Hypothalamic Deep Brain Stimulation in Positron Emission Tomography

Recently, functional imaging data have underscored the crucial role the hypothalamus plays in cluster headache, one of the most severe forms of primary headache. This prompted the application of hypothalamic deep brain stimulation. Yet, it is not apparent how stimulation of an area that is thought t...

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Bibliographic Details
Published in:The Journal of neuroscience 2006-03, Vol.26 (13), p.3589-3593
Main Authors: May, Arne, Leone, Massimo, Boecker, Henning, Sprenger, Till, Juergens, Tim, Bussone, Gennaro, Tolle, Thomas R
Format: Article
Language:English
Subjects:
Adult
Brain Mapping - methods
Brief Communications
Cluster Headache - diagnostic imaging
Cluster Headache - physiopathology
Cluster Headache - therapy
Deep Brain Stimulation - methods
Female
Humans
Hypothalamus - diagnostic imaging
Hypothalamus - physiopathology
Male
Middle Aged
Nerve Net - diagnostic imaging
Nerve Net - physiopathology
Positron-Emission Tomography - methods
Treatment Outcome
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Summary:Recently, functional imaging data have underscored the crucial role the hypothalamus plays in cluster headache, one of the most severe forms of primary headache. This prompted the application of hypothalamic deep brain stimulation. Yet, it is not apparent how stimulation of an area that is thought to act as a pace-maker for acute headache attacks is able to prevent these attacks from occurring. We addressed this issue by examining 10 operated chronic cluster headache patients, using H2(15O)-positron emission tomography and alternately switching the hypothalamic stimulator on and off. The stimulation induced activation in the ipsilateral hypothalamic gray (the site of the stimulator tip), the ipsilateral thalamus, somatosensory cortex and praecuneus, the anterior cingulate cortex, and the ipsilateral trigeminal nucleus and ganglion. We additionally observed deactivation in the middle temporal gyrus, posterior cingulate cortex, and contralateral anterior insula. Both activation and deactivation are situated in cerebral structures belonging to neuronal circuits usually activated in pain transmission and notably in acute cluster headache attacks. Our data argue against an unspecific antinociceptive effect or pure inhibition of hypothalamic activity. Instead, the data suggest a hitherto unrecognized functional modulation of the pain processing network as the mode of action of hypothalamic deep brain stimulation in cluster headache.
ISSN:0270-6474
1529-2401
DOI:10.1523/JNEUROSCI.4609-05.2006