The association between diabetes and A3243GmtDNA mutations dates back to 1984 when Pavlakis first described MELAS syndrome, and Hirano and Pavlakis had reported that 5% of patients with MELAS also had diabetes. Studies have reported 32.4% of ECG abnormalities, including cardiomyopathy, pre-excitation syndrome or heart block. One study reported that 18% of patients with MELAS had cardiomyopathy or congestive heart failure. Mitochondrial encephalomyopathy is a maternally inherited disorder with a combination of mtDNAA3243G mutations. Studies have reported short stature and mental retardation in 38.8% and 43.3% of cases, respectively, as these disorders affect aerobic metabolism in the brain and skeletal muscle by affecting the structure or function of the mitochondria. Although CT is commonly used in patients with MELAS, MRI is more powerful in diagnosing MELAS. Although the pathology is not demonstrated on MRI, the migratory nature of the lesions and the inconsistency with the distribution of cerebral arteries are also strongly suggestive of metabolic or mitochondrial disorders, rather than being caused by arterial occlusion. One study reported that MRI of MELAS patients showed multilobar onset, with lesions mostly located in the cortex and subcortical white matter, lesion distribution inconsistent with the distribution of cerebrovascular blood supply, with low signal on TWI and high signal on TW2 and FIAIR, and in addition, most lesions were symmetrically distributed, multiple and migratory. One report suggests the highest prevalence of occipital lobe on MRI, followed by temporal lobe, parietal lobe, frontal lobe, cerebellum, basal ganglia, hypothalamus, brainstem, and meninges in that order. GMT staining reveals broken red fibers (RRF), SDH staining reveals deeply stained fibers, and electron microscopy reveals a large number of abnormal mitochondria. The positivity rate of muscle biopsy in MELAS patients was nearly 90%, while the domestic literature reported 63.6%.