Rashed Hebatallah R, Milone Margherita
Department of Neurology, Mayo Clinic, Rochester, Minnesota, USA.
Muscle Nerve. 2025 Jan;71(1):9-21. doi: 10.1002/mus.28270. Epub 2024 Oct 6.
Rippling muscle disease (RMD) is a rare disorder of muscle hyperexcitability. It is characterized by rippling wave-like muscle contractions induced by mechanical stretch or voluntary contraction followed by sudden stretch, painful muscle stiffness, percussion-induced rapid muscle contraction (PIRC), and percussion-induced muscle mounding (PIMM). RMD can be hereditary (hRMD) or immune-mediated (iRMD). hRMD is caused by pathogenic variants in caveolin-3 (CAV3) or caveolae-associated protein 1/ polymerase I and transcript release factor (CAVIN1/PTRF). CAV3 pathogenic variants are autosomal dominant or less frequently recessive while CAVIN1/PTRF pathogenic variants are autosomal recessive. CAV3-RMD manifests with a wide spectrum of clinical phenotypes, ranging from asymptomatic creatine kinase elevation to severe muscle weakness. Overlapping phenotypes are common. Muscle caveolin-3 immunoreactivity is often absent or diffusely reduced in CAV3-RMD. CAVIN1/PTRF-RMD is characterized by congenital generalized lipodystrophy (CGL, type 4) and often accompanied by several extra-skeletal muscle manifestations. Muscle cavin-1/PTRF immunoreactivity is absent or reduced while caveolin-3 immunoreactivity is reduced, often in a patchy way, in CAVIN1/PTRF-RMD. iRMD is often accompanied by other autoimmune disorders, including myasthenia gravis. Anti-cavin-4 antibodies are the serological marker while the mosaic expression of caveolin-3 and cavin-4 is the pathological feature of iRMD. Most patients with iRMD respond to immunotherapy. Rippling, PIRC, and PIMM are usually electrically silent. Different pathogenic mechanisms have been postulated to explain the disease mechanisms. In this article, we review the spectrum of hRMD and iRMD, including clinical phenotypes, electrophysiological characteristics, myopathological findings, and pathogenesis.
波纹肌病(RMD)是一种罕见的肌肉过度兴奋疾病。其特征为机械性牵张或自主收缩后紧接着突然牵张所诱发的波纹状肌肉收缩、肌肉疼痛性僵硬、叩击诱发的快速肌肉收缩(PIRC)以及叩击诱发的肌肉隆起(PIMM)。RMD可分为遗传性(hRMD)或免疫介导性(iRMD)。hRMD由小窝蛋白3(CAV3)或小窝相关蛋白1/聚合酶I和转录释放因子(CAVIN1/PTRF)的致病变异引起。CAV3致病变异为常染色体显性遗传,较少为隐性遗传,而CAVIN1/PTRF致病变异为常染色体隐性遗传。CAV3 - RMD表现出广泛的临床表型,从无症状的肌酸激酶升高到严重的肌肉无力。重叠表型很常见。在CAV3 - RMD中,肌肉小窝蛋白3免疫反应性通常缺失或弥漫性降低。CAVIN1/PTRF - RMD的特征为先天性全身性脂肪营养不良(CGL,4型),常伴有多种骨骼肌外表现。在CAVIN1/PTRF - RMD中,肌肉小窝蛋白1/PTRF免疫反应性缺失或降低,而小窝蛋白3免疫反应性降低,通常呈斑片状。iRMD常伴有其他自身免疫性疾病,包括重症肌无力。抗小窝蛋白4抗体是血清学标志物,而小窝蛋白3和小窝蛋白4的镶嵌表达是iRMD的病理特征。大多数iRMD患者对免疫治疗有反应。波纹、PIRC和PIMM通常无电活动。人们推测了不同的致病机制来解释疾病机制。在本文中,我们综述了hRMD和iRMD的谱系,包括临床表型、电生理特征、肌病理发现和发病机制。