Michele Tinazzi1, Giovanna Maddalena Squintani2, Kailash P Bhatia3, Alessia Segatti2, Francesco Donato4, Massimiliano Valeriani5, Roberto Erro6. 1. Department of Neuroscience, Biomedicine and Movement Science, University of Verona, Verona, Italy. 2. Neurology Unit, Department of Neuroscience, AOUI Verona, Verona, Italy. 3. Department of Clinical and Movement Neurosciences, Institute of Neurology, University College London, London, UK. 4. Department of Neurology, SS Giovanni e Paolo Hospital, 30122, Venice, Italy. 5. Neurology Unit, Ospedale Pediatrico Bambino Gesú, Rome, Italy. 6. Center for Neurodegenerative Diseases (CEMAND), Department of Medicine, Surgery and Dentistry "Scuola Medica Salernitana", Universitá di Salerno, Baronissi, SA, Italy. Electronic address: rerro@unisa.it.
Abstract
INTRODUCTION: Several observations would suggest that dystonic pain is not simply muscular in origin. While ascending nociceptive pathways are normal in cervical dystonia, it is unknown whether descending inhibitory pain pathways are also normal. METHODS: We applied a conditioned pain modulation protocol and concomitantly recorded laser evoked potentials in patients with cervical dystonia (n = 15), blepharospasm (n = 15) and healthy volunteers (n = 15). RESULTS: During the application of a heterotopic noxious conditioning stimulation, patients with cervical dystonia, but not with blepharospasm, lacked the physiological reduction of the perceived intensity of a painful test stimulus as well as of the related evoked potential. This was observed in cervical dystonia patients regardless of the presence of clinical pain. CONCLUSIONS: Our results suggest that pain in CD is not simply muscular in origin but it also possibly reflects a dysfunction of the descending pain inhibitory control, thus providing a novel venue to explore the pathophysiology of pain in CD.
INTRODUCTION: Several observations would suggest that dystonic pain is not simply muscular in origin. While ascending nociceptive pathways are normal in cervical dystonia, it is unknown whether descending inhibitory pain pathways are also normal. METHODS: We applied a conditioned pain modulation protocol and concomitantly recorded laser evoked potentials in patients with cervical dystonia (n = 15), blepharospasm (n = 15) and healthy volunteers (n = 15). RESULTS: During the application of a heterotopic noxious conditioning stimulation, patients with cervical dystonia, but not with blepharospasm, lacked the physiological reduction of the perceived intensity of a painful test stimulus as well as of the related evoked potential. This was observed in cervical dystoniapatients regardless of the presence of clinical pain. CONCLUSIONS: Our results suggest that pain in CD is not simply muscular in origin but it also possibly reflects a dysfunction of the descending pain inhibitory control, thus providing a novel venue to explore the pathophysiology of pain in CD.
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