Our objective was to determine the clinical spectrum of pediatric hemiparesis by identifying the relative frequency of various diagnoses and comorbid conditions seen in these children. Case records of all patients with hemiparesis in a single practice over an 11-year period were reviewed with reference to clinical features, etiologic determination, and comorbid conditions. Ninety-two children were identified: 73 (79.3%) had a congenital hemiparesis and 19 (20.7%) had an acquired hemiparesis. An abnormal perinatal history ( P = .003), prematurity ( P = .016), and younger age at onset of symptoms ( P < .001) were associated with a congenital hemiparesis. The overall etiologic yield was 83.7% (82.2% in the congenital and 89.5% in the acquired). The top four etiologic entities were cerebrovascular ischemia (40.2%), periventricular leukomalacia (18.5%), intracranial hemorrhage (16.3%), and cerebral dysgenesis (13%). Factors predictive of establishing an underlying etiology included birth prior to 34 weeks' gestation ( P = .034), global developmental delay ( P = .048), epilepsy ( P = .024), and having appropriate imaging modalities ( P = .001). Half of these children had a concurrent global developmental delay, associated epilepsy (odds ratio 3.67; 95% confidence interval 1.40—9.72), and prematurity (odds ratio 5.41; 95% confidence interval 1.56—18.80). A third of these children developed epilepsy. Multivariate predictive factors for epilepsy included global developmental delay (odds ratio 4.20; 95% confidence interval 1.44—12.27), cerebrovascular ischemia (odds ratio 5.10; 95% confidence interval 1.76—14.77), and term birth (odds ratio 3.87; 95% confidence interval 1.20—12.56). The majority of children with hemiparesis have a congenital etiology. The diagnostic yield is higher than previously reported; however, specific underlying etiologies need to be better determined. Comorbid conditions of global developmental delay and epilepsy have a high prevalence in this population, contributing to overall morbidity. ( J Child Neurol 2005;20:471—476).