(BQ) Part 2 book Current practice of clinical electroencephalography presents the following contents: Pediatric epilepsy syndromes, EEG in adult epilepsy, EEG voltage topography and dipole source modeling of epileptiform potentials, subdural electrode corticography, evoked potentials overview, neurophysiologic intraoperative monitoring.
10 Pediatric Epilepsy Syndromes DOUGLAS R NORDLI Jr Introduction: Differential Diagnosis of Epilepsy According to Prominent EEG Features The Familial Epilepsies (Epilepsies with Frequently Normal Interictal Backgrounds) Benign Familial Neonatal Epilepsy Benign Familial Infantile Epilepsy Autosomal Dominant Nocturnal Frontal Lobe Epilepsy Familial Lateral Temporal Lobe Epilepsy or Autosomal Dominant Epilepsy with Auditory Features Familial Mesial Temporal Lobe Epilepsy Genetic Generalized Spike-Wave Epilepsies Myoclonic Epilepsy in Infancy Myoclonic-Astatic Epilepsy (Doose Syndrome) Childhood Absence Epilepsy Epilepsy with Myoclonic Absences Juvenile Absence Epilepsy Juvenile Myoclonic Epilepsy Masquerading Conditions Self-limited Epilepsies with Focal Spikes Panayiotopoulos Syndrome Benign Childhood Epilepsy with Centrotemporal Spikes or Rolandic Epilepsy Late-Onset Occipital Lobe Epilepsy Conditions Masquerading as Self-limited Epilepsies with Focal Stereotyped Spikes Epilepsies with Encephalopathy (Epilepsies with Slowed Backgrounds and Multifocal Pleomorphic Spikes) Epileptogenic Encephalopathies Epileptic Encephalopathies West Syndrome Late Infantile Epileptic Encephalopathy Lennox-Gastaut Syndrome Focal Structural Epilepsies Infantile Seizures are Often Subtle The Terms, “Simple” and “Complex” Are Difficult to Apply Infantile Focal Seizures May Have “Generalized” Clinical Features Difficulty Lateralizing Based upon Clinical Features Types of Infantile Focal Seizures and Their Electroclinical Correlations Conclusions References 283 284 Pediatric Epilepsy Syndromes INTRODUCTION: DIFFERENTIAL DIAGNOSIS OF EPILEPSY ACCORDING TO PROMINENT EEG FEATURES An unconventional but effective starting point for an organization of pediatric epilepsies is the interictal EEG As shown in Table 10.1, the various patterns encountered in clinical practice may be reduced to five discrete interictal EEG groups There are two major domains: the organization of the background and the characteristics of the epileptiform activity, most importantly the morphology of the interictal epileptiform discharges (IEDs) By considering the age of onset, one can narrow down the epilepsy syndromes to two or three possibilities, and the predominant seizure type will easily guide one to the final diagnosis In a minority, most particularly the familial epilepsies, verification of other similarly affected family members is critical TABLE 10.1 Organization of the Epilepsies by EEG Characteristics Name EEG background Epileptiform activity Familial epilepsies Normal None or rare Autosomal dominant Genetic Normal generalized spikewave epilepsies Stereotyped generalized spike waves Spikes are strongly inherited; epilepsy less so Self-limited epilepsies with focal spikes Normal Stereotyped focal and multifocal spikes Spikes are strongly inherited; epilepsy is minimally 4a Epileptogenic encephalopathy Slowed 4b Epileptic encephalopathies Slowed and often discontinuous (at least in parts) Pleomorphic If genetic, often de novo multifocal mutations, spikes some autosoPleomorphic mal recessive multifodisorders; usucal spikes; ally not familial electrodecremental responses Focal structural epilepsies Focal slowing, attenuation, or both Inheritance Pleomorphic Minimal genetic focal spikes contribution for diagnosis These groupings provide some powerful information: if there are genetic predispositions, they predict the mode of inheritance, they inform about the general prognosis, they have strong treatment implications, and they could be used as the basis for referral to tertiary epilepsy centers Of course, this is the opposite of the way we as clinicians normally conduct our evaluations A precise history and physical examination should always come first It is the sine qua non portion of the epilepsy evaluation, the basis of all we do, and the most important daily activity of the child neurologist A thorough history elicited with minimal interruption accompanied by close observation of the child and family allows us to make the interpersonal connections that are critical for trust and healing The interictal EEG, however, is a remarkably powerful tool and even though it sits in second place to our clinical assessment, it nevertheless informs us about the underlying pathophysiology in a manner that our naked senses never could For many years, our predecessors have appreciated that the various epilepsy syndromes have different relative contributions of genetic and structural components These thoughts were codified in the 2010 publication of the International League Against Epilepsy’s Classification Committee (1) In this chapter, we will see how the interictal EEG informs us about these fundamental characteristics The premise is simple: genetic and structural factors have markedly different EEG signatures, which allows the EEG to effectively categorize the epilepsies Indeed, the EEG findings can be used as an endophenotype to explore the genetic basis of susceptibility to epilepsy (2) This type of epilepsy syndrome organization is highly practical and simultaneously it reveals some fundamental principles about the causes of the epilepsies Another remarkable fact is that this can be usually accomplished with a relatively brief sample of the awake and sleep interictal EEG THE FAMILIAL EPILEPSIES (EPILEPSIES WITH FREQUENTLY NORMAL INTERICTAL BACKGROUNDS) One of the five broad categories of EEG features seen in children with epilepsy is a normal tracing The precise percentage of normal EEGs seen in patients with epilepsy is difficult to determine, but it may be as low as 8% (3) One reason for a repeatedly normal tracing may be a remote location of an epileptogenic lesion—one that does not readily allow for detection using conventional scalp recording electrodes Normal tracings are also seen in certain distinctive epilepsy syndromes that share a common characteristic: they are familial epilepsies that are inherited in an autosomal dominant Pediatric Epilepsy Syndromes fashion These may be considered the best examples of familial epilepsies Why these epilepsies most often present with normal interictal backgrounds is not entirely clear, but certainly, the normal background rhythms speak to the absence of cognitive impairment and disability in the vast majority of individuals with these epilepsies Here we encounter the first EEG-epilepsy paradox: even though these epilepsies are strongly genetically determined and spikes in other conditions have a strong genetic component (vide infra), the most conspicuous feature of the background is the lack of interictal epileptiform activity in these familial epilepsies There are familial epilepsies for every epoch of pediatric life starting with the neonatal period, and continuing to infancy, childhood, and adolescence These include benign familial neonatal epilepsy (BFNE), benign familial infantile epilepsy (BFIE), autosomal dominant nocturnal frontal lobe epilepsy (ADNFLE), autosomal dominant epilepsy with auditory features (ADEAF), and other autosomal dominant temporal lobe epilepsies It is obvious from the titles of these epilepsies that they vary in age of presentation, the brain region commonly involved, and the clinical manifestations Generally, the combination of the clinical features and family history, along with the mostly normal interictal EEG data, is sufficient to make a diagnosis, but if confirmation is required, genetic testing can help By and large, the outcome is favorable, although there are published cases of severe phenotypes (4) Benign Familial Neonatal Epilepsy BFNE usually begins on the second or third day of life and resolves within the first few months During seizures, neonates may have tonic posturing, automatisms, apnea, or focal or generalized clonic activity The seizures may rarely persist into adulthood Typically, the interictal EEG is normal, though it may have focal or multifocal sharp waves, an excessively discontinuous tracing for age or the theta-pointu alternant pattern The latter is characterized by rhythmic 4- to 7-Hz activity, with admixed sharp waves, with shifting laterality across the hemispheres, but it is by no means specific for this disorder Authors describe a clinical sequence starting with hypertonia and followed by apnea, autonomic signs, facial movements, and limb clonus (5) In some of the recorded seizures, an electrodecrement heralds the event and may last up to 19 seconds, followed by 1- to 2-minute bilateral spikes or sharp waves (6), but focal seizures (7) and focal seizures with secondary spread have also been recorded (8) The disorder has been associated with mutations in the KCNQ2 and KCNQ3 voltage-gated potassium 285 channels, responsible for the M-current (9) This slowly activating current regulates subthreshold neuronal excitability and therefore raises the possibility that a medication like retigabine may be helpful since it blocks the M-current A closely related syndrome of benign neonatal-infantile seizures has been associated with a missense mutation in the SCN2A gene, which encodes the alpha-2 subunit of the voltage-gated sodium channel (2q24) (10) Benign Familial Infantile Epilepsy BFIE and sporadic forms (which may be similar disorders) have been reported by several different investigators working in different regions of the world (11–14) Affected infants have focal seizures, which may present with subtle behavioral arrest or, on the other extreme, apparent bilateral convulsive features Eye version, staring, oral automatism, and oxygen desaturation are other common elements, and these are commensurate with the location of onset of the seizures The interictal EEG is usually normal, though some BFIEs may have peculiar low- or medium-voltage vertex spikes or sharp waves followed by a slow wave with a dome-like morphology (12,15) Ictal discharges often arise from the temporal region or posterior quadrant This finding is relatively nonspecific, since many focal seizures in infants arise from the same region These disorders are inherited in an autosomal dominant fashion and several genes have been discovered, which often involve ion channels, but importantly, sometimes not (16) Defects in the ATP1A2 gene may cause familial hemiplegic migraine and associated infantile seizures (17) When there is associated paroxysmal kinesigenic dyskinesia, mutations in the proline-rich transmembrane protein (PRPT2) have been reported (18) Similar mutations have been identified in Japanese children (19) and even, rarely, have been found in sporadic cases (20) The fact that only of the 16 probands in the Japanese study tested positive indicates that there are clearly other genetic causes of BFIE still to be discovered Autosomal Dominant Nocturnal Frontal Lobe Epilepsy Patients with ADNFLE have sudden awakenings with dystonic movements (tonic posturing) or violent movements Since the EEG findings are usually relatively bland, the seizures may be mistaken for sleep disorders, nocturnal paroxysmal dystonia, or nonepileptic seizures Rarely, the interictal EEG may show focal features such as slowing and spikes (21) Ictal recordings 286 Pediatric Epilepsy Syndromes Figure 10.1: Ictal recording in a 10 year old boy with ADNFLE Note the sudden change in the background as he awakens from sleep There is some admixed low-voltage rhythmic fast activity in the frontal regions are more distinctive and are characterized by bifrontal beta activity or other rhythmic discharges (22) (Fig 10.1) The ictal discharges may lateralize or even localize to a region, suggesting a focal structural lesion, and therefore, a careful family history is warranted before considering focal respective surgery in patients with nocturnal frontal lobe seizures Genetic screening for the associated nicotinic acetylcholine receptor gene mutation (CHRNA4 and CHRNB2) is commercially available symptoms is usually in adolescence of early adult life, but childhood onset is also possible It is characterized by subtle seizures with auditory hallucinations, infrequent nocturnal convulsions, and a good response to medications Seizures may be triggered by voices or noises The auditory hallucinations may be humming, clicking, ringing, or other noises Other sensory phenomena may also occur The interictal EEG is usually normal, though, as in the other familial disorders, IEDs may rarely be found and sporadic cases appear to have a higher incidence of epileptiform discharges (25,26) Familial Lateral Temporal Lobe Epilepsy or Autosomal Dominant Epilepsy with Auditory Features Familial Mesial Temporal Lobe Epilepsy Ottman described a pedigree in 1995 where most affected members reported seizures with auditory symptoms and named the syndrome autosomal dominant partial epilepsy with auditory features (ADPEAF [OMIM 600512]) (23) Subsequently, it was found that mutations of the leucine-rich glioma-inactivated LGI1 gene caused this disorder (24) The onset of The precise genetic cause of familial mesial temporal lobe epilepsy is not yet known This disorder usually presents in adults, never before age 10 years, and therefore, it will be only briefly mentioned here Seizures tend to be infrequent, mild, and easily controlled with medication, contrasting them to other forms of mesial temporal lobe epilepsy (27) Seizures without alteration Pediatric Epilepsy Syndromes of consciousness are more common than those with dyscognitive features Many cases show normal imaging and EEG findings, and the presence of MR changes or interictal epileptiform activity appears to predict intractability (28) GENETIC GENERALIZED SPIKE-WAVE EPILEPSIES Individuals with these forms of epilepsy have normal interictal backgrounds with superimposed generalized spike-wave discharges (SWDs) These discharges will usually be Hz or greater, though, at times, some slower spikewave activity, circa 2.5 Hz may be seen, particularly in the younger child In all cases, these occur on the backdrop of a normally developing child There may be associated photoparoxysmal responses and some of these epilepsies will show activation of spike waves with hyperventilation Spikes may appear more irregular and demonstrate fragmentation in the sleep record It is not unusual to see focal features (focal slowing and focal spikes), but these will show shifting laterality from study to study As stated, the interictal EEG background is normal, but there may be some important exceptions: rhythmic activity may intermittently punctuate the record This may be seen as either intermittent rhythmic theta activity, which is often in the biparietal regions (prominent in many cases of myoclonic-atonic epilepsy described by Doose) or as intermittent rhythmic delta, seen in either the occipital or the frontal regions (occipital intermittent rhythmic delta activity [OIRDA] and frontal intermittent rhythmic delta activity [FIRDA], respectively) Generalized spike waves and other paroxysmal features found in the EEGs of individuals with these epilepsies have been known for some time to be inherited in an autosomal dominant fashion with variable penetrance so that a high proportion of family members of individuals with primary generalized epilepsy will have generalized spike waves (29,30) The clinical tendency toward epilepsy has genetic contributors as well, but these are more complex than the inheritance of the EEG trait Although the concordance rate for primary generalized epilepsy in twin studies are high (31), the recurrence risks in first-degree relatives of patients with primary generalized epilepsies are much lower than the truly familial epilepsies with monogenic transmission (32) This argues for a more complex polygenic or oligogenic mode of inheritance A wide variety of epilepsies are seen and the prognosis is generally very favorable, although some will require treatment for prolonged periods Associated epilepsies include myoclonic epilepsy in infancy (MEI), childhood absence epilepsy (CAE), epilepsy with myoclonic-atonic seizures (EMA) (as described by Doose), epilepsy with myoclonic absence, epilepsy with eyelid 287 myoclonia (Jeavons syndrome), juvenile absence epilepsy (JAE), juvenile myoclonic epilepsy (JME), and epilepsy with generalized tonic-clonic seizures alone Treatment is generally with broad-spectrum agents, with the exception of ethosuximide for CAE Patients in this category will also usually not require referral to a tertiary center, unless complications arise or special circumstances present themselves Myoclonic Epilepsy in Infancy The predominant seizure seen in MEI is myoclonus, as the name suggests Infants who are developing normally have myoclonic jerks mostly of the head and proximal arms, occurring in isolation or in brief runs of recurrent jerks The ictal EEG shows a burst of generalized or diffuse spike-wave activity with the myoclonia, otherwise the interictal EEG is normal (33) (Fig. 10.2) Myoclonic-Astatic Epilepsy (Doose Syndrome) Myoclonic-astatic epilepsy may occur between late infancy and years, but most often starts between and years Many children will have antecedent febrile seizures The prototypic seizure is a myoclonic-astatic attack, or now known as a myoclonic-atonic seizure (34) The seizure begins with a sudden jerk of the head or body followed by a sudden loss of tone, causing a head drop or body drop This may easily result in injury because of the combination of the sudden propulsion from the myoclonus, the subsequent loss of postural tone, and the inability to have a protective reflex In addition to this seizure type, atonic seizures, isolated myoclonic jerks, absence seizures, and generalized clonic-tonic-clonic seizures occur Daytime tonic seizures are considered exclusionary by some, but nocturnal tonic seizures occur, even in patients with excellent outcome The interictal EEG may show biparietal rhythmic theta activity, and this may be the only abnormality early in the course of the illness (Fig 10.3) Bursts of 2- to 3-Hz generalized spike and polyspike-wave discharges follow and are often frequent These occur in brief bursts, usually consisting of isolated spike waves, couplets, or triplets The repetition rate is therefore difficult to accurately measure, but it is often variable between the bursts Photosensitivity is common The ictal accompaniment of the myoclonic-astatic seizure is a burst of generalized polyspike-wave discharge, where the after-going slow-wave discharge appears to have some high-frequency attenuation or diminished high-frequency activity (Fig 10.4) 288 Pediatric Epilepsy Syndromes Figure 10.2: Benign myoclonic epilepsy of infancy This infant had repeated myoclonic jerks associated with this burst of generalized spikewave activity Generalized spike waves are very rarely seen in infants, and this is one notable exception Figure 10.3: Myoclonic-atonic epilepsy as described by Doose This tracing was obtained in a 4-year-old and was punctuated by runs of biparietal rhythmic theta activity that occurred when the patient was clearly not drowsy Pediatric Epilepsy Syndromes A B Figure 10.4: Doose syndrome A: This youngster had a myoclonic-atonic seizure accompanied by this EEG correlate Note the burst of generalized polyspike activity is followed by a brief epoch of relative attenuation B: A 4-year-old with Doose syndrome had a clonic-tonic-clonic seizure, which is the typical type of convulsive event Note the rhythmic spike waves at the start of this page corresponding to the clonic phase of the seizure, which give way to the more rapid ictal discharges corresponding with the transition to the vibratory tonic phase 289 290 Pediatric Epilepsy Syndromes Childhood Absence Epilepsy Epilepsy with Myoclonic Absences CAE generally begins between and 10 years of age, with a peak in the early school-age years From the very early observations of this form of epilepsy, it was appreciated that absences are usually frequent, with scores to hundreds of seizures in a day This gave rise to the name pyknolepsy, signifying many seizures (35) Each individual seizure is typically brief, usually less than 10 seconds The clinical onset and offset is abrupt, with brief impairment of consciousness associated with unresponsiveness and interruption of the ongoing activity Some rhythmic eyeblinking may occur, but more pronounced myoclonus of the face or other body parts suggests a myoclonic form of epilepsy The interictal EEG is normal except that rhythmic delta activity may be seen (Fig 10.5) The attacks are accompanied by bursts of generalized 3-Hz SWDs These often have a frontal predominance and may have up to two spikes per complex The frequency may slow slightly as the ictal discharge continues Typical absence attacks often begin and end with rhythmic slowing with a more restricted topography (Fig 10.6) Seizures are easily activated by hyperventilation, and are more frequent with lower blood glucose levels (36,37) Ethosuximide is the most effective medication with the least side effects (38) Epilepsy with myoclonic absences is a rare form of genetic generalized epilepsy (39) It may occur at any time in infancy to adolescence, with a peak in the early school-age child, usually around years (40) Myoclonic absences are characterized by tonic elevation of the arms, with repeated myoclonia of the shoulders, arms, and legs The events may be asymmetric or even unilateral with resultant head deviation Approximately two-thirds of children will also have tonic-clonic seizures The interictal EEG is normal at onset and about half of the cases show brief generalized spike-slow-wave discharges, sometimes with fragmentation The ictal EEG shows rhythmic 3-Hz generalized polyspike-wave discharges (Fig 10.7) Juvenile Absence Epilepsy JAE and JME are both discussed in the chapter on adult epilepsy and are therefore only briefly mentioned here for completeness This epilepsy has a peak onset between and 13 years of age and most often absence attacks precede myoclonic jerks and generalized tonic-clonic seizures The prognosis is not as favorable as CAE (41) Figure 10.5: CAE This 8-year-old child has associated OIRDA Pediatric Epilepsy Syndromes A B Figure 10.6: A: CAE The classic 3-Hz SWD is evident This was associated with unresponsiveness, confirming that it was a clinical absence attack B: Same ictal discharge displayed with a longer page duration to reveal the whole discharge Note how the first few discharges and last discharges are different than the main ictal pattern (Dr Solomon Moshé—personal comments.) 291 292 Pediatric Epilepsy Syndromes Figure 10.7: Myoclonic absence This 6-year-old had an absence with repeated subtle head nods and arm myoclonia Note the slight stiffening of the arm evident in the deltoid recording There is an accompanying burst of generalized spike-wave activity The interictal EEG background is normal, upon which are superimposed fragments of diffuse spikes and polyspikes During absence attacks, there are 3- to 4-Hz generalized polyspike-wave discharges (Fig 10.8) Juvenile Myoclonic Epilepsy The history of JME has been recently reviewed (42) In 1957, Janz and Christian (43) established the essential components of JME and paid tribute to Herpin’s work dating back to 1867 with the name “Impulsiv Petit Mal.” JME is characterized by mild myoclonic, generalized clonic-tonic-clonic seizures, and absence seizures Delgado-Escueta and Greenberg (44) searched for the genetic cause and in doing so highlighted the importance of this syndrome in the United States Onset is typically in adolescence, with myoclonic seizures The myoclonic seizures are usually bilateral but mild to moderate, in the sense that they may cause objects to drop but usually not result in falls They typically occur after awakening and may precede or lead directly Figure 10.8: JAE Bursts of generalized SWDs are present 632 Index Anterior ischemic optic neuropathy (AION), 458 Anterior tibialis EMG, in polysomnography, 603, 604f Antialiasing filter, 56f, 61 Antiepileptic drugs (AEDs), 373 discontinuation of, 574 effects on EEG activity, 214 AOXD See Acyl-coenzyme A oxidase deficiency (AOXD) Apnea, sleep, diagnosis of, 617–618 Arousal activity of, 193–194 in infants and children, 192 polysomnographic scoring of, 612–613, 613–615f postarousal hypersynchrony, 194–195, 194–195f spontaneous, 195 Arterial oxygen assessment, for ventilatory monitoring in polysomnography, 607–608 Arteriovenous malformation (AVM), focal encephalopathies in, 239t, 254 Artery of Adamkiewicz, 490 Artifact(s) in continuous EEG in ICU, 551, 554–560f environmental, 234 eye movement, 240, 242f high-frequency ventilator, in infant with persistent pulmonary hypertension, 173f instrumental, 417, 419f interpretation of EEG data, 417–418, 419f in intracerebral depth electrodes EEG, 417–418, 419f nonphysiological, 551 patting, in infant with sepsis, apnea, and seizures, 142 physiological, 234 rhythmic extracerebral, 177 sucking, 142 ASDA See American Sleep Disorders Association (ASDA) Asynchrony, 131, 132f Atonic seizures, 334, 335f Atypical absence seizures, 334 Auditory nerve action potential, 521 Autosomal dominant epilepsy with auditory features (ADPEAF), 286 Autosomal dominant nocturnal frontal lobe epilepsy (ADNFLE), 285–286, 286f Awakening(s), polysomnographic scoring of, 612–613, 613–615f Axial electromyogram, in polysomnography, 603 Axonal plexus, B Baltic myoclonus epilepsy, 275 Bancaud phenomenon, 240, 242f Bandwidth(s), frequencies in EEG and, 92t alpha rhythm, 92–94, 94f beta rhythm, 96, 96f, 97f delta frequency, 97–98, 99f, 100f mu rhythm, 94–96, 95f theta frequency, 97, 98f Basket cells, parvalbumin-expressing, 6, 8–9 gamma activity, gap-junction coupling in, in high-frequency oscillations, BCSSS See Benign Childhood Seizure Susceptibility Syndrome (BCSSS) Behavioral arrest with version, 310 BEM See Boundary element model (BEM) Benign childhood epilepsy with centrotemporal spikes, 295, 296–297, 298f Benign Childhood Seizure Susceptibility Syndrome (BCSSS), 295 Benign epileptiform transients of sleep (BETS), 109–110, 113f Benign familial infantile epilepsy (BFIE), 285 Benign familial neonatal epilepsy (BFNE), 285 Benign variants of uncertain significance, 104, 106, 108–112, 110–115f Beta activity, 154–155 focal attenuation of, 240 focal enhancement of, 239–240 Beta coma frequency pattern, 225–226 Beta rhythm, 96, 96f, 97f BETS See Benign epileptiform transients of sleep (BETS) BFIE See Benign familial infantile epilepsy (BFIE) BFNE See Benign familial neonatal epilepsy (BFNE) # 151788 Cust: LWW Au: Ebersole Pg No 632 Bilateral independent temporal lobe seizures, 408 Bilateral latency prolongations, 453 Bilateral periodic lateralized epileptiform discharges (BIPLEDs), 245, 248f Bilateral rhythmic central theta activity, 156 Binding problem, 12 Biotin metabolism, disorders of, 267 Biotinidase deficiency, 269 BIPLEDs See Bilateral periodic lateralized epileptiform discharges (BIPLEDs) Bipolar montages, 40, 41f, 42f, 86, 89, 98f with subdural electrodes, 374 Bipolar stimulation, 533 Bit-depth, 56 Black box, Blood glucose level, to hyperventilation response, 187 Blood pressure See Anoxia Boundary element model (BEM), 349 Brachial plexus trauma, 539 Brain abscess, focal encephalopathies in, 239t, 249, 250f electrical activity, 394 electrical flow in, 2, 3f action potential currents, 4–5 active conductances, gap-junction coupling, 6–7 nonneuronal currents, synaptic currents, maps, 36 stem injury, 516 stem lesions, EEG correlation with, 253 tumors focal encephalopathies in, 239t infratentorial, 247, 249 large hemispheric, 247 Brain death BAEPs in, 469 checklist for, 234t electrocerebral inactivity, 233–234 clinical correlation, 234 technical requirements, 234–235 in infants, 161, 164f Brainstem auditory evoked potentials (BAEPs), 459–460 abnormalities K DESIGN SERVICES OF absolute latency, 466–467 amplitude in, 468 interpeak latency in, 465–466, 465–467f obligate wave absence in, 464, 464f in acoustic stimulation, 459 in alcoholism, 469 anatomy and physiology, 512, 512t anatomy and waveform generators, 460, 460t anesthetic considerations, 513 in Arnold-Chiari malformations, 469 auditory nerve action potential, 521 in brain death, 469 in cerebellopontine angle tumors, 469 change, mechanisms of, 513–520, 515t, 516–520f physiological changes, 516–518 surgery-induced changes, 514–516 technical issues, 518–520 clinical applications, 521 clinical correlations, 468–470 in coma, 469 interpretation, 462–464, 462f, 463t latency/intensity series, 470 methodology, 512–513, 514f, 515f recording technique, 461–462, 462t, 513 stimulating techniques, 460–461, 513 in multiple sclerosis, 468–469 in myelomeningocele, 469 in neurodegenerative disorders, 469 pediatric considerations, 468 warning criteria, 520–521 Brainstem dysfunction, EEG manifestations of, 214 Breach rhythm, 239, 240f, 241f Breathing, sleep-disordered, pediatric, polysomnographic scoring of, 618–619 Brief ictal rhythmic discharges (BIRDs), 177 Brushes See Delta brushes, in neonatal EEG interpretation Burst-suppression pattern, 159, 160f, 232, 233f C C5S electrode, 474 CAE See Childhood absence epilepsy (CAE) CAI See Composite alpha index (CAI) 633 Index Calibration, 81–82 Capacitance (C), 47, 47f, 49, 66 Capacitor(s), 47–48, 47f, 49 Carbon dioxide detectors, for airflow monitoring in polysomnography, 606 CDG See Congenital disorders of glycosylation (CDG) Cellular basis of EEG See Electroencephalogram (EEG), cellular basis of Central cortex seizures, 411–412, 412f Centrotemporal delta activity, in neonatal EEG interpretation, 147 Cerebellopontine angle tumors, BAEPs in, 469 Cerebral blood flow, on EEG, 547t Cerebral death, technical standards for EEG recording in, 235t Cerebral edema, 373 Cerebral function monitors (CFMs), 547 Cerebral sources, dipole models of, 341–342 Chattering neurons, 22 Cherry-red spot (myoclonus syndrome), 274 Childhood and adolescence, metabolic disorders of See Metabolic disorders, of childhood and adolescence and infancy, EEG background activity in See Pediatric EEG, infancy and childhood progressive encephalopathy See Progressive childhood encephalopathy Childhood absence epilepsy (CAE), 290, 290f, 291f Children alpha rhythm frequency in, 148 brainstem auditory evoked potentials in, 468 fast activity during early stages of sleep in, 200 flash visual evoked potentials in, 457–458 hyperventilation response in, 186–187, 187f paroxysmal slow bursts during drowsiness in, 188, 191–192, 193f with perinatal injury, 484 sharp-wave, vertex transients in, 195–196, 196–201f, 198, 200, 202 sleep-disordered breathing in, polysomnographic scoring of, 618–619 somatosensory evoked potentials in, 482–483 spikes and sharp waves in, 186–187 Ciganek rhythm, 114 Circuit(s) differential amplification, 50–51, 50f filters, 52, 52–54f impedance and alternating (sinusoidal), 52, 52f input impedance, 50, 50f time-varying, 51–52, 51f voltage divider, 49, 49f CJD See Creutzfeldt-Jakob disease (CJD) Clonic seizures, 334 Clonic-tonic-clonic seizures, 334 CMRR See Common-mode rejection ratio (CMRR) CN See Cranial nerve (CN) Cochlear injury, 514–515 Collodion, 59 Coma alpha, 224–225, 224f BAEPs in, 469 beta, 225–226 sleep See Spindle coma Common-mode rejection ratio (CMRR), 50, 444–445 Common reference montage, 41 Complex focal seizures, 325–326 Composite alpha index (CAI), 581 Conceptional age, 126 excessive discontinuity for, 159, 161t in neonatal EEG interpretation 24 to 29 weeks, 131, 134 30 to 32 weeks, 134–135, 136f 33 to 34 weeks, 135 35 to 36 weeks, 135, 137f, 138 37 to 40 weeks, 138, 139f, 140f 41 to 44 weeks, 138 45 to 46 weeks, 138, 141f Condensation, definition of, 461 Conductance, 2, 47, 48 Cone waves, 140 Congenital disorders of glycosylation (CDG), 273 Constant-voltage stimulators vs constant-current stimulators, 533 # 151788 Cust: LWW Au: Ebersole Pg No 633 Continuity, of EEG background, 207–208 Continuous EEG monitoring artifacts in, 551, 554–560f clinical applications of, 569–575 anoxic brain injury, 581–587, 587–589f, 590–593f hypothermia, 581–587, 587–590f ischemia, 581 nonconvulsive seizures, 572t, 578–581 status epilepticus, 575–578 clinical factors confounding, 551–553, 561f data review, 553–555 electrodes in, 550–551 future directions, 590 historical context, 547–548 in ICU See Intensive care unit (ICU), continuous EEG monitoring in interpretation and nomenclature, 555–561, 562t, 563–571f, 573f montages in, 551, 552–553f multimodal brain monitoring, 587–590, 594f personnel requirements, 549–550 quantitative analysis of, 562–569, 574–578f scientific basis, 546–547, 547t technical considerations for, 548–549, 548f Continuous spindling, 198 Corkscrew electrodes, 491, 492f Cortical after discharges, 389 Cortical currents, anatomical organization of basket cells, 8–9 hippocampal anatomy, 7–8 neocortical anatomy and thalamic connections, 9–11 Cortical generators and EEG voltage fields EEG source characterization, 34–37 potentials, 28–30, 29–30f effect of reference on EEG fields, 42, 43f, 44 electrode location and nomenclature, 38, 39–40f, 40 factors determining scalp EEG, 30–34, 32–35f montages, 40–42, 41f from specific cortical regions, 37–38, 38–39f Cortical interictal spikes, 367–368, 374 Cortical seizure propagation, character of, 381 K Cortical source factors, and scalp EEG potentials, 339–341, 340f, 341f Cortical spike sources, 375 Cortical waveforms, 444 Cranial nerve (CN) surgery, 538–539 VIII injury, 515–516 Creutzfeldt-Jakob disease (CJD), 220–221 Ctenoids, 109, 113f Currents, nonneuronal, Cz-A1/Cz-A2 montages, 460 D Daytime sleepiness, excessive, evaluation of, 624–626, 625f Decibel normal hearing level, 461 Deep hypothermic circulatory arrest (DHCA), 525 Deep sleep, 103 Delta brushes, in neonatal EEG interpretation, 144–147f, 148 Delta frequency(ies), 97–98, 99f, 100f Dentatorubral-pallidoluysian atrophy, 276–277 Depressed and undifferentiated background, 161, 161f Depth electrodes, 60, 368 subdural vs., 369 DHCA See Deep hypothermic circulatory arrest (DHCA) Diffuse tonic-focal clonic seizure, 310 Digital EEG, 40, 82 recording, 81 technology for PSG, 600 Digital filters, 82 Digital recording, issues related to, 80–81 Digitization, 81 digitizer electronics, 57, 57–58f of signals, 54 time discretization, 55–56, 55–56f voltage discretization (signal resolution), 56–57, 57f Digitizer digital processing, 62 digital transfer/storage, 62 electronics, 57, 57–58f finite impulse response filtering, 62, 63 infinite impulse response filtering, 62, 63 DESIGN SERVICES OF 634 Index Dipole localization techniques, 341–342, 346 Dipole patch model, 358, 361 Dipole source modeling, of epileptiform potentials, 338–364 assumptions of, 342 of cerebral sources, 341–342 clinical studies using, 361, 363–364 coregistering EEG data with MRI, realistic head models, and spatial sampling, 347, 349–350, 349f, 350f, 351f for extratemporal sources, 353, 359–363f interpretation of, 346–347, 347f, 348f of seizures, 350, 352f, 353, 354f single-moving, 342, 343f, 344f spatiotemporal multiple, 342–343, 345f, 346 for temporal lobe sources, 353, 355–358f Discontinuous EEG, in premature infant, 157 Doose syndrome See Myoclonic-astatic epilepsy Double-grounding, electrical safety, 66, 68, 68f Double train stimulation, 504 Down syndrome, 205, 278 Dravet disease, 300, 301f Drowsiness, 208 defined, 187 monorhythmic slow activity, 187–188, 189–190f paroxysmal slow activity, 188, 191–192, 192f, 193f Dysrhythmia, anterior, 148, 149f E Early infantile epileptic encephalopathy (EIEE), 303, 304f Early myoclonic encephalopathy (EME), 260–261, 260f, 302, 303f cause of, 260–261 diagnostic test for, 261t inborn error of metabolism causing, 261t Early onset epileptic encephalopathy (EOEE), 262 Early onset multiple carboxylase deficiency, 267 ECI See Electrocerebral inactivity (ECI) ECoG See Electrocorticography (ECoG) EEG See Electroencephalogram (EEG); Electroencephalography (EEG) EGA See Estimated gestational age (EGA) EIEE See Early infantile epileptic encephalopathy (EIEE) Electric charge, 46 Electric potential, 46 Electrical fields, 78–89 calibration in, 81–82 cerebral generators of EEG potentials in, 78–79, 79f conventions and sensitivity/filter settings, 80–85 electrode placement in, 79–80, 80f filters in, 82, 82–85f, 85 issues related to digital, 80–81 montages in, 85–86, 87–88f, 89 See also Montage(s) polarity conventions in, 81 sensitivity in, 81–82 Electrical flow, in brain, 2, 3f action potential currents, 4–5 active conductance, gap-junction coupling, 6–7 nonneuronal currents, synaptic currents, Electrical safety, 64, 68t double-grounding, 66, 68 exacerbating factors in, 68, 68t improper grounding, 65 leakage currents, 66 regulations, 68 Electrical stimulation, 470 for functional localization, 388–389 intracerebral depth electrodes EEG and, 433–435, 434f of peripheral nerves, 489 Electro-oculogram, in polysomnography, 602–603, 602f Electrocerebral inactivity (ECI), 233–235, 523 brain death, checklist for, 234t clinical correlation, 234 technical requirements, 234, 235t Electrocerebral silence See Electrocerebral inactivity # 151788 Cust: LWW Au: Ebersole Pg No 634 Electrocorticography (ECoG) technique, 394, 395 See also Intracranial EEG Electrode(s), 58–59, 59f anterior cervical, 473 common types of, 59–60, 60f continuous EEG in ICU and, 550–551 corkscrew, 491, 492f depth, 60, 368 for electroencephalography, 522–523 epidural, 369, 491–492, 492f grid, 60 high-resolution, flexible, active electrode array, 61, 61f intracranial, 60 localization of, 371, 371f, 372f for motor evoked potentials recording, 504–505 stimulating, 490f, 491–492t, 503 needle, 535, 535f nomenclature and location, 38, 39–40f, 40 pattern reversal visual evoked potentials recording, 451t placement of, 79–80, 80f platinum vs stainless steel, 369 potential, 58 scalp cup, 59, 60f silver chloride, 58 for somatosensory evoked potentials recording, 491–492, 492f stimulating, 490–491, 490f, 491t subdermal, 535, 535f subdural, 60 bipolar montages with, 374 depth vs., 369 in intracranial EEG, 367–389, 370f, 371f, 372f, 375f, 376f, 377–380f, 382–388f surface, 534–535, 535f Utah Intracortical Electrode Array, 60–61, 61f Electrodecrement, 305 Electroencephalogram (EEG) See also Encephalopathy, generalized cellular basis of, 1–27 cortical currents, anatomical organization of, 7–11 electrical flow in brain, 2–7, 3f, 6f K DESIGN SERVICES OF epileptiform activity microelectrode arrays, ictal discharges and penumbra, 17–19, 18f neural activity during epileptiform discharges, 14–17, 15f, 16f surround inhibition, 19, 20f, 21f oscillations, 11–12 and cellular activity, relationship between, 13–14 hierarchical phase-amplitude coupling, 14 high-frequency, EEG markers of ictal territories, 19–24, 20f, 23f structure of, 12–13 uses of, continuous monitoring See Continuous EEG monitoring; Intensive care unit (ICU), continuous EEG monitoring in description and interpretation, 214 localization, 214 reactivity, 215–217 digital, 40, 82 recording, 81 technology for PSG, 600 engineering aspects of, 46 focal, 238–255 See also Focal encephalopathies, EEG in monitoring, utility of, 213 for normal adult, 90–124, 91t activating procedures, 99–101, 101f, 102f bandwidths in alpha rhythm, 92–94, 94f beta rhythm, 96, 96f, 97f delta frequency, 97–98, 99f, 100f mu rhythm, 94–96, 95f theta frequency, 97, 98f benign variants of uncertain significance, 104, 106, 108–112, 110–115f misinterpreted, 114–115, 117–122t, 120, 122 parameters of recording, 91–92 sleep architecture, 101–104, 103–109f variations of, 112, 114, 116f safety rules for performing, 68t source characterization propagation, 37 voltage field analysis, 34–36 635 Index -specific acquisition antialiasing filter, 61 electrodes, 58–59, 59f common types of, 59–60, 60f high-resolution, flexible, active electrode array, 61, 61f Utah Intracortical Electrode Array, 60–61, 61f preamplifiers, 61 spindle coma frequency pattern, 225–226, 226f in ventilatory monitoring in polysomnography, 608 warning signs for an over interpreted EEG report, 122t waveform characteristics and identifying suspicious features in, 122t Electroencephalography (EEG), 188, 521–522 adult epilepsy in, 315–336 anatomy and physiology, 522 anesthetic considerations, 523–524, 524–527f change, mechanisms of, 524–526, 527–528t, 529–530f, 532t hypothermia, 525–526 ischemia, 524–525 other factors, 526 clinical applications, 530–531 hyperventilation for, 526 intracerebral depth electrodes, 393–437 intracranial, 367–389 methodology, 522–523 electrodes, 522–523 machine, 522 montages, 523 neonatal See Neonatal EEG ontogeny, overview of, 134f adolescence, 143 childhood, to 10 years, 142 conceptional age 24 to 29 weeks, 131, 134 30 to 32 weeks, 134–135, 136f 33 to 34 weeks, 135 35 to 36 weeks, 135, 137f, 138 37 to 40 weeks, 138, 139f, 140f 41 to 44 weeks, 138 45 to 46 weeks, 138, 141f early infancy, 46 weeks to year, 138, 140, 142 late infancy, to years, 142 pediatric See Pediatric EEG potential, cerebral generators of, 78–79, 79f quantitative analysis, 531 sleep recording, 601–603, 601f, 602f voltage topography cortical source factors and scalp potentials, 339–341, 340f, 341f other source models, 353, 358, 361 spike and seizure sources, 339 warning criteria, 526–530 Electrographic neonatal seizures (ENSs), and clinical correlations, 177–205 activity of drowsiness, arousal and sleep, 187–205, 188–204f characteristics amplitude, 182, 185f, 186 duration, 177, 181–182f, 182 location, 177, 179–180f morphological appearance, 182, 183–184f computer-based, 186 sharp waves and spikes in infant and child, 186–187, 187f Electromyography (EMG) anterior tibialis, in polysomnography, 603, 604f axial, in polysomnography, 603 clinical applications, 538–539, 538t cranial nerve surgery, 538–539 peripheral nerve surgery, 538–539 spinal surgery with instrumentation, 538 free running, 535–536 intercostal, for ventilatory monitoring in polysomnography, 607 interpretation of, 536–537, 537f stimulated, 534–535 Electronics, digitizer, 57, 57–58f Electroretinogram (ERG), 120, 456–457 EME See Early myoclonic encephalopathy (EME) EMG See Electromyography (EMG) Encephalitis, 249 causes of, 249–250 focal encephalopathies in, 239t # 151788 Cust: LWW Au: Ebersole Pg No 635 in neonates, 250 viral, 251 Encephalogram (EEG) acquisition, 373–374 association and electrographic neonatal seizures, 186t disc electrodes, 472 fields, effect of reference on, 42, 43f, 44 intracranial recording, 374–377, 375f, 376f, 377–380f isoelectric, 206 markers of ictal territories, 19–24, 20f, 23f neonatal, background, classification and implications of, 205–206, 205t organized approach to visual analysis of, 207–209 abnormalities, 208–209 continuity and state concordance, 207–208 gradient and principal components, 208 special features, 208 symmetry and synchrony, 208 potentials, sources of, 28–30, 29–30f Encephalopathy(ies), 208 epilepsies with, 299–308 epileptic encephalopathies, 301–308 epileptogenic encephalopathies, 300–301 focal, 238–255, 239t generalized, 213–236 caveats in using EEG for prognosis, 232–233 clinical correlations of encephalopathic EEG patterns, 215t EEG description and interpretation localization, 214 monitoring, utility of, 213 patterns associated with, 214t reactivity, 215–217, 216f, 217f electrocerebral inactivity, 233–235, 234t, 235t fast frequency patterns, 224 alpha coma, 224–225, 224f beta coma, 225–226 spindle coma, 226–227, 226f ICTAL patterns, 227 nonconvulsive status epilepticus, 227–231, 228t, 229–231f K low-voltage and suppressed patterns, 232 burst-suppression, 232, 233f generalized suppression, 232 parameters for, 215t periodic patterns, 220 generalized periodic discharges, 220–222, 221f triphasic waves, 222–224, 223f slow patterns, 217 generalized high-voltage delta activity, 219 generalized slowing, 217–218 generalized theta activity, 218–219, 218f intermittent rhythmic delta activity, 219–220, 219f glycine, 260–261 progressive childhood, 258–280 Encoches frontales, 165, 167, 167f, 208 Engineering principles, 45–77 aliasing in, 55, 55f circuits and, 49–54, 49–54f digital EEG, 40 digitization, 54–57, 55–58f digitizer, 62–64, 63–66f display considerations, 64, 67f EEG-specific acquisition, 58–61, 59–61f electrical basics, 46–47, 46t electrical safety, 64–66, 68, 68f, 68t evoked potentials See Evoked potentials fundamental electrical components, 47–49, 47–48f ENSs See Electrographic neonatal seizures (ENSs) Environmental artifacts, 417 EOEE See Early onset epileptic encephalopathy (EOEE) Ephaptic interactions, Epidural electrodes, 491–492, 492f in intracranial EEG, 369 EPIFOCUS technique, 358 Epilepsy, 367, 373 See also Seizure(s) adult, 315–336 ictal EEG, 324–336 interictal epileptiform discharges, 315–324, 335–336 clinical studies of, 361, 363–364 DESIGN SERVICES OF 636 Index Epilepsy (continued ) EEG in diagnosis and treatment of, 368 with encephalopathies, 299–308 epileptic encephalopathies, 301–308 epileptogenic encephalopathies, 300–301 extratemporal, 353, 409–415 familial, 284–287 focal structural, 308–310 generalized, 330 idiopathic generalized, 330–334 interictal regional delta activity in, 376 juvenile myoclonic See Juvenile myoclonic epilepsy lesional and nonlesional focal epilepsies, 415 with myoclonic absences, 290 pediatric See Pediatric epilepsy syndromes surgery, 368 symptomatic generalized, 334–335 temporal lobe, 377 focal onset in, 381 indications for SEEG in, 407–409 Epileptic encephalopathies, 301–308 background slowing and disorganization in, 301–302 early, 302–304 late infantile epileptic encephalopathy, 306, 306–307f Lennox-Gastaut syndrome, 307, 308f in newborn, 262t West syndrome, 304–306, 305f Epileptic spikes, 30 Epileptiform activity abnormalities of, 239, 243–244, 315 cellular basis of, 14 microelectrode arrays, ictal discharges and penumbra, 17–19, 18f neural activity during epileptiform discharges, 14–17, 15f, 16f surround inhibition, 19, 20f, 21f depth electrodes for, 369 potentials, dipole source modeling of, 338–364 Epileptiform potentials, dipole source modeling of See Dipole source modeling, of epileptiform potentials Epileptogenic encephalopathies Dravet disease, 300, 301f malignant migrating focal seizures in infancy, 300–301, 302f EPM2 gene, 275 EPs See Evoked potentials (EPs) EPSPs See Excitatory postsynaptic potentials (EPSPs) Equivalent dipoles, 342, 347 ERG See Electroretinogram (ERG) Esophageal pressure monitors, for ventilatory monitoring in polysomnography, 606–607 Estimated gestational age (EGA), 126 Evoked potentials (EPs), 442–484 basics of abnormalities, 446–447 interpretation, 445–446 naming convention, 443 normative data, 446 recording, 444–445 stimulation, 444 waveforms, 443–444 brainstem auditory, 459–460 abnormalities, 464–468, 464–467f anatomy and waveform generators, 460, 460t clinical correlations, 468–470 interpretation, 462–464, 462f, 463t latency/intensity series, 470 methodology, 460–462, 462t pediatric considerations, 468 somatosensory abnormalities, 476–480, 477–482f anatomy and waveform generators, 470–471, 471t clinical correlations, 483–484 interpretation, 474–476, 475f, 476t methodology, 471–474, 472t, 473f, 474t pediatric considerations, 480–483 visual anatomy and waveform generators, 447–448 clinical correlations, 458–459, 459f flash, 456–457, 457f pattern reversal, 448–456, 449–456f, 451–453t pediatric considerations, 457–458 Exaggerated spindles, 198 # 151788 Cust: LWW Au: Ebersole Pg No 636 Excessive asynchrony, 165 Excessive daytime sleepiness, evaluation of, 624–626, 625f Excessive discontinuity, of abnormal pediatric EEG backgrounds, 157, 158f, 159 abnormal asymmetry, 161, 165 abnormal interhemispheric asynchrony, 165 abnormal maturation, 165, 166f abnormal voltage, 159, 161 for age, 159, 161t burst-suppression pattern, 159, 160f isoelectric tracing, 161, 164f persistent low voltage, with or without lack of differentiation, 161, 162f, 163f Excitatory postsynaptic potentials (EPSPs), 14, 29 Extracellular secondary current, 29 Extracellular transfer functions, Extratemporal complex focal seizures, 328–330, 329–332f Extratemporal epilepsy, 353 Extratemporal lobe epilepsy, indications for SEEG in, 409–415 F Facilitation, 504 Familial epilepsies, 284–287, 286f Familial lateral temporal lobe epilepsy, 286 Familial mesial temporal lobe epilepsy, 286–287 Fast activity, of sleep, 200, 201f, 202 Fast frequencies See Beta rhythm Fast-spiking interneurons, Fatal familial insomnia, 250 Field(s), EEG, effect of reference on, 42, 43f, 44 Filters, 52–54, 52–54f, 61, 63–64, 63–65f, 82, 82–85f, 85 Finite-element methods, 349 Finite impulse response filtering, 62 vs infinite impulse response (IIR) filtering, 63 FIRDA See Frontal intermittent rhythmic delta activity (FIRDA) Firing patterns, in neuronal classes, Flash analog-to-digital converter, 57, 57f K DESIGN SERVICES OF Flash visual evoked potentials (FVEPs), 456–457, 457f fMRI See Functional magnetic resonance imaging (fMRI) Focal brain injury, 161 Focal clonic seizure, 310 Focal cortical dysplasia, 239t, 255 Focal encephalopathies, EEG in, 238–255, 239t epileptiform abnormalities, 243–244 focal cortical dysplasia, 255 historical background of, 238–239 nonepileptiform abnormalities, 239–243 background rhythms, changes in, 239–241 focal slow-wave activity, 241–243 periodic lateralized epileptiform discharges, 244–245, 247f specific pathologies, 239t, 245 brain abscess, 249 brain tumors, 245–249 encephalitis, 249–251 hemispheric stroke, 251–252, 252f, 254f subarachnoid hemorrhage, 254 subdural hematoma, 251 thalamic hemorrhage, 254 transient ischemic attack, 251 vertebrobasilar ischemia, 252–254 stroke, 254–255 Focal polymorphic delta activity, 241–242 Focal spikes/sharp waves, 316–317 Focal structural epilepsies, 308–310 Focal tonic-clonic seizure, 310 with secondary generalization, 310 Focal tonic seizure, 310 Forward solution, 342 Four-channel montages, for PRVEP, 450, 472 4-hydroxyphenylpyruvate dioxygenase deficiency See Tyrosinemia type III 14- and 6-Hz positive bursts, 109, 113f Fragile X syndrome, 277, 299 Free running electromyography, 535–536 Friedreich ataxia, 483 Frontal intermittent rhythmic delta activity (FIRDA), 219f, 220, 242, 243f, 245f, 253f Frontal lobe seizures, 409, 410–411, 410f Frontal sharp waves, 167 Frontal spindles, 198, 200 637 Index Frontal theta activity, 155–156 Frontocentral theta activity, 155–156 Full-field stimulation, 447 Functional localization, electrical stimulation for, 388–389 Functional magnetic resonance imaging (fMRI), 371 Fusiform bursts, in sleep, 200 FVEPs See Flash visual evoked potentials (FVEPs) G Galactosylceramidase, 268 Gamma activity, Gamma rhythm, 16f Gap-junction coupling, 6–7, Gaucher disease, 274 Generalized atypical spike-and-slow-wave discharges, 321, 321f Generalized epilepsies, 330 Generalized epileptiform discharges, 142 Generalized high-voltage delta activity, 219 Generalized periodic discharges (GPEDs), 221f clinical correlation, 220–221 pathophysiology, 222 prognosis, 221 Generalized repetitive fast discharge (GRFD), 322–323, 323f Generalized seizures, 330 Generalized slowing electroencephalogram, 217–218 Generalized suppression pattern, 232 Generalized theta activity, 218, 218f Generalized tonic-closure seizures, 333–334 on awakening, 334 Generator(s), cortical See Cortical generators Genetic generalized spike-wave epilepsies, 287 childhood absence epilepsy, 290, 290f, 291f epilepsy with myoclonic absences, 290 juvenile absence epilepsy, 290, 292f juvenile myoclonic epilepsy, 292–293, 293f masquerading conditions, 293 myoclonic-astatic epilepsy, 287, 288–289f myoclonic epilepsy in infancy, 287, 288f Glial syncytial networks, Globoid cell leukodystrophy See Krabbe disease Glucose transporter (GLUT-1) deficiency syndrome, 269, 270f, 293, 294f Glycine encephalopathy, 260–261 GM1 gangliosidosis, type I and type II, 268–269 GM2 gangliosidosis, 268 GPEDs See Generalized periodic discharges (GPEDs) GRFD See Generalized repetitive fast discharge (GRFD) Grid electrodes, 60 Ground fault, 66 Ground loop, 66, 68, 68f GSW See 6-Hz generalized spike-and-wave discharges (GSW) H Head models, realistic, coregistering EEG data with, 347, 349–350, 349f, 350f, 351f Head trauma, 227 Head ultrasound examinations, for premature infants, 206 Hearing screening, 469 Hematomas, subdural, 372–373 Hemifield stimulation, 447 Hemispheric stroke, focal encephalopathies in, 239t, 251–252, 252f, 254f Herpes encephalitis, focal encephalopathies in, 239t See also Encephalitis Herpes simplex virus (HSV), 249, 250 High-frequency oscillations (HFOs), 19–24, 20f, 23f, 384, 388f High-pass filter, 85 High-resolution, flexible, active electrode array, 61, 61f HIHA See Hyperinsulinemia and hyperammonemia (HIHA) Hippocampal anatomy, 7–8 Hippocampal ripples, 22 Hjorth source montages, 44 Hodgkin-Huxley model, 4, Holocarboxylase synthetase deficiency, 267 Homocystinuria, 273–274 HSV See Herpes simplex virus (HSV) # 151788 Cust: LWW Au: Ebersole Pg No 637 Hyperglycinemia, nonketotic, 260–261, 261f Hyperinsulinemia and hyperammonemia (HIHA), 293 Hypermotor focal seizure, 310 Hyperphenylalaninemias, 270–271 Hyperventilation, 526 response, in children, 186–187, 187f Hypnagogic state, 187–188 Hypothalamic hamartoma, 249 Hypothermia clinical applications of, 581–587, 587–590f EEG changes with, 528t mechanisms for electroencephalography, 525–526 Hypsarhythmia, 304, 305f I Ictal discharges, 17–19, 18f Ictal EEG, 324 dipole models, 364 in focal epilepsy, 325 complex focal seizures, 325–326 extratemporal complex focal seizures, 328–330, 329–332f simple focal seizures, 325 temporal lobe complex focal seizures, 326–328, 327–329f in generalized epilepsy, 330 idiopathic generalized epilepsy, 330–334 symptomatic generalized epilepsies, 334–335 intracranial, 377, 381, 382–384f, 384, 385–387f limitations of, 336–337 scalp-recorded ictal discharges, 324–325 Ictal penumbra, 17–19, 18f ICU See Intensive care unit (ICU) Idiopathic generalized epilepsy, 330–334 absence seizure, 331 clonic-tonic-clonic seizures, 334 generalized tonic-closure seizures, 333–334 on awakening, 334 juvenile myoclonic epilepsy, 332–333, 333f IEC 60601 standards, for electrical safety, 68 IEDs See Interictal epileptiform discharges (IEDs) IEM See Inborn error of metabolism (IEM) K IFCN See International Federation of Clinical Neurophysiology IIR filtering See Infinite impulse response (IIR) filtering Impedance and alternating (sinusoidal) circuits, 52, 52f Improper grounding, electrical safety, 65 Impulsiv Petit Mal, 292 Inborn error of metabolism (IEM), 259 causing EME, 261t nonsyndromic infantile epilepsies with, 268 seizures in newborns and, 262–267 acyl-coenzyme A oxidase deficiency in, 265 biotin metabolism, disorders of, 267 Leigh syndrome, 267 maple syrup urine disease in, 265 molybdenum cofactor deficiency, 263–264 neonatal adrenoleukodystrophy in, 264–265 organic acidurias in, 265, 266–267 peroxisomal disorders, 264–265 pyridoxine dependency, 262–263, 263–264f pyruvate carboxylase deficiency, 267 pyruvate dehydrogenase deficiency in, 267 sulfite oxidase deficiency, 263–264 urea cycle disorders in, 265 Zellweger syndrome in, 264 Inductive plethysmography, for ventilatory monitoring in polysomnography, 606, 607f, 608f Inductor(s), 48, 48f, 49 Infant(s) See also under Neonate(s); Pediatric EEG Alpers disease, 272–273 aminoacidurias in, 270 congenital disorders of glycosylation, 273 fast activity during early stages of sleep in, 200 glucose transporter (GLUT-1) deficiency syndrome, 269 GM1 gangliosidosis, type I and type II in, 268–269 Krabbe’s disease in, 268 DESIGN SERVICES OF 638 Index Infant(s) (continued) lysosomal disorders in, 268–269 Menkes’ disease in, 271 metachromatic leukodystrophy in, 271 mucopolysaccharidoses in, 271–272 neuronal ceroid lipofuscinoses in, 272, 272f organic acidurias in, 269–270 PEHO syndrome in, 271 Schindler’s disease in, 271 sharp waves and spikes in, 186–187 Tay-Sachs disease in, 268 vitamin metabolism disorders in, 269 West syndrome in, 267–268 Infantile focal seizures clinical features of, 309–310 simple and complex, 309 as subtle, 309 types and electroclinical correlations of, 310 Infantile spasms, in infancy, 304 Infinite impulse response (IIR) filtering, 62 finite impulse response (FIR) filtering vs., 63 Infratentorial brain tumors, 247, 249 Inhalational agents, 523 for motor evoked potentials, 506–507 for somatosensory evoked potentials, 494 Inhibitory postsynaptic currents (IPSCs), Inhibitory postsynaptic potentials (IPSPs), 29 Insomnia, evaluation of, 627 fatal familial, 250 Instrumental artifacts, 417 Instrumental phase reversal, 40 Instrumentation amplifier, 51 Insular lobe seizures, 413, 414f, 415 Insulator(s), 47f, 48 Intensive care unit (ICU), continuous EEG monitoring in, 543–594, 544f, 545f, 546f artifacts in, 551, 554–560f clinical applications of, 569–575 anoxic brain injury, 581–587, 587–590f hypothermia, 581–587, 587–590f ischemia, 581 nonconvulsive seizures, 572t, 578–581 status epilepticus, 575–578 clinical factors confounding, 551–553, 561f data review, 553–555 electrodes in, 550–551 future directions, 590 historical context, 547–548 interpretation and nomenclature, 555–561, 562t, 563–571f, 573f montages in, 551, 552–553f multimodal brain monitoring, 587–590, 594f personnel requirements, 549–550 quantitative analysis of, 562–569, 574–578f scientific basis for, 546–547, 547t technical considerations for, 548–549, 548f Intercostal electromyography, for ventilatory monitoring in polysomnography, 607 Interhemispheric asynchrony, abnormal in neonatal EEG, 165 Interhemispheric fissure, 340 Interhemispheric symmetry amplitude, 129, 129f, 130f, 206 waveform composition, 129 Interhemispheric synchrony, in neonatal EEG interpretation, 131, 133f, 165 Interictal epileptiform activities, 271, 304 in extratemporal neocortical epilepsy, 424 Interictal epileptiform discharges (IEDs), 13, 186, 315, 374 focal, spikes/sharp waves, 316–317, 316f generalized, 320 atypical spike-and-slow-wave discharges, 321, 321f photo-epileptiform discharges (photoparoxysmal response), 323, 324f repetitive fast discharge, 322–323, 323f slow spike-and-wave discharge pattern, 322, 322f 3-Hz spike-and-wave discharges, 320–321, 320f limitations of, 336–337 multifocal spikes, 317–318, 317f periodic lateralized epileptiform discharges, 318–319, 318f temporal intermittent rhythmic delta activity, 319–320, 319f Interictal regional delta activity, 376–377 # 151788 Cust: LWW Au: Ebersole Pg No 638 Intermittent rhythmic delta activity, 219–220, 219f, 242–243 International 10–20 system of electrode placement, 38, 39–40f, 40, 79–80, 80f, 126, 151f, 550 International Federation of Clinical Neurophysiology (IFCN), 79, 556 Interpeak latency (IPL) in BAEPs, 445 Intracerebral depth electrodes encephalography, 393–437 electrical stimulation, 433–435, 434f historical perspective, 394–395 indications for SEEG, 407t in extratemporal lobe epilepsy, 409–415 in lesional focal epilepsies, 415 in nonlesional focal epilepsies, 415 scheme for intracranial EEG in temporal lobe, 407t in temporal lobe epilepsy, 407–409 interpretation of EEG data, 415–416 abnormal interictal EEG activity, 418–425, 420–425f artifacts, 417–418, 419f normal physiological EEG activity, 416, 417–418f propagation, 425–433 seizure-onset zone, 425–433 study protocol during EEG, 416t recording procedure, 402 practical aspects, 404, 405–406f, 407 technical aspects, 402, 403–404f stereotactic radiofrequency thermocoagulation lesioning, 435, 436f technical considerations advantages of, 398, 400–401, 400f characteristics, 396–397 drawback of, 401 insertion and removal, 397 intracranial electrodes, 395–396 location, 398, 399f placement, 397–398 risks and complications, 401–402 scalp electrodes, 398, 400f types of, 397f Intracortical EEG (ICE), multimodal brain monitoring, 587–588 Intracranial aneurysm, 254 K DESIGN SERVICES OF Intracranial EEG, 367–389 acquisition, 373–374 chronic, 368 electrical stimulation and functional localization, 388–389 electrodes, 60 high-frequency oscillations, 384, 388f historical perspectives, 368–369 ictal, 377, 381, 382–384f, 384, 385–387f interictal, 374–377, 375f, 376f, 377–380f localization of intracranial electrodes, 371, 371f, 372f normal physiological, 374 postoperative care, 373 recordings, of seizure activity, 326 subdural electrodes characteristics of, 369, 370f vs depth electrodes, 369 EEG recording, clinical indications of, 373 placement, risks and complications of, 371–373 Intracranial electrodes, 60 characteristics of, 395, 396t localization of, in intracranial EEG, 371, 371f, 372f Intracranial IEDs, 374, 375, 376 Intraoperative digital photography, 371, 372f Intraoperative ECoG, 368 See also Electrocorticography (ECoG) technique Intraoperative monitoring, neurophysiologic See Neurophysiologic intraoperative monitoring Intravenous (IV) agents for motor evoked potentials, 507 for somatosensory evoked potentials, 494 Invasive EEG, 92, 409, 415, 436 clinical indications for, 393, 394t complication of, 373 motivation to use, 394 recordings, 407 Inverse solution, 342, 346, 367 IPL in BAEPs See Interpeak latency (IPL) in BAEPs, 445 IPSCs See Inhibitory postsynaptic currents (IPSCs) IPSPs See Inhibitory postsynaptic potentials (IPSPs) 639 Index Ischemia, 498 and anoxia/blood pressure, 495, 507 chronic, 251 clinical applications of, 581 mechanisms of for electroencephalography, 524–525 motor evoked potentials change, 507 somatosensory evoked potentials change, 495 vertebrobasilar, 252–253, 255f Isoelectric EEG, 206 Isoelectric tracing, 161, 164f Isolation amplifier, 51 Isovaleric aciduria, symptoms of, 265 IV agents See Intravenous (IV) agents J Jackbox, 59 JAE See Juvenile absence epilepsy (JAE) JME See Juvenile myoclonic epilepsy (JME) Juvenile absence epilepsy (JAE), 290, 292f Juvenile myoclonic epilepsy (JME), 292–293, 293f, 332–333, 333f K K complexes, 612 in adolescence, 143 in sleep, 103, 107f and vertex transients, 196 Kainate, Kaplan-Meier survival curve, 206f Kinky hair disease, 260, 271 Kirchhoff’s current law, 49 Kirchhoff’s voltage law, 49 Krabbe disease, 268, 458 in BAEP, 469 Late-onset batten disease, 274–275 Late-onset multiple carboxylase deficiency, 268, 269 Late-onset occipital lobe epilepsy, 297, 299, 299f Lateral lemniscus, 460, 460t, 512 Laura technique, 358, 364 Leakage currents, 66, 522 LED goggles See Light emitting diode (LED) goggles Leigh syndrome, 267 Lennox-Gastaut syndrome (LGS), 249, 259, 300, 307, 308f, 322 Lesional and nonlesional focal epilepsies, indications for SEEG in, 415 Leukodystrophy(ies), 458, 484 metachromatic, 271 LGS See Lennox-Gastaut syndrome (LGS) LIEE See Late infantile epileptic encephalopathy (LIEE) Light emitting diode (LED) goggles, 456 LKS See Landau-Kleffner syndrome (LKS) Loop of Meyer, 447 LORETA See Low-resolution tomography (LORETA) Low-pass filter, 52–54f, 53, 82 Low-resolution tomography (LORETA), 24, 358 Lowered seizure threshold, 169 Lysosomal disorders of childhood and adolescence, 274 of early infancy, 268–269 M L Lafora disease (EPM2), 275 Lambda waves, 101, 115, 119f, 120 Landau-Kleffner syndrome (LKS), 295, 297, 299 Laplacian montages, 44 Large hemispheric brain tumors, 247 Late infantile epileptic encephalopathy (LIEE), 259, 300, 306, 306–307f Macula, 447 Magnetic resonance imaging (MRI), coregistering EEG data with, 347, 349–350, 349–351f Magnetoelectroencephalography, 369, 371 Magnetoencephalography, 13, 29 Maintenance of wakefulness test (MWT), 600, 622 interpretation, 623 procedure, 623 Malignant migrating focal seizures in infancy, 300–301, 302f Maple syrup urine disease, 265, 279 # 151788 Cust: LWW Au: Ebersole Pg No 639 Masking, for BAEPs, 461, 513 Median nerve stimulation (MNS), 480 MEI See Myoclonic epilepsy in infancy (MEI) MELAS syndrome, 245, 267, 275–276, 277f Menkes disease, 260, 271 MEPs See Motor evoked potentials (MEPs) MERRF syndrome, 275 Mesial vs neocortical temporal lobe seizures, 408, 408f Metabolic disorders of childhood and adolescence, 273–277 adrenoleukodystrophy, 274 dentatorubral-pallidoluysian atrophy, 276–277 homocystinuria, 273–274 lysosomal disorders, 274 neuroaxonal dystrophies, 274 neuronal ceroid lipofuscinosis, type III, 274–275 progressive myoclonus epilepsies, 275–276 of early infancy aminoacidurias, 270 glucose transporter deficiency syndrome, 269 lysosomal disorders, 268–269 Menkes Disease, 271 organic acidurias, 269–270 progressive encephalopathy with edema, hypsarhythmia, and optic atrophy, 271 vitamin metabolism, disorders of, 269 West syndrome, 267–268 of late infancy Alpers disease, 272–273 congenital disorder of glycosylation, 273 metachromatic leukodystrophy, 271 mucopolysaccharidoses, 271–272 neuronal ceroid lipofuscinoses, 272 Schindler disease, 271 Metachromatic leukodystrophy, 271 Methylene tetrahydrofolate reductase (MTHFR) deficiency, 262, 269 Methylmalonicacidemia, 265, 266 Mg2+ ions, Microelectrode arrays, 61 lessons from, ictal discharges and ictal penumbra, 17–19, 18f K Midline central (Cz) theta activity, 156–157 Midline theta rhythm, 114, 116f MNS See Median nerve stimulation (MNS) Molybdenum cofactor deficiency, 260, 263–264, 279 Monomorphic, rhythmic 6- to 7-Hz voltage activity, 156, 156f, 157f Monorhythmic occipital delta activity, in neonatal EEG interpretation, 135, 143, 144f Monorhythmic slow activity, 187–188, 189–190f Montage(s), 44, 472t, 504t, 505t bipolar, 40–41, 41f, 42f, 86, 89, 98f, 222, 374, 404 Cz-A1/Cz-A2, 460 display conventions for, 86 for displaying EEG data, 523 four-channel, for PRVEP, 450, 472 MSLT, 621t, 623 paired-channel, 86 paired-group, 86 PSG, 608–609, 609t in quantitative EEG, 551, 552–553f recording, for ventilatory monitoring in polysomnography, 608–609, 609t referential, 41, 86, 87–88f, 374, 404 selection of, 89 SEP, recording, 456, 474t, 493, 493t standard neonatal, 126 transverse vertex, 601 unpaired, 86 used for BAEP, 461 voltage fields in EEG traces, display of, 40–42, 41f Motor evoked potentials (MEPs), 501t anatomy and physiology, 501–502 anesthetic considerations, 505–507, 506f inhalational agents, 506–507 intravenous agents, 507 neuromuscular junction blocking agents, 507 change, mechanisms of, 507–509, 508f acute trauma, 507 anesthetics, 507, 509 ischemia and blood pressure, 507 technical issues, 509 temperature, 507 DESIGN SERVICES OF 640 Index Motor evoked potentials (MEPs) (continued ) clinical applications, 511 methodology, 502–505, 503t, 503f, 505t, 506f recording techniques, 504–505 stimulating techniques, 502–504 safety, 509–511, 511t warning criteria, 509, 510f Motor unit action potentials (MUAP), 533 Movement-associated arousals, effects on polysomnographic scoring, 620 Movement(s), effects on polysomnographic scoring, 619–620 MS See Multiple sclerosis (MS) MSLT See Multiple sleep latency test (MSLT) MTHFR deficiency See Methylene tetrahydrofolate reductase (MTHFR) deficiency Mu rhythm, 118f adult EEG, normal, 94–96, 95f in neonates and children, 153–154, 154f MUAP See Motor unit action potentials (MUAP) Mucopolysaccharidoses, 271–272 Multifocal spikes, 317–318, 317f Multimodal brain monitoring, 587–590, 594f Multiple fixed-dipole models, 353 Multiple sclerosis (MS) BAEP in, 468–469 SEP in, 483 Multiple sleep latency test (MSLT), 600, 624 interpretation of, 621–623, 622t procedure for, 620–621, 621t, 621f Muscle artifacts, 82, 417 Muscle MEP recordings, 504, 505, 505t MWT See Maintenance of wakefulness test (MWT) Myoclonic-astatic epilepsy, 156, 272, 287, 288–289f Myoclonic-atonic seizure, 287, 306, 307f Myoclonic epilepsy in infancy (MEI), 287, 288f Myoclonic-tonic seizures, 306 Myoclonus, 221, 274, 293, 302 baltic myoclonus epilepsy, 275 progressive myoclonus epilepsies, 275–276, 295f Myotome, 531 N N-methyl-d-aspartate (NMDA) receptors, 5, NALD See Neonatal adrenoleukodystrophy (NALD) Nasal pressure transducer, for airflow monitoring in polysomnography, 605– 606, 605f NCLs See Neuronal ceroid lipofuscinoses (NCLs) NCS See Nerve conduction studies (NCS) NCSE See Nonconvulsive status epilepticus (NCSE) Needle electrodes, 535, 535f Negative centrotemporal SETs, 169 Neocortical anatomy, and thalamic connections, 9–11 Neonatal adrenoleukodystrophy (NALD), 264–265 Neonatal EEG, 165, 166f anterior dysrhythmia in, 148, 149f, 150f background, classification and implications of, 205–206, 205t biobehavioral state in, 135 centrotemporal delta activity in, 147 conceptional age in, 131 continuity in, 126–127, 128f delta brushes in, 144–147f, 148 in excessive discontinuity, 157, 158f, 159 abnormal asymmetry, 161, 165 abnormal interhemispheric asynchrony, 165 abnormal maturation, 165, 166f abnormal voltage, 159, 161 for age, 159, 161t burst-suppression pattern, 159, 160f isoelectric tracing, 161, 164f persistent low voltage, with or without lack of differentiation, 161, 162f, 163f interhemispheric synchrony in, 131, 165 monorhythmic occipital delta activity in, 143, 144f montage selection in, 126 ontogeny, overview of See Ontogeny, overview of positive sharp waves, 169, 172, 176–178f rhythmic occipital theta activity in, 143, 145f # 151788 Cust: LWW Au: Ebersole Pg No 640 rhythmic temporal theta activity in, 143, 146, 146f sharp EEG transient in, 169, 172, 174–178f trace alternant in, 135 trace discontinu in, 135 visual analysis of, 126–131, 128–133f, 207–209 Neonatal epilepsy syndrome, 260 Neonatal seizures See Seizure(s), neonatal Neonate(s) with clinically diagnosed seizures, 186 electrographic neonatal seizures, 177–205 neonatal electroencephalographic background, 205–206, 205t with occult seizures, 177 sharp electroencephalographic transients in frontal, 165, 167–168, 167f negative, 169, 174f, 175f positive sharp waves, 169, 172, 176f, 177f, 178f temporal and central negative, 168–169, 170–173f Nerve action potential (NAP), auditory, 513, 521 Nerve conduction studies (NCS) anatomy and physiology, 531–533 anesthetic considerations, 536 clinical applications, 538–539, 538t cranial nerve surgery, 538–539 peripheral nerve surgery, 538–539 spinal surgery with instrumentation, 538 interpretation of, 536–537, 537f methodology, 533–534, 534f, 535f Neuroaxonal dystrophies, 274 Neurointensive care unit (NICU), EEG monitoring in, 373 Neuromuscular junction blocking agents (NMJBA) for motor evoked potentials, 507 for somatosensory evoked potentials, 494–495, 496f Neuronal ceroid lipofuscinoses (NCLs), 272, 272f type III, 274–275 Neuronal specific enolase (NSE), 580 K DESIGN SERVICES OF Neurophysiologic intraoperative monitoring, 489–539 brainstem auditory evoked potentials anatomy and physiology, 512, 512t anesthetic considerations, 513 auditory nerve action potential, 521 change, mechanisms of, 513–520, 515t, 516–520f clinical applications, 521 methodology, 512–513, 514f, 515f warning criteria, 520–521 electroencephalography, 521–522 anatomy and physiology, 522 anesthetic considerations, 523–524, 524–527f change, mechanisms of, 524–526, 527–528t, 529–530f, 532t clinical applications, 530–531 methodology, 522–523 quantitative analysis, 531 warning criteria, 526–530 electromyography free running, 535–536, 535f stimulated, 534–535, 535f motor evoked potentials, 501t anatomy and physiology, 501–502 anesthetic considerations, 505–507, 506f change, mechanisms of, 507–509, 508f clinical applications, 511 methodology, 502–505, 503t, 503f, 505t, 506f safety, 509–511, 511t warning criteria, 509, 510f nerve conduction studies anatomy and physiology, 531–533 anesthetic considerations, 536 clinical applications, 538–539, 538t interpretation of, 536–537, 537f methodology, 533–534, 534f, 535f somatosensory evoked potentials anatomy and physiology, 489–490, 490t anesthetic considerations, 494–495, 494t, 495–496f change, mechanisms of, 495–498, 497–501f clinical applications, 500 methodology, 490–494, 490f, 491–493t, 492f warning criteria, 498–500 641 Index Neurotransmitters, Newborn(s) See also under Neonate(s) acyl-coenzyme A oxidase deficiency in, 265 biotin metabolism, disorders of, 267 epileptic encephalopathies in, 262t IEM causing seizures in, 262 Leigh syndrome, 267 maple syrup urine disease in, 265 molybdenum cofactor deficiency in, 263–264 neonatal adrenoleukodystrophy in, 264–265 nonketotic hyperglycinemia in, 260–261, 261f organic acidurias in, 265, 266–267 peroxisomal disorders in, 264–265 pyridoxine dependency in, 262–263, 263–264f pyruvate carboxylase deficiency, 267 pyruvate dehydrogenase deficiency in, 267 sulfite oxidase deficiency in, 263–264 urea cycle disorders in, 265 Zellweger syndrome in, 264 nHL See Normal hearing level (nHL) NICU, EEG monitoring in See Neurointensive care unit (NICU), EEG monitoring in NMDA receptors See N-methyl-d-aspartate (NMDA) receptors NMJBA See Neuromuscular junction blocking agents Nocturnal behavioral events, evaluation of, 626–627, 626t Non-Ohmic conductances, Noncerebral artifacts, 40 Nonconvulsive seizures, continuous EEG in, 572t, 578–581 Nonconvulsive status epilepticus (NCSE) algorithm for diagnosis of, 231f clinical signs associated with, 227, 228t controversy topics, 228 duration of monitoring, 230 generalized nonconvulsive ictal activity, 229f interictal-ictal continuum, 228 prevalence range of, 227 proposed criteria for, 228–230 seizure termination in patients with, 230f Nonketotic hyperglycinemia, 260–261, 261f Nonneuronal currents, Nonsyndromic infantile epilepsies, 268 Normal hearing level (nHL), 461 Normal physiological intracranial EEG, 374 Notch/bandstop filter, 54, 54f NSE See Neuronal specific enolase (NSE) Nyquist limit, 55 O Obligate wave absence, in BAEPs, 464, 464f Occipital alpha rhythm, in children, 188 Occipital intermittent rhythmic delta activity (OIRDA), 242 Occipital lobe seizures, 328 Occipital sharp waves, 103 Occipital slow transients, 204f, 205 Ohmic conductances, Ohm’s law, 5, Ohtahara syndrome, 259, 260 OIRDA See Occipital intermittent rhythmic delta activity (OIRDA) Ontogeny, pediatric EEG See Pediatric EEG, ontogeny Optic nerve fibers, anatomy and waveform generators, 447 Optic neuritis, for visual evoked potentials, 458, 459f Organic acidurias, 265–267, 269–270 Ornithine transcarbamylase deficiency, 265, 266f Oscillation(s), 11 and cellular activity, relationship between, 13–14 hierarchical phase-amplitude coupling, 12f, 14 high-frequency, EEG markers of ictal territories, 19–24, 20f, 23f structure of EEG, 12–13, 12f P P100 waveform latency, 447, 448, 452 Paired-channel montages, 86 Paired-group montages, 86 Panayiotopoulos syndrome (PS), 296, 296–297f Paradoxical alpha, 94 # 151788 Cust: LWW Au: Ebersole Pg No 641 Paradoxical arousal response, 194 Parasomnia(s), evaluation of, 626–627, 626t Parietal lobe seizures, 328 Paroxysmal depolarizing shift (PDS), 14–15 Paroxysmal hypnagogic hypersynchrony, 191, 191f, 192f Paroxysmal slow activity, 188, 191–192, 192f, 193f Parvalbumin positive neurons, Passband, 53 Pattern reversal visual evoked potentials (PRVEP), 448–456, 449–456f, 451–453t abnormalities, 453–456 interpretation, 451–453 methodology, 448 recording, 449–451 stimulation, 448–449 Patting artifacts, 142 PDE See Pyridoxine-dependent epilepsy (PDE) PDS See Paroxysmal depolarizing shift (PDS) Peak latency See Absolute latency Pediatric acute encephalopathy, 161 Pediatric EEG, 125–209 electrographic neonatal seizures and clinical correlations arousal, activity of, 193–194 characteristics amplitude, 182, 185f, 186 duration, 177, 181–182f, 182 location, 177, 179–180f morphological appearance, 182, 183–184f drowsiness, activity of monorhythmic slow activity, 187–188, 189–190f paroxysmal slow activity, 188, 191–192, 192f, 193f postarousal hypersynchrony, 194–195, 194–195f sharp waves and spikes in older infant and child hyperventilation response, 186–187, 187f photic stimulation, 187 sleep, activity of, 195–196, 196–204f, 198, 200, 202, 205 K infancy and childhood alpha rhythm (alpha activity), 148 alpha variants, 151, 152f, 153 beta activity, 154–155 distribution, 151 frequency of posterior dominant rhythm, 148, 148f, 151 frontal theta activity, 155–156, 156f, 157f frontocentral theta activity, 155–156, 156f, 157f midline central theta activity, 156–157 mu rhythm, 153–154, 154f symmetry, 151 voltage of posterior dominant rhythm, 151 introduction to, 126 neonatal classification and implications of, 205–206, 205t, 206f, 207f composition of, 143, 144–147f, 146– 148, 149f, 150f ontogeny, 134f adolescence, 143 childhood, to 10 years, 142 conceptional age 24 to 29 weeks, 131, 134 30 to 32 weeks, 134–135, 136f 33 to 34 weeks, 135 35 to 36 weeks, 135, 137f, 138 37 to 40 weeks, 138, 139f, 140f 41 to 44 weeks, 138 45 to 46 weeks, 138, 141f early infancy, 46 weeks to year, 138, 140, 142 late infancy, to years, 142 types and significance of abnormal, in neonates and children excessive discontinuity, 157, 158f, 159, 160f, 161, 161t, 162f, 163f, 164f, 165, 166f sharp electroencephalographic transients, 165, 167–169, 167f, 168f, 170–178f, 172 visual analysis, in neonates and children abnormalities in, 131, 208–209 continuity, 126–127, 128f, 207–208 gradient and principal components, 208 DESIGN SERVICES OF 642 Index Pediatric EEG (continued ) interhemispheric symmetry, 129, 129f, 130f, 131 interhemispheric synchrony, 129, 131, 132f, 133f, 208 organization and principal components, 128 organized approach to, 207–209 special features in, 131, 208 state, 126–127, 128f, 207–208 symmetry, 208 Pediatric epilepsy syndromes, 283–312 diagnosis of epilepsy, based on EEG features, 284, 284t epilepsies with encephalopathies, 299–308, 301–308f epileptic encephalopathies, 301–308 epileptogenic encephalopathies, 300–301 late infantile epileptic encephalopathy, 306, 306–307f Lennox-Gastaut syndrome (LGS), 307, 308f West syndrome, 304–306, 305f familial epilepsies, 284–287, 286f autosomal dominant nocturnal frontal lobe epilepsy, 285–286, 286f benign familial infantile epilepsy, 285 benign familial neonatal epilepsy, 285 familial lateral temporal lobe epilepsy, 286 familial mesial temporal lobe epilepsy, 286–287 focal structural epilepsies, 308–310 genetic generalized spike-wave epilepsies, 287–293, 288–293f childhood absence epilepsy, 290, 290f, 291f epilepsy with myoclonic absences, 290 juvenile absence epilepsy, 290, 292f juvenile myoclonic epilepsy, 292–293, 293f masquerading conditions, 293 myoclonic-astatic epilepsy, 287, 288–289f myoclonic epilepsy in infancy, 287, 288f by interictal EEG characteristics, 311t self-limited epilepsies with focal spikes, 293–299, 296–299f benign childhood epilepsy with centrotemporal spikes, 295, 296–297, 298f conditions masquerading, 299 late-onset occipital lobe epilepsy, 297, 299f panayiotopoulos syndrome, 296, 296–297f Periodic lateralized epileptiform discharges (PLEDs), 244–245, 247f, 248f, 249 in focal interictal epileptiform discharges, 318–319, 318f Periodic leg movements (PLMs), effects on polysomnographic scoring, 619–620 Periodic pattern, 220 Peripheral nerve surgery, 538–539 Peripheral nervous system (PNS), 480 Peripheral waveforms, 444 Peroxisomal disorders, 264–265 Persistent low voltage, with or without lack of differentiation, 161, 162f, 163f PET See Positron emission tomography (PET) Phantom spike-and-wave, 108 Phase progression, 11 Phase reversal, 37, 40, 86, 89 Phenylketonuria, 270–271 Phosphomannomutase-2 deficiency, type Ia, 273 Photic driving response, 100 Photic stimulation, in normal pediatric EEG, 187 Photo-epileptiform discharges, 323, 324f Photomyoclonic response, 101 Photoparoxysmal response (PPR), 100–101, 323, 324f Piezoelectric belts, for ventilator monitoring in polysomnography, 607 Place cells, 11 PLEDs See Periodic lateralized epileptiform discharges (PLEDs) Plethysmography, inductive, for ventilatory monitoring in polysomnography, 606, 607f, 608f PLP-DE See Pyridoxal 5′-phosphatedependent epilepsy (PLP-DE) Pneumotachography, for airflow monitoring in polysomnography, 606, 607f, 608f, 609t arterial oxygen assessment in, 607–608 ECG in, 608 # 151788 Cust: LWW Au: Ebersole Pg No 642 esophageal pressure monitors in, 606–607 inductive plethysmography, 606, 607f, 608f intercostal EMG, 607 piezoelectric belts in, 607 recording montage in, 608–609, 609t ventilatory effort monitoring, 606 PNPO See Pyridoxine 5′-phosphate oxidase (PNPO) PNS See Peripheral nervous system (PNS) Point source dipole model, 346 Polarity convention for BAEPs, 461 in recording techniques, 81 Poliodystrophy, progressive infantile, 272–273, 273f Polymorphic delta activity, 279 Polyphasic waves, 151 Polysomnography, 600–610, 601–608f, 609t, 611f, 612t, 613–615f, 618f airflow monitoring by, 604–609, 605–608f, 609t alternatives to, 606 anterior tibialis EMG in, 603, 604f axial EMG in, 603 basic sleep scoring with, 611–612, 611f, 612t carbon dioxide detectors in, 606 and computer-assisted scoring, 610 and EEG sleep recording, 601–603, 601f, 603f electro-oculogram in, 602–603, 602f inductive plethysmography, 606, 607f, 608f interpretation of, 610–620, 611f, 612t, 613–615f, 618f arousals and, 612–613, 613–615f awakenings and, 612–613, 613–615f EEG-related variables in, 611–613, 611f, 612t, 613–615f movement-related variables in, 619–620 in pediatric sleep-disordered breathing, 618–619 respiration-related variables in, 616–619, 618f in sleep apnea diagnosis, 617–618 nasal pressure transducer in, 605–606, 605f pneumotachography in, 606, 607f, 608f, 609t recording, ambulatory, 609–610 K DESIGN SERVICES OF respiratory monitoring with, 604–609, 605–608f, 609t thermistors in, 604–605 thermocouples in, 604–605 Positive occipital sharp transients of sleep (POSTs), 103, 105f, 202, 202f, 203f Positive rolandic sharp waves (PRS), 169, 172, 176f Positive sharp waves, neonatal, 169, 172, 176f, 177f, 178f Positive temporal sharp waves (PTS), 169, 172, 178f Positive vertex sharp wave (PVS), 169, 172, 177f Positron emission tomography (PET), 363, 371 Postarousal hypersynchrony, 194–195, 194–195f Posterior dominant rhythm, 96 frequency of, 148, 148f, 151 voltage of, 151 Posterior quadrant seizures, 412–413, 413f Posterior slow-wave transients, associated with eye movements, 153 Posterior slow waves of youth (PSWY), 97–98, 142, 151 POSTs See Positive occipital sharp transients of sleep (POSTs) Posttetanic stimulation, 504 Potential(s), sources of, 28–30, 29–30f Power, 565–566 PPR See Photoparoxysmal response (PPR) Preamplifiers, 61 Precision, 56 Primary current, 29 Prion diseases, 250 Progressive childhood encephalopathy, 258–280 age categorization, 260 early myoclonic encephalopathy, 260–261, 260f EEG hallmark of, 259 inborn error of metabolism, 259 causing seizure in newborn, 262–267, 263–264f, 266f limited repertoire of immature EEG, 259 metabolic disorders, 267–279 of childhood and adolescence, 273–279, 275f, 276f of early infancy, 267–271, 270f of late infancy, 271–273, 271f, 273f 643 Index role of EEG in child with suspected, 279–280 spectrum of epileptic encephalopathies, 259 Progressive Encephalopathy with Edema, Hypsarhythmia, and Optic Atrophy (PEHO Syndrome), 271 Progressive infantile poliodystrophy, 272– 273, 273f Progressive myoclonus epilepsies (PME), 275–276, 295f Progressive neurological syndrome, in infancy, 269 Propagation, EEG source characterization, 36f, 37 Propionic acidemia, 265 PRS See Positive rolandic sharp waves (PRS) PRVEP See Pattern reversal visual evoked potentials (PRVEP) PS See Panayiotopoulos syndrome (PS) Pseudo petit mal, 191, 192 Pseudo-temporal epilepsy, 409, 410f PTS See Positive temporal sharp waves (PTS) Pulsation artifacts, 417 PVS See Positive vertex sharp wave (PVS) Pyknolepsy, 290 Pyramidal cells, 6, 8, 29 Pyramidal neurons, 29, 522 Pyramidal somata, Pyridoxal 5′-phosphatedependent epilepsy (PLP-DE), 263 Pyridoxine 5′-phosphate oxidase (PNPO), 263 Pyridoxine dependency, 261t, 262–263, 263–264f Pyridoxine-dependent epilepsy (PDE), 263 Pyruvate carboxylase deficiency, 267 Pyruvate dehydrogenase deficiency, 267 Q QEEG See Quantitative EEG (qEEG) Quantitative EEG (qEEG), 95, 252 in intensive care unit, 562–563, 565–569, 574–578f neurophysiologic intraoperative monitoring, 531 Queen Square method, 449–450 R Rarefaction, 461, 513 Reactance, 52 Reactivity of alpha rhythm, 92, 251 EEG, in encephalopathic patients, 215– 217, 216f of mu rhythm, 95 Recording(s) auditory nerve action potential, 521 cerebral death, technical standards for EEG, 235t derivation, in visual evoked potentials, 448 differential amplifier, 444 digital, issues related to, 80–81 EEG clinical indications of subdural electrode, 373 sleep, 601–603, 601f, 602f electrodes for motor evoked potentials, 504–505 for somatosensory evoked potentials, 491–492, 492f in evoked potentials, 444–445 intracranial, in EEG, 374–377, 375f, 376f, 377–380f MEP muscle, 505, 505t spinal cord, 505, 505t montage, 608–609, 609t parameters of, normal adult EEG, 91–92 pattern reversal visual evoked potentials, 449–451 procedure for intracerebral depth electrodes encephalography See Intracerebral depth electrodes encephalography, recording procedure referential, 86, 374 spinal cord MEP, 505, 505t techniques, 78–89 for brainstem auditory evoked potentials, 459–460, 513 calibration in, 81–82 cerebral generators of EEG potentials in, 78–79, 79f conventions and sensitivity/filter settings, 80–85 EEG derivations in, 78 # 151788 Cust: LWW Au: Ebersole Pg No 643 electrode placement in, 79–80, 80f filters in, 82, 82–85f, 85 issues related to digital, 80–81 montages in, 85–86, 87–88f, 89 for motor evoked potentials, 504–505 polarity conventions in, 81 for PRVEP, 449–451 sensitivity in, 81–82 for somatosensory evoked potentials, 491–494, 492f Referential montages, 41, 86, 87–88f Referential recordings, 86, 374 Reformatting, 40 REM sleep (R sleep), in sleep architecture, 104, 108f, 109f Resistor(s), 46t, 47, 47f, 48, 48f Respiration(s), effects on polysomnographic interpretation, 616–619, 618f Respiratory artifact, 235t Respiratory monitoring, polysomnography in, 604–609, 605–608f, 609t Retina, anatomy and waveform generators, 447–448 Rett syndrome, 278, 279f Reye syndrome, 270 Rhythmic bursting (Ih), 10 Rhythmic delta activity, 219–220, 219f Rhythmic midtemporal theta bursts of drowsiness (RMTD), 106, 111f bilateral independent, 110f Rhythmic occipital theta activity, in neonatal EEG interpretation, 143, 145f Rhythmic temporal theta activity, in neonatal EEG interpretation, 143, 146, 146f Ripples, 21 of prematurity See Delta brushes, in neonatal EEG interpretation RMTD See Rhythmic midtemporal theta bursts of drowsiness (RMTD) Rolandic epilepsy (RE) See Benign childhood epilepsy with centrotemporal spikes S Safety, electrical See Electrical safety Sampling rate, in digitization, 55 Sandhoff disease, 268 K Scalp cup electrodes, 59, 60f Scalp EEG pattern, 37, 376 artifacts for, 417 in assessment of normal EEG, 90 factors in determination of, 30, 32–35f amplitude, of cortical activity, 32–33 source area, 31, 32–33f source location, 31 source orientation, 31–32, 34f synchrony, of cortical activity, 33–34, 35f ictal, 335–336 potentials, 339–341, 340f, 341f recordings, 335 Scalp electrodes, 59, 78, 335, 473 Schindler disease, 271 SEEG See Stereo-electro-encephalography (SEEG) SEF See Spectral edge frequency (SEF) Seizure(s) See also Epilepsy absence, 331 atonic, 334, 335f atypical absence, 334 bilateral independent temporal lobe, 408 central cortex, 411–412, 412f clonic, 334 clonic-tonic-clonic, 334 complex focal, 325–326 diffuse tonic-focal clonic, 310 dipole source modeling of, 350, 352f, 353, 354f EEG-confirmed neonatal, 186 for EEG voltage topography, 339 electrographic neonatal, 177–205 extratemporal complex focal, 328–330, 329–332f focal clonic, 310 focal tonic, 310 focal tonic-clonic, 310 frontal lobe, 409, 410–411, 410f generalized, 330 generalized tonic-clonic, 333–334 generalized tonic-closure, 333–334 hypermotor focal, 310 infantile focus, 309–310 insular lobe, 413, 414f, 415 malignant migrating focal, in infancy, 300–301, 302f DESIGN SERVICES OF 644 Index Seizure(s) (continued) mesial vs neocortical temporal lobe, 408, 408f myoclonic-atonic, 287 myoclonic-tonic, 306 neonatal disorders associated with, ambulatory EEG monitoring in, 628 EEG-related, 177–186, 181–185f, 186t amplitude of, 182, 185f, 186 duration of, 177, 181–182f, 182 location in, 177, 179–180f morphological appearance of, 182, 183–184f in newborns and, 262–267 occipital lobe, 328 parietal lobe, 328 posterior quadrant, 412–413, 413f sensorimotor, 411–412, 412f simple focal, 325 symptomatic generalized tonic-clonic, 334 tonic, 334 unilateral mesial temporal lobe, 407 Seizure-onset rhythms, 377, 381 Seizure-onset zone (SOZ), 425–433, 427–433f definition, 425 epileptogenicity index, 430 epileptogenicity maps, 433, 433f intracerebral ictal-onset patterns, 427, 427t, 428–430f symptomatogenic zone, 425 Self-limited epilepsies with focal spikes, 293–299 benign childhood epilepsy with centro temporal spikes, 295, 296–297, 298f conditions masquerading, 299 late-onset occipital lobe epilepsy, 297, 299f panayiotopoulos syndrome, 296, 296–297f Sensitivity, recording conventions and, 80–85 Sensorimotor seizures, 411–412, 412f Sensory-evoked potentials, 30 SEPs See Somatosensory evoked potentials (SEPs) Sharp-and-slow-wave complexes, 322 Sharp EEG transients (SETs) frontal, in neonates, 165, 167–168, 167f negative, 169, 174f, 175f positive sharp waves, 169, 172, 176f, 177f, 178f temporal and central negative, 168–169, 170–173f Sharp waves in SETs, 165 and spikes in older infant and child, 186–187 vertex transients, 195–196, 196–201f, 198, 200, 202 Shunting inhibition, Sialidosis type I, 274 type II, 274 Sigma-delta converter, 57, 58f Signal analysis, 92 Signal resolution, 56–57, 57f Silver chloride electrodes, 58 Simple filters, 52–54, 52f, 53f, 54f Simple focal seizures, 325 Single-moving dipole model, 342, 343f, 344f Single-photon emission computed tomography (SPECT), 371 Sinusoidal alpha rhythm, 14 SIRPIDs See Stimulus-induced rhythmic, periodic or ictal discharges 6-Hz generalized spike-and-wave discharges (GSW), 108, 112f Sleep active, in newborn, 127, 128f activity of occipital slow transients, 204f, 205 positive occipital sharp transients, 202, 202f, 203f sharp-wave, vertex transients, 195–196, 196–201f, 198, 200, 202 fast activity, 200, 201f, 202 K complexes and vertex transients, 196, 198f spindles, 198, 198f, 199f, 200, 200–201f apnea, diagnosis of, 617–618 continuous slow-wave, in newborns, 138 deprivation of, activation by, 102, 622 EEG during, 196 effects on BAEPs, 460 effects on EEG in juvenile myoclonic epilepsy, 293 vertex sharp-wave transients during, 195–196, 196–201f, 198, 200, 202 vertex transients during, 196, 197f video-EEG monitoring during, 609 # 151788 Cust: LWW Au: Ebersole Pg No 644 Sleep architecture, 101–104, 103–109f in late infancy, 142 in older infants, 131 Sleep-disordered breathing, pediatric, polysomnographic scoring of, 618–619 Sleep disorders, 599–627 ambulatory PSG recording in, 609–610 clinical evaluation of, 623–624, 625f, 626t excessive daytime sleepiness, evaluation of, 624–626, 625f insomnia, evaluation of, 627 laboratory evaluation of, 599–627 See also specific test, e.g., Polysomnography maintenance of wakefulness test, 623–627 multiple sleep latency test in, 620–623, 621t, 621f, 622t parasomnias, evaluation of, 626–627, 626t polysomnography in, technical aspects, 600–610, 601–608f, 609t, 611f, 612t, 613–615f, 618f See also Polysomnography Sleep Disorders Task Force of the American Sleep Disorders Association, 613 Sleep patterns, 227, 241 Sleep scoring, with polysomnography, 611– 612, 611f, 612t Sleep spindles, 10, 103, 131, 165 Sleepiness, daytime, excessive, evaluation of, 624–626, 625f Slow activity evaluating amount and duration of, 153 monorhythmic, 187–188, 188f, 189f, 190f paroxysmal, 188, 191–192, 191f, 192f, 196f Slow alpha variant pattern, 142 Slow spike-and-wave discharge pattern, 322, 322f Slow-wave activity, 241–243 Slow-wave sleep, in sleep architecture, 103–104, 107f Small sharp spikes, 109, 165 Somatosensory alpha rhythm See Mu rhythm Somatosensory evoked potentials (SEPs) abnormalities, 476–480, 477–482f in adrenoleukodystrophy, 484 amplifier setting for, 474 in amyotrophic lateral sclerosis, 483 anatomy, 470–471, 471t, 489–490, 490t K DESIGN SERVICES OF anesthetic considerations, 494–495, 494t, 495–496f inhalational agents, 494 intravenous agents, 494 neuromuscular junction blocking agents, 494–495 change, mechanisms of, 495–498, 497–501f acute trauma, 495–496 ischemia and anoxia/blood pressure, 495 technical issues, 496–498 temperature, 496 in Charcot-Marie-Tooth disease, 484 clinical applications, 500 clinical correlations, 483–484 in Friedreich ataxia, 483 interpretation, 474–476, 475f, 476t Krabbe disease, 484 maturational issues of, 481 median nerve, 473f, 475f, 477f, 480, 481 dorsal column pathway, 483, 489, 501 short-latency cortical potentials and, 470 metachromatic leukodystrophy, 484 methodology, 472t, 473f, 474t, 490–494, 490f, 491–493t, 492f recording techniques, 472–474, 491–494 stimulating techniques, 471–472, 490–491 pediatric considerations, 480–483 Pelizaeus-Merzbacher disease, 484 physiology, 489–490, 490t as predictors of outcome in coma, 483 recording montage for, 493, 493t parameters for, 493–494 stimulation for eliciting, 471 of peripheral nerves by, 480 warning criteria, 498–500 waveform generators, 470–471, 471t Sound intensity methods, for BAEPs, 461 Source analysis, EEG, 249 SOZ See Seizure-onset zone (SOZ) Spasm(s) with focal features, 310 infantile, video-EEG monitoring in, 227 645 Index Spatial sampling, coregistering EEG data with, 347, 349–350, 349f, 350f, 351f Spatiotemporal multiple dipole model, 342–343, 345f, 346 Spectral edge frequency (SEF), 566 Sphenoidal electrodes, 80, 328f Spherical head models, 349 Spielmeyer-Vogt disease, 274–275 Spike-and-slow-waves, generalized atypical, 321 Spike and wave discharges (SWDs), 10 Spike sources, for EEG voltage topography, 339, 340, 363 Spikelets, Spikes in basal temporal cortex, 363 intracranial interictal, role of, 376 in SETs, 165 sharp waves and, 316, 316f in older infant and child, 186–187 -sorting algorithms, -wave discharges, triphasic waves vs., 222 Spinal cord function, intraoperative monitoring of MEP monitoring in, 505, 505t SEP monitoring in, 489 Spinal surgery, with instrumentation, 538, 538t Spinal waveforms, 444 Spindle coma, 198 frequency pattern, 225–226, 226f Spindle-like fast rhythms See Delta brushes, in neonatal EEG interpretation Spindles, sleep, 198, 198f, 199f, 200, 200–201f Spontaneous arousal, 195 Spontaneous modulation, 14 Stage sleep (N1 sleep), in sleep architecture, 102, 104f Stage sleep (N2 sleep), in sleep architecture, 103, 105f, 106f Stage sleep (N3 sleep), in sleep architecture, 103–104, 107f Stage W (wakefulness), in sleep architecture, 102, 103f Status epilepticus, continuous EEG in, 575–578 Stereo-electro-encephalography (SEEG), 395 in extratemporal lobe epilepsy, indications for central cortex seizures, 411–412, 412f frontal lobe seizures, 409, 410–411, 410f insular lobe seizures, 413, 414f, 415 posterior quadrant seizures, 412–413, 413f guided radiofrequency thermocoagulation, 435–436, 436f in lesional and nonlesional focal epilepsies, indications for, 415 in temporal lobe epilepsy, indications for bilateral independent temporal lobe seizures, 408, 408f pseudo-temporal seizures, 409, 410f temporal plus epilepsy, 408–409, 409f unilateral mesial temporal lobe seizures, 407 Stereo-encephalography See Intracerebral depth electrodes encephalography Stereotactic radiofrequency thermocoagulation (RFTC), 435–436, 436f Stimulated electromyography, 534–535 Stimulation, procedure of, 434, 435 Stimulus(i), acoustic, for BAEPs See Acoustic stimulation, for BAEPs Stimulus-induced rhythmic, periodic or ictal discharges, 216, 217f, 561 Stimulus polarity, for BAEPs, 461 Stopband, 53 Stray capacitance, 66 Stray inductances, 66 Stroke, role of EEG in, 254–255 Subacute necrotizing encephalomyelopathy See Leigh syndrome Subacute sclerosing panencephalitis (SSPE), 220, 250–251 Subarachnoid hemorrhage, 239t, 254, 563 Subclinical rhythmic electrographic discharge in adults (SREDA), pattern in EEG, 111–112, 115f Subcortical waveforms, 444 Subdermal electrodes, 535, 535f Subdural electrode corticography See Intracranial EEG Subdural electrodes characteristics of, 369, 370f clinical indications of, in EEG recording, 373 # 151788 Cust: LWW Au: Ebersole Pg No 645 vs depth electrodes, 369 in intracranial EEG, 367–389, 370–372f, 375–380f, 382–388f risks and complications of placement, 371–373 Subdural hematoma, 372 focal encephalopathies in, 239t, 251 PLEDS in, 251 Subdural strips electrodes, 60 Successive-approximation converter, 57, 58f Sucking artifact, in infant, 142 Sulfite oxidase deficiency, 263–264 “Supernormal” EEG, for age, 152f, 153 Superposition principle, 52, 342 Surface electrodes, 504, 534–535, 535f Surface ground electrode, 472 Surface-positive sharp transients, 202 Surround inhibition, epileptiform activity, cellular basis of, 19, 20f, 21f SWDs See Spike and wave discharges (SWDs) Sylvian fissure, 340 Symmetry, in neonatal EEG interpretation, 208, 215f, 562f Symptomatic generalized epilepsies atonic and akinetic seizures, 334, 335f atypical absence seizures, 334 clonic seizures, 334 symptomatic generalized tonic-clonic seizures, 334 tonic-clonic seizures, 334 tonic seizures, 334 Synaptic activity, as source of extracellular current flow, 79, 79f Synaptic currents, Synchrony, 165 of cortical activity, 33–34, 35f interhemispheric, in neonatal EEG interpretation, 129, 130f, 131 T Tay-Sachs disease, 268 TBI See Traumatic brain injury (TBI) TCAs, effects on EEG activity See Tricyclic antidepressants (TCAs), effects on EEG activity K Temperature effects on BAEPs, 516, 517f effects on MEP, 507 effects on nerve conduction and SEP, 496 Temporal intermittent rhythmic delta activity (TIRDA), 242, 244f in focal interictal epileptiform discharges, 319–320, 319f Temporal lobe complex focal seizures, 326–328, 327–329f seizures, 353 sources, dipole source modeling of, 353, 355–358f spikes, 349 Temporal lobe epilepsy (TLE), 368, 377 familial lateral, 286 familial mesial, 286–287 focal onset in, 381 ictal EEG changes in, 326 indications for SEEG in, 407–415, 409f, 411–413f Temporal plus epilepsy, 408–409 TES See Transcranial electrical stimulation (TES) Thalamic connections, neocortical anatomy and, 9–11 Thalamic hemorrhage/stroke, focal encephalopathies in, 239t, 254 Thalamocortical circuit, 10 Therapeutic hypothermia (TH), 582 Thermistor(s), for airflow monitoring in polysomnography, 604–605 Thermocouple(s), for airflow monitoring in polysomnography, 604–605 Theta activity frontal, 155–156, 156f, 157f frontocentral, 155–156, 156f, 157f midline central, 156–157 Theta frequency(ies), 97, 98f Third rhythm, 94 3D CT/MRI co-registration technique, 371 3-Hz spike-and-wave discharges, 320–321, 320f Threshold intensity, 472 Time constant, 51 Time discretization, 55–56, 55–56f Time domain analysis, 563, 565 Time-frequency analysis, 566 DESIGN SERVICES OF 646 Index Time-varying circuits, 51–52, 51f TIRDA See Temporal intermittent rhythmic delta activity (TIRDA) TLE See Temporal lobe epilepsy (TLE) Tonic seizures, 334 Total conductance, Total throughput, for digitizer, 57 Toxic encephalopathies, 238 Trace alternant pattern, 135, 137f Trace deflection, 40 Trace discontinu (discontinuous tracing) EEG pattern, 135, 136f Transcranial electrical stimulation (TES), 502 Transfer function, Transient evoked otoacoustic emissions, 470 Transient ischemic attacks (TIAs), focal encephalopathies in, 239t, 251 Transmembrane current, Trauma acute, 495–496, 507 brachial plexus, 539 head See Head trauma nerve, 521 Traumatic brain injury (TBI), 226, 580 Tricyclic antidepressants (TCAs), effects on EEG activity, 622 Triphasic waves, 222–224 in hepatic encephalopathy, 223f spike-wave discharges vs., 222 Tumor(s) brain, 245–247 epileptiform abnormalities in, 243–244 infratentorial, 247, 249 large hemispheric, 247 cerebellopontine angle, BAEPs in, 469 in median and tibial SEP, 483 of optic nerve, VEPs in, 458 Two-point moving average, 62 Type I glutaric acidemia, 270 Tyrosinemia type III, 271 U UIEA See Utah Intracortical Electrode Array (UIEA) Unilateral mesial temporal lobe seizures, 407 Unilateral P100 waveform latency, 453 Unpaired montages, 86 Unverricht-Lundborg progressive familial myoclonic epilepsy See Baltic myoclonus epilepsy Urea cycle disorders, 265 Utah Intracortical Electrode Array (UIEA), 60–61, 61f V VA See Visual analysis (VA), of pediatric EEG VARETA technique, 358 Vascular diseases, BAEPs in, 469 Vasospasm, 214, 515 Ventilatory efforts, 604 monitoring of, 606 VEPs See Visual evoked potentials (VEPs) Vertebrobasilar ischemia, 252–253, 255f Vertebrobasilar stroke, focal encephalopathies in, 239t, 252–253 # 151788 Cust: LWW Au: Ebersole Pg No 646 Vertex transients K complexes and, 196 sharp-wave, 195–196, 196–201f, 198, 200, 202 Vertex waves (V-waves), 131, 165 in sleep architecture, 102, 104f Video-EEG monitoring absence seizures with JME, 333 for recording seizures, 609 role of, 177 Viral encephalitis, in EEG abnormalities, 251 Visual analysis (VA), of pediatric EEG abnormalities in, 131, 208–209 continuity, 126–127, 128f, 207–208 gradient and principal components, 208 interhemispheric symmetry, 129, 129f, 130f, 131, 208 interhemispheric synchrony, 129, 131, 132f, 133f, 208 organization and principal components, 128 organized approach to, 207 special features in, 131, 208 state, 126–127, 128f, 207–208 Visual cortex, primary, 447 Visual evoked potentials (VEPs) anatomy and waveform generators, 447–448 clinical correlations, 458–459, 459f flash, 456–457, 457f luminance and, 448 pattern reversal, 448–456, 449–456f, 451–453t pediatric considerations, 457–458 K DESIGN SERVICES OF Visual sleep scoring, 610 Visual system, 443 Vitamin metabolism, disorders of, 269 Voltage See also Cortical generators and EEG voltage fields discretization (signal resolution), 56–57, 57f of posterior dominant rhythm, 151 sources, in electrical circuit theory, 48 Voltage-dependent Ca2+ channels, W Wakefulness test, maintenance of See Maintenance of wakefulness test (MWT) Waking EEG, in newborns, 138 WAR pattern, 523, 524f Waveform composition symmetry, 129 Waveforms, definition of, 443–444 West syndrome, 259 in epileptic encephalopathies, 304–306, 305f metabolic disorders of early infancy, 267–268 Wicket spike (wickets) waveforms, 110, 111f, 114f X X-linked adrenoleukodystrophy, 264 Z Zellweger syndrome, 264 ... epilepsy: a video-polysomnographic and genetic appraisal of 40 patients and delineation of the epileptic syndrome Brain 1998; 121 (Pt 2) :20 5 22 3 22 Raju GP, Sarco DP, Poduri A, et al Oxcarbazepine in... Neurology 20 00;54 :21 73 21 76 26 Bisulli F, Tinuper P, Avoni P, et al Idiopathic partial epilepsy with auditory features (IPEAF): a clinical and genetic study of 53 sporadic cases Brain 20 04; 127 :1343–13 52. .. Clin 19 82; 12( 1) :21 25 72 Scheffer IE Does genotype determine phenotype? Sodium channel mutations in Dravet syndrome and GEFS+ Neurology 20 11;76(7):588–589 doi:10. 121 2/ WNL.0b013e31 820 d8b51 Epub