A Carotenuto1, R Iodice1, M Petracca1,2, M Inglese2, I Cerillo1, S Cocozza3, C Saiote4, A Brunetti3, E Tedeschi3, F Manganelli1, G Orefice1. 1. Department of Neurosciences, Reproductive and Odontostomatological Sciences, Federico II University of Naples, Naples, Italy. 2. Department of Neurology, Radiology, Neuroscience, Icahn School of Medicine, Mount Sinai, NY, USA. 3. Department of Advanced Biomedical Sciences, Federico II University of Naples, Naples, Italy. 4. Department of Neurology, Icahn School of Medicine, Mount Sinai, NY, USA.
Abstract
BACKGROUND: Spasticity in multiple sclerosis (MS) results from an imbalance of inputs from descending pathways to the spinal motor circuits, as well as from a damage of the corticospinal tract (CST). OBJECTIVES: To assess CST impairment in MS patients with and without spasticity and to evaluate its evolution under Sativex® treatment. METHODS: Ten MS patients with spasticity ("cases") underwent clinical (EDSS, 9-hole Peg, Ashworth scale, Timed 25-Foot Walk, and NRS for spasticity), MRI (CST fractional anisotropy [FA]), and electrophysiological (central motor conduction time [CMCT] and H/M ratio) evaluations at baseline and after 12 months. We selected 20 MS patients without spasticity as control group at baseline. RESULTS: At baseline, cases showed a lower CST FA (0.492±0.045 vs 0.543±0.047; P=.01) and a higher CMCT (P=.001) compared to the control group. No correlations were found between clinical, electrophysiological, and MRI features. After 12 months, cases showed a decrease in non-prevalent degree of impairment (PDI) side FA (0.502±0.023 vs 0.516±0.033; P=.01) without differences for electrophysiological features compared to baseline. Treatment with Sativex® resulted in a reduction of NRS for spasticity (P=.01). CONCLUSIONS: We confirm the presence of CST impairment in MS patients with spasticity. We did not identify structural/electrophysiological correlates that could explain Sativex® clinical effect.
BACKGROUND:Spasticity in multiple sclerosis (MS) results from an imbalance of inputs from descending pathways to the spinal motor circuits, as well as from a damage of the corticospinal tract (CST). OBJECTIVES: To assess CST impairment in MSpatients with and without spasticity and to evaluate its evolution under Sativex® treatment. METHODS: Ten MSpatients with spasticity ("cases") underwent clinical (EDSS, 9-hole Peg, Ashworth scale, Timed 25-Foot Walk, and NRS for spasticity), MRI (CST fractional anisotropy [FA]), and electrophysiological (central motor conduction time [CMCT] and H/M ratio) evaluations at baseline and after 12 months. We selected 20 MSpatients without spasticity as control group at baseline. RESULTS: At baseline, cases showed a lower CST FA (0.492±0.045 vs 0.543±0.047; P=.01) and a higher CMCT (P=.001) compared to the control group. No correlations were found between clinical, electrophysiological, and MRI features. After 12 months, cases showed a decrease in non-prevalent degree of impairment (PDI) side FA (0.502±0.023 vs 0.516±0.033; P=.01) without differences for electrophysiological features compared to baseline. Treatment with Sativex® resulted in a reduction of NRS for spasticity (P=.01). CONCLUSIONS: We confirm the presence of CST impairment in MSpatients with spasticity. We did not identify structural/electrophysiological correlates that could explain Sativex® clinical effect.
Authors: Antonio Carotenuto; Teresa Costabile; Mario De Lucia; Marcello Moccia; Fabrizia Falco; Martina Petruzzo; Marcello De Angelis; Cinzia Valeria Russo; Francesco Saccà; Roberta Lanzillo; Vincenzo Brescia Morra Journal: J Neurol Date: 2020-03-02 Impact factor: 4.849