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Sources & Resources

• wikipedia: https://en.wikipedia.org/wiki/Electroencephalography
• Rowan's
• Dr. Tatum's book
• EEG atlas
• AAN EEG course: https://tools.aan.com/education/webcme/index.cfm?event=neurolearn:info&PROGRAM_ID=52
• recommended by Dr. Shuster: https://www.amazon.com/Atlas-EEG-Patterns-John-Stern/dp/1451109636

Summary/Abstract/Intro

Welcome to the EEG Wiki! Following is introductory material on the basics of how EEGs work and how to read them!

To do

• remove any copyrighted material that may have persisted in the setup
• parse the notes into the skeleton sections
• incorporate more material from sources section
• find or generate free & open source EEG pictures
• ensure to NOT incorporate any copyrighted material

History

• 1929 - Hans Berger developed EEG with interest in elucidating physiology of emotion
• Late 1700s - Galvani's experiments with frogs demonstrating electrochemical nature of nerve transmission
• 1800s - Richard Caton - captured electrical activity in animals
• 1902 - Galvinometer and development of EKG

Basic Setups and Montages

basic conventions

• odd numbers on left, even on right
• Letters = LOBES (F=frontal, P=parietal, t=temporal, o=occipital, c=central)

Artifacts

Physiologic

• eye movement
• EKG
• pulse
• muscle

 * 15 Hz filters can help but a pitfall is that some amplitude can still pass and make normal background seem abnormal
 * better to have patient relax than use filters
 * subtypes: chewing, swallowing, glossokinetic

• respiratory - low frequency posterior-leads, lateralized if laying on side
• toothbrushing
• sweat artifact

Non-Physiologic

• electrode pop
• environmental:

 *power-line: 60 Hz
 *ventilator
 *IV drip
 *movement
 *touching jack box
 *phone ring

Activating Procedures

hyperventilation

• normally mild symmetric increase in amplitude & mild slowing that should resolve in ~1 min
• abnormal: may see e.g. asymmetry, induction of spike-wave discharges

photo stimulation

• normal driving response usually most prominent in intermediate frequencies
• lack of driving can be normal
• can induce photomyogenic response / artifact

 *time-locked muscle contractions

• photo-electric artifact (less latency vs. photomyogenic)
• abnormal: photoparoxysmal response

contraindications

• pregnancy: do not perform hyperventilation or photics
• do not perform hyperventilation with: stroke/tia, cardiopulmonary disease, sickle cell, inability to cooperate

Normal Sleep EEG

transition to drowsiness

• slowing PDR by ~1 Hz, attenuation of background amplitude, dropout of muscle artifacts/blinking, frontal beta may be more prominent, slow pendular rolling eye movements

stage I or N1

• POSTS, which can carry into stage II

surface positive (upgoing in T-O bipolar, down-going in O-Ref referential), upside-down checkmark morphology, bi-occipital and can have some degree of asymmetry

• vertex, carry into stage II - surface negative, maximal at vertex (consider using transverse montages for these), can be repetitive

stage II or N3

• K complex - midline phase-reversing slow wave, can be evoked with sounds
• sleep spindles - maximal fronto-central, symmetric, short bursts (usually half to few seconds), usually fusiform morphology
• continued POSTS & vertex (see above)

stage III or N2 or slow wave sleep

• 25-50% background delta activity
• no longer separate stage IV

REM sleep

• phasic eye movements
• muscle movement:

   * eye/respiratory muscle movement
   * brief phasic muscle twitches
   * otherwise continued atonia

• sawtooth: bursts, centrally, precede rapid eye movements

arousal responses

• typically fronto-central head regions
• can be rhythmic

below content yet to be parsed/filtered/edited

• Standard system of electrode placement is the 10-20 electrode system
  • 10 and 20% measurements are taken throughout the head, marked, electrodes glued. This is used internationally.
  • It is hard to correctly place the electrodes
  • A newer system exists, which is called 10-10 and uses 256 leads. Double-density recording, which can use tangential dipoles too. The principle is the same.
  • Nets are being developed for high-density recording, which are easy to place. They are saline soaked. The nets are easy to place, can be used at home for ambulatory monitoring, can be used in the ICU setting.

Normal EEG - Recording 23 - 7/12/2016 (http://eegatlas-online.com/index.php/en/)

http://socrates.mayo.edu/man-neuroeeg/adulteeg.html

• EEG later became one of the most abused tests in medicine and cause of much suffering.
  • Calling a normal EEG abnormal leads to unnecessary treatments and missed treatments of psychogenic problem
  • EEG remains a qualitative test, unless in the ICU setting with quantitative EEG
• All tissues in the body act as bioelectric generators
  • They have a positive end and a negative end, leading to electrochemical changes, allowing nerve conduction
• In EEG, we are trying to define in 2D what happens in the 3D brain. We predicate the interpretation on the principles of CNS electrical properties:
  • All nerve cells are polarized - Resting membrane potentials maintained by charge separation.
  • Causes polarity and electrical field effect
  • Understanding this separates pattern recognizer from a true EEGer
  • EEG has many patterns and variations that interfere and integrate with each other. These can be called abnormal incorrectly
• Most EEG is measured by a PERPENDICULAR DIPOLE - summation of small post-synaptic excitation potentials. These are LONGER than action potentials and summate in groups.
  • Summation of POOLS OF NEURONS - millions of neurons are required to generate a visible discharge. 10 cm2 is needed to be seen on a surface EEG
  • Small pools of neurons can-t be seen in surface EEG. These cannot be in a gyrus, cannot be deep. Otherwise you can-t see them on a surface EEG.
  • Direct cranial recording is much different, includes different principles. The appearance of the rhythms changes when there is no scalp.

• Flowsheet for determining a problem:
  • Electrodes are the number 1 problem site - This is the weakest interface
  • Electrodes-jackboxcablePCreader stationremote accessepileptologist
  • They think through this flowsheet to debug problems
• Polarity convention:
  • Relative negativity is the key notion here
  • G1 relatively more negative: Deflection is UP
  • G2 relatively more negative: Deflection is DOWN
  • Remember, IF G2 IS MORE NEGATIVE THAN G1, DEFLECTION IS DOWN
  • Note that it is the relative negativity that matters. The absolute values of the voltage could be positive or negative at either spot
  • The polarity convention helps us distinguish cerebral from extracerebral signals
• Montages:
  • Bipolar montage: Look for phase reversals at maximum electronegativity. Like a ripple effect. The smallest circle is at the center, then it spreads out like a wave.
  • Reference montage: Maximum negativity has the highest amplitude. Referential compares all sites to one point.
  • Finding the most negative site helps find location to place an intracranial recording grid or find places to perform surgery
  • Bipolar: Look for phase reversal
  • Referential: Look for absolute voltage
  • Also pay attention to the field effect. Does the area you are looking at have a believable field across several electrodes or does it only involve a single electrode?
  • The field of negative potential may be visualized by its appearance at adjacent electrodes, with a smooth fall-off at electrodes increasingly distant from an area of maximum electronegativity.
  • Polarity, localization, and field are important for deciding if something is normal or abnormal.
• Look at the background first, then the salient features. Use an orderly process.
  • Number one: Parameters of recording. Filter settings. Paper speed. Display speed.
    • Make sure you know if it-s standard or not.
  • Number two: Montage. State of the patient.
    • Suggest looking up the age and state. Then look at the EEG and develop an impression. Then look at the clinical information and adjust your impression if needed.
  • Number three: Frequency, voltage. Waveform montage. Polymorphic or monomorphic. How often is the thing we are looking at happening? Is it 3 in one second? Does it react? If 3 in one second in the right setting, such as an ICU patient, you might be seeing status.
  • Confirming your initial impression to the clinical history helps you develop skills.
• Frequencies:
  • Scalp EEG:
    • Alpha: 8-12 Hz
    • Beta: >12-30 Hz
    • Theta: >3.5-8
    • Delta: 3.5 Hz or less
  • More likely on intracranial EEG:
    • Gamma: >30
    • Ripples: 80-200
  • Fast ripples: 250 and up
  • Between one and thirty Hz is the bulk of what we see on scalp EEG (alpha through delta)
  • Intracranial EEG will have non-Berger bands - gamma, ripples, fast ripples
  • On intracranial EEG, the readings are a little different
• Standard EEG filter: 1 Hz to 70 Hz recorded, outside of that is removed
• General interpretation of the frequencies:
  • Alpha: Relaxed wakefulness in the posterior head region. Not necessarily occipital, because if you cut out the occipital lobe, it is still seen. It is a POSTERIOR, bihemispheric phenomenon.
    • Alpha rhythm is what we expect as the posterior rhythm in a relaxed awake pt
    • Alpha rhythm develops after age 3
    • Even after age 60, you still expect an alpha background rhythm. In the 7^th, 8^th, or 9^th decade a slower background is possible. However, in general, if you see less than 8Hz background in an adult awake patient, consider it abnormal.
    • In patients that have arrhythmias that undergo pacemaker placement, we actually see an improvement in the alpha rhythm. Having some type of arrhythmia seems to impact heart brain interaction.
    • In about 10% of people, alpha background can-t be found.
  • Alpha rhythm attenuates when the eyes are open. When you close the eyes, the alpha rhythm comes back. When you close the eyes, there may be a brief faster frequency, which can be called an alpha squeak.
  • Reactivity is absolutely key. Reactivity of the background is an important prognosticator of the ultimate outcome. If you stimulate and nothing happens, that is a poor background.
  • Modulation over time is a reflection of normal biorhythm.
  • Alpha starts in wakefulness, but it can persist in drowsiness. If you see vertical eye blink artifacts, you can think the patient is awake.
  • In drowsiness, you can see rhythms appear that are one half of the normal rhythms, which is referred to as subharmonics. So the frequency drops to theta range, but it actually is still an alpha rhythm.
    • To prove it is an alpha subharmonic, have them open their eyes and it should go away
    • The subharmonics happen with eye closure

Alpha activity: Refers to activity in the range of 8-13 Hz

Alpha rhythm: 8-13 Hz activity occurring during wakefulness over the posterior head regions, which is present when the eyes are closed and the patient relaxed, and which is attenuated by eye opening or alerting of the patient. The lower limit of alpha activity (8Hz) is reached by age 3 and progressively increases until 9-12 Hz reached by adolescence. 10% of adults have no alpha. A difference of greater than 1 Hz between hemispheres is significant.

Typical alpha rhythm amplitude is 20-60 microvolts. The alpha voltage is increased in younger children and adolescents, progressively decreasing with increasing age. Failure of the alpha rhythm to attenuate on one side with either eye opening or mental alerting indicates an abnormality on that side.

The following is an example of the posterior dominant alpha rhythm. See how the P-O lead turns into an alpha frequency when the eyes are closed. The rhythm disappears with eyes open (attenuates). The rhythm is reactive to eye opening.

The presence of a normal reactive posterior dominant rhythm is indicative of a well-functioning brain and automatically rules out all sorts of pathology. In a patient with altered mental status where the differential includes seizures, encephalopathy, or something psychogenic, the presence of a normal reactive PDR is a very strong argument against the first two.

The following is an example of alpha squeak. Just after eye closure, there is a brief period (one second ish?) during which the posterior dominant alpha rhythm may be higher in amplitude and in frequency than is otherwise the case. This phenomenon is known as alpha squeek. The frequency of the PDR should not be calculated during this period.

Slow alpha variant is a subharmonic pattern consisting of dicrotic or notched waveforms having a frequency of one half the resting alpha rhythm, usually in the range of 4-5 Hz, and which alternates or is mixed with the alpha activity. The following example shows a subharmonic of the posterior dominant rhythm, being half its frequency. Note how it goes away when eyes are open, proving it-s alpha subharmonic.

• To bring out the posterior dominant rhythm, techs will often ask the patients to close their eyes and relax. That is when you can see the normal posterior alpha or the alpha subharmonics. It is important to keep in mind that alpha frequency can be seen in alpha coma too.
  • Keep the patient-s overall state before you decide the alpha frequency is totally normal
  • The ultimate clinical outcome is based on cause
  • Lack of reactivity in general predicts a poor outcome
  • Alpha coma can be a manifestation of the subcortical/brainstem damage, releasing the cortex
• Intermittent photic stimulation at 10 Hz can bring out a supraharmonic alpha rhythm. It does not mean anything. It is not a seizure. It is not epileptic. It is a normal variant.

The fast alpha variant is a frequency which is twice the resting alpha and looks like beta activity, but occurs over the posterior head regions and reacts to eye opening. This is just like the alpha subharmonics mentioned earlier, just a faster version of a similar phenomenon. The fast alpha variant can be called a supraharmonic.

• Beta frequencies:
  • Beta is defined as >13 Hz.
  • These are usually activated rhythms by exposure to medication such as benzodiazepines, barbituates, anesthetics. CNS depressant drugs create beta frequencies.
  • Very low amplitude alphas, less than 15 microvolts for an adult, is considered abnormal. With beta frequencies, the amplitude is not interpreted as much.
  • When you have a breach of the skull due to a procedure, you can also see beta frequencies, typically in the 14-18 Hz range.
  • Think of faster diffuse frequencies being caused by drugs.
  • Think of slower faster frequencies being caused by breach.

• Mu rhythm: Can be unilateral and be mistaken for epileptiform discharges because they can be 20-70 msec, stand out of the background. You can differentiate them using their location. Mu is found in the center of the head. The mu rhythm is reactive to contralateral, ipsilateral movement. It reacts to thought of movement too.

The mu rhythm (has also been called precentral alpha or rolandic alpha) is present in 19-34% of individuals. Consists of arch-shaped waveforms, which occur unilaterally or bilaterally over the central regions. Appears to be related to function of the sensorimotor cortex, attenuated by active or passive movement of the extremities, thought of movement, or tactile stimuli. It can occur in an asymmetric fashion. It can be striking if there is an overlying skull defect.

• Theta: Can be normal or abnormal. Theta is activity >4 and less than 8 Hz. Theta can be normal in a younger population, when it is low amplitude and has a fronto-central field. Has been associated with concentration and meditation. Buddhist monks having training/meditation sessions can go into these rhythms. However, when you see theta diffusely, it is typically indicative of abnormality. Diffuse theta is non-specific.
  • Theta in the most awake state is abnormal
  • Can be seen in sleep-deprived individuals
• Always try to make an EEG normal until you can-t. The greatest misjustice is to call a normal result abnormal. 50 subsequent normal EEGs does not take it away.

Theta rhythm occurs as a normal rhythm during drowsiness. In young children, this occurs with a predominance over the fronto-central regions during drowsiness between ages of 4 months to 8 years of age. In adolescents, sinusoidal theta activity can occur over the anterior head regions during drowsiness. In adults, theta can occur diffusely or over the posterior head regions during drowsiness. Single transient theta waveforms or mixed alpha-theta waves can be present over the temporal regions in older adults.

• Lambda waves: Sharp waves that stand out from the background. They are found in the occipital head region. They are normal. LAMBDA WAVES INDICATE POSITIVITY IN G2 (THE OCCIPITAL LEAD)
  • Lambda is a POSITIVE occipital sharp transient, similar in appearance to a POST (seen in sleep), but found in an awake patient with eyes open as they focus on something visually
  • When you see lambda waves on an EEG, you can see eye movement from the frontal leads as well
  • Eye movements are picked up on the frontal part of the head.
  • When you see vertical eye blink artifact, you can almost always assume patient is awake
  • The lambda wave is an evoked potential. It is a normal finding.

The following is an example of a lambda wave. Looks a lot like POSTS. Surface positive. Bioccipital. Sharply contoured theta, usually higher amplitude than the posterior dominant rhythm. May be elicited by visual scanning of a complex or textured image; may be eliminated by placing a white sheet of paper in front of the individual.

Lambda waves are present over OCCIPITAL head regions when the subject is actively engaged in looking at something that arouses interest. The waveforms are monophasic or biphasic waveforms with the most prominent component being a SURFACE POSITIVE waveform over the occipital head regions. Typically 20-50 microvolt amplitude with a duration of 100-250 microseconds. These are more likely to be seen on scalp EEG if the subject is relaxed and interested in the image. Think of it as an evoked potential produced by shifts of images across the retina in the course of saccadic eye movements.

• Delta: Unlikely to be normal.
  • One exception is where there is delta mixed in with alpha in a young individual, called a posterior slow wave of youth. If the normal variant, goes away with eye opening.
  • Delta is less than 3.5 Hz
  • In a young patient, this can be a normal finding if it comes in mixed with alpha and then goes away with eye opening.
  • Buildup: A buildup of slow frequency high amplitude discharges, seen in hyperventilation. Can be seen in hypoglycemia.
• Normal sleep:
  • Drowsiness: Theta range like we talked about
  • N1 - intermixed theta, POSTs
  • N2 - Defining characteristic is spindles
  • N3 - Slow-wave sleep - delta sleep
  • REM sleep will have lateral eye movements, increased central theta
• Vertical eye blink artifact:
  • We see an EEG deflection in response to eye blink because the eye is a dipole
  • Cornea is more positive. Retina is more negative.
  • When you blink the eyes, the eye ball rolls up, which is called Bell-s phenomenon.
  • The Bell-s phenomenon is the reason we have vertical eye blink artifact:
    • The cornea is more positive than retina
    • When we blink, the cornea comes closer to the frontal leads
    • The frontal leads see the positive cornea coming close
    • If G1 is more positive compared to G2 (that is, G2 is relatively more negative), then the deflection is downward
    • As such, with positive cornea coming close to the frontal leads, a downward deflection is produced
  • We KNOW that cornea being positive MUST be producing the downward deflection with the eye blink because of the nature of the field effect.
    • For instance, say you see a downward deflection at Fp1 when there is a blink. In that setting, G1 is the cornea and Fp1 is G2.
    • A downward deflection means either cornea is positive OR Fp1 is negative
    • However, if Fp1 were negative, then when comparing Fp1 to say F3, you would ALSO see a positive deflection, producing a phase reversal. That does NOT happen. The only way that wouldn-t happen is if cornea is positive and there is no extra negativity in Fp1. The lack of a phase reversal within the scalp electrodes proves the discharge is due to something in the eye.

Hyperventilation: Hyperventilation in adults often produces little change in EEG. If there is a change, this usually consists of generalized slowing. Hyperventilation response may be gradual or abrupt onset of slow wave activity in the theta or delta range, which may continue as series of rhythmic slow waves or consist of repeated bursts of flow waves at irregular intervals. The degree of response depends on the vigor of hyperventilation, age, blood sugar levels, and posture. Response is more pronounced and more abrupt in children compared to adults. If one sees a marked buildup or early onset of slowing with hyperventilation, one should check and see when the patient last ate as relative hypoglycemia may potentiate slowing during hyperventilation.

Important note: Rhythmic fast activity such as those produced by drugs may be quite prominent, and when mixed with high-voltage smoother-contoured slow waves produced by hyperventilation, may look like a spike-and-wave-like waveform.

Contraindications to hyperventilate: Recent stroke, intracranial hemorrhage, significant cardiac or cerebrovascular disease, or respiratory dysfunction.

Photic stimulation: Complex waveforms may be produced with photic stimulation. Pay attention to the photic stimulation flash frequency. You can see halving of the flash frequencies with driving in the theta or delta range. You can also see doubling or tripling of the flash frequency. The driving can assume a spiky appearance. The following is an example of photic driving.

Drowsiness: In adults, drowsiness is often associated with slowing of the background, dropout of alpha activity, and attenuation of the background, or the occurrence of theta over the posterior regions. Bursts of moderate to high amplitude rhythmic theta can be present. Some admixed sharply contoured waveforms may be present over temporal regions, as well as wicket waves. This can be asymmetric.

During drowsiness there may be occurrence or persistence of alpha over temporal regions after the occipital alpha disappears.

Stage I sleep is also referred to as drowsiness or presleep and is the first or earliest stage of sleep. One of the most sensitive signs of drowsiness is the disappearance of mini eye blinks and the onset of slow eye movements.

Slow rolling eye movements: Usually the first evidence of drowsiness seen on EEG. Most often, these are horizontal movements, but can be vertical. They disappear in stage II and deeper sleep. Attenuation of the alpha rhythm typically occurs together with or nearby slow rolling eye movements. The following is an example of slow rolling eye movements in early sleep.

POSTs (Positive Occipital Sharp Transients of Sleep): Sharp-contoured surface-positive transients occurring singly or in trains of 4-5 Hz over the occipital head regions. These may have a similar appearance to the lambda waves during the awake record, but are of higher voltage and longer duration. POSTs are usually bilaterally synchronous, but may be asymmetric. Predominantly seen in drowsiness and light sleep. POSTs are: surface positive over occipital head regions, monophasic, can occur in trains of 4-5 Hz, and are bilateral.

POSTs start to occur in healthy people at age 4 years, become fairly common by 15, remain common through 35, and start to disappear by 50. They have a positive maximum at the occiput, are contoured sharply, and occur in EARLY SLEEP - stages 1 and 2. Their morphology has been described as a reverse check mark. The following is an example of POSTs.

Vertex Waves: Vertex sharp transients or V waves are almost universal. Just like the name implies, vertex waves are maximum at the VERTEX - CENTRAL MIDLINE (Cz). Amplitude 50-150 microvolts. Can be contoured sharply and occur in repetitive runs, especially in children. Can be seen in stage 1 and 2 sleep, but disappear in subsequent stages. They are narrower and more focal than K-complexes.

Vertex waves may have sharp or spiky appearance and attain high voltages in young adults. During the earlier stages of sleep, these may occur in asymmetric fashion. Sometimes trains or short repetitive series can occur. May be more blunted in older adults. This example has some vertex waves:

Hypnagogic hypersynchrony: Hypnagogic hypersynchrony (first described by Gibbs and Gibbs, 1950 [3] ) is a well-recognized normal variant of drowsiness in children aged 3 months to 13 years. This is described as paroxysmal bursts (3-5 Hz) of high-voltage (as high as 350 -V) sinusoidal waves, maximally expressed in the prefrontal-central areas, that brake after the cerebral activity amplitude drops during drowsiness.

Stage II is the predominant sleep stage during a normal night's sleep. The distinct and principal EEG criterion to establish stage II sleep is the appearance of sleep spindles or K complexes. The presence of sleep spindles is necessary and sufficient to define stage II sleep. Another characteristic finding of stage II sleep is the appearance of K complexes, but since K complexes are typically associated with a spindle, spindles are the defining features of stage II sleep. Except for slow rolling eye movements, all patterns described under stage I persist in stage II sleep.

Sleep spindles normally first appear in infants aged 6-8 weeks and are bilaterally asynchronous. These become well-formed spindles and bilaterally synchronous by the time the individual is aged 2 years. Sleep spindles have a frequency of 12-16 Hz (typically 14 Hz) and are maximal in the central region (vertex), although they occasionally predominate in the frontal regions. They occur in short bursts of waxing and waning spindlelike (fusiform) rhythmic activity. Typically occur every 5-15 seconds and last 0.5-1.5 seconds. More prolonged trains can be seen with benzos. Amplitude is usually 20-100 -V. Extreme spindles (described by Gibbs and Gibbs) are unusually high-voltage (100-400 -V) and prolonged (>20 s) spindles located over the frontal regions.

K complexes (initially described by Loomis) are high amplitude (>100 -V), broad (>200 ms), diphasic, and transient and are often associated with sleep spindles. Location is (central midline placement of electrodes [Cz] or frontal midline placement of electrodes [Fz]). They occur spontaneously and are elicited as an arousal response. They may have an association with blood pressure fluctuation during sleep.

The following shows typical sleep spindles with short-lived waxing and waning 15-Hz activity maximum in the frontocentral regions. Associated slow (theta) activity also characterizes stage II sleep.

The following is an example of a K complex, with its typical characteristics: high-amplitude, widespread, broad, diphasic slow transient with overriding spindle. On the longitudinal montage (left), the K complex appears to be generalized. However, the transverse montage clearly shows that the maximum (phase reversal) is at the midline (Fz and Cz). K complexes can be linked to an arousal response.

• The key difference between frequency and rhythm is reactivity. Alpha coma has alpha frequency, but does not have alpha rhythm, because it does not react.
• As you transition from awake to drowsy, you have loss of vertical eye blink artifact, loss of muscle artifact, more of a diffuse anterior spread of the background, slow rolling eye movements.
• In transition to drowsy, you may see bursts of theta and delta called hypnogogic bursts. This is very common in young individuals and is normal.
  • When you see a burst like that, don-t immediately call it abnormal. Check to see if it just represents a state change.
  • Hypnogogic burst can be associated with a superimposed beta and can look very abnormal. You have to analyze it very carefully.
• In awakening, you can similarly see a burst of theta. This is a hypnopompic burst on awakening.
• Occipital sharp waves seen in wakefulness while patient is looking at a complex image are called lambda waves.
• Occipital sharp waves seen in sleep are called POSTs and indicate N1 sleep. The lambda and POSTs are similar in appearance, but are seen in different states.
• Be suspicious of a lesion on the side of the brain that does not have the typical sleep changes.
• Vertex sharp transients are seen in the midline. Transverse montage helps visualize these better. Normal phenomenon, signify N1 sleep.
• Calling it N2 sleep requires sleep spindles to be present. Sleep spindles are found in the center of the head.
• N3 and N4 sleep are together called just N3 sleep now. This is theta and delta activity.
• Mittens: Superimposition of frequencies. One thumb and mitten for the other fingers.

Mittens: Variant of sleep activity consisting of a fast and slow-wave component, which resembles a mitten with the thumb formed by the last wave of a slow spindle wave, which is followed by a V-wave. This occurs in bilaterally synchronous fashion over the fronto-central regions.

REM sleep: REM sleep normally is not seen on routine EEGs, because the normal latency to REM sleep (100 min) is well beyond the duration of routine EEG recordings (approximately 20-30 min). The appearance of REM sleep during a routine EEG is referred to as sleep-onset REM period (SOREMP) and is considered an abnormality. While not observed on routine EEG, REM sleep commonly is seen during prolonged (>24 h) EEG monitoring.

During REM sleep, the EEG shows a low-voltage pattern which has some similarities with an awake pattern when the eyes are open. In addition, saw-toothed waves are intermittently present in the frontal and central leads before, during, or after rapid eye movements. The main distinguishing feature is the intermittent occurrence of rapid eye movements, which are seen in lateral frontal leads.

The following is rapid eye movement sleep with rapid (saccadic) eye movements. While muscle "atonia" cannot be proven without a dedicated electromyogram (EMG) channel, certainly EMG artifact is absent with a "quiet" recording. Also, no alpha rhythm is present that would suggest wakefulness.

• Lateral rectus spikes: Normal motor units generated by the lateral rectus. Can be seen in REM sleep.

• Spike: 20-70 msec duration
• Sharp wave: 70-200 msec duration
• Calling something a spike or a sharp wave does not say anything about whether something is abnormal.
• Lambda waves are due to eye movements, focusing on a complex image.
• Vertical eye blink artifacts are seen throughout the routine EEG in an awake patient.
• Horizontal eye movements can be determined via frontal electrodes
  • Cornea is positive
  • If you look up, deflection produced is down
  • If you look left, there is a positive phase reversal at F7, which is left frontal lead and you also have a negative phase reversal at F8

The eye is an electric dipole, with an anterior positive charge and posterior negative charge. During a normal eye blink, the eyes look upwards, creating a positive charge at the anterior frontal leads. This movement is known as Bell's phenomenon.

The following is EMG artifact from the lateral rectus muscle ipsilateral to the direction of movement . There is positive potential ipsilateral to the direction of eye movement . There is negative potential contralateral to the direction of eye movement. The eye is an electric dipole, with an anterior positive (cornea) charge and posterior negative charge. When the eye moves towards (away from) an electrode, a positive (negative) voltage field is generated at that electrode.

• Normal variants: Most normal variants go away in sleep.
• Older people have Wicket spikes and SRIDA - very commonly misinterpreted as abnormal.
• Rhythmic midtemporal theta of drowsiness: Rounded, notched, or sharp. When sharp and temporal, they can look like temporal sharp waves and can be misdiagnosed as abnormal.

Rhythmic mid-temporal theta of drowsiness RMTTD: These are MIDTEMPORAL, unilateral, bisynchronous, or bilaterally independent discharges. They consist of THETA frequency bursts lasting 1-10 seconds. Notched, flat topped, or sharply contoured. Amplitude is medium to high.

RMTTD waves can have a flat-topped or notched appearance. Rhythmic appearance occurs as a result of the combination of two or more different frequencies in the alpha and theta range. The bursts occur predominantly over temporal regions, but may be reflected in adjacent parasagittal regions. Do not confuse RMTTD with a seizure. RMTTD has a MONOMORPHIC pattern which does NOT evolve into other frequencies or waveforms. Present during RELAXED WAKEFULNESS OR DROWSINESS, primarily seen in adolescent and adult age group with an incidence of 0.5%.

• RMTD-like pattern has been described in the central region, which is also non-epileptic. There have been similar waves described in the parietal region, again a normal variant with no significance for epilepsy.
• 14 and 6 Hz positive spikes: A 14 Hz and 6 Hz discharge can be seen. 14 is more common. Called positive spikes, because they have accompanying positive phase reversals. This can be seen with Benadryl, hepatic encephalopathy, uremia, systemic illness. This is however a normal variant. Cetenoids is another name for it. Again, a normal variant that shouldn-t be confused with epileptic discharge.

14 and 6Hz Positive Spike Bursts: Associated with a variety of symptoms in the past, including headache, dizziness, vertigo, abdominal complaints. Normative studies however, showed that the pattern occurs in a NORMAL population, typically 12-20 years of age. These occur in DROWSINESS and LIGHT SLEEP, consisting of negative arciform waveforms with alternating positive spiky components. They are best seen on referential montages and have a maximal amplitude over the posterior temporal region. The bursts occur at a rate of 14 Hz or 6-7 Hz, ranging from 0.5 to 1 second. Usually independently over two hemispheres.

14 and 6 Hz positive spike bursts: Sharp positive component, rounded negative component . Predominantly in light sleep . Runs usually less than 2 seconds . Posterior temporal, unilaterally or bilaterally. Medium amplitude: 20-60 uV . Seen predominantly in adolescents, especially age 13-14 years, although it can be seen at any age . 6-Hz positive spikes: predominate in children < 1 year and adults > 40 years . 14-Hz positive spikes: predominate or combine with 6-Hz spikes in other age groups.

The images show the 14 & 6 positive spike bursts. Referential montage. The spikes point down because T6 is positive, making A2 more negative. If A2 (G2 in this instance) is relatively more negative compared to T6 (which is positive here), the deflection will be down.

• 6 Hz spike and wave: John Hughes described two variants of this, which were called WHAM and FOLD. WHAM is waking high amplitude in males and frontal predominant. WHAM does have a higher association with epilepsy, especially genetic generalized epilepsy. FOLD is female occipital low-amplitude in drowsiness, which is less-associated with epilepsy.

6 Hz spike and wave: The pattern has also been called the phantom spike and wave because the brief low amplitude spike is less prominent than the higher amplitude and more widely distributed slow-wave component. At times it may be difficult to detect the spike. The 6 Hz spike and wave consists of brief bursts or serial trains of spike and wave discharges having a repetition rate ranging from 5-7 Hz but usually occurring at a frequency of 6 Hz. The bursts usually last less than 1-2 seconds in duration. The benign 6 Hz spike and wave pattern is seen in adolescents and adults with an overall incidence of 2.5%. Occurs mainly during relaxed wakefulness and drowsiness and disappears during deeper levels of sleep, and this may be another helpful way of making the distinction between the benign 6 Hz spike and wave pattern and a more significant epileptogenic spike and wave discharge

The discharges usually occur in a bilaterally synchronous and diffuse manner. On occasion the bursts occur in a more asymmetric fashion or predominate over the anterior and posterior head regions. Hughes has used the acronyms of FOLD and WHAM to describe two different variants:

FOLD=Female, Occipital Predominance, Low Amplitude Drowsiness to characterize the more benign variants of 6 Hz spike and wave bursts.

WHAM=Wake, High Amplitude Anterior Predominance, and Male to describe the second form of 6 Hz spike and wave bursts which may overlap with more potentially epileptogenic spike and wave discharges. More likely to be assoc with seizures if the frontally dominant spikes are high in amplitude and repetition rate is slower than 5-6 Hz, and the spike/wave discharges present during deeper sleep.

• Small sharp spikes: Disappear in N3 sleep.

Small sharp spikes: Small Sharp Spikes (SSS) is the term given by Gibbs to the waveform. These have also been referred to as Benign Sporadic Sleep Spikes (BSSS) (View Image) or Benign Epileptiform Transients (BETS). SSS are usually of low voltage (50 microvolts) and are of short duration (<50 msec).

Usually SSS are monophasic or diphasic spikes with steep ascending and descending limbs. The SSS may have a single after-coming slow-wave component, but they do not distort the background nor are they associated with rhythmic slow-wave activity as are temporal sharp waves. The SSS occur mainly during drowsiness and light sleep in the adult age group. The incidence in normal control or asymptomatic subjects has been reported as 25%.

They are widespread but best seen in temporal and ear leads and, provided enough recording is obtained, almost always have a bilateral representation, occurring either independently or synchronously over the two hemispheres.

Ways of distinguishing small sharp spikes from more pathologic temporal spike or sharp wave discharges include the: Morphology of the waveform. Brief duration and low amplitude of the SSS. Lack of a disturbance of the background or associated focal abnormality in the EEG. Bilateral occurrence of SSS. Have a steep descending limb. Disappear during deeper levels of sleep

Key features: Occur in stage 1 or 2 NREM sleep. Usually monophasic, occasionally diphasic. Temporal with broad field of distribution. There is typically no disturbance of the background, although there is sometimes a single aftergoing slow wave. Typically less than 50 mV, less than 50 msec

• As you have seen, most of these benign variants occur in the temporal region, where they are misinterpreted. Wickets are another example of temporal discharges that can be confused with pathologic discharges.
• Wicket waves are typically in alpha frequency. Wickets typically run in bursts, but can be isolated. They are bilateral if you record long enough, but typically asynchronous, occur on one side and then the other. This is the number one thing confused as epileptic discharges.

Wickets: Single spike-like waveforms or trains or clusters of monophasic waveforms. Frequency of 6-11 Hz and amplitude from 60-200 microvolts. Can be mistaken for a temporal spike or discharge. However, wickets are not accompanied by a distortion of the background or a significant after-coming slow wave component. Wicket spikes are mainly seen in older adults. They occur in drowsiness and light sleep. They become apparent when the alpha and other awake patterns drop out. Wicket spikes are present over temporal regions, occurring bilaterally or independently over the two temporal regions, and they occur more frequently on the left side.

• SREDA: Two forms exist. One can be central at Cz. More typical is posterior temporal, seen in hyperventilation, build up. Bilateral. No post-ictal state. Triggered by hyperventilation. Seen more commonly in older individuals. This is a rare variant. Evolving theta frequency after a periodic sharp wave, triggered by hyperventilation.

SREDA (Subclinical Rhythmic Electrographic Discharge of Adults): Rhythmic pattern that is seen in the adult age group. SREDA may occur at rest but often is seen during hyperventilation and consists of a mixture of frequencies, often predominating in the theta frequency range.

The rhythmic pattern may range from 20 seconds to a few minutes in duration with an average duration of a burst being 40-80 seconds. Although widespread in its distribution, the activity is often maximal over the parieto-posterior temporal regions. At times SREDA may occur in a more focal or asymmetric fashion. SREDA may have an abrupt onset in which the resting record is suddenly replaced by repetitive monophasic sharp waveforms or the discharge may begin with a single, high voltage, monophasic sharp or slow-wave component which is followed one to several seconds later by other sharp waves, progressively reoccurring at shorter intervals and then merging into a sustained, rhythmic, sinusoidal pattern of 5-7 Hz.

Although the pattern looks like a subclinical EEG seizure discharge, it does not correlate with clinical seizures, and the patient does not complain of any signs or symptoms when the pattern is present. Although the mechanism of the pattern is unclear, it appears to represent a benign EEG phenomena which is of little diagnostic significance.

Key features: Abrupt onset and termination, unlike seizures which evolve. Rhythmic, sharply contoured theta. 5-6 Hz. Duration: 20 sec to minutes. Widespread or bilateral, maximal posteriorly. At rest or in drowsiness.

Pitfalls in EEG - Last lecture from 7/12/2016:

• Psychogenic non-epileptic event: Formerly known as psuedoseizures. The sample video showed a flashing light followed by the patient having a spell. The trigger of light shows suggestability.
• We stopped using the pseudoseizure term. Psychogenic nonepileptic event has been used more recently. Diagnostic error in these is common.
• Some clues: Out of phase movements in different limbs. Suggestability.
• In epilepsy, the eye is driven to the opposite side by frontal eye fields.
• The head is driven to a side by contralateral supplementary and premotor cortex.
• Huge numbers of patients with psychogenic attacks are diagnosed as epilepsy. Commonly in the setting of a misread EEG. The treatments can do significant harm to these patients. Steven-Johnson syndrome, neural tube defects are all important issues.
• Fear of missing the diagnosis of epilepsy is a fallacy in epilepsy. The harm of treatment often far exceeds the harm from missed epilepsy. If someone comes with a known diagnosis of epilepsy, it is hard to question it and get people off medications. Have confidence in the clinical history.
• Many EEGs are done each year. Quite a few are misdiagnosed.
• Reasons for misdiagnosis:
  • Fear of missing the diagnosis of epilepsy, which may lead to death
    • However, the truth is that most patients don-t die. Even chronic epileptics have a 1 in 50 chance of death, in the setting of many treatments not working.
    • Do everything you can before you diagnose people with epilepsy. Use smart phone videos. Most of the people that bring a video appears to be psychogenic.
    • History and physical is about 90% sensitive for real epilepsy.
    • Specificity of the smart phone is good when you look at psychogenic spells.
• When you see somebody and you are not sure, future EHRs will include videos as well as EEGs, which can be reviewed and reconsidered
• Sample case: A patient had a fall. She had head injury. They performed an EEG and called P3 and P4 spikes. Parietal lobe spikes are very rare on scalp EEG. If you see a report with P3 spikes, beware. The patient was diagnosed with a seizure disorder. As it turned out, the filter setting was at 15 Hz. Normal filters are less than 1 Hz and more than 70 Hz. Once you removed the 15 Hz filter, the discharge was clearly a myogenic artifact. The interpreter did not pay attention and called it a pathologic spike. The patient continued to have spells. Another EEG got done and they read T3 and T5 spikes. They added a second drug, sent the patient to an EMU. Patient ended up getting implanted with a vagus nerve stimulator. As it turned out, the temporal sharps were wicket waves. Seen in temporal, drowsiness. She sued the hotel chain and got 6 million dollars.
• A pediatric neurologist overtreating children. He thought 14 and 6 Hz spikes were epileptic discharges. There was a huge settlement for this.
• Remember that calling something normal, nothing is going to go wrong. Normal EEG does not rule out subclinical seizures from a deeper EEG. As such, the clinician will take over and make the decision based on their history and physical anyway.
• Calling an EEG normal is likely to do less harm.

Series of EEG Lectures from 7/19/2016 - Includes multiple talks by Dr. Tatum and one by Dr. Freeman

Recording 27 - Dr. Tatum Lecture - Seizures and Epilepsy:

• Within seizures, there is an electroclinical diagnosis that requires knowledge about semiology.
• Top 3 chronic neurologic diagnoses: Stroke, dementia, epilepsy
• Non-epileptic events are more common than autism, Parkinson disease, multiple sclerosis, trigeminal neuralgia
• Often epilepsy is a clinical diagnosis, but EEG helps. Structural brain MRI can be helpful as well, especially in frontal lobe epilepsy.
• Gamma frequency >30 Hz. Ripple is even faster. Fast ripples 250 Hz and above.
  • These may be a marker for epileptogenicity
• The goal is no seizures and no side effects
  • Epileptologists are most likely to identify no seizures as the goal
  • General practitioners considered that less of an overall goal
• We use EEG, but it supports our clinical diagnosis
• When we look at recordings for first-time seizure patients, most of them come back with a normal EEG.
  • 29-55% of patients can have a normal EEG after their first seizure
  • Tell people that most of the time it will come back as normal
  • If the first EEG is normal, then you can consider sleep EEG
  • You can also do video monitoring if needed
• 1.9-3.5% of normal people can have an abnormal discharge
• When you see a true epileptiform discharge though, then you become concerned that seizures might be very subtle and avoid detection by the patient.
  • Older patients with subtle findings and without awareness - fairly common scenario for epilepsy that can go unrecognized for a long time
  • In the older patient group, there is more jerking
  • In older life, patients are less aware of the episodes. He caretakers are often unaware too. There is just less attention paid compared to infants.
• Frontal lobe epilepsy is the second most common type of epilepsy. 30 percent of patients with this do not have epileptiform discharges on their EEG on repeat tracings.
• Temporal lobe epilepsy coming from the hippocampus can likewise be undetectable on the scalp EEG, though easily identified on intracranial epilepsy.
• Video monitoring is extremely useful in settings we can-t get data from scalp EEG alone.
• For video monitoring, we need to have a patient. A caregiver is helpful, but not mandatory.
  • The caregiver may click the button many times with nothing going on in EEG. This helps identify an overly vigilant caregiver
• Differential diagnosis for epilepsy
  • Psychogenic non-epileptic events
  • Psychophysiologic changes - someone that may have epilepsy presents with an aura, then they blow it up into something bigger. We can only identify this with monitoring.
  • Cardiovascular
  • Migraine
  • TIA
  • Sleep disorder
  • Movement disorder - In particular, non-epileptic myoclonus may be confused
• Sometimes even when we look at the video of the event, it is very hard to know what we are seeing. If you watch it long enough, sometimes it might be enough.
• Clinical history is good, but sometimes it is hard to tease apart the psychogenic spells and the simple partial seizures. Clinical assessment is good at telling -it sounds like a seizure-
• Psychogenic non-epileptic spells (or attacks):
  • Video EEG is the gold standard for diagnosis
  • Behavior plus a normal or baseline EEG without a change  diagnosis made
  • These used to be called pseudoseizures, but patients did not like that term. Psychogenic non-epileptic attack is the most preferred term. It gets confusing if you call them psychogenic non-epileptic seizures.
  • Calling them psychogenic non-epileptic attacks provides more clarity, puts a diagnosis on the entity, and avoids confusion.
  • There can be a 7-10 year delay to diagnosis. Patients often come in for EMU stay as a last hope. They stay on medications.
  • More common in women, in the third decade
  • No leg movement, extensor flexion movement, opposite of agonist/antagonist movement in real seizures.
• 3-4% with psychogenic non-epileptic attacks do have epilepsy. Official number in literature is 2%. These are very rare.
• Psychogenic attacks commonly have a component of suggestability too
• In a real seizure, more common to have eyes open and have an agonist/antagonist movement
• In the clinic, show the patient and family variations of the movements. This can help us understand what they are seeing. You can even ask the patient or family to mimic it. The patient and family may not be able to verbalize it, but may be able to show it very well. Video is especially helpful since verbal descriptions are difficult.
• In psychogenic non-epileptic attacks: Depression, anxiety, PTSD. In children bullying, academic stressors can be contributing. Depression is the most common, PTSD is also common. There may be different techniques and treatments for different types of attacks. For instance, if PTSD is the problem, eye movement desensitization can be a good technique.
• Wicket waves: Brief burst of activity, bilateral, seen in drowsiness. Temporal localization. Many people do not recognize these.
• Muscle artifact - myogenic spikes can be seen in the context of photic stimulation
• Epilepsy:
  • All ages
  • Occurs out of sleep - if it occurs directly out of sleep, think seizure
  • Durations are brief
  • Post-ictal state - critical in separating from syncope
  • STEREOTYPY: The same thing happens every time. EXACTLY the same.
  • No suggestability
  • Tongue bite can be very specific on the side of the tongue
• In contrast, the psychogenic events tend to have suggestability. Even if they occur out of sleep, they may be in pseudosleep, which you can figure out by EEG.
  • If there is a psychogenic attack, the tongue bite or lip bite is on the front
  • Look for lateral head movements
  • Look for asynchronous hand movements
  • Look for starting and stopping activity
  • Look for lack of post-ictal state
  • Out of phase movements
• Activation is a very important and helpful process. Some think this is unethical, but if you can trigger the episode and then record it, showing suggestability, you can make a diagnosis.
  • If you capture the one event and they only have that one type of event, you are done
• Remember that the patient may not be able to receive the data in the way it is presented to them. If you deliver the information in the correct way, up to 15% never have another event.
  • Be clear about the diagnosis - tell them if you are not sure
  • If there is an axis 1 diagnosis, get psychiatry to help
  • Psychology - cognitive behavioral therapy tremendously helps
  • SSRIs may be less effective than 12 weeks of CBT
  • Putting SSRI and CBT together may be most helpful
  • Kids with psychogenic episodes tend to do great. Adults have a harder time.
  • It is important to tell them the spells may not go away immediately. Explain to them that as we wean you off the medication you don-t need, we will make sure nothing new is emerging. Taking the medication off in this setting is the right thing to do. Of course, the exception is when we are using a seizure medication with the goal of treating their psychiatric condition such as valproic acid for a bipolar patient.
• The goal of an EMU admission is to capture every single type of event they have. You can only comment on the events reproduced. Sometimes you capture several events that are non-epileptic, start a taper and then they seize. That also helps. You understand they had both types.
• Convulsive syncope is another entity crucial to know about. Can be brought out by rising. Patient has a syncopal episode, stiffens or jerks a few times.
  • In syncope, the EEG is FLAT
  • You can see a few jerks with this
• Be very conservative for new-onset seizures in the hospital, unless it is status.
• The percentage of people with psychogenic events with real epilepsy is a bit more than 2%, I think 3-6% per lecture notes.
• Like the EEG, MRI is not always going to show abnormality in real epilepsy. Tell people this as you order the test.
• Use the term anti-seizure drugs rather than anti-epileptic drugs. We are preventing seizures, we are not curing their epilepsy.
• Functional classification system:
  • Generalized
  • Multifocal
  • Hemispheric
  • Multilobar
  • Focal
• The functional classification is helpful in choosing treatment - keep it simple, think FOCAL or GENERALIZED. This will help you determine the course of treatment.
• Most of what we see in clinic is uncontrolled.
• Likelihood of first seizure going on to become epilepsy - it depends. General number we can quote is 21-45%.
  • However, if there is an abnormal MRI OR abnormal epileptiform EEG, then the risk is double. In the setting of abnormal MRI or EEG, you can give the diagnosis of epilepsy after first seizure
• Most common reason for failed treatment is misdiagnosis - using a focal seizure drug for generalized seizure WORSENS generalized epilepsy
  • Be sure to choose the right type of medicine for the right type of epilepsy
  • In status epilepticus, it is also important to use the right dose of medication
  • Lifestyle changes are very important
• Generalized epilepsies:
  • Absence
  • Myoclonic seizures
  • Tonic seizures
  • Clonic-tonic-clonic seizures
  • Semiologies are such that half of these people can have falsely lateralizing features. For instance, the head may turn a little to the side. You need the EEG to help figure out which one they have.
• 3 Hz spike and wave pattern is typical of absence seizures
  • There can be polyspike patterns just before the 3 Hz spike and wave begins
  • What makes a given episode a seizure rather than an interictal epileptiform discharge is TIME and INDIVIDUAL
  • 3 seconds is a cut off for this type. Clinical symptoms is also important.
• Remember that a lot of the interictal patterns are also seen as ictal discharges
• Polyspike and wave is a pattern seen in myoclonic seizures

3 Hz spike and wave: This consists of a stereotyped, generalized and bisynchronous, symmetric, 3 Hz spike and wave pattern. The discharges, although generalized, often have a maximal amplitude over the superior frontal regions.

There is often some variability in the typical pattern. Frequency is usually 3 Hz; however, at the beginning of a discharge, it may be faster, 4 Hz, and in the end, slower, at a rate of 2.5 Hz. Although usually symmetric, there may be some shifting minor asymmetries in the spike-and-wave complexes over homologous regions, and there may be double spikes associated with slow-wave complexes.

The pattern is enhanced by hyperventilation and hypoglycemia. The 3 Hz spike-and-wave discharges often occur in rhythmic serial trains. If the discharge lasts longer than 3-4 seconds in duration, then one usually sees some type of clinical accompaniment, staring, clonic movements, motor arrest, and unresponsiveness.

he interictal record is usually normal. However, 20% of patients with absence seizures may show the presence of rhythmic bisynchronous slow waves over the posterior head region. During sleep the discharges occur in a more fragmented and less sustained fashion and often consist of single spike and wave or multispike-and-wave discharges of varying complexity. The 3 Hz pattern is associated with absence (petit mal) seizures (95%). The pattern is most often seen in children between the ages of 3-15. The clinical seizures and EEG pattern often resolve spontaneously after adolescence. Usually children with absence seizures and 3 Hz spike-and-wave pattern are otherwise normal, mentally and neurologically, and usually do not have any underlying organic pathology.

Polyspike and wave: Generally epileptiform; usually seen in the context of JME, in which case you expect to find 4 Hz, generalized, bifrontally predominant polyspike and wave. However, focal onset epilepsy can sometimes fool you when there is rapid secondary bisynchrony. The first EEG below is from a patient with JME. A referential montage is showing polyspike and wave pattern that is generalized, byt is predominant in frontal areas.

The polyspike is a little easier to see in the example below. Pay attention to the first few seconds of the spike and wave - it would be easy to confuse that with the 3Hz pattern, but later into the recording, there are several clear polyspikes that come in.

• Sturge-Weber: Port wine stain needs to involve the V2 distribution to try to diagnose Sturge-Weber. These patients have EEG abnormalities, cognitive abnormality, seizures.
• When you look at an EEG, always consider:
  • Parameters of recording
  • Background
  • Most salient feature
• We are often not told the parameters of recording, but the standard settings are:
  • 1-70 Hz
  • 30 mm/sec paper speed
  • 7 microvolts/millimeter sensitivity
• Hypsarrrhythmia: High amplitude discharges. Areas that are slow. Some intermixed spike and wave. It is a very chaotic background.

Hypsarrhythmia is actually a multifocal pattern rather than a generalized and bisynchronous pattern. The term hypsarrhythmia was introduced by Gibbs and refers to a high amplitude arrhythmic pattern consisting of a chaotic admixture of continuous, generalized, high amplitude, multifocal spike-and-sharp-wave discharges and arrhythmic slow waves ("the scrambled-eggs pattern").

The hypsarhythmic pattern is mainly seen between the ages of four months and two years of age and reflects severe cerebral damage which has occurred in early infancy. It is a pattern characteristic of early childhood, reflecting an insult or disease process occurring at an early age. Hypsarrhythmia is rarely seen beyond four to five years of age.

Electrodecremental seizure patterns often occur in patients with hypsarrhythmia. This consists of a decrement in the ongoing activity and which consists of trains of low voltage fast activity at the onset of the decrement in the EEG. This may be preceded by a high amplitude sharp and/or slow wave complex. The electrodecremental pattern is often accompanied by infantile spasms but can occur without a clinical accompaniment, particularly if it occurs during sleep.

During sleep the hypsarrhythmic pattern can occur in an intermittent fashion and almost resembles a burst suppression pattern.

The hypsarrhythmic pattern is often associated with infantile spasms, which is sometimes referred to as West syndrome. The symptom complex is not a specific disease entity but reflects a severe cerebral insult or dysfunction occurring at an early age, usually before one year of age. In about 25% of the patients the cause is unknown. In the other patients this symptom complex may occur as a result of prenatal, perinatal or postnatal difficulties, encephalitis, congenital defects, tuberous sclerosis, or various biochemical or metabolic derangements that occur in the young child.

The patients often have frequent infantile spasms or myoclonic jerks. The myoclonic jerks are very brief, lasting less than a second, and consist of a sudden flexion of the head, body, and extremities. Often they are associated with generalized, high amplitude spike or spike-and-wave discharges in the EEG. True infantile spasms, on the other hand, are of longer duration and may last from 3-5 seconds. These often consist of tonic flexion of the neck, body, and legs with the arms extending forward and outward. The EEG accompaniment usually consists of an initial, high amplitude spike and/or slow wave, followed by an abrupt decrement or flattening of the EEG with low amplitude fast rhythms termed electrodecremental pattern. The infantile spasms can occur in clusters, particularly after arousal from sleep.

• Broad spectrum anti-seizure medications
  • Levetriacetam - Keppra
  • Lamictal
  • Depakote
• Side note: Potega is an anti-seizure drug that causes blue eyes, urinary retention, bluish skin discoloration. Also has 3 times of day dosing. Not used currently.
• Slow spike and wave: Dr. Tatum-s sample showed a burst of paroxysmal fast activity, generalized spike and wave, and then slow spike and wave. This looks like an encephalopathic generalized epilepsy, the most common type of which is Lennox-Gestaut. Seizure type going along with the slow spike and wave is also the most common type of seizure in Lennox-Gestaut syndrome, which is generalized tonic.

Slow spike and wave: This pattern has also been termed "sharp and slow wave complexes" as the duration of the spike component resembles more that of a sharp wave. The pattern consists of slow-spike-and-wave discharges occurring with a frequency of 1-2.5 Hz. Discharges may occur singly or in serial trains. The serial trains of slow-spike-and-wave discharges are often not associated with any apparent clinical accompaniment. However, if appropriate testing is done, there may be some type of subtle impairment of psychomotor performance.

The spike-and-wave pattern may have a variable distribution. At times it occurs in a generalized and symmetric fashion; on other occasions the discharges may be asymmetric and even have a shifting focal emphasis. The slow-spike-wave discharges tend to be accentuated during drowsiness and are less likely to be activated by hyperventilation, hypoglycemia, or photic stimulation. The interictal background in between the spike-and-wave bursts is often abnormal. This may consist of focal spikes, generalized and/or focal slowing, or asymmetry of background activity. During sleep the EEG may show the presence of generalized spikes and multispike-and-wave discharges or bursts of generalized, paroxysmal fast activity, reflecting serial spike discharges.

The seizures in these patients can be varied and usually consist of: Tonic seizures #1 most common, but also atypical absences, tonic-clonic seizures, akinetic seizures, myoclonic seizures

The slow-spike-and-wave pattern is most often seen between 2-6 years of age, but it may persist through adolescence. The slow spike and wave is of significance in that it usually occurs in patients with some type of underlying organic pathology and who have signs of cerebral damage.

Many patients with this pattern have: A severe convulsive disorder, poor response to anticonvulsants, Signs of mental and motor dysfunction, Slow-spike-and-wave pattern on the EEG. This constellation of clinical signs and EEG pattern has been referred to as the Lennox-Gastaut syndrome.

In contrast to the 3 Hz spike-and-wave pattern, the slow-spike-and-wave pattern is often associated with an abnormal background and is usually seen in patients with an organic disturbance of cerebral function and who have poorly controlled seizures. Therefore, this pattern has a poorer prognostic implication than the 3 Hz spike-and-wave pattern, which is usually associated with a normal interictal background and is seen in children with a benign seizure disorder and who are otherwise normal neurologically and mentally.

• Sample video showed a generalized TONIC seizure - very strongly suggests Lennox-Gestaut syndrome, especially if there are other seizure types. It CAN be focal epilepsy and have a midtemporal focus, but Lennox-Gestaut is much more common.
• Side note: Onfi is a more recently approved drug for L-G, but we actually use it for focal seizure
• In neonates, you have to go off label for pretty much everything.
• Lennox-Gestaut triad: Cognitive impairment. Slow spike and wave pattern on EEG. Multiple seizure types.
• HLA-B1502 - can be used to predict risk of Stevens-Johnson syndrome.
  • In Taiwan, they have modified approach to treatment, they avoid carbamazepine in these patients with the HLA
  • The reason is mortality rate is high in Steven Johnson syndrome
  • When they stopped carbamazepine, they started to use valproate
• Patient with atonic seizure - had high fever and status epilepticus at age 1. Then had cognitive impairment and multiple seizures. Test for SCN1A.
  • SCN1A has been associated with atonic seizures - sodium channel
• Patients may have full unawareness much of the time they are having seizures.
• Look for evidence of EVOLUTION when you decide something is a seizure. Look for spread in TIME AND SPACE - evolution over time and space helps confirm seizures.
• It may be interesting to do prolonged EEG on patients with dementia. It is easy to miss seizures in this population. We already know half the people are unaware of their seizures and they are more subtle in older people.
  • Important to recognize this in elderly as 2/3 would respond to ASD and improve
• Hippocampal sclerosis of epilepsy and Alzheimer disease are different. In epilepsy, CA1 and CA3 are involved. In dementia, it is a more global process. It would be interesting to know how many of those have seizures. Most common substrate for most human epilepsy is the hippocampus.
  • 70% of adults have focal epilepsy
  • 70% of those is temporal onset
  • 70% of those have hippocampal onset
  • Overlap is significant too - anxiety spells, dementia, epilepsy
  • One common way to separate them out is duration and clinical course. As you get to be more episodic, think anxiety and epilepsy. The epileptic episodes though last a lot shorter. Anxiety episodes tend to last much longer.
  • Shorter episode strongly argues for epilepsy
• Ask people if it-s like a lightswitch when there is an episode. If it hits you fast, you will think more readily as seizures.
• Focal seizure with or without impairment of awareness is the new term
• Focal seizure evolving into bilateral convulsion is also the new term
• Even if we know seizure happened in the setting of alcohol withdrawal, an epileptiform EEG diagnoses epilepsy. Remember that seizures can be alcohol precipitated.
• Focal epilepsy:
  • Lamictal and Keppra are good choices of medication, especially for a female. These are the least teratogenic drugs.
  • Carbamazepine and Oxcarbamazepine are possible choices, but less preferable as they are enzyme inducers and are much more likely to interact with oral contraceptives as well as other medications.
• Absence seizures: Ethosuximide is #1, valproic acid is #2, lamotrigine is #3
  • If you try all three and absence is still not controlled, you may need to reconsider
  • Test the patient for Glut-1 deficiency syndrome - they respond to KETOGENIC diet
  • So a resistant absence - consider Glut-1 deficiency, if you prove it, then ketogenic diet
• Sample video with eyes open, lip smacking. Stiff on right, automatisms on the left. This is LEFT TEMPORAL SEIZURE. Left temporal origin helps explain why she is not talking (aphasic during event).
• Focal epilepsy is more difficult to control for genetic generalized epilepsy
  • 2/3 respond for focal epilepsy
  • 85% respond for genetic generalized epilepsy
• Temporal epilepsy is the most common epilepsy
  • The most reliable predictor of lack of response is a temporal lobe lesion on MRI
  • When MRI is abnormal, they may not respond to medications and surgery can be considered for these people
  • They may respond well to surgery too
• Sample video with horrible screaming episode. This was real epilepsy.
  • Brief episode, post-ictal state  The two best reasons why it-s real seizure
  • This was a FRONTAL LOBE seizure - oligodendroglioma
  • After her surgery, the seizures went away
• Abrupt-onset, brief duration, spontaneous, accompanied by an impaired responsiveness and a post-ictal state are critical features. Stereotypical episodes also help tremendously.
• There is such a thing called pseudo-pseudo seizures - these look non-epileptic, but end up being epileptic. Be careful. Diligently look for stereotypy, abrupt onset, altered mentation, brief duration, and post-ictal confusion.
• Side note: Modified Atkins diet can work similar to the Ketogenic diet. It is a little easier to do.
• If you are up to three drugs and it-s not working, start thinking about other treatments like vagus nerve stimulators and surgery.
• A significant improvement in quality of life scores has been reported in the surgical group. Epilepsy surgery is effective.
• It can be difficult to separate frontal and temporal lobe epilepsies clinically. Frontal lobe epilepsy tends to be brief, bizarre, bimanual automatisms.
• Be careful when you are looking for zebras that we may simply be wrong.
  • Neurologists are wrong 15% of the time when they diagnose conversion disorder
  • Remember that EEGs may be normal in 10-15% of the time even with repeated recording. The more you sample, the more likely you are to catch an event
• Cortical dysplasia can cause seizures. MRI shows hyperintensity that follows the contours of the gyrus.
• Tuberous sclerosis complex is autosomal dominant.
• 30% of the time, frontal lobe seizures are accompanied by use of actual words - cursing.
• Important note: Seizure classification is a prerequisite to treatment of epilepsy. You need to have a sense for what you are treating. You have to have a sense for focal and generalized.
  • Of course, you can use a broad-spectrum drug, but there is the potential to use the wrong drug, which can actually make them worse
• Everything that shakes is not epilepsy

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