Epilepsy (EP) is one of the most common chronic nervous system disease in childhood and adolescence, with a prevalence rate of 7.6‰. About 3/4 of epilepsy patients begin to get sick in childhood. At present, there are many ways to treat epilepsy, such as oral anti-seizure medications (ASMs), surgical treatment, ketogenic diet, etc. However, ASMs are the preferred treatment for most epilepsy patients and the most important and basic treatment. Oxcarbazepine (OXC) and Lacosamide (LCM) are both sodium channel blockers. The former is a second-generation ASMs, a fast sodium channel blocker, while the latter is a third-generation ASMs, a slow sodium channel blocker. The rapid inactivation of sodium channel is mediated by the inner pore ball chain mechanism in milliseconds, which is helpful to the termination of action potential and the regulation of refractory period. It is the main inactivation mode under normal physiological conditions. Different from the rapid inactivation of sodium channels, the slow inactivation is in seconds per minute, which may involve the rearrangement of the inner pore structure and increase the excitability of the action potential threshold regulating membrane. Generally, under pathological conditions, sodium channels are more likely to enter the slow inactivation state. Now, OXC and LCM have been approved by the US Food and Drug Administration, the European Union Drug Administration, and the National Drug Administration of China for monotherapy or additive therapy of focal origin (with or without secondary generalized seizures) in epilepsy patients aged 4 years and above. This article will focus on the pharmacokinetics, efficacy, and safety of LCM and OXC in the treatment of childhood epilepsy.