Infantile spasms, also known as West syndrome (WS) and nodding-like epilepsy, is an epilepsy syndrome of multiple etiologies and is the most common refractory epilepsy of infancy, accounting for about half of all severe epilepsy in infancy, with an incidence of 0.016% to 0.042% in live births. It is an age-dependent epilepsy, and the earlier the onset, the worse the prognosis. 95% of children have intellectual deficits, most of which are severe; in addition, mental and behavioral disorders are also common, such as hyperactivity syndrome, autism, and secondary epilepsy. Most of them start within 1 year of age, and their peak age of onset is 3 to 6 months. The seizures tend to occur before going to sleep and just after waking up, with several to dozens, or even hundreds of seizures per day. Infantile spasms can be classified as symptomatic, cryptogenic, or idiopathic according to the cause. Symptomatic infantile spasms account for 85% to 90% of cases. The clinical manifestations are recurrent spastic seizures, usually in clusters (series); disturbances in the peak rhythm of the EEG, characterized by random, high-amplitude spikes and slow waves; and significant psychomotor developmental delays (80%-90%). Although some common factors associated with WS have been summarized, the pathogenesis of WS is poorly understood. There have been many views on the etiology of WS, but currently there are two opinions: the brainstem or the cerebral cortex. It is believed that the brainstem is the responsible structure for WS; WS in infancy has both cortical damage and abnormal brainstem function and structural changes; however, severe brainstem disorders are more closely related to mental retardation and cognitive dysfunction in WS. More than 100 causes are known to cause infantile spasms. Possible causes of infantile spasms before birth include: genetic mutations, chromosomal abnormalities, congenital brain developmental abnormalities (cortical dysplasia, corpus callosum dysplasia, megalencephaly), neurocutaneous syndromes (tuberous sclerosis, etc.), metabolic factors [amino acid metabolic disease (phenylketonuria)], infections, etc.; possible causes of infantile spasms at birth include: ischemic-hypoxic encephalopathy, birth injuries, intracranial hemorrhage, etc. Possible etiologies of postnatal pathogenesis include: central nervous system infection, traumatic brain injury, etc. Features of clinical spastic seizures: Spastic seizures are characterized by brief, synchronized movements of the head, trunk, and limbs, and sometimes independent movements of the head, trunk, or limbs. Such movements can be flexors, extensors, or a mixture of flexors and extensors [3]. The EEG is characterized by typical or variant peak rhythm disturbances. The typical peak rhythm disorder is characterized by almost continuous disorganized irregular spikes, multi-spikes, spikes and slow waves, spikes and slow waves, and slow waves. Variable peak rhythm disturbances may manifest as asymmetric peak rhythm disturbances, where one side has lower wave amplitude or slower wave rate than the opposite side; or they may manifest as relatively symmetric peak rhythm disturbances; or they may manifest as focal abnormal peak rhythm disturbances with focal spike and sharp wave activity; or they may manifest as peak rhythm disturbances on one side, or EEG resembling burst-inhibition, etc. Although the treatment of infantile spasticity has progressed considerably, the application of various treatment options has improved the effective control of spasticity. However, the delayed intellectual-motor development of the child after the onset of the disease still does not improve and is worse than before the onset of the disease. The side-effects of western drug treatment seriously affect the growth and development of the child.