Multiple sclerosis is the most common inflammatory demyelinating disease of the central nervous system, caused by an autoimmune response against myelin that eventually leads to progressive neurodegeneration and disability. Although the knowledge on its underlying neurobiological mechanisms has considerably improved, there is a still unmet need for new treatment options, especially for the progressive forms of the disease. Both preclinical and clinical data suggest that cannabinoids, derived from the Cannabis sativa plant, may be used to control symptoms such as spasticity and chronic pain, whereas only preclinical data indicate that these compounds and their endogenous counterparts, i.e. the endocannabinoids, may also exert neuroprotective effects and slow down disease progression. Here, we review the preclinical and clinical studies that could explain the therapeutic action of cannabinoid-based medicines, as well as the medical potential of modulating endocannabinoid signaling in multiple sclerosis, with a link to other neuroinflammatory disorders that share common hallmarks and pathogenetic features.

多发性硬化症是中枢神经系统最常见的炎症性脱髓鞘疾病，由针对髓磷脂的自身免疫反应引起，最终导致进行性神经变性和残疾。尽管对其潜在的神经生物学机制的了解已大大改善，但仍未满足对新治疗方案的需求，特别是对于疾病的进展形式。临床前和临床数据均表明，源自大麻的大麻素植物，可用于控制诸如痉挛和慢性疼痛等症状，而只有临床前数据表明，这些化合物及其内源性对应物，即内源性大麻素，也可能发挥神经保护作用并减慢疾病进程。在这里，我们回顾了可以解释基于大麻的药物的治疗作用的临床前和临床研究，以及在多发性硬化症中调节内源性大麻素信号传导的医学潜力，以及与具有共同特征和致病特征的其他神经炎性疾病的联系。