Ebook Practical guide for clinical neurophysiologic testing EEG (2/E): Part 1

PracticalGuideforClinical
NeurophysiologicTesting•EEG
SECONDEDITION

ThoruYamada,MD
ProfessorEmeritus,DepartmentofNeurology
CarverCollegeofMedicine
UniversityofIowa
IowaCity,Iowa

ElizabethMeng,BA,R.EEG/EPT.
EEGTechnologist-DepartmentofNeurology
AbrazoMaryvaleCampus
Phoenix,Arizona


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Names:Yamada,Thoru,1940-author.|Meng,Elizabeth,author.
Title:Practicalguideforclinicalneurophysiologictesting.EEG/ThoruYamada,ElizabethMeng.
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Description:Secondedition.|Philadelphia:WoltersKluwerHealth,[2017]|Includesbibliographical
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To electroneurodiagnostic technologists/students, neurology residents, and
clinicalneurophysiologyfellows,andthepatientswhomtheyserve


ContributingAuthors
MICHAELCILBRERTO
AssistantClinicalProfessor,DepartmentofPediatrics-Neurology
CarversCollegeofMedicine
UniversityofIowa
IowaCity,Iowa
ELIZABETHMENG,BA,R.EEG/EPT.
EEGTechnologist-DepartmentofNeurology
AbrazoMaryvaleCampus
Phoenix,Arizona
PETERSEABA,MS
SeniorEngineer,DivisionofClinicalElectrophysiology
DepartmentofNeurology
UniversityofIowaHospitalandClinics
IowaCity,Iowa
THORUYAMADA,MD
ProfessorEmeritus,DepartmentofNeurology

CarverCollegeofMedicine
UniversityofIowa
IowaCity,Iowa
MALCOLMYEH,MD
AssociateClinicalProfessor,DepartmentofNeurology
CarverCollegeofMedicine
UniversityofIowa
IowaCity,Iowa


Foreword
It is with pleasure that I prepare this foreword to a work by a couple of my
friendsinIowa,whoseprofessionalaccomplishmentsIhavewitnessedfirsthand
forthepast40years.Dr.Yamada,asDirectoroftheEEGLaboratory,hasproven
hisproficiencyinclinicalneurophysiologywithhisinsatiabledesiretolearnand
toteach.ElizabethMengexcelledasthechiefEEGtechnologistandaprincipal
instructorforourEEGtechnologycoursecosponsoredbytheUniversityofIowa
and Kirkwood Community College. Their joint collaboration early on
culminatedinthepublicationofthebookentitled“PracticalGuideforClinical
NeurophysiologicTesting”whichwasreceivedwellbytheEEGcommunity.The
firstedition,thoughoriginallyintendedforusebyEEGtechnologists,enjoyeda
veryfavorablereceptionfromneurologyresidentsandclinicalneurophysiology
fellows, who prepare for the qualification examination by American Board of
ClinicalNeurophysiology(ABCN).
Iwelcomethetimelypublicationofthesecondeditionwiththeadditionofa
newchapter,ContinuousEEGMonitoringforCriticallyIllPatients,tomeetthe
currenttrendsandincreasingdemandstouseEEGinthisdevelopingfield.The
booknowincludesvideo-EEGrecordings,whichshowvarioustypesofseizures
and artifacts as well as changing EEG patterns in real time sequence. The
readers,regardlessofthepriorexperience,willenjoythevisuallyalluringEEG

recordingandthecorrespondingpatient’sbehaviorthatserveasasimpleguide
to correlate clinical and neurophysiological abnormalities. Both novice and
expert will benefit from the numerous aids to the examination of waveform
abnormalities.TheneweditionalsoincorporatesthecurrentEEGterminologies
recently proposed by American Clinical Neurophysiology Society (ACNS),
whichshouldprovehandyforthoseneedingaquickaccesstoproperdescription
informulatinganEEGreport.
ThisbookmeetsthepracticalneedsofphysicianswhoperformEEG,evoked
potentials, and bedside monitoring, providing a commonsense approach to
problemsolvingforfrequentlyencounteredcorticallesions.Thoughtful,expert
commentspertinenttoEEGpatternswillhelpeasethebeginner’sanxietyabout
performing EEG monitoring. The more experienced electroencephalographer
will appreciate the well-organized, practical outlines of clinical conditions and


electrodiagnosticfeatures.Ihavenodoubtthatthesecondeditionwillreceiveas
favorable reception as the first by technologists and practitioners alike. I
anticipatethatthebookwillgainanexcellentreputationasastandardguidein
electrodiagnosticmedicine.Itakegreatprideinknowingthatthevolumeisthe
productofmycolleaguesinIowaandhopethatitsusewillnotonlyenhancethe
electrodiagnosticevaluationbutalsoencourageresearchandteachinginthefield
ofclinicalneurophysiology.
JunKimura,MD
ProfessorEmeritus
KyotoUniversity,Kyoto
ProfessorEmeritus
DepartmentofNeurology
UniversityofIowaHospitalsandClinics
IowaCity,Iowa

Preface
OurinvolvementinteachingbothNDT(electroneurodiagnostictechnology)and
Neurologyresidencyprogramssincethe1970shasenabledustoexperiencethe
evolutionandprogressionofelectroencephalography(EEG)andrelatedfields.It
istothatendthatwehaveseentheneedforasecondeditionofPracticalGuide
toClinicalNeurophysiologicTesting–EEG.Inrecentyears,anewsubspecialty
hasevolvedinNeurodiagnosticscalledContinuousCriticalCareEEG(CCEEG)
monitoring. There has been a tremendous call for this long-term recording
especiallysincetheadventofdigitalEEGequipment.Inthissecondedition,we
includedmanyvideo-EEGrecordingssinceEEGofanytypeisaverydynamic
science,therefore,toviewitasa“movingpicture”ratherthanasatimelimited,
staticpresentationisimportant.Studieshavedocumentedthatmanypatientsin
theICU,bothcomatoseandawake,haveintermittentneurologiceventsthatcan
be captured with this new technology, thus improving patient outcomes. We
hopethisnewchapterwillbeusefulasyoubegintodelveintoCCEEG.
Thesecondeditionofthetextbookalsogaveusanopportunitytoaddnew
nomenclature and new standards recommended by The American Clinical
NeurophysiologySociety(ACNS).Youwillbeabletoaccessabout60videoson
topicsfromartifactstoseizures.Thevideosareonline,andyouhavetheaccess
codeunderthescratchofftaginsidethefrontcover.
Initially,thefirsteditionofthisbookwasintendedprimarilyforeducationof
EEG/NDT technologists, but we realized that the book was also useful for
neurology residents, clinical neurophysiology fellows, and also general
neurologistsbecauseanyphysicianswhointerpretsEEGsshouldalsoknowthe
technical aspects of the recording in order to provide accurate and appropriate
interpretationandtoavoidmisinterpretationofEEGdata.
We would like to thank Malcom Yeh, MD, the late Peter Seaba, MS, and
Michael Ciliberto, MD, who provided their expertise and experience in
particularchapters.Additionally,thebookwouldbenothingifnotfortheEEG

samples recorded by the very talented University of Iowa neurodiagnostic
technologists:MarjorieTucker,CNIM/CLTM/R.EEGT./EPT.,DeanneTadlock,
R.EEG T./CLTM, Jada Frank, R.EEG T./CNIM, Prairie Seivert, R.EEG T.,
CNIM,TomWiersema,R.EEGT./CNIM,KassyJacobs,R.EEGT./CNIM,Sara


Davis,R.EEGT.,HollyHeiden,R.EEGT.,LoriGrant,R.EEGT.
Wearealsoindebtedtoourpatientswhoprovidedimportantandusefuldata
which we use for teaching and the advancement of clinical neurophysiological
science.
Lastly, we would like to acknowledge our spouses, Patti and John, whose
loveandsupportallowedusthetimeweneededtoworkonthisproject.
ThoruYamada,MD
ElizabethMeng,BA,R.EEG/EPT.


Contents
ContributingAuthors
Foreword
Preface
OnlineVideos
1 Introduction: History and
NeurophysiologicDiagnosticTests

Perspective

of

THORUYAMADAandELIZABETHMENG

2BasicEEGTechnology
THORUYAMADAandELIZABETHMENG

3BasicElectronicsandElectricalSafety
PETERSEABAandTHORUYAMADA

4DigitalEEG
MALCOLMYEH

5NeuroanatomicalandNeurophysiologicBasisofEEG
THORUYAMADAandELIZABETHMENG

6PrinciplesofVisualAnalysisofEEG
THORUYAMADAandELIZABETHMENG

7CharacteristicsofNormalEEG
THORUYAMADAandELIZABETHMENG

8TheAssessmentofAbnormalEEG
THORUYAMADAandELIZABETHMENG

Clinical


9ActivationProcedures
THORUYAMADAandELIZABETHMENG

10EEGandEpilepsy
THORUYAMADAandELIZABETHMENG

11DiffuseEEGAbnormalities
THORUYAMADAandELIZABETHMENG

12FocalEEGAbnormalities
THORUYAMADAandELIZABETHMENG

13ContinuousEEGMonitoringforCriticallyIllPatients(CCEEG)
THORUYAMADAandELIZABETHMENG

14BenignEEGPatterns
THORUYAMADAandELIZABETHMENG

15ArtifactRecognitionandTechnicalPitfalls
THORUYAMADAandELIZABETHMENG

16EEGofPrematureandFull-TermInfants
THORUYAMADA,ELIZABETHMENG,andMICHAELCILIBERTO

Index


OnlineVideos:PracticalGuidefor
ClinicalNeurophysiologicTesting
•EEG


Chapter4
Video 4-1 For a more dynamic view of alias signals, view the video that
demonstrates how analogue signals are recorded and represented in digitized
form.

Chapter7
Video7-1AAnexampleofunusuallyprominentandfrequentLambdawavesin
30-year-old woman when she was reading a brochure. Note repetitive sharply
contouredpositivedischargesatO1andO2electrodes(channelsshownwithred
tracings)
Video7-1BThisisthesamepatientasinVideo7-1A,showingfrequentPOST
in stage 2 (N2*) sleep. Note the similarity of Lambda in awake and POST in
sleep.
Video 7-2 An example of K-complex triggered by click noise during stage
2(N2*)sleep.


Chapter9
Video 9-1 Subject is a normal 25 year old woman. Hyperventilation produced
prominent delta build-up, which is a normal finding, although the degree of
build-upwasmoreprominentthanusuallyseenforthisagesubject.
Video 9-2 An 8-year-old otherwise healthy girl presenting with staring spell
noted by teacher and parents. Technologist asked her to hyperventilate. She
started to hyperventilate (frame 12:42:55). Within 20 seconds of the start of
hyperventilation, EEG started to show 3 Hz, generalized rhythmic spike-wave
bursts (frame 12:42:12). This is typical EEG feature for absence seizure. She
then stopped hyperventilation and her eyes were open with a staring gaze.
Technologist asked the patient to remember the word “butterfly” during the
episode. The spike-wave burst lasted about 20 seconds and the patient quickly
returned to a normal state but she was unable to recall the correct word
(butterfly)givenduringtheepisode.Video9-3Patientwasa12-year-oldfemale
withahistoryofgeneralizedshakingsincetheageof15months.Heroldersister
wasdiagnosedwithabsenceseizures.EEGshowedphotoparoxysmaldischarges

with generalized spike-wave burst at 9 Hz photic stimulation. The photic
stimulationwasquicklystoppedafterthedischarges.Noteslow-wavedischarges
continued after the cessation of photic stimulation. The photoparoxysmal
dischargeswererepeatedlyproducedby9Hzphoticstimulation.NootherEEG
abnormalitywasfound.


Chapter10
Video 10-1 Patient was a 30-year-man with a diagnosis of complex partial
epilepsy (focal seizure with impaired awareness) since age 14. MRI showed
right hippocampal sclerosis. The ictal discharges started with rhythmic sharply
contoureddeltaofabout3Hzarisingfromrighttemporalregion.Withinafew
seconds,thepatientwasawareofimpendingseizure(aura)andpushedtheevent
button. By then the rhythmic delta activity was more widely spread, yet still
right>left.TheEEGtechnologistcameinandaskedseveralquestionstowhich
thepatientseeminglyrespondedcorrectlybuthisbehaviorwasnotquitenormal.
Video 10-2 Patient was a 62-year-old woman presenting with episodes of
confusionwhichstartedabout3yearsago.Shewasamnesticfortheseepisodes.
MRI was unremarkable. Interictal discharges consisted of well-defined spike
discharges from right temporal region, maximum at the anterior temporal
electrode (see Fig. 10-9). Seizure started while she was talking on the phone.
The ictal discharges started with rhythmic,sharplycontouredthetaburstsfrom
righthemisphere(frame16:55:24).Thethetaburstsprogressivelybecamelarger
toward the end of seizure. The seizure ended at frame 18:55:50. During the
event, she continued to talk on the phone carrying on a seemingly normal
conversation.
Video10-3A&BPatientwas35-year-oldwomanwithalonghistoryofcomplex
partial seizure. MRI showed left hippocampal atrophy (shown by circles;
compare left and right), consistent with mesial sclerosis (Video 13A). EEG
showed ictal discharges started with beta activity, maximum at left posterior

temporalregion(firstframe)withsubsequentspreadalongwithbilateraldiffuse
rhythmic sharp discharges from parasagittal region (2nd frame). This was
followed by left>right rhythmic sharply contoured delta activity (middle of 3rd
frame to 5th frame). The ictal event stopped at 6th frame (Video110-3A). The
samepatienthadanotherseizurewhileinsleep(Video110-3B).Theictalevent
startedshortlyaftertheinterictalspikefromlefttemporalregion(middleof2nd
frame)withbetaactivityfromrighthemisphere.Thiswasfollowedbyrhythmic
spikes involving mainly right hemisphere (3rd frame) when the patient raised
right arm with repetitive hand motion (automatism). Subsequently the ictal
discharges evolved to right>left rhythmic delta/theta pattern. The ictal event
stoppedat7thframe.


Video 10-4 Patient was a 16 year old boy presenting with episodes of body
stiffening,staringandlipsmackingwhichstartedabout2yearsago.Thespells
usually occurred during sleep. The seizure captured during this EEG started
shortly after arousal from N3 sleep. The ictal discharges started with 2.5 Hz
rhythmicdeltaoffrontaldominance,alongwithincreasedtonicmuscleartifact
(the patient was not moving during the onset of ictal delta activity). Then the
patient showed rhythmic axial body shaking. Although EEG was partly
contaminatedbymovementandmuscleartifacts,therhythmicdeltaactivitywas
notartifactsbecausethedeltafrequencywasnotsynchronouswithmovements.
The delta discharges became progressively slower toward the end of seizure t
artifacts.Theseizurelastedabout30secondsandpostictalEEGshoweddiffuse
slow delta (~1Hz) which was slower than expected for N3 sleep. About ~1
minute after the seizure, the EEG seemed to return to N3 sleep. This type of
seizurecannotbedifferentiatedfromatypeofparasomniasuchasbodyrocking
withoutcapturingthespellbyvideoEEGrecording.
Video10-5A Patient was a 53-year-old man with a history of traumatic brain
injuryinchildhood.Thefirstseizurewas7yearsagowithapparenttonic–clonic

convulsion. Most of his seizures were preceded by visual hallucination. MRI
was unremarkable. EEG showed mild delta slowing at the occipital region,
left>right.WhenEEGstartedtoshowsmallspikesfromleftoccipitalregion,he
feltthesensationofseizureandpushedtheeventmarker(frame17:00:55)and
he prepared himself by lowering the head of bed for impending seizure.
Recurrentspikedischargesfromleftoccipitalregionbecameclearwhenmuscle
artifacts decreased (frame 17:01:29). The nurse’s appropriate questions and
interactionwiththepatienthelpedtorecognizehisseizuresemiology.Hestated
to the nurse “Light show is going” pointing the right lower visual field (frame
17:01:38).Hewasabletodescribeclearlywhathewasseeing.Also,hewasable
tofollowthenurse’scommandswhilerepetitiverecurringspikescontinued.Up
to this point, the seizure can be classified as simple partial seizure or focal
seizurewithawareness*.
Video10-5BThisiscontinuationofthesameseizureofVideo10-5A(3minutes
and 16 seconds after the last frame). EEG now changed to slower and larger
spike-waveburstsassociatedwiththemoregeneralizedtheta/deltaslowwaves.
Thepatientthenbecameconfusedanddidnotrespondtothenurse’squestions.
Along with increased generalized rhythmic spike-wave bursts, his face started
twitching (not seen) (frame 17:07:56). This case shows an example of simple
partial seizure (focal seizure with awareness**) changing to complex partial


seizure(focalseizurewithimpairedawareness**).
Video 10-6 Patient was an 11-year-old boy with initial presentation of tonic–
clonic convulsion at school. His mother also noted occasional spells of staring
whichstartedabout6monthsago.Shestatedthathecouldspeakthroughthese
spells and continues his activities with eyelid fluttering. Shortly after
hyperventilation, EEG started to show generalized rhythmic polyspike-wave
burstswithinitialfrequencyof4to5Hz,whichprogressivelysloweddownto2
to3Hzspike-wavebursts.Thispatternischaracteristicforjuvenileabsenceand

different from classical absence seizures (compare with Video 9-2). Also, the
patientwasnottotallyoutofcontactduringthisepisode.Notealso,occipitally
predominantRDA*orOIRDjustbefore(frame09:08:34)andrightafter(frame
09:08:51)thespike-wavebursts.
Video10-7Patientwasa7-year-oldboywithspellsofunresponsivenesswhich
can be self-induced by looking at flashing light or interrupting bright light by
shakinghandwithspreadfingersinfrontofhim.Theparentsalsonoticedeyelid
fluttering, especially with eye closing. EEG showed episodes of bifrontally
dominantpolyspike-wavebursts,whichwereconsistentlyexacerbatedbyphotic
stimulation. Immediately after the 5 Hz photic stimulation, there was a brief
generalized polyspike-wave burst, which was followed by slight arm jerking.
With continued photic stimulation, generalized 2.5 Hz spike-wave burst
appeared, which was associated with eyelid twitching (not shown). These
featureswerecharacteristicforJeavonssyndrome.
Video 10-8 Patient is a 47-year-old man with a long history of tonic–clonic
convulsions since the age of 14. MRI was normal. EEG for seizure onset was
totallyobscuredbytonicmuscleartifacts.Thepatientvocalizedwithtoniclimb
posturing, which was followed by clonic movement. In-between the muscle
artifacts, EEG appeared to show diffuse slowing. Postictally, the patient was
unresponsivewithsomebackgroundslowing.
Video10-9 Patient was a 10-month-old baby girl presenting with episodes of
“tensesupherwholebody”notedbyherparents.MRIshoweddiffusecortical
atrophyanddelayedmyelination.Priortoseizure,EEGshowedhighamplitude
anddiffuseirregulardeltaslowwaves(frame13:35:59).Therewerelargedelta
slow waves followed by sudden flattening EEG pattern (electrodecremental
seizure)whenbabyshowedsuddenforwardmotionwitharmbendingposturing
(Salaamspasms)atframe13:36:07.


Video 10-10 Patient was a 44-year-old woman presenting with a history of

generalized tonic–clonic convulsions which started at the age of 22. Patient
deniesanywarningsign(aura)beforeseizure.MRIwasunremarkable.Priorto
seizure,EEGshowedbilaterallydiffuse,frontaldominantpolyspikeswhichare
slightlyright>left(note phase reversalatFP2 inframe09:57:26).Withseizure
onset, the patient vocalized with head turning to right and right arm jerking
(frame09:57:37).EEGwasthenobscuredbyclonicthentonicmuscleartifacts.
During clonic phase (frame 09:58:34), diffuse delta/theta slowing was evident,
seen during artifact free moments. Postictally, EEG showed marked flattening.
Thisislikelyfocalonsetsecondarygeneralizedtonic–clonicconvulsion.
Video10-11 Patient was a 20-year-old man who had first seizure 2 years ago,
presenting with initial dizziness followed by loss of consciousness and
generalizedtonic–clonicconvulsion.MRIwasunremarkable.Theseizurestarted
when the technologist was present. Just prior to the onset of seizure, EEG
showed right>left frontal dominant generalized spikes (frame 08:58:28). The
ictalonsetwassuddengeneralizedflatting,whichwasfollowedbygeneralized
spike-wavebursts(right>left)andsomewhatirregulardiffusedeltaslowwaves
(frame 08:58:33). This was followed by rhythmic right>left sharp delta bursts.
At this moment, the astute technologist noticed that the patient started having
seizureandaskedquestions(frame08:58:39).Thepatientwasunresponsive,and
EEG was showing generalized rhythmic spike-wave bursts (frame 08:58:56),
which became progressively more prominent subsequently, changing to
polyspike-wave bursts (08:59:02). His head started turning to right (frame
08:59:07), which was followed by generalized clonic convulsion (frame
08:59:13) and then tonic posturing (frame 08:59:30). EEG was then totally
obscured by muscle artifacts. Postictally, EEG changed to burst suppression
pattern with bursts consisting of generalized irregular polyspike waves. This
case is an example of partial complex seizure (focal seizure with impaired
awareness**)withsecondarygeneralizedtonic–clonicconvulsion.
Video 10-12 Patient was a 22-year-old woman with a long history of seizure
since the age of 2 when she had an intraparenchymal hemorrhage. CT scan

showedscatteredareasofincreasedattenuationconsistentwitholdcalcifications
likelyfromherintraparenchymalhemorrhageatage2.IctalEEGcapturedwhile
the patient was sleeping showed the onset of ictal event started with gamma
range fast activity initially arising from left frontotemporal region (frame
13:18:21).Thiswasfollowedbybetaactivitythenevolvingtorepetitivespikes
with wider spread. The ictal discharges quickly generalized but maintained


left>right prominence. Toward the end of seizure, the ictal pattern changed to
repetitive spike-wave bursts, left>right, which progressively slowed down
(frame 13:18:38). The ictal event lasted less than 30 seconds. Despite ictal
discharges becoming generalized, the patient showed no observable clinical
change.Thepatientmovedslightlyaftertheseizureended(frame13:18:46).
Video 10-13 Patient was a 22-year-old male with history of focal onset
secondarygeneralizedtonic-clonicconvulsions.Inaddition,thepatienthasbrief
but frequent partial seizures consisting of giggling and laughing with some
confusion or unresponsiveness. These spells occur either in sleep or in awake
state. Neurological examination and Brain MRI were normal. The ictal event
captured in awake state showed the onset of bi-frontal dormant beta with
progressiveslowinginfrequency.Theseizurelastedonlyabout10seconds.The
patientshowedsmilingwithgigglingsound.
Video10-14 Patient was a 52-year-old man with a long history of intractable
epilepsy, with mostly generalized tonic–clonic convulsions. MRI was
unremarkable except for mild cortical atrophy. EEG showed intermittent brief
episodes of sudden onset of generalized beta activity followed by rhythmic,
sharply contoured theta discharges changing to rhythmic sharp-wave bursts
(frame01:29:35)beforeendingtheictaldischarges(frame01:29:44).EKGrate
was60/minute(1/1second)beforetheictaleventwhichprogressivelyslowedto
20/minute (1/3 seconds). The ictal event lasted about 10 seconds, and EEG
quicklynormalizedwithrecoveryofEKGrate(frame01:29:44).

Video 10-15 Patient was an 18-year-old female presenting with syncopal
episodes often preceded by dizziness. These episodes tended to occur while
standingup.About1½minutesaftertiltingtableraisedup,EKGratestartedto
drop from approximately 100 beats/minute to 30 beats/minute (with 2 seconds
asystole) when her head dropped (frame 11:11:15). EEG then started to show
diffuse, bifrontal dominant delta. The prominent delta activity continued for
about 25 seconds, and then EEG activity started to recover, though EKG rate
remained bradycardia (~60/second) for a while as compared to the rate before
syncope.


Chapter11
Video 11-1A An example of EEG changes due to cerebral ischemia shown by
ligation of internal carotid artery during endarterectomy surgery. The right
internalcarotidwasclampedatthemark“Clampon”inthefirstframe10:46:28.
Within 20 seconds after the clamp, EEG started to be depressed on the right
hemisphere(frame10:46:48).
Video 11-1B The surgeon placed ashunt in at frame 10:50:28 to restore the
carotid circulation. EEG then gradually recovered and returned nearly to
baselineatframe10:52:05.
Video11-2AnexampleofEEGchangesafterPropofolinjectionforinductionof
anesthesia. EEG started with waking record. In the middle of first frame
(09:47:13), anesthesia staff started IV injection of Propofol. Within a few
seconds of the injection, EEG started to show slowing and prominent diffuse
deltaslowwaves(middleofframe09:47:21).Deltawavesbecameprogressively
slower(from3to0.5Hz)(frame09:47:21to09:47:47),andthenEEGchanged
toburstsuppressionpattern(frame09:47:55).Ittookonlyabout40secondsafter
theinjectiontoachieveburstsuppression.

Chapter13
Video13-1Patientwasa69-year-oldfemalepresentingwithshortnessofbreath
andmentalstatuschanges.CTscanshowedmultiplescatteredinfarctionsinthe
posterior fossa as well as left and right middle cerebral and anterior cerebral
arteryterritories,consistentwithembolicinfarcts.EEGstartedonthesameday
of admission. While the patient remained in coma, EEG showed continuous,
generalizedsharpdischargeswithoutevolutionorsignificantincidences(GPD*).
Video 13-2A Patient was a 78-year-old male with a history of left middle
cerebral artery aneurysm clipping 20 years ago with subsequent right
hemiparesis,expressiveaphasia,andseizuredisorder.Priortothisadmission,he
was found to be confused and had generalized tonic–clonic convulsion. EEG
recording started on the day of admission. EEG showed periodically recurring
burstsofirregularpolyspike-wavesfromlefthemisphere(PLEDs/LPD+F*)with
greaterprominenceinthetemporalregion.Occasionally,theburstshadalonger
duration, becoming close to a BIRD pattern (frame 03:31:21). The ictal events
started with continuously recurring polyspike-wave bursts from left temporal
region (03:31:38). This evolved to a greater degree of polyspike-waves,
involving also the parietal region (frame 03:31:55). Subsequently, the ictal
dischargesfaded,firstattheparietaldischarges(frame03:32:29)andthenatthe
temporalregion(frame03:32:37).Therewasnoobservableclinicalchange,and
therefore,thiswasconsistentwithnonconvulsiveseizure.
Video 13-2B Patient was a 57-year-old male found unconscious at home. He
wasfoundtohaveleftintraparenchymalhemorrhage.EEGstartedaftersurgical
evacuationofhematoma.EEGshowedcontinuousPLEDs/LPD+F*patternfrom
left hemisphere. Periodic discharges from parietal and temporal regions were
asynchronous but time locked between the two discharges with temporal
dischargesconsistentlyleadingparietaldischargesby200to500msec.Theictal
event started with serial polyspike-wave discharges from left temporal region
while the parietal discharges maintained a periodic pattern (frame 15:39:43).
Whentemporaldischargesstartedtoslowdown,parietaldischargeschangedto

anictalpatternwithserialpolyspike-wavebursts(frame15:40:00).Astemporal
ictaldischargesfurthersloweddown,parietaldischargesalsosloweddownand
ended at almost the same time (15:40:51). There was no observable clinical
change,andtherefore,thiswasconsistentwithnonconvulsiveseizure.


Video 13-3A Patient was a 63-year-old female with a history of high-grade
follicularlymphomaadmittedwithmentalstatuschangesandpossibleseizures.
The diagnosis was chemotherapy (Ifosfamide)-induced encephalopathy. EEG
started on the second day of admission. Before SIRPID started, EEG showed
diffuseslow(0.5to1Hz)deltawithintermittentlow-voltagethetawaves(frame
18:01:10).Withtheincreasedmuscleartifactandarousal(frame18:01:27),EEG
started to show more theta background activity. Subsequently, diffuse and
intermittent triphasic sharp-wave discharges appeared. Unlike the patient in
Video13-3B,thetriphasicdischargesremainedsporadicandneverbecamefully
rhythmic or continuous. The triphasic discharges progressively decreased, and
eventually,EEGreturnedclosetobaselinewiththedecreaseofmuscleartifact
(afterframe18:04:09).
Video13-3B Patient was an 89-year-old female presenting with confusion and
wasfoundtohaveintraparenchymalhemorrhage.EEGstartedonthesameday
of admission. EEG showed diffuse theta/delta slowing with some interspersed
scatteredminorsharptransientswhenthepatientwasrestingquietly.Whenever
shewasarousedbyothersorspontaneouslyevidencedbyanincreaseinmuscle
artifact, EEG showed initially brief generalized suppression, followed by
recurrent generalized triphasic sharp-wave discharges (frame 22:59:05). These
triphasic discharges became progressively more prominent, rhythmic and
continuous as the patient became more aroused evidenced by seemingly
purposefulmovement(adjustingpillowatframe22:59:48).Thetriphasicwaves
becamemore“spiky”consistingofspike-waveburstsandcouldbeconsideredto
be nonconvulsive seizure (frame 23:00:30 to 23:01:01). As the muscle artifact

decreased,theparoxysmaldischargessubsided(afterframe23:01:13).
Video 13-4 Patient was a 52-year-old male presenting with a problem in
speakingandfoundtohaveintracranialhemorrhageintheleftfrontallobe.EEG
showed semirhythmic delta from the left frontal region, which became
progressivelymorerhythmic andhigheramplitudewithwider spread (LRDA).
Thefocaldeltaactivitybecamemoresharplycontouredandeventuallyevolved
toasharpandwavecomplex.Sincethepatientdidnotshowanymotorsign,the
patternwasconsistentwithnonconvulsivefocalseizure.
Video 13-5 Patient was a 57-year-old male presenting with confusion and
difficulty with complex tasks and found to have a brain tumor in the right
temporal region originating from the right sphenoid. EEG was started one day
after surgery. The EEG showed frequently recurring irregular polyspike-wave


burstsfromtherightcentralandmid-temporalregion.Eachburstlasted2to4
seconds (BIRD). The similar discharges became intermittently more prolonged
and more rhythmic, consistent with electrographic seizure. Note that DSA
indicatednumerousBIRDsinterspersedbytrueictaleventsexpressedbythicker
lines during a 4-hour segment. There was no observable clinical change
associatedwithictaldischargesandthereforeitisconsistentwithnonconvulsive
seizure.
Video13-6A&B Patient was a 65-year-old man with a history of brain tumor
resection from the left temporal lobe about 30 years ago and subsequent
seizures. He was admitted with acute encephalopathy and the EEG showed
recurrent electrographic seizures. Initially, 2 to 5 ictal events were recorded
every4hours.Eachictaldischargestartedwithsharplycontouredrhythmictheta
bursts from the left temporal region, maximum at the anterior temporal
electrode. Shortly after the onset of ictal discharges, apparently there was a
changeinrespirationgivinganalarmsignal.Afterthealarmsignal,therewasan
increaseofmuscleartifact,andtheEEGstartedtoshowincreasedslowertheta

slow waves bilaterally. Each ictal event lasted about ½ to 1 second, and the
sequenceofeacheventwassimilarfromoneseizuretoanother(A&B).Inthis
case,theonlyclinicalsignsofseizurewereachangeinrespirationpatternand
increaseofmuscletone.
Video 13-7 Patient was a 61-year-old male who had cardiac arrest following
cervical trauma. EEG showed burst suppression pattern with prolonged
suppression period lasting 20 to 50 seconds. The burst was associated with
vigorousheadjerking;thus,itwasnotpossibletodifferentiateEEGburstsfrom
themovementartifacts.Aparalyzingagent(Rocuronium)wasgivenattheframe
of 10:43:02. After muscle artifacts were completely eliminated, the bursts
consisting of generalized polyspike and spike-wave continued without muscle
artifacts, verifying that the patient was having myoclonic seizures associated
withburstsuppressionpattern.
Video13-8 Patient was a 65-year-old male with a history of stroke in the left
hemisphere 2 years ago who presented with right arm twitching. EEG showed
diffuse slowing in the background activity and intermittent, nearly periodically
recurring well-defined focal spikes from the left hemisphere, maximum at the
parietal region. Associated with each spike, right arm jerking occurred,
consistentwithepilepsiapartialiscontinua.Theeventscontinuedforhours.