Seizures are the first sign of neurological dysfunction in newborn but their clinical expression at this age is quite variable, poorly organized and often subtle, where prompt diagnostic and therapeutic plans are necessary; a delay in therapy often results in poor neurological outcome.1 Volpe has classified seizures into five clinical types, viz. subtle, multifocal, clonic, focal clonic, generalized tonic and myoclonic. Neonatal seizures can be due to various causes like hypoxic-ischemic encephalopathy, intracranial hemorrhage, meningitis, hypoglycemia, hypocalcemia, congenital malformation, etc, Immature brain is uniquely vulnerable to develop seizure, because the development of inhibitory neuronal circuits lag behind the excitatory network While this imbalance between excitatory and inhibitory processes promote early neuronal development, it also leaves the brain more susceptible to seizures. Neonatal seizures are always "secondary to 'or' 'symptomatic of an underlying cerebral insult or stress. Animal data suggest that the neonatal seizure have a deleterious impact on later development and that these seizures may exacerbate underlying injury from hypoxia.2 Seizures occur when a large group of neurons undergo excessive synchronized depolarization. Depolarization can result from excessive excitatory amino acid release (eg, glutamate) or deficient inhibitory neurotransmitter (eg, gamma amino butyric acid [GABA]). Another potential cause is disruption of ATP-dependent resting membrane potentials, which causes a flow of sodium into the neuron and potassium out of the neuron. Hypoxic-ischemic encephalopathy disrupts the ATP- dependent sodium-potassium pump and appears to cause excessive depolarization. It as an important cause of neonatal seizures. The biochemical effects of neonatal seizures included derangements of energy metabolisın. Energy-dependent ton pumps are compromised and ADP levels rise. The rise in ADP stimulates glycolysis with the ultimate increase in pyruvate, which accumulates as a result of compromised mitochondrial function.3,.

Methods of Collection of Data: The present study included 11 neonates presenting with seizures admitted to NICU. (A) Baseline characteristics: These includes sex, gestational age, intrauterine growth status, maternal education and the socioeconomic status (Kuppuswami scale), weight, head circumference and length. (B) Clinical profile of seizures: Each seizure episode reported by mother and subsequently observed in the NICU was recorded and relevant information was gathered: age at onset of seizure, duration of seizure in minutes, associated autonomic changes (HR, RR, 02 Saturation), medication required to control seizures and response time to medication. (C) Determination of etiology: Relevant clinical information, antenatal history of infection including TORCH, drug intake, chorioamnionitis, fetal distress (fetal heart rate abnormalities or meconium stained liquor). (D) Investigations: Essential investigations including blood glucose, ionized sernm calcium, serum sodium, arterial pH and USG of cranium .Additional investigation as guided by history, physical examination and essential investigations. These include sepsis screen, blood culture, cerebrospinal fluid (CSF) examination, haematoc t, serum bilirubin level, serum urea and creatinine, "TORCH"serology, serum calcium/magnesium, metabolic profile for inborn error of metabolism and CT scan. Inclusion Criteria: All neonates presenting with seizures or developing clinically identifiable seizures before 28 days of life were included in the study. Exclusion criteria: Neonates with doubtful seizures were excluded. Neonates with jitteriness were excluded by holding the limb to determine whether the movement could be stopped. Detailed antenatal, natal and post natal history were taken as per the proforma enclosed. Antenatal History: History of medical illness like fever with rash, Asthma, Tuberculosis, cardiac diseases, diabetes Mellitus were asked. History of obstetric complications like Pili, Sudden increase in fetal movement were taken. Regarding Antenatal Registration, Inj. TI, Iron and folic acid were also asked. Perinatal History: History of PROM, Prolonged Jabour, repeated per vaginal examinations, foul smelling liquor, place of delivery, type of delivery and indication for caesarean section, were enquired. Accidental injection of the local anaesthetic into the fetal scalp After delivery whether baby cried immediately or not, cord around the neck, cord prolapse, fetal distress, Mcconium stained liquor, mcconium aspiration and any resuscitation done, were enquired.The neonate was diagnosed with birth asphyxia if baby did not cry for more than three minutes after birth or documented APGAR score was :S 3 at one minute and< 7 at 5 minutes of birth. Post-natal History: History of lethargy, poor activity, poor feeding, jaundice, excessive cry, vomiting and seizures were taken. History of Seizures: The day of onset of seizures, type of seizures, the duration of seizures, number of seizures and consciousness during and between seizures were taken after appropriate history, detailed examination of neonate was done. Examination: The vitals of the baby (Heart Rate, Respiratory Rate, Peripheral pulses, Blood pressure, temperature, Capillary filling time) were recorded. General physical examination of neonate was done according to the proforma and any disparity in Head size and Shape, Skin lesions were noted. Anthropometry of the neonate was recorded & gestational age was assessed according to New Ballard scoring. CNS examination was done as per the proforma and HIE was staged according to modified Sarnat staging in to stage I, II and Ill. Other systems were also examined.

Table 1: Mortality Outcome Count Column n% Improved and discharged 98 89.1% Expired 6 5.5% DAMA 6 5.5% Total 110 100.0% Mortality in our study was 6 cases (5.45%) and birth asphyxia was the commonest cause seen in 4 cases (66.66%). Hyponatremia and hypernatremia: Two cases of hyponatremia associated with neonatal meningitis had seizures in our study. In a study by Ashok Kumar et al 6(%) of the 7 neonates with birth asphyxia showed a combination of biochemical disturbances hyponatremia and hypoglycemia occurred in 2 cases. Hyponatremia with birth asphyxia and meningitis may have hyponatremia due to fluid overload as a result of renal compromise, or due to inappropriate secretion of antidiuretic hormone. Some of these biochemical disturbances may trigger seizures, or potentiate further brain damage in asphyxiated infants. Therefore, strict biochemical monitoring of infants with asphyxia is suggested for appropriate management. Intracranial hemorrhage: In the present study 2(1.82%) babies had intracranial hemorrhage in that one had SAH and another one had SDH. Baby with SAH was AGA presented with seizure on the 4th day of life it was multifocal clonic type and baby with EDH was AGA present with seizure on the 1st day of life it was subtle type was diagnosed by IVH on ultrasound cranium and CSF study. Preterm neonates are prone for intraventricular hemorrhage because of fragile blood vessels and ineffective supporting structures for periventricular blood vessels. In a study by A.R. Moayedi et al intra cranial hemorrhage (ICH) seen (2.7%) neonates with seizures. In a study by Raj D.Sheth et al Intraventricular hemorrhage was the principal etiology underlying the higher seizure rate for infants, 30 weeks (p<0.001) occurred in 16% (57) if patients with sezures.5 CNS infection:6 Neonatal meningitis is one of the important causes of neonatal seizures. 7(6.36%) babies were diagnosed as neonatal meningitis in our study and was the 4th most common cause of neonatal seizures. 2(33.33%) cases had hyponatremia with neonatal meningitis. One neonate presented with seizures on 1st day, 4 neonates presented between 4th to 7th day and remaining 2 neonates presented between 8th to 28th day of life. Multifocal clonic type is more common seen in 4(57.14%) cases of meningitis. In a study by Ajay kumar et al 18 seizure episodes were noticed in 7 babies with meningitis, out of which 7 were multifocal clonic seizure. In a study by Michael Mizraiki et al The main diagnosis in neonates with seizure were sepsis in 85 (56%), neonatal encephalopathy in 36 (21%) and meningitis in 21 (13%), but only neonatal encephalopathy and bacterial meningitis were independently associated with seizures. Neonatal sepsis:7 11(10%) babies were diagnosed as sepsis in our study and was the 3rd most common cause of neonatal seizures. One neonate presented with seizure on 2nd day of life, 5 neonates presented between the 3rd and 7th day of life and remaining 5 neonates presented between 8th to 28th day of life. In babies with sepsis 5 babies had multifocal clonic seizures, 2 had subtle seizure and 4 had focal clonic seizure. 8 babies were AGA and 3 babies were SGA. In study by A.R. Moayedi et al seizure were due to infections (19.1%). Mortality: Mortality in our study was 5.45% in which birth asphyxia (66.66%), sepsis (33.34%) was the commonest cause. Mortality in studies by Sandhu Ravneet et al and Ronen Gabriel et al were 11.25% and 9% respectively and birth asphyxia was the commonest cause. Mortality rate in a study by A.R. Moayedi et al was 13.6% the most common etiology leading to death was HIE (60%), followed by infection (20%) and ICH (6.7%)..

Mortality in our study was 6 cases (5.45%) and birth asphyxia was the commonest cause seen in 4 cases (66.66%).

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