posterior hypothalamus and ventral midbrain was noted during untreated PH.
Conclusions:
- The posterior hypothalamus and ventral midbrain are implicated in the pathophysiology of paroxysmal hemicrania.
- These subcortical structures likely play a crucial role in the syndrome.