1. Neonatal Seizures
Dr. Kalpana Malla
MD Pediatrics
Manipal Teaching Hospital
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2. INTRODUCTION
• Not uncommon
•Always due to some underlying cause
•25% cases cause – unknown
•Often first sign of neurological disorders
•Powerful predictors of long term
cognitive and developmental impairement

3. Pathophysiology
1.Large group of neurons undergo
excessive, synchronized depolarization which
results from –
a) Increase in excitatory
neurotransmitters (glutamate)
b) Decrease in inhibitory
neurotransmitters (gamma amino
butyric acid- GABA

4. PROBABLE MECHANISMS
c. Disruption of ATP – dependent resting
membrane potentials - Failure of Na - K
pump – flow of sodium into the neuron
& potassium out of neuron
d. Membrane alteration - Increased Na
permeability

5. Incidence
• 1 in 200 healthy newborns
• 0.5 -0.8% Term babies
• 6-12% <1.5 kg (1 in 4 premature and
LBW
• Many seizures are very subtle – go
undetected

6. SEIZURE PATTERN
1. Subtle seizure: 50%of seizures
- Tonic horizontal deviation of eyes,
staring look,Repetitive blinking /
fluttering of eyelids
- Oro- buccal movements-chewing,
lip smacking, sucking, yawning
- Tonic posturing of a limb
- Apnea
- Swimming/ bycycling movements

7. SEIZURE PATTERN
2.Clonic - Focal / Multifocal –
twitching migrate haphazardly
from one limb to another,
occur due to HIE & birth
trauma
3.Generalised seizure - rare

8. SEIZURE PATTERN
4. Focal clonic –
Localized & often assoc with loss of
consciousness
They are signs of bilateral c’bral disorder
Common in metabolic disorder, birth
trauma and c’bral infarction

9. SEIZURE PATTERN
5. Tonic seizure –
- Stiffening similar to decerebrate
posture but with eye signs and
heavy breathing
- Often associated with apnea
- Seen in IVH, preterm and
Kernicterus

10. SEIZURE PATTERN
6.Myoclonic seizures
• Rare in newborns
• Single/multiple flexion
movements, slow and jerky
• Seen in developmental defects and
anencephaly

11. Features Jitteriness Seizure
Stimulus ++ _
sensitive
Cessation Passive flexion -
Gentle grasp
Rhythmicity Rhythmic Fast & slow
oscillation components

12. Features Jitterine Seizure
ss
Frequency of jerks 5-6 / sec 2-3 / sec
Abnormal gaze-Eye Nil Present
movement
Autonomic disturbance Nil Increase HR, BP)
EEG Normal Abnormal

13. ETIOLOGY
A. Perinatal causes
1. Neonatal encephalopathy - 20-
40% of seizures
2. Intracranial hemorrhages- CNS
trauma, SAH, PVH,

14. B. METABOLIC CAUSES
• Hypoglycemia
• Hypocalcemia – most common metabolic
cause for NNS
• Hypomagnesemia
• Hypo / Hypernatremia
• Pyridoxine dependency
• IEM - Disorders of amino acid
metabolism

15. C. Infections
• Intracranial
- Meningitis
- encephalitis – herpes, coxachie, echo, CMV,
- Toxoplasmosis
Extracranial
– septicemia
- Tetanus
- Severe rep distress

16. D. Developmental defects
– Cerebral Dysgenesis
– Hydrocephalus
– Microcephaly
– Neuronal migration defects-
Lissencephaly,pachygyria,schizenceph
aly

17. Others
E. Drugs- prolonged maternal
administration
- Vit B6-pyridoxin dependancy
- Narcotic withdrawal
- Theophylline
F. Polycythemia
G. Focal infarcts

18. Others
H .Hypertensive encephalopathy
I . Benign familial epilepsy – does not
continue after neonatal period
J .Unknown(Idiopathic : 3-25%

19. Diagnosis – time of onset
• 1st day – birth asphyxia (HIE)
- C’bral trauma
- Pyridoxin dependancy
- Narcotic withdrawal
- IEM

20. Diagnosis – time of onset
• 1-3 days –
- ICH
- Hhypocalcemia
- Hypoglycemia
- Hypo & hypernatremia
- Pyridoxin deficiency
- Cong C’bral malformations
- Narcotic withdrawal

21. Diagnosis – time of onset
• 4-7 days –
- Meningitis
- Encephalitis
- Hypomagnesemia
- TORCH infection
- Developmental malformations
- Kernicterus
- IEM
- Pyridoxin dependancy
- Tetanus

22. Refractory seizures
• IEM –
• Developmental defects of CNS
• Narcotic withdrawal
• Pyridoxin dependancy
• Kernicterus
• Benign familial seizures

23. Investigations
• CBC
• Blood – glucose, calcium, electrolytes, Mg,
bilirubin, ABG
• CSF analysis
• Blood C/S , urine C/S
• Cranial USG

24. Second line investigations
• TORCH screening
• IEM screening – urine organic acids
• - S. amino acid assay
• Imaging – CT scan
- MRI
- EEG brain

25. Management
• Collect all samples
• IV line
• Thermoneutral environment
• Glucose 10% - 2-4ml/kg as bolus followed by
10% glucose as drip @ 8mg/kg/min
• IV calcium – gluconate 2ml/kg

26. ANTICONVULSANTS
Phenobarbitone
15 - 20mg / kg IV loading dose
3.5 - 5mg / kg / day maintenance dose
Phenytoin
15 - 20 mg / kg IV at 1mg / kg / min
4 - 8 mg / kg day maintenance dose
Midazolam 0.02 - 0.4 mg/kg IM
0.02 - 0.1mg/kg IV
0.06 - 0.4mg/kg/hr
Others Lorazepam, diazepam, Paraldehyde

27. ANTICONVULSANTS
• Phenobarbitone
↓↓
• Phenytoin
↓↓
• Lorazepam, midazolam drip – 48 hrs
↓↓

28. ANTICONVULSANTS
↓↓
• Barbiturate coma – pentobarbital& thiopental
on ventilator – try to wean every 24 hrs
↓↓
• GA with isoflurane or halothane +
neuromuscular blockade (muscle paralysis)

29. TREATMENT
1. Optimise ventilation
Maintain CO, BP, Serum electrolytes & pH
2. Treat underlying diseases- Metabolic abnor
malities,meningitis,Narcotic withdrawal
3. Pyridoxine dependency- 50mg IV, repeat
every 10 min till control- maintenance dose –
5mg/kg PO daily
6. Hyperbilirubinemia –phototherapy,
exchange transfusion

30. Benign familial neonatal seizure
• Typically occur in first 48- 72 hrs of life
• Disappear by age 2-6 months
• A family history seizures is usual
• Development - normal

31. Benign idiopathic NNS
• Typically Presents at day 5 of life
• Also called 5th day fits
• Multifocal in type
• No cause detected

32. FOLLOW UP -
ANTICONVULSANTS
1. Stop all others except maintenance PB
2. Maintenance PB : 2wks - 2months
3. Risk of recurrence
Little: transient metabolic abnormalities
30-50% : HIE
High : Cortex malformations

33. PROGNOSIS
Normal Outcome: 56%
Neurological sequelae: 30 - 40%
Death : 15-25%
Chronic seizure disorder: 15-20%
Outcome depends on
1. Level of maturity
2. Etiology
3. Neurological examination
4. EEG / Imaging studies

34. GOOD PROGNOSIS
• Uncomplicated hypoglycemia
• Narcotic withdrawal
• SAH

35. POOR PROGNOSIS
• Low APGAR score ≤ 6 at 5min
• Onset o seizures within 24 hrs of life
• Presence of myoclonic attacks
• Abnormal EEG
• 3 or more days of uncontrolled seizures

36. Thank you
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Medical Post [ www.themedicalpost.net ]