NEONATAL SEIZURE

TUTOR E

TUTOR E

Ligia Riesky Banche (41120003)

Andyta Kartikawati (41120044)

Bernadus Chrisna Bayu (41120015)

Anissa Cintyaning (41120037)

Vincent Exel Susanto (41120016)

Yudha Hadi K. (41120101)

Teresa Nadia Iriani (41120038)

Gusti Ayu Putu Ika BSA (41120048)

Yulianti Wenas (41120043)

Kristina Elizabeth (41120104)

BACKGROUND

Seizure is the physical findings or changes in behavior that occur after an

episode of abnormal electrical activity in the brain

The neonatal period is limited to the first 28 days of life in a term infant
Determining the underlying etiology for neonatal seizures is critical. Etiology

determines prognosis and outcome and guides therapeutic strategies.

SEIZURE CHARACTERISTICS
Most neonatal seizures occur over only a few days, and fewer than half of

affected infants develop seizures later in life.

Seizures in neonates are relatively common, their presence is often the first

sign of neurologic dysfunction, and they are powerful predictors of long-term

cognitive and developmental impairment.
Most seizures in the neonate are focal.

NEONATAL SEIZURE CLASSIFICATION

1. Clonic Seizure

2. Tonic Seizure
3. Myoclonic Seizure

CLONIC SEIZURE

These movements most commonly are associated with electrographic

seizures.
They often involve 1 extremity or 1 side of the body.
The rhythm of the clonic movements is usually slow, at 1-3 movements per

second.

TONIC SEIZURE

These may involve 1 extremity or the whole body. Focal tonic seizures

involving 1 extremity often are associated with electrographic seizures.

Generalized tonic seizures often manifest with tonic extension of the upper

and lower limbs and also may involve the axial musculature in an opisthotonic
fashion

MYOCLONIC SEIZURE

These may occur focally in 1 extremity or in several body parts (in which case

they are described as multifocal myoclonic seizures).

Generalized myoclonic jerks are possibly the clinical equivalent of infantile

spasms.

ETIOLOGY
Seizures occur when a large group of neurons undergo excessive, synchronized depolarization.

Depolarization can result from excessive excitatory amino acid release, such as glutamate, or deficient

inhibitory neurotransmitter, such as gamma amino butyric acid (GABA)

Etiology
1. Hypoxic-ischemic encephalopathy
2. Hemorrhage
3. Metabolic disorders
4. Intracranial infections
5. Malformation syndromes
6. Benigna neonatal seizures

PATHOGENESIS
Potential mechanisms of brain injury with repeated neonatal seizures include:
Hypoventilation/apnea

Causing hypoxia (leading to cardiovascular collapse, diminished cerebral blood flow [CBF]
and
increased risk of
hypoxic ischemic injury), or hypercarbia (leading to a rise in CBF
and increased risk of intracranial hemorrhage (ICH).
Elevated blood pressure increases CBF and risk of ICH.
Increased glycolysis leading to hypoglycemia which exacerbates seizure induced brain injury.
Excitatory amino acids (increased release) resulting in excitotoxic brain injury.

PRESENTATION
Infants with neonatal seizures are frequently lethargic between seizures and often appear ill.
Findings of the neurologic examination between seizures may be normal. Abnormalities findins may

be seen correlating with a focal or generalized neurologic syndrome.

Family history genetic syndrome
Pregnancy history TORCH Infections, fetal distress, pre-eclampsia, maternal infections
Delivery history Apgar scores may offer some guidance concerning etiology
Postnatal history drug withdrawal, neonatal hypocalcemia, infections, sepsis

WORKUP
Imaging Studies
Cranial USG

It is a valuable tool for quickly ascertaining whether intracranial hemorrhage, particularly intraventricular hemorrhage, has
occurred

A limitation of this study is the poor detection rate of cortical lesions or subarachnoid blood

Cranial CT Scanning

It is a much more sensitive tool than ultrasonography in detecting parenchymal abnormalities.

Cranial CT scan can delineate congenital malformations. Subtle malformations may be missed on CT scan, requiring a
magnetic resonance imaging (MRI) study.

MRI

Cranial MRI is the most sensitive imaging study for determining the etiology of neonatal seizures, particularly when
electrolyte imbalance has been excluded as the seizures cause.

A major disadvantage is that MRI cannot be performed quickly and, in an unstable infant, it is best deferred until the
acute clinical situation resolves.

Ecocardiography

This study can rule out cardiac hypomotility as a result of more diffuse hypoxia

WORKUP
Approach considerations
Tests to ascertain the cause of neonatal seizures include the following:
Serum glucose and electrolytes - Transient neonatal hypocalcemia is a cause of neonatal seizures

during the first 3 weeks of life; hypocalcemia associated with chromosome 22q11 deletion syndrome
may also be a consideration
TORCH (toxoplasmosis, rubella, CMV, herpes) infection studies
Urine organic acids
Serum amino acid assay
Renal function tests - These tests rule out posthypoxic renal dysfunction; hypoxic damage to multiple

organ systems may also be suggested by elevated liver transaminase levels.

DIFFERENTIAL DIAGNOSES
Benign sleep myoclonus
Jitteriness
Anoxia
Benign epilepsy syndromes
Mitochondrial cytopathies

Myoclonic epilepsy
Myoclonus
Organic acidurias

Pyridoxine-dependent epilepsy

Subarachnoid hemorrhage
Subdural hematoma
Tuberous sclerosis
Vein of Galen malformation
Viral encephalitis
Viral meningitis

MEDICATION
Anticonvulsants
Phenobarbital :

Depresses sensory and motor cortex, cerebellum. Antiseizure activity occurs primarily where GABA mediates
neurotransmission

Phenytoin :

It should be added to phenobarbital if seizures persist. Phenytoin may act in the motor cortex, where it may inhibit the
spread of seizure activity.

Lorazepam :

It is a benzodiazepine anticonvulsant. It is used in cases refractory to phenobarbital and phenytoin. By increasing the
action of GABA, which is a major inhibitory neurotransmitter in the brain, lorazepam may depress all levels of the CNS,
including the limbic and reticular formations.

Vitamins, Water-soluble
Pyridoxine (vit. B6) :

Pyridoxine should be tried in patients not responding to the above regimen. Deficiency vit.B6 rarely cause seizure. It
functions is cofactor in enzymatic reactions

PROGNOSIS

Prognosis is determined by etiology for neonatal seizures. If the EEG background is normal, the

prognosis is excellent for seizures to resolve; normal development is likely

Severe EEG background abnormalities indicate poor prognosis; such patients frequently have cerebral

palsy and epilepsy. The presence of spikes on EEG is associated with a 30% risk of developing future
epilepsy.

PROGNOSIS
Scoring system :
-

Pisani et al devised a scoring system for early prognostic assessment after neonatal seizures.

There are 6 independent risk factors for adverse outcome:

(1) birth weight

(2) Apgar score at 1 minute
(3) neurologic examination at seizure onset
(4) cerebral ultrasonogram
(5) efficacy of anticonvulsant therapy
(6) presence of neonatal status epilepticus
-

Each variable was scored from 0 to 3 to represent the range from normal to severely abnormal. These were
then added together to produce a total composite score, ranging from 0 to 12.

A cutoff score of 4 or higher provided the greatest sensitivity and specificity for prediction of adverse
neurologic outcome

COMPLICATIONS
Complications of neonatal seizures may include the following :
Cerebral palsy
Cerebral atrophy
Hydrocephalus ex-vacuo
Epilepsy
Spasticity
Feeding difficulties

REFERENCES

http://emedicine.medscape.com/article/1177069-overview#aw2aab6b2b5aa

http://www.nlm.nih.gov/medlineplus/ency/article/003200.htm
Intensive Care Nursery Manual Neonatal Seizure USCFs Children Hospital