Continuum: Eeg And Epilepsy Monitoring

Front 1

2 EEG hallmarks of focal epilepsy

Back 1

interictal spike

interictal sharp wave

Front 2

EEG hallmark of generalized epilepsy

Back 2

frontocentral spike-wave

Front 3

spike part of spike-wave is from ___

Back 3

surge of thalamic input to cortex

Front 4

wave part of spike wave is from ___

Back 4

inhibition

Front 5

___ of ___ cortex is required to record spike or sharp wave

Back 5

6 cm2

gyral

Front 6

___ may turn out to be specific EEG marker for epileptogenicity

Back 6

HFOs

Front 7

interictal epileptiform discharges are present in EEGs of ___% of non-epileptic patients

Back 7

0.2--3

Front 8

5 drugs associated with epileptiform discharges

Back 8

cefepime

bupropion

Li

tramadol

clozapine

Front 9

3 metabolic d/os a/w epileptiform discharges

Back 9

uremia

thyrotoxicosis

Hashimoto encephalopathy

Front 10

photoparoxysmal response is ___ or ___

it is located ___ly

Back 10

generalized spike-wave

polyspike-and-wave

anterior or posterior

Front 11

T/F: consciousness can be preserved in photoparoxysmal response

Back 11

true

Front 12

photoparoxysmal response is a/w ___ epilepsy,

especially ___

Back 12

generalized

childhood absence

Front 13

5 EEG patterns which are abnormal but nonspecific

Back 13

focal slowing

diffuse slowing

focal voltage asymmetry

FIRDA

triphaisc waves

Front 14

focal slowing may be caused by ___ or ___

Back 14

focal lesion

diffuse process

Front 15

3 diffuse processes a/w focal slowing

Back 15

dementia

postictal state

migraine

Front 16

ddx of diffuse slowing

Back 16

TBI

SAH

encephalopathy

Front 17

ddx of focal voltage asymmetry

Back 17

infarct

subdural hematoma/hygroma

skull hyperostosis (or defect)

Front 18

ddx of FIRDA

Back 18

hyperventilation

sleep

lesion

high ICP

metabolic derangement

Front 19

2 kinds of lesion a/w FIRDA

Back 19

deep midline

diffuse subcortical

Front 20

ddx of triphasic waves

Back 20

metabolic encephalopathy

other diffuse process

Front 21

3 signs that triphasic waves may be epileptiform

Back 21

local phase reversal

u/l

reduced background slowing

Front 22

triphasic waves are suppressed by ___ (2)

and activated by ___

Back 22

benzos

sleep

stimulation

Front 23

spike duration

Back 23

<70 ms

Front 24

sharp wave duration

Back 24

80-500 ms

Front 25

spikes/sharp waves normally have ___ dipole
except in ___ when it is ___

Back 25

radial
benign rolandic
tangential/rorizontal

Front 26

absence epilepsy has ___ on EEG
it is a/w ___

Back 26

3 Hz generalized spike and wave
OIRDA

Front 27

atypical absence has ___ on EEG

Back 27

2-2.5 Hz generalized spike

Front 28

atypical absence differs from typical in ___ (3)

Back 28

developmental delay present
longer Sz with gradual onset/offset
a/w atonia

Front 29

JME has ___ on EEG

Back 29

4-6 Hz generalized spikes/polyspikes

Front 30

catastrophic epilepsy syndromes have ___ on EEG

Back 30

slow spike + wave

Front 31

slow spike + wave frequency

Back 31

1.5-2.5 Hz

Front 32

interictal ___ is highly specific for temporal lobe epilepsy

Back 32

TIRDA

Front 33

6 epileptic encephalopathies in order of age of onset

Back 33

Ohtahara
West syndrome
Dravet
Lennox-Gataut
Landau-Kleffner
progressive myoclonic epilepsy

Front 34

Ohtahara syndrome has ___ on EEG

Back 34

burst suppression

Front 35

West syndrome has ___ on EEG

Back 35

hypsarrhythmia

Front 36

West syndrome is ___ (3)

Back 36

spasms

arrest of psychomotor development

hypsarrhythmia

Front 37

Landau-Kleffner has ___ on EEG

Back 37

continuous spike and wave in slow-wave sleep

Front 38

Dravet syndrome has ___ (3)

Back 38

progressive background slowing
generalized/multifocal spike-wave
photosensitivity

Front 39

PME has ___ (3)

Back 39

3-6 Hz polyspike and wave
slow background
photosensitivity

Front 40

6 normal variant EEG patterns confused for epilepsy

Back 40

rhythmic midtemporal theta
small sharp spikes
wicket spikes
phantom spike and wave
14 and 6 positive spikes
subclinical rhythmic electrographic discharges of adults

Front 41

small sharp spikes have amplitude ___
and phase reverse at ___
they are located ___ly

Back 41

<50 uV
temporal leads
unilateral or bilateral

Front 42

phantom spike and wave has frequency ___
occur in bursts of ___
2 variants are ___

Back 42

6 Hz
1-2 s
FOLD (female, occipital predominant, low amplitude and drowsiness)
WHAM (wake, high amplitude, anterior and male)

Front 43

14 and 6 positive spikes have frequency ___
occur in bursts of ___
are maximal at ___
are seen in ___ (state)
are seen in ___ (population)

Back 43

14 or 6 Hz
0.5-1 s
temporal leads
drowsiness
adolescent

Front 44

SREDA consists of ___
occurs in bursts of ___
onset/offset is ___
predominance is ___
is seen in ___ (population)

Back 44

bursts of theta and delta
10-40s
abrupt
temporal or diffuse
older adults

Front 45

5 EEG stages of status

Back 45

discrete seizures
merging of discrete seizures
continuous ictal discharges
continuous ictal discharges with flat periods
periodic epileptiform discharges

Front 46

EEG stage in status predicts ___

Back 46

responsiveness to treatment

Front 47

T/F: in comatose pt, periodic discharges imply status epilepticus

Back 47

F: not always

Front 48

6 periodic EEG patterns seen in comatose patients

Back 48

PLEDs
BIPLEDs
GPEDs
SIRPIDs
triphasic waves
burst suppresssion

Front 49

ddx of PLEDs (6)

Back 49

HSV
grey matter lesion
white matter lesion
HONK
EtOH w/d
theophylline

Front 50

PLEDs are ___
frequency range is ___
spatial distribution i s___
association with seizures is ___

Back 50

sharp-wave + slow-wave complexes
1-2 Hz
unilateral
strong

Front 51

ddx of BIPLEDs (3)

Back 51

anoxic brain injury
CNS infection
chronic epilepsy

Front 52

mortality is higher with PLEDs/BIPLEDs

Back 52

BIPLEDs

Front 53

ddx of GPEDs (5)

Back 53

anoxic brain injury
SSPE
CJD
known epilepsy (?)
acute neurologic events

Front 54

ddx of SIRPIDs

Back 54

critically ill patients with or without neurologic injury

Front 55

SIRPIDs are triggered by ___

Back 55

alerting stimuli

Front 56

ddx of triphasic waves

Back 56

metabolic encephalopathy
NCSE

Front 57

triphasic waves of metabolic encephalopathy can reliably be distinguished from NCSE based on ___

Back 57

nothing

Front 58

triphasic waves have ___ amplitude
___ frequency range
___ spatial distribution

Back 58

medium to high
1.5-2.5 Hx
bilateral synchronous or unilateral

Front 59

ddx of burst suppression (3)

Back 59

anoxic injury
severe encephalopathy
drug-induced

Front 60

2 drug families a/w burst suppression

Back 60

propofol
barbiturates

Front 61

burst suppression has alternating ___ and ___

Back 61

high-amplitude slow waves
flat EEG

Front 62

4 ILAE indications for long-term EEG ambulatory monitoring

Back 62

spells
uncertain dx of epilepsy
epilepsy syndrome classification
electroclinical localization in surgical candidate

Front 63

2 problems with outpatient EEG

Back 63

low quality
inability to re-attach leads quickly

Front 64

prevalence of PNES without epilepsy in EMU

Back 64

25%

Front 65

prevalence of PNES with epilepsy in EMU

Back 65

9-15%

Front 66

___ is pathognomonic for PNES

Back 66

normal EEG during spell

Front 67

___ may be abnormal in PNES, however ___

Back 67

PDR during spell
it normalizes immediately at termination of spell

Front 68

___ may be confused for PNES

Back 68

surface-negative seizures

Front 69

2 epilepsies which are commonly surface negative

Back 69

simple gelastic
frontal lobe

Front 70

5 characteristics of PNES

Back 70

lack of stereotypy
long duration
gradual onset/offset
stop-and-go progression
pelvic thrusting