Table 1.

Disease timeline and therapeutic interventions/outcomes.

Age	Clinical descriptions
At birth	The patient was born at 40 weeks by natural delivery, with a weight of 3320 g and height of 50 cm, passing newborn screenings of foot blood and hearing. The mother of the patient had hypothyroidism and was treated with oral Eucalyptus during pregnancy. The patient was breastfed for 1 month after birth, and then on artificial feeding. Immunization was performed according to local regulations, without any noted adverse reactions. His parents were healthy and there was no family history of epilepsy or other genetic disorders.
Shortly after birth	Clustered seizures like nodding and hugging multiple times a day, more than 10 at a time and each lasting 1–2 min.
1.5 months	Bilateral or unilateral limb tonic seizures or tonic-clonic seizures occurred, more than 10 times a day and each time lasting 2–10 s.
2 months	Hospital admission and diagnosis of Ohtahara syndrome based on burst-suppression electroencephalogram (EEG). Physical examination at admission revealed consciousness, poor response, ability to suck, inability to eye-track or to hold the head up. Eye examinations revealed slight esotropia, pupils on both sides of equal size and circle, diameters at about 2 mm, and with light reflex. Further tests showed stable breathing, inspiratory depression in the suprasternal fossa, normal heart and lung auscultation, soft abdomen, and no palpable enlargement of the liver or spleen under the ribs. Besides, the neck was soft, the muscle strength and muscle tone of the limbs were low, the bilateral Babinski sign was negative, and there was a livedo about 2 cm*2 cm on the back. Blood biochemical examinations and genetic metabolism screening also revealed nothing remarkable in lactate, blood ammonia, ceruloplasmin, thyroid function, blood liver and kidney function, electrolytes, and blood sugar. Treatment with oral Adrenocorticotropic Hormone (ACTH), topiramate, and valproic acid.
2 months and 3 weeks	Poor outcome (EEG) and severe pulmonary infection resulted in admission to the Pediatric Intensive Care Unit; ACTH ended and prednisone acetate tablets added; topiramate and valproic acid continued.
	One STXBP1 variant identified through genetic testing; oral levetiracetam and midazolam micropump added, prednisone acetate and topiramate continued, valproic acid reduced and withdrawn.
3 months	Seizures under control (EEG) and reduced to 1–3 times a day; midazolam withdrawn and oral clonazepam tablets added (both midazolam and clonazepam are benzodiazepines).
	Discharge from hospital with prednisone acetate tablets, topiramate, levetiracetam oral liquid, and clonazepam tablets; seizures under control.
4 months	Seizure attacks were in the form of binocular staring, with or without rigidity of both upper limbs, 3–4 times a day.
5 months	The symptoms were similar to those at 4 months, with reduced seizure attacks at once every 2–3 days and improved EEG; prednisone acetate tablets withdrawn and topiramate gradually reduced, whereas oral levetiracetam liquid and clonazepam continued.
6 months	Seizures were under control and occurred once every 10 days. EEG findings significantly improved, but the development was still markedly behind. The muscle strength and muscle tone of the limbs were low.