Finsterer Josef, Zarrouk-Mahjoub Sinda
Department of Neurology, Krankenanstalt Rudolfstiftung, Vienna, Austria;
Genomics Platform, Pasteur Institute of Tunis, Tunis, Tunisia.
Sultan Qaboos Univ Med J. 2016 Feb;16(1):e92-5. doi: 10.18295/squmj.2016.16.01.017. Epub 2016 Feb 2.
Similarities between a mitochondrial disorder (MID) and amyotrophic lateral sclerosis (ALS) fade with disease progression and the development of mitochondrial multiple organ dysfunction syndrome (MIMODS). However, with mild MIMODS, a MID may still be misinterpreted as ALS. We report a 48-year-old male who presented to the Neurological Hospital Rosenhügel, Vienna, Austria, in February 2001 with slowly progressive weakness, wasting and left upper limb fasciculations which spread to the shoulder girdle and lower limbs. Additionally, he developed tetraspasticity and bulbar involvement. He had been diagnosed with ALS a year previously due to electrophysiological investigations indicative of a chronic neurogenic lesion. However, a muscle biopsy revealed morphological features of a MID and a combined complex-II/III defect. Nerve conduction studies were performed over subsequent years until February 2011. This case demonstrates that MIDs may mimic ALS at onset and begin as a mono-organ disorder but develop into a multi-organ disease with long-term progression. A combined complex II/III defect may manifest with bulbar involvement.
线粒体疾病(MID)与肌萎缩侧索硬化症(ALS)之间的相似性会随着疾病进展以及线粒体多器官功能障碍综合征(MIMODS)的发展而减弱。然而,在轻度MIMODS的情况下,MID仍可能被误诊为ALS。我们报告了一名48岁男性,他于2001年2月前往奥地利维也纳的罗森许格尔神经医院就诊,表现为缓慢进展的肌无力、消瘦以及左上肢肌束震颤,并蔓延至肩胛带和下肢。此外,他还出现了四肢痉挛和延髓受累症状。一年前,由于电生理检查提示慢性神经源性病变,他被诊断为ALS。然而,肌肉活检显示出MID的形态学特征以及复合酶II/III缺陷。在随后的几年直至2011年2月期间,均进行了神经传导研究。该病例表明,MID在发病时可能会模仿ALS,起初表现为单器官疾病,但随着病程的长期进展会发展为多器官疾病。复合酶II/III缺陷可能会伴有延髓受累症状。