Neonatal seizure

Seizures in the neonatal population often present differently than in other age groups due to brain immaturity.{{Cite journal|last1=Al-Fraik|first1=Nasren Gamal Saleh|last2=Al-Khurum|first2=Khadeejah Miftah Ali|title=Neonatal Seizure in Tobruck Medical Center|date=2020-09-27|journal=Scientific Journal of Applied Sciences of Sabratha University|volume=3|issue=2|language=en|pages=13–24|doi=10.47891/sabujas.v3i2.13-24|s2cid=229010547|issn=2708-7301|doi-access=free}} Electroclinical seizures are defined by evidence of seizure activity on electroencephalogram as well as clinical signs or symptoms.{{Cite journal|last1=Pressler|first1=Ronit M.|last2=Cilio|first2=Maria Roberta|last3=Mizrahi|first3=Eli M.|last4=Moshé|first4=Solomon L.|last5=Nunes|first5=Magda L.|last6=Plouin|first6=Perrine|last7=Vanhatalo|first7=Sampsa|last8=Yozawitz|first8=Elissa|last9=Vries|first9=Linda S. de|last10=Vinayan|first10=Kollencheri Puthenveettil|last11=Triki|first11=Chahnez C.|date=2021|title=The ILAE classification of seizures and the epilepsies: Modification for seizures in the neonate. Position paper by the ILAE Task Force on Neonatal Seizures|url=https://onlinelibrary.wiley.com/doi/abs/10.1111/epi.16815|journal=Epilepsia|language=en|volume=62|issue=3|pages=615–628|doi=10.1111/epi.16815|pmid=33522601|hdl=10138/341148 |s2cid=231762346|issn=1528-1167|hdl-access=free}}

Classification systems have been developed based on neonatal seizure motor manifestations, summarized below.{{Cite journal|last=Scher|first=Mark S.|date=December 1998|title=Diagnosis and management of neonatal seizures.By Eli M. Mizrahi and Peter Kellaway Philadelphia, Lippincott-Raven, 1998 192 pp, illustrated, $79.00|journal=Annals of Neurology|volume=44|issue=6|page=988|doi=10.1002/ana.410440628|issn=0364-5134}}

• Focal or multifocal clonic

Clonic seizures are defined by repetitive contractions of groups of muscles, typically of the limbs, face, or trunk.{{Citation|last1=Abend|first1=Nicholas S.|title=Chapter 12 - Neonatal Seizures|date=2018-01-01|url=https://www.sciencedirect.com/science/article/pii/B9780323428767000120|work=Volpe's Neurology of the Newborn (Sixth Edition)|pages=275–321.e14|editor-last=Volpe|editor-first=Joseph J.|publisher=Elsevier|language=en|doi=10.1016/b978-0-323-42876-7.00012-0|isbn=978-0-323-42876-7|access-date=2022-02-06|last2=Jensen|first2=Frances E.|last3=Inder|first3=Terrie E.|last4=Volpe|first4=Joseph J.|editor2-last=Inder|editor2-first=Terrie E.|editor3-last=Darras|editor3-first=Basil T.|editor4-last=de Vries|editor4-first=Linda S.|url-access=subscription}} These may involve one group of muscles (focal) or multiple groups of muscles (multifocal). An isolated focal seizure can move or spread, and can even alternate from one side of the body to the other. If they occur on both sides of the body, they may occur simultaneously in an asynchronous manner.{{Cite book|author1=Blaise F. Bourgeois|url=https://books.google.com/books?id=47fckyBY2XwC|title=Pediatric Epilepsy: Diagnosis and Therapy|author2=Edwin Dodson|author3=Douglas R. Nordli Jr|author4=John M. Pellock|author5=Raman Sankar|date=2007-12-16|publisher=Demos Medical Publishing|isbn=978-1-934559-86-4|language=en}} If a multifocal seizure, is limited to muscles of one side of the body, it may occur synchronously or asynchronously. Focal clonic seizures cannot be suppressed by repositioning of limbs or by physical suppression.{{Cite journal|last=Volpe|first=Joseph J.|date=1989-09-01|title=Neonatal Seizures: Current Concepts and Revised Classification|journal=Pediatrics|volume=84|issue=3|pages=422–428|doi=10.1542/peds.84.3.422|pmid=2671912|s2cid=39194127|issn=0031-4005}} Due to the neonatal brain's immaturity, the typical Jacksonian march may not occur. Focal seizures typically have very close correlates on EEG, with measurable EEG abnormalities with each seizure movement. The rhythm of the clonic movements and EEG abnormalities is usually slow, at 1-3 movements per second.

• Focal tonic

Focal tonic seizures are characterized by sustained muscle contraction of facial, limb, axial, and other muscle groups. It often involves asymmetric positioning of the neck and trunk and appears as abnormal posturing of a single limb. Horizontal eye deviation may or may not be involved. They may be symmetric, asymmetric, focal, or multifocal. Such seizures cannot be provoked by stimulation or suppressed by restraint.

• Generalized tonic

A focal tonic seizure can generalize, or the first seizure can occur as a generalized seizure, or seizures that impair the neonate's level of consciousness. Generalized tonic seizures typically appear as symmetric and sustained posturing of limbs in either an extensor or flexor distribution. Generalized tonic seizures often manifest with the 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.Such seizures can be initiated by stimulation and can be suppressed by restraint.

• Myoclonic

Myoclonic movements can either be caused by seizures or be benign neonatal sleep myoclonus, a common mimicker of seizures in neonates. Myoclonic seizures are characterized by isolated and fast contractions of muscle groups that are non-repetitive. It generally involves flexor muscle groups of upper extremities- trunk, diaphragm, face.{{Citation|last1=Krawiec|first1=Conrad|title=Neonatal Seizure|date=2022|url=http://www.ncbi.nlm.nih.gov/books/NBK554535/|work=StatPearls|place=Treasure Island (FL)|publisher=StatPearls Publishing|pmid=32119422|access-date=2022-02-06|last2=Muzio|first2=Maria Rosaria}} These movements typically occur in the limbs or face. Stimulation can provoke myoclonic seizures.

• Spasms

Spasms include either flexor or extensor or both flexor and extensor. These occur in clusters and cannot be provoked by stimulation or suppressed by restraint.

Some clinicians use the term subtle seizures to describe seizures that appear to be more normal and there is an absence of distinct tonic or clonic movements but the presence of abnormal eye movements, stereotyped lip-smacking, or apneic events.{{Cite book|last=Panayiotopoulos|first=C. P.|url=https://www.ncbi.nlm.nih.gov/books/NBK2599/|title=Neonatal Seizures and Neonatal Syndromes|date=2005|publisher=Bladon Medical Publishing|language=en}} They may be difficult to diagnose clinically due to the subtleness of symptoms. Sometimes in subtle seizures complex limbic hyperactivity that is purposeless along with crying could be observed.

Benign neonatal seizures are not classified as epilepsy and the seizures usually resolve after 1–4 months.{{cite book|title=The Epilepsies: The diagnosis and management of the epilepsies in adults and children in primary and secondary care|publisher=National Clinical Guideline Centre|chapter=9|pages=119–129|chapter-url=http://www.nice.org.uk/nicemedia/live/13635/57784/57784.pdf|author=National Institute for Health and Clinical Excellence|date=January 2012}} A benign familial neonatal seizure onsets as early as 3 days of birth and may involve one or both sides of the brain. Recurrent seizure episodes are observed to occur in neonates. Electroencephalogram of infants with BFNS often have normal readings. Sometimes, they may show theta pointy, a specific abnormality. They usually begin with tonic stiffening accompanied by apnea. Later clonic jerks are witnessed. It occurs in 1 in every 1,00,000 newborns.{{Cite web|title=Benign familial neonatal seizures: MedlinePlus Genetics|url=https://medlineplus.gov/genetics/condition/benign-familial-neonatal-seizures/|access-date=2022-02-13|website=medlineplus.gov|language=en}}

This condition is usually inherited and is passed on in autosomal dominant manner. This condition is also caused due to mutation in KCNQ2 or KCNQ3 gene that may be carried by people bearing no family history of benign familial neonatal seizure. Mutation in these genes lead to excessive excitability of neurons.

Most of the infants with BFNS develop normally but some neonates with it may later develop intellectual disability which becomes evident in early childhood. In some patients approximately 15%, epilepsy recurs later in life. Myokymia is also witnessed in a few cases.

Seizures in the developing brain are more common than in a mature brain for several reasons. First, the developing brain is hyperexcitable due to excess in excitatory glutaminergic neurons and immaturity of inhibitory gamma-amino butyric acid (GABA) neurons. Preterm infants are at especially high risk for seizures for this reason. During the neonatal developmental stages, numerous pathophysiological mechanisms, lead to excessive excitation and reduced inhibition, which lowers their seizure threshold when compared with that of adults. This has been proved in animal (rodent) models wherein the adult and infant models are administered with the chemoconvulsant agent and their threshold seizure potential is compared.{{Cite journal|last1=Stafstrom|first1=Carl E.|last2=Thompson|first2=James L.|last3=Holmes|first3=Gregory L.|date=February 1992|title=Kainic acid seizures in the developing brain: status epilepticus and spontaneous recurrent seizures|journal=Developmental Brain Research|volume=65|issue=2|pages=227–236|doi=10.1016/0165-3806(92)90184-x|pmid=1572066|issn=0165-3806}} This lowered seizure threshold potential makes the neonatal brain susceptible to acute symptomatic seizures.

• Seizure risk due to decreased inhibition: Gamma-butyric acid (GABA) is the main inhibitory neurotransmitter in adult humans. Upon binding with its receptor i.e. GABAa, it causes hyperpolarisation of the neuronal membrane by causing the net influx of chloride ions. This hyperpolarisation leads to inhibition of further action potentials. However, in neonates, there is a relatively high expression of NKCC1(sodium-potassium-chloride cotransporter 1) than KCC2(potassium-chloride cotransporter 2). NKCC1 causes net efflux of chloride ions{{Cite journal|last1=Dzhala|first1=Volodymyr I.|last2=Talos|first2=Delia M.|last3=Sdrulla|first3=Dan A.|last4=Brumback|first4=Audrey C.|last5=Mathews|first5=Gregory C.|last6=Benke|first6=Timothy A.|last7=Delpire|first7=Eric|last8=Jensen|first8=Frances E.|last9=Staley|first9=Kevin J.|date=November 2005|title=NKCC1 transporter facilitates seizures in the developing brain|journal=Nature Medicine|volume=11|issue=11|pages=1205–1213|doi=10.1038/nm1301|issn=1078-8956|pmid=16227993|s2cid=25348736}} while KCC2 is responsible for causing a net influx of chloride ions. Increased expression of NKCC1 leads to depolarisation of the neuronal membrane. This depolarisation removes voltage-dependent Mg from N-methyl-D-aspartate(NMDA) receptors and triggers calcium influx. The binding of calcium to the receptors causes the generation of secondary messengers that increases the risks of seizures and increase the excitability of the brain.{{Cite journal|last1=Nardou|first1=Romain|last2=Ferrari|first2=Diana C.|last3=Ben-Ari|first3=Yehezkel|date=2013-08-01|title=Mechanisms and effects of seizures in the immature brain|url=https://www.sciencedirect.com/science/article/pii/S1744165X13000115|journal=Seminars in Fetal and Neonatal Medicine|series=Neonatal seizures|language=en|volume=18|issue=4|pages=175–184|doi=10.1016/j.siny.2013.02.003|pmid=23702158|issn=1744-165X|url-access=subscription}}{{Cite journal|last1=Rivera|first1=C.|last2=Voipio|first2=J.|last3=Payne|first3=J. A.|last4=Ruusuvuori|first4=E.|last5=Lahtinen|first5=H.|last6=Lamsa|first6=K.|last7=Pirvola|first7=U.|last8=Saarma|first8=M.|last9=Kaila|first9=K.|date=1999-01-21|title=The K+/Cl- co-transporter KCC2 renders GABA hyperpolarizing during neuronal maturation|journal=Nature|volume=397|issue=6716|pages=251–255|doi=10.1038/16697|issn=0028-0836|pmid=9930699|bibcode=1999Natur.397..251R|s2cid=7687596}}
• Seizure risk due to increased activation: Glutamate is the primary excitatory neurotransmitter and the expression of its receptor is developmentally regulated.{{Cite journal|last1=Monyer|first1=Hannah|last2=Burnashev|first2=Nail|last3=Laurie|first3=David J.|last4=Sakmann|first4=Bert|last5=Seeburg|first5=Peter H.|date=March 1994|title=Developmental and regional expression in the rat brain and functional properties of four NMDA receptors|journal=Neuron|volume=12|issue=3|pages=529–540|doi=10.1016/0896-6273(94)90210-0|pmid=7512349|s2cid=26733598|issn=0896-6273}} It binds to NMDA receptors, kainite receptors, and AMPA receptors. In course of the developmental stages, in several parts of the brain, a subunit of NMDA receptor-GluN2B is highly expressed which increases calcium influx. This mechanism increases the duration of postsynaptic currents in the immature brain in comparison to adult brains.{{Cite journal|last1=Carrasco|first1=Melisa|last2=Stafstrom|first2=Carl E.|date=2018|title=How Early Can a Seizure Happen? Pathophysiological Considerations of Extremely Premature Infant Brain Development|journal=Developmental Neuroscience|volume=40|issue=5–6|pages=417–436|doi=10.1159/000497471|issn=1421-9859|pmid=30947192|s2cid=96432850|doi-access=free}}

Neonatal seizures have a number of causes. Determining the cause of a confirmed seizure is important because treatment and prognosis vary based on underlying etiology of the seizure. In contrast to seizures that occur in other age groups, seizures that occur during the neonatal period are most often caused by the following processes:

• Hypoxic-ischemic encephalopathy: This is the most common cause of seizures in the neonatal period,{{cite journal | vauthors = Vasudevan C, Levene M | title = Epidemiology and aetiology of neonatal seizures | journal = Seminars in Fetal & Neonatal Medicine | volume = 18 | issue = 4 | pages = 185–91 | date = August 2013 | pmid = 23746578 | doi = 10.1016/j.siny.2013.05.008 }} causing approximately 33% of neonatal seizures. The onset of seizure associated with it occurs within first 12 to 24 hrs of life.{{Citation needed|date=October 2023}} Delays in diagnosis may further increase the brain injury.{{Citation needed|date=October 2023}} Seizure semiology and severity varies with the location and size of injured region of the brain.
• Perinatal arterial stroke: Arterial stroke can be caused by intra-arterial thrombosis or embolism from the heart or placenta. The risk for perinatal arterial stroke increases with a variety of conditions that occur due to material factors during birth (oligohydramnios, chorioamnionitis, placental abnormalities) or neonatal factors (clotting disorders, congenital heart defects, coagulation problems, systemic infection, male sex, placental abnormalities). The onset of seizures associated with focal strokes begin after 24hrs to 48 hrs of birth. Focal clonic seizure is generally associated with it due to involvement of motor cortex in middle cerebral artery region.{{Citation needed|date=October 2023}}
• Intraventricular hemorrhage: This consists of bleeding in the ventricles, which are interior chambers of the brain. This is the most common cause of neonatal seizures in preterm infants.
• Central nervous system infection: CNS Infection are found in 3-10% of neonates who seize. Bacterial meningitis and viral meningoencephalitis are most prevalent, though fungal infections can occur as well. Infections caused by Group B streptococcus and herpes simplex virus are also possible causes. Seizures related to it persist longer than those associated with HIE or ICH.{{Citation needed|date=October 2023}}
• Congenital central nervous system malformations: lissencephaly, polymicrogyria, and tuberous sclerosis are specific entities known to cause seizures due to defects in brain tissue development. These are responsible for approximately 9% of cases of neonatal seizures.
• Inborn errors of metabolism: Inborn errors of metabolism can cause physiologic conditions that result in seizures. These errors are genetic and often are accompanied by other symptoms such as lethargy, poor feeding, and low tone. Diagnosis often involves specific laboratory tests of metabolic products as well as genetic tests. Several classification systems exist for seizures caused by inborn errors of metabolism, one of which separates causes into problems with neurotransmitter metabolism, energy production, and biosynthetic substances crucial for brain formation.{{cite journal | vauthors = Van Hove JL, Lohr NJ | title = Metabolic and monogenic causes of seizures in neonates and young infants | journal = Molecular Genetics and Metabolism | volume = 104 | issue = 3 | pages = 214–30 | date = November 2011 | pmid = 21839663 | doi = 10.1016/j.ymgme.2011.04.020 }}
• Electrolyte abnormalities: Metabolic abnormalities such as hypoglycemia, hyponatremia, and hypocalcemia can manifest as seizures.
• Substance-related: neonatal abstinence syndrome occurs when maternal drug use before birth results in a fetal withdrawal syndrome. Substances include alcohol, cocaine, narcotics, tricyclclic antidepressants, or other sedatives. Seizures can be prevented from occurring if the symptoms of withdrawal are recognized and treated early.

File:Normal CFM trace.jpg

Seizure activity in a neonate is difficult to diagnose, as many seizures have subtle clinical symptoms. Diagnosis relies on a combination of brain monitoring (electroencephalography)(EEG) and observing clinical signs or symptoms of a seizure. EEG may be continuous or intermittent, and it may also be combined with video recording of the infant to correlate any seizure movements with EEG recordings.

There are several modes of EEG that are commonly used to diagnose neonatal seizures. Conventional continuous multichannel conventional EEG is the gold standard for diagnosis of epileptiform activity, but requires expert interpretation. Newer amplitude integrated EEG (aEEG) (also termed cerebral function monitoring, or CFM) allows easier monitoring of brain activity, but may not allow identification of short duration, low amplitude, or very high frequency seizure activity.{{cite journal | vauthors = Boylan GB, Stevenson NJ, Vanhatalo S | title = Monitoring neonatal seizures | journal = Seminars in Fetal & Neonatal Medicine | volume = 18 | issue = 4 | pages = 202–8 | date = August 2013 | pmid = 23707519 | doi = 10.1016/j.siny.2013.04.004 }} Often, both modes are displayed concurrently.

Evaluation for infection (often with blood counts, blood cultures, or lumbar puncture) may be done to determine if there is a secondary cause of seizures. Blood glucose and electrolyte testing can identify metabolic problems that can be corrected. Further testing includes evaluation for genetic causes and other more rare metabolic causes.{{cite journal | vauthors = Glass HC | title = Neonatal seizures: advances in mechanisms and management | journal = Clinics in Perinatology | volume = 41 | issue = 1 | pages = 177–90 | date = March 2014 | pmid = 24524454 | pmc = 3925308 | doi = 10.1016/j.clp.2013.10.004 }} Genetic testing may be done with an epilepsy gene panel to determine presence of neonatal primary genetic epilepsy syndromes. Brain injury such as cerebral infarction or hemorrhage can be evaluated with imaging techniques such as magnetic resonance imaging (MRI) and brain ultrasound.

Infants can exhibit stereotyped movements that may be hard to distinguish from seizure activity. Since many of these non-seizure movements are not dangerous and require no treatment, differentiation from actual seizure activity is useful.{{Citation needed|date=October 2023}} Jitteriness is common in the neonatal period and is seen in upwards of 2/3 of neonates. It is characterized by a tremor that is especially prominent during sleep or periods of agitation.

{{Citation needed|date=October 2023}} Gaze deviation or eye movements do not occur. Benign neonatal sleep myoclonus (BNSM) is another common movement that can be mistaken for a seizure. It is characterized by jerking limb movements only during sleep, and stop with waking of the infant.

Once diagnosis is made, the goals of management are to identify the cause of the seizure, stop the seizure activity, and maintain physiologic parameters such as oxygenation, ventilation, blood glucose, and temperature.

Treatment greatly depends on the cause of the seizure. For example, infectious causes of seizures (meningitis, meningoencephalitis), are often treated with antimicrobials. Similarly, electrolyte or glucose abnormalities are treated by correcting the underlying abnormality.

If the cause of the seizures are unlikely to be easily or quickly corrected, once diagnosis of a seizure is made, the mainstay of treatment is pharmacotherapy with anti-epileptic drugs. Phenobarbital is the first line anti-seizure medication in neonatal seizures, regardless of the cause of the seizure. Phenytoin, levetiracetam, midazolam and lidocaine are used as second line agents. Almost 66% of patients with acute symptomatic seizures, don't have a complete response to the initial dose administered regardless of the medication.{{Cite journal |last1=Ziobro |first1=Julie |last2=Shellhaas |first2=Renée A. |date=April 2020 |title=Neonatal Seizures: Diagnosis, Etiologies, and Management |url=http://www.thieme-connect.de/DOI/DOI?10.1055/s-0040-1702943 |journal=Seminars in Neurology |language=en |volume=40 |issue=2 |pages=246–256 |doi=10.1055/s-0040-1702943 |pmid=32143234 |s2cid=212621495 |issn=0271-8235|url-access=subscription }}

Term or near term infants with moderate to severe hypoxic ischemic encephalopathy causing neonatal seizures may be treated with therapeutic hypothermia.

With prompt diagnosis, mortality after diagnosis of neonatal seizures has decreased dramatically from an estimated 33% in the 1990s to around 10% in the 2010s.{{cite journal | vauthors = Uria-Avellanal C, Marlow N, Rennie JM | title = Outcome following neonatal seizures | journal = Seminars in Fetal & Neonatal Medicine | volume = 18 | issue = 4 | pages = 224–32 | date = August 2013 | pmid = 23466296 | doi = 10.1016/j.siny.2013.01.002 }} Underlying cause of the seizure remains the greatest predictor of ongoing seizures and neurologic problems later in life. Controversy remains with the extent of damage the seizures themselves cause. Clinician consensus is that frequent or intractable seizures (status epilepticus) leads to neuronal damage and are associated with later neurodevelopment problems.{{cite journal | vauthors = Clancy RR, Legido A | title = Postnatal epilepsy after EEG-confirmed neonatal seizures | journal = Epilepsia | volume = 32 | issue = 1 | pages = 69–76 | date = February 1991 | pmid = 1985832 | doi = 10.1111/j.1528-1157.1991.tb05614.x | s2cid = 25884790 }}

Infants that are premature, have hypoxemic ischemic encephalopathy, CNS infection, severe intraventricular hemorrhage, structural central nervous system defect, or severely abnormal EEG tracings have a worse prognosis.

Low Apgar scores, need for resuscitation at birth, and perinatal distress place the neonate at greater risk for seizures{{Cite journal|title=Elsevier Enhanced Reader|url=https://reader.elsevier.com/reader/sd/pii/S1525505020302547?token=99482587F0CBB3FA939B7A2DBD3927F5D85C6878E9F3F40601702A429C1186C76BF4B2D93FFD0816FFD905D4D89F8E1D&originRegion=us-east-1&originCreation=20210921135122|access-date=2021-09-21|journal=Epilepsy & Behavior|date = June 2020|volume = 107|page = 107075|doi = 10.1016/j.yebeh.2020.107075|language=en|last1 = Pisani|first1 = Francesco|last2 = Facini|first2 = C.|last3 = Bianchi|first3 = E.|last4 = Giussani|first4 = G.|last5 = Piccolo|first5 = B.|last6 = Beghi|first6 = E.|pmid = 32304988|s2cid = 215767632|url-access = subscription}}".

For all infants with neonatal seizures  regardless of cause, the rate of subsequent seizures during childhood is estimated between 10 and 20%.{{cite journal | vauthors = Tekgul H, Gauvreau K, Soul J, Murphy L, Robertson R, Stewart J, Volpe J, Bourgeois B, du Plessis AJ | s2cid = 31487112 | title = The current etiologic profile and neurodevelopmental outcome of seizures in term newborn infants | journal = Pediatrics | volume = 117 | issue = 4 | pages = 1270–80 | date = April 2006 | pmid = 16585324 | doi = 10.1542/peds.2005-1178 }} Infants who survive severe global HIE have the highest rate of epilepsy later in life.

Untreated or repeated neonatal seizures, especially prolonged seizures or status epilepticus, are associated with hippocampal sclerosis later in life.

It is difficult to determine the incidence of seizures in the neonatal period. Estimations range between 1-5 per 1,000 live births, with other estimates being 1.1 cases per 1,000 live births in full term infants and 14 cases per 1,000 live births in preterm infants.{{cite journal |last1=Yozawitz |first1=Elissa |title=Neonatal Seizures |journal=New England Journal of Medicine |date=4 May 2023 |volume=388 |issue=18 |pages=1692–1700 |doi=10.1056/NEJMra2300188|pmid=37133587 |s2cid=258463345 }} The actual rate of seizures during the neonatal period may be higher due to a lack of accurate diagnosis of sub-clinical seizure activity without continuous EEG monitoring. The epidemiology moreover varies in high-income countries (HIC) from that in low-income ones (LIC). The incidence is estimated to be 1-3 per 1000 live births in HIC whereas it ranges from 36 to 90 per live birth in LIC.{{Citation needed|date=October 2023}} Acute causes of seizures (hypoxemic ischemic encephalopathy, infection, intracranial hemorrhage, stroke, etc.) are more common than the first episode of neonatal epilepsy syndromes.{{Citation needed|date=October 2023}}

Since interpretation of continuous EEG monitoring requires a trained neurologist, automated interpretation software has been proposed. Algorithms and machine learning have been studied, however logistical and mathematic challenges remain.{{Citation needed|date=October 2023}}

• Epilepsy in children

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{{Seizures and epilepsy}}

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Category:Epilepsy

Category:Symptoms and signs

Category:Neonatology