In order to identify the brain lesions of symptomatic/cryptogenic partial epilepsies (S/CPEs) in infants and children, magnetic resonance imaging (MRI) studies, thorough encephalographic (EEGic) studies, and detailed clinical and neurologic evaluations were obtained in 300 infants and children who were diagnosed to have S/CPEs with onset before the age of 13 years during the past 7 years. The overall detection rate of brain lesions by MRI was 41.7% (125/300). Congenital malformations (18 cases), vascular malformations (9 cases), neurocutaneous syndromes (13 cases), and space-taking lesions (20 cases) constitute a large percentage of SPEs in infants and children. A variety of insults such as infection, ischemia, hemorrhage, trauma and metabolic disorders can result in destructive parenchymal loss lesions including porencephaly, focal atrophy, hemiatrophy, and diffuse brain atrophy (20 cases). Major etiologic factors leading to infarction, encephalomalacia, leukomalacia, included trauma, hvpoxicischemic encephalopathy (HIE), systemic lupus erythematosus (SLE), encephalitis, vasculitis, venous thrombosis, vasculopathies, and heart problems (22 cases). Mesial temporal sclerosis (MTS) could be evidenced in around 20% (18/95) of cases with temporal lobe epilepsy (TLE), which was strongly associated with past histories of febrile seizures and encephalitis complicated by status epileptics. However, cases with porencephaly, global atrophy or delayed myelination of unilateral temporal lobe on MRI were more related to HIE. With the advent of neuroimaging techniques, particularly MRI, a wide variety of underlying pathology can be detected as a cause of symptomatic partial epilepsies in pediatric patients. The occurrence of S/CPE indicates the presence of localized brain dysfunction, and many of the causes are potentially treatable. An orderly and thorough clinical and laboratory investigations, as well as neuroimaging studies should be made to diagnose and treat any underlying conditions.