This document discusses neonatal seizures, including their incidence, causes, clinical presentation, investigations, and management. Some key points include: - Seizures affect 0.1% of term infants and up to 10% of very low birth weight infants. Common causes include hypoxic ischemic encephalopathy, infection, hemorrhage, and congenital malformations. - Presentation depends on etiology but may include oculo-facial, central/autonomic, clonic, tonic, or myoclonic seizures. Investigations include bloodwork, imaging, EEG, and metabolic screening. - Management involves treating any underlying cause, starting anticonvulsants if seizures are prolonged or frequent, and

1. By
Dr. Asmaa Abd El wakeel I brahim
Lecturer of Pediatrics/Neonatology
Al-Azhar Faculty of Medicine for Girls

2. Neonatal seizures
Seizure: abnormal electrical brain activity causing
neurological dysfunction.
Incidence
Seizures affect around 0.1% of all term infants and up
to 10% of very low birth weight (VLBW) infants—
newborns have a predominance of excitatory synapses
relative to adults and alongside other molecular factors
are more prone to seizures.

3. Causes of neonatal seizures
 Hypoxic ischaemic encephalopathy
 Sepsis (meningitis, encephalitis)
 Intracranial haemorrhage (intraventricular,
parenchymal, subarachnoid, or subdural)
 Cerebral infarction (stroke, venous sinus
thrombosis)
 Congenital brain malformations.

4. Rarer causes
 • Metabolic (hypoglycaemia, hypocalcaemia,
hypomagnesaemia, hypo/hypernatraemia,
hyperbilirubinaemia/ kernicterus,
hyperammonaemia,
 Inborn errors of metabolism as(hyperglycinaemia,
pyridoxine deficiency)
 •Maternal substance abuse/ neonatal abstinence
syndrome
 Epilepsy syndromes(Benign non- familial neonatal
seizures (5th day fits) ,Benign familial neonatal
seizures,…)
 • Hypertension.

5. Clues to etiology
 HIE is the most common cause of seizures in term
babies and characteristically presents in the first 24
hours with a history of fetal distress, need for
resuscitation at birth, and decreased conscious
level.
 Group B streptococci and E. coli are the commonest
infective causes, andpresent from the end of the
first week onwards, as does Herpes simplex.
 Intrauterine toxoplasmosis and cytomegalovirus
(CMV) infection present in the first 3 days.

6. Clues to etiology
 Cerebral infarction (stroke) often presents with focal
seizures at 24– 72hours of age in an otherwise well
infant.
 IUGR and preterm infants are at risk of
hypoglycaemia.
 Poor feeding and weight loss may lead to
hypernatraemic dehydration.
 Severe unconjugated jaundice and kernicterus—
decreased consciouslevel, abnormal neurology, and
typically opisthotonic posture.

7. • Clues to etiology
 Preterm infants may have subtle seizures following
intraventricular haemorrhage (IVH) in the first 72
hours, with decreased Hb.
 Neonatal abstinence syndrome— history of
maternal substance abuse, presents in first week
with other signs of withdrawal.
 Inborn errors of metabolism: at least 1% of cases
of seizures in the newborn. caused by an enzyme
defect in the metabolic pathways of carbohydrates,
proteins, or fat, many cause disease due to
accumulation of toxic products unable to proceed
along the appropriate metabolic pathways.

8. • Clues to etiology
 Inborn errors of metabolism:.
 In these disorders, infants initially appear well, due
to the benefits of placental clearance of toxins until
birth, and only become encephalopathic and have
seizures after 2 to 3 days.
 Biochemical markers for these disorders include
hypoglycemia, metabolic acidosis,
hyperammonemia, as well as specific patterns of
alteration in amino acid or organic acid profiles.

9. • Clues to etiology
 Inborn errors of metabolism:.
 Among metabolic disorders,Hyperglycinaemia—
increased fetal movements, intractable seizures,
commonly causes myoclonic events,
encephalopathy with depressed sensorium,
respiratory compromise, and hypotonia, burst
suppression on EEG, raised plasma and
cerebrospinal fluid (CSF) glycine levels.

10. Clues to etiology
 Pyridoxine deficiency— intractable seizures with
dramatic resolution following pyridoxine
administration
 which results in deficiency of alpha amino-adipic
semialdehyde (α-AASA) dehydrogenase and
accumulation of α-AASA in blood, urine, and CSF,
 thus providing a biologic marker for the disorder.
 This enzyme is involved in lysine breakdown in the
brain and is believed to impact the metabolism of
the neurotransmitters glutamate and GABA.

11. Clues to etiology
 Epilepsy syndromes.
 Benign familial neonatal seizures— autosomal
dominant channelopathy, presents at 3– 7 days with
clonic seizures
 Benign infantile neonatal seizures(“fifth day fits”)
present suddenly on days 4 to 6 of life, often with
frequent seizures leading to status epilepticus.
Seizures are initially focal clonic often with apnea.
Seizures usually cease within 2 weeks. The etiology
is unknown.

12. Clues to etiology
 Epilepsy syndromes.
Early myoclonic epilepsy (EME),
 often presenting in the first few days of life with
focal motor seizures andmyoclonus, which may be
subtle and erratic and usually affects the face and
limbs.
 The seizures are very refractory to medications.
 The EEG is characterized by aburst-suppression
pattern, which may only be seen in sleep, and, if
present throughout the sleep-wake cycle, is
exacerbated by sleep.

13. Clues to etiology
 Epilepsy syndromes.
Early myoclonic epilepsy (EME),
 This syndrome is often associated with underlying
metabolic disorders, for instance, glycine
encephalopathy (described earlier). Development is
severely affected, and many infants die, often within
 their first year.

14. Clues to etiology
 Epilepsy syndromes.
Early infantile epileptic encephalopathy (EIEE; Ohtahara
syndrome)
 is also associated with very refractory epilepsy. In
contrast to EME, it is characterized by early onset of
tonic spasms along with focal motor seizures.
 It, too, is associated with a burst-suppression
pattern on EEG, which is relatively invariant.
 EIEE is more likely to be associated with structural
lesions.
 Developmental prognosis is also poor in this
syndrome.

15. Clues to etiology
 Malformations/structural lesions. Five percent of
neonatal seizures are caused by cerebral dysgenesis.
 Cerebral dysgenesis can cause seizures from the first
day of life. This is most likely with the more severe
 disorders such as hemimegalencephaly,
lissencephaly, and polymicrogyria. Seizures are
often refractory to medications.

16. Cerebral infarct.
Diffusion-weighted MRI
brain scan showing
restricted diffusion
(bright) corresponding to
a large left middle
cerebral artery territory
infarct involving much of
the frontal lobe.

17. MRI scan showing the
characteristic smooth
brain of an individual
with lissencephaly. It is a
basket term for a number
of congenital cortical
malformations
characterised by absent
or minimal sulcation.

18. Clues to etiology
 Clues to neurocutaneous diseases may be apparent
on the newborn examination—for instance, the
hemangioma in the distribution of cranial nerveV1
in Sturge-Weber syndrome, which can occasionally
cause seizures in the newborn period.
 Hypopigmented“ash-leaf” macules of tuberous
sclerosis may be seen, although neonatal seizures
are rare in this disorder.
 Neuroimaging is primary in making these diagnoses.

19. Seizures in newborns are varied and subtle due to the
relative immaturity of the nervous system, and
generalized tonic– clonic seizures are rare.
Patterns of clinical seizures are:
 Oculo- orofacial: eye rolling, eye deviation, staring,
nystagmus, chewing, sucking, lip smacking, smiling,
and blinking.
 Central/ autonomic: change in breathing, apnoea,
desaturation, bradycardia.

20. Patterns of clinical seizures are:
 Clonic: cycling or boxing movements, usually one
limb or side, may migrate to other limbs, 2– 4 Hz,
sharp- slow wave pattern on EEG, may be due to an
underlying focal lesion or a metabolic cause
 Tonic: stiffening of the limbs or trunk usually
symmetrically and sometimes decerebrate or
opisthotonic posturing
 Myoclonic jerks: fast movement, flexor muscles
 Multifocal: more than one site, asynchronous,
migratory

21.  •Generalized: bilateral, synchronous, non- migratory
 Seizures must be differentiated from jitters.
 •Jitteriness is a common, often normal finding, 5 Hz,
symmetrical tremor ofthe limbs, exacerbated by
startling, and terminated by holding/ flexing
thelimb, no ocular phenomena, no autonomic
changes, normal EEG.

22. Investigations
 Bloods: glucose, blood gas, U&Es, Ca, Mg, FBC +
differential WCC, CRP, blood culture, congenital
infection screen.
 Urine toxicology.
 CSF (delay LP if baby is unstable) glucose, protein,
Gram stain, culture, viral PCR.
 EEG (distinguish from non- seizure activity):
newborns often exhibit electro- clinical dissociation,
that is poor correlation between EEG changes and
clinical events. See Fig. 11.3.

23. Investigations
 Neuroimaging: cranial USS (haemorrhage) and
consider CT/ MRI(cerebral malformations and
infarcts) if etiology remains unclear. SeeFig. 11.4
 Consider genetic testing and referral if dysmorphic
or family history.
 Consider metabolic screen if acidotic or family
history: ammonia, aminoacids, lactate, urine amino
and organic acids, +/ – CSF glucose, lactate,
 and amino acids.

24. Management
 Monitor breathing, which may be compromised
during seizures and following anticonvulsant
administration.
 Rapidly identify and treat reversible causes
Hypoglycemia Dextrose 10%, 2-3 mL/kg IV
Hypocalcemia Calcium gluconate, 5% (50 mg/mL)
100-200 mg/kg IV; 10% (100 mg/mL) 50-100 mg/kg
IV if inadequate time for dilution Hypomagnesemia
Magnesium sulphate, 12.5% (125 mg/mL) 50-100
mg/kg IV
 Commence antibiotics and add aciclovir if there is
any suspicion of herpes infection (e.g. maternal

25. Management
 Commence antibiotics and add aciclovir if there is
any suspicion of herpes infection (e.g. maternal
infection, rash, abnormal LFTs).

26. Management
• Anticonvulsants
• The threshold for starting anticonvulsants is based on
both clinical condition and seizure duration and
frequency.
• Start an anticonvulsant if there are: prolonged
desaturations, haemodynamic instability, seizure
lasting>5 minutes, or brief but frequent seizures >3
per hour.

27. Management
• Anticonvulsants First- line:
 phenobarbital ‘full’ loading dose (20 mg/ kg IV) • if
seizures continue for 30 min: give a further ‘half ’
loading dose of phenobarbital (i.e. 10mg/ kg IV) and
take blood for aphenobarbital level.
 If seizures remain uncontrolled: either give further
‘half ’ loading dose of phenobarbital if blood levels
are low or consider adding another anticonvulsant.
 Phenobarbital terminates seizures in up to 50% of
cases within a few hours.

28. Management
• Anticonvulsants Second- line:
 phenytoin, loading dose (20 mg/ kg IV over 30 min),
may cause hypotension and arrhythmias if cardiac
function is impaired.
 Give second dose if seizures not controlled after 20
min.
 Phenytoin stops a further 15% of seizures.

29. Management
• Anticonvulsants Third- line:
 clonazepam (10– 60 μg/ kg/ h IVI), midazolam (30–
50 μg/kg/ h IVI), lidocaine (4– 8 mg/ kg/ h IVI) NB
should not be used with phenytoin)), or
levetiracetam (initial dose 7 mg/ kg once daily).
 It remains unclear which is the most effective agent
and the management of difficult to control seizures
should be discussed with a paediatric neurologist.

30. Management
• Anticonvulsants Fourth- line:
• consider 1 week trial of pyridoxine (100 mg od, po) if
• EEG shows a persistent spike and wave pattern and
poor response toprevious treatment.
• One week trial of pyridoxal phosphate (30 mg/
• kg/ 24 h po) if there is no response to pyridoxine.
Trial of creatine (300mg/ kg/ 24 h) + folinic acid (2.5
mg bd) + biotin (10 mg od) if seizures remain
uncontrolled

31. Management
if seizures remain uncontrolled
 Use the minimum number of anticonvulsants
required to maintain seizure control
 Some anticonvulsants cause respiratory depression
so breathing must bemonitored carefully.

32. Management
 Maintenance treatment is not usually needed unless
there is evidence of an underlying seizure disorder:
 If seizures persist use phenobarbital 3– 5 mg/ kg/
24 h IV or po in divided doses.
 Most babies can stop anticonvulsants before
discharge home. However, those with persistent,
abnormal neurology may need to continue.

33. Outcome
 Prognosis depends upon the underlying cause.
There is evidence that seizures in themselves and
status epilepticus in particular, are associated with
adverse neurodevelopmental sequelae.

34. toxins/Poisons
 Toxic ingestions are uncommon in this age group,
but occasionally result from a maternal ingestion in
a breastfeeding mother, homeopathic remedies, or
overuse of accepted medications.
 Although teething does not occur in the first month
of life, colic is a common concern at this point and
results in lost sleep and frustration.
 Teething gels may be used as an attempt to relieve
distress for both parents and neonates.
 Note that teething gels often contain benzocaine
which may cause methemoglobinemia with
overuse.

35. toxins/Poisons
Star anise tea:-
 Used for relief of infantile colic.
 Neurotoxicity.
 Unexplained irritability.
 Vomiting.
 Seizures.
 Baking soda:-
 Used for intestinal gas cause serious toxicity.

36. toxins/Poisons
Management:-
 ED management is primarily supportive, and will
depend on the clinical presentation.
 Hospitalization for monitoring and observation is
recommended .

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