Movement Disorders (revue)

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Botulinum toxin modulates basal ganglia but not deficient somatosensory activation in orofacial dystonia

Identifieur interne : 001781 ( Main/Exploration ); précédent : 001780; suivant : 001782

Botulinum toxin modulates basal ganglia but not deficient somatosensory activation in orofacial dystonia

Auteurs : Christian Dresel [Allemagne] ; Ferdinand Bayer [Allemagne] ; Florian Castrop [Allemagne] ; Christoph Rimpau [Allemagne] ; Claus Zimmer [Allemagne] ; Bernhard Haslinger [Allemagne]

Source :

RBID : ISTEX:91DBF2C6A18BF93D45B3BE466A7D0C92D1F21C28

Descripteurs français

English descriptors

Abstract

The etiology of idiopathic orofacial dystonia is incompletely understood. Neurophysiological studies indicated that a sensory dysfunction could play a key role in the pathophysiology of focal dystonia. To explore if central sensory processing is abnormal in patients with blepharospasm and Meige's syndrome and to study the effects of botulinum toxin (BTX) treatment, we systematically mapped the somatotopic representations of punctate tactile stimuli in these patients before and after therapy. Methods:: Standardized tactile stimuli were pseudorandomly applied to the forehead, upper lip, and hand by a MR‐compatible stimulation device during event‐related fMRI. Results:: Patients showed a deficient activation in primary and secondary somatosensory representations of affected and unaffected (right hand) body regions compared to healthy controls. Although clinically effective BTX treatment did not modulate this impaired cortical activation, it reduced the activation of the thalamus and contralateral putamen during forehead stimulation. Conclusions:: This study reveals a more generalized dysfunction of the somatosensory cortex including asymptomatic body representations in orofacial dystonia. Deficient cortical sensory activation may be due to a dedifferentiation of somatosensory representations and could represent a critical functional change within the basal ganglia‐thalamocortical loops facilitating dystonic movements. Modulation of basal ganglia activation might reflect an indirect remote effect of BTX treatment on these sensorimotor circuits. © 2010 Movement Disorder Society

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DOI: 10.1002/mds.23497


Affiliations:


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<div type="abstract" xml:lang="en">The etiology of idiopathic orofacial dystonia is incompletely understood. Neurophysiological studies indicated that a sensory dysfunction could play a key role in the pathophysiology of focal dystonia. To explore if central sensory processing is abnormal in patients with blepharospasm and Meige's syndrome and to study the effects of botulinum toxin (BTX) treatment, we systematically mapped the somatotopic representations of punctate tactile stimuli in these patients before and after therapy. Methods:: Standardized tactile stimuli were pseudorandomly applied to the forehead, upper lip, and hand by a MR‐compatible stimulation device during event‐related fMRI. Results:: Patients showed a deficient activation in primary and secondary somatosensory representations of affected and unaffected (right hand) body regions compared to healthy controls. Although clinically effective BTX treatment did not modulate this impaired cortical activation, it reduced the activation of the thalamus and contralateral putamen during forehead stimulation. Conclusions:: This study reveals a more generalized dysfunction of the somatosensory cortex including asymptomatic body representations in orofacial dystonia. Deficient cortical sensory activation may be due to a dedifferentiation of somatosensory representations and could represent a critical functional change within the basal ganglia‐thalamocortical loops facilitating dystonic movements. Modulation of basal ganglia activation might reflect an indirect remote effect of BTX treatment on these sensorimotor circuits. © 2010 Movement Disorder Society</div>
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