Neonatal EEG and Neonatal Seizures
Kohilavani Velayudam MD
Assistant Professor
Department of Pediatric Neurology
Vanderbilt University
October 10, 2013
Objectives






Introduction
Technical aspects - Neonatal EEG
Common Artifacts
Normal developmental landmarks
Abnormal neonatal EEG findings
Neonatal Seizures
Introduction
 Objective methods - Functional integrity of immature
cortex and its connection
 Interpretation: Recognition of EEG changes from
CA < 28 weeks through 44 weeks
 Rapid rate of cerebral development - Neonatal period
 Identifying age dependent findings - critical
 Quick clinical state change - parallel EEG changes happens
 Assessing prognosis - neonates at risk for neurological
sequelae
 Exact generators - unknown
Technical Information
Information prior to interpretation
 Post Conceptional Age :
• Gestational age at birth (weeks)+ chronological age
 Behavioral State of the infant
 Medications
 Location (isolette versus open bed)
 Recent medical procedure
 Topographic - Caput or cephalhematoma
Neonatal Montage
Neonatal Montage
 Modified standard 10-20
system
 Minimum 9 electrodes small head size
 Single bipolar montage
 16 channels
 2 or more non-cerebral
channels
Non- Cerebral Electrodes
EKG: HR and rhythm
 One electrode - midline chest
 Another electrode referenced to ear.
EMG: helps - sleep staging
 Oral-lingual - pharyngeal
movements
 Bilateral symmetric - under
jaw
EOG: Each eye - one
electrode nasion and one outer
canthus
 Characterize eye movements
 Staging sleep
Basic EEG Settings
Non- cerebral Electrodes
Physiological
Measures
Awake
Active Sleep
Quiet Sleep
EMG (chin)
Phasic and
tonic
Phasic
Tonic
Respiration
Irregular
Irregular
Regular
Eye movements
Random or
pursuits
Rapid eye
movements
Absent
Body movements
Facial, limbs
and body
Sucking and
irregular limb
movements
None
Duration
 60 minutes recording - mandatory
 Sleep cycle: 45 to 60 minutes
 Sampling of all neonatal sleep stages:
 Active sleep: 25 mins
 Quiet sleep: 20 mins
 Intermediate sleep: 15 mins
Active sleep - Term infant
Quiet sleep - Term infant
Artifacts
Artifacts
 Various artifacts - affects interpretation NEEG
 Simultaneous occurrence of unusual appearing activity
in the extra cerebral electrodes
 Peculiar morphology
Sucking - Artifact
Sweat - Artifact
Head Movement associated with sobbing- Artifact
Eye movement - Artifact
Limb clonic movement - Artifact
Ventilator - Artifact
Ballistocardio - Artifact
Hiccups - Artifact
Multiple artifacts
Depressed BG
EKG artifact
IV drip
Patting - Artifact
Mechanical Device - Artifact
Normal Neonatal EEG
Normal developmental landmarks
 Continuity and discontinuity
 Synchrony
 Age appropriate landmarks:
 Delta brushes
 Frontal sharps
 Temporal theta and alpha burst
< 30 weeks CGA
Trace Discontinue
 Discontinuous EEG - “Trace Discontinu”
 EEG signal with high amplitude burst “ON”
Periods followed low amplitude burst “OFF”
periods (Interburst Interval IBI)
 Amplitude of IBI : > 5 but < 25 microvolts
 < 28 weeks - 34 weeks
Trace Discontinue - 26 weeker
Burst “ON”
Burst “OFF”
Interburst Interval
 GA increase the IBI decreases
 > 30 weeker or older: 8 seconds or less
 Determinant of IBI:
 Conceptional age
 Prolonged IBI : Medical illness, elevated ammonia,
hypoxia
Maximal Acceptable Single Interburst
Interval Duration
Conceptional
< 30 Weeks
age
Maximal
IBI
30-35 s
31-33
Weeks
34-36
Weeks
37-40
Weeks
20 s
10 s
6s
31 - 37 Weeks CGA
Development
Active Sleep
Awake
Quiet Sleep
Continuous Activity
• EEG signal with steady amplitude throughout the recording
• Seen > 30 weeks CGA
Development of Continuity
Quiet Sleep “ Trace Alternant”
 36-38 weeks - Quiet sleep - mature pattern - TA
 High amplitude burst of mixed frequencies for 3-10
seconds -> followed by 3-5 seconds of low amplitude
burst
 Low amplitude burst > 25 and < 50 microvolts
Trace Alternant (Quiet sleep) - 38 weeker
Synchrony
 Asynchrony: burst of morphological similar activity in the homologous head
regions separated by > 1.5 to 2 seconds
 < 27 weeks: burst are synchronous
Delta Brushes
 Prime landmark - Prematurity
 0.3 to 1.5 hz delta slowing superimposed with fast activity
18-22 hz
 central  temporal 
occipital
 Peak age: 32 - 34 weeks
 Active sleep  awake  quiet sleep (37 weeks) 
disappear
 44 weeks - completely disappear
Delta Brushes
Temporal Theta and Alpha burst
• Developmental marker
• First appears: 26 weeks temporal theta burst
• 33 weeks - temporal
alpha burst
• Disappear after 34 weeks
Frontal Sharps
 Blunt isolated sharp waves in the frontal region
 Initial Negative (200 msec) --> Positive phase (longer)
 Frequently seen: Transitional stage of Sleep
 33 weeks - 46 weeks
 Symmetric and synchronous
 Sometimes seen with mixed rhythmic bi-frontal delta
Frontal Sharps
Awake stage - 30 Weeks CGA
35 weeker - Awake state
Continuous
activity
35 weeker - Awake state
Continuous
Activity
35 weeker - Quiet Sleep
discontinuous
activity
38 - 42 weeks CGA
38 weeker - Quiet sleep
Continuous Activity
38 weeker - Quiet sleep
Trace Alternant
44 Weeker - Sleep
Rudimentary Spindles
Developmental EEG Markers
Weeks
Continuity
Synchrony
EEG Awake/
sleep
diff
R/Nr
Components
A
QS
(NREM
)
AS
(REM)
A
QS
(NREM)
D
D
D
S
S
S
No
NR
DB (central); TT
27-29
D
D
D
As
As
As
No
NR
DB; TT ( theta)
30-33
C
D
D
S+
As
As
No
NR
DB (temp, occ) ; TA ( alpha);
FS
34-35
C
C
D
S ++
S+
As
No
R
DB (Occ), FS
36-37
C
C
D
S
++++
S
+++
S
++
Yes
R
DB (Occ) disappear – awake ,
FS, RFD
37- 40
C
C
TA
S
++++
S
++++
S
++++
Yes
R
DB (Occ) (TA – Qs)
C
CSWS
Sleep
spindles
S
S
S
Yes
R
FS disappear after 44 weeks
AS
(REM)
24-26
41- 44
C
Developmental Landmarks
Abnormal EEG findings
Asymmetry
• Subdural
infarction
• Cyst
• Caput
• Cephalhematoma
• Subgaleal
Hemorrhage
Def : Persistent interhemispheric amplitude difference of
background rhythms > 50%
FT Baby with Congenital heart diseases – ECMO
Asymmetry of BG
Positive Sharp waves
 Positive polarity
 Rolandic (PRS) and central vertex regions (PVS)
 Electrographic markers - Parenchymal injury - deep WM
injury
 IVH, PVL, Hydrocephalus, HIE
 5th to 8th postnatal day and disappear in 3-4 weeks
29 weeker with IVH – Positive Sharp waves
Sharp Electroencephalographic
transients ( SETs)
 Frequently seen - Frontal, central, temporal
 Less frequent: Vertex and occipital
 Frontal sharps versus Abnormal Frontal SET:
 Associated with frontal slowing
 Asymmetric
 Increased in active sleep and awake
Focal Sharp activity
 NORMAL
Bitemporal, central
Amp: < 75 micro volts
Duration < 100 msec
SW, Sync or async,
randomly
 > 1/minute
 Monophasic or diphasic
 Polarity: Negative
 Quiet Sleep
 Normal BG




 ABNORMAL
 One persistent location
 Amp > 150 microvolts
 Duration > 150 msec
 spikes, long runs
 several times/min
 Variable and polyphasic
 Polarity: Neg or positive
 Awake and QS
 Abnormal BG
Normal and Abnormal SET
Excessive Discontinuity
 Maximum Acceptable single IBI - Hahn et al
 CNS insults
 Sedative agents
Conceptional
age
< 30 Weeks
31-33
Weeks
34-36
Weeks
37-40
Weeks
Maximal
IBI
30-35 s
20 s
10 s
6s
Excessive Discontinuity
Excessive Discontinuity
Diffuse Abnormalities
 Excessive Discontinuity
 Depressed or undifferentiated EEG
 Burst suppression
 Electro-cerebral silence
Depressed and Undifferentiated
 Depressed EEG activity - marker abnormal cortical
function
 Undifferentiated: virtual or complete disappearance of
polyfrequency
 Some normal developmental landmarks - can be present
 Indicates - brain insult has occurred
 Persists > 24 hours after the insult - poor prognosis
 HIE, Meningitis, Encephalitis, IVH
39 weeker Congenital heart diseases - Hypoxia
FS
UD BG
Depressed and Undifferentiated EEG
Burst Suppression
 Burst of delta and theta frequency with SW and spikes
followed by severe background suppression (< 5
microvolts)
 No Reactivity
 Burst - can be associated with Myoclonic jerks
(Non-ketotic hyperglycinemia).
40 weeker - NKH - Burst suppression
Electro-cerebral Silence
 No EEG activity > 2 microvolts – isoelectric
 Severe encephalopathy
 Indicates - Death of the cortex
 Severe HIE with multi-organ failure
40 weeker - Electrocerebral silence - Severe HIE
Timing - Neonatal EEG
 Timing of the EEG - 24 hours following the insult
 Changes happens in hours
 Follow up EEG very important - Prognosis
Dyschronism
Disordered Maturational development
External
 Discrepancy between clinically
determined CA and EEG
derived CA
 2 weeks or < - Transient
CNS dysnfunction
 > 3 weeks - Persistent
impairment of CNS function
Internal
 The developmental
characteristics of Q sleep more
immature than the awake and
active sleep state
 3 weeks or more - significant
brain injury
Neonatal Seizures
Neonatal Seizures – Introduction




Neonatal Seizures - sign of acute brain injury
3 types : Electrographically; electroclinical and clinical only.
Usually happens within first week of life
Scher et al :
 < 30 weeks – higher incidence ~ 3.9 %
 > 30 weeks – 1.5 %
 Pathophysiology : Imbalance between inhibition and
excitation
Neonatal Seizures - Etiology
Classification of neonatal Seizures
ILAE neonatal syndromes:
 Benign neonatal convulsions
 Benign familial neonatal convulsions
 Early myoclonic encephalopathy
 Early infantile epileptic encephalopathy
 Migrating partial seizures of infancy
Other way of classifications:
 Clinical manifestations
 Relationship bet EEG and clinical sz
 Sz pathophysiology
Clinical Manifestations





Focal clonic
Focal tonic
Myoclonic
Multifocal clonic
Subtle seizure pattern:







Apnea
Tonic deviation of the eyes
Eye lid fluttering
Drooling, Sucking and chewing
Swimming movements of the arm
Pedaling movements of the legs
Paroxysmal Laughing
Clinical Manifestations
Tonic seizures – Intraventricular hemorrhage
Multifocal clonic – Hypoxic Ischemic encephalopathy
Focal clonic – Infarction
Infantile spasms – Poor prognosis
Myoclonic jerks with decreased state of consciousness –
Metabolic – inborn errors of metabolism
 Apneic spells + tonic deviation of eyes  seizures
 Apneic spells + tachycardia  Seizures
 Apneic spells - commonly seen during – active sleep





Ictal Neonatal EEG
 Electrographic and clinical seizures in neonatal age unique
 EEG seizure patterns vary widely
 Not always accompanied with clinical signs
 Electrical Seizure activity - rare before 34 weeks
 Most of EEG seizures - Focal
 Generalized EEG activity - infantile spasm and
Myoclonic jerks.
Ictal Neonatal EEG
 Most of the seizure originated - central and temporal
regions
 Same EEG seizures - Morphology, frequency and evolution
pattern - Varies
 Minimal Ictal Duration : 10 seconds
 < 10 seconds : BIRDS (Significance - unclear)
 Ictal patterns : Sinusoidal patterns to complex bizarre
 Evolution - differentiates from artifacts
 Alpha Seizures – Poor prognosis – Seen in severe HIE
 Burst suppression – Metabolic diseases
Ictal EEG
Ictal EEG
Ictal EEG
Ictal EEG
BIRD
Seizures in Depressed Brain
Alpha Seizure Discharge
Generalized Seizure Activity - Myoclonus
Electrodecremental Pattern
Clinical Sz : Infantile spasms
Neonatal Seizures – Management
 Neonatal seizures  requires urgent treatment
 First line Phenobarbital – 82%  Lorazepam – 9% Phenytoin
– 2%
 Second line therapy : lorazepam 50 %  phenytoin(39%) 
phenobarbital (20%)
(Neonatal Seizures: Multicenter variability in current treatment
practices : Ped Neurol 2007)
~ 58% continued to have EEG seizures after administration of
AED and stopped the clinical seizures.
(Uncoupling of EEG – clinical seizures after AED use) (Ped
Neurol 2003)
Neonatal Sz  Postnatal Epilepsy
~ 20 % neonatal seizures survivors  postnatal epilepsy
Atleast 1 or more seizures up to 7 years of age
2/3 occur within first 6 months
Neonatal Seizures due to acute encephalopathy 
decreases in 7 to 14 days
 Perinatal Asphyxia  post natal Epilepsy ~ 30%
 Cerebral Dysgenesis  Post natal Epilepsy ~ 80%




( Age at onset of seizures in young children : Ann Neuol
1984)
References
 Atlas of Neonatal Electroencephalography, Third Edition,
Eli M. Mizrahi
 Current Practice of Clinical Electroencephalography,
Timothy A Pedley
 Levin & Luders Comprehensive Clinical Neurophysiology
 Neonatal Neurology Fourth edition Gerald M. Fenichel
 Visual Analysis of Neonatal EEG, Koszer et al Holmes et
al, 2010