Each Tech Tips article focuses on a special topic and is written by ASET members who are a subject-matter expert on a given topic in Neurodiagnostics. This Issue’s article focuses on working in an Epilepsy Monitoring Unit (EMU) with PNES patients.
Working in an Epilepsy Monitoring Unit (EMU) brings many opportunities to perform Video EEGs (VEEGs) on unusual or unique patients. Most techs have distinct memories about many of the patients they have worked with, especially those patients who presented with an interesting history or had unusual EEG findings. Often these memories lead to excellent extemporaneous tech educational sessions. The patient with psychogenic non-epileptic seizures (PNES) can and should be a topic worthy of such discussions.
Data indicate that approximately 20–30% of admissions to an EMU can consist of patients with a known or suspected diagnosis of PNES, so it is highly likely that every EMU tech will eventually set up and monitor such a patient1. While we should treat all of our patients with dignity and respect, it is especially important to do so with this type of patient. Some background into the disorder highlights common denominators for patients with PNES: the majority are female, their events started in their teens to twenties, a significant percentage of patients have some type of psychiatric or unexplained medical disorder such as fibromyalgia/asthma/gastroesophageal reflux or headaches, and there is usually a history of some type of emotional or physical abuse2, 5, 7. Additionally, 10–30% of patients with PNES can also have a diagnosis of true epileptic seizures5, 7, further complicating diagnosis and treatment. Many of these patients have been or are currently taking more than one antiepileptic drug (AED), but they continue to have multiple events5, 7.
There are some characteristics that tend to occur more frequently or even exclusively in patients with PNES. The frequency of events in PNES is usually greater than those of patients with epilepsy5. Being in a stressful situation, or undergoing routine Photic Stimulation (PS) and Hyperventilation (HV) during an EEG is more likely to trigger an event of PNES5. Technologists should be aware of these precipitating factors, and plan accordingly.
Differentiating a PNES event from an epileptic event based solely on clinical information is very difficult. By description, it is easy to confuse a PNES event with a generalized tonic-clonic or frontal lobe seizure5, 7. Although a typical PNES event often consists of asynchronous thrashing movements or periods of unresponsiveness with an EEG that shows no correlating abnormalities, by the description the patient is having shaking of extremities or staring. Similar descriptions can be applied to tonic-clonic or absence seizures. Therefore, the differential diagnosis of PNES will often depend on the actions of the EEG technologist when these events occur.
If a patient is having a PNES event which consists of motor activity, it is important to observe the sequence of events which occur. A typical true generalized tonic-clonic seizure will start with a period of stiffness, progressing to a period of strong, rhythmic, synchronous clonic activity which gradually lessens in intensity and frequency. The duration is usually less than 3 minutes and there can be other clinical signs such as cyanosis or incontinence that are difficult or impossible to voluntarily perform. Comparatively, a PNES event will often consist of arrhythmic, asynchronous movements that will wax and wane in both intensity and frequency. The patient may close their eyes during the event and/or move their head from side to side5. These events can last for long periods of time, and when completed, the patient is completely responsive7 with no post ictal fatigue or confusion. Patients with PNES may coherently answer questions and obey commands during the event5, whereas patients with tonic clonic or absence seizures are unable to respond to questions or commands. If the PNES event is one of unresponsiveness, it is important to stimulate the patient to demonstrate responsiveness. Holding the patient’s arm above their face or head and letting the arm fall is a good indication of whether the patient is aware of their surroundings. A patient with PNES will usually let their arm fall to the side, avoiding their hand striking their face7. If the patient’s eyes are open during the event, look for voluntary fixation of their gaze by holding a mirror in front of the patient. If the eyes fixate on their reflection this is an indication of voluntary eye control7.
What circumstances contribute to a patient developing PNES? Many authors feel that these patients have not developed adequate coping skills to deal with stress or adverse events1, 5, 6, 7. Patients all over the world, regardless of culture, are affected by PNES5. PNES is usually considered a type of somatoform disorder called a conversion disorder. This means that the patient shows clinical symptoms that resemble a physical disorder but does not have corroborating physical findings. A conversion disorder is a type of somatoform disorder in which these clinical findings have a psychologic rather than physical origin4. Many PNES patients have also been diagnosed with anxiety, depression, borderline personality disorders or post-traumatic stress disorder (PTSD)6.
Psychogenic symptoms (symptoms that are perceived as real but don’t have an organic cause) can take multiple forms, including vomiting, diarrhea, stomach pain, non-cardiac chest pain, shortness of breath, etc.3. These findings could be diagnosed, based on a description of the symptoms, as irritable bowel syndrome, heart disease or asthma. But what if there are no substantiating physical findings? No cardiac issues, no lung inflammation, no findings on endoscopy or colonoscopy? Are the symptoms any less real to the patient? Absolutely not! Apply this thought process to the patient with PNES. Although the EEG is normal during the event, with no evidence of epileptic abnormalities, to the patient their symptoms (the event) are real. Remember, if you haven’t experienced it firsthand, it is impossible to judge how another person responds to a significant event.
What does this mean for us as EEG techs? First of all, compassion is required and judgment should be suspended. The patient should be treated with respect and dignity. It is important to realize that these patients are not “faking it”. While there are indeed some patients who find any diagnosis of illness to have advantages such as receiving extra attention, or avoiding social and societal responsibilities7, the majority of patients with PNES sincerely want to “be cured”. They are individuals who have most likely already suffered a severe emotional or physical trauma. Many of these patients have willingly complied with an unhelpful AED regime (some for many years)7. These patients continue to seek medical help, going from physician to physician; hospital to hospital. They find their symptoms to be physically and socially debilitating. They deserve our help and our compassion, not our judgment and dismissal.
VEEG is the procedure most often credited with diagnosing a patient with PNES. During the event, the EEG will not show any of the changes associated with a true epileptic seizure (spikes, sharp waves, spike, and waves). Often, the EEG is obscured with muscle or movement artifact. Utilizing the midline electrodes (Fz, Cz, Pz) can usually provide good information regarding the level of consciousness and the presence or absence of epileptiform activity. The emergence of a normal background rhythm at the end of the event argues against a true epileptic seizure.
Some patients with PNES will state that their events occur only in sleep. VEEG can accurately display the patient’s state of consciousness at the onset of the event. Frontal lobe seizures usually arise directly from sleep, whereas patients who are experiencing a PNES event will show arousal and a portion of waking background before the event begins (7).
Performing activation procedures such as HV and PS are acceptable methods for inducing an event of PNES5. Additionally, sometimes simply explaining to the patient that it is important to achieve a correct diagnosis so that appropriate treatment can be instituted and un-needed and potentially harmful medications can be eliminated or adjusted, is all that is needed to provoke a typical event. Regardless of which method is used, it is important that the tech be completely honest with the patient at all times. It is never acceptable to “lead a patient on” with false comments about the EEG findings, for example: “Your EEG is looking like you’re about to have an event…”, or “Your EEG is showing some funny activity so I think you should be getting ready to have your spell”. Remember, a percentage of PNES patients actually have a diagnosis of epilepsy, so their interictal EEG may actually be abnormal. Only the findings of the ictal EEG during the typical event are diagnostic. Many patients will actually have their PNES event within the first few hours of VEEG5. Once an event is recorded, it is important to verify that the event is representative of the patient’s typical spell5. If the patient has more than one type of spell, try to capture each type during the VEEG.
Patients with simple partial seizures have been known to have normal EEGs during their seizures. Likewise, patients with frontal lobe epilepsy often have normal waking EEGs. And, patients with a true diagnosis of epilepsy have normal interictal routine EEGs up to 30% of the time7. It is essential that both the VEEG findings as well as the clinical event be utilized equally to provide a correct diagnosis of PNES5.
So, what happens after the EEG technologist has done their job and successfully recorded a typical PNES event? First of all, the patient must be told their “new” diagnosis. The process for doing this varies widely and often comes down to how comfortable a neurologist is at explaining this change in diagnosis and treatment. Unfortunately, the average length of time between PNES onset and PNES diagnosis is 5–7 years 2, 6. Obviously, it would be very difficult for a patient who has spent years feeling as if their events were a medical condition to suddenly be told their problems are psychiatric. The patient’s care will usually be transferred from the Neurology service to the Psychiatry service. If both the neurologist and the psychiatrist can be present during this initial informational meeting with the patient, the patient will have more confidence that their transfer of care will be seamless6.
Describing the patient’s events and noting that there are no corroborating EEG abnormalities is usually the first step in discussing the diagnosis of PNES with a patient6, 7. Much reassurance is given to the patient that they are not “crazy”, and that their experiences, while not epileptic, are most certainly real6, 7. The physician can then explain the relationship between stress and PNES6, 7. Understanding the underlying cause of their PNES events is difficult for most patients1. One study utilizes the example of “switching off” your brain, for example when driving home but not remembering the trip, or the way a child who is being repeatedly abused may “switch off” or dissociate their brain during their abuse, as a way of explaining why the patient may not understand what their “trigger” is for precipitating PNES events7. The need for tapering AEDs is explained to the patient6, 7. Finally, a psychiatric treatment plan is drawn up, and the need for compliance in following the plan is stressed6, 7. Usually the patient is referred for some type of cognitive behavioral therapy, although group therapy, antidepressants, hypnotherapy, and eye movement desensitization and reprocessing have also been used with varying degrees of success6.
How does the patient cope with this new information? PNES patients need a great deal of time to process and understand this change to their self-image, and much support to ensure that they continue to maintain a good level of trust with their healthcare provider1. Patients can feel as if the responsibility for the resolution of their problems had been shifted to them, rather than being the responsibility of the health care professional 1. Helping them understand what precipitates their events, and having the health care professional take them seriously were the two most important factors identified by PNES patients as a requirement to get them started on the road to recovery1.
Unfortunately, a large percentage of patients who receive a diagnosis of PNES have a poor outcome. Some studies relate this to the delay between PNES onset and PNES diagnosis, stating that the longer the delay the less effective the treatment7. Some patients may simply have a difficult time accepting a psychiatric diagnosis over a medical one. Regardless, this patient population represents a challenge to the EEG technologist as well as the neurologist and psychiatrist. Creating a safe and compassionate environment is the single best thing the EEG technologist can do for the patient with PNES. After that, it is up to the physicians, and the patient, to understand and hopefully conquer this difficult condition.
This article was written by Pat Lordeon, R. EEG T., FASET.
- Karterud HN, Knizek BL, Nakken KO. Changing the diagnosis from epilepsy to PNES: Patients’ experiences and understanding of their new diagnosis. Seizure 19 (2010) 40-46. doi:10.1016/j.seizure.2009.11.001.
- Dixit R, Popescu A, Bagic A, Ghearing G, Hendrickson R. Medical comorbidities in patients with psychogenic nonepileptic spells (PNES) referred for video-EEG monitoring. Epilepsy & Behavior 28 (2013) 137-140. http://dx.doi.org/10.1016/j.yebeh.2013.05.004.
- Benbadis SR, Lutsep HL et al. Psychogenic Nonepileptic Seizures. https://emedicine.medscape.com/article/1184694-overview.
- The Truth about Psychogenic Nonepileptic Seizures. https://www.epilepsy.com/article/2014/3/truth-about-psychogenic-nonepileptic-seizures. Epilepsy Foundation.
- LaFrance WC, Baker GA, Duncan R, Goldstein LH, Reuber M. Minimum requirements for the diagnosis of psychogenic nonepileptic seizures: A staged approach. Epilepsia 54(11):2005-2018, 2013. doi: 10.1111/epi.12356.
- Baslet G. Psychogenic nonepileptic seizures: a treatment review. What have we learned since the beginning of the millennium? Neuropsychiatr Dis Treat. 2012; 8: 585-598. doi: 2147/NDT.S3230 https://www.ncib.nlm.nih.gov/pmc.articles/PMC3523560/.
- Mellers JDC. The approach to patients with “non-epileptic seizures” Postgrad Med J 2005;81:498-504. doi: 1136/pgmj.2004.029785.
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.
Intraoperative Neurophysiological Monitoring
Nerve Conduction Studies
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
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.
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.
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:
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.
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.
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?!
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.
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.
- Clifton, J. “Millennials: How They Live and Work.” May 11, 2016. http://news.gallup.com/opinion/chairman/191426/millennials-live-work.aspx
- “Simon Sinek on Millennials in the Workplace.” Online video clip. October 29, 2016. https://www.youtube.com/watch?v=hER0Qp6QJNU Web. Accessed June 1, 2018
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 [email protected].
I look forward to hearing from you.
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.
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).
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.
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.
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.
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Hartings JA, Watanabe T, Dreier JP, Mojor S, Vendelbo L, Fabricius M, Recovery of Slow Potentials in AC-Coupled Electrocorticography: Application to Spreading Depolarization in Rat and Human Cerebral Cortex J. Neurophysiol. 2009,102: 2563-2575.
Kim W, Miller JW, Ojemann JG, Miller KJ, Icta Locaization by Invasive Recording of Infraslow Activity with DC-Coupled Amplifiers, J Clin Neurophsiol. 2009, 26(3):135-144.
Nasretdinov A, Lotfullina N, Vinokurova D, Lebedeva J, Burkhanova G, Chernova K, Zakharov A, Khazipov R, Direct Current Coupled Recordings of Cortical Spreading Depression Using Silicone Probes. Frontiers in Cell. Neuroscience, 2017, 11: 1.00408- 11.00408.
Modur, PN, High Frequency Oscilations and Infraslow Activity in Epilepsy, Ann Indian Acad Neurol. 2014 Mar: 17(suppl 1): S99-S106.
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Thompson, SA, Krishnan B, Gonzalez-Martinez J, Bulacio J, Jehi L, Mosher J, Alexopoulos A. Burgess RC, Interictal Infraslow Activity in Stereoelectroencephalography: From Focus to Network. J Clin Neurophysiol. 2016, Apr;33(2):141-8
Vanhatalo S, Tallgren P, Andersson S, Sainio K, Voipio J, Kaila, K, DC-EEG Discloses Prominent, Very Slow Activity Patterns During Sleep in Preterm Infants, Clin. Neurophysiol. 2002 Nov 113(11): 1822-1825
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!
Welcome from the Interest Section Chair
By Petra Davidson, R. EEG/EP T., FASET, BS
Greetings Fellow ASET member,
Happy Spring! Hopefully, you are enjoying spring wherever you reside. We are not yet there in Minnesota. Currently, nearly 18 inches of snow coat my yard. Tiny bunny tracks dotted across the glittery, diamond like snow suggest that spring is in fact on its way.
Recently, I changed employment. After 20 years as a clinical technologist, I am now a remote technologist. Everything I do resides behind a computer screen and headset. As I reconfigure my elevator speech to fit my new role, I called on our Special Interest Section Leaders to do the same. There are a few surprises in the articles that follow. I hope that you enjoy them as much as I did.
It is always intriguing to me to hear how others in the field describe what we do. I ask that you read these carefully and let us know what you find interesting or how you might change things to fit your unique role. That is the beauty of our field, each of us has a unique position! Happy reading!
Acute/Critical Care Neurodiagnostics
By A. Todd Ham, R. EEG T., CLTM, BS
For this section, I’ve prepared an “All Things EEG, 2nd Edition” crossword puzzle for you to exercise your brain muscles. To view the crossword puzzle, click here.
By Jennifer Carlile, R. EEG T.
Because I wear a few hats in my position, here is how I describe my job is: First, I always start with how much I love what I do. I’ve been in the Neurodiagnostic field for almost 30 years and I help Neurologists make a diagnosis for their patients who might have epilepsy. The other way I describe my job is: I offer a service to physicians, helping them determine whether their patients have epilepsy, seizures, or brain injury. I have been able to say for the past 29+ years that I love what I do and still love this field. How many people can honestly say that? I have been so blessed. In the beginning of my career journey, I started working in a major hospital system that saw the worst-case scenarios of brain-related issues, followed by selling equipment that helps detect brain-related issues, and now, full circle, I have the best of both worlds, offering an amazing service to these physicians and taking care of their patients. Love, love, love, love in honor of Valentine’s Day. Sounds sappy, but it is the truth! #blessed#lucky!
By Emily Scanlan, R. EEG T., BS
When asked about what I do, I try and relate it in terms that are appropriate to my audience. If I am talking to another healthcare professional, I will tell them that I monitor brainwaves of patients and look for any seizure-like activity or any abnormalities. Now, if I am talking to a non-healthcare person, I try and make my description fit their intellectual capabilities. My dad was a professor at the University of Minnesota and likes to know the little details of my job, so I will go into more details including why I may see certain things and how it may impact a patient’s prognosis. On the other hand, if I am talking to my sons (mind you, they have helped me as subjects for marking with my students), I go really high-level and say that I am monitoring their brain to see if anything is wrong. There is no need to go into detail as they won’t get it, which will, more than likely, just confuse them.
By Vicki Sexton, R. EEG/EP T., R.NCS.T., CNCT, CLTM, BS
My 5-second elevator speech to my patients who do not speak English and who have no one to translate, or a patient who is developmentally delayed is to say what I am going to do and act out what I am saying at the same time. As I explain what I am going to do, I do part of it on myself, then I show them either on their head (with marker and tape measure), or I show them on their hand. I will mark their hand, then rub with the prep, then apply an electrode so they know how it feels before I apply it their head. As I perform the test, I act out what I want the patient to do while speaking English. They usually start to understand as I repeat common commands, such as open eyes and close eyes. With the hyperventilation, I usually do it along with the patient, so they understand.
Taking the little extra time to explain, while acting out the steps usually gives a thorough study and calms the patient at the same time.
By Stephanie Jordan, R. EEG/EP T., CNIM, CLTM
One thing I certainly enjoy teaching the NDT students at our lab is how to communicate with our patients and put them at ease for their procedure no matter the challenge. We are fortunate here to have a diverse patient population with different ages, cultures, and ability to comprehend. For many, it is their first EEG and the patient arrives to the lab apprehensive and uncertainty.
First things first is to make the patient comfortable in their physical surroundings then explain what the EEG is. I avoid calling it a test because so many are apprehensive about “taking tests”. I tell the patient that the EEG is a recording of their brain cell activity in waveform, recorded by electrodes pasted onto the scalp. At this point I show them the electrodes and how they lay flat on the scalp by pasting an electrode on my hand. Speaking slowly and allowing time for the patient to ask questions as they occur helps to relax them. It is helpful to let the patient know that the test is non-invasive by telling them “I am not putting anything into or out of your brain, just recording the activity that naturally occurs there.” For young children, a simpler way is to say, “I am going to put these golden buttons on your head and take pictures of your brainwaves.” Children know they need to stay still for pictures and most enjoy it, so this is a good strategy. For all patients showing the entire bunch of electrodes and letting them know you will measure and mark with a crayon for each one gives them an idea of how the set up will go. Show the measuring tape and marker to the patient and let them know when you are going to touch their head. After the marking, let them know you are going to clean each spot and paste the electrode on there (show the cotton swab and cleanser). Letting the patient know that everything washes off with water when done can also put them at ease. For older patients who are familiar with EKGs, letting them know that the EEG is for recording brain activity like the EKG is for recording heart activity gives them a familiar comfort. For my 5-second elevator speech – my job is to get the best brain cell recordings for each patient I serve.
By Patricia Lordeon, R. EEG T., FASET
We frequently hear about and discuss how important communication is within our work space, but even then most of us don’t really communicate well. For example, we lament when a new policy is implemented, and we feel that insufficient information has been communicated to us about the change. We assume that our coworkers know what we mean without us having to actually utter the words. We think that everyone knew about that “something” being changed and are surprised to realize that some individuals were unaware (you mean the grapevine let us down??). And work issues are only the tip of the iceberg of communications. Don’t even get me started on communication in politics!
When you are trying to communicate with someone and there is a language barrier, the stakes are increased exponentially. At our hospital, we are fortunate to have the “blue phone”. It is a device that has two hand sets and plugs into a jack on the side of our existing hospital phone. Via the magic of technology, we can choose from a large variety of languages and dialects, and have a real-time, three-way conversation between tech, patient and translator. The company maintains a staff of translators available to speak with and translate for healthcare professionals. This luxury is obviously not available for every hospital and clinic setting, and we are blessed to have this advantage when working with non-English speaking patients. If you have to make do without this marvel of modern technology, you can prepare for these situations in advance by making a picture book of the application process. YouTube is another great resource, and of course, Google Translator makes everyone an instant linguist.
When I was a young tech, none of this technology existed (gives you a hint of how old I am). So, we had nothing to use or help us when working with patients who did not speak our language. Pantomime and picture drawing were our only resources when faced with this situation. It was far from optimal, and we have come a long way from those days. Obviously, communicating with non-English speaking patients and families is not an issue for us in our current work environment.
Back in those days, we were sometimes fortunate enough to test patients who had some small understanding of English, or even better, we had some small understanding of their native language. One day, long ago, I had the pleasure of working with a four-year-old patient and her mother who were at our facility for long-term video EEG monitoring. The patient and her mother spoke French exclusively. I was thrilled to be able to use my four years of high school French to help comfort them and assist in achieving good quality testing. I quickly realized that my school-taught French was no match for a native French speaking parent. I was able to communicate much better with the four-year-old patient (which told me that four years of high school French puts you on par with the conversational level of a four-year-old, French speaking child).
Despite our language barrier, we soldiered on with the testing. We made due with a smattering of French (on my part), lots of head nodding and pantomime, and some diagram drawing. This patient continued to travel to our hospital for the next twelve years, and we forged a strong bond during that time. The fact that the patient took an English class at home in her grade and high schools helped tremendously in our being able to communicate over the years. Her English was excellent, while I am sad to confess my French never really progressed beyond the four-year-old level I started with.
For me, determination and good humor were the two most influential factors in establishing a communication process with this patient. While there are certainly easier methods available now, nothing can replace the shared trial-and-error that made us laugh and smile and learn together. This family never forgot how, during the patient’s first-ever video EEG, I asked, in all seriousness, to “Ferme tes oeufs” (Close your eggs) instead of the intended “Ferme tes yeux” (Close your eyes). And I will tell you that I never, ever had the opportunity to use the only French phrase I recall from those four years of French class. “Ou est la piscine?” (Where is the pool?) is not something I have ever needed to ask when obtaining a medical history.
By Susan Hollar, R. EEG T., BA
There are many approaches to describing what an EEG technologist does each day. Of course, you should tailor your description based on your audience. Children tend to be very literal in their interpretation of what adults say. I have encountered more than one child, including my own grandson, who thought we sucked out the brains of children with our electrodes! There have been many who believed we could tell what they were thinking. I, personally, am glad that is not the case! My explanation has evolved as I have witnessed what seemed to work and what fell totally flat.
My typical, quick explanation for what an EEG tech does is: We make a recording of how your brain is working. We do that by placing recording wires called electrodes on your head (scalp). My main job is to make sure the recording is free from artifact or noise. We will have you do some activities to help the Neurologist see how your brain works. Those activities will include some special breathing, opening and closing of your eyes, and a special flashing light. All of this helps us see how your brain works.
I also really like the explanation (when appropriate) that it is like looking for a bolt of lightning or listening for thunder to see if there is likely to be a storm coming in the future.
It is also important to ask what the patient knows about EEG and then build on their knowledge.
Intraoperative Neurophysiological Monitoring
By Jeffrey R. Balzer, Ph.D., FASNM, D.ABNM
“So, What Is It You Do for a Living?”
In 26 years of performing IONM, if I had a quarter for every time someone asked me “what do you do at work?” I could have retired 10 years ago. Unlike other professions where people say, “I’m a pharmacist” or “I’m a mechanic” we typically answer, “I am a neurophysiology technologist” or a “surgical neurophysiologist” and that’s where people stop and look at us like we are speaking a different language. It is at this point that we often default to saying “oh, I work in the operating room” in an attempt not to go into detail of what we do. What we fail to realize is that we are missing the perfect opportunity to create and deliver a succinct layman’s explanation of what IONM is and what role we play in the care of our patients. Our answer should be almost reflexive and polished so that we can clearly convey what we do and how we generally perform IONM.
Typically answers begin with “I monitor the spine and brain during surgery in the operating room.” Family members then say, “so you are a surgeon”? Our answers concerning what we do should attempt to be more detailed while maintaining a level of basic verbiage. I begin by explaining that most, if not all surgical procedures, pose some level of risk. I then, for example, talk about the ideal situation for detecting complications during surgery. I tell people that if every spine or brain surgery could be done awake to allow for a continuous assessment of neurological function, we would do it that way. The confounding factor is that our patients are under general anesthesia, so a traditional neurological examination is impossible to perform. As such, we use specific tools that reflect an awake neurological examination and reliably provide information to the surgical team so that interventions might occur, thereby potentially preventing or lessening complications.
The next thing to describe are the tools we use and how we perform IONM. Depending on where and what the surgery is, I say we use tools to stimulate the nervous system and record activity that is generated. I often attempt to use analogies that most people understand to describe what we do. A basic description involving electricity and wiring is often very useful in these instances. I tell folks that what we do is analogous to us generating an electrical signal that travels along a wire. We continuously watch the signal moving along the wire measured at different points. If the wire (the spinal cord being the wire, for example) is interrupted, then we know when and where the problem occurred along the length of the wire. Once we detect an interruption, we immediately inform the surgical team who, in turn, investigates the potential cause. This typically gets the message across particularly for cases involving spine monitoring. As IONM become more complex our explanations need to be a bit more complex as well, and using these types of analogies is often very useful.
We should be using the opportunity with friends and family to polish our explanation of IONM testing so that we can utilize the explanation with patients and patient’s families when we are explaining the details of IONM to them or more importantly, acquiring an informed consent. The explanation needs more detail but still be succinct and accurate as patients and their families are often under far more stress than a family member who is casually asking what we do in the operating room.
One of the major components of informed consent is that information is given about a treatment or test so that the patient can decide if they wish to undergo a treatment or test. This process of understanding the risks and benefits of treatment is known as informed consent. The key component is that the patient must understand the relevant information. Decision-making capacity is also referred to as competency. Competency may be the most important components of informed consent. There are several different components of decision-making capacity:
- Ability to understand options
- Ability to understand consequences of choosing the options
- Ability to evaluate costs and benefits of consequences and relate them to personal values and priorities
The key to decision-making capacity or competency is predicated on the patient understanding the IONM, the risks and the options. We therefore need to ensure that our patients understand exactly why we are there and what we are going to do.
The explanation during informed consent should be more formalized, but nonetheless, basic enough for the patient to understand. If need be, similar analogies to those described above are perfectly fine to use conversationally. As for the written IONM consent, the following is an excerpt from a typical IONM consent form:
“Intraoperative neurophysiological monitoring is performed during a variety of surgical procedures to measure the function of the brain, brainstem, cranial nerves, spinal cord, spinal nerve roots and peripheral nerves depending on the type(s) of testing performed and the surgery. Electrophysiological measurements provide information to the surgeon in the operating room that may assist in identifying neural structures, aid in performing the surgical procedure itself and in detecting and preventing injury to the nervous system.
Central and peripheral nervous system function is measured using electroencephalography (EEG, an electrical map of the brain), electromyography (EMG, measurement of electrical energy to the muscles) and/or evoked potentials (EP, stimulated electrical activity) recordings. The surgical procedure and the parts of the nervous system at risk will determine which of these tests will be monitored. In some cases, these will be recorded simultaneously.
After the induction of general anesthesia but before the start of surgery, small, sterile subdermal (under the skin) needle electrodes will be placed and used as stimulating and recording devices. Baseline recordings will be made so that differences during the surgical procedure can be detected. Once the surgery has begun, recordings will be monitored continuously or near-continuously throughout the procedure and any significant changes will be reported to the surgical team. The information will be interpreted by a board-certified Neurophysiologist and recommendations will be made. Prior to you awakening from anesthesia, all the electrodes will be removed.”
Once an explanation, such as the one above has been given, the patient should be given a detailed description of what the potential morbidities are as they relate to performing IONM. In addition to the potential morbidities, quoting incidence as a percent is important. This can be based on the literature or on personal institutional experience. Some examples of these include the following:
- Infection. Infection may occur at the site of electrode application in the skin (estimated risk <0.1%).
- Burns. Burns at electrode site caused using electrical equipment such as cautery or by a malfunction of the neurophysiological monitoring equipment (estimated risk <0.1%).
- Hematoma. Because a needle is placed beneath the skin, blood may collect to form a hematoma (bruise or blood clot) (estimated risk <0.1%).
It is important that this list be complete and describe all possible instances in a succinct and understandable manner. This is all part of a complete description of IONM that needs to be provided to the patient and their families prior to the procedure.
Regardless of who we are explaining IONM to, whether family, friends or patients, we need to take great care to provide accurate and succinct information. Perhaps most important, particularly with patients and their families, we must make sure they understand the information and details because without this fundamental understanding, a legitimate decision cannot be made about the IONM.
Nerve Conduction Studies
By Jerry Morris, MS, R.NCS.T., CNCT, FASET
Hey, everyone! I hope everyone had a wonderful holiday season. I know I did. January and February are usually the dreariest months around Louisiana. Usually by March things start to brighten up and spring is around the corner. It’s still a good time to be inside, and my northern and eastern friends have so many colder and drearier days and nights ahead.
Having said that, I am writing this article during my fourth week of rehabbing from right knee replacement surgery. I finally bit the bullet and had it surgically repaired the second week of January. The surgery went great; only two nights in the hospital in a room right down the hall from my EMG lab. Great nurses, therapists, the works… They had me up and walking on a walker less than 24-hours post-op and with very little pain. NOTE: I got rid of the walker and the cane 6-days post-op. Debby, my wife, said I was showing off. The only drawback was that they ran bags of D5W continuously for two days. I have never gone to the bathroom that much in my entire life! Fluids were going in my arm and seemingly going right through me. I think I slept in 30-minute shifts during those two days. Discontinuing the IV was a significant highlight of my stay, but it did feel humbling to see the patient care and staff interaction from the other side of the fence. Once I got home, I began going to physical therapy (PT) two days later. For what it’s worth, the surgery was a piece of cake compared to the PT. For an hour, two to three days a week, I got pushed and shoved and flexed and extended until I was ringing wet with sweat. One of the patients who was there at the same time called them “physical terrorists”. They said it, not me! Then I got to do the same thing at home on my off days. By the time you read this I should be back at work, either on light duty or full time. Four to six weeks off is pretty normal for this type of surgery. Debby is being a jewel at taking care of me since it was my right knee I cannot drive until I get clearance, she has become my chauffeur. Being stuck at the house has given me time to work on projects for ASET and AANEM, as well as the “Honey Do” lists Debby writes out for me each morning! I miss my patients, doing clinical work, and the day-to-day routine, but keeping busy at home has eased my boredom. If I get tired of my computer work, I just turn on the sports talk shows for a while. I could really get used to this, but I still want to get back to my work routine. Can’t change 43 years of working habits in only three to four weeks…
For this article, I have been asked to give a quick explanation of what I do when I do nerve conduction studies and how I go about that explanation. I can probably safely say that NCS/EMG can be, and probably are, the most painful modalities of neurodiagnostic technologies, with the possible exception of SSEPs. EEGs and LTM, BAERs, VEPs, sleep studies are relatively painless unless you scrub and prep the skin too hard. IOM studies are started and finished under sedation, and therefore not painful, unless your anesthesia person likes to wake the patient up a tad too early. EMG/NCS procedures are a bit more painful, depending on the patient’s sex, age, pain tolerance, attitude, and overall general health. Although an explanation of the procedures is supposed to be done by the referring physician, more often than not, an explanation is never given. So, as I am getting the patient ready for the NCS procedure, I explain to them, and their family if present, what I am going to be doing in the next 30 minutes or so. This involves answering any questions they have and trying to calm any anxiety they have about having the test. If I don’t know the answer to one of their questions, I tell them I will find out the answer as soon as I can and get back with them once the test is over. Once I start the test, I try to talk them through the process of cleaning their skin, putting on the electrodes, performing the actual stimulation, measuring distances, and marking for conduction velocities, etc. After doing this once or twice, most patients learn what the routine is, and any further detailed explanation is usually unnecessary, although there are always patients who need to have further details given to them. At all times, be POSITIVE! Every patient is different and needs to be treated with care, no matter how challenging they are personally. Technical challenges are often less difficult to deal with than personal ones. We, as techs, don’t really know what our patients go through day to day, so trying to be tuned-in to their feelings really helps a lot, no matter how difficult the situation. Once the NCS is completed, I start a simple and preliminary explanation of the EMG study if it is being performed. I try not to go into a lot of detail because the physician performing the EMG will do that. During the study, the doctor will adjust his explanation to his specific study criteria for that patient. Once the study is completed, any unanswered questions will try to be resolved. If the patient asks specific diagnostic questions, it is the doctor who will answer them. If no EMG is performed, I tell the patient and their family that the study will be given to the interpreting physician and that a final report will then go to the patient’s referring physician, even though at times this answer is frustrating to the patient. Remember that you are doing a painful and difficult test to a hurting and anxious patient. A good bedside manner, a sympathetic ear, and a willingness to listen often is the difference between a good and a mediocre study, no matter how technically sound you are.
Please have a wonderful spring and summer. Stay tuned in to ASET for the latest and greatest things in neurodiagnostics.
By Anna-Marie Beck, MOL, R. EEG T.
As I look back at all the times I have attempted to explain what I do to people I have to giggle. I have said things such as:
“Have you seen an ECG? What I do is similar, but I work with the brain, not the heart.” I overheard a physician explain it to a patient this way, and they understood it, so I used it.
“I put ‘buttons’ on a person’s head and watch their brain waves.” I have used this especially with children.
“I teach students how to perform tests on the nervous system, primarily the brain.”
“I work with neurologists.”
If I am speaking to someone who knows a little more about allied health, or health care in general, I give a few more details. However, it is usually simplified for them as many do not know or understand the scope of what we do and who we work with. While this is frustrating to me, especially as an educator and a parent of a child with epilepsy, I must remember not every person in health care is exposed to everything in health care.
Recently some of my students and I were speaking with local high school students about a career in neurodiagnostics. I loved hearing my students tell the high school students that this field is full of possibilities as we don’t know all there is to know about the brain and nervous system and if you want to be a part of something bigger than yourself, neurodiagnostics is a great way to do that. My 5-second blurb regarding our field: “If you have a passion for working with people, learning something new daily, being a detective for physicians, providing answers to the puzzle a physician is trying to figure out; then maybe neurodiagnostics is something you might be interested in. We work closely with physicians and direct patient care staff, but we all work together to ‘solve the puzzle’ for the patient. No two days are the same. I have always enjoyed what I do. The field of neurodiagnostics is ever changing and in that I take comfort. As I near 20 years in the field, I can honestly say that I have not regretted one day of my choice for neurodiagnostics.”
By Mark Ryland, AuD, R. EP T., RPSGT, R.NCS.T., CNCT, FASET
I consider myself to be one of the most fortunate people in the known universe as I have the honor and privilege to be part of an awesome team of dedicated individuals who are responsible for educating and training the next generations of Neurodiagnostic Technologists in our area of Ohio. Our field provides an enormous contribution to patient care, which is so very important. Because the field is changing, growing, and expanding so much, formal education of future technologists is an absolute necessity.
By Bill Coslett, Ph.D., CNIM, BCIA, EEG-C
“……Sleep that knits up the raveled sleeve of care. The death of each day’s life, sore labor’s bath. Balm of hurt minds, great nature’s second course. Chief nourisher in life’s feast…..”
William Shakespeare, one the world’s most prolific dramatist, was a very keen observer of human behavior. Many of his protagonists were afflicted with the pains of life including problems with sleep and vivid dreams. There are those today who say that Shakespeare’s lavish descriptions of character afflictions sets the foundation for many of our present sleep disorders such as night terrors, sleep paralysis, and insomnia. According to Shakespeare, sleep was a “blessing” given to many, but also serves as a curse to those with “restless minds.” Shakespeare understood how sleep effected the immune system as well as our overall general health and wellness. He understood how anxiety/stress and our ability to calm the mind prevents sleep onset and uninterrupted sleep.
Shakespeare’s observation in early 1600 rings true today. It is estimated that insomnia and daytime drowsiness affect 35–40% of the adult population annually and are a significant cause of morbidity and mortality (Ncbi.nlm.nih.gov). The untold impact of insomnia is staggering in terms of loss of productivity, increased risk of chronic health conditions, as well as increased negative impact of our mental health.
Today’s sleep industry is enormous, with billions of dollars in revenues being spent each year to combat the effects of our inability to get and stay sleep. Sleeping medications, such as Lunesta and Ambien, are one of the most widely prescribed prescriptions for general practitioners. Although these medications are safer now than were the benzodiazepines of years ago, there still are concerns about side effects, as well as issues of dependence.
There are so many over-the-counter sleep aids that a comprehensive listing would be impossible for this article. Although many times these medications may help bring about restorative sleep patterns, there remains issues of undesirable and possibly dangerous side effects.
An area that has received a lot of attention in sleep medicine is Neurofeedback. NF is a powerful tool that can help people with difficulties in getting and staying asleep. Studies are beginning to emerge demonstrating that neuro training impacts the sleep regulatory mechanisms in the brain. Many clinicians have documented that the first noticeable change with NF training is an improvement of sleep quality. This seems to hold true whether training is done for ADHD, chronic pain, and/or substance abuse.
The sensory motor rhythm (SMR) is an oscillatory brain wave noted over the sensory motor strip. It is considered by many to an idle rhythm of the brain. For most individuals, this frequency oscillates in the range of 12-15 Hz and is produced with a quieting of the motor cortex. Motion or the thought of movement diminishes the sensory motor rhythm. Another name for this oscillation is the Mu rhythm or what is commonly referred to as a Wicket Rhythm.
In 1963, Barry Sternman, a pioneer in the field of neuroscience, was doing some research involving a Pavlov-like experiment training the brains of cats. Sternman was the first to show that instrumental condition of the SMR was possible. Two very interesting observations were made by Sternman in his research of cats:1) SMR training selectively enhanced spindle activity in subsequent sleep and 2) SMR training produced longer periods of undisturbed sleep.
It is hypothesized that SMR training impacts sleep by increasing sleep spindle density, which results in a normalization of sleep onset. Others suggest that the rationale for SMR training is that increased relaxation combined with inhibition of motor activity should counteract the hyperarousal associated the problems of sleep onset.
Generally, training is placed with one electrode placed on the sensory/motor strip (C3 or C4) and the other electrode placed as a reference over the ear (A1/A2). As a general rule, training from the right side at C4-A2 produces a calming and relaxed affect while left hemisphere (C3-A1) training produces a more energizing and focused affect. The goal of the training is to increase the amplitude of the SMR with auditory and or visual feedback given as a reward when amplitudes exceed a specific threshold. Some NF therapists incorporate a reward for inhibition of Beta along the sensory motor strip. As a general rule, changes in sleep patterns can emerge in as quickly as 6–10 sessions.
Any comprehensive treatment of sleep insomnia should include incorporating positive sleep hygiene practices, general physical exercises, as well as cognitive behavior strategies. It is now being recognized that neurofeedback can be added to help those individuals who have trouble in getting and staying sleep.
By Janna Cheek, R. EEG T., CNIM
Ideas and maneuvers to translate our job and its description to patients by being able to relate to generational phrases or activities to help with communication:
NeuroLinks provides multiple NDT procedures to both in- and outpatients; to the young and old, which at times becomes challenging to explain exactly what we are doing to their head. We commonly answer questions, such as, “Do earlobes have brainwaves in them?” or “Can you read my mind or see what I’m thinking?”
I have explained to the elderly females that it is like the perms their moms use to give them, but this one won’t damage their hair. Another comical explanation I have given elderly men is that I am just needing to confirm that your brain is “clicking on all cylinders” and if not, we have an extra supply of them (cylinders) at a discount price in our backroom.
But I think the most memorable and precious explanation came from a little 6-year-old girl many years ago who told me to please send pretty music to her brain to listen to when she went to sleep. I explained to her that I would do my best, but that this test doesn’t send things into her brain, only records what comes out of her brain. If she likes pretty music, then this test can write down the pretty music she likes to hear on a piece of paper (analog back then) in a language that that the doctor can read.
At the end of her test, I tore off the first couple of pages of recording (BioCal), folded it up, drew a heart on the outside of it with my red china marker, wrote her name on it, and handed it to her on her way out of the exam room letting her know that this was the music her brain wrote down for her doctor to see. That easy little gesture made this little girl so happy and proud. You would have thought I’d given her the moon. She showed it to everyone in the waiting room and her mom called the next week to let me know that she was still sleeping with her “mind’s music waves”.
It takes a lot of creativity and thinking outside the box many times to be able to get your patient to relate, relax, and understand what an EEG is all about and why they need these wires placed on their head.