Chapter 135: Seizures in Infants and Children

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

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 the approach to febrile seizures, neonatal seizures, and seizures in special populations (e.g., children with epilepsy, neurologic shunts, and trauma) are discussed under Special Considerations/Populations.

The incidence of new-onset pediatric seizure in the United States is approximately 120,000 cases per year and is highest in children <2 years and in certain high-risk groups.² Febrile seizures are the most common type of pediatric seizure, affecting 2% to 5% of all children between 6 months and 5 years of age.³ Epilepsy is diagnosed when a patient has one or more unprovoked seizures.^4,5 Roughly 326,000 children <15 years have epilepsy, and 1% of the population can be expected to have epilepsy by the age of 20.² The incidence of status epilepticus in developed countries is between 17 and 23 cases per 100,000 and is higher for younger children.⁶

PATHOPHYSIOLOGY

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 gamma-aminobutyric-acid, and failure of this inhibition facilitates seizure spread.⁷ Incomplete myelination of the brain may limit secondary generalization of seizure activity in young infants, and a relative imbalance between glutamate and gamma-aminobutyric-acid with paradoxical excitation from gamma-aminobutyric-acid makes younger children more susceptible to seizure activity.

Seizures can be primary (intrinsic) or secondary (the result of another process). Primary seizures are often idiopathic or may be caused by congenital developmental abnormalities, in utero central nervous system 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.

CLINICAL FEATURES

TYPES OF SEIZURE

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. ...