NEONATAL

SEIZURES

By:

SITI NURAISYAH BT ABDUL AZIZ

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.

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.

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.

CLASSIFICATION

ETIOLOGY

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.

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

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

METABOLIC DISORDERS

Common metabolic causes of seizures include

hypoglycemia, hypocalcemia, hypomagnesemia.

Rare causes include pyridoxine deficiency and

inborn errors of metabolism (IEM).

SEIZURES VERSUS JITTERINESS AND OTHER

NON-EPILEPTIC MOVEMENTS

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.

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

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,

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

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.

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).

GENERAL EXAMINATION

CNS EXAMINATION

BLOOD INVESTIGATIONS

ULTRASOUND CRANIUM

EEG (ELECTROENCEPHALOGRAPHY)

SPECIFIC INVESTIGATIONS

CT SCAN OR MRI

MANAGEMENT

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.

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.

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.

PROGNOSIS

Thank you