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Epileptic seizures are the most frequent neurological emergency in the neonatal period. In contrast to seizures in older children and adults they are mostly acute symptomatic seizures as a response to a prenatal or perinatal acute brain injury; less commonly epilepsy is already manifested in the neonatal period. Previous classifications systems were purely based on the clinical observation of behavior despite increasing evidence that the correct diagnosis based on the clinical symptoms is extremely unreliable. In 2021 the Neonatal Task Force of the International League against Epilepsy (ILAE) published a new classification system for neonatal seizures with implications for the clinical management of neonates with presumed or at risk of seizures. This classification emphasizes the importance of electroencephalography (EEG) or amplitude-integrated EEG (aEEG) in making the diagnosis and presumes a predominantly local onset of seizures in the neonatal period. Seizures are classified into motor (automatisms, clonic, epileptic spasms, myoclonic or tonic), nonmotor (autonomic or behavioral arrest), sequential or unclassifiable. Combining clinical observation with EEG or aEEG can help to determine the etiology and ultimately avoid overdiagnosis and underdiagnosis of neonatal seizures with the overall aim to improve the treatment and prognosis of seizures in neonates.
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Seizures occur more frequently in neonates than in children or adults. The incidence is between 2 and 20/1000 live births, and epileptic seizures are even more common in extremely preterm neonates (up to 50/1000 live births). The incidence also depends heavily on the demographic region [1].
Most cases involve acute symptomatic (or provoked) seizures in the context of a serious illness in the neonate, whereas neonatal-onset epilepsy is less common [2, 3].
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Neonatal seizures are associated with significant mortality and morbidity. The underlying disease plays a decisive role here; however, the seizures themselves can also be immediately life-threatening for the neonate, for example, due to apnea resulting in hypoxia. Moreover, the epileptic activity itself appears to be a risk factor for the child’s development. Several studies have shown that a high seizure burden is associated with poorer treatment outcomes in individual patients [4]. Conversely, it has been shown that rapid, accurate diagnosis and thus early initiation of effective therapy can significantly reduce seizure burden [5, 6].
Etiologies
Seizures can occur in neonates in the context of a wide variety of diseases, but the majority of cases are caused by the following known factors (Table 1; [1, 2]): In full-term neonates, hypoxic–ischemic encephalopathy (HIE) is the most common cause. In such cases, seizures typically occur 8–24 h after the hypoxic–ischemic event and almost always cease after 2–4 days. In preterm neonates, intraventricular hemorrhage is the primary cause. Infections, focal circulatory disorders, and acute metabolic events such as hypoglycemia or electrolyte imbalances can also trigger neonatal seizures even after an uncomplicated pregnancy and birth. Only 10–15% of all neonatal seizures are an expression of neonatal-onset epilepsy. Rapid diagnosis of epilepsy in such cases is extremely important for the infant’s treatment and long-term prognosis. Neonatal-onset epilepsy is usually caused by genetic factors, such as ion channelopathy or metabolic disorders, in which an excess of a toxic metabolite (such as ammonia) or a deficiency of a cofactor (such as vitamin B6) can lead to encephalopathy with seizures. By contrast, congenital cortical malformations rarely present with seizures in the neonatal period.
Table 1
Etiology of neonatal seizures
Etiology
Proportion (%)
Common specific disorders
Acute symptomatic (provoked) seizures
Acute neonatal encephalopathy
30–50
Hypoxic–ischemic encephalopathy, pre- and postnatal hypoxic events
Depending on clinical presentation, neonatal seizures can be classified into:
Electroclinical seizures, in which abnormal clinical behavior correlates with an electrographic pattern
Electrographic seizures, which can only be detected on electroencephalography (EEG) or amplitude-integrated EEG (aEEG) without reliable accompanying clinical signs
At least half of all seizures in neonates are purely electrographic [7, 8]. A purely clinical diagnosis of neonatal seizures is therefore not possible. In addition, the following limiting factors must be taken into account:
1.
Clinically, seizures in neonates are often difficult to distinguish from non-epileptic phenomena, creating the risk of misdiagnosis [9]. Fragmentary movement patterns such as sucking, licking, rowing movements, blinking, nystagmus, fixed gaze, hiccups, and bilateral/generalized tonic extension posturing are typically non-epileptic [7, 8]. Neonates with HIE, in particular, very often also exhibit non-epileptic movement abnormalities [7].
2.
The clinical symptoms of neonatal seizures are often subtle and therefore easily overlooked. Generalized tonic–clonic seizures almost never occur in the neonatal period, as incomplete dendritic arborization, synaptogenesis, and myelination limit the spread of cerebral excitation.
3.
Autonomic phenomena, such as apnea, are very rarely a manifestation of epileptic seizures in both preterm and full-term neonates. Ictal apnea is usually accompanied by tachycardia and/or other motor symptoms, which, however, may easily be overlooked.
4.
Treatment of seizures often leads to electroclinical dissociation (uncoupling), i.e., electroclinical seizures transition into purely electrographic (subclinical) seizures [10]. This is particularly likely in critically ill preterm and term neonates.
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Therefore, an EEG is required for the reliable diagnosis or exclusion of neonatal seizures. In routine clinical practice, an assessment of diagnostic certainty [1] can be useful in determining whether a neonate is experiencing seizures (Fig. 1): The gold standard is a seizure “confirmed” by continuous video EEG (cEEG; level 1). When documented on aEEG, seizures should be considered “probable” (level 2a). Purely clinically observed focal clonic or focal tonic seizures can also be considered “probable,” as a strong correlation between clinical observation and electrographic confirmation has been demonstrated for these (level 2b; [9, 11]). A neonatal seizure should be classified as a “possible seizure” if symptoms other than focal clonic or tonic seizures have been observed by experienced personnel but an ictal EEG is not available (level 3); a diagnosis of cerebral seizure is unlikely if none of the above criteria are met (level 4). The absence of a correlate on cEEG during a clinically suspected seizure event excludes neonatal seizures (level 5; [1, 12]).
Fig. 1
Brighton Collaboration algorithm for determining diagnostic certainty in neonatal seizures. EEG electroencephalography, aEEG amplitude-integrated EEG. (Courtesy of [1, 12])
Role of electroencephalography and amplitude-integrated electroencephalography in neonatal seizures
All neonates with clinically suspected seizures or a high risk of seizures due to HIE or a vascular event should undergo EEG monitoring for 24 h [13, 14]. The gold standard for this is cEEG [15]; if this is not available, at the very least an aEEG should be performed, ideally supplemented by a routine video EEG for at least 1 h, with additional electromyographic recordings from both deltoid muscles [16]. During therapeutic hypothermia, EEG monitoring is also required to assess background activity; if seizures have been observed, monitoring should be continued for up to 24 h after completion of therapeutic hypothermia [17].
The International League Against Epilepsy (ILAE) defines epileptic seizures as a transient occurrence of signs and/or symptoms due to abnormal excessive or synchronous neuronal activity [18]. This definition does not take electrographic events into account, thereby overlooking more than half of all seizures in the neonatal period. Therefore, experts recommend defining or confirming neonatal seizures on the basis of abnormal electrographic activity. The American Clinical Neurophysiology Society describes electrographic seizures as sudden, abnormal electrographic events with a clearly recognizable onset, evolution, and termination, characterized by a repetitive and evolving pattern lasing at least 10 s and an amplitude of at least 2 μV [16]. The electrographic pattern should show modulation in frequency, amplitude, morphology, or location. The morphology, spatial distribution, and temporal dynamics of seizure patterns can vary both between and within individual patients.
The “typical” neonatal seizure often begins electrographically with low-amplitude, rhythmic, or sinusoidal waveforms that often lack typical spikes or spike–wave complexes. As the seizure evolves, the amplitude of the ictal activity increases while the frequency slows down. Any rhythmic activity—regardless of its frequency—can form part of the ictal EEG pattern, provided that a clear pattern of evolution can be identified.
Neonatal seizures usually arise focally and propagate only to a limited extent to other brain regions. Interhemispheric spread is rare, especially in preterm infants [19]. Occasionally, simultaneous, independent focal seizures occur that appear to spread throughout the entire brain and can create the false impression of a generalized seizure. In such cases, however, the ictal event does not have a generalized origin, but rather two independent focal origins. Diffuse causes of encephalopathy—such as meningitis, hypoglycemia, or hypoxic–ischemic damage—can trigger focal seizures or cause multiple seizures, each originating in different regions of the scalp. Multifocal seizures are also possible in such cases. By contrast, lateralized or unifocal seizures often indicate a focal structural lesion—such as a stroke—as they reflect a localized functional disorder.
The typical duration of a single electrographic neonatal seizure is between 1 and 2 min and is generally shorter in preterm infants [19, 20]. Typically, repetitive short series of seizures occur rather than long-lasting continuous seizures. Although individual seizures are brief, neonatal seizures usually occur in multiple episodes over a period of several hours. Therefore, they can account for a significant proportion of the EEG recording.
Neonatal seizures occur against a background of highly variable baseline EEG activity, which depends heavily on the conceptional age of the infant and can range from normal to predominantly discontinuous or suppression–burst patterns. The interictal EEG can provide clues to the etiology and prognosis. Persistent unifocal sharp waves originating from a limited cortical area may indicate focal lesions such as intracranial hemorrhage, venous thrombosis, or ischemic stroke. A predominance of multifocal sharp waves, on the other hand, suggests a more diffuse event.
Neonates with normal EEG background activity have a significantly lower risk of developing seizures than those with pronounced background changes. A severely abnormal EEG with no clinical signs of acquired brain injury may indicate a metabolic or genetic cause or a cerebral malformation.
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Today, aEEG is standard in the care of critically ill neonates [21‐23]. It was developed primarily to assess background activity and prognosis in neonates following HIE. However, the aEEG pattern also allows seizures to be detected, especially when not only the amplitude-integrated trace but also the conventional EEG trace is analyzed. Separate recording of both hemispheres, including the central region, is always required. In this way, approximately 50–70% of seizures can be correctly detected [24]. Seizures that do not involve the central region, last less than 30 s, or are characterized by low-amplitude discharges are not detected [25]. However, the risk of overinterpretation is also high [23, 24].
Clinical presentation and classification of neonatal seizures
Although neonatal seizures cannot be reliably diagnosed on the basis of clinical presentation alone, they should be classified according to seizure semiology. In 2021, the ILAE published a classification (Fig. 2) derived from those used in older children and adults [12, 26]. This required adaptation in several key respects for use in neonates:
Since the onset of a seizure in neonates is often difficult to determine, the predominant symptom observed during the seizure is used for classification rather than the initial clinical symptom.
Since seizures in neonates are always focal in origin, it is not necessary to distinguish them from generalized seizures.
Since an alteration of consciousness cannot be reliably assessed in neonates, it cannot serve as a criterion for classification.
Neonatal seizures sometimes show a complex course with different, successive elements; sequential seizures have therefore been newly included in the classification.
There is no uniform definition for neonatal status epilepticus [27]. Therefore, the definition of the American Clinical Neurophysiology Society (ACNS) is often used, according to which status epilepticus is present if the electrographic seizure activity on EEG persists for at least 30 min within a 1‑h recording [16].
Fig. 2
Diagnostic flowchart for seizures in neonates, including seizure classification. Neonates exhibit discrete events suspected to be of epileptic origin, or they are critically ill (often ventilated, sedated, and treated with muscle relaxants in the intensive care unit). Asterisk If electroencephalography (EEG) is not available, see algorithm for diagnostic certainty (see Fig. 1). (With kind permission from [12])
The classification is useful in neonates at high risk for seizures or who have exhibited abnormal clinical events suggestive of seizures. The presence of neonatal seizures is then confirmed by means of an EEG (either routine EEG or cEEG monitoring) or, if not available, an aEEG. If neither EEG nor aEEG is available, the recommendations for diagnostic certainty in neonatal seizures should be followed (Fig. 1).
The clinical features of electroclinical events are classified into motor, nonmotor, sequential (multiple consecutive clinical features during a seizure), or unclassifiable. Motor events are classified into automatisms, clonic, epileptic spasms, myoclonic, or tonic. Non-motor events are classified into autonomic or with pauses (Fig. 2). Table 2 describes the seizure types in detail.
Table 2
Description of seizure types in neonates based on the ILAE [29] seizure definitions and specific aspects in neonates
Seizure type
Description
Special aspects in neonates
Automatisms
A more or less coordinated motor activity that typically occurs in cases of impaired consciousness. It often resembles a voluntary movement and may consist of an inappropriate continuation of a pre-critical motor activity
Typically oral and usually associated with other features. Normal and abnormal behaviors in term and preterm neonates can mimic ictal automatisms
Clonic
Rhythmic movements (2–3 Hz), symmetrical or asymmetrical, that occur regularly and affect the same muscle groups
Clinically most easily recognizable seizure type. Sometimes slower in neonates
Epileptic spasms
A sudden flexion, extension, or mixed flexion–extension movement of predominantly proximal and trunk muscles, lasting 0.5–2 s. Limited forms may occur: grimacing, head nodding, or subtle eye movements. May occur in clusters
Rare. Difficult to distinguish from myoclonic seizures without surface EMG channel
Myoclonic
Sudden, brief (< 100 ms) involuntary single or multiple contraction(s) of muscle(s) or muscle groups, variably localized (axial, proximal extremities, distal)
Clinically difficult to distinguish from non-epileptic myoclonus
Sequential
Events that show a sequence of signs, symptoms, and EEG changes at different times
No predominant feature can be identified. Several features typically occur in sequence, often with changing lateralization within or between seizures
Tonic
A sustained increase in muscle tone lasting from a few seconds to minutes
Usually focal, unilateral, or bilaterally asymmetrical. Generalized tonic posturing is of nonepileptic origin
Autonomic
A marked change in the function of the autonomic nervous system, which may affect cardiovascular, pupillomotor, gastrointestinal, sudomotor, vasomotor, and thermoregulatory functions
May also include respiration (apnea). Typically observed in combination with other seizure manifestations. EEG confirmation is mandatory
Behavioral arrest
Cessation (pause) of activities, freezing, immobility, as in a behavioral arrest seizure
May be focal and/or followed by apnea, other autonomic manifestations, and motor seizures
Unclassifiable
Cannot be otherwise classified due to insufficient information or unusual clinical signs
–
EEG electroencephalography, EMG electromyogram, ILAE International League Against Epilepsy
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The clinical classification allows important conclusions to be drawn about the probable etiology for further diagnosis and therapy [11, 26]: Focal clonic seizures often occur after vascular events (ischemic stroke or hemorrhage), spasms may indicate vitamin B6-dependent epilepsy, while myoclonic seizures occur in neonates with metabolic or genetic epilepsies. Ion channelopathies (and other genetic neonatal epilepsies) often manifest as tonic or sequential seizures. However, these are only indications; in principle, any seizure may be observed in association with any etiology.
Etiological clarification
In addition to EEG and aEEG for establishing the diagnosis, imaging and laboratory investigations are required for etiological evaluation to enable targeted, coordinated treatment (Fig. 3). Hypoglycemia and electrolyte imbalance should always be ruled out; today, this can usually be achieved immediately using point-of-care methods. A complete blood count and analysis of inflammatory markers such as interleukin (IL)-6 and C‑reactive protein (CRP) should also be performed immediately. If there are clinical indications of infection, a lumbar puncture is necessary, possibly after imaging and provided the infant’s condition is sufficiently stable. Cranial ultrasound, if possible magnetic resonance imaging (MRI), is performed primarily to exclude hemorrhage.
Fig. 3
Flowchart of the initial diagnostic approach in neonatal seizures. CRP C-reactive protein, IL6 interleukin‑6, Hst urea, AP alkaline phosphatase, MRI magnetic resonance imaging, cEEG continuous electroencephalogram, aEEG amplitude-integrated electroencephalogram
If seizures do not respond to first-line pharmacotherapy or if there are additional signs of encephalopathy, further laboratory investigations are recommended to rule out a metabolic disorder, particularly with regard to potentially treatable diseases (such as pyridoxine-dependent seizures, metabolically induced seizures in maple syrup urine disease, etc.).
Differential diagnosis
Paroxysmal non-epileptic phenomena [28] must be distinguished from epileptic seizures in neonates in order to avoid misdiagnosis and consequently unindicated drug therapy. Table 3 lists the most important differential diagnoses.
Table 3
Key differential diagnoses for neonatal seizures
Diagnosis
Description
Normal movement patterns
Healthy neonates exhibit a wide array of fragmentary movements and lively spontaneous motor activity, as well as primitive reflexes. These can usually be modified by stimulation or changes in position
Abnormal movement patterns
Tremors, jitteriness, myoclonus, and oral non-epileptic automatisms are common in neonates with mild HIE or acute metabolic disorders. EEG is essential to differentiate these from epileptic seizures
Benign sleep myoclonus
These often occur in clusters and are multifocal. They can be clinically differentiated from epileptic seizures in that they usually persist when touched or when the position is changed but cease promptly with a change in arousal
Apnea
Most apneas in preterm infants, as well as in full-term infants, are not of epileptic origin, but are caused by immaturity of the respiratory center or occur as part of a systemic disease, such as sepsis or an inborn error of metabolism
Hyperekplexia
This disorder is caused by impaired inhibition due to a genetic defect in the glycine receptor α1 subunit or a glycine transporter. Affected infants exhibit a markedly exaggerated startle response, followed by sustained increases in muscle tone. A violent backward head movement in response to tapping the tip of the nose (nose-tapping phenomenon) is almost pathognomonic. Since the tonic phenomena pose a risk of life-threatening apnea, rapid diagnosis should be sought
HIE hypoxic–ischemic encephalopathy, EEG electroencephalography
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Practical conclusion
Epileptic seizures are the most frequent neurological emergency in the neonatal period.
Neonates with medical illness, in particular, also frequently present with abnormal non-epileptic phenomena.
Many neonatal seizures are electrographic, i.e., without apparent clinical signs.
To improve diagnosis, and thus also treatment, precise clinical and electroencephalographic (EEG) classification is required, for which important guidelines have been developed in recent years.
Continuous EEG video monitoring is particularly important in neonates at high risk of seizures or after clinically suspected seizure episodes in order to avoid misdiagnosis.
Acknowledgements
I would like to express my sincere thanks to Prof. Hans Hartmann for his helpful revision of the manuscript.
Declarations
Conflict of interest
R.M. Pressler is Associate Editor at Epilepsia Open, serves as an investigator for studies with UCB Pharma, and has received honoraria from Longboard, Natus, Kephala, Autifony, and UCB Pharma for activities on advisory boards, teaching courses, or consulting services. She is supported in part by the National Institute for Health Research (NIHR) Biomedical Research Centre at Great Ormond Street Hospital (NIHR GOSH BRC), the Evelyn Trust, the Cambridge Biomedical Research Centre, and the NIHR. The views expressed are those of the author and not necessarily those of the NHS, the NIHR, or the UK Department of Health.
For this article no studies with human participants or animals were performed by any of the authors. All studies mentioned were in accordance with the ethical standards indicated in each case.
The supplement containing this article is not sponsored by industry.
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Pellegrin S, Munoz FM, Padula M, Heath PT, Meller L, Top K et al (2019) Neonatal seizures: Case definition & guidelines for data collection, analysis, and presentation of immunization safety data. Vaccine 37(52):7596–7609CrossRefPubMedPubMedCentral
2.
Glass HC, Chang T, Shellhaas RA, Wusthoff CJ, Abend NS, Bonifacio SL et al (2015) Contemporary profile of neonatal seizures: A prospective cohort study of the neonatal seizure registry. Ann Neurol 78:S185–S186
3.
Shellhaas RA, Wusthoff CJ, Tsuchida TN, Glass HC, Chu CJ, Massey SL et al (2017) Profile of neonatal epilepsies: Characteristics of a prospective US cohort. Neurology 89(9):893–899CrossRefPubMedPubMedCentral
4.
Pinchefsky EF, Hahn CD (2017) Outcomes following electrographic seizures and electrographic status epilepticus in the pediatric and neonatal ICUs. Curr Opin Neurol 30(2):156–164CrossRefPubMed
5.
Wusthoff CJ, Sundaram V, Abend NS, Massey SL, Lemmon ME, Thomas C et al (2021) Seizure Control in Neonates Undergoing Screening vs Confirmatory EEG Monitoring. Neurology 97(6):e587–e596CrossRefPubMedPubMedCentral
6.
Pavel AM, Rennie JM, de Vries LS, Blennow M, Foran A, Shah DK et al (2022) Neonatal Seizure Management: Is the Timing of Treatment Critical? J Pediatr 243:61–68.e2CrossRefPubMedPubMedCentral
7.
Mizrahi EM, Kellaway P (1987) Characterization and classification of neonatal seizures. Neurology 37(12):1837–1844CrossRefPubMed
8.
Murray DM, Boylan GB, Ali I, Ryan CA, Murphy BP, Connolly S (2008) Defining the gap between electrographic seizure burden, clinical expression and staff recognition of neonatal seizures. Arch Dis Childhood: Fetal Neonatal Ed 93(3):F187–F191CrossRef
9.
Malone A, Ryan AC, Fitzgerald A, Burgoyne L, Connolly S, Boylan GB (2009) Interobserver agreement in neonatal seizure identification. Epilepsia 50(9):2097–2101CrossRefPubMed
10.
Boylan GB, Rennie JM, Pressler RM, Wilson G, Morton M, Binnie CD (2002) Phenobarbitone, neonatal seizures, and video-EEG. Arch Dis Child Fetal Neonatal Ed 86(3):F165–F170CrossRefPubMedPubMedCentral
11.
Nunes ML, Yozawitz EG, Zuberi S, Mizrahi EM, Cilio MR, Moshe SL et al (2019) Neonatal seizures: Is there a relationship between ictal electroclinical features and etiology? A critical appraisal based on a systematic literature review. Epilepsia Open 4(1):10–29CrossRefPubMedPubMedCentral
12.
Pressler RM, Cilio MR, Mizrahi EM, Moshé SL, Nunes ML, Plouin P et al (2021) The ILAE classification of seizures and the epilepsies: Modification for seizures in the neonate. Position paper by the ILAE Task Force on Neonatal Seizures. Epilepsia 62(3):615–628CrossRefPubMed
13.
Malfilâtre G, Mony L, Hasaerts D, Vignolo-Diard P, Lamblin MD, Bourel-Ponchel E (2021) Technical recommendations and interpretation guidelines for electroencephalography for premature and full-term newborns. Neurophysiol Clin 51(1):35–60CrossRefPubMed
14.
Wusthoff CJ, Numis AL, Pressler RM, Chu CJ, Massey S, Clancy RR et al (2025) The American Clinical Neurophysiology Society Guideline on Indications for Continuous Electroencephalography Monitoring in Neonates. J Clin Neurophysiol 42(1):1–11CrossRefPubMed
15.
Boylan GB, Stevenson NJ, Vanhatalo S (2013) Monitoring neonatal seizures. Semin Fetal Neonatal Med 18(4):202–208CrossRefPubMed
16.
Tsuchida TN, Wusthoff CJ, Shellhaas RA, Abend NS, Hahn CD, Sullivan JE et al (2013) American clinical neurophysiology society standardized EEG terminology and categorization for the description of continuous EEG monitoring in neonates: report of the American Clinical Neurophysiology Society critical care monitoring committee. J Clin Neurophysiol 30(2):161–173CrossRefPubMed
17.
Pavel AM, Rennie JM, de Vries LS, Mathieson SR, Livingstone V, Finder M et al (2024) Temporal evolution of electrographic seizures in newborn infants with hypoxic-ischaemic encephalopathy requiring therapeutic hypothermia: a secondary analysis of the ANSeR studies. Lancet Child Adolesc Health 8(3):214–224CrossRefPubMedPubMedCentral
18.
Fisher RS, van Emde BW, Blume W, Elger C, Genton P, Lee P et al (2005) Epileptic seizures and epilepsy: definitions proposed by the International League Against Epilepsy (ILAE) and the International Bureau for Epilepsy (IBE). Epilepsia 46(4):470–472CrossRefPubMed
19.
Janackova S, Boyd S, Yozawitz E, Tsuchida T, Lamblin MD, Gueden S et al (2016) Electroencephalographic characteristics of epileptic seizures in preterm neonates. Clin Neurophysiol 127(8):2721–2727CrossRefPubMed
20.
Pisani F, Statello R, Pedrazzi G, Miragoli M, Piccolo B, Turco EC (2022) The duration of successive epileptic seizures is monotonically correlated in neonates. Neurophysiol Clin 52(6):472–481CrossRefPubMed
21.
Hellström-Westas L (2018) Amplitude-integrated electroencephalography for seizure detection in newborn infants. Semin Fetal Neonatal Med 23(3):175–182CrossRefPubMed
22.
El-Dib M, Abend NS, Austin T, Boylan G, Chock V, Cilio MR et al (2023) Neuromonitoring in neonatal critical care part II: extremely premature infants and critically ill neonates. Pediatr Res 94(1):55–63CrossRefPubMed
23.
El-Dib M, Abend NS, Austin T, Boylan G, Chock V, Cilio MR et al (2023) Neuromonitoring in neonatal critical care part I: neonatal encephalopathy and neonates with possible seizures. Pediatr Res 94(1):64–73CrossRefPubMed
24.
Rakshasbhuvankar A, Paul S, Nagarajan L, Ghosh S, Rao S (2015) Amplitude-integrated EEG for detection of neonatal seizures: A systematic review. Seizure 33:90–98CrossRefPubMed
25.
Shellhaas RA, Soaita AI, Clancy RR (2007) Sensitivity of amplitude-integrated electroencephalography for neonatal seizure detection. Pediatrics 120(4):770–777CrossRefPubMed
26.
Yozawitz EG, Cilio MR, Mizrahi EM, Moon JY, Moshé SL, Nunes ML et al (2025) ILAE neonatal seizure framework to aide in determining etiology. Epileptic Disord 27(1):64–70CrossRefPubMed
27.
Nunes ML, Yozawitz EG, Wusthoff CJ, Shellhaas RA, Olivas-Peña E, Wilmshurst JM et al (2025) Defining neonatal status epilepticus: A scoping review from the ILAE neonatal task force. Epilepsia Open 10(1):40–54CrossRefPubMed
28.
Cross JH (2013) Differential diagnosis of epileptic seizures in infancy including the neonatal period. Semin Fetal Neonatal Med 18(4):192–195CrossRefPubMed
29.
Fisher RS, Cross JH, French JA, Higurashi N, Hirsch E, Jansen FE et al (2017) Operational classification of seizure types by the International League Against Epilepsy: position paper of the ILAE Commission for Classification and Terminology. Epilepsia 58(4):522–530CrossRefPubMed
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