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Botulinum toxin modulates basal ganglia but not deficient somatosensory activation in orofacial dystonia
Author(s) -
Dresel Christian,
Bayer Ferdinand,
Castrop Florian,
Rimpau Christoph,
Zimmer Claus,
Haslinger Bernhard
Publication year - 2011
Publication title -
movement disorders
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.352
H-Index - 198
eISSN - 1531-8257
pISSN - 0885-3185
DOI - 10.1002/mds.23497
Subject(s) - somatosensory system , basal ganglia , neuroscience , dystonia , psychology , focal dystonia , thalamus , deep brain stimulation , movement disorders , putamen , sensory system , sensory stimulation therapy , medicine , central nervous system , parkinson's disease , pathology , disease
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