After the first month of life, a baby graduates from being a neonate to an infant, and thus also graduate from the neonatal montage to a standard 10-20 montage in terms of electrode placement. Just as with neonates, though, infants and children—particularly the first few years—have an evolving EEG that requires a good understanding of its normal timeline for proper interpretation. A key part of the pediatric EEG is its evolving PDR, discussed in detail below, but summarized as follows:
4-5 by 6 months
6 by 1 year
7 by 2 years
8 by 3 years
9 by 8 years
10 by 10 years
The first year of life on EEG is characterized a preponderance of slow, high amplitude delta activity. The recording should be continuous and symmetric, but not particularly reactive to eye opening until 2-4 months. After this point, a PDR of 4-5 Hz arises by 6 months of age during wakefulness. Early in this timeframe, there is significant amounts of delta activity, but as baby's approach one year of age theta frequencies become increasingly admixed. In drowsiness, though, the background is usually still very slow and high amplitude, with a lot of 1-2 Hz activity up to 200uV in amplitude, particularly early on in the first year of life. By 1 year of age, the expected PDR is 6 Hz.
Below are a few examples of normal waking tracings at various time points for infants; note the general trend, over time, of less delta and more theta, and a better formed anterior-posterior gradient. These tracings have their sensitivities lowered from the standing 7uV/mm to between 10-20uV/mm for clarity as, generally, pediatric tracings are higher amplitude than adults.
Regarding sleep, by 2 months of age stage II sleep spindles develop; initially they can be very prolonged (up to 15 seconds at a time), and can remain asynchronous till up to 2 years of age. With spindles, vertex waves in stage I, and K complexes in stage II arise, and can be extremely prominent in children; vertex waves, in particular, can be very sharp appearing and come in long runs, so don’t confuse them for B(I)RDs or seizures.
In the first months of life, up to half a baby's sleep time can be REM sleep, but this proportion decreases to about a third by 1-2 years of age. The example below is from a 4 month old healthy baby; note the high amplitude vertex wave, rather prolonged spindle in the first half of the page, and the asynchronous and poorly formed spindle near the end of the page.
You won't often try activation techniques in babies, but prolonged crying can cause a hyperventilation response, and if you do attempt photic stimulation, a slow driving response of 1-3 Hz is seen starting around 6 months of age.
First of all note that this tracing is in the awake state, given multiple eye blinks across the page. This tracing shows a PDR of 3-4 Hz, which would be normal for a 2 or 3 month old awake baby, and maybe even the lower limit of normal for a 6 month old (their normal is 4-5 Hz), but by 1 year of age you should be seeing an awake PDR of at least 6 Hz.
After the first year of life, the PDR continues to evolve, reaching 8 Hz by 3 years of age, and remains higher voltage than you'll see in adults. Most of the delta activity seen in infants' background evolves to theta in this timeframe, and alpha frequencies gradually come into the mix too. You'll also start to see some of benign variants and rhythms found in adult tracings, including lambda waves with visual scanning, and the mu rhythm as the idling activity of the sensorimotor cortex. Sleep remains very high amplitude, especially slow wave sleep.
In the set of examples below, focus on the overall progression of the gestalt background, as it moves from mostly theta at 3 years to much more alpha and beta (similar to adult tracings) by 8 years of age. Again, note that these tracings have a lowered sensitivity (10uV/mm) to allow for better clarity.
From 3-6 years of age, a new waveform also arises, posterior slow waves of youth. These are rather high amplitude, spike-like waveforms that exist within the PDR and similarly attenuate with eye opening; they are often but not requisitely bilateral in appearance, and can predominate on one side or the other. Along the same vein, there can arise slow alpha variants, which are essentially two waves from the PDR combining into one, which is thus about half the frequency of the usual PDR. Below are examples from a 5 year old patient, with a PDR of 9 Hz (normal for age). Note how the posterior slow wave of youth has a delta frequency is surrounded by the PDR without really interruping the PDR's pattern, and how the slow alpha variant has a notched appearance that should not be mistaken for an epileptiform discharge.
Note that drowsiness in children may not be accompanied by the classic slow, roving eye movements seen in adults. Throughout this time period, sleep architecture should be synchronous and essentially in line with what you see in adults, although generally more prominent and high amplitude, with vertex waves often coming in runs. You can also see hypnagogic or hypnapompic hypersynchrony, in which high amplitude, synchronized slow waves arise in the transitions from waking to sleep and sleep to waking, respectively.
The tracing below is from a 7 year old patient. Given that, is the background normal or is there generalized slowing?
First of all, we know this patient is awake because we see eye blinks and a lot of frontal myogenic artifact. Second of all, this tracing has a lot of delta and theta activity, which might be normal for a very drowsy 7 year old, but in an awake patient of this age we expect to see much more alpha activity with a PDR of at least 8-9 Hz. Here, though, the PDR doesn't get past 6 Hz, and that with the excess delta and theta activity merits a call of mild generalized slowing. There is also a right temporal spike, although this patient has multifocal spikes seen elsewhere in the tracing too.
By the time kids reach adolescence, their EEG looks quite similar to adults, with a PDR that usually approaches 10 Hz and with a dominant mixture of alpha and beta throughout. However, unlike in adults, adolescents can have some admixed theta in their waking background, but this should fade away into the teen years.
In adolescence, the prominent hypnagogic and hypnapompic hypersynchrony of the early years recedes, and as teens grow into adults they lose posterior slow waves of youth. Sleep architecture remains quite prominent in teenagers and young adults, with vertexes continuing to often come in runs even into some patient's thirties; the example below is from a 15 year old patient.
Recall that by 6 months of age a baby should have a PDR of 4-5 Hz. Here, we see on the right side a PDR of about 3 Hz, which is age appropriate. However, on the left side there is broad hemisphere polymorphic delta slowing, suggestive of an underlying structural abnormality. On top of that, we see a few left temporal spikes, phase reversing at T5 suggesting focal cortical hyper excitability from that area. The high amplitude, messy activity toward the end of the page is mostly movement artifact.
From infancy into adulthood, there are a number of classic EEG patterns and syndromes that you should be familiar with, because each has different treatment requirements and prognosis. Here we'll give a brief overview on the more common ones that have a particular EEG signature.
Ohtahara syndrome, now termed early infantile epileptic encephalopathy (EIEE) is a devastating diagnosis of early infancy. On EEG, its characterized by a burst suppression pattern, with high amplitude, multifocal spikes embedded within the bursts of activity. Multiple seizure types, most often tonic seizures or spasms, are seen along with significant intellectual disability and developmental delay. EIEE often leads to early death, but if not can progress into West Syndrome or Lennox Gastaut Syndrome.
Hypsarrhythmia describes a characteristic EEG background that is very high amplitude, disorganized, slow and with multifocal epileptiform discharges throughout. As you'd expect, its a highly concerning pattern seen most often in infants in the setting of infantile spasms, or West Syndrome. This syndrome describes a triad of clinical findings including hypsarrhythmia on EEG, epileptic spasms, and developmental delay/regression. Urgent treatment is critical for this in order to prevent long term developmental sequelae and intractable seizures.
Lennox Gastaut Syndrome (LGS) can evolve from EIEE or West Syndrome, or arise on its own. Similar to the other two, it is a severe form of epileptic encephalopathy with multiple seizure types and intellectual impairment. The classic LGS tracing is marked by diffuse, prominent slowing and slow (2.5-3 Hz) generalized spike wave discharges.
Benign (rolandic) epilepsy with centrotemporal spikes (BECTS) is a common, descriptive and often self-limiting disorder, marked electrographically by the aforemented centrotemporal spikes, which can be unilateral or bilateral. This condition usually emerges from 1-4 years of age, and remits by adolescence. Seizures in BECTS classically are focal nocturnal, and consist of unilateral facial spasms that can progress to involve the ipsilateral arm and leg.
While you can see absence seizures with multiple types of generalized epilepsy, the classic absence seizure, marked by 2.5 Hz generalized spike and slow waves, is seen with the syndrome of absence epilepsy. These seizures tend to be very brief and have rapid on and offset, without any postictal state; they can often be provoked by hyperventilation. The 2.5 Hz spike wave pattern is important to recognize because absence epilepsy is the only epilepsy syndrome treated first line with ethosuximide.
Electrical status epilepticus of sleep (ESES)--also called continuous spike and waves during slow wave sleep (CSWS)--describes a dramatic increase in interictal activity during sleep, such spikes are present in at least 85% of non REM sleep. ESES is commonly found in Landau Kleffner Syndrome, in which children have seizures and language regression after an initially normal development, due to the presence of ESES on a nightly basis. In the example below, this patient has occasional left hemispheric predominant discharges when awake, which increase in frequency too essentially continuous as soon as she falls asleep.
Juvenile myoclonic epilepsy is among the more common pediatric epilepsy syndromes, arising in adolescence with possible persistence into adulthood. Clinically it is marked by myoclonic jerks, more often in the morning, and on EEG you may see a classic, intermittent 4-6 Hz generalized spike or polyspike and slow wave pattern.
Note that this page is captured at a very, very low sensitivity for (scalp EEG) of 70uV/mm, so on the usual reading sensitivity of 7uV/mm, all the activity here would be so high amplitude as to be unreadable. Understanding that, this tracing shows a very high amplitude, disorganized background with multifocal epileptiform discharges, consistent with hypsarrhythmia.
After the neonatal phase, babies' records are dominated by delta activity the first few months, with a PDR that is often incomplete and, when present, quite slow in the delta frequency. Eye blinks may not be seen yet.
As babies approach 6 months of age, their background shows more theta frequencies amongst the still predominant delta, and the AP gradient can start to become more apparent.
By 6 months, the PDR should be 4-5 Hz, and by 1 year its 6 Hz. Between that time, the trend of increasing theta activity, with delta activity less apparent in wakefulness but still predominant in drowsiness, continues.
At one year, the PDR should be 6 Hz with a clear AP gradient. In this tracing note that F7 and T3 are too close together; if two electrodes see the same voltage on bipolar montage, the difference between their voltages is zero, and you'll get a flat tracing line for that pair.
While the awake tracing for babies becomes more filled with theta and alpha towards one year, drowsiness is still dominated by higher amplitude delta activity; despite this slow activity, note the good AP gradient here.
By 2 years old, the PDR should be at least 7 Hz, with an awake background mostly of theta, alpha and beta. Posterior slow waves of youth--posterior delta waves with the PDR embedded in them--can be seen.
By 3 years old the PDR should be at least 8 Hz, and the background continues to accommodate more alpha amongst the expected theta and, to a less extent, delta activity.
From 3 years to 10 years old, the PDR changes slower than it does in the first few years, going from 8 Hz at 3 years to 10 Hz by 10 years. Throughout childhood, amplitudes tend to be higher than in adults, especially in sleep.
By 8 years old, the PDR should reach 9 Hz and the background can look pretty similar to an adult, except with more theta than an adult should have.
Drowsiness in children can still have significant amounts of delta activity, and you'll start to see other benign variants that are most often seen when drowsy in adults, such as the mu rhythm or temporal wicket waves.
Ohtahara syndrome is a very early infantile epileptic encephalopathy marked by discontinuity and high amplitude bursts of multifocal discharges. It often leads to an early death; if not, it can develop into infantile spasms with significant intellectual impairment.
Hypsarrhythmia describes an extremely high amplitude, extremely disorganized background with multifocal spikes. It is most often seen in the setting of infantile spasms (West Syndrome), and can progress into Lennox Gastaut Syndrome.
Lennox Gastaut Syndrome (LGS) is marked by a very disorganized and slow background with diffuse and/or multifocal epileptiform discharges. Classically, you can see runs of 2.5-3Hz discharges.
Benign (rolandic) epilepsy with centrotemporal spikes is a well named syndrome that usually resolves on its own by the teenage years. Its marked by centrotemporal spikes (bilateral or unilateral) with nocturnal seizures that start with hemifacial spasms, and can progress into GTCs.
Absence epilepsy is marked by absence seizures of 2.5 Hz generalized spike/polyspike wave complexes, which are usually brief and rapid in onset and offset. It is important to recognize this distinct pattern because absence epilepsy is the only type of epilepsy treated with ethosuximide.
ESES occurs when baseline epileptfirom discharges are greatly activated by sleep, and seen in >85% of the sleeping record. It can lead to developmental regression, such as with Landau Kleffner Syndrome. Here the first page is awake, with a rare discharge, and the second page is asleep, with continuous discharges.