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Neonatal Seizures

  • Author: Raj D Sheth, MD; Chief Editor: Amy Kao, MD  more...
 
Updated: Apr 15, 2016
 

Background

The most prominent feature of neurologic dysfunction in the neonatal period is the occurrence of seizures. Determining the underlying etiology for neonatal seizures is critical. Etiology determines prognosis and outcome and guides therapeutic strategies.[1] (See Etiology, Prognosis, Treatment, and Medication.)

The neonatal period is limited to the first 28 days of life in a term infant. For premature infants, this term usually is applied until gestational age 44 weeks; ie, the age of the infant from conception to 44 weeks (ie, 4 wk after term).

Seizure characteristics

Most neonatal seizures occur over only a few days, and fewer than half of affected infants develop seizures later in life. Such neonatal seizures can be considered acute reactive (acute symptomatic), and therefore the term neonatal epilepsy is not used to describe neonatal seizures.[2]

Seizures in neonates are relatively common, with variable clinical manifestations. Their presence is often the first sign of neurologic dysfunction, and they are powerful predictors of long-term cognitive and developmental impairment. (See Prognosis.)

Most seizures in the neonate are focal, although generalized seizures have been described in rare instances.

Subtle seizures are more common in full-term than in premature infants. Video electroencephalogram (EEG) studies have demonstrated that most subtle seizures are not associated with electrographic seizures. Examples of subtle seizures include chewing, pedaling, or ocular movements.[3]

Neonatal seizure classification

Clonic seizures

These movements most commonly are associated with electrographic seizures. They often involve 1 extremity or 1 side of the body. The rhythm of the clonic movements is usually slow, at 1-3 movements per second.

Tonic seizures

These may involve 1 extremity or the whole body. Focal tonic seizures involving 1 extremity often are associated with electrographic seizures.

Generalized tonic seizures often manifest with tonic extension of the upper and lower limbs and also may involve the axial musculature in an opisthotonic fashion. Generalized tonic seizures mimic decorticate posturing; the majority are not associated with electrographic seizures.

Myoclonic seizures

These may occur focally in 1 extremity or in several body parts (in which case they are described as multifocal myoclonic seizures).

Focal and multifocal myoclonic seizures typically are not associated with electrographic correlates. Generalized myoclonic jerks are possibly the clinical equivalent of infantile spasms.

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Pathophysiology

The biochemical effects of neonatal seizures include derangements of energy metabolism. Energy-dependent ion pumps are compromised, and adenosine diphosphate (ADP) levels rise. The rise in ADP stimulates glycolysis with the ultimate increase in pyruvate, which accumulates as a result of compromised mitochondrial function.

Patient education

For patient education information, see the Brain and Nervous System Center, as well as Seizures in Children and Seizures Emergencies.

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Etiology

Seizures occur when a large group of neurons undergo excessive, synchronized depolarization. Depolarization can result from excessive excitatory amino acid release (eg, glutamate) or deficient inhibitory neurotransmitter (eg, gamma amino butyric acid [GABA]).

Hypoxic-ischemic encephalopathy

Another potential cause is disruption of adenosine triphosphate (ATP) ̶ dependent resting membrane potentials, which cause sodium to flow into the neuron and potassium to flow out of the neuron. Hypoxic-ischemic encephalopathy disrupts the ATP-dependent sodium-potassium pump and appears to cause excessive depolarization. It is an important cause of neonatal seizures.[1, 4]

Seizures resulting from hypoxic-ischemic encephalopathy may be seen in term and premature infants. They frequently present within the first 72 hours of life. Seizures may include subtle, clonic, or generalized seizures.

Hemorrhage

Intracranial hemorrhage occurs more frequently in premature than in term infants. Distinguishing infants with pure hypoxic-ischemic encephalopathy from those with intracranial hemorrhage often is difficult.

Subarachnoid hemorrhage is more common in term infants. This type of hemorrhage occurs frequently and is not clinically significant. Typically, infants with subarachnoid hemorrhage appear remarkably well.

Germinal matrix-intraventricular hemorrhage is seen more frequently in premature than in term infants, particularly in infants born prior to 34 weeks' gestation. Subtle seizures are seen frequently with this type of hemorrhage.

Subdural hemorrhage is seen in association with cerebral contusion. It is more common in term infants.

Metabolic disorders

Metabolic disturbances include hypoglycemia, hypocalcemia, and hypomagnesemia. Less frequent metabolic disorders, such as inborn errors of metabolism, are seen more commonly in infants who are older than 72 hours. Typically, they may be seen after the infant starts feeding.

Intracranial infections

Intracranial infections (which should be ruled out vigorously) that are important causes of neonatal seizures include meningitis, encephalitis (including herpes encephalitis), toxoplasmosis, and cytomegalovirus (CMV) infections. The common bacterial pathogens include Escherichia coli and Streptococcus pneumoniae.

Malformation syndromes

While most cerebral malformations present with seizures at a later age, major malformation syndromes are important to consider. Lissencephaly, pachygyria, polymicrogyria, and linear sebaceous nevus syndrome can present with seizures in the neonatal period.

Benign neonatal seizures

Benign neonatal seizure syndromes can be characterized by familial or idiopathic seizures. Benign familial neonatal seizures typically occur in the first 48-72 hours of life; the seizures disappear by age 2-6 months. A family history of seizures is usual. Development is typically normal in these infants.

Benign idiopathic neonatal seizures typically present at day 5 of life (ie, fifth day fits), with the vast majority presenting between days 4 and 6 of life. Seizures are often multifocal. Cerebrospinal fluid (CSF) analysis is usually unremarkable.

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Epidemiology

The incidence of neonatal seizures in the United States has not been clearly established, although an estimated frequency of 80-120 cases per 100,000 neonates per year has been suggested. The incidence of seizures is higher in the neonatal period (ie, the first 4 wk after birth) than at any other time of life.[5]

Age-related demographics

Neonatal seizures by definition occur within the first 4 weeks of life in a full-term infant and up to 44 weeks from conception for premature infants. Seizures are most frequent during the first 10 days of life.

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Prognosis

Prognosis is determined by etiology for neonatal seizures. If the EEG background is normal, the prognosis is excellent for seizures to resolve; normal development is likely.[6, 7]

Severe EEG background abnormalities indicate poor prognosis; such patients frequently have cerebral palsy and epilepsy. The presence of spikes on EEG is associated with a 30% risk of developing future epilepsy.

The prognosis following neonatal seizures that result from isolated subarachnoid hemorrhage is excellent, with 90% of children not having residual neurologic deficits.

Scoring system

Pisani et al devised a scoring system for early prognostic assessment after neonatal seizures. Analysis of 106 newborns who had neonatal seizures and were followed prospectively to 24 months' postconceptional age identified 6 independent risk factors for adverse outcome: (1) birth weight, (2) Apgar score at 1 minute, (3) neurologic examination at seizure onset, (4) cerebral ultrasonogram, (5) efficacy of anticonvulsant therapy, and (6) presence of neonatal status epilepticus.

Each variable was scored from 0 to 3 to represent the range from normal to severely abnormal; these were then added together to produce a total composite score, ranging from 0 to 12. A cutoff score of 4 or higher provided the greatest sensitivity and specificity for prediction of adverse neurologic outcome.[8]

Morbidity and mortality

Neonatal seizures are a risk factor that markedly increases rates of long-term morbidity and neonatal mortality. The presence of neonatal seizures is the best predictor of long-term physical and cognitive deficits. Complications of neonatal seizures may include the following:

  • Cerebral palsy
  • Cerebral atrophy
  • Hydrocephalus ex-vacuo
  • Epilepsy
  • Spasticity
  • Feeding difficulties
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Contributor Information and Disclosures
Author

Raj D Sheth, MD Chief, Division of Pediatric Neurology, Nemours Children's Clinic; Professor of Neurology, Mayo College of Medicine; Professor of Pediatrics, University of Florida College of Medicine

Raj D Sheth, MD is a member of the following medical societies: American Academy of Neurology, American Academy of Pediatrics, American Epilepsy Society, American Neurological Association, Child Neurology Society

Disclosure: Nothing to disclose.

Chief Editor

Amy Kao, MD Attending Neurologist, Children's National Medical Center

Amy Kao, MD is a member of the following medical societies: American Academy of Neurology, American Epilepsy Society, Child Neurology Society

Disclosure: Have stock from Cellectar Biosciences; have stock from Varian medical systems; have stock from Express Scripts.

Acknowledgements

Robert Stanley Rust Jr, MD, MA Thomas E Worrell Jr Professor of Epileptology and Neurology, Co-Director of FE Dreifuss Child Neurology and Epilepsy Clinics, Director, Child Neurology, University of Virginia; Chair-Elect, Child Neurology Section, American Academy of Neurology

Robert Stanley Rust Jr, MD, MA is a member of the following medical societies: American Academy of Neurology, American Epilepsy Society, American Headache Society, American Neurological Association, Child Neurology Society, International Child Neurology Association, and Society for Pediatric Research

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

References
  1. Volpe JJ. Hypoxic-Ischemic Encephalopathy: Biochemical and Physiological Aspects. Neurology of the Newborn. 4th ed. Philadelphia: WB Saunders; 2000. 217-276.

  2. Lombroso CT. Neonatal seizures: gaps between the laboratory and the clinic. Epilepsia. 2007. 48 Suppl 2:83-106. [Medline].

  3. Sheth RD. Electroencephalogram confirmatory rate in neonatal seizures. Pediatr Neurol. 1999 Jan. 20(1):27-30. [Medline].

  4. Silverstein FS, Jensen FE. Neonatal seizures. Ann Neurol. 2007 Aug. 62(2):112-20. [Medline].

  5. Sheth RD, Hobbs GR, Mullett M. Neonatal seizures: incidence, onset, and etiology by gestational age. J Perinatol. 1999 Jan. 19(1):40-3. [Medline].

  6. Sheth RD. Frequency of neurologic disorders in the neonatal intensive care unit. J Child Neurol. 1998 Sep. 13(9):424-8. [Medline].

  7. Sheth RD, Bodensteiner JB. Delayed postanoxic encephalopathy: possible role for apoptosis. J Child Neurol. 1998 Jul. 13(7):347-8. [Medline].

  8. Pisani F, Sisti L, Seri S. A scoring system for early prognostic assessment after neonatal seizures. Pediatrics. 2009 Oct. 124(4):e580-7. [Medline].

  9. Vigevano F. Benign familial infantile seizures. Brain Dev. 2005 Apr. 27(3):172-7. [Medline].

  10. Sheth RD, Buckley DJ, Gutierrez AR, et al. Midazolam in the treatment of refractory neonatal seizures. Clin Neuropharmacol. 1996 Apr. 19(2):165-70. [Medline].

  11. Cherian PJ, Deburchgraeve W, Swarte RM, De Vos M, Govaert P, Van Huffel S, et al. Validation of a new automated neonatal seizure detection system: a clinician's perspective. Clin Neurophysiol. 2011 Aug. 122(8):1490-9. [Medline].

  12. Sheth RD. Electroencephalogram in developmental delay: specific electroclinical syndromes. Semin Pediatr Neurol. 1998 Mar. 5(1):45-51. [Medline].

  13. Peliowski-Davidovich A,. Hypothermia for newborns with hypoxic ischemic encephalopathy. Paediatr Child Health. 2012 Jan. 17(1):41-6. [Medline].

  14. Shah DK, de Vries LS, Hellström-Westas L, Toet MC, Inder TE. Amplitude-integrated electroencephalography in the newborn: a valuable tool. Pediatrics. 2008 Oct. 122(4):863-5. [Medline].

  15. Natalucci G, Leuchter RH, Ulrich Bucher H, Latal B, Koller B, Hüppi PS, et al. Functional brain maturation assessed during early life correlates with anatomical brain maturation at term equivalent age in preterm infants. Pediatr Res. 2013 Apr 5. [Medline].

  16. Scher MS, Trucco GS, Beggarly ME, et al. Neonates with electrically confirmed seizures and possible placental associations. Pediatr Neurol. 1998 Jul. 19(1):37-41. [Medline].

  17. Sankar R, Painter MJ. Neonatal seizures: after all these years we still love what doesn't work. Neurology. 2005 Mar 8. 64(5):776-7. [Medline].

  18. Painter MJ, Scher MS, Stein AD, et al. Phenobarbital compared with phenytoin for the treatment of neonatal seizures. N Engl J Med. 1999 Aug 12. 341(7):485-9. [Medline].

  19. Sheth RD. Frequency of neurologic disorders in the neonatal intensive care unit. J Child Neurol. 1998 Sep. 13(9):424-8. [Medline].

 
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Onset of neonatal seizure demonstrating a focal onset in the right frontal (FP4) region. At this point, the child had head and eye deviation to the left.
Twenty seconds into a seizure that had focal onset in the right frontal (FP4) region, the seizure shows a rhythmic buildup of activity in the right frontocentral region.
This seizure had focal onset in the right frontal (FP4) region and subsequent buildup of activity in the right frontocentral region. As the seizure evolves, the electroencephalogram shows diffuse involvement of both cerebral hemispheres.
 
 
 
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