The pathogenesis of zygomatic-frontal subluxation, like facial lateral atrophy, is unknown. It is thought to be related to sympathetic nerve disorders leading to vasomotor and nutritional dysfunction; others have suggested that it is related to traumatic infections of the face, skull or neck, trigeminal neuropathy, fetal injury or endocrine dysfunction. What are the causes of zygomatic-frontal bone subsidence? Zygomatic-frontal subluxation is one of the clinical symptoms of crossed lateral atrophy. Crossed lateral atrophy is extremely rare in clinical practice. The disease is a subtype of facial lateral atrophy, such as facial lateral atrophy involving the ipsilateral trunk atrophy (TotalHemiatrophy), combined with the contralateral trunk atrophy is called CrossedHemiatrophy, the former is relatively rare, the latter is even rarer. The clinical manifestations of Crossed Hemiatrophy are mostly atrophy in the upper orbital region or zygomatic region of the face, with the lesion slowly developing to half of the face, occasionally spreading to the skull, neck, and contralateral torso, with skin atrophy and wrinkling, often accompanied by hair loss, hyperpigmentation, white scarring, capillary dilation, increased or reduced sweat gland secretion, sunken zygomatic frontal bones, and well-defined skin boundaries with the healthy region. Some patients may have pupillary changes, decreased iris pigmentation, Horner’s sign, and a few have epilepsy and endocrine disorders. Some patients may have pupillary changes, decreased iris pigmentation, Horner’s sign, and in some cases, epilepsy and endocrine disorders. Crossed lateral atrophy is difficult to diagnose clinically because it is not covered in general neurological monographs, and should be differentiated from unilateral mandibular hypoplasia and lateral hypertrophy, as well as from infantile hemiplegia and fat metabolism disorders.