Hemifacial atrophy is one of the more common types of disorders seen in plastic surgery. However, patients who come to the clinic are often already in their post-adolescent years. These children have suffered from localized facial atrophy since childhood, but parents and doctors in some remote areas do not recognize this disease, so they have done a lot of tests including whole body CT, MRI, and even pathological examinations, but in the end, no cause can be found, and some are even misdiagnosed as immune system diseases such as scleroderma. Patients take a lot of drugs and spend a lot of money, but the atrophy continues. To recognize hemifacial atrophy and avoid unnecessary overtreatment, the following will introduce you to the characteristics of this disease. Progressive unilateral facial atrophy syndrome is a relatively common craniofacial deformity, an acquired soft tissue disorder of the face, first described by Parry (1825), Romberg (1846) and Eulenburg (1871) and named Romberg Disease. The onset of the disease is slow but progressive and usually begins at the age of 5-15 years, with some onset at the age of 1 or 2 years, and lasts for 2-10 years. It is more common in females than males, 1.5:1, and is characterized by partial atrophy of half of the face or parts of the face, usually confined to one side of the body. The prevalence is the same on both sides, unilateral prevalence is 95%, bilateral prevalence is about 5%, and about 7% of patients show symptoms of atrophy of one limb or trunk. Pensler reported that 15% of the patients have pure soft tissue atrophy and depression, and 85% of the patients have shortened bone atrophy along with soft tissue atrophy. After puberty, the atrophy gradually stabilizes. At the beginning of the disease, there is often an increase or decrease in pigmentation in certain areas of the face, such as the upper eyebrow, forehead or lower orbital area, and the skin becomes brown or white, and then gradually expands and shows depression of subcutaneous tissues until it disappears completely, and is related to the distribution of the trigeminal nerve. The clinical manifestations of facial nerve palsy are not present. In patients with longer disease duration, thinning and drying of the skin, scleroderma-like symptoms, and even association with muscles and bones, forming obvious deformities can be seen. There is a distinct depression at the junction of detection. In some patients, the affected side of the tongue, nasal cartilage, ear cartilage and mucosa of the hard palate, tongue and mouth and lips can be affected. In addition, there may be significant changes in the skin and hair. Hair thinning, loss or gray hair, sweat glands, salivary glands, and hair follicles may also be affected. In severe cases, the ipsilateral skull and orbital contents may be affected, causing sunken eyes, reduced or no vision, and drooping eyelids. Patients also often have epilepsy and trigeminal neuritis lesions. In cases with onset within 10 years of age, the patient’s facial skeleton is not yet well developed, often producing severe deformities and causing deformation and displacement of facial organs. After the age of 10, the soft tissues are predominantly involved. To date, the etiology of progressive hemifacial atrophy remains unclear. in 1964 Rogers observed 773 cases of hemifacial atrophy and concluded that the pathogenesis was unknown. The four main possible pathogenetic theories are as follows 1. Infection theory Mobius believes that this disease is due to the sympathetic nervous system to certain inflammatory processes produced by tissues such as certain infectious diseases such as scarlet fever, measles, dengue, tuberculosis, etc., such as alveolar swelling, periodontal inflammation, etc. 2. Sympathetic theory Patients with hemifacial atrophy often have sympathetic hyperexcitability, which can lead to vasoconstriction disorders, neurokeratitis, The trigeminal nerve theory Mondel reported by autopsy that tissue atrophy in the trigeminal nerve distribution area is associated with trigeminal neuritis.4. Scleroderma theory Peskovo Stockar reported in 1961 from the perspective of histological examination that the skin, subcutaneous tissue, often showed chronic inflammatory progressive necrotic lesions, eventually leading to scar formation, epidermal Many patients have facial, brain, and neck trauma, or cervical sympathetic nerve stimulation caused by thyroid surgery that induces hemifacial atrophy. Although the etiology is unknown, hemifacial atrophy is still a self-limiting benign disease, atrophy basically ceases after puberty, and treatment is mainly for cosmetic improvement. Compared with traditional free autologous tissue transplantation, autologous fat transplantation is the most preferred treatment option for hemifacial atrophy because it is less invasive and faster to recover, and the post-operative expression is natural and the surgical traces cannot be seen by bystanders.