scholarly journals Neonatal seizures and epilepsies

2014 ◽  
Vol 01 (02) ◽  
pp. 075-083 ◽  
Author(s):  
Kollencheri Vinayan ◽  
Solomon Moshé
Keyword(s):  
Motor Behavior ◽  
Neonatal Seizure ◽  
Neonatal Seizures ◽  
Immature Brain ◽  
Accurate Identification ◽  
Central Nervous System Dysfunction ◽  
Ictal Eeg ◽  
Neurologic Function ◽  
Eeg Recordings ◽  
Cerebral Insult

AbstractNeonatal seizure is the most frequent clinical manifestation of central nervous system dysfunction in the newborn. It is defined as a paroxysmal alteration in neurologic function that include motor, behavior and/or autonomic functions occurring in the first 28 days after birth of a term neonate or before 44 weeks of gestational age in a preterm infant. Seizures in the presence of encephalopathy are the most important clinical pattern of an acute cerebral insult in the immature brain. Chronic epileptic disorders very rarely may have their onset in the neonatal period and may persist well into infancy and later childhood. Structural brain defects and metabolic disorders constitute a substantial proportion of this group. Ictal EEG recordings remain the gold standard for the accurate identification of neonatal seizures of cortical origin and for the distinction from non-epileptic paroxysmal events. This review focuses on the electroclinical patterns of neonatal seizures and epilepsies with an emphasis on the classification and terminologies. The current therapeutic options are also highlighted briefly.

Time Varying Neonatal Seizure Localization

2010 ◽  
Vol 49 (05) ◽  
pp. 473-478 ◽  
Author(s):  
P. J. Cherian ◽  
M. Vos ◽  
R. M. Swarte ◽  
J. H. Blok ◽  
G. H. Visser ◽  
...  
Keyword(s):  
Spatial Information ◽  
Neonatal Seizure ◽  
Neonatal Seizures ◽  
Neonatal Brain ◽  
Cp Decomposition ◽  
Neurologic Disorders ◽  
Eeg Recordings ◽  
Value Decomposition ◽  
Seizure Localization ◽  
The Brain

Summary Background: A common cause for damage to the neonatal brain is a shortage in the oxygen supply to the brain or asphyxia. Neonatal seizures are the most frequent manifestation of neonatal neurologic disorders. Multichannel EEG recordings allow topographic localization of seizure foci. Objectives: We want to objectively determine the spatial distribution of the seizure on the scalp, the location in time and order the dominant sources in the brain based on their strength. Methods: In this paper we combine a method based on higher order CP-decomposition with subsequent singular value decomposition (SVD). Results: We illustrate the abilities of the method on simulated as well as on real neonatal seizure EEG. Conclusions: The proposed method provides reliable time and spatial information about the seizure, gives a clear overview of what is going on in the EEG and allows easy interpretation.

scholarly journals Electroencephalographic Features of Temporal Lobe Epilepsy

2010 ◽  
Vol 37 (4) ◽  
pp. 439-448 ◽  
Author(s):  
Mohammed M. Jan ◽  
Mark Sadler ◽  
Susan R. Rahey
Keyword(s):  
Temporal Lobe Epilepsy ◽  
Surgical Management ◽  
Temporal Lobe ◽  
Seizure Onset ◽  
Resective Surgery ◽  
Accurate Localization ◽  
Epileptiform Discharges ◽  
Ictal Eeg ◽  
Temporal Lobe Seizures ◽  
Eeg Recordings

Electroencephalography (EEG) is an important tool for diagnosing, lateralizing and localizing temporal lobe seizures. In this paper, we review the EEG characteristics of temporal lobe epilepsy (TLE). Several “non-standard” electrodes may be needed to further evaluate the EEG localization, Ictal EEG recording is a major component of preoperative protocols for surgical consideration. Various ictal rhythms have been described including background attenuation, start-stop-start phenomenon, irregular 2-5 Hz lateralized activity, and 5-10 Hz sinusoidal waves or repetitive epileptiform discharges. The postictal EEG can also provide valuable lateralizing information. Postictal delta can be lateralized in 60% of patients with TLE and is concordant with the side of seizure onset in most patients. When patients are being considered for resective surgery, invasive EEG recordings may be needed. Accurate localization of the seizure onset in these patients is required for successful surgical management.

Electroencephalographic Recordings of Focal Seizures in Patients Affected by Periventricular Nodular Heterotopia: Role of the Heterotopic Nodules in the Genesis of Epileptic Discharges

2004 ◽  
Vol 19 (3) ◽  
pp. 369-377
Author(s):  
Giorgio Battaglia ◽  
Silvana Franceschetti ◽  
Luisa Chiapparini ◽  
Elena Freri ◽  
Stefania Bassanini ◽  
...  
Keyword(s):  
Brain Regions ◽  
Periventricular Nodular Heterotopia ◽  
Focal Seizures ◽  
Ictal Eeg ◽  
Epileptic Discharges ◽  
Nodular Heterotopia ◽  
Eeg Recordings ◽  
Drug Resistant Epilepsy ◽  
Video Eeg

Patients affected by periventricular nodular heterotopia are frequently characterized by focal drug-resistant epilepsy. To investigate the role of periventricular nodules in the genesis of seizures, we analyzed the electroencephalographic (EEG) features of focal seizures recorded by means of video-EEG in 10 patients affected by different types of periventricular nodular heterotopia and followed for prolonged periods of time at the epilepsy center of our institute. The ictal EEG recordings with surface electrodes revealed common features in all patients: all seizures originated from the brain regions where the periventricular nodular heterotopia were located; EEG patterns recorded on the leads exploring the periventricular nodular heterotopia were very similar both at the onset and immediately after the seizure's end in all patients. Our data suggest that seizures are generated by abnormal anatomic circuitries, including the heterotopic nodules and adjacent cortical areas. The major role of heterotopic neurons in the genesis and propagation of epileptic discharges must be taken into account when planning surgery for epilepsy in patients with periventricular nodular heterotopia. ( J Child Neurol 2005;20:369—377).

scholarly journals Canonical Decomposition of Ictal Scalp EEG and Accurate Source Localisation: Principles and Simulation Study

2007 ◽  
Vol 2007 ◽  
pp. 1-10 ◽  
Author(s):  
Maarten De Vos ◽  
Lieven De Lathauwer ◽  
Bart Vanrumste ◽  
Sabine Van Huffel ◽  
W. Van Paesschen
Keyword(s):  
Simulation Study ◽  
Seizure Activity ◽  
Canonical Decomposition ◽  
Scalp Eeg ◽  
Activity Frequency ◽  
Ictal Eeg ◽  
Single Dipole ◽  
Eeg Recordings ◽  
Frequency Changes ◽  
Dipole Localisation

Long-term electroencephalographic (EEG) recordings are important in the presurgical evaluation of refractory partial epilepsy for the delineation of the ictal onset zones. In this paper, we introduce a new concept for an automatic, fast, and objective localisation of the ictal onset zone in ictal EEG recordings. Canonical decomposition of ictal EEG decomposes the EEG in atoms. One or more atoms are related to the seizure activity. A single dipole was then fitted to model the potential distribution of each epileptic atom. In this study, we performed a simulation study in order to estimate the dipole localisation error. Ictal dipole localisation was very accurate, even at low signal-to-noise ratios, was not affected by seizure activity frequency or frequency changes, and was minimally affected by the waveform and depth of the ictal onset zone location. Ictal dipole localisation error using 21 electrodes was around 10.0 mm and improved more than tenfold in the range of 0.5–1.0 mm using 148 channels. In conclusion, our simulation study of canonical decomposition of ictal scalp EEG allowed a robust and accurate localisation of the ictal onset zone.

scholarly journals Targeting ischemia-induced KCC2 hypofunction rescues refractory neonatal seizures and mitigates epileptogenesis in a mouse model

2020 ◽  
Author(s):  
Brennan J. Sullivan ◽  
Pavel A. Kipnis ◽  
Brandon M. Carter ◽  
Shilpa D. Kadam
Keyword(s):  
Mouse Model ◽  
Neonatal Seizure ◽  
Seizure Susceptibility ◽  
Neonatal Seizures ◽  
First Line ◽  
Chloride Homeostasis ◽  
Epilepsy Models ◽  
And Function ◽  
Ischemic Encephalopathy

AbstractNeonatal seizures pose a clinical challenge for their early detection, acute management, and mitigation of long-term comorbidities. A major cause of neonatal seizures is hypoxic-ischemic encephalopathy that results in seizures that are frequently refractory to the first-line anti-seizure medication phenobarbital (PB). One proposed mechanism for PB-inefficacy during neonatal seizures is the reduced expression and function of the neuron-specific K+/Cl− cotransporter 2 (KCC2), the main neuronal Cl− extruder that maintains chloride homeostasis and influences the efficacy of GABAergic inhibition. To determine if PB-refractoriness after ischemic neonatal seizures is dependent upon KCC2 hypofunction and can be rescued by KCC2 functional enhancement, we investigated the recently developed KCC2 functional enhancer CLP290 in a CD-1 mouse model of refractory ischemic neonatal seizures quantified with vEEG. We report that acute CLP290 intervention can rescue PB-resistance, KCC2 expression, and the development of epileptogenesis after ischemic neonatal seizures. KCC2 phosphorylation sites have a strong influence over KCC2 activity and seizure susceptibility in adult experimental epilepsy models. Therefore, we investigated seizure susceptibility in two different knock-in mice in which either phosphorylation of S940 or T906/T1007 was prevented. We report that KCC2 phosphorylation regulates both neonatal seizure susceptibility and CLP290-mediated KCC2 functional enhancement. Our results validate KCC2 as a clinically relevant target for refractory neonatal seizures and provide insights for future KCC2 drug development.

scholarly journals P.052 Benign spasms of infancy - a mimicker of infantile epileptic disorders

2019 ◽  
Vol 46 (s1) ◽  
pp. S28
Author(s):  
J Ghossein ◽  
D Pohl
Keyword(s):  
Epileptiform Activity ◽  
Positive Family History ◽  
Myoclonic Epilepsy ◽  
First Year ◽  
Neurodevelopmental Outcomes ◽  
Epileptic Spasms ◽  
Ictal Eeg ◽  
Interictal Eeg ◽  
Eeg Recordings ◽  
First Year Of Life

Background: Benign spasms of infancy (BSI), previously described as benign non-epileptic infantile spasms or benign myoclonus of early infancy, are non-epileptic movements manifesting during the first year of life and spontaneously resolving in the second year of life. BSI are characterized by spasms typically lasting 1-2 seconds, involving to varying degrees the head, neck, trunk, shoulders and upper extremities. Ictal and interictal EEG recordings are normal. BSI are not associated with developmental retardation and do not require treatment. Distinction between BSI and infantile epileptic disorders, such as epileptic spasms or myoclonic epilepsy of infancy, can be challenging given the clinical similarities. Moreover, interictal EEGs can be normal in all conditions. Epileptic spasms and myoclonic epilepsy require timely treatment to improve neurodevelopmental outcomes. Methods: We describe a 6-month old infant presenting with spasm-like movements. His paroxysms as well as a positive family history for epileptic spasms were in keeping with a likely diagnosis of West syndrome. Results: Surprisingly, ictal video EEG did not reveal epileptiform activity, and suggested a diagnosis of BSI. Conclusions: We emphasize that ictal EEG is the gold standard for classification of infantile paroxysms as either epileptic or non-epileptic, thereby avoiding overtreatment of BSI and facilitating timely targeted treatment of infantile epilepsies.

scholarly journals Etiology and Immediate Outcome of Neonatal Convulsions : A Hospital Based Study

2020 ◽  
Vol 19 (1) ◽  
pp. 8-14
Author(s):  
Salina Haque ◽  
Shahadat Hossain ◽  
Mitra Datta ◽  
Mohammed Maruf Ul Quader
Keyword(s):  
Important Determinant ◽  
Neonatal Seizure ◽  
Neonatal Seizures ◽  
Newborn Period ◽  
Primitive Reflexes ◽  
Neonatal Convulsions ◽  
Normal Body Weight ◽  
The Mean ◽  
Very High ◽  
Common Manifestation

Background: Neonatal seizures are the most common manifestation ofneurological disorders in the newborn period and an important determinant ofoutcome To evaluate the causes and immediate outcome in hospital of neonatalconvulsions. Materials and methods: This hospital based prospective study was conducted inSpecial Care Neonatal Unit (SCANU) Department of Paediatrics and Child HealthBangabandhu Memorial Hospital (BBMH) USTC, including 30 neonates sufferingfrom convulsion from 1 to 28 days of age during the period of 1st July to 30thOctober, 2003. Results: Twenty-four (80%) cases were under 5 days age, 4 (13.33%) cases wereranged 6 to 15 days age. The mean age of the patients was 3 days. 18 (60%)babies were male and 12 (40%) were female. Male:female ratio was 1.5:1.Twenty (66.67%) babies had normal body weight (2500-4000 g). Maternalcomplications during pregnancy were present in 10 (33.33%) cases. Convulsionwas present in all 30 (100%) cases. Depressed primitive reflexes were found 16(53.33%) cases, cyanosis in 5 (16.67%) cases, fever in 7 (23.33%) cases. Subtleseizures were present in 16 (53.33%) cases, focal clonic and focal tonic seizureswere present in 7 (23.33%) and 4 (13.33%) cases, respectively. Generalized tonicseizures were present in 3 (10%) cases and none (0%) cases had myoclonicseizure. Onset of convulsion in relation to age revealed that 13 (43.33%) caseshad convulsion before 24 hours of age, 10 (33.33%) developed convulsionbetween 1-3 days of age, 5 (16.67%) and 2 (6.67%) had convulsion between 4-7days and 8-21 days of age respectively. Commonest cause of neonatalconvulsion was found to be Hypoxic-Ischaemic Encephalopathy (HIE). It wasfound in 17 (56.67%) patients. Hypoglycaemia as primary metabolic cause wasfound in 4 (13.33%) patients, and septicaemia was found in 3 (10%) patients.Eighteen (60%) cases stayed in hospital for 7-10 days, out of which 16 (53.33%)were cured and 2 (6.67%) died. Three (10%) cases stayed in hospital for 4-5days, all of them were cured, Two (6.67%) cases stayed in hospital for 3 daysand among them 1 (3.33%) died and another was cured and discharged onrequest. Five cases (16.67%) stayed for 11-14 days in hospital, out of them 3(10%) were cured and 2 (6.67%) expired. Only 1 case (3.33%) stayed for morethan 14 days and died at day 20. The mortality rate in this study is 20%. Conclusion: The most common cause of neonatal seizure was HIE (56.67%).Other causes of neonatal convulsions are septicaemia, meningitis, primarymetabolic disorders like hypoglycaemia and hypocalcaemia, intraventricularhaemorrhage and some causes are still unknown. Mortality due to neonatalconvulsion is still very high, and in this series, it was found to be 20 percent.Survival while staying in hospital occurred in 24 (80%) cases. Chatt Maa Shi Hosp Med Coll J; Vol.19 (1); January 2020; Page 8-14

scholarly journals Profile of neonatal epilepsies

Neurology ◽  
2017 ◽  
Vol 89 (9) ◽  
pp. 893-899 ◽  
Author(s):  
Renée A. Shellhaas ◽  
Courtney J. Wusthoff ◽  
Tammy N. Tsuchida ◽  
Hannah C. Glass ◽  
Catherine J. Chu ◽  
...  
Keyword(s):  
Genetic Testing ◽  
Diagnostic Testing ◽  
Epileptic Encephalopathy ◽  
Neonatal Seizure ◽  
Neonatal Seizures ◽  
Epileptic Encephalopathies ◽  
Brain Malformations ◽  
Symptomatic Seizures ◽  
Acute Symptomatic Seizures ◽  
Structural Brain

Objective:Although individual neonatal epilepsy syndromes are rare, as a group they represent a sizable subgroup of neonatal seizure etiologies. We evaluated the profile of neonatal epilepsies in a prospective cohort of newborns with seizures.Methods:Consecutive newborns with seizures were enrolled in the Neonatal Seizure Registry (an association of 7 US children's hospitals). Treatment and diagnostic testing were at the clinicians' discretion. Neonates with seizures related to epileptic encephalopathies (without structural brain abnormalities), brain malformations, or benign familial epilepsies were included in this analysis.Results:Among 611 consecutive newborns with seizures, 79 (13%) had epilepsy (35 epileptic encephalopathy, 32 congenital brain malformations, 11 benign familial neonatal epilepsy [BFNE], 1 benign neonatal seizures). Twenty-nine (83%) with epileptic encephalopathy had genetic testing and 24/29 (83%) had a genetic etiology. Pathogenic or likely pathogenic KCNQ2 variants (n = 10) were the most commonly identified etiology of epileptic encephalopathy. Among 23 neonates with brain malformations who had genetic testing, 7 had putative genetic etiologies. Six infants with BFNE had genetic testing; 3 had pathogenic KCNQ2 variants and 1 had a pathogenic KCNQ3 variant. Comorbid illnesses that predisposed to acute symptomatic seizures occurred in 3/35 neonates with epileptic encephalopathy vs 10/32 with brain malformations (p = 0.03). Death or discharge to hospice were more common among newborns with brain malformations (11/32) than those with epileptic encephalopathy (3/35, p = 0.01).Conclusions:Neonatal epilepsy is often due to identifiable genetic causes. Genetic testing is now warranted for newborns with epilepsy in order to guide management and inform discussions of prognosis.

NEONATAL SEIZURE STATES

PEDIATRICS ◽  
1970 ◽  
Vol 45 (4) ◽  
pp. 650-650
Author(s):  
L. Rose ◽  
Cesare T. Lombroso
Keyword(s):  
Congenital Heart ◽  
Normal Development ◽  
Sporadic Case ◽  
Neonatal Seizure ◽  
Unknown Etiology ◽  
Hemorrhagic Disease ◽  
Neonatal Seizures ◽  
Line Section ◽  
Pathologic Findings ◽  
Made In

In the March issue of Pediatrics two corrections should be made in the article by Drs. Rose and Lombroso: Page 406: Table III, second footnote should read † 1. Two siblings with seizures which continued and were accompanied by mental retardation. 2. A case of transient familial neonatal seizures occurring in three generations and followed by normal development. 3. One sibship and a sporadic case of pyridoxine dependency. 4. A case of hypernatremia associated with hypocalcemia of unknown etiology. 5. A case of hemorrhagic disease of the newborn. 6. A case of congenital heart disease with transient seizures. Page 418: Table referred to in second line, section on Pathologic Findings, should be XII rather than II.

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