neonatal seizures by Farshid Mokhberi

1. NEONATAL SEIZURES
By: Farshid Mokhberi
Shahid beheshti University of medical sciences and health services

2. 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.

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

4. TYPES OF NEONATAL SEIZURES
1. Subtle seizures
2. Clonic seizures
3. Tonic seizures
4. Myoclonic seizures

5. SUBTLE SEIZURES
1) Ocular - tonic horizontal deviation of eyes or
sustained eye opening with ocular fixation or cycled
fluttering.
2) Oral facial lingual movements - chewing, tongue
thrusting, lip smacking etc.
3) Limb movements - cycling, paddling, boxing etc.
4) Autonomic phenomena-tachycardia or bradycardia.
5) Apnea may be a rare manifestation of seizure.

6. 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.

7. 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

8. 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

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

10. 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.

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

12. 5.MISCELLANEOUS
 Passive drug withdrawl
 Accidental injection of local anesthetic
into fetal scalp.
 Neonatal epileptic syndromes
 Benign familial neonatal convulsions
 Benign idiopathic neonatal convulsions
 Early myoclonic encephalopathy
 Early infantile epileptic encephalopathy
 Malignant migrating partial seizures in
infancy

13. 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

14. 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.

15. 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

16. APPROACH TO NEONATAL SEIZURES

17. 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 .

18.  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.

19. EXAMINATION
 Vitals : HR, RR, 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.

20.  CNS examination – presence of bulging AF may be
suggestive of meningitis or ICH
- consciousness
- tone
- 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 .

21.  Additional
 Hematocrit
 Serum bilirubin
 Serum magnesium
 Arterial blood gas and anion gap
 Imaging: CT and/or MRI (if no etiology found
after essential investigations)
 TORCH screen for congenital infections
 Work-up for inborn errors of metabolism

22. INVESTIGATIONS
 Essential
- Blood sugar
- Serum electrolytes
- CSF examination
- Cranial ultrasound
- EEG

23.  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.

24. Acute management of seizures

25. 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

26. 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

27. 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

28. 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.

29. 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.

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

31. REFERENCES
 MANUAL OF NEONATAL CARE - CLOHERTY
 NELSON TEXTBOOK OF PEDIATRICS

32. THANK YOU