The most common types of muscular dystrophy are: pseudohypertrophy, tonic muscular dystrophy and facioscapulohumeral muscular dystrophy, followed by limb-girdle muscular dystrophy, congenital muscular dystrophy in children or infants, and the less common oculopharyngeal muscular dystrophy. Each kind of myotonic dystrophy is named according to its clinical characteristics, such as pseudohypertrophy of the muscles in the posterior group of calves in pseudohypertrophy, muscle straightening after cold or repeated exercise in ankylosing myotonic dystrophy, and atrophy and weakness of shoulder girdle muscles, humerus muscles and facial muscles in face-shoulder-brachial myotonic dystrophy. Nevertheless, myotonic dystrophy is a genetic disease, and most of the genes and proteins that cause the disease have been identified, but only a few pathogenesis is not yet clear. Pseudohypertrophic myotonic dystrophy can be divided into two clinical types according to different age of onset and severity of the disease: Duchenne’s muscular dystrophy and Baker-type muscular dystrophy. Duchenne muscular dystrophy mostly starts within 5 years of age, manifesting as weakness of the extremities, mainly in the lower extremities, which may progress to the upper extremities, and the ability to walk independently is lost around 12 years of age. Baker-type myotonic dystrophy has a later onset, and a few patients may retain the ability to walk even in adulthood. Pseudohypertrophic myotonic dystrophy is caused by mutations in the Dystrophin gene located on the X chromosome and is inherited in a consensual manner, so that the vast majority of patients are male and their mothers are carriers. In very rare cases, female carriers may also present with limb weakness. Patients with this type of myotonic dystrophy may present with cardiac involvement, so it is important to monitor cardiac function. Early diagnosis can also be very helpful for the mother’s reproduction, allowing for better eugenics. Gene therapy is being studied for site-specific mutations in the Dystrophin gene. Ankylosing muscular dystrophy is an autosomal dominant disorder in which patients usually have family members with similar symptoms, but the severity of the onset may not be consistent from generation to generation due to different episodic rates. In addition to muscle tonus induced by cold and after repeated exercise, over time, patients develop symptoms of muscle atrophy and weakness in the extremities. Depending on the clinical manifestations, it can be divided into ankylosing muscular dystrophy type 1 and type 2. type 1 patients may also develop premature baldness, cataracts and cardiac conduction disorders, which require early screening to prevent and treat complications. For patients with ankylosing symptoms, Mesilac is partially effective. Patients with face-shoulder-brachial muscular dystrophy are autosomal dominant and may develop atrophy and weakness of the shoulder girdle and brachialis muscles in the early stages, and gradually develop facial muscle weakness. Due to the involvement of the facial muscles, the patient’s lips pucker forward, resulting in “fish lips” and inability to whistle. Symptoms such as incomplete eyelid closure may also occur. Limb-girdle muscular dystrophy is a large group of diseases, with more than 20 subtypes identified so far. According to the mode of inheritance, they can be divided into autosomal dominant (type 1) and autosomal recessive (type 2), and most of them are found and reported to be type 2. Some patients with limb-girdle muscular dystrophy type 2 have a history of consanguineous parentage, and the disease begins in adolescence or youth, with atrophy and weakness of the shoulder girdle and pelvic girdle muscles as the main manifestations. Each subtype is caused by a different protein lesion, and the diagnosis depends on muscle pathology, immunoblotting and genetic testing. Currently, the more common types of muscular dystrophy in China are limb-girdle muscular dystrophy type 2B and type 2A. Regardless of the type of myotonic dystrophy, there is no very effective treatment. However, functional rehabilitation exercises and gene therapy are among the rapidly developing tools.