Brum Marisa, Semedo Cristina, Guerreiro Rui, Pinto Marques José
Neurology Department, Centro Hospitalar de Setúbal, Rua Camilo Castelo Branco, 2910-446 Setúbal, Portugal ; Instituto de Medicina Molecular, Faculty of Medicine of Lisbon University, 1649-028 Lisbon, Portugal.
Neurology Department, Centro Hospitalar de Setúbal, Rua Camilo Castelo Branco, 2910-446 Setúbal, Portugal.
Case Rep Neurol Med. 2014;2014:701761. doi: 10.1155/2014/701761. Epub 2014 Dec 8.
Background. The mutation 9185T>C in ATP6 gene, associated with Leigh syndrome, was reported in only few families. Motor neuron disease (MND), both clinically and electrophysiologically, was not previously described in association with this mutation. Case Report. 33-year-old male, with family history of mitochondrial disease, presented with cognitive impairment, exercise intolerance, and progressive muscle weakness. Examination revealed global hypotonia, and proximal tetraparesis, without atrophy or fasciculation, pyramidal signs, or sensory symptoms. The laboratory findings revealed an increase of lactate and lactate/pyruvate ratio; electromyogram showed chronic neurogenic compromise; muscle biopsy was suggestive of spinal muscular atrophy and mitochondriopathy; genetic study of SMN1 was negative but detected a homoplasmic mutation 9185T>C in ATP6 gene. His younger sister, with the same mutation, had cognitive impairment, ataxia, and muscle weakness. EMG showed axonal peripheral neuropathy. Conclusion. This case is unique because of the benignity and the coexistence of clinical, neurophysiological, and pathological findings suggestive of MND that, although described in mitochondrial disease, have not yet been reported in association with 9185T>C mutation. The present case contributes to the expansion of the phenotypic expressions of this particular mutation.
背景。ATP6基因中的9185T>C突变与 Leigh 综合征相关,仅在少数家族中有报道。运动神经元病(MND),无论是临床还是电生理方面,此前均未被描述与该突变有关。病例报告。一名33岁男性,有线粒体疾病家族史,出现认知障碍、运动不耐受和进行性肌肉无力。检查发现全身肌张力减退和近端四肢轻瘫,无萎缩、肌束震颤、锥体束征或感觉症状。实验室检查结果显示乳酸和乳酸/丙酮酸比值升高;肌电图显示慢性神经源性损害;肌肉活检提示脊髓性肌萎缩和线粒体病;SMN1基因研究为阴性,但检测到ATP6基因中的纯合突变9185T>C。他的妹妹有相同突变,有认知障碍、共济失调和肌肉无力。肌电图显示轴索性周围神经病。结论。该病例独特之处在于其良性以及临床、神经生理和病理表现提示MND的共存,尽管在线粒体疾病中有所描述,但尚未报道与9185T>C突变相关。本病例有助于扩展这一特定突变的表型表达。