INTRODUCTION AND EPIDEMIOLOGY
Unusual movements and changes in behavior in children often lead to an ED visit. Most seizure activity stops before the child is seen in an ED; therefore, history is key to the correct diagnosis. Although seizures account for many of these events, as many as 30% or more of paroxysmal events may be misdiagnosed as seizures.1,2
There are many different causes of pediatric seizures. The goal is to identify and treat the underlying cause. Some seizures require emergency management and extensive evaluation (e.g., status epilepticus, neonatal seizures), whereas others are common, benign, and need little or no ED evaluation (e.g., febrile seizures, first-time seizure in an otherwise well child). This chapter focuses on the diagnosis and management of ongoing seizures first and then discusses the approach to febrile seizures, neonatal seizures, and seizures in special populations (e.g., children with epilepsy, neurologic shunts, and trauma) under “Special Considerations/Populations.”
The prevalence of pediatric seizures in the United States is approximately 1% of all children up to the age of 14 years and is highest in children <1 year old (120 cases per 100,000) and in certain high-risk groups.2-4 Febrile seizures, the most common type of pediatric seizure, affect 3% to 4% of all children between 6 months and 5 years of age.5 Epilepsy is defined as recurrent unprovoked seizures.4,5 Roughly 326,000 American children <15 years old have epilepsy, and the lifetime prevalence of epilepsy is roughly 1%.3 The incidence of status epilepticus in developed countries is between 18 and 23 cases per 100,000 and is higher for younger children.6
Seizures represent abnormal, excessive, paroxysmal neuronal activity in the brain, primarily the cortex. Glutamate released from firing neurons activates N-methyl-D-aspartic acid receptors that subsequently initiate and propagate seizure activity.7 Seizures are inhibited by γ-aminobutyric acid, and failure of this inhibition facilitates seizure spread.8 Incomplete myelination of the brain may limit secondary generalization of seizure activity in young infants, and a relative imbalance between glutamate and γ-aminobutyric acid with paradoxical excitation from γ-aminobutyric acid makes younger children more susceptible to seizures.2,7
Seizures can be primary (unprovoked) or secondary (provoked).9,10 Primary seizures are often idiopathic or may be caused by congenital developmental abnormalities, in utero CNS insult (e.g., infection, infarct), or genetic factors. Secondary seizures may result from trauma or injury, infection, metabolic abnormalities (e.g., hypoglycemia, electrolyte abnormalities, inborn errors of metabolism), toxins, or systemic illness.10
The clinical manifestation of seizures depends on the area(s) of the brain that are affected and whether the seizure activity is localized (focal) or widespread (generalized). Generalized seizures involve both hemispheres of the brain and lead to loss of consciousness, usually followed by a period of postictal drowsiness. In convulsive generalized seizures or grand mal seizures, rhythmic motor activity affects both sides of the body.7 Nonconvulsive generalized seizures produce loss of ...