CASE

OF
NE0NATAL
CONVULSIONS
Dr. Balakrishna
2nd year Postgraduate
Dept of pediatrics
 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.
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 seizures are common in preterm
neonates ?

Incidence of Neonatal seizures is 2.8 per 1000

in infants with birth weight >2.5kg. It is higher
in preterm LBW neonates as high as 57.5 per
1000.

Myelination, dendritic processes, arborization

starts to develop at term.
Why generalised seizures are rare in
neonates ?

Neonatal brain has reduced connectivity,

therefore electrical discharges spread
incompletely, so generalised seizures are
rare in neonates.
TYPES OF NEONATAL
SEIZURES
There are 5 subtypes of neonatal seizures
1. Subtle seizures
2. Clonic seizures
3. Tonic seizures
4. Myoclonic seizures
5. Spasms
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.
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.

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.
 SPASMS
Sudden generalised jerks lasting for 1-2sec.

Distinguished from generalised tonic spells by

their short duration and they are usually
associated with single very brief generalised
discharge.
CAUSES OF NEONATAL SEIZURES
AGES 1 - 4 DAYS

HIE ( most common )

IVH

Acute metabolic disorder

hypocalcemia
hypoglycemia
hypomagnesemia
hypo/ hypernatremia
Drug withdrawl maternal drug use of
narcotics or barbiturates.

Drug toxicity- lidocaine, penicillin.

Inborn errors of metabolism

galactosemia, hyperglycinemia, urea cycle
disorders.

Pyridoxine deficiency (must be considered

at all ages).
 AGES 4 - 14 DAYS

Infection meningitis (bacterial) , encephalitis

(enteroviral, herpes simplex).
Metabolic disorders hypocalcemia,
hypoglycemia
Drug withdrawal
Kernicterus, hyperbilirubinemia
Benign neonatal convulsions
Developmental delay, epilepsy, neonatal
diabetes syndrome- DEND syndrome
 AGES 2 - 8 WEEKS

Infection
Head injury subdural hematoma
Inherited disorders of metabolism -
aminoacidurias , organic aciduria, urea cycle
defects
Malformations of cortical developments
lissencephaly, focal cortical dysgenesis.
Tuberous sclerosis
Sturge weber syndrome
 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 : RBS level <40mg/dl in the first

24 hours and <50mg/dl after 24 hours.

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 REM
sleep disappear when baby is awake, EEG is
normal and seizures spontaneously resolve by
2 months of age.
CLINICAL CHARACTER SEIZURE
JITTERINESS
rare
Increases with
common
stimulation
Suppress with absent
passive flexion present
Autonomic
accompanimen present
ts absent
Predominant
movement clonic jerking
tremor
APPROACH TO NEONATAL
SEIZURES
 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
- Neuroimaging (CT, MRI)
- Screen for congenital infections (TORCH)
- Screen for IEM
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.
Acute management of
seizures
 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 (blood sugar <40 mg/dl): 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
Seizures
continue
Repeat phenobarbitone in 10 mg/kg/dose
aliquots until 40 mg/kg dose is reached
Seizures continue

Administer phenytoin 20 mg/kg IV slowly

over 20 minutes under cardiac monitoring
Seizures continue

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
 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 ]

Seizures controlled

Wean AEDs slowly to maintenance

phenobarbitone
 MAINTENANCE DOSES
Phenobarbitone or phenytoin after
loading dose maintenance dose 3-5
mg/kg/day divided in bd .
Start weaning if baby convulsion free
for 72 hours .
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

Wean all antiepileptic drugs except phenobarbitone once

seizure controlled

Perform neurological examination prior to discharge

Normal Abnormal
Stop
phenobarbitone Continue phenobarbitone for 1 month
prior to
discharge
Repeat neurological examination at 1 month

Normal examination Abnormal examination

Stop Evaluate EEG

phenobarbiton Abnormal EEG
e. Normal EEG Continue drug;
Stop reassess at 3
phenobarbitone
 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
PGEI NICU PROTOCOL
MANUAL OF NEONATAL CARE - CLOHERTY
NELSON TEXTBOOK OF PEDIATRICS
CARE OF THE NEWBORN MEHARBAN SINGH
PRACTICAL PEDIATRIC NEUROLOGY VEENA
KALRA
IAP TEXT BOOK OF PEDIATRICS
THANK YOU