Neonatal Seizures: Priscilla Joe, MD Children's Hospital & Research Center at Oakland

Neonatal Seizures
Priscilla Joe, MD
Childrens Hospital & Research Center at Oakland
Pathophysiology
Abnormal synchronous depolarization from
large group of neurons
Excessive excitatory amino acid release
(glutamate)
Lack of inhibitory systems (GABA)
Depolarization results from Na influx into
cells; repolarization from outflux of K+
Disruption of Na/K ATP pump
Basic Mechanisms of Seizures

Abnormal energy production (hypoxemia,
hypoglycemia)
Alteration in neuronal membrane
(hypocalcemia, hypomagnesemia)
Relative excess of excitatory versus
inhibitory neurotransmitters (GABA)
Biochemical Changes with Seizures
ATP
phosphocreatine
Pyruvate converted to lactate
brain glucose
Increased production of pyruvate from ADP
Incidence
Higher in neonates than any other age group
Most frequent in the first 10 days of life
Do Prolonged Seizures Harm the

Developing Brain?
Animal studies:
Persistent neonatal seizures in rats induce neuronal
death and changes in hippocampus
Chronic seizures in adults associated with memory

impairment and poor psychosocial outcome
Permanent reduction in seizure threshold
associated with significant deficits in learning and
memory
Causes of Neonatal Seizures
HIE (32%)
Intracranial hemorrhage (17%)
CNS infection (14%)
Infarction (7%)
Metabolic disorders (6%)
Inborn errors (3%)
Unknown (10%)
Drug withdrawal (1%)
Adverse Effects of Seizures
Cell division and migration

Formation and expression of receptors
Synaptogenesis and apotosis
Long term effects: seizure threshold,
learning, and cognition
Ferriero D. N Engl J Med 2004;351:1985-1995
Subtle Seizures
More common in premature infants
Most frequently observed type of seizure
Clinical manifestations: Bicycling
movements, lip smacking, apnea, and eye
movements or staring, unresponsiveness
Typically have no electrographic correlate,
are likely primarily subcortical
Clonic Seizures
Focal or multifocal, rhythmic movements
with slow return movement
May be associated with generalized or focal
brain abnormality
Most commonly associated with
electrographic seizures
Tonic Seizures
Sustained flexion or extension of one
extremity or the whole body
Extensive neocortical damage with
uninhibited subcortically generated
movements
May or may not have electrographic
correlate
Myoclonic Seizures
Rapid, isolated jerks which lacks the slow
return phase of clonic movements
Typically not associated with electrographic
correlate
Myoclonic movements may be normal in
preterm or term infants
Nonepileptic movements
Benign sleep myoclonus
Tremulousness or jitteriness
Stimulus evoked myoclonus from metabolic
encephalopathies, CNS malformation
Benign Sleep Myoclonus

Onset 1st week of life
Synchronous jerks of upper and lower extremities
during sleep
No EEG correlate
Provoked by benzodiazepines
Ceases upon arousal
Resolves by 2 months
Good prognosis
Jitteriness vs. Seizures
No ocular phenomena
Stimulus sensitive
Tremor
Movements cease with passive flexion
Hypoxic Ischemic Encephalopathy
Seizures begin within 24-72 hours after birth

Accounts for 50-60% of all neonatal seizures
Most asphyxia occurs before or during birth
Arterial cord pH < 7.0, base deficit < -10
60% develop seizures within 1st 12 hours
Recent stress: hypotonia and unresponsiveness
Longer standing dysfunction: hypertonia with cortical thumbing,
joint contractures or conversely hypotonia with encephalopathy
Meningitis/ Encephalitis
Accounts for 5-10% of all neonatal seizures
TORCH, enterovirus, parvovirus
Usually present by day 3 of life, except for HSV
which may present in 2nd week of life
GBS, listeria, E coli, strep pneumoniae

Presents at end of 1st week to 3 months of age
Intracranial Hemorrhage
Accounts for 10% of all seizures

Grade IV IVH/PVH
Subarachnoid/subdural hemorrhage
Cerebral infarction (ischemia, dehydration,
infection, polycythemia)
Cerebral Infarction
Most frequently involves middle cerebral
artery
Focal, clonic seizures common
At risk for spastic hemiparesis
Venous sinus thrombosis may cause
hemorrhage stroke
ECMO
Etiologies: CNS malformations

Lissencephaly, pachygyria, linear sebaceous
nevus syndrome, polymicrogyria
Present with seizures at a later age
Etiologies: Metabolic
Hypoglycemia, hypocalcemia, hypomagnesemia,
hyper/hyponatremia
Inborn errors of metabolism (>72hrs of age):
Aminoacidopathies, urea cycle disorders,
biotinidase deficiency, mitochondrial disorders,
beta oxidation disorders, glucose transporter
deficiency, peroxisomal disorders
Epileptic syndromes-benign
Benign familial neonatal seizures
Autosomal dominant
Inter-ictal exam is normal
Long term outcome is good
Unusual tonic-clonic pattern
Benign idiopathic neonatal seizures

Term, normal birth
Normal inter-ictal state, EEG
Clonic, occur day 5, may be Zn deficiency
Epileptic syndromes-malignant
Neonatal Myoclonic encephalopathy
Fragmentary partial seizures, massive myoclonus
Metabolic disorders, abnormal EEG
Poor prognosis
Ohtahara syndrome
10d -3 mo
Numerous brief Tonic seizures
Dysgenesis is cause, prognosis very poor
Metabolic Evaluation
Blood: glucose, lytes, BUN, creatinine,
lactate, pyruvate, ammonia, biotinidase,
quantitative amino acids, very long chain
fatty acids
Urine: quantitative amino acids
CSF: cell count, glucose, protein, pyruvate,
lactate, quantitative amino acids, HSV PCR
EEG
Scalp recordings measure discharges that
spread to the surface
Discharges from frontal or temporal regions
may not spread to the surface
More common in the newborn
Clinical Seizures Without EEG

Correlate
May represent uninhibited brainstem
reflexes
Discharges from deep cerebral structures
and brainstem may not reach the cortical
surface
Treatment
More difficult to suppress than in older
children
Treatment is worthwhile because seizures:
May cause hemodynamic or respiratory
compromise
Disrupt cerebral autoregulation
May result in cerebral energy failure and
further injury
Treatment
Stabilize vital signs and treat underlying
hypotension
Correct transient metabolic disturbances
Phenobarbital is first line agent
Lorazepam
Phenytoin
Prognosis based on etiology
Hypoxia-ischemia
Meningitis
Hypoglycemia
Early Hypocalcemia
Subarachnoid hemorrhage
Late Hypocalcemia
50% normal outcome
Almost all are normal
Prognosis based on etiology

Cerebral dysgenesis has grave prognosis,
almost none are normal
Prematurity and seizures associated with
high risk of death or very poor outcome
Prognosis based on type

Subtle
Clonic
Generalized Tonic
Myoclonic
Depends on cause,
other seizure types
Better prognosis
Poor
Poor
Prognosis by EEG
Severe inter-ictal EEG background associated
with adverse outcome
Normal EEG background at presentation
associated with good outcome
Ictal features less reliable
Better outcome when clinical and EEG seizures
correlate
Increased number and frequency may relate to
worse outcome
Conclusions
Neonatal seizures are often subtle
Close examination and characterization
important for prognosis and evaluation
Treatment usually successful in stopping
seizures, but risk of neuro-developmental
abnormalities remains high
Prevention of causes remains a priority

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Neonatal Seizures

Basic Mechanisms of Seizures

Biochemical Changes with Seizures

Do Prolonged Seizures Harm the

Chronic seizures in adults associated with memory

Causes of Neonatal Seizures

Adverse Effects of Seizures

Cell division and migration

Ferriero D. N Engl J Med 2004;351:1985-1995

Benign Sleep Myoclonus

Jitteriness vs. Seizures

Hypoxic Ischemic Encephalopathy

Seizures begin within 24-72 hours after birth

GBS, listeria, E coli, strep pneumoniae

Accounts for 10% of all seizures

Etiologies: CNS malformations

Benign idiopathic neonatal seizures

Clinical Seizures Without EEG

Prognosis based on etiology

50% normal outcome

Almost all are normal

Prognosis based on etiology

Prognosis based on type

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