Clinical and etiological profile of neonatal seizures: a tertiary care hospital based study

Asif Aziz, Imran Gattoo, Munazza Aziz, Ghulam Rasool


Background: The most vulnerable period of life to develop seizures is the neonatal period. These events very often signify serious damage or malfunction of the immature developing central nervous system. Neonatal seizures may arise as a result of diverse etiologies and can have varied presentations. Objective: Our study was aimed at finding the incidence, etiological factors, and time of onset, clinical types and various biochemical abnormalities in neonatal seizures.

Methods: A hospital based prospective observational study was undertaken in a tertiary care paediatric hospital of Government Medical College Srinagar. A total of 100 consecutive neonates presenting with seizures from September 2013 to August 2014 were enrolled in the study. Detailed antenatal history and baseline characteristics of convulsing neonate were recorded at admission. Clinical details of each seizure episode reported by the mother and subsequently observed by the resident doctors on duty were recorded. Venous blood was collected as soon as possible and blood glucose, total serum calcium levels, Na+, K+, Mg and P-levels were done immediately after baby had seizures and before instituting any treatment. Data was described as mean ± SE and %age. SPSS 16.0 and MS Excel software were used for data analysis.

Results: Cumulative frequency of 3.9% was recorded in neonatal seizures in our setup. Hypoxic ischemic encephalopathy was the commonest etiology of neonatal seizures. Intracranial haemorrhage followed by Hypoxic ischemic encephalopathy was the commonest seizure etiology in preterm neonates. Majority of Hypoxic ischemic encephalopathy patients presented with seizures in the first 72 hrs. of life. Focal clonic and subtle seizures were the commonest seizure types encountered. 17 neonates (31%) had primary metabolic seizures. Hypocalcaemia was the commonest biochemical abnormality in primary metabolic seizures and was present in 70% neonates in this group. Hypoglycaemia was the next commonest abnormality and was present in 41% neonates within this group.

Conclusions: Hypoxic ischemic encephalopathy was the commonest etiology with focal clonic and subtle seizures being the commonest clinical types encountered. Hypocalcaemia was the most frequent biochemical abnormality found.



Hypoglycaemia, Hypocalcaemia, Intracranial haemorrhage, Non-metabolic seizures, Primary metabolic

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Volpe JJ. Neonatal seizures. Neurology of the new-born. Philadelphia, PA: WB Saunders, 2001;178-214.

Airede KI, Neonatal seizures and a two year neurological outcome. J Trop Pediatr 1991;37:313-17.

Nunez JL, Alt JJ, McCarthy MM. A novel model for prenatal brain damage. Long term deficits in hippocampal cell number and hippocampal-dependent behaviour following neonatal GABA receptor activation. ExpNeurol. 2003;181:270-80.

Sarnat HB, Sarnat MS. Neonatal encephalography following foetal distress. A clinical and encephalographic study. Arch Neurol 1976;33:696-705.

Mercuri E, Cowan M, Rutherford D, Pennoch J, Dubowitz L. Ischemic and haemorrhagic brain lesions in new-borns with seizures and normal Apgar scores. Arch Dis Child 1995;73:F67-F74.

Scher MS. Destructive brain lesions of presumed foetal onset: Antepartum causes of cerebral palsy. Paediatrics. 1991;88:896-906

Scher MS, Hamid MY, Steppe DA. Ictal and interictal durations in preterm and term neonates. Epilepsia 1993;34:284-8.

Sheth RD, Hobbs GR, Mullett M. Neonatal seizures: Incidence onset and etiology by gestational age. J Perinatol. 1999;19:40-3.

Kairam R, De Vivo DC. Neurologic manifestations of congenital infection. Clin Perinatol. 1981;8:455-65.

Brown JK, Cockburn F. Clinical and chemical correlates in convulsions of the new-born. Lancet. 1972;1;135-9.

Sood A, Grover N, Sharma R. Biochemical abnormalities in neonatal seizures. Indian Journal of Paed. 2003;70(3):221-4.

Keen JH, Lee. Sequelae of neonatal convulsions. Study of 112 infants. Arch Dis Child 1973. Jul; 48(7):542-546

Rose AL, Lombroso. CT: A study of clinical, pathological and electroencephalographic features in 137 full term babies with a long term follow up. Paediatrics 1970;45:404-425.

Mark S. Scher. Avery’s Disease of New-born 8thed. Elsevier Health Sciences; 2005. Chapter 66, Neonatal seizures, p1020.

Carole Kenner, Judy, Wright Lott. Comprehensive neonatal care 4th ed. Elsevier Health Sciences; 2007. Chapter 8, 95.

Kumar A, Gupta V, Singla: Biochemical abnormalities in neonatal seizures. Indian Paed. 1995;32(4):424-8.

Ment LR, Freedman RM. Neonates with seizures attributed to perinatal complications. Am J Dis Child 1982;136:548-50.

Asindi AA, Antia Obong OE, Ibia EO. Neonatal seizures in Nigerian infants. Afr J Med Sci 1995;24:243-8.

Taksande AM, Krishna V, Manish Jain, Mahaveer L. Clinico-biochemical profile of neonatal seizures. PaedOncall Journal 2005 October;2(10).

Coen RW, Mc Cutchen CB, Wermer D, Snyder J, Gluck FE. Continuous monitoring of EEG following perinatal asphyxia. J Pediatr 1982;100:628-30.

Holden KR, Mellitis ED, Freeman JM. Neonatal seizures: correlation of prenatal and perinatal events with outcome. Pediatrics 1982;70:165-76

Legido A, Clancy RR. Neurologic outcome after EEG proven neonatal seizures. Paediatrics 1991;88:583-96.

Bushra AM, Butt MA. Seizure etiology in the new-born period. Journal of College of Physicians and Surgeons Pakistan 2005;15:786-90.

Scher MS. Controversies regarding the neonatal seizure recognition. Epileptic disord. 2002;4:139-58.