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Clinical Evoked Potentials An Illustrated Manual Omkar N Markand 123 Clinical Evoked Potentials Omkar N. Markand Clinical Evoked Potentials An Illustrated Manual Omkar N. Markand, MD, FRCP(C), FACP Professor Emeritus of Neurology Department of Neurology Indiana University School of Medicine Indianapolis, IN USA ISBN 978-3-030-36954-5    ISBN 978-3-030-36955-2 (eBook) https://doi.org/10.1007/978-3-030-36955-2 © Springer Nature Switzerland AG 2020 This work is subject to copyright All rights are reserved by the Publisher, whether the whole or part of the material is concerned, specifically the rights of translation, reprinting, reuse of illustrations, recitation, broadcasting, reproduction on microfilms or in any other physical way, and transmission or information storage and retrieval, electronic adaptation, computer software, or by similar or dissimilar methodology now known or hereafter developed The use of general descriptive names, registered names, trademarks, service marks, etc in this publication does not imply, even in the absence of a specific statement, that such names are exempt from the relevant protective laws and regulations and therefore free for general use The publisher, the authors and the editors are safe to assume that the advice and information in this book are believed to be true and accurate at the date of publication Neither the publisher nor the authors or the editors give a warranty, expressed or implied, with respect to the material contained herein or for any errors or omissions that may have been made The publisher remains neutral with regard to jurisdictional claims in published maps and institutional affiliations This Springer imprint is published by the registered company Springer Nature Switzerland AG The registered company address is: Gewerbestrasse 11, 6330 Cham, Switzerland With gratitude and love, I dedicate this book to the memory of my wife, Pramila Lal Markand In her last years of life, she encouraged me to work on the manuscript of this book even when it may have cut into a portion of our time together Her constant belief in me was unending I also would like to dedicate this book to my two daughters, Vaneeta M. Kumar and Sandhya M. Graves Their belief in me and constant support inspired me to put my clinical experience of evoked potentials over the past several decades in the form of a book Foreword It was 1976, the second year of Medical School at Indiana University, and the course was an Introduction to Clinical Medicine On that day, the lecture was on epilepsy: a complex topic, especially for students knowing so little about clinical semiology, neurophysiology, and the world of EEG. In that hour, Dr Omkar Markand calmly, with reassurance and certainty, laid out the world of neurophysiology and epilepsy in a clear, logical, and clinically valuable fashion Amazingly, organized and complete, we all paid attention and processed his wisdom and understanding Something so complex for us became something understandable and a framework for building an interest and a career in neurology We immediately, as students, understood that he was more than a great neurologist and expert in neurophysiology He was a teacher in the truest sense – an amazingly, wonderful teacher who would affect so many of us and contribute to so many careers in neurology In 1984, while taking my oral boards in neurology, I was presented with a patient having an acquired spastic paraparesis The discussion was intense, and the examiners turned to the diagnostic workup for multiple sclerosis The back and forth was challenging, and I had an uneasy feeling about the outcome of the entire session My learned examiners brought up the topic of spinal fluid studies and evoked potentials and wanted to know just how good these studies were in providing evidence for MS. At that moment, my fortunes turned, and I calmly began my response with, “according to Markand et  al as just recently published in the green journal (Neurology), the sensitivity and specificity for these are…,” and his data flowed into the discussion Hearing Markand’s name, the examiners finally relaxed and smiled, and for the first time in the session, they seemed comfortable that I knew something of importance (Bartel et al 1983) Being on the faculty in the Department of Neurology at Indiana University since 1985, I have acquired an understanding and complete appreciation for the tremendous professional and personal qualities that lead to Dr Markand being viewed uniformly by his colleagues and his students as a unique treasure and gift to the world of neurology He knows his field to depths unmatched His work ethic is inspirational And, Dr Markand, to this day, remains one of the most gifted teachers of neurology and neurophysiology that the field has ever seen In an ocean of many great teachers in neurology, there is none any better than Omkar Markand We are so fortunate that he has chosen to share his vast knowledge of evoked potentials with the neurophysiology and neurology world There is no greater vii viii Foreword authority on this topic than Omkar Markand From the fundamental neurophysiology and technology to the anatomic considerations to the clinical applications, Dr Markand has gathered his experience and understanding from 50 years in the field to provide the reader with a complete and cogent tour de force of evoked potentials in clinical medicine – a tremendous resource for practitioners and neurophysiologists and for those clinicians seeking to apply these important techniques to the evaluation and management of their patients Dr Markand has not only devoted his career to Indiana University and to the Department of Neurology but also to our patients He is an integral part of the very fabric of what makes us special He is Professor Emeritus of Neurology and Director EEG/Evoked Potentials/Epilepsy at Indiana University School of Medicine and is one of the most remarkable educators at Indiana He continues to provide exceptional training for our residents and fellows in EEG, evoked potentials, and epilepsy He is viewed as the ultimate source of truth Of his numerous awards and honors, I point to his receiving the Health Care Hero Award for his lifelong work in epilepsy in Indiana And, on a national level, Dr Markand received the annual Jasper Memorial Award in 2009 from the American Clinical Neurophysiology Society for lifelong work in clinical neurophysiology On the international stage, he received a Lifetime Achievement Award of the Association of Indian Neurologists in America (AINA) given by the American Academy of Neurology And he has received the “Certificate of Medical Excellence” awarded by the Epilepsy Foundation of Indiana for high values, commitment to public service, community involvement, leadership, and dedication to those with epilepsy The terms “role model” and “mentor” as well as the discussions of “professionalism” are often emphasized, defined, and applied to talented and accomplished individuals in the medical profession; yet, rarely there comes along a person for whom these terms are insufficient Professionals like Dr Markand are the stimuli for which such words are created For me, this has always been the case I love being able to call Omkar Markand my friend and colleague, and am so thankful he was in my brain during the oral board exams His many years of trainees and professional colleagues are grateful for his production of this valuable book of truth on evoked potentials Reference Bartel DR, Markand ON, Kolar OJ.  The diagnosis and classification of multiple sclerosis: evoked responses and spinal fluid electrophoresis Neurology 1983;33:611–7 Robert M. Pascuzzi, MD Professor and Chair Department of Neurology Indiana University School of Medicine Indianapolis, IN, USA Preface With the introduction of evoked potentials (EPs) in clinical medicine in the mid-­ 1970s, visual, brainstem auditory, and somatosensory EPs played a major role in the diagnosis of suspected demyelinating disorder Although their applications have significantly changed since magnetic resonance imaging became a major diagnostic modality for multiple sclerosis, the use of EPs continues in order to exclude, detect, or confirm conduction abnormalities involving major afferent systems in the central nervous system In addition, somatosensory EPs, along with the transcranial motor EPs, have established themselves as a standard of care for intraoperative monitoring during various spinal and intracranial surgeries The major role the EPs play during intraoperative monitoring is reflected in several excellent texts, published over the last few decades on the subject of monitoring during surgery But only a few texts have appeared which have devoted themselves exclusively to diagnostic applications of EPs in clinical medicine At the Indiana University School of Medicine, Department of Neurology, there has been a strong clinical neurophysiology section for the last five decades As the only university medical center in the State, all the attached hospitals have been an excellent source of neurologic referrals This has provided me with a large collection of abnormal EPs, which I was able to use for teaching purposes Because of my interest in EPs, I have been the sole clinical neurophysiologist at the institution who has had the distinct privilege of interpreting almost all of the diagnostic EPs, in addition to directing this subspecialty of clinical neurophysiology at the institution I also developed a handout on “clinical evoked potentials” for the neurology residents and the clinical neurophysiology fellows to help them learn the basics of EPs This handout has been updated on several occasions and is still used today Many of the fellows in the past encouraged me to publish a book on clinical EPs based on this handout, as well as include a large number of EP illustrations I had in my collection So during my semiretirement, I decided to undertake their request for writing this book One of the problems facing the writer was to limit the area of his presentation Evoked potentials are utilized extensively in the operating room, as well as in the clinical diagnostic laboratories Because there have been excellent texts already available on EPs for intraoperative monitoring, I decided to limit myself essentially to the diagnostic applications of EPs in my work Thus, this book represents an attempt to provide essential basic knowledge pertinent to all modalities of the ix x Preface evoked potentials as they are practiced by clinical neurophysiologists in the diagnostic laboratories The role of EP intraoperative monitoring is dealt with only in a minor way In addition, a large number of illustrations depicting various types of EP abnormalities are also included in this book Thus, the reader may find this book not only as a basic text but also as an atlas of evoked potentials This book is divided into five major chapters The first chapter discusses relevant material on the techniques of EP recordings, the basics of the analog to digital conversion, the principles of signal averaging, and how to gather normative data in a laboratory Second to fifth chapters survey, respectively, the brainstem auditory, the visual, the somatosensory, and the motor EPs Chapters on auditory, visual, and somatosensory EPs include six case studies at the end of each chapter based on actual clinical cases with reasons for ordering the test, the EP findings, their interpretation, and discussion A format of generating EP reports is provided to help the reader acquire basic skills in typing or dictating clinical reports on EP studies I sincerely hope that this book will be informative for practicing neurologists, clinical neurophysiologists, psychiatrists, and others who request and/or interpret EPs in their clinical practice It may also serve as a basic text and atlas of major EP abnormalities for the neurology residents and fellows of clinical neurophysiology There are several people who helped me directly and indirectly to bring this book in the present format I am thankful to many neurophysiology fellows at the University who made several helpful suggestions over the past several years and who inspired me to undertake this work My special thanks are to Christopher Brown, BFA, MS, Medical Illustrator, Indiana University School of Medicine, who helped me with all the illustrations and figures of this book In many instances, he retraced the EP graphs, making them visibly more clear without ever altering the details of the waveform I not think I could have put the book together without his tremendous assistance My thanks are to Glenda Shaw, BA, Medical Editor and Communications Specialist, Indiana University School of Medicine, who edited the manuscript Finally, I am indebted to the many technologists performing diagnostic EPs at the Indiana University-affiliated laboratories who helped me acquire the normative data and assisted in identifying and obtaining graphs of the EPs on many of my patients Indianapolis, IN, USA October 2019 Omkar N. Markand, MD, FRCP(C), FACP Contents 1Basic Techniques of Evoked Potential Recording ������������������������������������   1 Basic Principals of EP Recording����������������������������������������������������������������    1 Stimulus Characteristics��������������������������������������������������������������������������    2 Amplification ������������������������������������������������������������������������������������������    2 Filtering of the Analog Signal������������������������������������������������������������������    3 Analog to Digital Conversion������������������������������������������������������������������    3 Signal Enhancement��������������������������������������������������������������������������������    6 Limitation of Signal Averaging����������������������������������������������������������������    8 Strategies to Improve EP Recording��������������������������������������������������������    9 Common Problems Encountered During EP Recordings������������������������    9 Final Recording, Display, and Storage of EPs����������������������������������������   11 Nomenclature of EP Components����������������������������������������������������������������   11 Measurements����������������������������������������������������������������������������������������������   11 Appropriate Use of Certain Stimulating and Recording Parameters ����������   14 Analysis Time������������������������������������������������������������������������������������������   14 Stimulus Rate ������������������������������������������������������������������������������������������   15 Filters ������������������������������������������������������������������������������������������������������   16 Sampling Rate������������������������������������������������������������������������������������������   17 AD Convertor������������������������������������������������������������������������������������������   17 Number of Averages��������������������������������������������������������������������������������   18 Recording Montage����������������������������������������������������������������������������������   18 Utility of EPs�����������������������������������������������������������������������������������������������   22 References����������������������������������������������������������������������������������������������������   23 2Brainstem Auditory Evoked Potentials������������������������������������������������������  25 Overview of the Technique of Recording BAEPs����������������������������������������   26 Normal BAEPs��������������������������������������������������������������������������������������������   28 Generators of BAEP Components ��������������������������������������������������������������   30 BAEP Evaluation and Criteria of Abnormalities ����������������������������������������   34 Evaluation of BAEPs ������������������������������������������������������������������������������   34 Criteria for Clinically Significant BAEP Abnormality����������������������������   36 Factors Affecting BAEPs ����������������������������������������������������������������������������   37 Clinical Applications of BAEPS������������������������������������������������������������������   48 Coma������������������������������������������������������������������������������������������������������������   48 xi Applications of TCMS 227 Fig 5.5 Schematic diagram of transcranial magnetic stimulation (A) followed by magnetic stimulation of the spine (B) generating the muscle MEPs (a) and the CMAP (compound muscle action potentials) (b), respectively From these two recordings, the central motor conduction time is determined Also note the silent period following MEP (a) However, if CMCT is measured by the foraminal stimulation technique, it may be prolonged due to intraspinal nerve root lesion The CMCT has been noted to be 2–3 times higher in infants and gradually decrease with maturity reaching adult value around the age of 3–5 years (Garvey and Mall 2008) after which it remains stable throughout adulthood The CMCT to the upper limb muscles is not related to height but to the lower limb muscles it does There are no significant gender or side-to-side differences Amplitude of MEP: The amplitude of MEP is much variable and significantly less than that of compound muscle action potential (M-wave) obtained by supramaximal stimulation of the peripheral nerve It is also more polyphasic and of longer duration than the M waves MEP amplitude is usually measured peak-to-­peak from the highest amplitude response elicited by five to six consecutive MEP traces MEPs can be enhanced by several techniques but particularly by exerting a background voluntary contraction A slight voluntary contraction (at a level of 5–20% of maximum effort) generates MEPs of shorter latencies (by 1–3 msec) and of  higher amplitudes (severalfolds, often as much as the amplitude of 228 5  Motor Evoked Potentials M-wave) in normal subjects When the target muscles are paralyzed or weak so that they cannot be contracted voluntarily, other types of facilitation techniques have been utilized such as vibration of the muscles, prestimulation of the mixed nerves innervating the muscle, intention to contract the muscle (mental simulation), or a contraction of the homologous muscle of the opposite limb (Rossini and Rossi 1998) These MEPs are often referred to as “contracted MEPs” compared to the “relaxed MEPs.” The contacted MEPs, being shortest in latency, are utilized for CMCT or MEP latency measurements Besides the absolute amplitude of the contracted MEPs, an MEP/M amplitude ratio is often used It is expressed as percentage of the MEP amplitude to the M-wave amplitude obtained by supramaximal stimulation peripherally of the nerve innervating the muscle This ratio is the preferred measure of MEP amplitude because it has lesser intersubject variability than the absolute amplitude The MEP/M ratio in ABP muscle in normal subjects is reported to be 91.5% ± 7.2% in the contracted state (Uozumi et al 1991) Triple stimulation technique (TST): Magistris et  al (1999) developed a triple stimulation technique which, through two collisions, synchronizes the transcranially induced discharges of spinal motor neurons The smaller amplitude of the MEP compared to the M-wave is mostly due to phase cancellation of the action potentials caused by the desynchronization occurring within the corticospinal tract or at the spinal motor neuron level Similarly, the variability from one stimulus to another among normal subjects is mostly due to variability of this desynchronization The amplitude of MEP recorded with TST matches very closely to the M wave; therefore, the MEP/M ratio is 1 in normal subjects Applying TST, which allows a technical “resynchronization” of the spinal motor neuron discharge, the conduction failure of various degrees was detected 2–3 times more often in patients suspected of corticospinal dysfunction than by evaluating conventional MEPs (Magistris et al 1999; Bühler et al 2001) Even though TST is somewhat challenging to perform, it is recommended as a diagnostic method of choice for upper extremity MEPs Cortical motor threshold: With TCMS, cortical motor threshold for eliciting MEP in a given muscle is evaluated during complete relaxation This so-called resting motor threshold is defined as the intensity of stimulation required to get a 50 μv MEP appearing with 50% probability Another threshold measure is “active motor threshold” defined as intensity required to obtain a MEP of about 100–200  μv in slightly contracted muscle (20% of maximum effort) Besides absolute threshold values, which are more variable among subjects, the interhemispheric thresholds in one individual are quite similar The latter parameters can, therefore, be utilized in disorders affecting one cerebral hemisphere (e.g., strokes) Although the method proposed by Rossini et al (1994) is commonly utilized to measure cortical motor threshold, there are several technical details which have not yet been standardized Furthermore, the threshold is not a static measure because it depends upon several variables, such as target muscle, age, drug effect, Applications of TCMS 229 patient’s posture (lying or seated), and wake-sleep cycles More work is needed to standardize the method of measurement if corticomotor threshold could be utilized effectively for diagnostic purposes Silent period: Besides excitatory effects, TCMS, also, elicits inhibitory effects, e.g., silent period (SP) When the motor cortex is stimulated while the subject maintains a voluntary tonic contraction of a muscle, a pause in the ongoing EMG activity follows the evoked MEPs The mechanism of this SP is unknown, but perhaps multifactorial, occurring both at the segmental and suprasegmental levels The H-reflex (segmental reflex) is found to be depressed during the early phase (first 100 msec) of the SP, but not during the later phase suggesting that the initial portion of the SP may be due to segmental factors (reduction in spinal motor neuron excitability), whereas the latter phase may be suprasegmental, e.g., lack of cortical drive Both in the normal subjects and in patients (e.g., with spasticity), it is possible to record a SP in the absence of preceding MEP. If a muscle is weak, TCMS may not elicit an MEP but may still demonstrate SP if the patient can maintain some contraction of the muscle The SP is considered a physiologic phenomenon distinct from MEP. The SP duration increases linearly with the stimulus intensities Even with maximum stimulator output, the duration of SP in normal hand muscles has a wide range (100–300  msec) but has low intraindividual variability and a high interside symmetry (less than 25 msec) SP is commonly measured as the duration from the onset of the MEP to the resumption of sustained EMG activity during tonic voluntary activation of the target muscle There are several limitations associated with SP determination, which are discussed, and appropriate strategies suggested by Groppa et  al (2012) The SP may provide helpful information regarding intracortical inhibition in the primary motor cortex Transcallosal inhibition has also been demonstrated by applying a single pulse which produces transient suppression of the EMG activity ipsilateral to the TCMS.  This has been used to evaluate interhemispheric connectivity and conduction time Measures to evaluate cortical inhibition and facilitation: TCMS technique using paired-stimuli paradigms has been used to study cortical inhibitory and facilitatory mechanisms Since this application is primarily a research tool to understand pathophysiologic basis of neurological disorders and presently has little clinical utility, only a brief description follows Paired TCMS stimuli consist of an initial conditioning stimulus followed after a variable interval by a test stimulus Using such a protocol, it is shown that a subthreshold conditioning stimulus suppresses the MEP in response to a subsequent suprathreshold stimulus (test stimulus) delivered after 2–5  msec This inhibition is called short-interval intracortical inhibition (SICI) It demonstrates that a cortical stimulus, which is not strong enough to evoke an MEP, may still generate a strong intracortical inhibition SICI is of intracortical origin, possibly GABAergic, and considered a useful measure for assessing even minor changes in cortical excitability in normal and pathological conditions 230 5  Motor Evoked Potentials Using this measure, patients with JME have been found to show a unique pathophysiology (Caramia et al 1996) Long-interval intracortical inhibition (LICI) is demonstrated when a suprathreshold conditioning stimulus is followed in 50–200 msec by a decrease of the test MEP amplitude This again is a cortical phenomenon but mediated by a different set of inhibitory neurons than for SICI Not only inhibitory but facilitatory influences have been described using paired stimuli protocols At short and discrete interstimulus intervals (1.1–1.5, 2.3–3.0, and 4.1–4.3 msec) with both the conditioning and the test stimuli close to the threshold or suprathreshold conditioning stimulus and subthreshold test stimulus, a facilitatory effect is seen for the test stimulus This short interval intracortical facilitation is again due to intracortical mechanisms Paired magnetic stimulation with conditioning stimulus below and test stimulus above threshold at an interstimulus interval of 8–30 msec causes an increase in the test MEP amplitude (compared to the test stimulus alone) This is called intracortical facilitation and appears to be due to intracortical, possibly glutamatergic-­mediated, mechanisms Paired-stimuli paradigm has, also, been used such that the conditioning and the test stimuli are delivered over the opposite hemispheres A mild interhemispheric facilitation is produced at short interstimulus interval (4–6  msec), whereas a potent interhemispheric inhibition results from longer intervals (8–50 msec) between the two stimuli Table 5.4  Common diagnostically utilized parameters following TCMS of motor cortex Description Response of target muscle – shortest latency, highest amplitude, and MEP/M amplitude ratio are evaluated 2. Central motor Time from motor cortex to LMN, derived from MEP latency by conduction time (CMCT) subtracting peripheral transit time Measure 1.  Muscle MEP Physiologic significance Evaluates integrity of the system including UMN, corticospinal tract, and LMN – latency denotes time from motor cortex to target muscle Diagnostically most evaluated measure of conduction in fast conducting pathway between upper and lower motor neuron Utilizes MEP and double collision TST/M ratio is directly related to the 3. Triple number of activated LMNs technique to “resynchronize” stimulation  Better measure of central conduction LMN discharge technique than CMCT (TST) Excitability measure of the pyramidal 4. Resting motor Intensity required to get a threshold 50 μV MEP appearing at least half neurons and the excitatory interneurons in the motor cortex of the time Related both to the cortical and 5. “Silent” Suppression of the tonic EMG segmental inhibitory processes period following the MEP or without a proceeding MEP LMN lower motor neuron, UMN upper motor neuron, MEP motor evoked potential, M compound muscle action potentials Applications of TCMS 231 Clinical Applications Table 5.5 summarizes the diagnostic utility and the MEP findings in major neurologic disorders: Multiple sclerosis (MS): Hess et al (1987) conducted an extensive study on 83 patients with MS evaluating CMCT from the abductor digiti minimi (ADM) muscles to magnetic stimulation of the motor cortex and electrical stimulation at C7–T1 interspace The CMCT was abnormal in 60 patients (72%) The incidence was higher in those with weakness of the ADM, but arms out of 32 with normal examination had abnormal CMCT, thus detecting subclinical lesions The sensitivity of the test was slightly better than with VEPs and SSEPs MEP abnormalities which have been reported in  MS include prolonged CMCT, prolonged MEP latencies, MEP dispersion, reduced MEP amplitude (MEP/M ratio), or absence of MEPs Several studies have shown that prolonged CMCT is seen in 56–93% of patients with MS, a higher sensitivity if lower limb muscles are included (Chen et  al 2008) and if there are clinical motor deficits The recently introduced TST revealed that there is a high incidence of central conduction abnormalities in MS patients (Bühler et al 2001; Humm et al 2003) and that this method is more superior compared to the conventional MEP technique Caramia et al (1991) also found an increased threshold for eliciting MEPs in relaxed muscles of the upper and lower extremities in over two-thirds of their 34 patients with MS. Britton et al (1991) in a study found an increased onset variability of MEPs as an additional abnormal parameter in almost half of the first dorsal interosseous muscles tested in 21 patients with MS. In conclusion, various TCMS measures provide clinically useful information regarding the functional status of corticospinal tracts including detection of subclinical lesions and possible reclassification of MS Amyotrophic lateral sclerosis (ALS): Unequivocal diagnosis of ALS depends upon the presence of both upper and lower motor neuron dysfunction LMN involvement is easy to demonstrate by conventional EMG studies, but the concomitant presence of UMN degeneration may be elusive and often obscured by the LMN signs TCMS has been utilized in patients with motor neuron disorder (MND), who may have either questionable or total absence of UMN signs The goal is to detect subclinical signs of UMN dysfunction so that a reliable diagnosis of ALS may be established Several TCMS parameters have been evaluated in patients with MND. Schriefer et  al (1989) demonstrated abnormal findings in 14/22 patients with MND on TCMS of the motor cortex Prolonged CMCT and absence of response to brain stimulation were more frequent than the low amplitude MEP without prolonged CMCT. Subsequent studies have shown abnormal TCMS findings in 50–100% of ALS patients (Claus et al 1995; Eisen et al 1990); the variable sensitivity is most likely related to the proportion of patients with definite UMN signs and also to different diagnostic parameters utilized for TCMS testing 232 5  Motor Evoked Potentials Schulte-Mattler et al (1999) studied 39 patients with MND; 19 patients had definite UMN signs, had probable UMN signs, and had no UMN signs MEPs were elicited from ADM and anterior tibial muscles TCMS was considered abnormal if there was no response to cortical stimulation (but a response present to peripheral stimulation) and if the CMCT was abnormal All patients with definite UMN signs had abnormal findings, but over two-thirds with the probable or absent UMN signs also had abnormal studies They concluded that TCMS helped to establish the diagnosis of ALS more reliably in patients without definite UMN signs Other studies have emphasized parameters other than the CMCT to detect UMN dysfunction in patients with MND, e.g., resting motor threshold, small or unobtainable MEPs, prolonged latencies of MEPs, and decreased MEP/M ratio during voluntary contraction (Eisen et  al 1990; Uozumi et  al 1991) Triple stimulation technique by demonstrating reduced TST response size has been claimed to detect varying degrees of conduction failure more frequently as an indicator of pyramidal tract involvement particularly if both upper and lower extremity muscles are evaluated (Bühler et al 2001) Probably, the largest clinical study is by Triggs et al 1999, who studied 121 patients with MND. They divided their patients into following four groups with corresponding incidence of abnormal findings (a) ALS, definite (UMN +, LMN +): 41 patients (34 or 83% had abnormal studies) (b) ALS, PUMNS (LMN +, UMN probable): 40 patients (30 or 75% had abnormal studies) (c) Pure LMN syndrome: 22 patients (6 or 27% had abnormal studies) (d) Progressive bulbar palsy: 18 patients (14 or 78% had abnormal studies) Increased motor thresholds were the most common abnormality observed The threshold in some patients was so high that no MEPs could be elicited with maximum stimulation In addition, the duration of SP was reduced in ALS. Moreover, SP could be elicited in some patients in whom MEPs could not be recordable even at a maximal stimulator output In the most recent study, Wang et  al (2019) applied TST, CMCT, MEP latency, and resting motor threshold in 50 patients with ALS, 28 with and 22 without UNN signs The incidence of abnormality in TST amplitude ratio, resting motor threshold, CMCT, and the MEP latency was 89.3%, 78.6%, 64.3%, and 64.3%, respectively, in those with UMN signs Abnormal TST ratio was detected in 27.3% of 22 patients without UMN signs, whereas other parameters were abnormal in only 13.6% in this group The authors concluded that TST was a more sensitive measure for detecting UMN conduction failure in ALS and contributed to an early diagnosis by providing evidence of subclinical UMN dysfunction so that the diagnosis of ALS could be made with a higher degree of confidence Caramia et  al (1991) found increased excitability threshold and prolonged CMCT both for upper and lower limb MEPs in three out of the four patients with Applications of TCMS 233 primary lateral sclerosis One patient without MEP abnormalities had a long duration condition, probably a mild form of the disorder One can conclude that TCMS is a useful clinical tool in detecting UMN dysfunction in patients with MND presenting essentially with LMN signs if multiple parameters such as CMCT, excitation threshold, SP, and MEP characteristics are evaluated Movement disorders: In various movement disorders, TCMS has contributed to better understanding of the pathophysiology, but the technique has attained no diagnostic application so far This application has been well discussed by Cantello (2002), and the author emphasized that in most movement disorders, the CMCT and threshold studies have been essentially normal On the other hand, SP, SICI, LICI, and other parameters have shown abnormalities MEP studies may also be helpful in differentiating classic Parkinson’s disease in which CMCT is normal from other atypical parkinsonian disorders in which a prolonged CMCT may provide a useful evidence of subclinical UMN involvement Strokes: In severely affected muscles, the MEPs are often non-recordable, whereas in less severely affected muscles, they may be elicitable but are low in amplitude and prolonged in latency with elevated excitable threshold TCMS studies have been utilized in stroke patients to predict the outcome Absence of MEPs in the paralyzed limb and an increased MEP amplitude in the unaffected limb on contralateral hemispheric stimulation are findings which suggest poor functional recovery (Trompetto et al 2000) On the other hand, recordable MEP in the paralyzed limb on stimulation of the affected hemisphere is a favorable predictor (Hendricks et al 2003) Motor assessment by MEPs may be more sensitive than clinical examination to detect residual corticospinal function which may be a better predictive parameter for motor recovery after stroke Myelopathy: Cervical spondylosis commonly results in radiculopathy, but more severe neurologic complication is cord compression, which can be evaluated functionally with TCMS. A large study reported by Lo et al (2006) evaluated MRI and TCMS findings in 231 patients with cervical spondylosis with different grades of cord compression TCMS showed 98% sensitivity and 98% specificity for cord abnormality using MRI as reference standard They concluded that while TCMS is not a substitute for MRI scan, TCMS is of value as a rapid, inexpensive, and noninvasive technique for screening spondylotic patients prior to MRI studies TCMS may also detect evidence of spinal cord compression before clinical signs become evident Travlos et al (1992) evaluated this area of utility in 23 patients with cervical radiculopathy None had overt myelopathic features MEP recorded from hand muscles showed prolonged CMCT and/or reduced MEP/M ratio in 65% They suggested that such findings may direct a more timely surgical intervention Assessing the functional state of the corticospinal tracts and predicting the extent of recovery after spinal cord injury using different experimental treatment 234 5  Motor Evoked Potentials modalities are areas of intense interest TCMS has a place in the research protocols investigating spinal cord trauma Epilepsy: TCMS stimulation has been used to identify basic mechanism underlying epilepsy, particularly in idiopathic generalized type Threshold for TCMS using single pulses has been shown to be an important indicator of cortical excitability Patients with untreated generalized epilepsy show a lower threshold to TCMS suggesting an increased cortical excitability In treated patients, however, the TCMS threshold is higher than for normal persons due to the suppressive action of antiepileptic drugs Caramia et al (1996) used paired TCMS of the motor cortex to assess the role of cortical inhibition In paired stimulation paradigm, it has been demonstrated that a subthreshold conditioning stimulus suppresses the MEP (in relaxed hand muscles) generated in response to a subsequent suprathreshold test stimulus delivered after 1–6 milliseconds This inhibition is due to intracortical inhibitory mechanisms mediated by GABAergic inhibitory system Patients with JME showed findings dissimilar to other forms of idiopathic generalized epilepsy using this paired stimulation technique They did not exhibit MEP suppression and showed a progressive amplitude increase of MEPs to the test stimulus over the course of a series of consecutive paired stimuli This was in contrast to a normal healthy person who usually shows a slight decrease in the MEP to the test stimulus over a course of consecutive stimuli implying a progressive inhibition to ongoing stimulation The author postulated that impaired MEP suppression may be due to loss of intracortical inhibition By contrast, no such loss of inhibition to paired stimulation was found in patients with sporadic grand mal epilepsy They concluded that a JME marker may be loss of MEP inhibition 7. Psychiatric applications: TCMS has emerged as one of the treatment options for resistant depression disorder, which accounts for one-third of all cases of major depression (Garnaat et al 2018) TCMS is physically delivered in trains of pulses (usually 10 Hz for 4 seconds) separated by periods of rest Figure-of-eight coil is commonly used for stimulation This is called repetitive TMS (rTMS) In 2008, the Federal Drug Administration cleared the first TMS device to treat major depression, and now multiple devices have been approved Meta-analysis and large randomized control trials have usually shown beneficial effects The mechanism of action is considered to be the ability of rTMS to modulate neuronal firing in both excitatory and inhibitory circuits Depression has been linked to a dysfunction in a network of dorsolateral prefrontal cortex, and this is the area of the brain which is targeted by magnetic stimulation Success in treating depression has led to a growing interest in its application as a therapeutic tool in a variety of neuropsychiatric conditions such as schizophrenia, obsessive-­ compulsive disorder, posttraumatic stress disorder, attention-deficit/hyperactivity disorder, substance abuse disorder, autism spectrum disorder, anxiety/panic disorder, bipolar disorder, and even in patients with refractory epileptic seizures It has also been used in pediatric seizure disorder The therapeutic utility of rTMS in all of these conditions has yet to be clearly defined Applications of TCMS 235 Pillai et  al (1992) described normal SSEPs as well as normal MEPs and CMCT in two patients with  psychogenic paralysis; an expected finding Schönfeldt-­Lecuona et al (2006) investigated the effect of rTMS in four patients with nonorganic limb paralysis; three were diagnosed with conversion disorder and one with malingering Stimulation frequency was 15  Hz, train length 2 seconds, intertrain interval 4 seconds, and daily total of 4000 stimuli All three who had conversion disorder had complete recovery or marked improvement in a few weeks, but the malingerer did not respond The author concluded that rTMS may have therapeutic effect in motor conversion disorder, but not in simulated paralysis or malingering The rTMS is very safe The degree of cortical excitation depends upon the frequency as well as the intensity of stimulation The major concern, therefore, is the triggering of seizures in epileptic patients with rTMS. This is extremely infrequent with single pulses or lower frequency (
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