Neonatal seizures

NEONATAL
SEIZURES
Dr. VENKATESH
Postgraduate
Dept of Pediatrics
S V medical college

OBJECTIVES
 To familiarize the varied presentations of neonatal
seizures.
 To distinguish non seizure states from seizures.
 To recognize the unique etiology of neonatal
seizures.
 To familiarize the algorithm of management specific
to neonatal seizures.
 To be able to decide the duration of antiepileptic
therapy and followup.

OVERVIEW
 DEFINITION OF SEIZURE
 TYPES OF NEONATAL SEIZURES
 CAUSES OF NEONATAL SEIZURES
 SEIZURE MIMICS
 APPROACH TO NEONATAL SEIZURES
 DURATION OF ANTICONVULSANT THERAPY
GUIDELINES
 PROGNOSIS

 SEIZURE is defined clinically as paroxysmal alteration in
neurologic function ie., motor, behaviour and/or
autonomic function.
It includes
1. Epileptic seizures - phenomenon associated with
corresponding EEG seizure activity.
Eg: clonic seizures.
2. Nonepileptic seizures - clinical seizures without
corresponding EEG correlate.
Eg: subtle and generalised tonic seizures.
3. EEG seizures - abnormal EEG activity with no clinical
correlation.

EPIDEMIOLOGY- INDIA(NNPD;2002-03)
 Incidence : 10.3 per 1000 live births
 The incidence is high in PRETERM
neonates (2 fold), VLBW( 4 fold) compared
to TERM neonates.
 Term neonates- 8.4
 Preterm neonates-20.8
 VLBW-36.1

Why seizures are common in neonatal period ?
 Seizures are common in neonatal period than any other
time in life due to decreased seizure threshold.
 Transient overdevelopment of excitatory system than
inhibitory system.

Why generalised seizures are rare in neonates
?
 Neonatal brain has reduced connectivity due to
incomplete myelination, so electrical discharges
spread incompletely.

TYPES OF NEONATAL SEIZURES
Four types of neonatal seizures
1. Subtle seizures
2. Clonic seizures
3. Tonic seizures
4. Myoclonic seizures

SUBTLE SEIZURES
 Most common form(>50%)
 It includes
a) Ocular - tonic horizontal deviation of eyes or sustained
eye opening with ocular fixation or cycled fluttering.
b) Oral facial lingual movements - chewing, tongue
thrusting, lip smacking etc.
c) Limb movements - cycling, paddling, boxing etc.
d) Autonomic phenomena-tachycardia or bradycardia.
e) Apnea may be a rare manifestation of seizure.

CLONIC SEIZURES
 Rhythmic movements of muscle groups.
 Have both fast and slow movements with frequency of 1-
3 jerks per second.
 Commonly associated with EEG changes.
 May be unifocal or multifocal.
 Focal clonic has good prognosis.

TONIC SEIZURES
 Pattern is sustained posture of limbs or
asymmetrical truncal postures.
 cause: diffuse neurological injury or IVH in preterm
or postasphyxial.
 Usually no EEG changes.
 Prognosis is poor except for postasphyxial cases.

MYOCLONIC SEIZURES
 Non rhythmic lightning fast contraction.
 Seen in diffuse brain damage as in perinatal
asphyxia, inborn errors of metabolism, cerebral
dysgenesis.
 Worst prognosis in terms of neurodevelopmental
outcome and seizure recurrence.

ETIOLOGY
1.Perinatal events:
 Hypoxic ischemic encephalopathy
 Intracranial hemorrhage: Germinal
matrix intraventricular hemorrhage,
subdural hemorrhage, primary
subarachnoid hemorrhage (well baby
seizures)

ETIOLOGY
2. METABOLIC
 Hypoglycemia
 Hypocalcemia
 Early: preterm, asphyxia, IDM
 Late: Top feeding
 Hypomagnesemia
 Hyponatremia / hypernatremia
 Pyridoxine deficiency
 IEM: non-ketotic hyperglycinemia, urea cycle
defects, maple syrup disease, glutaric aciduria,
propionic aciduria,methyl malanoic aciduria,
mitochondrial disease.

ETIOLOGY
3.INFECTIONS:
 Bacterial meningitis
 Non-bacterial infections: toxoplasmosis,
herpes simplex, rubella,cytomegalovirus
4.DEVELOPMENTAL PROBLEMS:
 Cerebral cortical dysgenesis
 Neuronal migration disorders
 Pachygyria, polymicrogyria

ETIOLOGY
5.MISCELLANEOUS
 Passive drug withdrawl
 Accidental injection of local anesthetic
into fetal scalp.
 Neonatal epileptic syndromes
Benign familial neonatal convulsions
Benign idiopathic neonatal convulsions
(fifth day fits)
Early myoclonic encephalopathy
Early infantile epileptic encephalopathy
(Ohtahara’ssyndrome)
Malignant migrating partial seizures in
infancy( coppola syndrome)

NEONATAL SEIZURES – TIME OF ONSET
Time of
onset
Etiology
< 24 hrs HIE, severe birth trauma, hypoglycemia, hypocalcemia,
drug withdrawl, congenital CNS anomalies,
intracranial hemorrhage
1-3 days All above , subarachnoid hemorrhage, IEM, benign
familial neonatal seizures
> 3 days sepsis ,meningitis, progressive hydrocephalus,
epileptic syndromes, herpes encephalitis, IEM

SPECIFIC ETIOLOGIES
Hypoxic Ischemic Encephalopathy
 Most common cause of neonatal seizures usually
in the first 24 hours.
 In perinatal asphyxia, seizures occur in context of
history of difficulty during labour , delivery with fetal
HR alterations, low Apgar scores.

Intra cranial hemorrhages
 Sub arachnoid hemorrhages cause seizures
usually on second day and have a very good
outcome.
 In preterm infant, seizures occur with extension
of germinal matrix hemorrhage to parenchyma
typically after 3 days of life and it is not
assosciated with good outcome.

Acute metabolic disorders
 Hypoglycemia
 Hypocalcemia : Whole blood ionized calcium is the best
measure.
ionised calcium < 1.1 mmol/lit in > 1500gm.
ionised calcium < 1 mmol/lit in < 1500gm.
 Hypomagnesemia: Levels < 1.4mg/dl (0.6 mmol/lit ) are
considered low.
 Hypo/Hypernatremia

Neonatal seizure syndromes
 Benign familial neonatal seizures
 Benign idiopathic neonatal seizures ( fifth day fits )
 Early infantile epileptic encephalopathy ( Ohtahara
syndrome )
 Malignant migrating partial seizures ( Coppala syndrome
)

SEIZURE MIMICS
1. Jitteriness – suppress with passive flexion,
increases with stimulation, not associated with
autonomic accompaniments and eye movements.
2.Epileptic apnea – associated with tachycardia.
3.Benign neonatal sleep myoclonus - occur as
synchronus myoclonic jerks during non REM sleep
disappear when baby is awake, EEG is normal and
spontaneously resolve by 2 months of age.

Clinical
character
seizures jitteriness
Increases with
stimulation
rare common
Suppress with
passive flexion
absent present
Autonomic
phenomena
present absent
Eye or facial
movements
present absent
Rate of
movement
Clonic seizures show
rapid alteration of fast
and slow phase of
movements
Rate of movement
is identical in
either direction.
EEG
abnormalities
Yes No

HISTORY
 Seizure history – regarding type of seizure , associated
movements , day of onset.
 Antenatal history - intrauterine infection , maternal
diabetes , narcotic addiction.
 Perinatal history - H/o fetal distress, instrumental
delivery, need for resuscitation in labour room, apgar
scores .

 Feeding history – appearance of lethargy, poor activity
and vomiting after initiation of breast feeding may be
suggestive of IEM.
 Family history – H/o consanguinity in parents , family
h/o seizures or MR , early fetal or neonatal deaths would
be suggestive of IEM.
H/o seizures in either parent or sibling in neonatal period
may be suggestive of benign familial neonatal
convulsion.

EXAMINATION
 Vitals – HR, RR, CRT, Temp, BP.
 General examination – gestation , birth wt and wt for
age
- Seizures in term well baby may be due to SAH.
- Seizures in large for date babies may be due to
hypoglycemia.

 CNS examination – presence of bulging AF may be
suggestive of meningitis or ICH
- consciousness (alert /drowsy/comatose).
- tone (hypo/hyper).
- fundus examination for chorioretinitis.
 Systemic examination – presence of
hepatosplenomegaly or abnormal urine odour may
be suggestive of IEM
- skin should be examined for neurocutaneous
markers .

INVESTIGATIONS
 Essential
- Blood sugar
- Serum electrolytes
- CSF examination
- Cranial ultrasound
- EEG

 Additional
 Hematocrit (if plethoric and/or at risk for
polycythemia)
 Serum bilirubin (if icteric)
 Serum magnesium
 Arterial blood gas and anion gap (lethargy,
vomiting, family history, etc.)
 Imaging: CT and/or MRI (if no etiology found
after essential investigations)
 TORCH screen for congenital infections
 Work-up for inborn errors of metabolism

 NSG - excellent tool for detection of IVH and
parenchymal hemorrhage.
 CT - diagnostic in SAH and developmental
malformations.
 MRI - diagnostic in cerebral dysgenesis, lissencephaly
and other neuronal migration disorders.
 EEG - diagnostic and prognostic role in seizures and
should be done in all neonates who need anticonvulsant
treatment.

Neonate with seizures
•Identify and characterize the seizure
• Secure airway and optimize breathing, circulation, and temperature
• Secure IV access and take samples for baseline investigations
•If hypoglycemic : administer 2 ml/kg of 10% dextrose as
bolus followed by a continuous infusion of 6-8 mg/kg/min
• If serum calcium is abnormal, 2 ml/kg of calcium gluconate
(10%) should be given IV under cardiac monitoring
Seizures persist

Administer phenobarbitone 20mg/kg IV stat
over 20 minutes
Repeat phenobarbitone in 10 mg/kg/dose
aliquots until 40 mg/kg dose is reached
Seizures
continue
Seizures continue
Administer phenytoin 20 mg/kg IV slowly
over 20 minutes under cardiac monitoring
Lorazepam: 0.05 mg/kg IV bolus over 2-5 minutes; may be repeated
Midazolam: 0.15 mg/kg IV bolus followed by infusion of 1-7 mcg/kg/min
Clonazepam 0.1mg/kg;Consider ventilation.
Seizures continue
Seizures continue

Second line drugs like
Lidocaine[4mg/kg f/b 2mg/kg/hr]
Paraldehyde[0.1-0.2ml/kg/dose IM]
sodium valproate[20-25mg/kg f/b 5-10mg/kg/12h]
Topiramate(20mg/kg/day)
Levetiracetam(10-30mg/kg/day)
Vigabatrin(50mg/kg/day) Pyridoxine(100mgIVtestdose)
exchange transfusion[IEMs,drug toxicity,bilirubin encephalopathy]
Wean AEDs slowly to maintenance
phenobarbitone
Seizures controlled

MAINTENANCE DOSE
Phenobarbitone or phenytoin after
loading dose maintenance dose 3-5
mg/kg/day in two divided doses.
Wean slowly in a way, taper the last
given anti convulsant first and first
given phenobarbitone in last.

DURATION OF ANTICONVULSANT
THERAPY GUIDELINES

Newborn on anticonvulsant therapy
Stop
phenobarbitone
prior to discharge
Evaluate EEG
Normal
Normal examination
Taper drugs over
2 weeks
Abnormal EEG
Continue drug;
reassess at 3
Normal EEG
Taper drugs over 2
weeks
Wean all antiepileptic drugs except phenobarbitone once seizure
controlled
Perform neurological examination prior to discharge
Abnormal
Continue phenobarbitone for 1 month
Repeat neurological examination at 1 month
Abnormal examination

PROGNOSIS
 Focal clonic seizures carry the best prognosis.
 Myoclonic seizures carry the worst prognosis in
terms of neurodevelopmental outcome and seizure
recurrence.
 Seizures due to SAH and late onset hypocalcemia
carry best prognosis in terms of long term
neurodevelopmental outcome.
 Seizures related to hypoglycemia,cerebral
malformations and meningitis have adverse
outcome.

Neurological Disease Normal
Development
 Hypoxic-ischemic encephalopathy 50%
 Primary subarachnoid hemorrhage 90%
 Hypocalcemia
Early-onset 50%
Later-onset 100%
 Hypoglycemia 50%
 Bacterial meningitis 50%

SUMMARY
 Seizures are common in neonatal period than any
other period of life.
 Subtle seizures are the most common type of
neonatal seizures.
 Hypoxic ischemic encephalopathy is the most
common cause of neonatal seizures.
 Phenobarbitone is the drug of choice for neonatal
seizures.
 Focal clonic seizures and seizures due to
subarachnoid hemorrhage and late onset
hypocalcemia carries best prognosis.

REFERENCES
 AIIMS NICU PROTOCOL -2014
 MANUAL OF NEONATAL CARE - CLOHERTY
 NELSON TEXTBOOK OF PEDIATRICS
 CARE OF THE NEWBORN – MEHARBAN SINGH
 IAP TEXT BOOK OF PEDIATRICS

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