Cause Of Neonatal Seizures Research Articles

Sturge–Weber syndrome without facial nevus: An unusual cause of neonatal seizures

Sturge-Weber syndrome is a neurocutaneous syndrome characterised by facial port wine stain, ipsilateral leptomeningeal angioma and vascular eye abnormalities. We report a rare case of Sturge-Weber syndrome without facial nevus presenting with neonatal seizures.

Epileptogenesis in the immature brain: Neonatal seizures in hypoxic/ischemic encephalopathy

SummaryNeonatal hypoxic/ischemic encephalopathy is the most common cause of neonatal seizures, and these seizures are refractory to conventional antiseizure drugs and can lead to later life epilepsy and congitive deficits. Data from human tissue studies as well as rodent models suggest unique age‐specific mechanisms underlying these neonatal seizure and their consequences, and are leading to a number of new therapeutic targets. For an expanded treatment of this topic see Jasper’s Basic Mechanisms of the Epilepsies, Fourth Edition (Noebels JL, Avoli M, Rogawski MA, Olsen RW, Delgado‐Escueta AC, eds) published by Oxford University Press (available on the National Library of Medicine Bookshelf [NCBI] at http://www.ncbi.nlm.nih.gov/books).

Early continuous video electroencephalography in neonatal stroke

Perinatal stroke is the second most common cause of neonatal seizures, and can result in long-term neurological impairment. Diagnosis is often delayed until after seizure onset, owing to the subtle nature of associated signs. We report the early electroencephalographic (EEG) findings in a female infant with a perinatal infarction, born at 41 weeks 2 days and weighing 3.42 kg. Before the onset of seizures, the EEG from 3 hours after delivery demonstrated occasional focal sharp waves over the affected region. After electroclinical seizures, focal sharp waves became more frequent, complex, and of higher amplitude, particularly in 'quiet sleep'. In 'active sleep', sharp waves often disappeared. Diffusion-weighted imaging confirmed the infarct, demonstrating left frontal and parietal diffusion restriction. At 9 months, the infant has had no further seizures, and neurological examination is normal. To our knowledge, this report is the first to describe the EEG findings in perinatal stroke before seizures, and highlights the evolution of characteristic background EEG features.

Management of Neonatal Seizures

Seizures in the newborn period constitute a medical emergency. Subtle seizures are the commonest type of seizures occurring in the neonatal period. Myoclonic seizures carry the worst prognosis in terms of long-term neurodevelopmental outcome. Hypoxic-ischemic encephalopathy is the most common cause of neonatal seizures. Multiple etiologies often co-exist in neonates and hence it is essential to rule out common causes such as hypoglycaemia, hypocalcemia, and meningitis before initiating specific therapy. A comprehensive evidence based approach for management of neonatal seizures has been described in this protocol.

Neonatal Seizures: When to Consider and How to Investigate for an Inborn Error of Metabolism

Seizures occur more frequently in the neonatal period than in the remainder of childhood. Neonatal seizures can have different aetiologies. Inborn errors of metabolism are rare causes of seizures in the newborn. However, they are an important cause of intractable neonatal seizures, accounting for 30% of cases. Diagnosis is necessary for timely institution of appropriate treatment and is important in determining clinical outcome. As these are genetic conditions, it allows for appropriate genetic counselling. We describe the clinical presentation of neonatal seizures and the investigation findings in symptomatic neonatal seizures and epilepsy syndromes that arise in the neonatal period. The approach in diagnosis and investigation of an underlying inborn error of metabolism is described and inborn errors of metabolism that are important causes of neonatal seizures are reviewed.

Pattern of neonatal seizures in Osogbo, south-western Nigeria

Objectives. A study to determine the pattern and outcome of neonatal seizures. Design. A prospective descriptive study. Setting. Special Care Baby Unit, Ladoke Akintola University of Technology Teaching Hospital, Osogbo, Nigeria. Subjects. All newborn infants with observed seizures admitted between January 2006 and December 2008. Results. Of 866 neonates admitted, 59 (6.8%) had seizures; of these 43 (72.9%) had been born outside our health facility (outborn). Babies with seizures had a higher birth weight than babies without seizures (p=0.008), and the incidence of seizures had a linear relationship increasing with the weights of the babies and inverse to their ages. Of the 59 babies with seizures, 37 (62.7%) were considered to have had birth asphyxia. Meningitis, hypoglycaemia, and hypocalcaemia occurred in 7 (11.9%), 6 (10.2%) and 2 (3.4%) of cases, respectively, and 7 (11.9%) had undiagnosed causes. Forty-two (71.2%) of the 59 babies had both subtle and generalised seizures. Twenty-seven babies with seizures died (45.8%) compared with 131 of 807 babies without seizures (16.2%, p=0.0001). Babies with seizures and asphyxia or who had been outborn had the highest risk of death (59.5% and 48.8%, respectively). Recommendations. The major causes of neonatal seizures and death are potentially preventable. Comprehensive and vigorous efforts are needed to achieve safe delivery, prevent birth asphyxia and improve care and transport of sick neonates at the primary care level. In view of the high prevalence of seizures among severely asphyxiated neonates and those with meningitis, anticonvulsant chemoprophylaxis is recommended in these groups.

Intracranial Cavernous Hemangioma and Seizures in a Newborn Infant

A 3.28-kg male infant was delivered at 40 week's gestation by means of cesarean delivery for a non-reassuring CTG, after an uncomplicated pregnancy. After successful transition, he was transferred to the post-natal ward for routine newborn care. At 50 hours of age, the infant had a left-sided tonic-clonic seizure. With non-contrast axial computed tomography (Figure, A), high attenuation areas in the right frontal lobe and germinal matrix adjacent to the right lateral ventricle (arrows) were shown, consistent with an intracerebral haemorrhage. With axial T2-weighted magnetic resonance imaging (Figure, B), a low signal was shown in the right frontal lobe and adjacent to the right lateral ventricle (arrows) at the sites of the intra-parenchymal hemorrhage. A vascular channel connecting these 2 separate lesions (arrowhead) showed no communication with the main circulation. In conjunction with magnetic resonance angiography and MRV imaging (not shown), the appearances represent 2 separate cavernous hemangioma isolated from the intracranial circulation and complicated by a parenchymal hemorrhage. Cavernous hemangiomas of the central nervous system are benign vascular malformations that are best imaged with magnetic resonance imaging.1Ng B.H. Mulyadi E. Pereira J.K. Ghedia S. Pinner J. Mowat D. et al.Familial cerebral cavernous haemangioma diagnosed in an infant with a rapidly growing cerebral lesion.Australas Radiol. 2006; 50: 583-590Crossref PubMed Scopus (14) Google Scholar These vascular lesions of the brain are uncommon, rarely present in the first year of life, and represent only a small proportion of all central nervous system vascular anomalies.2Sakai N. Yamada H. Nishimura Y. Shirakami S. Futamura A. Andoh T. Intracranial cavernous angioma in the 1st year of life and a review of the literature.Childs Nerv Syst. 1992; 8: 49-52Crossref PubMed Scopus (24) Google Scholar Clinical manifestations most often associated with intracranial cavernous hemangiomas include: seizures, hemorrhagic syndrome, and mass lesion effect with hydrocephalus or focal neurological deficits. A congenital intracranial cavernous hemangioma is particularly rare and an unusual cause of neonatal seizures. Complete surgical resection yields an excellent outcome for large hemangiomas, but the optimum treatment for smaller lesions remains unclear. Spontaneous regression of extracranial cavernous hemangiomas during childhood is common, but the natural progression of intracranial cavernous hemangiomas is less well-described.3Prensky A.L. Gado M. Angiographic resolution of a neonatal intracranial cavernous hemangioma coincident with steroid therapy. Case report.J Neurosurg. 1973; 39: 99-103Crossref PubMed Scopus (5) Google Scholar This infant has been treated conservatively and remains seizure free with medication. Intracranial cavernous hemangiomas of infancyThe Journal of PediatricsVol. 157Issue 1PreviewTo the Editor: Full-Text PDF

Prenatal Ischemic Stroke as a cause of Neonatal Seizure Diagnosed by Magnetic Resonance Diffusion-Weighted Imaging

Perinatal ischemic stroke is a serious complication of pregnancy that may be attributed to certain specific risk factors associated with either some maternal or some infantile characteristics. While the occurrence of perinatal stroke may develop during the prepartum, intrapartum, or postpartum period, it is difficult to determine the exact time of occurrence because of obscure clinical manifestations in newborn babies. Here, we present the case of a neonate suffering from focal clonic seizure 24 hours after birth. The neonate was diagnosed as having perinatal ischemic stroke, which may have been caused by prenatal ischemic insult, as judged from the characteristic features in magnetic resonance (MR) diffusion-weighted imaging (DWI) performed a week after his birth. Finally, we strongly suggest that neonatal focal seizures be immediately investigated by MRI, especially with MR DWI. This image modality provides not only early diagnosis of perinatal ischemic stroke, but also assists to clarify the specific time (prepartum, intrapartum, or postpartum period) of the stroke's occurrence.

Seizures in the newborn

Seizures in the newborn period constitute a medical emergency. Subtle seizures are the commonest type of neonatal seizures, other types being clonic, tonic, and myoclonic. Myoclonic seizures carry the worst prognosis in terms of long-term neurodevelopmental outcome. Hypoxic-ischemic encephalopathy is the most common cause of neonatal seizures. Multiple etiologies often co-exist in neonates and hence it is essential to rule out conditions such as hypoglycemia, hypocalcemia, and meningitis before initiating specific therapy. A comprehensive approach for management of neonatal seizures has been described.

Apneic Seizures: A Sign of Temporal Lobe Hemorrhage in Full-Term Neonates

Intracranial hemorrhage is a common cause of neonatal seizures in full-term infants. However, only some infants with intracranial hemorrhage come to clinical attention. A right temporal lobe hemorrhage with resulting apneic seizures was described previously in one neonate. In this case report, we review three full-term male neonates with no significant perinatal complications who presented with apneic events and temporal lobe hemorrhage. One neonate had apnea as the sole manifestation of a seizure that was confirmed electrographically. One neonate had motor manifestations of seizures, in addition to apnea, that were confirmed as seizures electrographically. The third neonate had pure apneic events before initiation of electroencephalogram monitoring which were presumed to be seizures, because the electroencephalogram demonstrated epileptiform abnormalities. At follow-up, all three children were neurodevelopmentally normal. This case report emphasizes that, although uncommon, full-term neonates may present with apnea as the initial manifestation of temporal lobe hemorrhage. Because apnea could be a manifestation of a seizure, continuous electroencephalogram monitoring should be considered in a full-term neonate with unexplained apnea.

Radiologic Findings of Neonatal Cerebral Infarction related with Portal Vein Thrombosis: Case Report

A cerebral infarction in a newborn infant is not uncommon and is major cause of neonatal seizure. The author encountered one case of cerebral infarction that was assumed to be related to a portal vein thrombosis, and reports the radiology findings of a neonatal cerebral infarction and portal vein thrombosis.

Persistently Decreased Basal Synaptic Inhibition of Hippocampal CA1 Pyramidal Neurons after Neonatal Hypoxia-Induced Seizures

Hypoxia is the most common cause of neonatal seizures and can lead to epilepsy, but the epileptogenic mechanisms are not yet understood. We have previously shown that hypoxia-induced seizures in the neonatal rat result in acutely decreased amplitudes and frequency of spontaneous and miniature inhibitory postsynaptic currents (sIPSCs and mIPSCs) in hippocampal CA1 pyramidal neurons. In the current study, we asked whether such changes persist for several days following hypoxia-induced seizures. Similar to the acute findings, we observed decreased frequency and amplitudes of sIPSCs and decreased mIPSC amplitudes in CA1 pyramidal neurons at 3–5 days after hypoxia. However, in contrast to the acute findings, we observed no differences between hypoxia-treated and control groups in mIPSC frequency. Additionally, by 7 days after hypoxia, sIPSC amplitudes in the hypoxia group had recovered to control levels, but sIPSC frequency remained decreased. These data indicate that the persistently decreased sIPSC frequency result from decreased firing of presynaptic inhibitory interneurons, with only transient possible changes in postsynaptic responses to GABA release.

Neonatal seizures from in utero venlafaxine exposure

Venlafaxine (Efexor), a selective noradrenergic reuptake inhibitor, is an important therapeutic option in the treatment of perinatal depression, but its effects on the newborn are uncertain. We present a report of two infants with neonatal seizures attributed to maternal use of venlafaxine. The first infant was hypotonic and required resuscitation at birth. The second was born in a good condition but developed clinically apparent seizures after the second day of life. Both infants responded rapidly to treatment with phenobarbitone that was weaned uneventfully by the first and second week of life. Both remain well at 1 year of age. Other causes of neonatal seizures were excluded and neurological investigations on these two infants were unremarkable. We suggest that all infants exposed to maternal venlafaxine, no matter their condition at birth, be monitored in hospital for at least 3 to 4 days in order to preempt and treat adverse neurological events.

Maternal Risk Factors for Term Neonatal Seizures: Population-Based Study in Colorado, 1989—2003

Neonatal seizures in term infants are rare but have important potential implications for brain development. Risk factors for neonatal seizures in term infants have been less well defined than those among preterm infants. To evaluate the relationship between maternal risk factors and neonatal seizures in the first 72 hours of life in term infants, a case-control study using the Colorado Birth Certificate Registry was conducted. Term neonates in all hospitals in Colorado with and without seizures in the first 72 hours were studied. After adjusting for vaginal delivery in the setting of herpes infection and post-term delivery, preexisting diabetes in the mother (odds ratio 4.30, 95% confidence interval 1.64-11.27, P < .01) and fetal distress (odds ratio 5.88, 95% confidence interval 4.60-7.13, P < .0001) were independent risk factors for neonatal seizures in term infants. These findings are confirmatory of previous reports that maternal preexisting diabetes and fetal distress increase the risk of neonatal seizure in term infants. Although we cannot establish the pathophysiology of neonatal seizures from this analysis, hypoxic-ischemic brain injury and hypoglycemia in infants of diabetic mothers are known causes of neonatal seizures that can be represented in this analysis by fetal distress and maternal preexisting diabetes, respectively. Maternal diabetic vasculopathy can also be a contributing factor.

279 The Role of 7-Nitroindazole in Prolonged Seizures Induced by Kainic Acid in Young Rats, Submitted to Hypoxia During the Perinatal Period.

Background: Perinatal hypoxia is one of the most common causes of neonatal seizures. Nitric oxide (NO) has been involved in the pathophysiology of seizures. Furthermore, NO as well as nuclear factor-kB (NF-kB) have been implicated in the oxidative stress-induced neurodegeneration, associated with hypoxia and/or kainic acid (KA). Objective: The aim of the present study is to examine the role of 7-Nitroindazole (7NI) on hypoxic (H) and KA-induced seizures during early life. The expression of NF-kB has been also examined. Methods: Wistar rats (P10–11) were divided into 4 groups: A (H), B (H/KA), C (H/KA and 7NI) and D (control, vehicle). Hypoxia was induced by decreasing O2 concentration from 7% to 4% within 15 minutes. At P21–22, rats of groups B and C were administered with KA (10mg/kg i.p). Animals of group C were pre-treated with 7NI (50mg/kg i.p). Histological assessment was performed at P24 with hematoxylin-eosin staining and cell counts in the hippocampal area. NF-kB expression was examined by immunohistochemistry. Results: Histologic evaluation revealed significantly decreased cell loss in 7NI treated group, compared with group B (10.1%±3.5 and 25.1%±10.5 respectively p<0.05). In control group NF-kB immunostaining was slight and restricted to the cytoplasm. In H/KA group over-expression of NF-kB was clearly observed at 4 hr, following KA administration, reduced in 24 hrs and almost totally abolished in 48 hrs. NF-kB immunoreactivity was localized mainly in the cytoplasm of neuronal, glial and endothelial cells. Dense nuclear immunostaining of NF-kB was observed in damaged neurons and reactive astrocytes of hippocampal area. There was no obvious difference in NF-kB staining between H/KA group and animals pre-treated with 7NI Conclusion: According to our results administration of 7NI, a selective inhibitor of nNOS, clearly diminished seizures-induced damage in the hippocampus, which might indicate a possible role of NO in the pathophysiology of prolonged seizures during infancy. Additionally, alteration of NF-kB expression points to a potential implication of NF-kB in mechanisms of seizures that may be correlated with NO.

Maternal water intoxication as a cause of neonatal seizures

A term infant was admitted at 6 h of age with seizures related to hyponatraemia. During the last hours of labour the infant's mother had drunk 3 L of water. After delivery the serum sodium was 121 mmol/L in the mother and 126 mmol/L in the infant. Both resolved spontaneously. We discuss this case and the impact of maternal fluid intake during labour on the fetus and neonate. Women should be advised that excessive oral fluid intake during labour could adversely affect both mother and infant.

Impaired SynGAP expression and long-term spatial learning and memory in hippocampal CA1 area from rats previously exposed to perinatal hypoxia-induced insults: beneficial effects of A68930

Hypoxic encephalopathy is a common cause of neonatal seizures and long-term neurological cognitive deficits. In rats at postnatal days 10–12 (P10–P12), global hypoxia induced spontaneous seizures and chronic brain injury, mimicking clinical aspects of neonatal hypoxia. Synaptic Ras-GTPase activating protein (SynGAP) has important roles in RAS/MAPK-dependent synaptic plasticity and mammalian learning. We investigated possible alterations of SynGAP expression occurring in memory-impaired animals previously exposed to perinatal hypoxia insults. We also evaluated the therapeutic efficacy of A68930, a selective agonist of dopamine D1/D5 receptors, on perinatal hypoxia insults. In the hippocampal CA1 region, perinatal hypoxia insults (P10) led to a reduction in SynGAP expression associated with impairment in long-term spatial learning and memory performance at P45. The use of A68930 (at a dose of 1, 2, 3 mg/kg, P17–P23) effectively attenuated the deleterious effects as described above. Our results may indicate the involvement of SynGAP in certain forms of brain injury, leading to long-term learning and memory deficits. A68930 may have clinical potential as a therapeutic agent for alleviation of long-term cognitive deficits in rats and other animal models.

Etiology of Neonatal Seizures

After completing this article, readers should be able to: 1. Name the primary causes of neonatal seizures today. 2. Describe the cerebral malformations associated with neonatal seizures. 3. Name the metabolic disorders that are associated with neonatal seizures. 4. Compare the characteristics of familial or idiopathic epilepsies. 5. List appropriate diagnostic tests for neonates who have seizures. 6. Provide a prognosis based on the cause of neonatal seizures. Neonatal seizures are a common problem in the newborn nursery and can occur in infants at any gestational age. Seizures in a newborn infant evoke a sense of urgency among neonatologists because they often indicate a disturbance of the central nervous system (CNS). Causes of neonatal seizures encompass virtually the entire spectrum of neurologic disorders of infancy, but most neonatal seizures today are due to hypoxic-ischemic brain injury and intracranial hemorrhage. The proper treatment of neonatal seizures depends on the cause. For example, neonatal seizures due to a transient metabolic disturbance, such as hypocalcemia or hypoglycemia, are treated by correcting the underlying metabolic derangement. However, seizures due to such transient disturbances are relatively infrequent today because of improved neonatal care. For neonates who have seizures caused by a systemic infection (sepsis) or CNS infection (meningitis and encephalitis), the underlying infection must be treated appropriately. The specific cause also has prognostic implications. More common etiologies of neonatal seizures are discussed in this review (Table 1). As discussed in the review on neonatal electroencephalography (EEG) in this issue of NeoReviews , proper identification of epileptic seizures is important. The most common seizure types are: focal or multifocal clonic, tonic, and myoclonic and subtle. Subtle seizures comprise a variety of motor and autonomic phenomena and are more common in neonates who have severe encephalopathies. However, neonates often have abnormal paroxysmal motor activity, such as oral-buccal-lingual movements, pedaling, stepping, and rotatory arm …

Index of Suspicion In the Nursery

A 9-day-old Hispanic boy presents to the emergency department with seizures and apnea. The seizure lasts for about 3 minutes and is characterized by stiffening of the body and laryngospasm. Laboratory evaluation reveals a serum calcium concentration of 6 mg/dL (1.5 mmol/L). Hypocalcemic tetany resolves after administration of intravenous calcium. The infant also has fever of 100.4°F (37.7°C). The infant was born at term, and his birthweight was 3.2 kg. He is the fifth child born of nonconsanguineous parentage. The antenatal period was uneventful. Because the family does not have insurance, the mother had not taken prenatal vitamins and supplements. The baby has been fed with human milk and formula. On physical examination upon admission to the hospital, his temperature is 99°F (36.9°C), pulse is 186 beats/min, respiratory rate is 54 breaths/min, blood pressure is 97/64 mm Hg, and weight is 3.83 kg. He has no dysmorphic features and is normocephalic, with an open and flat anterior fontanelle without craniotabes. No cataracts or Chvostek sign are present. Cardiovascular examination reveals a regular heart rate and rhythm, with no murmurs. The lungs are clear to auscultation bilaterally, and there is no hepatosplenomegaly. Neurologic findings are normal. Laboratory evaluation reveals: sodium, 136 mEq/L (136 mmol/L); potassium, 5.2 mEq/L (5.2 mmol/L); chloride, 101 mEq/L (101 mmol/L); bicarbonate, 26 mEq/L (26 mmol/L); blood urea nitrogen, 10 mg/dL (3.57 mmol/L); creatinine, 0.3 mg/dL (26.5 mcmol/L); glucose, 109 mg/dL (6.1 mmol/L); calcium, 6.6 mg/dL (1.65 mmol/L); phosphorous, 10.5 mg/dL (3.4 mmol/L); albumin, 3.0 g/dL (30 g/L); and magnesium, 2 mg/dL (0.82 mmol/L). The white blood cell count and differential count are normal. Findings on cerebrospinal fluid evaluation are normal. However, the 25-hydroxyvitamin D concentration is less than 7 ng/mL (17.5 nmol/L) (normal, 10 to 68 ng/mL [25 to 169.7 nmol/L]), the 1,25-dihydroxyvitamin D concentration is 45 …

Decreased Glutamate Receptor 2 Expression and Enhanced Epileptogenesis in Immature Rat Hippocampus after Perinatal Hypoxia-Induced Seizures

Hypoxic encephalopathy is the most common cause of neonatal seizures and can lead to chronic epilepsy. In rats at postnatal days 10-12 (P10-12), global hypoxia induces spontaneous seizures and chronically decreases seizure threshold, thus mimicking clinical aspects of neonatal hypoxia. We have shown previously that the acute and chronic epileptogenic effects of hypoxia are age-dependent and require AMPA receptor activation. In this study, we aimed to determine whether hypoxia-induced seizures and epileptogenesis are associated with maturational and seizure-induced changes in AMPA receptor composition and function. Northern and Western blots indicated that glutamate receptor 2 (GluR2) mRNA and protein expression were significantly lower in neocortex and hippocampus at P10-12 compared with adult. After hypoxia-induced seizures at P10, GluR2 mRNA was significantly decreased within 48 hr, and GluR2 protein was significantly decreased within 96 hr. AMPA-induced Co(2+) uptake by neurons in hippocampal slices indicated higher expression of Ca(2+)-permeable AMPA receptors in immature pyramidal neurons compared with adult. In slices obtained 96 hr after hypoxia-induced seizures, AMPA-induced Co(2+) uptake was significantly increased compared with age-matched controls, and field recordings revealed increased tetanus-induced afterdischarges that could be kindled in the absence of NMDA receptor activation. In situ end labeling showed no acute or delayed cell death after hypoxia-induced seizures. Our results indicate that susceptibility to hypoxia-induced seizures occurs during a developmental stage in which the expression of Ca(2+)-permeable AMPA receptors is relatively high. Furthermore, perinatal hypoxia-induced seizures induce increased expression of Ca(2+)-permeable AMPA receptors and an increased capacity for AMPA receptor-mediated epileptogenesis without inducing cell death.