A Buvanendran

A May

Arnaud Fumal

B Burns

D Borsook

D Magis

Delphine Magis

J Schoenen

Jean Schoenen

JM DeSantana

K Le Doare

KL Casey

M Leone

Marie-Aurélie Bruno

MS Matharu

MY Oh

N Morelli

O Sjaastad

P Irimia

Pierre-Yves Gérardy

PJ Goadsby

RC Kupers

Roland Hustinx

S Laureys

SL Owen

Steven Laureys

T Bartsch

T Sprenger

TP Jurgens

English

PubMed

Abstract Background Occipital nerve stimulation (ONS) has raised new hope for drug-resistant chronic cluster headache (drCCH), a devastating condition. However its mode of action remains elusive. Since the long delay to meaningful effect suggests that ONS induces slow neuromodulation, we have searched for changes in central pain-control areas using metabolic neuroimaging. Methods Ten drCCH patients underwent an 18FDG-PET scan after ONS, at delays varying between 0 and 30 months. All were scanned with ongoing ONS (ON) and with the stimulator switched OFF. Results After 6-30 months of ONS, 3 patients were pain free and 4 had a ≥ 90% reduction of attack frequency (responders). In all patients compared to controls, several areas of the pain matrix showed hypermetabolism: ipsilateral hypothalamus, midbrain and ipsilateral lower pons. All normalized after ONS, except for the hypothalamus. Switching the stimulator ON or OFF had little influence on brain glucose metabolism. The perigenual anterior cingulate cortex (PACC) was hyperactive in ONS responders compared to non-responders. Conclusions Metabolic normalization in the pain neuromatrix and lack of short-term changes induced by the stimulation might support the hypothesis that ONS acts in drCCH through slow neuromodulatory processes. Selective activation in responders of PACC, a pivotal structure in the endogenous opioid system, suggests that ONS could restore balance within dysfunctioning pain control centres. That ONS is nothing but a symptomatic treatment might be illustrated by the persistent hypothalamic hypermetabolism, which could explain why autonomic attacks may persist despite pain relief and why cluster attacks recur shortly after stimulator arrest. PET studies on larger samples are warranted to confirm these first results.</p

Laureys Steven

Hustinx Roland

Gérardy Pierre-Yves

Fumal Arnaud

Bruno Marie-Aurélie

Magis Delphine

Schoenen Jean

Directory of Open Access Journals

BMC Neurology

Central modulation in cluster headache patients treated with occipital nerve stimulation: an FDG-PET study

Springer - Publisher Connector

Abstract
          
            Background
            Occipital nerve stimulation (ONS) has raised new hope for drug-resistant chronic cluster headache (drCCH), a devastating condition. However its mode of action remains elusive. Since the long delay to meaningful effect suggests that ONS induces slow neuromodulation, we have searched for changes in central pain-control areas using metabolic neuroimaging.
          
          
            Methods
            Ten drCCH patients underwent an 18FDG-PET scan after ONS, at delays varying between 0 and 30 months. All were scanned with ongoing ONS (ON) and with the stimulator switched OFF.
          
          
            Results
            After 6-30 months of ONS, 3 patients were pain free and 4 had a ≥ 90% reduction of attack frequency (responders). In all patients compared to controls, several areas of the pain matrix showed hypermetabolism: ipsilateral hypothalamus, midbrain and ipsilateral lower pons. All normalized after ONS, except for the hypothalamus. Switching the stimulator ON or OFF had little influence on brain glucose metabolism. The perigenual anterior cingulate cortex (PACC) was hyperactive in ONS responders compared to non-responders.
          
          
            Conclusions
            Metabolic normalization in the pain neuromatrix and lack of short-term changes induced by the stimulation might support the hypothesis that ONS acts in drCCH through slow neuromodulatory processes. Selective activation in responders of PACC, a pivotal structure in the endogenous opioid system, suggests that ONS could restore balance within dysfunctioning pain control centres. That ONS is nothing but a symptomatic treatment might be illustrated by the persistent hypothalamic hypermetabolism, which could explain why autonomic attacks may persist despite pain relief and why cluster attacks recur shortly after stimulator arrest. PET studies on larger samples are warranted to confirm these first results.
          </jats:sec

Crossref

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http://orbi.ulg.ac.be/bitstream/2268/88843/1/PET-ONS%20-%20%20BMC%20Neurol%202011.pdf

Central modulation in cluster headache patients treated with occipital nerve stimulation: an FDG-PET study

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