INTRODUCTION A seizure is a paroxysmal manifestation ofneurological dysfunctionIncidence(overall):2 in 1000 to 14 in 1000 live births
PATHOPHYSIOLOGY Excessive depolarisation (excitation) ofneurons within the CNS.
Probable Mechanisms of SomeNeonatal SeizuresFailure of sodium potassium pump mechanismleading to depolarisation due to inward migrationof sodium and repolarisation due to efflux ofpotassiumRelative excess of excitatory neurotransmittersDeficit of inhibitory neurotransmitters
variable clinical manifestations.often the first sign of neurologic dysfunctionpredictors of long-term cognitive anddevelopmental impairment.
TYPES OF NEONATAL SEIZURES5 main seizure typesSubtleTonicClonicMyoclonicSpasms
TONIC SEIZURES May be focal or generalized Focal seizures –persistent posturing of a limb ortrunk with persistent horizontal eye deviation generalized seizures-bilateral tonic limbextension or tonic flexion of upper extremities withtonic extension of lower extremities
CLONIC SEIZURES Repetitive , rhythmic contractions of musclegroups of the limbs , face or trunk Consciousness may be preserved Signals focal cerebral injury
MYOCLONIC SEIZURES rare random , single , rapid contractions of musclegroups of the limbs , face or trunkTypically not repetitive or may recur at a slowrate
SPASMSSudden generalized jerks lasting 1-2 sec and areusually associated with a single , very brief,generalized discharge
D/DsJitterinessmust be differentiated from seizures inneonates. rapid motor activities such as a tremor or shake jitteriness is not associated with oculardeviation.-is stimulus sensitive (eg, easily stopped withpassive movement of the limb)
DIAGNOSISHISTORY:Family history may suggest genetic syndromeMany of these syndromes are benign In the absence of other etiologies, family historyof seizures may suggest good prognosis
Antenatal history is importantHistory of fetal distress, preeclampsia , maternalinfections or maternal diabetes
Delivery historyType of delivery and antecedent eventsApgar scores offer some guidanceLow Apgar score without the need forresuscitation and subsequent neonatal intensivecare is unlikely to be associated with neonatalseizures
INVESTIGATIONS: Lab studies-Blood count-Blood, urine & CSF culture-Serum IgM & IgG-specific TORCH titres-Blood biochem.->evaluation of Glu, Ca, Mg,electrolytes-Blood gas levels to detect acidosis & hypoxia.
EEG:Main tool for diagnosisIt is useful to confirm a clinically doubtfulconvulsion , to locate an epileptic focus andand to determine its anatomical basis Ultrasonography and CT scan of head:To detect subarachnoid /intraventricularhemorrhage
TREATMENTThe principles of Rx are:To control convulsionsTo treat the underlying pathology
To control convulsion:I.V. phenobarbitone 20 mg/kg body weight overa period of 10-15 minMaintenance dose-> 2.5 to 4 mg/kg b.w. per daygiven orally or I.M. for a pd. of 2 wks or longer.In resistant cases-> I.V. phenytoin 20 mg/kgb.w @ 1 mg/kg/min
Maintenance dose of 5-8 mg/kg/day divided 12hourly.Fosphenytoin is preferred.
To treat the underlying pathologyHypoglycemia : Glucose infusion 2 ml per kg of10% glucose, through an I.V. line is given over 2-3 minHypomagnesemia: MgSO4(0.4-0.8 mEq/kg);given IV every 12 hours until Mg level is normal.Infection: Appropriate antibiotics
Hypocalcemia: I.V administration of 2 ml/kg ofCalcium gluconate given over 5 min.- To be followed by oral Calcium Chloride250 mg with each feed for few days.Pyridoxine deficiency: IV administration of 50mg pyridoxine is effective.
PROGNOSIS:Varies with etiology.Hypocalcemic convulsions have an excellentprognosis.Neurological sequelae are still around 30-40%
References:Nelson textbook of pediatrics (19thedition) Averys diseases of newborn(8thedition)D.C.Dutta textbook of obstetrics(7thedition)