Oculoclonus-myoclonus syndrome (OMS), also known as oculoclonus-cerebellar-myoclonus syndrome or infantile polymyoclonus-oculoclonus syndrome. The etiology is unknown, and the possible causes include microcephaly or brainstem inflammation caused by viral infections, and in recent years, studies have found that it may be an autoimmune disease. The onset of the disease is usually between 1-2 years of age, mostly around 14 months of age; acute or subacute onset; the main manifestation is myoclonus, which is an involuntary, rhythmic, large, multidirectional, continuous, disorganized eye movement that is obvious when pursuing an object, and decreases when the eye has been fixed on the target; often accompanied by rapid eyelid flutter; multiple wandering myoclonias of the face, limbs, and trunk. Sleep may be reduced or absent; may be accompanied by cerebellar ataxia; behavioral changes, marked excitement and irritability; and sleep disturbances. Approximately 50% of the cases are combined with neuroblastoma. Neuroimaging, EEG and brain crest fluid are normal. There is no specific treatment for this disease. However, in the acute phase, adrenocorticotropic hormone (ACTH) and adrenocorticotropic hormone have a remitting effect. Some data suggest that IVIg, rituximab, etc. also have some efficacy. It is prone to recurrence; long-term follow-up may leave problems such as delayed motor development, language impairment, cognitive impairment or behavioral abnormalities. The disease may sometimes be misdiagnosed as myoclonic epilepsy or myoclonic persistence, but similar oculomotor features are rarely seen in true seizures.