Your Summer Reading: Our Favorite Cases


Welcome from the Interest Section Chair 

My kids know that I share the sentiment of a certain little snowman about winter. I would much rather be in summer all-year-round.  There is something so beautiful about the crack of a baseball bat on a ball, laughing children, birds, owls, crickets and splashes in pools.  The beautiful blue fish was last spotted at an aquarium I visited on the first of many summer mini-family vacations.  I am a summer person.   

I hope you all are finding ways to refresh yourself this summer. Take this newsletter on your favorite electronic gadget out to your favorite tree with a cool drink and enjoy as we walk you through some of our favorite cases. This edition brings you puzzling, interesting or just plain fun cases in our careers as Neurodiagnostic Technologist. Please feel free to write in with your own! We’d love to hear them. Or better yet, write it up for our journal or step up to teaching at a platform talk! For ease of reading we’ve provided anchors to each section, in the case that you’re short on time and would like to jump to a section that peaks your interest the most.

Acute/Critical Care
Ambulatory Monitoring
Autonomic Testing
Clinical EEG
Epilepsy Monitoring
Intraoperative Neurophysiological Monitoring
Nerve Conduction Studies
Neurodiagnostic Education
New Technologies & Research
Pediatrics & Neonatology

Take care, enjoy the read and have a wonderful summer. Hope to hear about your adventures at the upcoming conference in New Orleans!


Petra Davidson, R. EEG/EP T., BS, FASET

Acute/Critical Care Neurodiagnostics 

By A. Todd Ham, R. EEG T., CLTM, BS 

Though other methods have emerged which are less-invasive and carry lower risk (though not necessarily a substantially improved accuracy), the Wada procedure continues to be actively administered at many hospitals as an effective, relatively-safe procedure for lateralizing hemispheric dominance in refractory epileptic surgical candidates (Wellmer et al. 2005).  The EEG occupies a prominent role in the Wada, providing real time insight into the functioning of the cortex, including the expected sequential electrocortical changes (beta, theta, delta, etc.) associated with the administration of sedative medication (Sharbrough et al. 1973) – in this case, hemispheric – such as amobarbital.  It is crucial that the neuropsychologist performing the language and memory tests has knowledge of electrocortical changes secondary to sedation and when the patient’s background has returned to baseline (i.e. the slowing has resolved).  This information appropriately regulates the progression through the sequence of language and memory testing including when to procede with memory recall.  For example, it is necessary to ensure the patient has returned to baseline before contrasting sedated responses to baseline ones.

The inclusion of quantitative EEG (QEEG) software may ease the burden of the somewhat subjective task of determining notable background responses to amobarbitol, including identifying when the background has resolved (Tu et al. 2014).  Trends such as the proprietary Rhythmicity Spectrogram designed by Persyst as well as frequency spectrograms visually describe such changes across time and space in a coherent, comprehensively-consolidated language. Figure 1 is a 1 hour QEEG epoch of a Wada test; electrocortical responses throughout the procedure’s duration are  encapsulated.  As the right hemisphere is sedated first, tangible background changes can be observed in the peak evolution (bottom trend), amplitude EEG (second to last trend), fast Fourier transform spectrogram (top two trends), Rhythmicity Spectrogram (third and fourth from top), and Asymmetry Relative Spectrogram (ARS) (third from bottom).  The acute appearance of dark red shading within the ARS aligns with the moment in time when the sedation was administered intravenously.  With respect to the ARS, a return to baseline can be expected after the relative color intensities (red = right, blue = left) and spatial (with respect to frequency spectrum, y-axis) distributions gradually return to the pre-sedation presentation.  Note that the other trends can also indicate baseline return within their respective display parameters.

Consistent with expected sequential changes secondary to sedative medication, beta frequencies are one of the first indicators of the right hemisphere’s exposure to the sedative (Figure 2).  An essentially-concurrent (trends epoch is compressed as it represents one hour of data) appearance of delta and theta band activities within the Rhythmicity Spectrogram is also visible.  A gradual upward trend in the theta, alpha frequency bands which are representative of the induced slowing can be observed within the fast Fourier spectrogram (upward-pointing arrow) as the sedative is metabolized (Figure 3).  The initial broad white shading within the delta band indicates a high proportion of delta activity as the sedation is introduced.  This band and its intensity decrease across time (downward-pointing arrow), again, as the sedative is metabolized.

Left hemispheric sedation is then easily identified via the asymmetry spectrogram and associated heavy shading of blue.  A similar multi-trend response can be appreciated (refer back to Figure 1).

Increasing the trends timebase can reveal subtle progressions in sequence of frequency changes.  Figure 4 A. – C. presents a magnified Rhythmicity Spectrogram along with the concurrent EEG tracing at discrete points during right hemispheric sedation.  In Figure 4 A. below, the EEG captured copious right hemispheric beta while the trend indicated that this frequency band was the initial electrocortical response to sedation.  

Figure 4 B. shows that the induced activities over the right hemisphere are prominently in the alpha and theta range which is supported by the EEG data at that time. 

Figure 4 C. (below) captures a further slowing of the right hemispheric background evidenced by the prominent frequency bands (most heavily-shaded) being in the delta range.

As Persyst can be viewed in real time, its use during the Wada test may reduce subjective determination of both deviation from and return to baseline (the EEG acquisition was terminated just prior to the left hemisphere returning to baseline).  Essentially, the advantages to incorporating QEEG in such circumstances align well with the familiar phrase “You can’t see the forest for the trees”.

Sharbrough, F., Messick, J., Sundt, Jr., T.  Correlation of Continuous Electroencephalograms with Cerebral Blood Flow Measurements During Carotid Endarterectomy.  Stroke (1973); 4; 674-683.

Tu, B., Assassi, N., Bazil, C., Hamberger, M., Hirsch.  Quantitative EEG Is an Objective, Sensitive, and Reliable Indicator of Transient Anesthetic Effects During Wada Tests.  J Clin Neurophysiol 2015; 32(2); 152-158.

Wellmer, J., Fernandez, G., Linke, D., Urbach, H., Elger, C., Kurthen, M.  Unilateral Intracarotid Amobarbital Procedure for Language Lateralization.  Epilepsia 2005; 46(11); 1764-1772.

Ambulatory Monitoring 

By Christine Blodgett, MA, R. EEG/EP T., CLTM, FASET

I am lucky enough to come across interesting case studies all of the time in Ambulatory EEG since my primary role is to review studies and write technical impressions.  Our patients are set-up at home for their comfort and convenience.  A push button event system is available to mark events on the EEG at the time of their occurrence and a patient event diary is utilized for the patient to describe their symptoms.

This is the case of a 15-year-old right-handed male patient with normal birth and development with a past medical history of episodes described as blanking out for 6-7 seconds.  These occur approximately once per month and sometimes multiple times in one day.  He mumbles during them and afterwards he feels dizzy, lightheaded and tired.  He is not currently taking any medications.  A 48-hour Ambulatory EEG was ordered to capture and classify these events.

The background appeared normal with a posterior dominant rhythm of 9-11 hertz.  No interictal epileptiform discharges or focal slowing was noted throughout the recording and the patient did not press the event marker or notate any abnormal symptoms for the duration of the test.

Awake with Eyes Closed
Awake with Eyes Closed
Stage 2 Sleep
Stage 2 Sleep

However, 2 electrographic events were detected upon review.  Both occurred out of sleep with an arousal followed by rhythmic theta slowing in the left temporal region most focal over the T3 and A1 electrodes which evolved into high-amplitude rhythmic sharp waves and delta slowing lasting up to 90 seconds in duration with post-ictal slowing on the left afterwards.  On camera, there was some movement in bed under a blanket, but no clear clinical semiology.

*In the interest of space, the following are NOT consecutive pages of EEG:

Beginning of Seizure
Beginning of Seizure
Middle of Seizure
Middle of Seizure
Post-Ictal Slowing on Left
Post-Ictal Slowing on Left

This was an interesting case for several reasons.  First, we captured electrographic events that indicate this patient is having seizures, but these were not documented by the patient or his family and were probably not the same as the events he was describing.  Despite not capturing the target events, we can be assured that he is having seizures and treatment can be started.  Perhaps additional monitoring may be beneficial to capture and classify all of his events and determine the frequency in which they are occurring.

Also, in full disclosure – these events were almost missed by the technologist.  In a standard bipolar montage, there was muscle artifact and slowing that could have been mistaken for an arousal from sleep upon first glance.  Luckily, it was suspicious enough that I stopped and took another look.  While reviewing in any montage other than one that includes the A1 (mastoid, in this case) electrode; I may not have recognized these as seizures.  Coincidentally, I had just recently had a conversation with one of our reading physicians who had stressed the importance of utilizing a montage with the A1 and A2 electrodes in cases of suspected temporal lobe epilepsy.  This great advice certainly ended up making a difference!

Another benefit was that the automated seizure detection software identified these two events as seizures.  This software often shows false positives and we can sometimes be conditioned to rely on our own manual review and dismiss the seizure detections which are often due to chewing, muscle or various other artifacts.  This record indicates that the automated seizure detections can definitely be worth taking a look at!  Overall, the idea is to take your time, review the study methodically and utilize all of the tools available to you to ensure an accurate technical impression.

Autonomic Testing

By Marcia Hawthorn, R. EEG T., CAP

I would like to start off with introducing myself.  My name is Marcia Hawthorne and I have been in Neurodiagnostics for six years at Penn State Hershey Medical Center.  I am currently registered in EEG and certified in Autonomic Testing.  Currently, I am working on my certification in Long Term Monitoring and hope to accomplish that by the end of the year.  In August, I will have the privilege of presenting a paper at the ASET conference and am really looking forward to that.

I had the pleasure of participating in an Autonomic Workshop this past year, which really opened my eyes to the importance of technician and physician education in the Autonomic Lab to ensure accurate results.  Learning about the baroreceptor reflex was very helpful in performing the Valsalva Maneuver appropriately.   When performing Valsalva, explaining to your patients what is being done and how the test works is extremely beneficial.  The baroreceptor reflex (mechanisms that helps to maintain blood pressure at nearly constant levels) is located in the neck.  If a patient moves his head during or within the 30 seconds after the Valsalva Maneuver, he can actually inhibit this reflex which in turn gives inaccurate results.  Explaining to the patient how important it is to keep the head relaxed and still during this test is crucial in determining adrenergic function accurately.

Clinical EEG 

By Vicki L. Sexton, R. EEG/EP T., R.NCS. T., CNCT, CLTM, FASET

My interesting case study is about education.  A few years back while sitting on the ASET Board of Trustees, we happened to be talking about the book “Brain on Fire” and Anti-NMDAR encephalitis.  This disease was discovered at the place where I use to work, and I remember the first cases we saw and the EEGs that went with it, which typically showed at pattern coined Extreme Delta Brush.

Faye McNall, who is the Director for Education at ASET, asked me to do a poster on the disease because she found it very interesting.  A month later she asked if I could also do a talk on it, and I agreed.

In 2015, in Weston, Florida, I gave my first speech in front of around 100 people. I was very nervous and thought, “no one wants to hear me speak”.  When I finished my talk everyone was genuinely interested and had a lot of questions.  I also had at least two people in the crowd tell me that they, too, had a patient whose EEG showed the Extreme Delta Brush pattern and that the diagnosis was unknown.  I said to them, “Now that you have invested the time and your resources coming to the ASET Annual Conference, you will now be able to go back to your team, let them know about anti-NMDAR encephalitis, for which the patient might be tested and treated. You just might save their life!”

So, for all who think that it is a waste of time going to the annual or even local conferences, not only will you learn something new, get your continuing educational credits, but you might just save someone’s life. Isn’t that worth the trip?!

Epilepsy Monitoring  

By Magdalena Warzecha, R. EEG/EP T., CLTM

Right handed male in his fifties, with history of spells characterized by feeling of confusion, head rush, followed by dizziness. Patient was seen looking pale, arms and legs trembling, but did not report loss of awareness. Episodes of confusion lasted up to 45 seconds, but dizziness and head rush persisted for up to an hour after the spell.

At the onset of spells – three years ago, they occurred every 6-8 weeks. Recently, he reported new types of symptoms: spells of disorientation and confusion were now sometimes followed by loss of consciousness.  He would experience both types of spells, with and without loss of consciousness, always occurring while sitting in upright position. Frequency of episodes increased to 2-4 spells per month with and without loss of awareness. In addition, he reports having daily spells of disorientation for a few seconds at a time.

Patient had no family history of seizures, or head injury, but was positive for psychological trauma in childhood and adolescence. MRI and CT scan were both normal. He was evaluated by cardiology who did not think his events were cardiac. He was evaluated by neurology who thought his events were not epileptic.

Routine EEG and 24-hour EEG were both normal and did not capture events. He reported having an event right after the 24-hour EEG was disconnected. Diagnosis included syncope and psychogenic nonepileptic events. No AED medications were prescribed.

Last month this patient was seen by an epileptologist who ordered 72-hour in-home video EEG. On the second day of in-home video EEG study, two complex partial seizures were recorded lasting 40 and 45 seconds.  Event 1 started with rhythmic 3,5 Hz sharply contoured activity in right temporal area, spreading to left temporal lobe, evolving in morphology and amplitude. EKG rate was seen slowing down as seizure progressed. Event 2 began with rhythmic 4 Hz activity in left anterior temporal area (Figure 1). Over next epochs, the activity spread to the right temporal lobe and evolved (Figures 2, 3, and 4): increased in amplitude, decreased frequency to 2,5 Hz -1 Hz spike and wave and became bi-temporally asynchronous. EKG showed drop in heart rate followed by asystole lasting 10 seconds. Following epochs showed slowing of background and then gradual return to baseline for EEG and EKG.

Patient was seen on video sitting on the sofa during the episodes, no clinical symptoms were noted. He was not aware of these episodes and did not push the event button.

This is just one example of why long term, in-home video EEG recordings are useful and important diagnostically, especially for patients with normal baseline. Seizures and abnormalities do not appear on command and expecting to find them in routine EEG is unrealistic in many cases. Ictal asystole is a rare event mostly seen in patients with temporal lobe epilepsy and it is considered a potential contributor to sudden unexplained death in epilepsy. In this case, prolonged, in home EEG provided physician with valuable EEG and EKG data necessary for accurate diagnosis. Patient will now be treated for seizures and hopefully will be helped. Cases like this make our job truly rewarding and meaningful.

Figure 1
FIgure 1. Event 2. Seizure Onset
Figure 2
Figure 2. Event 2. Progression with asystole
Figure 3
Figure 3. Event 2. Spread
Figure 4
Figure 4. Event 2. Activity becomes bi-laterally asynchronous.

Intraoperative Neurophysiological Monitoring  

By Joshua Mergos, MS, CNIM

One of the greatest struggles in education of IONM is experiential learning of true changes.  Something I frequently stress to my students is how many true negatives are seen in IONM.  The explanation for this is simple: in a majority of the cases our field monitors, nothing goes wrong – there are no significant changes, we alert the surgeon of no changes, and the patient wakes up with no deficits.  This creates two challenges for the aspiring neuromonitorist.  First, it limits the degree to which he or she can learn the process of identifying a true change and how this unfolds in the OR, including rapid communication with the surgeon, anesthesiologist, and remote reading professional.  Second, it can create a growing skepticism of our value and efficacy in the OR.  While this second issue may seem inconsequential, I’ve found that it is playing a large role in the shaping of our field’s future, in more ways than one.  As an educator and engineer, I could write about new ideas for OR simulation environments, and IONM mannequins that have electronics embedded under real-to-the-touch skin that can be stimulated and carry signals to volumetric generators in an EEG model head, but for the time being these ideas are only conceptual and I hope that I will be able to talk about their existence and application ten years from now (or sooner).

I believe this second issue is just as great if not a greater obstacle to our field’s growth.  And the fundamental issue here boils down to one word: purpose.

I’ve had numerous conversations with colleagues as well as students about the Millennial generation and find myself in a unique position since I am very near the border of this generation and can relate to some of its characteristics.  When viewed from an employment perspective, purpose ranks as the most important factor of job satisfaction among millennials.  There are many reports on this, including one by Gallup1, and those of you who find yourselves struggling with managing/employing millennials, I’d encourage you to watch Simon Sinek’s viral talk on the generation2 (two of my students kindly shared this with me and I’m very grateful to them for this).  I can’t tell you how many times I’ve re-watched this.

Regardless of your view on this issue and a proper solution, when we see just how indispensable purpose is to today’s growing work force, we should contemplate the day to day application of our work specifically.  In a nutshell, neuromonitoring can be very mundane.  I will regularly talk with my students about percent risk or chance.  Our view of how probable something is changes based on what that thing is.  A 3% chance of rain won’t likely change our plans for an outdoor event; however, a 3% risk of permanent paralysis will more than likely make us give second thought to undergoing a procedure.  Further to this, the chances of seeing a significant intraoperative neuromonitoring change are very low in a majority of the procedures we monitor.  This can lead to extraordinarily long periods (weeks, months, perhaps a year) of monitoring without seeing any changes.  This can result in one believing that he or she is not adding value to the procedure, or that neuromonitoring is not necessary.  When considering our field’s growth, and investigating why some leave the field, I believe this perceived lack of value or purpose is a contributing factor.

Of course, there is always the added security many of our surgeons have when using neuromonitoring that we’re unaware of.  It’s a silently added value – those moments when retraction is held just a bit longer, or a clip is left on longer, or resection is carried out a bit more fully – and all we may hear is a brief inquiry of “how are the signals?”  But the large-scale interventions (catching an intraoperative stroke, identifying too much derotation, or verifying nerve fiber continuity) are rare to come by, and can leave us with months of what feels like lack of purpose.  I’ve encouraged my students to stay alert, knowing that their high-stress, one-in-a-thousand case could be any day, and when they encounter it, to frequently remind themselves of this and reflect on it.  The irony is that the ability to perform well in these tense situations only comes from countless hours of practice during uneventful cases, though a bit of encouragement and affirmation goes a long way through these dry spells.

We are fortunate to have a phenomenal group of surgeons and residents with whom we work that frequently voice their appreciation for our service and how it aids in their practice on a regular basis.  This reminds us of our purpose and is encouraging, regardless of how uneventful a particular case may be.


  1. Clifton, J. “Millennials: How They Live and Work.” May 11, 2016.
  2. “Simon Sinek on Millennials in the Workplace.”  Online video clip.  October 29, 2016. Web.  Accessed June 1, 2018

Nerve Conduction Studies 

By Jerry Morris, MS, R.NCS.T., CNCT, FASET 

Such a nice Memorial Day weekend here in north Louisiana. It’s hot and muggy (when isn’t it?) but with a little, and I do mean little, temperature drop in the evenings, which makes them more tolerable. All and all, it is a good time to spend with family and friends, either indoors or outdoors doing things like yardwork (just ask my wife, Debby!!!). It was also a good time to remember our heroes and patriots from Bunker Hill, the Battle of New Orleans, Gettysburg, San Juan Hill, the Somme, Normandy Beach and Iwo Jima, Choisin Reservoir, Khe Sanh, Iraq, Afghanistan, and wherever our brave men and women fought to preserve the freedom we have today. TIME TO REFLECT. TIME TO BE THANKFUL.

An offshoot of the word time is “timing”. Timing is defined as the choice, judgement, or control of when something is done. We use timing in all walks of life. A timing belt helps synchronize an engine. Timing is very important when we try for that first kiss, ask for that raise, or stand up to that bully down the street. Timing is crucial when a spacecraft attempts re-entry into the earth’s atmosphere or when an airplane takes off and lands safely. In athletics, the timing of a golf swing or a baseball swing is an integral part of the game. In football, timing patterns are run with regularity and their success depends on the practice put in before the actual game. WHEN to throw the ball, swing the bat or club, or pass the car ahead of you is often more important than HOW to complete the task.

Timing is just as important in EMG/NCS because it incorporates the concept of Wallerian degeneration. Wallerian degeneration is the process of nerve breakdown distal to the point of injury, insult, or pathology. In most cases this process begins from the point of injury distally 24-48 hours after the actual injury or insult to the nerve and takes 7-21 days to complete the degeneration process. Axonal breakdown begins first, followed by demyelination of the nerve. This degeneration is a length-dependent process depending on the length of the nerve segment distal to the injury site. Some abnormalities may show up soon after the injury with the EMG studies having the earliest abnormalities. One limitation in doing the NCS early is having to differentiate between a conduction block on an intact axon AND axonal degeneration from a completely transected nerve and axons. With that in mind, 14-21 days is usually used as the optimum time to perform the electrodiagnostic studies. After complete degeneration occurs, regeneration begins at the rate of 1 millimeter/day going toward the target muscle(s).

In our lab, the timing issue is usually not a problem, although there are exceptions. For inpatients, if the problem is <14 days, the study is done during the hospital stay. If the problem falls >14 days, the study is performed after the 14 days either in the hospital if still admitted or on an outpatient basis. This allows for maximum pathological deficits in both the nerve and muscle. It also prevents unnecessary studies to be performed too early that may cloud the data picture overall. Again, most of the inpatients we see have had the nerve problem for a while. The process of referring outpatients from their primary physician to the physician in the EMG lab ensures that the time frame is correct.

One particular patient that I had several years ago illustrates a similar timing principle very well in regard to the disease process. A patient was seen early Friday morning on the general medicine floor of one of our hospitals. The patient was in no acute distress but complained of numbness, tingling, and slight weakness spreading from the feet to just below the knees. X-rays and spine films were normal. Work-up otherwise was essentially normal. The patient did relate that about 2 weeks before he had come down with a stomach virus that had limited him for a couple of days. With that in mind, an NCS and a lumbar puncture was ordered with the preliminary diagnosis of Guillain Barre Syndrome (GBS). Preliminary medication was also begun. NCS was performed shortly after the physician’s examination. The NCS of upper and lower extremities showed normal CV, amplitudes, and latencies. “F” wave latencies were normal. No temporal dispersion was seen in any of the waveforms. Again this was on Friday at noon. When I left that afternoon, the patient was in little-to-no distress and was still on the general medicine floor.

Sunday morning I was called in to repeat the NCS on the patient from Friday. Evidently on Saturday afternoon the patient was found in respiratory distress, intubated, and transferred to the ICU. There was also more weakness and numbness in all four extremities. The NCS on Sunday showed a profound worsening from the Friday study, done less than 48 hours before. CVs were slow, latencies were prolonged, and amplitudes were low. “F” wave was markedly prolonged or totally absent. All waveforms both proximally and distally showed temporal dispersion. The NCS was essentially a 180 degree change from the previous study. Seemingly, the electrodiagnostic abnormalities presented during that 24–36-hour window between studies, along with the worsening of the patient’s physical condition. Since that patient, I’ve had one and possibly two patients presenting with that same scenario; normal NCS early with a rapid progression to a markedly abnormal study. Once again, the timing of the test was critical. Especially in a progressive disease such as GBS, the 1st study may well be essentially normal even with the physical symptoms there. It may be the 2nd study that catches those abnormalities. As always, there will be exceptions. For other diseases such as CTS, radial neuropathy or other entrapments, immediate studies may be normal and waiting and performing another study later during that 14–21-day period would be needed to see if any pathology has occurred.

I hope this helps someone in knowing when to do or not do a NCS. As in all other timing issues, knowing WHEN to do the NCS is almost as important as knowing HOW to do the study.

Have a great summer. If you have any questions please call me at 318-617-0970 or e-mail me at

I look forward to hearing from you.

Neurodiagnostic Education 

By Anna-Marie Beck, MOL, R. EEG T. 

I think we have all had those interesting cases. Those that make us scratch our head and make us think hard for the answer. One such patient for me was in the ED on a late Friday afternoon (just before on-call time began). I was the on-call tech that weekend and was with another patient while a coworker went to begin setting up the emergency patient. The room was small, the gurney was sideways at the end of the room, and the machine was in the doorway; hardly enough room for the two technologists and one patient. We began running the study and activity appeared that we couldn’t identify. It appeared to have a spike buried in the wave; it was very rhythmic and continuous. The patient was non-responsive. It was time to call the physician, as we assumed we had a patient in non-convulsive status epilepticus (NCSE). The physician came to look at the recording (long enough ago that they had to physically come to view the recording) and said that it wasn’t NCSE. We were completely taken aback. We were so confused; how could this not be NCSE? It was rhythmic, continuous, spikes and waves, after all. The physician skirted over to the patient, and did a quick neuro check on him. Then after his quick assessment, as we stood in the doorway watching him and still trying to figure out why this wasn’t NCSE, he opened the patient’s mouth to find his tongue ‘jerking’ (for lack of a better description) continuously. It was the strangest glossokinetic artifact we had ever seen! Apparently, the physician had seen something in his brief neuro exam that had provided him with the insight he needed to say it was not NCSE. He never did fully explain it to us, but I’ll never forget the way that glossokinetic artifact appeared. That one patient has provided me with the memory to check all things possible until I know it is something worth calling the physician over; a reminder we can all use every now and then.

New Technologies & Research 

By James Wadsworth, CNIM, BS

In the recent fast-changing technological world of electroencephalography (EEG) many advances have been achieved; High frequency amplifiers, HD Video, better IT infrastructure to name a few.  However, the typical technology used today for routine EEG, an AC-coupled amplifier recording at a bandwidth of 0.5 – 50Hz, has not significantly changed in 50 years. The advancements in amplifier and storage technology has seen the emergence of higher frequency recordings that have captured High Frequency Oscillations (HFO) which have shown to have credible information related the ictal onset zone (IOZ) in epilepsy. However, very little advancement or clinical use of infraslow frequency (<0.5Hz) EEG (isEEG) has taken place. Much of this limited advancement has been due to the fact that historically, initial EEG systems used AC-coupled EEG amplifiers that filter out the slow EEG components.  As new technology DC-coupled amplifiers have become available, researchers have recorded significant pathological low frequent EEG activity in pediatrics, epilepsy, sleep and ICU-EEG environments. In order to further study isEEG and understand the clinical relevance, there is a need for commercially available full spectrum EEG amplifiers that take advantage of the DC-coupling and high frequency sample rates. Both Infraslow frequency (isEEG) and high frequency (hfEEG) are needed today in the routine recordings of EEG without sacrificing performance of either.

EEG activity from the brain is electrically small and measured in µV. To be able to measure and record small signals in an electrically noisy clinical environment, a differential amplifier is used (Figure 1.).  This type of amplifier only amplifies the differences between two inputs while rejecting the similarities through a process of common mode rejection (CMR).

Figure 1
Historically, an EEG system consisted of a differential amplifier, galvanometer and a graphical pen.  The amplifier sends its output signal to the galvanometer that was a coil in a magnetic field.  This signal caused the pen to deflect and record the analog signal.  To attenuate unwanted noise from the signal, filters were used to limit what frequency spectrum was amplified.   Low frequency filters (LFF) (also called high pass filters) were used for the low end of the spectrum. High Frequency Filters (HFF) (also called low pass filters) were used for the high end of the EEG spectrum.  Because isEEG or DC offset was considered noise, the first commercially produced EEG amplifiers were AC-coupled.  The difference between an AC-coupled and DC coupled amplifier is simple.  The AC-coupled amplifier adds a hardware LFF circuit that removes the DC offset from the amplified signal.

FIgure 2

The DC offset is the voltage potential between the inputs and may be positive or negative, whereas the LFF of the AC-coupled amplifier removes the offset voltage so the signal is centered around zero volts.  The first EEG amplifiers used a time constant that is measured in seconds for the LFF which is an engineering term that represents the time it takes for the signal to settle within 63% of its final value.

  • Because there is no LFF that an AC-coupled amplifier uses, the down slope of the digital signal is not distorted (Figure 2). The precise LFF digital filter of the DC-Couple amplifier is designed to limit the DC-offset without the slow time-constant shift of the data. Figure 3

Today’s amplifiers are completely digital using Analog to Digital Conversion (ADC) to represent the analog signal.  A digital DC-coupled amplifier can take advantage in that a precise digital filter can be used to remove the DC-offset without distortion, allowing easy recording and interpretation of the routine EEG signal.  However, the same signal can be processed without the LFF digital filter to see the isEEG.   Using a full spectrum amplifier, a full recording of the EEG data can be accomplished without sacrificing any abilities to record and review high frequency data.The DC offset is the voltage potential between the inputs and may be positive or negative, whereas the LFF of the AC-coupled amplifier removes the offset voltage so the signal is centered around zero volts.  The first EEG amplifiers used a time constant that is measured in seconds for the LFF which is an engineering term that represents the time it takes for the signal to settle within 63% of its final value.

Being able to record isEEG allows for investigation of several interesting topics:

  • isEEG signal shift (DC-Shift) related to the Ictal onset of a seizure. Helping with location of the IOZ.
  • isEEG is needed to record Cortical Spreading Depression (CSD). CSD is seen in a number of pathologies of migraine, epilepsy, traumatic brain injury (TBI) and ischemia.
  • isEEG has shown an electrode correlation between contacts with stereotactic depth EEG electrodes.
  • Slow Activity in Preterm Human EEG patterns. Vanhatalo et. al. indicates that having the full spectrum of EEG allows seeing the slow frequency data that has been ignored.  Brain developmental abnormalities are just beginning to be understood in this area.
  • isEEG Oscillations during sleep. Slow oscillations that take place between 0.02–0.2 Hz that vary in amplitude are observed during REM.  This slow cyclic modulations may have higher clinical impact to neurophysiological as well as pulmonary clinical diagnosis.

In conclusion, as we collect data for patients with specific abnormal EEG, we do so with the intent to determine localization and or etiology with an intent for treatment. Full Spectrum EEG has become needed in many clinical settings to help with the wide range of diagnostic areas.  By having a non-distorted view of the EEG data, it is hoped that clinical evaluation of many patients will be clearer and less confusing.  It is likely that more information will emerge as commercial systems with this technology become more readily available and the use of full spectrum EEG becomes more common place in the clinical setting.

References –

Bauer H, Korunka C, Leodolter M. Technical requirements for high-quality scalp DC recordings” Electroencephalogr Clin Neurophysiol. 1989 Jun; 72(6):545-7.

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Pediatrics and Neonatology 

By Michelle Gregory, R. EEG T.

It’s never a dull moment at Seattle Children’s, so this provider’s request was not out of the overall norm.

History: 22-month old male that started having episodes of unresponsiveness, irregular respirations, starts to sway with stiffening at 4 months of age. The only caveat is that these symptoms occurred only when in water with a temperature is 96–97 degrees.

Mother had similar episodes at 8 years of age with no additional family history of seizures or episodes.

Request: Provider asked the EEG team if the patient could have an outpatient EEG study and have the EEG performed with the patient in a bathtub. The EEG team thought from a safety perspective it would be better to bring the patient in to our Epilepsy Monitoring Unit to attempt to capture an episode.

Conditions of Recording: The EEG tech transitioned the patient to ambulatory monitoring equipment as it was thought the safest. The epilepsy team (2 EEG techs, EMU attending, patient nurse, EMU ARNP and 2 parents) was able to get the water temperature to 102.5 degrees with the thinking that the water would cool down. The patient was placed in the tub and everyone waited for 2 separate trials.

Ictal /Events: At the beginning of the first trial, the patient exhibited what seemed to be the onset of one of his events – appearing dazed and somewhat unsteady but the episode did not progress from there and he quickly returned to his behavioral baseline. No clinical changes were noted with the second trial.

What we learned was that a simple request took a lot of preparation from determining if it is even feasible to where the safest place to perform this would be; the inpatient or outpatient area. Once that was vetted, the next challenges came during the procedure. The parents became frustrated when the toddler didn’t have an event right away and said that too many people were in the room and/or the water was not exactly at 97 or 98 degrees! We had most of the people leave and achieved the closest water temperature we could.

Would we do it again maybe, but I think that it’s always worth trying something different.

By Melanie Sewkarran, R. EEG T., CLTM, BS

We are pretty fortunate to get to see a wide variety of clinical presentations at our hospital, but I think most of us would agree that one of our favorites is the patient with the “tablet spikes.” We had a young boy (maybe 7 years old) admitted to our EMU with reports of staring spells and some episodes of lateralized extremity weakness. A routine EEG had shown left central sharp waves during sleep, so the suspicion was Benign Rolandic Epilepsy (BRE). Since the routine EEG did not show evidence of absence seizures and the mother continued to report episodes of staring and unresponsiveness, the patient was brought in for 24 hours of continuous EEG monitoring in our EMU. During that monitoring, our Neurophysiologist noted some long, semi-rhythmic runs of 200-400 µV left-central sharp waves while the patient was awake. When he looked at the video, he noticed that the sharp waves correlated with the times that the patient was playing a game on his tablet. Upon closer review, he noticed that whenever the patient would tap his index finger on the screen, we would see a sharp wave maximal at C3. One sharp wave for every tap. You can imagine that, at times during his game, the runs of sharp waves were so lengthy and rhythmic that we were concerned these were seizures. However, when reviewing the video, the sharp waves always stopped as soon as he stopped tapping his finger. In order to investigate further, I went into the patient’s room and asked him to do some finger exercises for me. I had him tap with each thumb, and then one finger at a time until he’d tapped with them all. The only finger that elicited the C3 sharp waves was his right index finger and the sharp waves occurred when he tapped anything – the tablet, the table, the bed, his own thumb. A little while later, a physician came in and tested this phenomenon a little differently. She tapped the tips of his fingers with her finger, one at a time, and the only EEG correlates were the C3 sharp waves when she tapped his right index finger. One sharp wave for every tap. She asked if he felt anything odd when she tapped his finger, and he said he just felt “tap, tap, tap.”

Since the staring episodes we captured were not absence seizures (and in no way related to the C3 discharges), the theory remains that these were some sort of exaggerated somatosensory response in the context of BRE.

To this day, I’m sure this patient still tells stories about how he went into the hospital for a brain test and he has no idea why a bunch of people we so fascinated with his finger!

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