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Epileptic seizures are among the most common neurological manifestations in the neonatal period. A distinction is made between acute symptomatic (provoked) and unprovoked neonatal seizures: the former arise from brain injuries, such as hypoxic-ischemic encephalopathy (HIE), intracerebral hemorrhages, infections or metabolic disturbances. Unprovoked neonatal seizures typically occur in the context of genetic disorders or structural brain malformations. This distinction as well as the underlying etiology, are crucial as both significantly influence the prognosis. This review summarizes the current state of knowledge regarding the long-term outcomes of neonatal seizures and their predictive factors. Long-term neurological deficits depend not only on the seizures themselves but primarily on the underlying cause. Hypoxic-ischemic encephalopathy is frequently associated with severe long-term consequences such as cerebral palsy and cognitive impairments. Genetic epileptic encephalopathies are usually associated with lifelong epilepsy and neurocognitive deficits, while the extent and localization of structural brain malformations determine the severity of cognitive and motor impairments. Early diagnosis and prompt initiation of treatment are essential. In the short term, mortality is the primary concern and in the long term, neurological sequelae such as cerebral palsy, cognitive deficits, or post-neonatal epilepsy may occur. Identified prognostic factors include the underlying etiology, electroencephalography (EEG) and magnetic resonance imaging (MRI) findings and perinatal risk factors. Further prospective long-term studies are needed to improve care for affected neonates and sustainably optimize their long-term outcomes.
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Epileptic seizures are among the most common neurological manifestations in the neonatal period. Common causes include hypoxic–ischemic encephalopathy (HIE), intracerebral hemorrhage, infections, as well as metabolic and genetic disorders [35, 50].
The neonatal period is a critical phase of brain development in which the brain grows rapidly, cortical neurons mature, and numerous synapses are formed. Synaptic plasticity, the maturation of chloride cotransporters, and the distribution of neurotransmitters increase neuronal excitability and make the immature brain particularly susceptible to epileptic seizures. The concept of “seizures beget seizures,” whereby early seizures increase the likelihood of further seizures, has also been discussed in the neonatal period. Neonatal seizures can potentially influence brain development and be associated with an increased susceptibility to seizures later in life. However, the underlying mechanisms are complex and not yet fully understood [33].
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Early diagnosis and prompt initiation of treatment are essential [33]. The diagnostic gold standard is continuous video electroencephalography (EEG; [37]), while amplitude-integrated EEG (aEEG) broadens the diagnostic spectrum. The distinction between acute symptomatic (provoked) and unprovoked seizures and the determination of etiology are essential, as these significantly influence treatment decisions and the course of the disease [8, 24]. Acute symptomatic seizures usually result from acute brain injury such as HIE, meningitis/encephalitis, or infarction; unprovoked seizures typically occur in cases of genetic alterations, structural brain malformations, or metabolic disturbances [33]. Antiseizure medications such as phenobarbital are primarily used. In specific etiologies such as HIE, hypothermia treatment can also have an antiseizure effect. In genetic alterations such as sodium channel mutations, sodium channel blockers are used in a targeted manner [33, 34].
Long-term neurological impairments including epilepsy, cognitive deficits, and cerebral palsy are usually attributable to the underlying disease rather than to the neonatal seizures themselves [33, 36]. Genetic encephalopathies are often associated with lifelong, treatment-resistant epilepsy and neurocognitive deficits. Structural brain malformations may be associated with motor and cognitive deficits, depending on their localization and severity, although in individual cases, favorable outcomes can be achieved through early epilepsy surgery [14, 19]. Typically, HIE is associated with severe acute and long-term sequelae. However, current studies are predominantly based on mixed cohorts of neonates with seizures, limiting the extent to which the specific effect of seizures on the long-term outcome of individual etiologies can be assessed.
This narrative review summarizes current knowledge on long-term neurological impairments following provoked and unprovoked neonatal seizures and their predictors.
Outcome following neonatal seizures: predictors
In the short term, there is a significantly increased risk of mortality following neonatal seizures, particularly in etiologies such as HIE or infections of the central nervous system [27]. In addition, the antiseizure medications used can impair vital functions such as feeding and respiration due to their side effect profile, as has been described particularly for phenobarbital [4]. In the long term, severe neurological impairments may occur, including post-neonatal epilepsy, cerebral palsy, and cognitive deficits ([30]; Fig. 1). The pathophysiology and specific characteristics of the immature neonatal brain influence both seizure susceptibility and the likelihood of long-term outcomes of this kind [46].
Fig. 1
Unfavorable short- and long-term outcomes following neonatal seizures. EEG electroencephalogram
Identified prognostic factors of long-term neurological impairment include the etiology of the seizures, abnormalities in background EEG activity and cranial imaging, and perinatal clinical variables such as birth weight and Apgar score [10, 20, 25, 26, 30]. A structured overview of the associations between these prognostic factors and long-term impairments described in the literature, based on studies with EEG- or aEEG-confirmed seizures [25‐27, 29, 31], is presented in Tables 1, 2, and 3.
“Unfavorable long-term outcomes” include various long-term neurological impairments such as post-neonatal epilepsy, cognitive deficits, cerebral palsy, and mortality [25, 26, 31]. In individual cases, blindness or deafness has also been included [26, 31]
* Significant in univariate analysis, ** significant in multivariate analysis
Mortality
Neonatal seizures are associated with a significantly increased risk of mortality in the neonatal period [30]. Preterm infants with a birth weight < 1000 g and a gestational age < 28 weeks are particularly at risk [6, 28]. In a study of EEG-confirmed seizures, mortality was higher in preterm infants (50%) than in full-term infants (40%; [32]). Predictive factors for increased mortality include certain etiologies such as cerebral hemorrhage and HIE [27]. Other risk factors include a 5-min Apgar score < 4, as well as abnormal neurological examination findings, EEG background activity, and cranial imaging results [20, 25, 27, 28]. In addition, the antiseizure medications used can impair vital functions such as respiration and feeding due to their side effect profile [4].
A comparison of two historical studies that also included purely clinically diagnosed neonatal seizures shows a decline in mortality over time: Between 1959 and 1966 and again between 1990 and 1994, mortality decreased from 35% to 24% [32]. This decline is most likely attributable to medical advances in the care of pregnant women and neonates [13].
Post-neonatal epilepsy
The development of epilepsy after the neonatal period (from the 29th day of life onward) is a common long-term neurological impairment following neonatal seizures. The risk is approximately 20%, which is significantly higher than in children without neonatal seizures [43]. In addition, post-neonatal epilepsy often occurs in association with cerebral palsy or cognitive deficits [30]. Severe epilepsy syndromes such as infantile spasms have also been frequently reported in this context.
Several predictors for the development of post-neonatal epilepsy have been documented in the literature. Neonatal status epilepticus and repetitive or prolonged seizures significantly increase the risk [11, 29]. The use of two or more antiseizure medications to control seizures is also considered a relevant risk factor [1, 9, 49]. Imaging findings—particularly lesions in the basal ganglia or thalamus—have been repeatedly associated with an increased risk of post-neonatal epilepsy [1, 25, 26, 29, 32]. Watershed infarcts, on the other hand, are more commonly associated with cognitive deficits—and less commonly with motor deficits—than with epilepsy [32]. Other risk factors include female sex [27], low birth weight, low Apgar score [43], abnormal EEG background activity [26, 29, 31], early onset of seizures [31], and lack of or incomplete response to antiseizure medication [29]. A recently published study involving 1998 children also confirmed the influence of etiology: ischemic cerebral infarction, cerebral hemorrhage, and structural brain malformations were significantly associated with an increased risk of post-neonatal epilepsy [43].
Cerebral palsy
The risk of developing cerebral palsy is significantly increased following neonatal seizures [32]. This risk is particularly high in preterm infants (53%) compared to full-term infants (17%; [38]). In a long-term study of 85 children (44 full-term, 41 preterm) who were followed up for 7 years, the overall incidence of cerebral palsy was 32%. In most cases, it was associated with additional neurological impairments: 15% of the affected children also developed post-neonatal epilepsy and intellectual disability [29]. By contrast, isolated cerebral palsy occurred in only 9% of cases [29]. Cerebral lesions, particularly in the basal ganglia or thalamus, can increase the risk of both cerebral palsy and post-neonatal epilepsy [11]. The few independent predictors for the development of cerebral palsy include neonatal status epilepticus and an absent or incomplete response to antiseizure medication [32].
Cognitive deficits
The prevalence of cognitive impairment following neonatal seizures has been systematically investigated in only a handful of studies to date. One study—which, however, also included neonatal seizures without EEG confirmation—reported a prevalence of approximately 20% [38]. Preterm infants are more frequently affected than full-term infants [32]. Etiology also plays an important role: Children with HIE, particularly those with prolonged neonatal status epilepticus, have an increased risk of cognitive impairment [2, 44]. In addition, an association has been found between certain magnetic resonance imaging (MRI) abnormalities, particularly watershed infarcts, and cognitive deficits [32].
Diagnosis
Seizure detection
The gold standard for diagnosing epileptic seizures in neonates is continuous video EEG [47]. This technique enables the objective assessment of seizure frequency, duration, type, onset and propagation patterns, as well as overall seizure burden, all of which are essential for optimizing treatment, evaluating treatment response, and estimating prognosis [17]. Neonates can have purely electrographic seizures that are often overlooked without EEG [9, 38]. Neurologically abnormal behavior is not always attributable to a seizure [37], which increases the risk of misdiagnosis when relying on clinical observation alone.
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The importance of EEG diagnosis is also underscored by the new International League Against Epilepsy (ILAE) classification of neonatal seizures [35]. This defines seizures primarily on the basis of an EEG correlate, while the clinical presentation serves to classify the semiology [17]. Since EEG patterns are often difficult to interpret in neonates, special expertise is required. The combination of clinical data with video EEG, imaging, and genetic information enables the differentiation between acute symptomatic and unprovoked seizures, as well as the identification of etiology-specific electroclinical syndromes and more targeted interventions.
The current guidelines of the American Clinical Neurophysiology Society (ACNS; [47]) recommend continuous video EEG for, among other things, confirming aEEG patterns suspicious for seizures, monitoring at-risk neonates without clinically apparent seizures, and assessing treatment success. The use of continuous video EEG has led to a paradigm shift in clinical practice—away from purely reactive confirmation toward proactive seizure detection in high-risk patients. Initial evidence suggests that early EEG-based seizure detection may be associated with better treatment response [22, 48], and that seizure burden correlates with prognosis and the severity of brain injury on MRI [18]. However, it has not yet been conclusively proven whether the use of continuous video EEG improves long-term neurological outcomes. The 2011 ACNS guidelines recommend a minimum monitoring period of 24 h or until seizure control is achieved [40], and up to 72 h in high-risk neonates (e.g., preterm infants or cases of suspected HIE; [40]). In some cases, the monitoring duration can be individually adjusted based on interictal EEG patterns in the first 24–48 h [5].
Since continuous video EEG involves considerable logistical and personnel resources, aEEG represents a resource-saving alternative in clinical practice. It is widely available and can broaden the diagnostic spectrum [17], particularly when video EEG—the recognized gold standard—is not available. However, its simplified use comes at the cost of reduced diagnostic accuracy [37]. Nevertheless, aEEG significantly outperforms a purely clinical assessment in the detection of neonatal seizures and provides considerable additional diagnostic value [37].
New technologies such as machine learning, artificial intelligence (AI), quantitative EEG, and automated seizure detection are increasingly being developed to support the evaluation of EEG data and enable faster and more targeted treatment.
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Etiological evaluation
Determining the underlying etiology is crucial for diagnosis, prognostic assessment, and treatment planning in neonatal seizures.
Imaging techniques such as cranial ultrasound and, in particular, MRI provide valuable information on structural causes such as hemorrhage, infarction, or malformation. In HIE, the identification of specific injury patterns is becoming increasingly important: Lesions in the deep gray matter and cerebellum are associated with unfavorable neurological outcomes, whereas cortical and periventricular white matter lesions have no demonstrable effect on long-term outcomes [3]. These patterns enable a more precise assessment of prognosis and form the basis for new diagnostic approaches, including AI-assisted methods [7].
Genetic testing also provides valuable information on the etiology and prognosis of neonatal seizures. Mutations in genes such as KCNQ2, KCNQ3, and SCN2A are often associated with an unfavorable neurological outcome and, in particular, an increased risk of post-neonatal epilepsy [41]. A positive family history should prompt targeted genetic and metabolic evaluation. Gene panels as well as next-generation exome and genome sequencing have identified numerous gene variants associated with early-onset epilepsy, including self-limiting forms and developmental and epileptic encephalopathies (DEEs). For some of these disorders, disease-modifying treatments are already available or in development. These targeted approaches address specific pathophysiological mechanisms and could significantly improve the treatment and prognosis of affected neonates.
Treatment optimization
Early seizure detection and prompt treatment initiation are crucial to achieving the best possible neurological outcome [17]. Immediate initiation of treatment is essential, as a higher seizure burden correlates with a lower response rate to antiseizure medications [4].
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The question of whether purely electrographic seizures should be treated in addition to electroclinical seizures remains open. Three small randomized studies [12, 39, 42] have investigated the prognostic significance of electrographic seizures in neonates with moderate to severe HIE. In one study, seizure burden was lower when both clinical and subclinical seizures were treated; in addition, a higher seizure burden was associated with a less favorable long-term neurodevelopmental outcome. A second study showed a trend toward lower seizure burden and less severe MRI changes when subclinical seizures were also treated. By contrast, a third study found no difference in seizure burden or in the rates of mortality or severe disability between groups with and without treatment of subclinical seizures. Numerous other studies have confirmed the association between high seizure burden and poor long-term outcomes [16, 23]. However, these studies primarily investigated the association between seizure burden and prognosis rather than the direct effect of seizure reduction on long-term outcomes. Therefore, based on the currently available data, it is not possible to conclusively determine whether the targeted reduction of subclinical seizures improves the long-term outcome in neonates [34].
Phenobarbital is the antiseizure medication of choice for neonatal seizures regardless of etiology (e.g., HIE, infarction, or intracerebral hemorrhage; [34]). In cases of familial predisposition or clinical evidence of a channelopathy, e.g., due to a KCNQ2 mutation, a sodium channel blocker such as phenytoin or carbamazepine may be initially used; oxcarbazepine and lacosamide are also potential alternatives, although fewer data are available on their use in neonates [34, 37]. If there is no response to phenobarbital, phenytoin or levetiracetam is available as second-line therapy [4, 34]; other options include midazolam or lidocaine [1, 15]. If a secondary channelopathy is suspected based on clinical or EEG findings, a sodium channel blocker may also be considered a second-line therapy [34]. The choice between phenytoin and carbamazepine depends on the clinical condition of the neonates (e.g., critically ill vs. stable) as well as on regional availability and the possibility of determining drug levels [34]. In cases of pre-existing cardiac conditions, levetiracetam is the preferred second-line therapy [34]. In neonates with clinical or EEG evidence of vitamin B6-dependent epilepsy, as well as in cases of seizures with no identified cause and no response to second-line therapy, a trial with pyridoxine (in addition to existing medication) may be attempted [1].
Hypothermia is an adjunctive, neuroprotective treatment for HIE-related seizures and can have a positive effect on long-term outcomes [1]. It is indicated in cases with a Thompson score ≥ 7 [45].
Outlook
In order to better assess the impact of neonatal seizures on long-term neurological development, future studies are needed that differentiate disease course according to the underlying cause. Differentiation of this kind would enable more accurate prognoses and more targeted therapeutic approaches.
Progress in several areas is needed in order to improve neonatal care. Researchers are currently investigating promising biomarkers for seizure detection and prognostic assessment. One example is high-frequency oscillations on EEG, which can be automatically detected using algorithmic approaches [7]. High-frequency oscillations occur more frequently in infants with neonatal seizures and could serve as an early warning sign for an increased risk of seizures [7]. These developments underscore the relevance of AI-assisted EEG analysis for more precise and earlier seizure detection. Initial studies on automated EEG evaluation are yielding promising results and form the basis for further research [21]. In addition, new therapies and neuroprotective strategies are being evaluated in clinical trials. These could significantly broaden the therapeutic spectrum for neonatal seizures and reduce long-term neurological impairments.
A key aspect remains the implementation of systematic long-term studies to better understand the effects of neonatal seizures and their treatment throughout development. These studies are essential for optimizing existing treatment concepts and sustainably improving the long-term prognosis and quality of life of affected children.
Practical conclusion
Early diagnosis: Continuous video electroencephalography (EEG) is the gold standard for detecting neonatal seizures. If availability is limited, amplitude-integrated EEG (aEEG) is a practical alternative.
Rapid initiation of treatment: Prompt treatment initiation with antiseizure medications such as phenobarbital is crucial, as a higher seizure burden is associated with a poorer response to treatment.
The following factors increase the risk of severe long-term neurological sequelae: prematurity; birth weight < 1000 g; low Apgar score; abnormal findings on neurological examination, EEG background activity, and magnetic resonance imaging (MRI); lack of response to medication; and neonatal status epilepticus.
Determining etiology: The underlying cause is central to prognosis and treatment. MRI and genetic testing can support a more precise assessment.
Acknowledgements
The authors would like to thank Panagiota Karatza for her assistance in preparing the figures and tables for this article.
Funding
This review article was supported by third-party funding from the Anna Mueller Grocholski Foundation, the Vontobel Foundation, and the Swiss National Science Foundation (SNSF: 208184) awarded to G.R. The funding organizations had no influence on the planning or preparation of the review article.
Declarations
Conflict of interest
A. Grubenmann, A. Rüegger and G. Ramantani declare that they have no competing interests.
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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Benedetti GM, Vartanian RJ, McCaffery H, Shellhaas RA (2020) Early Electroencephalogram Background Could Guide Tailored Duration of Monitoring for Neonatal Encephalopathy Treated with Therapeutic Hypothermia. J Pediatr 221:81–87.e1. https://doi.org/10.1016/j.jpeds.2020.01.066CrossRefPubMed
Garfinkle J, Shevell MI (2011) Prognostic factors and development of a scoring system for outcome of neonatal seizures in term infants. Eur J Paediatr Neurol 15:222–229. https://doi.org/10.1016/j.ejpn.2010.11.002CrossRefPubMed
Iams JD, Romero R, Culhane JF, Goldenberg RL (2008) Primary, secondary, and tertiary interventions to reduce the morbidity and mortality of preterm. birth, vol 371
14.
Kadish NE, Bast T, Reuner G et al (2019) Epilepsy Surgery in the First 3 Years of Life: Predictors of Seizure Freedom and Cognitive Development. Neurosurgery 84:E368–E377. https://doi.org/10.1093/neuros/nyy376CrossRefPubMed
Kharoshankaya L, Stevenson NJ, Livingstone V et al (2016) Seizure burden and neurodevelopmental outcome in neonates with hypoxic-ischemic encephalopathy. Dev Med Child Neurol 58:1242–1248. https://doi.org/10.1111/dmcn.13215CrossRefPubMedPubMedCentral
Kline-Fath BM, Horn PS, Yuan W et al (2018) Conventional MRI scan and DTI imaging show more severe brain injury in neonates with hypoxic-ischemic encephalopathy and seizures. Early Hum Dev 122:8–14. https://doi.org/10.1016/j.earlhumdev.2018.05.008CrossRefPubMed
Nagarajan L, Palumbo L, Ghosh S (2010) Neurodevelopmental Outcomes in Neonates With Seizures: A Numerical Score of Background Encephalography to Help Prognosticate. J Child Neurol 25:961–968. https://doi.org/10.1177/0883073809355825CrossRefPubMed
21.
Pavel AM, Rennie JM, De Vries LS et al (2020) A machine-learning algorithm for neonatal seizure recognition: a multicentre, randomised, controlled trial. Lancet Child Adolesc Health 2(0):740–749. https://doi.org/10.1016/S2352-4642CrossRef
Pinchefsky EF, Hahn CD (2017) Outcomes following electrographic seizures and electrographic status epilepticus in the pediatric and neonatal ICUs. Curr Opin Neurol 30:156–164. https://doi.org/10.1097/WCO.0000000000000425CrossRefPubMed
Pisani F, Facini C, Bianchi E et al (2018) Incidence of neonatal seizures, perinatal risk factors for epilepsy and mortality after neonatal seizures in the province of Parma, Italy. Epilepsia 59:1764–1773. https://doi.org/10.1111/epi.14537CrossRefPubMed
Pisani F, Prezioso G, Spagnoli C (2020) Neonatal seizures in preterm infants: A systematic review of mortality risk and neurological outcomes from studies in the 2000’s. Seizure 75:7–17. https://doi.org/10.1016/j.seizure.2019.12.005CrossRefPubMed
Pressler RM, Abend NS, Auvin S et al (2023) Treatment of seizures in the neonate: Guidelines and consensus-based recommendations—Special report from the ILAE Task Force on Neonatal Seizures. Epilepsia 64:2550–2570. https://doi.org/10.1111/epi.17745CrossRefPubMed
35.
Pressler RM, Cilio MR, Mizrahi EM 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 62:615–628. https://doi.org/10.1111/epi.16815CrossRefPubMed
36.
Ramantani G (2013) Neonatal epilepsy and underlying aetiology: to what extent do seizures and EEG abnormalities influence outcome? Epileptic Disord 15:365–375. https://doi.org/10.1684/epd.2013.0619CrossRefPubMed
van Rooij LGM, Toet MC, van Huffelen AC et al (2010) Effect of treatment of subclinical neonatal seizures detected with aEEG: randomized, controlled trial. Pediatrics 125:e358–366. https://doi.org/10.1542/peds.2009-0136CrossRefPubMed
40.
Shellhaas RA, Chang T, Tsuchida T et al (2011) The American Clinical Neurophysiology Society’s Guideline on Continuous Electroencephalography Monitoring in Neonates. J Clin Neurophysiol 28:611–617. https://doi.org/10.1097/WNP.0b013e31823e96d7CrossRefPubMed
Srinivasakumar P, Zempel J, Trivedi S et al (2015) Treating EEG Seizures in Hypoxic Ischemic Encephalopathy: A Randomized Controlled Trial. Pediatrics 136:e1302–1309. https://doi.org/10.1542/peds.2014-3777CrossRefPubMed
Vollmer B, Roth S Baudin J et al Predictors of Long-Term Outcome in Very Preterm Infants: Gestational. AGE (Versus Neonatal Cranial Ultrasound)
45.
Weeke LC, Vilan A, Toet MC et al (2017) A Comparison of the Thompson Encephalopathy Score and Amplitude-Integrated Electroencephalography in Infants with Perinatal Asphyxia and Therapeutic Hypothermia. Neonatology 112:24–29. https://doi.org/10.1159/000455819CrossRefPubMed
Wusthoff CJ, Numis AL, Pressler RM et al (2025) The American Clinical Neurophysiology Society Guideline on Indications for Continuous Electroencephalography Monitoring in Neonates. J Clin Neurophysiol 42:1–11. https://doi.org/10.1097/WNP.0000000000001120CrossRefPubMed
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