University of Rostock, Department of Physiology, Germany.
University of Rostock, Department of Neurology, Division of Neuroimmunology, Germany.
Autoimmun Rev. 2017 Sep;16(9):925-936. doi: 10.1016/j.autrev.2017.07.004. Epub 2017 Jul 8.
In contrast to other diseases that go along with spasticity (e.g. spinal cord injury), spasticity in chronic autoimmune diseases involving the CNS is complicated by the ongoing damage of neuronal networks that leads to permanent changes in the clinical picture of spasticity. Multiple sclerosis (MS) is the most frequent autoimmune disease of the central nervous system (CNS) and spasticity is one of the most disabling symptoms. It occurs in more than 80% MS patients at some point of the disease and is associated with impaired ambulation, pain and the development of contractures. Besides causing cumulative structural damage, neuroinflammation occurring in MS leads to dynamic changes in motor circuit function and muscle tone that are caused by cytokines, prostaglandins, reactive oxygen species and stress hormones that affect neuronal circuits and thereby spasticity. The situation is complicated further by the fact that therapeutics used for the immunotherapy of MS may worsen spasticity and drugs used for the symptomatic treatment of spasticity have been shown to have the potential to alter immune cell function and CNS autoimmunity itself. This review summarizes the current knowledge on the immunologic pathways that are involved in the development, maintenance, dynamic changes and pharmacological modulation of spasticity in MS.
与其他伴随痉挛的疾病（例如脊髓损伤）相反，涉及中枢神经系统的慢性自身免疫性疾病中的痉挛因神经元网络的持续损伤而变得复杂，从而导致痉挛的临床症状发生永久性变化。多发性硬化症（MS）是最常见的中枢神经系统（CNS）自身免疫性疾病，痉挛是最致残的症状之一。在疾病的某个阶段，超过 80%的 MS 患者会出现痉挛，并且与运动障碍、疼痛和挛缩的发展有关。除了导致累积的结构损伤外，MS 中发生的神经炎症会导致运动回路功能和肌肉张力的动态变化，这是由细胞因子、前列腺素、活性氧和应激激素引起的，这些物质会影响神经元回路，从而导致痉挛。更复杂的是，用于 MS 免疫治疗的疗法可能会加重痉挛，而用于痉挛症状治疗的药物已被证明有可能改变免疫细胞功能和中枢自身免疫本身。这篇综述总结了目前关于参与 MS 中痉挛的发展、维持、动态变化和药物调节的免疫途径的知识。
