This is a basic introduction to Pediatric EEG and part of the Neurophysiology Fellows teaching lecture series. This covers from 1 month to age 20. There is another presentation for Neonatal and Newborn EEG. Pediatric EEG like Pediatric Neurology differs from Adult EEG and Adult Neurology because the electrical activity of the brain changes during growth and development. Therefore, children develop different pathological conditions from adults that are often age specific. The EEG recording itself is different in children than adults because the brain, meninges, skull, scalp, head size as well as the child's behavior and ability to cooperate all change over time. Therefore, Pediatric EEGs must be recorded and interpreted with special attention given to the child's age and developmental level. An EEGer must possess knowledge of normal as well as abnormal features for each age. Interpretation of pediatric EEGs requires the understanding of what Blume calls:

1. Normalities
2. Curiosities
3. Abnormalities

I. Normalities: Normal Pediatric EEG

General Features to remember about Pediatric EEGs:
• Normal Pediatric EEG activity has more variation than adult EEG.
• Focalities are not always abnormal.
• EEG varies greatly by age, therefore interpretation needs to be age specific for the Conceptual Age.
• For a complete EEG, all states (Awake, Drowsy, and Sleep) should be recorded. Lack of state change is abnormal in infants.
• Dysmaturity is an non-specific abnormality; "baby encephalopathic slowing".

Gestational Age(GA) = time in weeks from conception based on LMP
Conceptual Age (CA) = gestational age + chronological age(time from birth)

Age catagories to consider for Pediatric EEG Interpretation:
• Pre-term: Below 38 weeks GA
• Neonatal: Less than 1 month CA (38 to 44 weeks GA)
• Infants: Age 1- 12 months
• Age 1 to 3 years
• Age 3 to 6 years
• Age 6 to 12 years
• Age 13 to 19

The ideal EEG should contain:
• Awake
• Drowsiness
• Transitions
• Sleep
• Arousal
• Activation
  • Hyperventilation: when able to cooperate and if not medically contraindicated (HgbSS, Congenital heart disease, CF or active asthma)
  • Photic Stimulation: if greater than 6 months of age

Infancy: Age 1 month to 12 months

Age 1 month to 12 months: Awake EEG
• Poorly defined "fast" 20 mV background while awake in the first 1-3 months.
• at 3 months: posterior dominant rhythm established at 3-4 Hz
• at 6 months: average posterior dominant posterior rhythm is 5 Hz, should be at least 4 Hz
• at 12 months: posterior dominant rhythm is 6 to 7 Hz.

Age 1 month to 12 months: Drowsy EEG
• EEG background may slow by 1-2 Hz from the waking frequency
• Transition
• may be gradual over several minutes
• evidenced by reduction in artifact
• multiple partial and full alertings common
• After 6 months a prominent mono-rhythmic theta may develop
• Fronto-central dominant and may reach 200mV

Age 1 month to 12 months: Sleep
• 44-48 week conceptual age may have a discontinuous looking trace alternans to spindle
• Spindles may develop in 2^nd month
• Spindles are 12 to 15 Hz and may last up to 10 seconds
• Spindles are asymmetrical at onset below 6-9 months
• Spindles frequently alternate from side of the head to the other below 6 months
• Spindles may be asymmetrical by 1 to 5 seconds at onset from 6 to 12 months then
• Spindles become increasingly symmetrical as sleep progresses
• Vertex sharp waves and K-complexes develop at 5 months
• Background is 0.75 to 3 Hz in sleep

Age 1 month to 12 months: Activation:

• Hyperventilation can not be performed. Crying in older infants often produces a HV response with slowing of the EEG background which should not be called abnormal.
• Photic Stimulation: Not done less than 6 months of age because of concern over retinal over-stimulation.
  • PS Response over 6 months of age at slow flash frequencies (1-3 Hz) is a VEP.
  • Response can be asymmetrical because of uneven stimulation of the visual fields.
  • Exaggerated response (very high voltage) with: infantile neuronal ceroid lipofusinosis, Gaucher's disease and biopterin deficiency.

Toddler/Early Childhood: 1-3 Years of Age:

1-3 years: Awake
• Posterior Dominant Rhythm at Age 1 is 6-7 Hz and gradually increases by Age 3 to 6-8 Hz
• Underlying diffuse 2 - 5 Hz activity
• Mu develops age 1 to 2 years
• Beta frequently occurs at 18 to 25 Hz
1-3 years: Drowsy
• Semi-rhythmic 4 to 6 Hz background
• Hypnagogic Hypersynchrony most prominent in the central and parietal areas
• Hypnagogic Hypersynchrony often occurs in burst and may resemble spike-and-wave activity (Phantom spike-wave)
1-3 years: Sleep
• 1 to 6 Hz background
• Bilaterally symmetrical spindles at 12 to 14 Hz
• Vertex often resemble high voltage frontal sharp waves
1-3 years: Activation
• Limited HV because of cooperation
• HV response with crying possible, especially at beginning of the recording if upset from electrode application
• Variable PS driving

Pre-school and Early Childhood: 3 to 6 Years of Age

3 to 6 Years: Awake
• Often 8 Hz by age 3, usually mixed theta and alpha
• Amount of alpha increases with age, often all 8-9 Hz by age 5-6
• Awake voltage frequently 100 mV range and above
• Posterior Slow waves of youth: 2.5 to 4.5 Hz slowing
• Anterior 6 to 7 Hz theta
• Rolandic Mu is frequent
3 to 6 Years: Drowsiness
• Alpha attenuation with background theta
• Hypnagogic Hypersynchrony present until age 11
• 14 and 6 Hz positive spikes begin but are uncommon
3 to 6 Years: Sleep
• Uniform sleep background unless reach slow wave sleep
• Very clear sleep spindles, V-waves (may be sequential) and K-complexes
3 to 6 Years: Activation
• HV: high amplitude slowing, often asymmetrical at onset
• Rapid return to baseline unless hypoglycemic (classical reports, but drowsiness can develop with rapid entry into sleep without return to baseline)
• PS: Prominent driving at slow flash frequencies

Elementary School Age/Late Childhood: 6 to 12 Years

6 to 12 Years: Awake
• 8 to 9 Hz by 7 years, 9 to 10 Hz by 9 or 10
• If not 8 Hz by 8 years then clearly abnormal allowing for slowing of drowsiness
• Posterior slowing remains prominent but is arrhythmic, attenuates with eye-opening
• Beta is normal in 25% of EEGs
• Rolandic Mu present
• Occipital lambda begins
• Burst of Anterior Rhythmic theta at 6 to 7 Hz begins
6 to 12 Years: Drowsiness
• Alpha is reduced and replaced by theta and some delta
• Hypnagogic hypersynchrony is less frequent with age
• Paroxysmal Hypnagogic hypersynchrony burst between ages 4 and 9 years
6 to 12 Years: Sleep
• Sleep spindles and vertex wave in stage 2
• POSTS (Positive Occipital Sharp Transients of Sleep) begin to appear
• 14 and 6 positive spikes may be present
6 to 12 Years: Activation
• HV: high voltage slow activity is common
• PS: maximal response at 6-16 Hz (medium flash rates)

Adolescence: 13 to 19 years:

13 to 19 years: Awake
• Well defined alpha 9-11 Hz (occasionally into 12-13 Hz Beta)
• Posterior consistently decreases with age
• Rolandic Mu common
• Lambda common
• Burst of Anterior Rhythmic theta at 6-7 Hz maximal at 13 to 15 years of age
13 to 19 years: Drowsy
• Low voltage Alpha with intermixed moderate to high voltage theta
13 to 19 years: Sleep
• Stage 2: spindles, vertex
• POSTS
• 14 and 6 positive sharp waves
• Deep sleep: delta and theta frequencies
13 to 20 years: Activation
• HV: moderate intermittent slowing
• PS: symmetrical driving

II. Pediatric EEG Curiosities

• Posterior Slow Activity (Waves) of Youth: Waking, sinusoidal 2.5 to 4.5 Hz slow wave that interrupts the background alpha with voltage similar to the alpha voltage.
• Mu Rhythm: Waking, central 9Hz (7-11 Hz) comb shaped that is blocked by movement (thought of movement) of the contra-lateral extremity.
• Lambda Waves: Waking, positive sharp waves over the occipital region from looking at a complex visual target. Usually 20 to 50 m V with a duration of 200 to 300 ms. Bilaterally synchronous with moderate voltage asymetries. Disappear with eye closure.
• Vertex: wider projection in children, usually fronto-central not just frontal as in adults. Often very high in voltage in early childhood, maximal ages 2-4. May appear on one side initially then be symmetrical once stage 2 sleep is well established. Repetitive or sequential at onset may look like fronto-central spikes.
• POSTS (Positive Occipital Sharp Transients of Sleep): Surface positive, occipital waves during stage 1 and 2 sleep, typically bilaterally synchronous (may have voltage asymmetries), that occur in runs of 4 to 5 Hz. Onset as young as 4 years, maximal at 15-35 years.
• 14 and 6 Positive Spikes: Onset at 3 or 4 years, peaks at 13-14 years, minimal by 17-18 years. Rhythmic trains of spikes followed by a smooth rounded component lasting 0.5 to 1 s. Occur most often in the posterior temporal regions and may be asynchronous or appear independently on the two sides. (COMMENT: I haven't seen in age of digital EEG! I'm not sure if the digital, referrential amplifiers fail to pick up the activity or if the CRT displays of the EEG machine alter the presentation of "14 and 6" so it is not recognizable)
• Psychomotor Variant is rhythmic theta (monomorphic and monorhythmic) burst often notched at 5 to 7 Hz. Psychomotor Variant occurs bilaterally and independently and may shift from side to side. Psychomotor Variant begins in late adolescence and continues into adulthood.

Photic Stimulation:
Photic stimulation (PS) is a very useful and important activation procedure in Pediatric EEG because of the activation of Generalized Spike-Wave activity. This is a common finding in children wiht Primary Generalized Epilepsy. Of note, children investigated after seizures caused by Pokemon TV episode in Japan were found to have partial (focal onset) seizures induced by photic stimulation.
The Photoparoxysmal Response (PPR) is bilaterally synchronous, generalized spike-and-slow-wave and can have multiple spike and slow wave complexes to repetitive flash stimulation (Chatrian et al., 1983), poly-spike waves are the most significant abnormality. Reilly and Peters (1973) report Prolonged PPR (spike-wave discharges outlasts the flash stimulus) associated with seizures in a significantly higher incidence than Self-Limited PPR (spike wave ceases when the flash stops).Jayakar and Chiappa (1990) found no difference in clinical seizures for individuals with prolonged PPS and self-limited PPS on EEG.
Puglia, Brenner and Soso: (Pittsburgh University and Western Psychiatric Institute) reviewd 9,738 EEGs recorded over 6 years for the effect of PS. 85 records in 71 patients contained a PPR (0.9%). Charts of 68 patients were analyzed (charts lost in 3): ages ranged from 7 years to 60 years. They also looked at age matched controls with EEGs performed in the same month. Overall conclusion was that individual with PPR and other Epileptiform EEG abnormalities are more likely to have seizures.

Puglia JF. Brenner RP. Soso MJ., Relationship between prolonged and self-limited photoparoxysmal responses and seizure incidence: study and review. Journal of Clinical Neurophysiology. 9(1):137-44, 1992 Jan.

Photoparoxysmal responses (PPRs) are generalized epileptiform abnormalities occurring during photic stimulation. Prolonged PPRs, which outlast the stimulus, can be distinguished from self-limited PPRs, which cease spontaneously or when the flashes stop. Reilly and Peters (1973) found a higher incidence of seizures in patients with prolonged, rather than self-limited, PPRs. More recently, Jayakar and Chiappa (1990) reported a similar seizure incidence in the prolonged and self-limited groups. In order to assess these discordant results, we reviewed EEG records performed in our laboratory from 1983 to 1988. Sixty-eight EEGs had PPRs (19 prolonged and 49 self-limited). Patients with PPRs had a significantly higher incidence of seizures than controls (total patients versus controls, p less than 0.001; prolonged subgroup compared to controls, p less than 0.001; self-limited subgroup versus controls, p less than 0.01). Comparing PPR groups, we found that a prolonged PPR was associated with a higher incidence of seizures than a self-limited response (p less than 0.05); however, patients with a prolonged PPR more often had other epileptiform abnormalities than the self-limited group (p less than 0.001). There was no difference in seizure incidence between the PPR groups when comparing patients whose EEGs also contained other epileptiform abnormalities. Meta-analysis suggests apparent differences among the three studies are superficial.

III. Pediatric EEG Abnormalities

Pediatric EEGs contain different abnormalities than adults because of the different pathological processes and different clinical epileptic syndromes that occur in childhood. Many of the pathological processes produce seizures. Therefore, most of the recognized pathological patterns in Pediatric EEG contain spike and spike-wave activity.

Abnormal Pediatric EEG patterns and Clinical Correlations

• Generalized 3-Hz spike-and wave complex is always abnormal. 3-Hz s-w activity may need to last 6 to 10 seconds before clinical absence seizure activity occurs. The generalized spikes may become poly-spikes in sleep and have a more variable frequency (especially in stage 3 and 4 sleep). During sustained burst of the "3-Hz" the frequency may begin closer to 3.5 to 4-Hz and slow to 2.5 to 3-Hz. Hyperventilation(HV) for 3 to 4 minutes usually will produce 3-Hz spike and wave activity if present. If 3-Hz activity is highly suspected based on history but does not occur than a second attempt at HV for 5 minutes should be performed. HV is as likely to record 3-Hz spike wave as 24 hours of continuous EEG. Onset of 3 Hz spike and wave with Absence seizures is commonly reported as most likely at 5-6 years of age. Often children have been having absence seizures for at least 6 months before diagnosis and occasionally have been having events consitently for year. Onset can occur before age 2. EEG in child of 23 months with 3-hz spike-wave and "pauses" in activity.




J. K. Penry, R. J. Porter & R. E. Dreifuss. Simultaneous recording of absence seizures with video tape and electroencephalography. A study of 374 seizures in 48 patients. Brain 98:427-440, 1975.

Forty-eight patients, 4 to 24 years of age, with recurring absence seizures were studied prospectively for twenty-seven months. Each patient and his EEG were recorded simultaneously by a multicamera videotape technique and each recording was repeatedly viewed and described in writing by two observers who subsequently resolved any differences by joint viewing. From the 48 patients, 374 clinical absence seizures were recorded and classified according to the International Classification of Epileptic Seizures. Automatisms accompanied at least one attack in 88 per cent of the patients. Mild clonic components occurred in 71 per cent, and decreased postural tone in 41 per cent. Only one patient experienced an attack comprising only "blank staring" accompanied by unawareness and amnesia, but 40 per cent of patients exhibited this type of attack in addition to more complex absence attacks. Seizures of ten seconds or less in duration occurred among 85 per cent of patients. Each of the 374 seizures were readily classified according to the International Classification, but simple absence constituted only 9-4 per cent of the seizures. The others most often contained, in order of prevalence, either automatisms, mild clonic components, or decreased postural tone, or a combination of two or more of these features. The relationship between increased duration of the seizures and the occurrence of automatisms was significant. The findings are discussed in relation to differential diagnosis and mechanisms of automatisms. Absence seizures differ from complex partial (temporal lobe, psychomotor) seizures because an aura does not precede the abruptly beginning absence attack, the seizure usually lasts less than ten seconds, and mental clarity returns instantly at the end of the seizure.

• Hypsarrhythmia is a term to describe an EEG with 0.5 to 3 Hz chaotic, asynchronous slow waves with voltages greater than 300 mV. Voltages of 1000 to 2000 mV can occur. Multifocal spikes and sharp and slow waves are also present. Intervals of attenuation can occur with and without clinical myoclonic activity or flexor spasms. Hypsarrhythmia can begin at 3 to 4 months of age and may persist into the 2nd year of life. Hypsarrhythmia is present in about 2/3 of infants with infantile spasms. Infantile Spasms is a clinical syndrome of clusters of axial myoclonic seizures that occur in infants from 2 to 18 months of age.
  
  

  Modified Hypsarrhythmia: Hrachovy RA., Frost JD Jr., and Kellaway P. (Baylor College of Medicine) Hypsarrhythmia: variations on the theme. Epilepsia. 25(3):317-25, 1984 Jun.

  Prolonged monitoring studies of patients with infantile spasms have shown that hypsarrhythmia is a highly variable and dynamic electroencephalographic pattern. Variations of the prototypic pattern (modified hypsarrhythmia) include hypsarrhythmia with increased interhemispheric synchronization, asymmetrical hypsarrhythmia, hypsarrhythmia with a consistent focus of abnormal discharge, hypsarrhythmia with episodes of attenuation, and hypsarrhythmia comprising primarily high-voltage slow activity with little sharp-wave or spike activity. Marked changes in the hypsarrhythmic pattern usually occur during sleep, chiefly during rapid eye movement sleep, when there is a marked reduction in, or total disappearance of, the hypsarrhythmic pattern. Relative normalization of the hypsarrhythmic pattern can also be seen immediately on arousal and during clusters of infantile spasms. Thus, the specific EEG features seen in a given patient depend on multiple factors, including the duration of the EEG recording, the clinical state of the patient, and the presence of various structural abnormalities of the brain.

  
  

  Infantile Spasms: Wong M., Trevathan E. (Pediatric Epilepsy Center, Washington University School of Medicine and St. Louis Children's Hospital, St. Louis, MO 63110-1093, USA.) Infantile spasms. Pediatric Neurology. 24(2):89-98, 2001 Feb.[Review]

  Infantile spasms constitute both a distinctive seizure type and an age-specific epilepsy syndrome that have been extensively described for over a century. Standardization of the classification of infantile spasms has evolved, culminating in recent recommendations for separately recognizing and distinguishing the seizure type (spasms or epileptic spasms) and the epilepsy syndrome of infantile spasms (West syndrome). More-detailed descriptions of the clinical and electrographic features of epileptic spasms and hypsarrhythmia have emerged. Advances in neuroimaging techniques have revealed clues about pathophysiology and increased the etiologic yield of the diagnostic evaluation of patients with infantile spasms. Adrenocorticotrophic hormone remains the treatment of choice for many neurologists. Recent controlled studies support vigabatrin as first-line therapy, and open-label studies suggest that topiramate, lamotrigine, and zonisamide may be useful in treating spasms. Recent reports of visual-field constriction with vigabatrin may limit its use. Surgical treatment has been used successfully in a select subgroup of patients with secondarily generalized spasms from a single epileptogenic zone. Although the prognosis for most patients with infantile spasms remains poor, further studies identifying predictors of favorable prognosis and recent advances in understanding the pathophysiology of infantile spasms offer hope of safer and more-effective therapies that improve long-term outcome. [References: 92]

• Slow Spike and Wave occurs at 1 o 2.5 Hz and may be widely distributed and synchronous over both hemispheres or may be asymmetric and present in only one hemisphere. Slow Spike and Wave is often seen for several seconds without any clinical change. There are usually other background abnormalities such as slowing and mutifocal spikes. Slow Spike and Wave usually appears between 2 and 6 years of age and activates with drowsiness and sleep. Slow spike and wave is not activated by HV and will block with eye opening. Slow spike and wave is one of 3 features of the Lennox-Gastaut Syndrome. The other 2 are refractory seizures and mental retardation.
• Multifocal Spike and Wave is defined as "spikes in 3 non-contiguous electrode positions with at least one focus in each hemisphere" (Blume 1982). Multifocal Spike and Wave activity is frequently seen in children with multiple seizure types and retardation.
• Rolandic Spikes occur exclusively in children with peak age of 6 to 10 years but may be present at age 2 or 3 years until age 12 to 15 years. Spikes are most commonly highest in voltage in the C3-C4 electrodes spreading into the T3-T4 electrodes. A horizontal dipole may be present with a surface positive field in the frontal-polar electrode. During drowsiness and sleep the Rolandic spikes increase in numbers and often cluster in trains of 3 to 6 over 1-2 second intervals. Rolandic spikes may be unilateral, bilateral synchronous or bilateral independent. Rolandic spikes frequently seen as an incidental finding and have only a 50% correlation with underlying seizure disorder. Begin Rolandic Epilepsy (BRE) is a syndrome where simple partial seizures occur early in sleep or on awakening. Many children may have just one such event. Occasionally secondary generalization and rarely prolonged seizures occur. Rolandic spikes are also present in children with other generalized epileptiform activity. Abstracts of BRE articles present more details on EEG features and variations for BRE.
• SSPE Subacute sclerosing panencephalitis produces double and triple sine waves at about 1 Hz that may occur in long runs superimposed on normal background. Early in the illness, short burst of slow sharp waves may be produced by noise. SSPE is a delayed onset, progressive measles encephalitis.
• Slowing may be present post-ictally or with underlying structural abnormality which usally has to be large in size and involves the white matter.

Topics from the Pediatric Neurology Teaching Syllabus on Seizures and Epilepsy
• Seizures and Epilepsy
       Overview
• Status Epilepticus
       Handout for the pediatric Acute Care Symposium. (July 11,2002)
• Pediatric Epilepsy
       Handout about Pediatric Epilepsy by Dr. Larry Olson. (PDF Format)
• Febrile Seizures
  • Febrile Seizures: Family Handout
• Benign Rolandic Epilepsy
• Neonatal Seizures and Febrile Seizures
       Handout Prepared for the 6th Annual Georgia Epilepsy Symposium. November 3, 2001.
• Diastat®
• Seizure First Aid Information Sheet
  • Seizure First Aid Information Sheet: HSCH
  • Seizure First Aid Information Sheet: Egleston EEG Lab
• Ketogenic Diet Information Sheet
• Non-Epileptic Paroxysmal Disorders
  • Breathholding

References:

• Blume, WT: Atlas of Pediatric Encephalography, Raven Press, New York, 1982.
• Holmes, GL: Diagnosis and Management of Seizures in Children, W.B.Saunders Company,Philadelphia, 1989.
• Hrachovy RA., Frost JD Jr., and Kellaway P. Hypsarrhythmia: variations on the theme. Epilepsia. 25(3):317-25, 1984 Jun.
• Mizrahi, EM: Avoiding the Pitfall of EEG Interpretation in Childhood Epilepsy. Epilepsia, 37(Suppl. 1):S41-51, 1996.
• Novotny EJ: The Role of Clinical Neurophysiology in the Management of Epilepsy, Journal of Clinical Neurophysiology, 15(2):98-108, 1998.
• Pampiglione, G: Some criteria of maturation in the EEG of children up to the age of 3 years, Electroencephalogr. Clin. Neurophysiol., 32:463, 1972.
• Penry JK,Porter RJ & Dreifuss RE. Simultaneous recording of absence seizures with video  tape and electroencephalography. A study of 374 seizures in 48 patients. Brain98:427-440, 1975.
• Petersen, I and O. Eeg-Olofsson: The development of the electroencephalogram in normal  children from the age of 1 through 15 years. Neuropaediatrie, 2:247-304, 1971.
• Puglia, JF, RP Brenner, and MJ Soso: Relationship Between Prolonged and Self-Limited  Photoparoxysmal Responses and Seizure Incidence: Study and Review, Journal of Clinical Neurophysiology, 9(1): 137-144, 1992.
• Wong M., Trevathan E. Infantile spasms. Pediatric Neurology. 24(2):89-98, 2001 [Review]