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Introduction to EEG UNIVERSITY OF NORTH CAROLINA – CHAPEL HILL CLINICAL NEUROPHYSIOLOGY LABORATORY

Preface This primer is written as a brief introduction to EEG that can be read on the first day as someone is exposed to an EEG for the first time. It is not meant to be a comprehensive text. There are many textbooks available that go into much more detail. The goal is to review the principles of EEG and give examples of EEG findings encountered on a routine day of EEG reading. Therefore, subjects such as neonatal EEG and full treatment of EEG interictal and ictal patterns are not included.

It is easy to read EEG, but difficult to read EEG well.

Contents: Introduction 1 Electrical Principles 2 Electrode Placement 2 Recording and display conventions 3 Montages: 4 EEG Analysis of Waveforms 8 Normal Waking EEG Background Organization 2 Normal Sleep EEG Background Organization 4 Normal Variants 11 Artifacts 26 Encephalopathic Patterns 39 Interictal Epileptiform EEG 50 Ictal Recordings 58 Critical Care EEG Quantitative EEG Appendix 1: Approach to a Normal EEG Report 59 INDEX 61

For Neurology Residents:

These are the Neurology Residency Milestones for EEG.

“Must Know” EEG findings for Adult and Child Neurology Residents

Introduction Electroencephalography (EEG) was first described by Hans Berger in 1929. He recorded brain waves from two electrodes placed at the back of the head and described the normal resting alpha rhythm. He also identified abnormal electrical patterns among brain injured subjects. Since then, EEG’s application in evaluating numerous clinical scenarios has been expanded and refined.

1st Recorded EEG -- ca 1928

Though a relatively old technology, EEG remains the best available noninvasive method for evaluating brain function in real time. EEGs are often requested to assess paroxysmal neurologic events, define and characterize seizure disorders, and determine how overall brain function correlates with a variety of clinical states.

Identification of interictal epileptiform discharges may help confirm a diagnosis of epilepsy or clarify the diagnosis of specific epilepsy syndromes. Differentiating between a generalized epilepsy syndrome and a localization-related epilepsy syndrome can be crucial in prognosis and decision making for medical and/or surgical management. EEGs are also used to help establish diagnosis and prognosis in certain encephalopathic or coma states. Commonly the EEG will reveal slowing to some degree paralleling the clinical examination. If a particular coma pattern is seen on the EEG, the pattern and its evolution over time may provide prognostic information to assist in clinical decision making for further treatment. One condition where the information provided by EEG is indispensable is nonconvulsive status epilepticus. This condition is difficult to diagnose unless the index of suspicion is high at the onset because the clinical presentation can be subtle. The morbidity and mortality of status epilepticus can be high if proper diagnosis and treatment are delayed.

Electrical Principles Surface electrodes are applied to the scalp to record the underlying cortical activity. Each electrode records the synchronized electrical activity arising from a population of neurons in an area of cortex in an angle subtended by the surface electrode of approximately 6 cm2, slightly more than the surface area of a quarter.

Since most of the neurons in the cerebral cortex are radially oriented, the synaptic events in the area just under the surface of the scalp tend to be negative in polarity, reflecting the electrical activity in the extracellular space around apical dendrites as positive ions rush into the cell during excitation. Electrical activity surrounding the soma is generally positive in polarity, but due to its depth, is not typically recorded by surface electrodes.

Electrode Placement - International 10-20 Electrode Placement System

        The surface electrodes are placed on the scalp in a systematic manner that   standardizes their position in relation to underlying brain regions and ensures a reproducible study between patients or for an individual patient across multiple recordings. 

EEG electrodes are placed according to an internationally agreed-upon system called the International 10-20 System. This system is based on measurements of the head that are divided into 10% and 20% fractions of the total circumference of the head, the ear to ear measurement and the anterior-posterior measurement from the nasion to the inion.

The electrodes are named based on convention, with letters that represent particular cerebral regions (Frontal, Temporal, Central, Parietal, Occipital), and numbers that represent sidedness. Odd numbered electrodes are on the left, even numbered on the right, and electrodes with a “z” designation at the midline.

Additional electrodes placed in between at the 10% locations to improve the ability to localize. This system is called the 10-10 electrode placement system. Electrodes F9/10, T9/10 and P9/10 are examples on this head diagram.

Recording and display conventions The EEG machine is a differential amplifier. It takes the electrical information from one signal source or electrode and compares it to another source, rejecting any common features (common mode rejection). The resulting signal reflects a measurement of the net difference in voltage between the two electrodes (here designated as gridpoints G1 and G2) over time. In this way the EEG displays a continuous tracing of the electrical activity from a particular region of the cortex in relationship to another cortical region or in relationship to a non-brain reference.

By convention, the tracing for each channel of the EEG reflects the electrical activity of the first electrode or grid point (G1) in reference to the second (G2). Again by convention, each derivation or channel displays a waveform with an upward deflection when the net difference of the voltage between the two electrodes is negative (G1-G2<0). If G1 is positive or less negative than G2 (G1-G2>0), then the waveform has a downward deflection. Thus, there are two possible interpretations for the waveform produced by each derivation pair. For example, if G1 is more negative than G2 or G2 is more positive than G1, then the waveform points upwards. It depends on which electrode is the active electrode and in what direction.

There is a rational basis for the convention of displaying electrically negative events as an upward deflection on the EEG. Epileptic discharges result in a paroxysmal negative charge at the surface of the cortex, and conventional EEG tracings produce a rapid upward deflection often described as a sharp wave or spike. This is why a transient negative potential at any given electrode is described as a surface negative event. Vice versa, a transient positive potential is described as a surface positive event.

Montages: A montage is the arrangement of channels on the EEG display or tracing, and each channel consists of paired signal sources. When channel derivations are arranged into montages their sequence provides information that identifies of polarity and location of the cortical activity of interest. Montages can be created in any array, though the most useful ones will be those that allow for rapid visual interpretation of the EEG signals. There are two types of montages: bipolar and referential. The rules for interpretation for each type of montage are different based on the way they display the information.

Bipolar montages are created by making chains of sequential channels where each channel consists of a pair of individual electrodes. In order to convey spatial resolution, the chains of sequential channels can be arranged in anatomically relevant directions. A new chain starts when the sequence begins in a new location. The chains can run in an anterior to posterior direction (AP Bipolar Montage also called the double banana), or in a transverse direction across the head; whatever manner that gives useful localizing information.

Rule for interpretation of a bipolar montage: A phase reversal in a chain identifies an area where the changes in electrical potential are maximal relative to the surrounding signals. Phase reversals can either be positive or negative in polarity. When there is a negative phase reversal, the waveforms appear to point toward each other; when there is a positive phase reversal the waveforms appear to point away from each other. Phase reversals often indicate a region of interest electrophysiologically, showing a particular spatial point on the EEG where voltage changes are maximal and/or the spatial extent of voltage changes that surround it, its field.

In this hypothetical bipolar example, systematically evaluating each channel will allow us to make an interpretation of the entire chain and by using the polarity conventions of EEG display, localize electrical events in space.

• In the first channel where a is compared to b, there is no large net difference in their electrical potentials so the display shows a relatively flat line.
• When b is compared to c, there is a small downward deflection. This finding suggests that either b is slightly more positive than c or c is more negative than b.
• When c is compared to d, there is another small deflection downwards also suggesting that c is slightly more positive than d or that d is more negative than c.
• There is a large deflection upwards when d is compared to e. In this case, d is either much more negative than e or e is much more positive than d.
• When e is compared to f, there is a small upward deflection suggesting e is either slightly more negative than f or f is slightly more positive than e.
• Finally, in the last channel f and g are equipotential and the tracing appears relatively flat.

The conclusion from this analysis suggests that either there are two positive generators on either side of the chain or electrode d is the region of maximum negativity and the potential of interest. Considering that most cortical events of interest are negative in potential, this finding would be the most logical conclusion. The deflections between channels c-d and d-e represent a negative phase reversal.

Referential montages give the same electrophysiological information but present the information in a slightly different format. The voltage at each electrode is compared to a common or neutral electrode or to mathematical average of a group of electrodes. In a referential montage, the area of highest amplitude is of the most interest because it represents the region most negative or positive in polarity. If there is an apparent “phase reversal” there are two potential interpretations: 1) The reference electrode is active or is involved in the area of interest, or 2) there is a horizontal dipole and that both ends of the dipole are apparent on the montage.

Referential montage Referential montage referenced to Cz referenced to the ipsilateral ear

Common referential montages: Ipsilateral ear reference – Each electrode over the left hemisphere is compared to the left ear electrode; each electrode over the right hemisphere is compared to the right ear electrode. Contralateral ear reference – Each electrode over one hemisphere is compared to the contralateral ear electrode. A1-A2 reference – Each electrode is compared to an average of the A1 and A2 electrodes Cz Reference – each electrode is compared to Cz Average reference – Each electrode is compared to the average signal of a group of electrodes (usually those least affected by eye movement or muscle artifact Laplacian anatomic average reference – Each electrode is compared to a weighted average of an immediately surrounding set of electrodes.

In this hypothetical referential example (which shows the same electrical event as the bipolar example), systematically evaluating each channel will allow us to make an interpretation of the entire EEG.

• In the first channel when a is compared with the reference electrode, there is no net difference between the electrical potentials so the display shows a relatively flat line.
• When b is compared to the reference electrode, there is also little net difference between the electrical potentials so the display also appears as a flat line. These findings suggest that neither a nor b is involved in the discharge of interest.
• When c is compared to the reference, there is a small deflection upwards, thus suggesting that c is slightly more negative than the neutral reference.
• There is a large deflection upwards when d is compared to the reference. This finding suggests that d is much more negative than the reference.
• When e is compared to the reference, there is a small upward deflection suggesting that e is slightly more negative that the reference.
• Finally, the last channel f is again equipotential to the reference electrode.

The conclusion from this analysis suggests that electrode d is the maximally negative electrode with a field that extends to the surrounding electrodes c and to a lesser extent e. This analysis of the same set of electrodes draws us to the same conclusion as when we the bipolar montage was analyzed systematically. A referential display also allows quantification of the events recorded since the voltage of each channel is being compared to a common reference.

EEG Analysis of Waveforms When approaching the evaluation of the EEG you will see continuous lines that represent fluctuating cerebral potentials and are composed of several types of waveforms. To describe a waveform in an organized and reproducible way, we break it down into its component dimensions of voltage, frequency and morphology.

Voltage: At the scalp surface, the amplitude of the cerebral activity is measured on the order of microvolts. This is in contrast to EKG potentials which are recorded in millivolts. The EEG waveform represents the summed electrical potential of a population of cortical neurons just below the electrode. This signal recorded at the scalp is attenuated by the cerebral tissue itself, the CSF, dura, skull and scalp and the EEG equipment before being displayed on the oscilloscope, paper or computer screen. The height of the waveform on the tracing or display depends of the sensitivity of the EEG amplifier, and is described in microvolts/mm.

Frequency: Many EEG patterns are rhythmic or semirhythmic in nature. Frequency is a measure of the number of repetitive waveforms with respect to time and is described in waves per second or Hertz. Frequencies are grouped into bands that are relevant to patterns of normal or abnormal brain activity. Physiological brain rhythms are rarely pure, and are usually composed of a mixture of frequency bands, but they can be described and assigned a frequency based on the relative dominance of one particular frequency band. .

Morphology: The morphology is the shape of a waveform. Descriptive adjectives used to characterize waveform morphology include monomorphic, sinusoidal, polymorphic, arciform, biphasic, triphasic, spiky, or sharp with or without slow wave components. These patterns may be incorporated into ongoing EEG activity, occur as bursts or as individual paroxysmal discharges that stand out from the background activity. Whether the morphology of a particular waveform on the EEG represents benign, normal activity or implies pathology depends on where and when it occurs in the context of the overall EEG.

Electrical events on the EEG are described in terms of timing, rhythmicity, quantity and location

Timing: It is important to describe the number of occurrences of a waveform that occurs paroxysmally during the EEG or the duration of a pattern. When the events occur is equally important. Some EEG events may occur more often or exclusively in association with other physiological events, changes in clinical state or induction procedures during the EEG such as eye closure, drowsiness, sleep, photic stimulation or hyperventilation.

Rhythmicity: Waveforms on the EEG can occur as isolated sporadic events but may also occur repetitively. When events are repetitious, they can be described in terms of their periodicity or regularity. Rhythmic events have a relatively consistent frequency. Some waveforms are less regular, but still have a periodicity. Certain periodic waveforms with particular frequencies are associated with specific disorders. For example, rhythmic 3 Hz spike and wave discharges are associated with Genetic/Idiopathic/Primary Generalized Absence Epilepsy. Slow Periodic Lateralized Discharges (LPDs) are associated with Sub-Sclerosing Panencephalitis (SSPE).

Quantity: An EEG pattern can be described as continuous or intermittent. If it is paroxysmal a qualitative or quantitative description of how often it occurs allows the next EEG reader to assess the degree of change without pulling up the original study. For example, if there slowing, what is the prevalence of the slowing Continuous: ≥ 90% of record/epoch, Abundant: 50% to 89% of record/epoch, Frequent: 10% to 49% of record/epoch, Occasional: 1% to 9% of record/epoch or Rare: <1% of record/epoch? If there are discharges, are they Abundant: ≥ 1 per 10 seconds, but not periodic ( estimated average and maximum number of spikes per 10-second epoch), Frequent: ≥ 1/minute but less than 1 per 10 seconds, Occasional: ≥ 1/hour but less than 1/minute, or Rare: <1/hour?

Location: The purpose of a montage is to help localize the region of the brain from which a particular waveform arises. The rules of localization are based on interpretation of bipolar and referential montages. EEG events are called generalized when they affect leads over both hemispheres of the EEG simultaneously. Lateralized features affect only one hemisphere. Regional events are seen in one region of the brain, typically affecting a group of contiguous electrodes. Focal events may be seen in only one or two electrodes at a time.

Normalcy of an EEG is dependent on patient characteristics and clinical state. Before interpreting an EEG, it is important to appreciate what is considered normal in reference to the patient’s clinical state and age. Identifying the state of the patient during the EEG is essential to the interpretation. Findings that might be considered normal during one state may be abnormal in another state. The age of the patient is also an important identifier. For instance, more slowing is allowed in as part of a normal pediatric EEG than is allowed in an adult EEG.

Normal Waking EEG Background Organization The normal waking EEG background is characterized by anterior-posterior voltage and frequency gradients. The EEG activity is generally lower in amplitude and faster in frequency anteriorly and higher in amplitude and slower in frequency posteriorly.

Another feature of a normal waking EEG background is the posterior dominant rhythm, sometimes called the alpha rhythm, which is best seen at O1 and O2 electrodes and is sinusoidal in morphology. This particular rhythm has other physiological characteristics which define it. It is most apparent in the relaxed wakeful state when the eyes are closed. It reacts to eye opening and mental concentration by attenuating or disappearing as the neuronal population responsible for its generation desynchronizes. This rhythm is present beginning at about 6 months of age and gradually increases in frequency with maturation (see table). Most adults have a posterior dominant rhythm in the range of 8.5 to 13 Hz. Slowing of the posterior dominant rhythm below what is considered appropriate for a given age is a potential indication of dysfunction. During childhood into adolescence this rhythm can be intermixed with delta waves on which the posterior rhythm rides. These underlying delta waves are called posterior slow waves of youth and should not be considered abnormal.

(b) 2 year old (a) 7 month old

In these examples we can appreciate a rudimentary ~5 Hertz posterior dominant rhythm in a 7-month-old (a) contrasted with the well-developed 7 Hz posterior rhythm of a 2-year-old (b) that emerges with eye closure and is intermixed with slower 2-3 Hz posterior slow waves of youth.

In both examples, there are well-developed anterior-posterior voltage and frequency gradients, and despite their overall difference in appearance, both show normal organization for the patient’s age.

8 year old EEG with less delta more theta compared to 2 year old EEG

95 year old EEG not much different

Normal Sleep EEG Background Organization Sleep is divided into two states: non-rapid eye movement (NREM) sleep and rapid eye movement (REM) sleep. NREM sleep is further subdivided into N1-3 based on the depth of sleep and certain EEG characteristics.

The onset of N1 sleep is characterized by an attenuation of the posterior dominant rhythm, increased theta activity, reduction in muscle movements and slow roving eye movements.

The appearance of hypnagogic hypersynchrony and triangular vertex waves that have a phase reversal across the midline also herald development of N1 sleep.

As sleep deepens into N2, vertex waves and sleep spindles become more apparent. Since sleep transients are best seen in the central regions, a transverse montage brings them out. During arousals K-complexes can appear (next page)

K-complexes during N2 Sleep are high voltage, broad, triangular, often biphasic deflections that are maximal in the frontal and vertex leads and often trailed by spindles. Also note sharp, triangular, monophasic waveforms in the occipital leads – Positive Occipital Sharp Transients of Sleep (POSTS) – a normal variant seen in N1 and N2 sleep.

N3 sleep is characterized by the increasing percentage of high voltage delta waves of >20% of the epoch. Previously these were divided into two stages: stage 3 and 4 sleep where the delta activity comprises approximately 20-50% of the record, and in stage 4 the delta activity comprises more than 50% of the record.

REM sleep has the electrophysiologic characteristics of a low voltage mixed frequency background without evidence of a posterior dominant rhythm, temporal theta called saw tooth waves and rapid eye movements that are usually lateral or oblique in direction. There is a noticeable lack of movement or muscle artifact during this period of time due to physiologic atonia.

Normal Variants There is a set of EEG waveforms that appear either sharp in contour or rhythmic in nature and may be mistakenly described as epileptiform or abnormal features. However, based on many years of experience and large studies of normal EEG, these patterns, though not evident on every normal EEG, are accepted as benign normal EEG variants. The importance of recognizing and describing these normal variants lies in not mistaking them for findings that raise suspicion of dysfunction.

Alpha Squeak This finding occurs immediately after eye closure during the waking state. The posterior dominant rhythm appears to transiently increase in frequency by approximately by 1 Hertz over the normal posterior rhythm.

Slow alpha variant This finding is a subharmonic of the normal posterior dominant rhythm. This rhythm is approximately half the normal frequency. The morphology of this waveform is typically notched, indicating a superimposition of the subharmonic rhythm and not a replacement of the normal occipital rhythm with slow frequencies that would suggest pathology.

Fast alpha variant This finding is a super harmonic of the normal posterior dominant rhythm and typically is about twice the normal frequency.

Mu rhythm This monomorphic rhythm is seen over the central region (here most prominent in the F3-C3 and F4-C4 derivations). Analogous to the resting occipital rhythm, this is an “idling” rhythm of sensorimotor cortex. It is arciform in morphology and can sometimes appear sharp in contour. The frequency is usually in the alpha range, and it can be seen in either hemisphere. This rhythm is reactive, attenuated by movement or thought of movement of the contralateral hand.

Central/Midline Theta Rhythm of Ciganek is a normal drowsy pattern seen most in children and adolescents. These regular, sinusoidal, theta range rhythms wax and wane in amplitude, and do not evolve in frequency or distribution (unlike electrographic seizures).

Breach rhythm Regionally increased waveform amplitude and increased frequency bands suggest that there has been a breach or a break in the skull as a result of a fracture or surgical procedure. An intact skull acts as a natural filter of EEG signals, reducing their amplitude and attenuating faster frequencies. When the integrity of the skull has been disrupted these waveforms are more easily detected at the scalp. Though the skull breach may be an abnormal phenomenon, the accentuation of normal underlying brain rhythms is not.

Lambda waves These waveforms are seen in the occipital regions of the brain. They are typically triangular, biphasic, positive in polarity and are seen in people who are actively scanning with their eyes during the EEG. They are thought to be related to a visual evoked potential as they are sensitive to visual stimuli. When the subject is asked to close their eyes or to defocus their vision, these waveforms disappear.

Positive Occipital Transients of Sleep (POSTS) These waveforms are also seen in the occipital regions but during sleep rather than wakefulness. They are indicative of stage 1 sleep, are positive in polarity and often occur in runs. The phenomenon of a positive signal displayed as an upward deflection on the EEG occurs on bipolar montages when the signal arises from an end-of-chain electrode. The POSTS on this example are surface positive at O1 and O2, and not surface negative at T5, T6, P3 or P4.

Small Sharp Spikes (SSS) also called Benign Epileptiform Transients of Sleep (BETS). As their name implies, these waveforms are seen during drowsiness and light sleep. They are temporal in location, are low voltage (<100 microvolts), needle-like in morphology (<100 msec) and spiky, sometimes multiphasic, and are distributed across a broad field with a shallow voltage gradient. They are often difficult to see in a bipolar montage but can be more easily detected in a referential montage. In contrast to temporal epileptiform discharges, they are not associated with any after going slow wave.

Wickets This alpha or theta (6-7 Hz) rhythm is seen in the temporal regions of adults during drowsiness. These monomorphic waveforms are arciform or notched in appearance and can occur in runs bilaterally or independently in each temporal region. When they occur singly (“wicket spikes”) they can appear sharp and high in voltage, but usually have a characteristically curved up- and down-slope, do not stand out from the background frequencies, and unlike epileptiform sharp waves, do not have after going slow waves.

Rhythmic Midtemporal Theta of Drowsiness (RMTD) Also known as psychomotor variant, this is another rhythm that is widespread over the temporal region in the 4-7 Hz theta range. They were thought to be related to seizures in the past but are now accepted as a benign variant seen during drowsiness or light sleep in children or adults. These monomorphic waveforms appear notched or are flat-topped and can be seen bilaterally or independently in the temporal regions. In contrast to the rhythmic discharges of a seizure, they do not evolve in frequency or spatial distribution.

14 and 6 Positive Bursts These bursts of activity are seen during drowsiness and are of positive polarity in the posterior or midtemporal regions bilaterally or independently. They tend to build in amplitude and are composed of two frequency bands of both 6 Hz and/or14 Hz.

6 Hertz Phantom Spike Wave Discharges These waveforms are low voltage 6 Hz discharges of small spike and higher voltage slow wave morphology that are best seen during drowsiness. They can be anteriorly or posteriorly predominant and are usually symmetric. In contrast to epileptic spike-wave discharges, they tend to build up and then taper gradually in amplitude.

Subclinical Rhythmic Epileptiform Discharges in Adults (SREDA) is a rhythmic, non-evolving discharge that begins and ends abruptly, can be unilateral or bilateral and is superimposed on a normal background. It is quite rare and of unclear significance.

Common Normal Variants

Pattern	Frequency	Morphology	Distribution	Duration	Age	State
14-and-6 Hz positive bursts	14 and 6 Hertz	Repetitive arch-shaped positive spikes	Posterior temporal/parietal; bilaterally synchronous or independent	<1-2 seconds	Adolescence (10-58%)	Stage I & II sleep
Midline theta rhythm (of Ciganek)	4-7 Hertz	Rhythmic trains of sinusoidal, spiky or arciform shape	Midline, usually central	4-20 seconds	Children and adults	Awake, drowsy
Phantom 6 Hz spike and wave	5-7 Hertz	Diphasic, small spike (<40 μV)and large aftergoing slow wave	FOLD: Female, Occipital, Low amp, Drowsiness WHAM: Waking, High-amp Anterior, Males† || <1 second || Adolescence/adults (2-5%) || Drowsy/awake, Stage I (not II)
Positive occipital sharp transients of sleep (POSTS)	Sporadic	Surface positive focal spikes and sharp waves up to 200 msecs	Occipital: unilateral or bilateral	Sporadic	Children	Drowsy, asleep
Rhythmic midtemporal discharge (RMTD) / “Psychomotor variant”	4-7 Hertz	Notched harmonic; abrupt onset and end	Midtemporal; unilateral, bilateral, independent or bisynchronous	Few-10 seconds	Young adult, middle aged females (1-2%)	Stage I sleep
Small sharp spikes (SSS) / Benign epileptiform transients of sleep (BETS)	Sporadic	<50 μV, <50 msec short spikes; broad shallow local gradient	Mid-/anterior temporal, shifting distribution, widespread bifrontal or bilaterally independent	Sporadic	Adults/Adolescents (20-25%)	Stage I & II sleep
Subclinical rhythmic EEG discharges of adults (SREDA)	5-6 Hertz	Mono-/biphasic sharp waves followed by rhythmic 4-7 Hertz waves – abrupt onset/offset	Symmetrical, posterior temporal/parietal maximally; may be unilateral or asymmetric	40-80 seconds	Older adults	Awake, Stage I, HV
Wicket spikes	6-12 Hertz	Monophasic arciform; no slow waves; notched harmonic	Midtemporal, bilateral independent	Rhythmic up to a few seconds	Adult (0.9%)	Awake, Stage I sleep
Hypnogogic/Hypnapompic hypersynchrony	3-5 Hertz	Moderate to high amplitude rhythmic bursts with intermixed spikes	Generalized, maximum anterior or posterior	1-6 seconds	Children	Drowsy/Arousals State transitions

†NOTE: Anteriorly predominant phantom 6Hz spike-wave variants have been reported by some as less than benign variants, and while a nonspecific finding, may have an association with a predisposition to seizures. Artifacts Artifacts are waveforms on an EEG caused by electrical sources other than the cortex. It is important to recognize and identify artifacts so that they are not confused with cerebral potentials. Artifacts can be generated by numerous sources, the most common of which is the body itself: the eyes, the heart, and muscle. Environmental artifacts such as the EEG machine, electrode placement or malfunction, and 60 cycle interference can also produce artifacts, particularly in “hostile” environments such as the ED, ICU and OR.

Physiologic Artifacts Ocular Artifact The globe of the eye has an electrical potential of about 50-100 microvolts with the cornea positive and the retina negative in polarity. Artifacts of eye movement are best seen in the frontal and temporal leads closest to the eyes. Specific electrodes can be placed above and below the outer canthus and are called electrooculograms (EOG). During eye closure, the eyes move upward (Bell’s phenomenon) and there is a large bifrontal positive deflection. With lateral movements, there is a positive deflection ipsilateral to the direction eye movement and a negative deflection on the contralateral side. An easy mnemonic is “look through the key hole” or in other words, a positive phase reversal (keyhole) on a bipolar EEG is the direction to which the eye is turned.

Electroretinogram Not only does the globe have electrophysiologic characteristics; the retina itself generates potentials in response to stimulation. This finding can be manifested during photic stimulation when the bright light stimulus causes a response from the retina that can be recorded from the frontal electrodes (here at FP1 and FP2). These deflections are typically positive in the frontopolar electrodes and have a slight delay from the stimulus of between 50 to 100 milliseconds.

Electrocardiographic Artifacts The QRS complex can be recorded as a far field potential over the scalp and seen best at the A1 or A2 electrode. This signal can be particularly prominent in patients with large volume conduction. Extra systolic beats can be confused with cerebral discharges due to their apparent paroxysmal nature and sharp contour.

Cardioballistogram occur in correlation with the QRS complex as the contraction of the heart generates vibration that can be recorded by the EEG electrodes. The peak of each waveform coincides with the QRS complex. These waveforms are typically seen when the sensitivity of the EEG is increased and there are no other features to detract from their presence (i.e., when there is minimal to no cerebral activity).

Pulse artifact This artifact is usually confined to a single electrode when that electrode is placed over a superficial artery. It appears as a slow rhythmic waveform that just lags behind the QRS complex.

Electromyographic Artifacts Lateral rectus spikes are generated by single muscle units during lateral eye movement.

Muscle Artifact Frontalis muscle artifact occurs especially with a photically stimulated photomyoclonic response and with forcible eye closure or opening. Temporalis muscle artifact occurs when a patient clenches his jaw or chews. When the muscle artifact is so dense, it obscures the EEG. A tech can ask the patient to open their mouth slightly to relax the muscles and minimize the artifact.

Glossokinetic Artifacts The tip of the tongue is negative and the base of the tongue is positive. When the tongue moves there can be a diffuse or unilateral activity depending on the direction of the movements.

Galvanic Skin Responses are high amplitude slow potentials also called sweat sway. The salt bridge that develops between electrodes “shorts” or decreases their differential impedances so that the amplifier cannot differentiate between the two electrodes and the potential difference between the two electrodes approaches zero. The resulting tracing is of a relatively flat line that undulates irregularly.

Physiologic Movements Tremors and myoclonic jerks can cause diffuse or focal sporadic or rhythmic artifacts in the EEG. Here, head tremor affect the A2 (ear) reference maximally. Most physiologic movements show nearly vertical deflections on the EEG, too steep to be caused by cerebral potentials.

Nonphysiologic Artifacts: Instrumental 60 cycle interference from other electrical equipment may interfere with an EEG and produces a characteristic pattern. This exogenous electrical artifact is accentuated when electrode impedances are high (poor scalp contact). The rules of interpretation for bipolar montages allow identification of the faulty electrodes on this tracing: P3 and O2.

A 60 Hz notch filter specifically reduces the interference of activity around 60 Hz but the resultant waveforms may be misleading. This is the same page of EEG as shown on the previous page, but now the notch-filtered 60 cycle interference appears to be a continuous alpha band rhythm. Frequency filters imposed on the EEG can be useful for visualizing underlying EEG rhythms when excessive artifact is present but can themselves produce artifactual findings.

Electrode pops. This artifact is generated by tapping on each electrode to ensure the integrity and placement of each electrode at the beginning of a study. Similar artifacts can be seen if the integrity of the electrode contact is not adequate, and the electrode intermittently discharges accumulated electrical static. Unlike most cerebral potentials, electrode pops are exclusively limited to a single electrode at a time, without a surrounding electrical field.

Abnormal EEG Patterns

Encephalopathic Patterns When a patient is unresponsive without lateralizing exam findings and the etiology of the coma is in question, an EEG can be helpful to further assess the degree of the coma and perhaps give insight into the etiology or localization of the underlying pathology. With repeated EEGs, just like with repeated physical examinations, the evolution of the EEG pattern can help determine prognosis.

In general, there is a continuum of EEG findings that correspond to the severity of a diffuse clinical encephalopathy. Extremes of normalcy or abnormality at both ends of this continuum are fairly easy to recognize, and what lies in between can be categorized as mild, moderate, or severe based on some basic reproducible EEG findings.

Mild: As the level of arousal becomes clouded there is corresponding mild slowing of the EEG. It may begin with slowing of the posterior dominant rhythm, but as the depth of encephalopathy increases, there are increasing amounts of theta and then delta activity intermixed with the background. These changes are independent of the etiology of the encephalopathy.

Moderate: With worsened cerebral function, there is increased theta and delta range slowing. Background organizational features such as anterior-posterior gradients and the posterior dominant rhythm become difficult recognize, but the EEG background retains some variability in response to stimulation and there is usually evidence of discernible state changes.

Severe: Eventually there is loss of normal state changes that control wakefulness and sleep, and the EEG becomes monotonous in appearance and unresponsive to external or internal stimulation. At the far extreme of a severe diffuse encephalopathy, there is a loss of all cortical activity and the EEG shows electrocerebral silence.

Within these general patterns of encephalopathy, there can be more specific findings that suggest particular etiologies.

Slow Posterior Dominant Rhythm

Diffuse theta slowing Diffuse delta slowing

Generalized Periodic Discharges with Triphasic Morphology, previously known as Triphasic Waves are a periodic pattern of waveforms that have three phases and are generally most prominent in the anterior leads.  These waveforms often have a subtle time lag between anterior and posterior regions.  Their presence tends to be associated with metabolic encephalopathy, often of hepatic or renal origin, but they are nonspecific and may be seen in a variety of toxic-metabolic encephalopathies.

Generalized Rhythmic Delta Activity (GRDA) frontally predominant – previously known as Frontal Intermittent Rhythmic Delta Activity (FIRDA): This is an intermittent pattern of rhythmic monomorphic delta waves seen with mild to moderate diffuse encephalopathies. It tends to occur with subcortical white matter disease more than cortical disease, but the etiology is usually nonspecific. It becomes more pronounced as the patient becomes drowsier.

Dominant Frequency is in the alpha range with loss of reactivity previously known as Alpha Coma This monomorphic pattern of diffuse alpha frequencies that are more prominent in the anterior than the posterior regions of the brain typically occurs in the setting of hypoxic-ischemic injury. It looks like a normally organized background turned upside-down (or more accurately, frontside-back). The prognosis for independent living following development of this EEG pattern is poor. It can also be seen with anesthetic sedation so the context matters.

Dominant Frequency is in the beta range but it is usually intermixed delta with loss of reactivity previously known as Beta Coma. This pattern of diffuse beta frequently is associated with a drug overdose. These faster frequencies seen can be seen with sedatives such as barbiturates and benzodiazepines. The overall prognosis is better compared to other coma patterns if the patient is supported through the overdose period assuming there is no other cerebral injury.

Dominant frequency is a beta delta pattern previously known as a Spindle Delta Coma In contrast to the beta predominant pattern, there are bursts of beta activity riding over large slow polymorphic delta waves that are maximal centrally and can be seen in encephalopathy from a variety of etiologies. It is a nonspecific pattern. Burst Suppression Pattern is an extreme pattern that can be seen in severe coma states or can be induced iatrogenically by anesthesia or for the treatment of status epilepticus. This is an alternating pattern of bursts of higher voltage activity separated by periods of relatively suppressed cerebral activity. This pattern is typically described by its ratio of burst period to suppression period. When the bursts are lost and the suppression periods become continuous, then the pattern is called background suppression with no apparent cerebral activity over 2 microvolts.

Electrocerebral Silence or Inactivity These studies, also called brain death studies, are now rarely used. They were frequently requested in transplant centers as a confirmatory test to document brain death in association with the clinical examination. The principal limitation EEG for the purpose of establishing a diagnosis of brain death is that it only records cortical activity and cannot reveal useful information about brainstem activity. Other tests such nuclear medicine test for cerebral perfusion or evoked potentials have largely supplanted the usefulness of the EEG. In addition, there are no EEG criteria for the very young, and the presence of small populations of cortex that cannot generate sufficient voltages above 2 microvolts cannot be revealed by an EEG.

When other ancillary tests are unavailable, an EEG for the purpose of establishing electrocerebral inactivity (ECI) is still sometimes performed. Reversible factors that suppress cerebral activity need to be excluded, and the study must be performed according to a strict criteria:

Exclusion Criteria:

• Overdose of CNS depressants
  • barbiturates, benzodiazepines, methaquinolone and meprobamate
• Hypothermia (T < 32.2C)
• Cardiovascular shock (BP < 80mmHg)
• Severe metabolic or endocrine disorders

Technical requirements of a brain death study.

• At least 8 scalp electrodes and reference electrodes
• Interelectrode impedance between 100-10,000 ohms
• Document testing integrity of entire system
• Interelectrode distances of > 10 cm
• Sensitivity < 2mV/mm
• Time constant 0.3-0.4 second
• EKG channel
• Test EEG reactivity to external stimulation
• Recording time at least 30 minutes
• Qualified technologist (rEEG,T)

Electrocerebral Inactivity (ECI) with respiratory and ECG artifacts. Note the scale legend shows a 40 microvolt amplitude. There is no waveform that could be considered generated by the cortex.

Periodic Discharges These discharges occur with a regular periodicity throughout the EEG and can be generalized, regional/lateralized, or bilateral and independent. Generalized periodic discharges (GPDs) are more frequently associated with severe encephalopathy and can been seen after a severe hypoxic/ischemic event. Lateralized Periodic Discharges (LPDs) are seen in a variety of clinical settings including herpes encephalitis, acute stroke, tumor, or as the aftermath of nonconvulsive status epilepticus. Bilateral independent lateralized discharges are rare and suggest that multifocal injury to the brain such as occurs in the setting of shower emboli resulting in multifocal strokes or aggressive metastatic brain cancer. While Periodic Discharges are not an epileptogenic pattern per se, they are associated with pathological processes where seizures often occur.

Generalized Periodic Discharges (GPDs) in the setting of a hypoxic ischemic injury after cardiac arrest

Right Temporal Lateralized Periodic Discharges (LPDs) in the setting of herpes encephalitis

LPD+ LRDA

Interictal Epileptiform EEG – outpatient or EMU

Epilepsy syndromes are classified as either Focal or Generalized epilepsies. They are differentiated by whether the seizures arise from a focal region of the brain or from activation of a generalized network. Epilepsy syndromes are also differentiated by their clinical characteristics, EEG patterns, prognosis and response to treatment. The EEG is used to differentiate focal from generalized epilepsy syndromes by the epileptiform discharges that are localized to a focal region versus a generalized pattern.

Generalized Epilepsy Syndromes The generalized epilepsy syndromes are further subdivided into Idiopathic/Primary and Secondary Generalized Epilepsies. Most generalized epilepsies share interictal findings of diffuse paroxysmal EEG changes and have similar appearing clinical manifestations and ictal EEG patterns. The EEG abnormalities have a generalized distribution; they are seen simultaneously at the surface electrodes of both hemispheres and have a diffuse spatial distribution.

It is thought primary/idiopathic/genetic generalized epilepsy syndromes are related to dysfunction in the circuitry between the thalamus and the cortex. Occasionally, patients show an EEG trait consistent with a primary generalized epilepsy syndrome yet may have never had a seizure in their life time. With detailed questioning, a family history of epilepsy may be uncovered. In general, these patients are of normal intellect and have normal neuroimaging. Most of these patients are easily treated when appropriate medications are used.

Secondary generalized epilepsy syndromes are associated with underlying dysfunction that is less clearly characterized since these patients tend to have diffuse or multifocal neurological dysfunction. They are typically developmentally delayed and have other neurologic disorders. They frequently have a variety of seizure types that can be very difficult to treat medically. Although they have EEG features similar to other generalized epilepsy syndromes, they also have other generalized or multifocal abnormalities indicating widespread abnormalities within the cortex.

Genetic/Idiopathic/Primary Generalized Epilepsy Syndromes Of the primary generalized epilepsy syndromes Childhood Absence Epilepsy and Juvenile Myoclonic Epilepsy are the most commonly encountered in an EEG lab. The EEG patterns are similar but differ in subtle ways.

Classically, Childhood Absence Epilepsy is associated with blank staring and unresponsiveness lasting seconds that can be induced by hyperventilation. The seizures begin at 5 years of age and tend to remit by 12 years of age. The EEG shows characteristic bursts of spikes followed by dome-shaped slow waves that occur in a rhythmic pattern at a frequency of 3 per second. The onset is synchronous in both hemispheres and tends to be predominant in both frontocentral regions, although in young children they may have a more posterior predominance. The EEG finding is a diffuse frontocentrally predominant 3 Hz Spike-Wave Complex. During hyperventilation, an activating procedure routinely performed during an outpatient EEG, absence seizures can often be provoked.

With Juvenile Myoclonic Epilepsy, the clinical onset is later in adolescence or early adulthood. This epilepsy syndrome is associated with early morning jerking and these patients can be photosensitive. The EEG also shows characteristic bursts of spike and slow waves that occur in a faster frequency of 4-5 per second compared to classic 3 Hz spike wave complexes. The spike components can also appear as a run of polyspikes. The onset is synchronous in both hemispheres and tends to be predominant in both frontocentral regions. The EEG finding is often described as diffuse frontocentrally predominant fast spike and polyspike and wave activity.

Photic stimulation, another routine induction used in the outpatient setting to increase the yield of an interictal EEG, can often induce discharges at particular flash frequencies. This phenomenon is called a photoparoxysmal response. Typically a technologist will repeat the photic stimulation to ensure that the discharges did not occur by chance but were a reproducible finding. It can then be concluded that this patient is photosensitive to a particular flash frequency range.

Developmental Epileptic Enephalopathy are typically secondary to some other neurological dysfunction of either known or unknown etiology. The patient is commonly clinically developmentally delayed and may have numerous seizure types. Often they are classified as West Syndrome or Lenox Gastaut Syndrome depending on the age of onset. The characteristic EEG pattern is called hypsarrhythmia This pattern is a chaotic one without any normal organization and is of high voltage with intermixed multifocal sharp waves and slow spike and wave activity. The Slow Spike and Wave is on the order of 1-2 discharges per second and can occur in prolonged runs lasting more than 20 seconds during which the clinical correlation is a protracted atypical absence seizure.

Focal Epilepsy Syndromes Localization-related epilepsies are a mixed bag of epilepsy syndromes that can be idiopathic or symptomatic in etiology. The clinical characteristics or semiology of the seizures is dependent on their region of onset or the symptomatogenic zone. The interictal EEG may provide evidence about the location of the epileptogenic zone responsible for the epilepsy syndrome. The epileptogenic zone is the region that demonstrates cortical irritability. This irritability is represented by spikes or sharp waves. Formally the definition of a spike is a paroxysmal discharge that stands out from the background and in amplitude and frequency. They are less than 70 msec and typically followed by a slow wave. Neurophysiologically, this discharge represents a brief synchronous depolarization in a population of cortical neurons followed by a zone of inhibition with hyperpolarization. Otherwise, the informal definition is that a spike looks like something that would hurt to sit on! A sharp wave is equally uncomfortable to sit on and is 70-120 msec in duration. Localization of the discharge determines the region of epileptogenic potential.

Self-Limited Idiopathic Focal Epilepsy Syndromes In the outpatient setting, the most common discharges seen are Benign Focal Epileptiform Discharges of Childhood (BFEDC). This type of discharge is often seen in the centrotemporal region near the Rolandic sulcus where the superior temporal bank of the temporal lobe is relatively perpendicular to the scalp surface. Classically there will be a horizontal dipole because of this localization. A negative charge is recorded from the central or temporal region with a simultaneous positive charge in the frontal region. Due to the orientation of the discharge, the EEG will be able to pick up both ends of the dipole. This is in contrast to typical discharges arising from the convexity when only the negativity is recorded and the positivity is buried deep within the brain (radially oriented dipole). At times, discharges of similar morphology can also be recorded from the occipital region. Only 40-60% of patients with BFEDC have or will have seizures. The the remainder have an asymptomatic EEG trait. When clinically manifested, BFEDCs are EEG finding of Benign Rolandic Epilepsy (BRE). The classic history is a child between the ages of 3-13 years who has a somatosensory aura around the face or hand with or without focal or generalized motor manifestations afterward. The seizures of BRE resolve spontaneously by adolescence, thus its “benign” designation. If the discharges are located in the occipital region, the clinical manifestations include visual alteration associated with headache and/or nausea or vomiting.

Benign Focal Epileptiform Discharges of Childhood (BFEDC) are most commonly seen in the centrotemporal region either unilaterally or bilaterally. In this average referential montage, a horizontal discharge dipole can be appreciated, with maximal surface positivity on the right at C4 and surface positive components at FP2 and F4. There is an independent discharging focus on the left at C3. BFEDCs are provoked by sleep, and may dissipate completely during wakefulness.

Focal Symptomatic Epilepsy Syndromes The interictal findings can manifest as slowing and sharp waves arising from a focal region of the brain. The most common symptomatic focal epilepsy syndrome involves the temporal lobe, specifically the mesial part of the temporal lobe, the hippocampus. Despite a clear clinical history the interictal EEG may remain normal. The clinical manifestations of temporal lobe epilepsy typically include an aura that may include a sensation in the abdomen, alteration in taste or smell, or a sense of fear. Loss of awareness typically follows with ipsilateral automatisms and contralateral dystonia. Should these findings or other focal findings be seen on an interictal EEG, further workup including imaging and treatment with medications most likely should be pursued.

The same focal epileptiform discharges in the right temporal lobe are shown in both of these examples, in a bipolar montage in the upper panel and an average reference montage in the lower panel. The discharges are maximal at F8 and T2, clearly set apart from the background, and are associated with after-going slow waves.

Ictal Recordings - cEEG

Ictal Recordings - EMU It is rare to capture a seizure during a routine EEG, because the study is a random sampling of someone who has paroxysmal events. For this is the reason, we tend to admit these patients to the hospital and reduce their medications in order to increase the chance of recording a typical event while they undergo prolonged monitoring with video and EEG to optimize the amount of information we can get about the seizures. Ictal patterns can vary widely. The rule of thumb is that a rhythmic pattern that varies in frequency, amplitude, and location is most likely a seizure. The onset of a seizure provides the most localizing information because it is most likely to represent the ictal onset zone. Any other focal pattern later in the seizure may simply represent a spread pattern. At the conclusion of an ideal neurophysiological evaluation the epileptogenic zone, symptomatogenic zone and the ictal onset zone should all overlap before we would consider them for a surgical resection.

Quantitative EEG Teaching the 6 EEG Spectrogram Patterns Using an Infographic | Neurology Education

Appendix 1: Approach to an EEG Report.

UNC EEG REPORT: {EEG title:29647}

Patient: @NAME@ Date of Birth: @DOB@ UNC MRN: @MRN@ Ordering Provider: @REFERPROV@ Identifiers: Patient and referring provider. If there is no referring provider, let staff know to manually fax the report.

Study Information Duration of the study has implications to the billing of the study. Date of Study: *** EEG Start: *** EEG End: ***

HISTORY: Per chart, @NAME@ is @AGE@ years old @SEX@ with ***

INDICATION: {eeg; indication for procedure:85577} History/Indication: a brief recapitulation that describes the clinical question that this EEG is meant to answer.

PATIENT STATE: {SML Patient State :74330}

PERTINENT MEDICATIONS: {seizure medications: 93165} The medications need to be documented because there are certain medications that can affect the EEG and may explain a particular finding, especially seizure medications.

TECHINCAL DESCRIPTION

Routine EEG was performed while awake utilizing 21 active electrodes placed according to the international 10-20 system. The study was recorded digitally with a bandpass of 1-70Hz and a sampling rate of 200Hz and was reviewed with the possibility of multiple reformatting. The first sentence describes the technical aspects of the EEG. It describes what electrodes were placed and if there were any technical difficulties. For example, patients who have just had a craniotomy, some electrodes need to be moved because of the incision.

EEG FINDINGS

The description of the EEG Findings should be detailed enough to allow another clinical neurophysiologist to picture the EEG without opening the study. Background: {UNC EEG background without sleep:110332} The next statement describes the general background of the patient. For a normal EEG we typically describe the normal organization and the posterior dominant rhythm and reactivity. The clinical state if the patient is not normal. Sleep: {UNC EEG Sleep:110331} What states were captured during the EEG as there are EEG findings that are seen predominantly during sleep. Describe the sleep transients that were observed and whether they were appropriate for stated age. Some findings occur during sleep.

Focal Features: There {Actions; were/were no:19617} focal slowing or interhemispheric asymmetries. Describe whether there are any focal features or epileptiform discharges. Location, frequency, morphology Epileptiform Activity: There {Actions; were/were no:19617} epileptiform abnormalities

Activating Procedures: {eeg hyperventilation:96586} {photo stim:96587} Activation procedures are also described such as hyperventilation or photic stimulation which may promote certain EEG findings. We restrict the use of hyperventilation in patients over the age of 70 and if they have cardiopulmonary disease, cerebrovascular disease or if they are pregnant.

Ictal Activity: {UNC ictal patterns:121894} Clinical Events: {UNC ictal patterns:121894} Single channel EKG: {Desc; regular/irreg:14544::"regular"} rhythm and normal rate

EEG SUMMARY

{Normal/Abnormal:58117} {PROCEDURE - EEG STATE:18081} EEG: For EEGs with any unusual or pathologic findings, the deliniates the EEG findings of interest

CLINICAL CORRELATION

This routine EEG is {normal/abnormal/---:49231}. There were no seizures or epileptiform activity. The clinical correlation draws together the history and EEG results for a clinical conclusion. {EEG comments:71738} It develops a clinical interpretation of those findings and their relationship to possible underlying disease states. Description of waveforms: Discharges: Localization: Focal: Field Generalized Diffuse Polarity (negative, positive or horizontal) Voltage Frequency Rare: < 1/hour Occasional >1/ hour but less than 1/min Frequent: > 1/min but less than 1/sec Morphology Sharp waves+/- slow wave Spikes Polyspike Activation: Hyperventilation Photic stimulation Accentuation with sleep Clinical correlation Context: Accompanied by slowing?

Slowing: Localization: Focal: Regional Hemispheric Diffuse Voltage: Very low: <20 microvolts Low: 20-49 microvolts Medium: 50-199 microvolts High: >200 microvolts Frequency: Theta or delta +/- superimposed faster frequencies Morphology: Polymorphic Monomorphic Continuity: Continuous Intermittent Reactivity: State changes Spontaneous Stimulation

INDEX

14 and 6 Positive Bursts 22 6 Hertz Phantom Spike Wave 23 60 cycle interference 36 alpha coma 42 alpha squeak 11 beta coma 43 benign epileptiform transients of sleep (BETS) 19 benign focal epileptiform discharges of childhood (BFEDC) 55, 56 benign rolandic epilepsy (BRE) 55 bipolar montage 4 breach rhythm 16 burst suppression 47 cardioballistogram 29 clectrocardiographic artifacts 28 childhood absence epilepsy (CAE) 51 Ciganek, central/midline theta rhythm 15 electroretinogram 27 encephalopathic patterns 39 electrocerebral inactivity (ECI) criteria and technical requirements 48 example 49 electrode pops 38 fast alpha variant 13 focal epilepsy syndromes 55 frontal intermittent rhythmic delta activity (FIRDA) 41 generalized periodic epileptiform discharges (GPEDs) 46 galvanic skin responses 34 glossokinetic artifact 33 hypnagogic hypersynchrony 6 hypsarrhythmia in Lennox Gastaut syndrome 54 interictal epileptiform patterns 50 juvenile myoclonic epilepsy (JME) 52 K-complexes 8 Lambda waves 17 lateral rectus spikes 31 Mu rhythm 14 muscle artifact 32 normal variants-table 25 ocular/eye movement artifact 26 photic stimulation 53 posterior dominant rhythm 2 posterior slow waves of youth 3 periodic discharges 45 periodic lateralized epileptiform discharges (PLEDs) 45 positive occipital sharp transients of sleep (POSTS) 18 pulse artifact 30 referential montage 6 rhythmic midtemporal theta of drowsiness (RMTD) 21 saw tooth waves 10 sleep REM 10 N1 5 N2 7 N3 9 sleep spindles 7 small sharp spikes (SSS) 19 spindle delta coma 44 slow alpha variant 12 sweat sway 34 temporal discharges 57 triphasic waves 40 vertex waves 6 wickets 20

References Beniczky S, Schomer DL. Electroencephalography: basic biophysical and technological aspects important for clinical applications. Epileptic Disord. 2020;22(6):697-715. doi:10.1684/epd.2020.1217

Peltola ME, Leitinger M, Halford JJ, et al. Routine and sleep EEG: Minimum recording standards of the International Federation of Clinical Neurophysiology and the International League Against Epilepsy. Clin Neurophysiol. 2023;147:108-120. doi:10.1016/j.clinph.2023.01.002

Nascimento FA, Jing J, Strowd R, et al. Competency-based EEG education: a list of "must-know" EEG findings for adult and child neurology residents. Competency-based EEG education: a list of “must-know” EEG findings for adult and child neurology residents. Epileptic Disord. 2022;24(5):979-982. doi:10.1684/epd.2022.1476

Marcinski Nascimento KJ, Westover MB, Nascimento FA. Teaching the 6 EEG Spectrogram Patterns Using an Infographic. Neurol Educ. 2024;3(4):e200158. Published 2024 Sep 25. doi:10.1212/NE9.0000000000200158

ACNSStandardizedCriticalCareEEGTerminology_rev2021.pdf ACNSNomenclature2021_ReferenceChart: _Présentation PowerPoint

Gaspard N, Hirsch LJ, LaRoche SM, Hahn CD, Westover MB; Critical Care EEG Monitoring Research Consortium. Interrater agreement for Critical Care EEG Terminology. Epilepsia. 2014;55(9):1366-1373. doi:10.1111/epi.12653 Interrater agreement for Critical Care EEG Terminology

Dhakar MB, Sheikh ZB, Desai M, et al. Developing a Standardized Approach to Grading the Level of Brain Dysfunction on EEG. 'J Clin Neurophysiol'. 2023;40(6):553-561. doi:10.1097/WNP.0000000000000919

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