Introduction

Aseizure is a result of sudden variations in neuronal electrical discharges in the central nervous system (CNS) that causes a behavioral or functional change in a neonate. A neonate has a decreased seizure threshold compared to other pediatric patients due to hyper-excitability of an immature brain.^1–3 In fact, neonatal seizures occur in 1.8 to 3.5 patients per 1,000 neonates. In very low birth weight neonates, the incidence increases drastically to 19 to 57.7 patients per 1,000 neonates.^4–6

Pathophysiology

There is a balance between excitatory and inhibitory neurotransmitters andelectrolyte-based pathways in mature brains. The immature brain pathways are imbalanced, promoting brain development and increasing risk of seizures.² The intrinsic factors related to excitatory pathways are increased N-methyl-D aspartate glutamate receptors, α-amino-3-hydroxyl-5-methyl-4-isoxazolepropionic acid glutamate receptors, metabotropic glutamate receptors, gamma-aminobutyric acid (GABA) transporters, and corticotropin-releasing factors. The inhibitory pathway intrinsic factors are decreased glutamate transporters, neuropeptide Y, and adenosine. There are also variable GABA_B receptors; the GABA_A receptors are depolarizing, which decreases the inhibitory pathway function.^2,3 Head traumas during delivery, neonatal CNS infections, metabolic abnormalities, intracranial hemorrhages,hypoxic-ischemic brain injuries, and toxin exposures or withdrawals are extrinsic factors that may lead to neonatal seizures.^1,3 (CNS infection treatments are discussed in Chapter 10 for group B Streptococcus and Escherichia coli and in Chapter 11 for toxoplasmosis, cytomegalovirus, and herpes simplex virus infections.) Metabolic abnormalities that increase the risk of neonatal seizures include hypocalcemia, hypoglycemia, hypomagnesemia, inborn errors of metabolism, and pyridoxine deficiency. Hypoxic-ischemic brain injuries and intracranial hemorrhages account for 50 to 65% and 15% of neonatal seizures, respectively.¹

Presentation

Distinguishing between seizures or jitteriness in neonates is often difficult. A simple approach to differentiating between the two is to suppress the movement. If the movement ceases, the neonate is not having a seizure. Jitteriness is also initiated by an acute stimulation event.⁷ Neonatal seizures are divided into five main categories or types:

1.clonic

2.myoclonic

3.spasms

4.subtle

5.tonic

Generalized clonic seizures are uncommon in neonates due to partial myelination in immature brains. Most clonic seizures in neonates are either focal or multifocal, resulting in jerking of limbs.

Myoclonic seizures are generalized, focal, or multifocal in nature. The rapidness and nonrhythmic jerkiness distinguishes myoclonic from clonic neonatal seizures. Generalized myoclonic seizures consist of bilateral jerking of mainly upper limbs. Focal myoclonic seizures typically affect upper extremities. Multi-focal myoclonic seizures involve multiple asynchronous movements. Generalized and focal myoclonic seizures often have an association with electroencephalogram (EEG) changes.

Spasms are short, generalized jerks associated with a single neuronal firing.

Subtle neonatal seizures involve abnormal movements of extremities, eyes, or mouth in a rhythmic pattern. Other characteristics of subtle seizures are brief periods of hypertension, apnea, and heart rate variation.

Generalized tonic neonatal seizures are more common than focal tonic seizures. Generalized tonic seizures include flexion or extension of both upper and lower limbs. Focal tonic seizures involve posturing of the neck, trunk, or extremity with eye deviation.^7,8

Evaluation and Diagnosis

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