Disclosure – Just here to help disseminate knowledge

○ I do not have any ties to any business.

○ I am not representing any entity.

Neonatal/Premie EEG Recordings

○ Help to determine treatment specific to “True” physiological age.

○ Help to determine brain maturation to better decide on intervention

○ Identify focal and/or generalized abnormalities and any subsequent treatment

○ Find and Classify epileptogenic foci and ongoing seizures to better determine proper anticonvulsant

○ Assists in predicting risks for neurological sequelae and course of treatment specific to child

EEG of the Newborn: from Isolette to Bassinet

Presenter: Henry Coet III, R.EEG T., BA

Neonatal Montage

Reduced number of electrodes because of newborn head circumference

Neonatal Montage “Extra” Physiological leads

○ 2 eye-movement electrodes -0.5 cm above/ below the outer canthus of either eye -Record differential field effects of dipoles between retina and cornea○ Electromyogram (EMG) electrodes -Help differentiate subcortical/ peripheral myoclonus from epileptiform movements○ EKG ○ Respiratory monitor electrodes (chest wall and/or nasal airflow)○ Sensitivity- Eye electrodes: 7 mV/mm ECG, EMG electrodes: 50 mV/mm

Neonatal EEG Recording○ Time constant: 0.3 seconds (to record slower

frequencies)○ Low-pass filter: 70 Hz○ Sensitivity of EEG electrodes: 7 mV/mm ○ Run for 45-60 minutes to record at least one change in

sleep state (neonatal sleep cycle: 50-60 min) ○ On paper, half the recording speed of a typical adult

record (15 mm/s instead of 30 mm/s)○ Enhances detection of asymmetries/asynchronies○ Changes waveform morphology○ Less of an issue with digital EEG acquisition (allows

post-recording review at various speeds)

Neonatal EEG Analysis

○ Knowledge of the post-conceptional age and topography of the infant's head

○ Identification of artifacts

○ Identification of sleep/awake states

○ Feature recognition

○ Classification of record as normal/ abnormal with clinical correlation

Age & Topography○ EEG features vary with age ○ Gestational age (GA) = number of weeks/months in the

womb○ Pre term (PT) = GA of less than 38 weeks○ Full term (FT) = GA of 38-42 weeks○ Post-conceptional age (PCA) = GA (in weeks) + weeks

since birth○ Description of skull and scalp topography - attenuation (increased inter-electrode resistance): scalp swelling, encephalocele, subdural/epidural fluid, - increased voltage (low-resistance pathway for electric fields): skull fractures - other: distorted cranial vaults (common after birth trauma)

Neonatal EEG Common Artifacts

○ Head in midline○ Identification of artifacts while EEG is recording

○ Cardiac: ECG and pulse, head movement with heartbeat○ Head: Head movements, electrode “pops”, fontanelle-related pulsations○ Face: Sucking, glossokinetic, eye movements/ blinks, fronto-temporal muscle contraction○ Body: Respiratory, twitches, tremor ○ Other: 60-Hz electrical, electromechanical devices ( ventilators, IV drips)

Artifact

Artifact

Artifact

Artifact

Identification of Sleep/Wake States

○ Determinants of neonate's state - Observation of infant's movements/ behavior by the technician - Analysis of non-cerebral electrodes -Lateral eye movements, ventilator rate, ECG, and EMG patterns (not reliable indicators of state until 34-36 weeks PCA)

Neonatal SleepMaturation

○ Prior to 28-30 weeks PCA○ discontinuity with inter-bursts of inactivity alternating with

higher amplitude mixed-frequency activity: tracé discontinu (TD)

○ At 28-30 weeks PCA○ some sleep-state differentiation with more continuous patterns

in active sleep than in quiet sleep○ Until 32-34 weeks PCA

○ sleep-state differentiation may be difficult○ decrease in inter-burst duration with change in amplitude

and morphologies○ By 34-35 weeks PCA

○ other physiological features help determine sleep state

Tracé Discontinu (TD)

○ prior to 28-30 weeks' postconceptional age

○ discontinuous, with interbursts of low voltage or inactivity alternating with higher amplitude and mixed-frequency activity

○ as the infant matures:○ interburst duration of TD decreases○ amplitude and morphologies of the interburst activity change

Tracé Discontinu (TD)

State-Related EEG Changes Awake Active Sleep Quiet Sleep

Eye Movements

Random Rapid Eye Movements

None

EMG Phasic/tonic

Phasic Tonic

Body Movements

Random Random None

Respiration Irregular Irregular Regular

Neonatal SleepActive Sleep

○ Analogous to REM sleep○ Low-to-moderate voltage, continuous EEG pattern with rapid

eye movements (Low Voltage Irregular)○ Irregular respirations and cardiac rate○ Decreased chin EMG activity○ Quick irregular movements of the fingers, hand, or face○ At sleep onset at full term

Low Voltage Irregular (LVI) Active Sleep

Active Sleep- 40 wks

Neonatal Sleep Quiet Sleep

○ Analogous to NREM sleep

○ Absence of lateral eye movements

○ Increased chin EMG activity

○ Regular respirations and ECG

○ Patterns

○ Tracé alternant (TA)○ Continuous Slow Wave Sleep (CSWS) or High

Voltage Slow (HVS)

Quiet Sleep Tracé Alternant (TA)

○ Discontinuous pattern of NREM○ Emerges by 36-38 weeks PCA ○ Replaced by 44-48 weeks PCA○ Bursts of slow activity (1-4 Hz) admixed with

random, faster frequencies at 50-200 mV○ Seen every 4-5 seconds○ last 2-4 seconds

○ Inter-burst pattern of low-voltage, continuous activity predominantly in the theta range at 20-50 mV

TA

TA

TA

Quiet Sleep Continuous Slow Wave Sleep (CSWS)High Voltage Slow (HVS)

○ Seen by 36 weeks PCA

○ Prominent diffuse delta with some theta rhythms

○ Gradually increases and replaces TA by 44-48 weeks PCA

Neonatal Sleep

Sleep/Wake States

○ Four EEG patterns in FT neonate related to the sleep/wake cycle:○ Low-voltage irregular (LVI) - continuous low-amplitude

(<50 µV) theta activity○ Mixed pattern - continuous moderate amplitude

(usually <100 µV) theta/delta activity○ Tracé alternant (TA) - 3 to 5 second bursts of high

amplitude (50 to 100 µV) slow activity (0.5 to 3.0 Hz), which occur at intervals of 3 to 10 seconds when the background is relatively low amplitude (10 to 25 µV) theta waves

○ High-voltage slow (HVS) - continuous, high amplitude (50 -150 µV), semi-rhythmic delta activity

Sleep/Wake States

○ LVI - wakefulness and active sleep

○ Mixed pattern- active sleep and relaxed wakefulness

○ TA and HVS-quiet sleep

○ At sleep onset-○ Active (REM) sleep in FT

○ Quiet (NREM) sleep 10 to 12 weeks

post-term

Feature Recognition Delta Brushes

○ Analogous to K complexes but occur asynchronously

○ Medium to high voltage delta activity with superimposed low to medium voltage 18-22 Hz fast activity, maximum centrally

○ Seen in PT infants beginning at 26 weeks PCA○ Prominent in active sleep by 29-33 weeks PCA○ Maximal in quiet sleep by 33-38 weeks PCA

Delta Brush32 week infant

Multifocal Sharp Transients

○ Frequent occurrence of multi-focal sharp transients during indeterminate and quiet sleep

○ First seen at 35 weeks CA○ Normal finding in full-term neonates○ Clinical significance: controversial○ Pathologic:

○ repetitive, periodic, or localized over one region ○ occur with increased frequency even during active

sleep and wakefulness○ suggestive of a nonspecific encephalopathic process

Positive Rolandic Sharp Waves

○ May be confined/more abundant in one hemisphere

○ Maximum at CZ but may be lateralized to C3/C4○ Seen in peri-ventricular leukomalacia,

intra-ventricular hemorrhage/parenchymal hemorrhage, hydrocephalus, hypoxic/ischemic insult

○ Represent a marker of white matter lesions ○ Positive sharp waves at other locations - no distinctive significance - may be multifocal sharp transients

Positive Rolandic Sharp Waves

Normal/Abnormal Discontinuous Patterns ○ Burst-Suppression pattern

○ invariant, non-reactive to stimulation○ signifies a severe encephalopathy (hypoxic/ischemic)○ seen with sedative/hypnotic medication

○ TA, TD○ state dependent, reactive to stimulation○ “30/20” rule: inter-burst interval < 30 seconds with < 30wksPCA < 20 seconds with > 30 wks PCA○ long recordings - transitions between wakefulness and

sleep with > 32 weeks PCA ○ over 6 weeks post-term, TA gradually replaced by CSWS (sole EEG pattern of quiet sleep)

Burst Suppression Pattern (Paroxysmal)

○ defined for the near and fullterm infant ○ difficult to distinguish from tracé discontinu in the preterm○ classically described as interbursts > 20 seconds without

reactivity and with disorganized bursts○ consider metabolic-toxic encephalopathies (asphyxia or other

etiologies)○ poor prognosis

Burst Suppression

• No reactivity to stimulation

• Not disease-specific

Electrocerebral Inactivity (Isoelectric Recording)

• Less than 5 µV• Lack of reactivity

– Consider• postictal state• hypothermia • metabolic/ toxic effects

– Poor prognosis– Not etiology or time specific

Background AbnormalitiesSevere

○ Persistance in serial EEGs○ Isoelectric EEG (below 5 µV) or low-voltage tracing (5-15 µV) with

poor variability or sleep/wake cycling

○ Paroxysmal tracing or burst-suppression pattern

○ Invariant high-amplitude generalized delta activity (0.5 to 3.0 Hz)

○ Gross asynchrony and asymmetry

Background AbnormalitiesMild

○ Presence of more than one mild abnormality in serial EEGs

- underlying encephalopathic process of varying severity - may be iatrogenic (medication effect)

○ more than the usual asynchrony and/or asymmetry ○ immature EEG for PCA○ lack of recognizable sleep states○ excessive discontinuity ("flat" periods longer than 30

seconds)○ abnormal mono-rhythmic activities○ excessive multi-focal sharp transients

See the Forrest AND the Trees.

Neonatal Seizures○ Estimated incidence in US: 80-120 /100,000

neonates per year ○ Occur within first 4 weeks of life in FT infant

and up to 44 weeks PCA for PT infants ○ Most frequent during first 10 days of life ○ Occur over a few days○ Less than 50% infants develop seizures later

in life○ Acute symptomatic rather than “ epilepsy" ○ Markedly increases rates of long-term

morbidity and neonatal mortality

Neonatal Seizures Etiology

○ History indicates likely etiology ○ Positive family history ○ Pregnancy history

○ TORCH infections (toxoplasmosis, rubella, cytomegalovirus, herpes)

○ history of fetal distress, pre-eclampsia, or maternal infection

○ Delivery history○ type of delivery and antecedent events ○ Apgar scores

Neonatal Seizures Etiology

○ Hypoxic-ischemic encephalopathy (FT,PT)○ present within 72 hours of life

○ Hemorrhage○ Subarachnoid (FT)○ Germinal matrix-intraventricular (PT>FT)○ Subdural (FT)

○ Metabolic (hypoglycemia, hypocalcemia, hypomagnesemia, inborn errors of metabolism)

○ Intracranial infections (TORCH, bacterial, Herpes)○ Major malformations (Lissencephaly, pachygyria,

polymicrogyria)

Neonatal Seizures○ Predominantly focal

○ Subtle (FT>PT)○ chewing, pedaling, or ocular movements○ no EEG correlate

○ Clonic ○ often involve one extremity or one side of the body○ positive EEG correlate

○ Tonic ○ Focal- positive EEG correlate○ Generalized (tonic extension)-no EEG correlate

○ Myoclonic ○ Focal and multi-focal myoclonic –no EEG correlate

○ Jitteriness○ not associated with ocular deviation○ stimulus sensitive (easily stopped with passive movement of limb)○ resembles a tremor○ no associated change in vital signs

EEG Ictal Pattern

○ Highly variable○ Rhythmic activity○ Localized to relatively small area○ Usually focal (uni-focal or multi-focal)○ Multi-focal

○ ictal pattern(s) over different regions at the same time ○ independent discharges (differing morphology & frequency)○ unique feature of neonatal epileptogenesis

EEG Ictal Pattern

EEG Ictal Pattern

EEG Ictal Pattern

Benign Neonatal Convulsions Benign Familial Neonatal Seizures (BFNC)Benign Idiopathic Neonatal Seizures (BINC)

○ Onset after birth through day 28 in a healthy infant

○ Familial or isolated○ Normal exam and development ○ Seizures

○ frequent and brief○ usually resolve within days but may continue for months

○ Status epilepticus ○ common in BINC ○ uncommon in BFNC

BFNC

○ Autosomal dominant ○ Voltage-gated potassium channel gene defect○ Seizures in the second or third day of life

○ tend to persist longer than in BINC○ disappear by age 2-6 months○ mainly clonic, sometimes with apneic spells○ rare tonic seizures

○ Normal background ○ Favorable outcome but higher risk for subsequent

epilepsy

BINC (Fifth-day fits)○ Occur around the fifth day of life (day 1- 7)○ Unknown etiology ○ Males > females ○ Seizures

○ clonic (partial) and/or apneic○ resolve within days

○ Variable inter-ictal EEG ○ Ictal recordings: unilateral or generalized

spikes or slow-waves○ Diagnosis of exclusion○ Good outcome but increased risk of minor

neurological impairment

Early Myoclonic Encephalopathy

○ Often associated with inborn errors of metabolism & cerebral malformations

○ Onset in first month○ Ictal manifestations:

○ partial or fragmented myoclonus○ massive myoclonias○ partial motor seizures○ tonic spasms

○ EEG:○ burst-suppression (sleep)○ evolves into atypical hypsarrythmia

○ Seizures resistant to treatment○ ACTH with temporary effect○ Poor outcome

Early Infantile Epileptic Encephalopathy (Ohtahara syndrome)

○ Age of onset- first three months of life○ Usually associated with cerebral malformations,

(Aicardi syndrome, porencephaly)○ Seizures

○ Tonic spasms (100 - 300 per day) in clusters○ Partial motor seizures-less frequent○ Resistant to treatment○ ACTH - some temporary effect

○ EEG- burst-suppression pattern (awake/asleep)○ Poor prognosis but better than for EME○ Evolution into infantile spasms

Ohtahara vs. EMEOhthara○ Etiology - structural brain

lesions

○ Seizure - tonic spasms

○ EEG - burst-suppression (BS) in both awake/sleep states

○ BS evolves to hypsarrhythmia

around 3-4 months of age, and sometimes further to diffuse slow spike-waves

○ Course: evolution to West syndrome, and further to LGS

EME○ Etiology - non-structural/

metabolic disorders

○ Seizure - myoclonia and partial motor seizures

○ EEG - BS more apparent in sleep

○ BS may persist up to late childhood after a transient evolution to hypsarryhthmia in middle to late infancy

○ Course: transient phase of West syndrome

Ohtahara SyndromeAwake & Asleep

EME

EME

Pyridoxine Dependency○ Autosomal recessive○ Rare but treatable seizures○ Can begin in utero○ Generalized clonic seizures shortly after birth○ Resistant to conventional antiepileptic drugs○ Burst-suppression pattern or other generalized

discharges○ Unknown mechanism

○ Pyridoxine needed for synthesis of gamma amino butyric acid (GABA)

○ 100–200 mg IV pyridoxine given during EEG

Guidelines for the Use of Neonatal EEG

Assessment of Neonatal Encephalopathy1) Medical frame of reference

○ GA, recording conditions, drugs etc.2) EEG abnormalities are NOT disease-specific

○ neonatal encephalopathy 3) EEG abnormalities are NOT time-specific

○ antepartum-intrapartum-neonatal4) Serial recordings superior to single

recordings5) Partial or complete normalization of EEG

disturbances commonly occur

Conclusions○ Long enough study to include sleep states

(45- 60 minutes)○ Presence of sleep differentiation - important

maturational feature○ Abnormal patterns (discontinuity,

asynchrony and asymmetry, multi-focal sharp transients, delta brushes) - evaluated best in quiet sleep

○ Physiologic variables (respiration, extra-ocular movements, EKG, EMG)- useful in identification of sleep/wake states and in recognition of artifacts

Conclusions

○ An EEG Technician is vital for an accurate EEG interpretation!

○ His/her observations & documentation are CRUCIAL for accurate interpretation.

○ Without his/her artifact recognition &

trouble-shooting during the recording itself,

possible artifacts cannot be proven.

Citations

Citations• Lombroso, C. T. (1985). Neonatal polygraphy in full-term and premature

infants: a review of normal and abnormal findings. Journal of Clinical Neurophysiology, 2(2), 105-156.Le Bihannic, A., Beauvais, K., Busnel, A., De Barace, C., & Furby, A. (2012). Prognostic value of EEG in very premature newborns. Archives of Disease in Childhood-Fetal and Neonatal Edition, 97(2), F106-F109.

• Schmitt, S. E., Pargeon, K., Frechette, E. S., Hirsch, L. J., Dalmau, J., & Friedman, D. (2012). Extreme delta brush A unique EEG pattern in adults with anti-NMDA receptor encephalitis. Neurology, 79(11), 1094-1100.

• Lanska, M. J., Lanska, D. J., Baumann, R. J., & Kryscio, R. J. (1995). A population-based study of neonatal seizures in Fayette County, Kentucky. Neurology, 45(4), 724-732.

• Spitzmiller, R. E., Phillips, T., Meinzen-Derr, J., & Hoath, S. B. (2007). Amplitude-integrated EEG is useful in predicting neurodevelopmental outcome in full-term infants with hypoxic-ischemic encephalopathy: a meta-analysis. Journal of child neurology, 22(9), 1069-1078.

• Selton, D., Andre, M., & Hascoet, J. M. (2000). Normal EEG in very premature infants: reference criteria. Clinical neurophysiology, 111(12), 2116-2124.

• Tharp, B. R., Cukier, F., & Monod, N. (1981). The prognostic value of the electroencephalogram in premature infants. Electroencephalography and clinical neurophysiology, 51(3), 219-236.