Carotenuto A, Iodice R, Petracca M, Inglese M, Cerillo I, Cocozza S, Saiote C, Brunetti A, Tedeschi E, Manganelli F, Orefice G
Department of Neurosciences, Reproductive and Odontostomatological Sciences, Federico II University of Naples, Naples, Italy.
Department of Neurology, Radiology, Neuroscience, Icahn School of Medicine, Mount Sinai, NY, USA.
Acta Neurol Scand. 2017 Apr;135(4):442-448. doi: 10.1111/ane.12660. Epub 2016 Aug 8.
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).
To assess CST impairment in MS patients with and without spasticity and to evaluate its evolution under Sativex treatment.
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.
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).
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.
多发性硬化症(MS)中的痉挛是由于下行通路至脊髓运动回路的输入失衡,以及皮质脊髓束(CST)受损所致。
评估有痉挛和无痉挛的MS患者的CST损伤情况,并评估其在使用Sativex治疗下的演变。
10例有痉挛的MS患者(“病例组”)在基线时和12个月后接受了临床评估(扩展残疾状态量表[EDSS]、9孔插钉试验、Ashworth痉挛量表、25英尺计时步行试验和痉挛数字评定量表[NRS])、MRI检查(CST各向异性分数[FA])以及电生理评估(中枢运动传导时间[CMCT]和H/M比值)。我们在基线时选择了20例无痉挛的MS患者作为对照组。
与对照组相比,病例组在基线时CST的FA较低(0.492±0.045对0.543±0.047;P = 0.01),CMCT较高(P = 0.001)。临床、电生理和MRI特征之间未发现相关性。12个月后,病例组患侧FA的非优势损伤程度(PDI)降低(0.502±0.023对0.516±0.033;P = 0.01),与基线相比电生理特征无差异。使用Sativex治疗使痉挛的NRS降低(P = 0.01)。
我们证实有痉挛的MS患者存在CST损伤。我们未发现可解释Sativex临床效果的结构/电生理相关性。