1. NEONATAL
SEIZURES
By:
SITI NURAISYAH BT ABDUL AZIZ

2. DEFINITION
 As a paroxysmal alteration in neurologic function, i.e.
motor, behavior and/or autonomic function.
 Neonatal seizures or neonatal convulsions are epileptic
fits occurring from birth to the end of the neonatal period.
 The neonatal period is the most vulnerable of all periods
of life for developing seizures, particularly in the first 1–2
days to the first week from birth.

3.  Seizures are the most frequent manifestation of
neonatal neurological diseases.
 It is important to recognize seizures, determine
aetiology and treat them as:
1. The seizures may be related to diseases that
require specific treatment.
2. The seizures may interfere with supportive
measures e.g. feeding and assisted respiration for
associated disorders.
3. The seizures per se may lead to brain injury.

4. PATHOPHSIOLOGY
 The early postnatal development time is a period of
increased susceptibility to seizures in relation to
other ages.
 This may be due to a combination of factors
specific to the developing brain that enhance
excitation and diminish inhibition.
 There is an unequal distribution of anticonvulsant
and proconvulsant neuro-transmitters and
networks.

5. CLASSIFICATION

6. ETIOLOGY

7. HIE
 Usually secondary to perinatal asphyxia is the
commonest cause of seizure in neonates,
constituting 50-65% of all seizures.
 Most seizures (50-65%) due to HIE start within 12
hrs, remaining have an onset within 24-48 hours.
 Subtle seizures are the most common type of
seizures following HIE.

8. INTRACRANIAL HEMORRHAGE
 Seizures due to sub-arachnoid, intraparenchymal or
subdural hemorrhage occur more often in term neonates,
while seizures secondary to intraventricular hemorrhage
(IVH) occur in preterm infants.
 Most seizures due to intracranial hemorrhage occur
between 2-7 days

9. Intracranial Infection
 Common organisms are group B streptococci, E.
coli., toxoplasmosis, herpes simplex, coxsackie B,
rubella and cytomegalovirus.
Malformations of cortical development
 Neuronal migration disorder resulting in cerebral
cortical dysgenesis

10. METABOLIC DISORDERS
 Common metabolic causes of seizures include
hypoglycemia, hypocalcemia, hypomagnesemia.
 Rare causes include pyridoxine deficiency and
inborn errors of metabolism (IEM).

11. SEIZURES VERSUS JITTERINESS AND OTHER
NON-EPILEPTIC MOVEMENTS

12.  Other normal movement during sleep (Myoclonic
jerks as infant wakes from sleep) or when awake/
drowsy (roving sometimes dysconjugate eye
movements, sucking not accompanied by ocular
fixation or deviation) in newborns may be mistaken
for seizures.

13. DIAGNOSIS/APPROACH
1) Seizure history
 eye movements
 restraint of episode by passive flexion of the
affected limb
 change in color of skin (mottling or cyanosis)
 autonomic phenomena
 infant was conscious/ sleeping at the time of
seizure should be elicited
 The day of life on which the seizure occurred

14. 2) Antenatal history
 Intruterine infection, maternal diabetes and narcotic
addiction
3) Perinatal history
 Perinatal asphyxia is the commonest cause of
neonatal seizures and a detailed history including
history of fetal distress, decreased fetal
movements, instrumental delivery,

15.  Need for resuscitation in the labor room, low Apgar
scores (<3 at 1 and/ or 5 minutes) and
 abnormal cord pH (≤7) and base deficit (> 10
mEq/L) should be obtained.
 Use of a pudendal block for mid-cavity forceps may
be associated with accidental injection of the local
anesthetic into the fetal scalp

16. 4) Feeding history:
 Appearance of clinical features including lethargy,
poor activity, drowsiness, and vomiting after
initiation of breast-feeding may be suggestive of
inborn errors of metabolism.
 Late onset hypocalcemia should be considered in
the presence of top feeding with cows’ milk.

17. 5) Family history
 History of consanguinity in parents, family history of
seizures or mental retardation and early
fetal/neonatal deaths would be suggestive of inborn
errors of metabolism.
 History of seizures in either parent or sib(s) in the
neonatal period may suggest benign familial
neonatal convulsions (BFNC).

18.  GENERAL EXAMINATION
 CNS EXAMINATION
 BLOOD INVESTIGATIONS
 ULTRASOUND CRANIUM
 EEG (ELECTROENCEPHALOGRAPHY)
 SPECIFIC INVESTIGATIONS
 CT SCAN OR MRI

19. MANAGEMENT

21. DURATION OF ANTICONVULSANT THERAPY
 Duration of therapy depends on :
1. the probability of recurrence of seizures if the drugs
are discontinued
2. the risk of subsequent epilepsy.
 This can be determined by considering the neonatal
neurological examination, cause of the seizure and the
EEG.

22. NEONATAL PERIOD
 If neonatal neurological examination becomes
normal discontinue therapy
 If neonatal neurological examination is persistently
abnormal 
1. Consider etiology and obtain
electroencephalogram (EEG).
2. In most cases – continue phenobarbitone,
discontinue phenytoin.
3. And re-evaluate in one month.

23. ONE MONTH AFTER DISCHARGE
 If neurological examination has become normal,
discontinue phenobarbitone over 2 weeks.
 If neurological examination is persistently abnormal,
obtain EEG.
1. If no seizure activity or not overtly paroxysmal on
EEG, discontinue phenobarbitone over 2 weeks.
2. If seizure activity is overtly paroxysmal continue
phenobarbitone until 3 months of age and
reassess in the same manner.

24. PROGNOSIS

25. Thank you