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The Journal of Neuroscience, March 29, 2006, 26(13):3589-3593; doi:10.1523/JNEUROSCI.4609-05.2006

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Brief Communications
Hypothalamic Deep Brain Stimulation in Positron Emission Tomography

Arne May,¹ Massimo Leone,² Henning Boecker,³ Till Sprenger,⁴ Tim Juergens,⁵ Gennaro Bussone,² and Thomas R. Tolle⁴

¹Department of Systems Neuroscience, University of Hamburg, D-20246 Hamburg, Germany, ²Instituto Neurologico Carlo Besta, 20133 Milano, Italy, Departments of ³Nuclear Medicine and ⁴Neurology, Technical University of Munich, 81657 Munich, Germany, and ⁵Department of Neurology, University of Regensburg, 93059 Regensburg, Germany

Correspondence should be addressed to Dr. Arne May, Assistant Professor of Neurology, Department of Systems Neuroscience, Universitäts-Krankenhaus Eppendorf, Martinistrasse 52, D-20246 Hamburg, Germany. Email: a.may{at}uke.uni-hamburg.de

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 H₂¹⁵O-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.

Key words: deep brain stimulation; hypothalamus; cluster headache; PET, pain; neuromodulation

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Received Oct. 27, 2005; revised Feb. 9, 2006; accepted Feb. 13, 2006.

Correspondence should be addressed to Dr. Arne May, Assistant Professor of Neurology, Department of Systems Neuroscience, Universitäts-Krankenhaus Eppendorf, Martinistrasse 52, D-20246 Hamburg, Germany. Email: a.may{at}uke.uni-hamburg.de

This article has been cited by other articles:

				R. Cordella, A. Franzini, L. La Mantia, C. Marras, A. Erbetta, and G. Broggi Hypothalamic stimulation for trigeminal neuralgia in multiple sclerosis patients: efficacy on the paroxysmal ophthalmic pain Multiple Sclerosis, November 1, 2009; 15(11): 1322 - 1328. [Abstract] [PDF]

				M. Leone, A. Franzini, G. Broggi, E. Mea, A. P. Cecchini, and G. Bussone Acute hypothalamic stimulation and ongoing cluster headache attacks Neurology, November 28, 2006; 67(10): 1844 - 1845. [Abstract] [Full Text] [PDF]

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