Seizures in neonates are common, with an incidence of 1 in 200 live births, and may represent primary central nervous system (CNS) disease or a systemic or metabolic disorder. Recent data suggest that seizure activity itself may adversely affect the growing brain. It is important to distinguish seizures from tremors or jitteriness, which may be seen in infants who have hypocalcemia, hypoglycemia, drug withdrawal, or no identifiable disease. Tremors are uniform, fine movements that respond to sensory stimuli, stop with manual stabilization, and do not occur spontaneously. They are not accompanied by eye, oral, or lingual movements. The types of neonatal seizures include subtle seizures, tonic seizures, multifocal clonic seizures, focal clonic seizures, and myoclonic seizures.
Subtle seizures occur in both preterm and term neonates. These seizures consist of ocular, facial, oral, or lingual movements and respiratory manifestations, such as apnea or stertorous breathing.
Tonic seizures are characteristic of premature infants. The seizures appear as decerebrate or decorticate posturing. There are sustained deviation of the eyes and assymetric posturing of the limbs and trunk.
Multifocal clonic seizures are seen in term infants. These are initially noted in one limb and migrate to another part of the body. There are rhythmic and slow movements at one to six times per second.
Focal clonic seizures are well localized and are accompanied by specific sharp activity on the electroencephalogram (EEG). These seizures occur more commonly in full-term infants.
Myoclonic seizures are expressed as single or multiple jerks of flexion of the upper or lower extremities. They are rare and occur in both premature and full-term infants.
CLINICAL FEATURES There are numerous causes of neonatal seizures. Hypoxic-ischemic encephalopathy is the most common cause of seizures. The seizures occur between 6 and 18 h of life. In full-term neonates, the hypoxic injury may result in a cerebral hemorrhage, watershed infarct, posterior fossa hematoma, or subarachnoid or subdural hemorrhage. In premature infants, hypoxic injury often results in periventricular-intraventricular hemorrhage. This type of seizure has a poor prognosis.
The metabolic disturbances associated with neonatal seizures include hypoglycemia, hypocalcemia, hypomagnesemia, hyperammonemia, hypernatremia, and hyponatremia. Hypoglycemia, hypocalcemia, and hypomagnesemia are often found in premature infants with perinatal asphyxia. Hypernatremia occurs in neonates with dehydration secondary to excessive fluid losses or treatment with large doses of sodium bicarbonate. Hyponatremia may be seen secondary to inappropriate ADH secretion or acute volume overload. Inborn errors of amino acid metabolism also may present as seizures.
Seizures can result from bacterial meningitis, and encephalitis associated with TORCH complex (toxoplasmosis, rubella, cytomegalovirus infection, and herpes simplex infection) or coxsackie B encephalitis. Developmental abnormalities including congenital hydrocephalus, microcephaly, and other congenital brain anomalies can cause seizures. Drug withdrawal from maternal use of methadone, barbiturates, alcohol, pentazocine (Talwin), and tripelannamine (Pyribenzamine) rarely presents as seizures. Pyridoxine dependence occurs rarely but must be considered in neonatal seizures unresponsive to standard therapy. A rare cause of neonatal seizures is inadvertent fetal scalp injection of maternal local anesthetic agents. Finally, neonatal stroke diagnosed by computed tomography (CT) has recently been described in term infants with focal motor seizures. Neonatal stroke may occur in the setting of diverse cerebrovascular disorders, such as hypoxic-ischemic encephalopathy, polycythemia, acute severe hypertension, and cocaine use.
A careful history, including intrapartum monitoring data and physical examination, is essential when considering drug withdrawal, birth asphyxia, or metabolic disorders as a cause of the seizures. A lumbar puncture with analysis of cell count, culture, and Gram stain along with blood specimens for culture and determinations of sugar, calcium, magnesium, and blood urea nitrogen (BUN) levels should be obtained. The skull x-ray, echoencephalogram, and EEG can be obtained after the seizures have been controlled. In a full-term infant, a CT scan of the head to look for ischemic injury may be necessary, since an echoencephalogram may not provide adequate visualization of the subarachnoid space or posterior fossa. Recently, positron emission tomography of the head has been utilized to evaluate the effects of asphyxia and seizures on cerebral blood flow.
TREATMENT Repeated seizures in neonates may be accompanied by hypoventilation and apnea, resulting in hypercapnia and hypoxemia. Increases in cerebral blood flow and arterial hypertension occur with neonatal seizures. Treatment of seizures should be initiated while awaiting results of laboratory data. An intravenous access route should be established immediately and the airway maintained; assisted ventilation should be initiated if apnea persists. Hypoglycemia and hypocalcemia should be treated as stated above. Hypomagnesemia is often associated with hypocalcemia and should be treated by intravenous administration of 2 to 4 mL of a 2 percent magnesium sulfate solution.
The anticonvulsant drugs used most frequently include phenobarbital and diphenylhydantoin. The loading dosage of phenobarbital is 20 mg/kg intravenously given slowly over 10 min, and the maintenance dose is 5 (mg/kg)/day intramuscularly or orally in two divided doses. If the initial 20 mg/kg dose of phenobarbital is not effective in controlling the seizures, additional doses of 5 mg/kg may be administered every 5 min until the seizures have ceased or the total dose of 40 mg/kg has been reached. In unresponsive cases, diphenylhydantoin may be administered with a similar loading dose followed by maintenance dose of 3 to 5 (mg/kg)/day by the intravenous route in only two divided doses 20 min apart to avoid disturbance of cardiac function. Lorazepam is recommended for status epilepticus as long as ventilation and blood pressure are supported. The dose of lorazepam is 0.01 mg/kg administered intravenously. Infants with pyridoxine dependence respond immediately to an intravenous injection of 50 to 100 mg of pyridoxine.
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