Table 2.

Summary of the Animal Models of Infantile Spasms

	How model is created	Age	Seizure/ictal EEG	Interictal EEG
CRH model	CRH intraperitoneally or intracerebroventricularly	P5-P22	Limbic seizure/show rhythmic, sharp activity
NMDA model	NMDA antagonist intraperitoneally	P10 and P15	Hyperflexion and tonic spasms of the entire body/generalized amplitude reduction	Large-amplitude, nonsynchronous waves	Spasms start earlier and occur in greater numbers when the rats are prenatally exposed to betamethasone or restraint stress
TTX model	Chronic intrahippocampal infusion of tetrodotoxin	28 Days of infusion starting at P10	P21: Flexor or extensor spasms/generalized slow wave followed by voltage attenuation and then low-voltage fast activity	High-voltage, slow waves and multi-spikes
Multiple hit model	Doxorubicin intraperitoneally and lipopolysaccharide intracerebral on P3, then p-chlorophenylalanine intraperitoneally on P5	Induction at P3-P5	P7-P12: clusters of spasms/EEG decrement
Ts65Dn mice	GABAB receptor agonists intraperitoneally to Ts65Dn mice	2 month-old mice	Clusters of extensor spasms/polyspike-wave bursts and electrodecrement
ARX mutation model	Targeted deletion of ARX gene from cortical interneurons	P12 start by partial seizure	Cluster of spasms/sharp spike-slow wave transients followed by attenuation of background activity	An increase in high-frequency background rhythmic activity

ARX = Aristaless-related homeobox; CRH = corticotropin-releasing hormone; EEG = electroencephalographic; GABAB = gamma-aminobutyric acid receptor type B; NMDA = N-Methyl-D-aspartate; TTX = tetrodotoxin