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NEONATAL CONVULSIONS
SANJAY RAO
(090101361)
INTRODUCTION
 A seizure is a paroxysmal manifestation of
neurological dysfunction
Incidence(overall):2 in 1000 to 14 in 1000 live births
PATHOPHYSIOLOGY
 Excessive depolarisation (excitation) of
neurons within the CNS.
Probable Mechanisms of Some
Neonatal Seizures
Failure of sodium potassium pump mechanism
leading to depolarisation due to inward migration
of sodium and repolarisation due to efflux of
potassium
Relative excess of excitatory neurotransmitters
Deficit of inhibitory neurotransmitters
variable clinical manifestations.
often the first sign of neurologic dysfunction
predictors of long-term cognitive and
developmental impairment.
TYPES OF NEONATAL SEIZURES
5 main seizure types
Subtle
Tonic
Clonic
Myoclonic
Spasms
SUBTLE SEIZURES
 Transient eye deviations (term)
 Nystagmus , fixed stare (preterm)
 Abnormal extremity movements ( rowing,
pedaling , swimming)
 Apnea , fluctuations in heart rate
TONIC SEIZURES
 May be focal or generalized
 Focal seizures –persistent posturing of a limb or
trunk with persistent horizontal eye deviation
 generalized seizures-bilateral tonic limb
extension or tonic flexion of upper extremities with
tonic extension of lower extremities
CLONIC SEIZURES
 Repetitive , rhythmic contractions of muscle
groups of the limbs , face or trunk
 Consciousness may be preserved
 Signals focal cerebral injury
MYOCLONIC SEIZURES
 rare
 random , single , rapid contractions of muscle
groups of the limbs , face or trunk
Typically not repetitive or may recur at a slow
rate
SPASMS
Sudden generalized jerks lasting 1-2 sec and are
usually associated with a single , very brief,
generalized discharge
D/Ds
Jitteriness
must be differentiated from seizures in
neonates.
 rapid motor activities such as a tremor or shake
 jitteriness is not associated with ocular
deviation.
-is stimulus sensitive (eg, easily stopped with
passive movement of the limb)
ETIOLOGY
Hypoxic-ischemic encephalopathy
Intracranial Hemorrhage
subarachnoid hemorrhage
germinal matrix –intraventricular hemorrhage
subdural hemorrhage
Metabolic disorders(hypoglycemia/
hypocalcemia /hypomagnesemia/hyponatremia)
CONTD..
Intracranial infections
bacterial meningitis
TORCH infections
 Pyridoxine dependency
Benign neonatal seizures
DIAGNOSIS
HISTORY:
Family history may suggest genetic syndrome
Many of these syndromes are benign
 In the absence of other etiologies, family history
of seizures may suggest good prognosis
Antenatal history is important
History of fetal distress, preeclampsia , maternal
infections or maternal diabetes
Delivery history
Type of delivery and antecedent events
Apgar scores offer some guidance
Low Apgar score without the need for
resuscitation and subsequent neonatal intensive
care is unlikely to be associated with neonatal
seizures
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 diagnosis
It is useful to confirm a clinically doubtful
convulsion , to locate an epileptic focus and
and to determine its anatomical basis
 Ultrasonography and CT scan of head:
To detect subarachnoid /intraventricular
hemorrhage
TREATMENT
The principles of Rx are:
To control convulsions
To treat the underlying pathology
To control convulsion:
I.V. phenobarbitone 20 mg/kg body weight over
a period of 10-15 min
Maintenance dose-> 2.5 to 4 mg/kg b.w. per day
given orally or I.M. for a pd. of 2 wks or longer.
In resistant cases-> I.V. phenytoin 20 mg/kg
b.w @ 1 mg/kg/min
Maintenance dose of 5-8 mg/kg/day divided 12
hourly.
Fosphenytoin is preferred.
To treat the underlying pathology
Hypoglycemia : Glucose infusion 2 ml per kg of
10% glucose, through an I.V. line is given over 2-
3 min
Hypomagnesemia: 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 of
Calcium gluconate given over 5 min.
- To be followed by oral Calcium Chloride
250 mg with each feed for few days.
Pyridoxine deficiency: IV administration of 50
mg pyridoxine is effective.
PROGNOSIS:
Varies with etiology.
Hypocalcemic convulsions have an excellent
prognosis.
Neurological sequelae are still around 30-40%
References:
Nelson textbook of pediatrics (19th
edition)
 Averys diseases of newborn(8th
edition)
D.C.Dutta textbook of obstetrics(7th
edition)
NEONATAL SEIZURE CAUSES AND TYPES

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NEONATAL SEIZURE CAUSES AND TYPES

  • 2. INTRODUCTION  A seizure is a paroxysmal manifestation of neurological dysfunction Incidence(overall):2 in 1000 to 14 in 1000 live births
  • 3. PATHOPHYSIOLOGY  Excessive depolarisation (excitation) of neurons within the CNS.
  • 4. Probable Mechanisms of Some Neonatal Seizures Failure of sodium potassium pump mechanism leading to depolarisation due to inward migration of sodium and repolarisation due to efflux of potassium Relative excess of excitatory neurotransmitters Deficit of inhibitory neurotransmitters
  • 5. variable clinical manifestations. often the first sign of neurologic dysfunction predictors of long-term cognitive and developmental impairment.
  • 6. TYPES OF NEONATAL SEIZURES 5 main seizure types Subtle Tonic Clonic Myoclonic Spasms
  • 7. SUBTLE SEIZURES  Transient eye deviations (term)  Nystagmus , fixed stare (preterm)  Abnormal extremity movements ( rowing, pedaling , swimming)  Apnea , fluctuations in heart rate
  • 8. TONIC SEIZURES  May be focal or generalized  Focal seizures –persistent posturing of a limb or trunk with persistent horizontal eye deviation  generalized seizures-bilateral tonic limb extension or tonic flexion of upper extremities with tonic extension of lower extremities
  • 9. CLONIC SEIZURES  Repetitive , rhythmic contractions of muscle groups of the limbs , face or trunk  Consciousness may be preserved  Signals focal cerebral injury
  • 10. MYOCLONIC SEIZURES  rare  random , single , rapid contractions of muscle groups of the limbs , face or trunk Typically not repetitive or may recur at a slow rate
  • 11. SPASMS Sudden generalized jerks lasting 1-2 sec and are usually associated with a single , very brief, generalized discharge
  • 12. D/Ds Jitteriness must be differentiated from seizures in neonates.  rapid motor activities such as a tremor or shake  jitteriness is not associated with ocular deviation. -is stimulus sensitive (eg, easily stopped with passive movement of the limb)
  • 13. ETIOLOGY Hypoxic-ischemic encephalopathy Intracranial Hemorrhage subarachnoid hemorrhage germinal matrix –intraventricular hemorrhage subdural hemorrhage Metabolic disorders(hypoglycemia/ hypocalcemia /hypomagnesemia/hyponatremia)
  • 14. CONTD.. Intracranial infections bacterial meningitis TORCH infections  Pyridoxine dependency Benign neonatal seizures
  • 15. DIAGNOSIS HISTORY: Family history may suggest genetic syndrome Many of these syndromes are benign  In the absence of other etiologies, family history of seizures may suggest good prognosis
  • 16. Antenatal history is important History of fetal distress, preeclampsia , maternal infections or maternal diabetes
  • 17. Delivery history Type of delivery and antecedent events Apgar scores offer some guidance Low Apgar score without the need for resuscitation and subsequent neonatal intensive care is unlikely to be associated with neonatal seizures
  • 18.
  • 19. 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.
  • 20. EEG: Main tool for diagnosis It is useful to confirm a clinically doubtful convulsion , to locate an epileptic focus and and to determine its anatomical basis  Ultrasonography and CT scan of head: To detect subarachnoid /intraventricular hemorrhage
  • 21. TREATMENT The principles of Rx are: To control convulsions To treat the underlying pathology
  • 22. To control convulsion: I.V. phenobarbitone 20 mg/kg body weight over a period of 10-15 min Maintenance dose-> 2.5 to 4 mg/kg b.w. per day given orally or I.M. for a pd. of 2 wks or longer. In resistant cases-> I.V. phenytoin 20 mg/kg b.w @ 1 mg/kg/min
  • 23. Maintenance dose of 5-8 mg/kg/day divided 12 hourly. Fosphenytoin is preferred.
  • 24. To treat the underlying pathology Hypoglycemia : Glucose infusion 2 ml per kg of 10% glucose, through an I.V. line is given over 2- 3 min Hypomagnesemia: MgSO4(0.4-0.8 mEq/kg); given IV every 12 hours until Mg level is normal. Infection: Appropriate antibiotics
  • 25. Hypocalcemia: I.V administration of 2 ml/kg of Calcium gluconate given over 5 min. - To be followed by oral Calcium Chloride 250 mg with each feed for few days. Pyridoxine deficiency: IV administration of 50 mg pyridoxine is effective.
  • 26. PROGNOSIS: Varies with etiology. Hypocalcemic convulsions have an excellent prognosis. Neurological sequelae are still around 30-40%
  • 27. References: Nelson textbook of pediatrics (19th edition)  Averys diseases of newborn(8th edition) D.C.Dutta textbook of obstetrics(7th edition)