Neonatal Seizures

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Dr. Kalpana MallaMD Pediatrics

Manipal Teaching Hospital

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

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

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

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

SEIZURE PATTERN1. 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

SEIZURE PATTERN

2.Clonic - Focal / Multifocal – twitching migrate haphazardly from one limb to another, occur due to HIE & birth trauma

3.Generalised seizure - rare

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

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

SEIZURE PATTERN

6.Myoclonic seizures• Rare in newborns• Single/multiple flexion movements,

slow and jerky• Seen in developmental defects and

anencephaly

Features Jitteriness Seizure

Stimulus sensitive

++ _

Cessation Passive flexion Gentle grasp

-

Rhythmicity

Rhythmic oscillation

Fast & slow components

Features Jitteriness

Seizure

Frequency of jerks

5-6 / sec

2-3 / sec

Abnormal gaze-Eye movement

Nil Present

Autonomic disturbance

Nil Increase HR, BP)

EEG Normal Abnormal

ETIOLOGY

A.Perinatal causes 1. Neonatal encephalopathy -

20- 40% of seizures2. Intracranial hemorrhages-

CNS trauma, SAH, PVH,

B. METABOLIC CAUSES

• Hypoglycemia • Hypocalcemia – most common

metabolic cause for NNS• Hypomagnesemia• Hypo / Hypernatremia• Pyridoxine dependency • IEM - Disorders of amino acid

metabolism

C. Infections

• Intracranial - Meningitis - encephalitis – herpes, coxachie, echo,

CMV, - Toxoplasmosis

Extracranial – septicemia - Tetanus - Severe rep distress

D. Developmental defects

–Cerebral Dysgenesis–Hydrocephalus–Microcephaly–Neuronal migration defects-

Lissencephaly,pachygyria,schizencephaly

Others

E. Drugs- prolonged maternal administration

- Vit B6-pyridoxin dependancy - Narcotic withdrawal - TheophyllineF. PolycythemiaG. Focal infarcts

Others

H .Hypertensive encephalopathy

I . Benign familial epilepsy – does not continue after neonatal period

J .Unknown(Idiopathic : 3-25%

Diagnosis – time of onset

• 1st day – birth asphyxia (HIE) - C’bral trauma - Pyridoxin dependancy - Narcotic withdrawal - IEM

Diagnosis – time of onset

• 1-3 days – - ICH - Hhypocalcemia - Hypoglycemia - Hypo & hypernatremia - Pyridoxin deficiency - Cong C’bral malformations - Narcotic withdrawal

Diagnosis – time of onset

• 4-7 days – - Meningitis - Encephalitis - Hypomagnesemia - TORCH infection - Developmental malformations - Kernicterus - IEM - Pyridoxin dependancy - Tetanus

Refractory seizures

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

Investigations

• CBC• Blood – glucose, calcium, electrolytes, Mg,

bilirubin, ABG• CSF analysis• Blood C/S , urine C/S• Cranial USG

Second line investigations

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

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

ANTICONVULSANTS

Phenobarbitone 15 - 20mg / kg IV loading dose 3.5 - 5mg / kg / day maintenance dosePhenytoin 15 - 20 mg / kg IV at 1mg / kg / min 4 - 8 mg / kg day maintenance doseMidazolam 0.02 - 0.4 mg/kg IM

0.02 - 0.1mg/kg IV0.06 - 0.4mg/kg/hr

Others Lorazepam, diazepam, Paraldehyde

ANTICONVULSANTS

• Phenobarbitone ↓↓• Phenytoin

↓↓• Lorazepam, midazolam drip – 48 hrs

↓↓

ANTICONVULSANTS

↓↓• Barbiturate coma – pentobarbital& thiopental

on ventilator – try to wean every 24 hrs

↓↓• GA with isoflurane or halothane +

neuromuscular blockade (muscle paralysis)

TREATMENT1. Optimise ventilation Maintain CO, BP, Serum electrolytes & pH2. Treat underlying diseases- Metabolic abnor malities,meningitis,Narcotic withdrawal3. Pyridoxine dependency- 50mg IV, repeat every 10 min till control- maintenance dose – 5mg/kg PO daily6. Hyperbilirubinemia –phototherapy, exchange transfusion

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

Benign idiopathic NNS

• Typically Presents at day 5 of life• Also called 5th day fits• Multifocal in type• No cause detected

FOLLOW UP - ANTICONVULSANTS

1. Stop all others except maintenance PB2. Maintenance PB : 2wks - 2months3. Risk of recurrence Little: transient metabolic abnormalities

30-50% : HIE High : Cortex malformations

PROGNOSISNormal Outcome: 56%Neurological sequelae: 30 - 40%Death : 15-25%Chronic seizure disorder: 15-20%

Outcome depends on1. Level of maturity2. Etiology3. Neurological examination4. EEG / Imaging studies

GOOD PROGNOSIS

• Uncomplicated hypoglycemia• Narcotic withdrawal• SAH

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

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