Transcript EEG/Epilepsy: High yield RITE review

EEG/EPILEPSY: HIGH
YIELD RITE REVIEW
Your Epi
Fellows
PRE-TEST
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What medications are contraindicated in CAE?
What stage of sleep suppresses 3 Hz spike and wave activity?
What is the mechanism of action of felbamate?
Which AEDs are not metabolized by the liver?
Where are the spikes in panayiotopoulos syndrome?
What is the MRI hallmark feature of Aicardi syndrome?
 What does this EEG show?
QUESTION 1
 A 10 yo boy with a hx of epilepsy and cerebral palsy is on
Phenytoin, Phenobarbital, and Valproate. He transitioned to a
new neurologist due refractory seizures. He was started on
Lamotrigine, Topiramate, Phenobarbital and Zonisamide, with
some improvement in seizure control. His vitals are 98F, pulse
75/minute, BP 100/82, he is drowsy and bedridden. Ct of the
brain done recently shows generalized atrophy. Which of the
following is a cause of his skin rash?
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A . Topiramate
B. Zonisamide
C. Lamotrigine
D. Phenobarbital
E. Phenytoin withdrawal
LAMOTRIGINE
 ~10% patient develop erythema and maculopapular rash.
 Develops during the first 2 -8 weeks of therapy
 Serious rashes—SJS, TEN, angioedema in 1% of cases.
QUESTION 2
22 yo man evaluated for seizures. Head CT
shows widespread rounded lesions:
What is the treatment?
 A. Acyclovir
 B. Steroids
 C. Aspirin
 D. Interferon
 E. Albendazole
QUESTION 3
Same 10 yo boy came in due to worsening
seizures. He is on Phenytoin, phenobarbital,
and topiramate. Felbamate is started.
What is the concern with starting this
medication?
 A. Drowsiness
 B. Dizziness and ambulatory difficulty
 C. Pancreatic dysfunction
 D. Aplastic anemia
 E. QRS prolongation and heart block
FELBAMATE
 NMDA blocker; potentiates GABA
 Partial seizures, approved in 1993
 Bad side effects: fulminant liver failure and aplastic
anemia
 Other side effects: mild drowsiness, ataxia,
nystagmus, tachycardia, N/V [anorexia]
QUESTION 4
 40 yo man w a hx of seizures described as
“flashes of light” from his right hemifield followed
by GTC. Current medications include lamotrigine,
HAART meds and multivitamins.
 What is the next best medication to add:
 A. Phenobarbital
 B. Levetiracetam
 C. Valproate
 D. Tiagabine
 E. Topiramate
LEVETIRACETAM
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If it’s a choice, it’s usually the answer
No drug interactions
Okay in pregnancy [as is lamotrigine]
What is not okay in pregnancy???
AEDS BAD IN PREGNANCY
Valproic acid
Spinal cord issues
Phenytoin
Topiramate
Fetal hydantoin
syndrome
Oral/cleft lip/palate
Phenobarbital
Low IQ
AEDS BAD IN PREGNANCY
Valproic acid
Spinal cord issues
Phenytoin
Topiramate
Fetal hydantoin
syndrome
Oral/cleft lip/palate
Phenobarbital
Low IQ
METABOLISM
Metabolized p450
 Topiramate
 Tiagabine
 Phenobarbital
P450 inhibitors
 Valproic acid
P450 inducer
 Phenobarbital
Liver:
betaoxidation/glucuronidation
 Valproic acid
METABOLISM
Metabolized p450
 Topiramate
 Tiagabine
 Phenobarbital
P450 inhibitors
 Valproic acid
P450 inducer
 Phenobarbital
Liver:
betaoxidation/glucuronidation
 Valproic acid
Non liver AEDs:
- Gabapentin
- Keppra
QUESTION 5
 55 yo woman here for f/u after being started on
carbamazepine for localization -related epilepsy. She initially
had no seizures for the first 2 months, but then started having
seizures 2 weeks ago.
 Why did this happen?
 A. she needs higher doses of carbamazepine given its level
likely decreased after initial stabilization
 B. Her epilepsy is becoming refractory to carbamezapine.
 C. She needs the addition of a second AED.
CARBAMAZEPINE
Auto-induces itself
Typically occurs 15-30 days after onset of treatment
Plasma clearance doubles
Pearl: Don’t restart someone’s carbamazepine at the same
dose when it was held
 Doesn’t apply to oxcarb or esclicarb
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QUESTION 6
CHILDHOOD ABSENCE EPILEPSY (CAE)
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Treat with ethosuximide
Less ef ficacious are lamotrigine and valproic acid
Induced by hyperventilation
Was asked about 5 times on my boards
What meds are contraindicated?
CHILDHOOD ABSENCE EPILEPSY (CAE)
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Treat with ethosuximide
Less ef ficacious are lamotrigine and valproic acid
Induced by hyperventilation
Was asked about 5 times on my boards
What meds are contraindicated?
 Carbamazepine, oxcarb, tiagabine, vigabatrin
CHILDHOOD ABSENCE EPILEPSY (CAE)
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Treat with ethosuximide
Less ef ficacious are lamotrigine and valproic acid
Induced by hyperventilation
Was asked about 5 times on my boards
What meds are contraindicated?
 Carbamazepine, oxcarb, tiagabine, vigabatrin
QUESTION 7
A 6 yo girl presents due to occasional
episodes of waking up, producing strange
gurgling noises and hemifacial twitching.
What is the next step in management?
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A . Psychiatry
B. Sleep study
C. Brain MRI
D. Reassurance
E. 24-EEG monitor
BENIGN CHILDHOOD EPILEPSY WITH
CENTROTEMPORAL SPIKES: BECTS/BRE
 One of the many childhood epilepsy syndromes where there is
an↑ in discharges during sleep
 Depending on % increase and where the spikes localize, you
can get a dif ferent syndrome/phenotype
BRE/BCECTS
LandauKleffner
Panayiotopoulos
Generalized + regression: CSWS
QUESTION 8
 A 3 yo girl presents to the ED with her fifth febrile seizure
over the past year. Each is described as a GTC which self resolved within 5 minutes. Her mother also had a history of 1
febrile seizure.
 What is the next step in management?
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A. Start Keppra
B. Reassurance because the child will likely not develop epilepsy.
C. DNA testing for SCN1A mutations
D. MRI brain
E. Routine EEG
FEBRILE SEIZURES
 Simple febrile sz: <15 minutes, does not recur within 24
hours, no focality
 Complex: does not fit above criteria
 Still low risk of developing epilepsy (2%)
 Though related to sodium channel mutations, typically not
tested at this point and would not change management
QUESTION 9
 Which of the following suppressed 3 Hz spike and wave
activity on EEG?
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A . Alkalosis
B. Hyperventilation
C. Hypoglycemia
D. Drowsiness
E. REM sleep
QUESTION 9
 Which of the following suppressed 3 Hz spike and wave
activity on EEG?
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A . Alkalosis
B. Hyperventilation
C. Hypoglycemia
D. Drowsiness
E. REM sleep [all of the above increase 3 Hz EEG activity]
QUESTION 10
A 10 yo child suf fered a TBI 2 days ago and remains
unresponsive. An EEG was obtained at 2 uV. What is the most
likely interpretation?
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A . Brain death
B. The electrode box is disconnected.
C. This patient is on benzos
D. This person likely has focal seizures.
E. There is some residual cortical activity, although the
prognosis is poor.
QUESTION 10
A 10 yo child suf fered a TBI 2 days ago and remains
unresponsive. An EEG was obtained at 2 uV. What is the most
likely interpretation?
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A . Brain death
B. The electrode box is disconnected.
C. This patient is on benzos
D. This person likely has focal seizures.
E. There is some residual cortical activity, although the
prognosis is poor.
QUESTION 11:
WHAT IS THE TREATMENT FOR THIS?
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Phenobarbital
Phenytoin
ACTH
Carbamezepine
Lamotrigine
QUESTION 12
 Regarding the pharmacokinetics of phyntoin, which of the
following is correct?
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A . It is renally metabolized
B. It is exclusively metabolized in the liver
C. It has zero-order (nonlinear) kinetics
D. It is a hepatic enzyme inhibitor
E. It has first-order kinetics
QUESTION 12
 Regarding the pharmacokinetics of phyntoin, which of the
following is correct?
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A . It is renally metabolized
B. It is exclusively metabolized in the liver
C. It has zero-order (nonlinear) kinetics
D. It is a hepatic enzyme inhibitor
E. It has first-order kinetics
QUESTION 13
 What is the MOA for benzos?
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A . Chloride channel antagonism
B. Chloride channel agonism
C. GABAa antag
D. GABAa agonist
E. GABAb agonism
QUESTION 13
 What is the MOA for benzos?
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A . Chloride channel antagonism
B. Chloride channel agonism
C. GABAa antag
D. GABAa agonist
E. GABAb agonism
QUESTION 14
 Where does the figure 4 localize?
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A. Mesial temporal lobe
B. Occipital lobe
C. Motor cortex
D. Supplementary motor cortex
E. Frontal lobe
QUESTION 14
 Where does the figure 4 localize?
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A. Mesial temporal lobe
B. Occipital lobe
C. Motor cortex
D. Supplementary motor cortex
E. Orbitofrontal lobe
QUESTION 15
 In a patient with CSF -positive HSV encephalitis, what would
you find on their EEG?
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A . Triphasic waves
B. Wicket spikes
C. Periodic lateralized epileptiform discharges (PLEDs)
D. Polyspikes
E. Fast spike-wave complexes
QUESTION 15
 In a patient with CSF -positive HSV encephalitis, what would
you find on their EEG?
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A . Triphasic waves
B. Wicket spikes
C. Periodic lateralized epileptiform discharges (PLEDs)
D. Polyspikes
E. Fast spike-wave complexes
QUESTION 15
 In a patient with CSF -positive HSV encephalitis, what would
you find on their EEG?
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A . Triphasic waves
B. Wicket spikes
C. Periodic lateralized epileptiform discharges (PLEDs)
D. Polyspikes
E. Fast spike-wave complexes
JME
 Myoclonic seizures
 GTCs
 Tx “life long”: Keppra, VPA, Lamotrigine
QUESTION 16
 12 yo boy with frequent falls, clumsiness, drops objects and
has frequent GTCs. Has a history of infantile spasms.
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A . Landau-Kleffner
B. Lennox-Gastaut
C. Myoclonic epilepsy
D. Doose syndrome
E. JME
QUESTION 16
 12 yo boy with frequent falls, clumsiness, drops objects and
has frequent GTCs. Has a history of infantile spasms.
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A . Landau-Kleffner
B. Lennox-Gastaut
C. Myoclonic epilepsy
D. Doose syndrome
E. JME
QUESTION 17
 What is the mechanism of action of lacosamide?
 A. Selectively enhances fast inactivation of voltage -dependent
sodium channels
 B. Stabilizes hyperexcitable neuronal membranes
 C. Inhibits repetitive neuronal firing
 D. Enhances slow inactivation of voltage -dependent sodium channels
 E. Binds to the collapsin response mediator protein 2 (CRMP2)
QUESTION 17
 What is the mechanism of action of lacosamide?
 A. Selectively enhances fast inactivation of voltage -dependent
sodium channels
 B. Stabilizes hyperexcitable neuronal membranes
 C. Inhibits repetitive neuronal firing
 D. Enhances slow inactivation of voltage -dependent sodium channels
 E. Binds to the collapsin response mediator protein 2 (CRMP2)
QUESTION 18
 A 2 month old girl has blindness, infantile spasms, and an
abnormal retinal examination. Her brain MRI shows agenesis
of the corpus callosum. What is the most likely cause?
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A . West syndrome
B. Ohtahara syndrome
C. Severe myoclonic epilepsy of infancy ( Dravet)
D. Aicardi syndrome
E. Myoclonic-astatic epilepsy (Doose)
QUESTION 18
 A 2 month old girl has blindness, infantile spasms, and an
abnormal retinal examination. Her brain is below. What is the
most likely cause?
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A . West syndrome
B. Ohtahara syndrome
C. Severe myoclonic epilepsy of infancy ( Dravet)
D. Aicardi syndrome
E. Myoclonic-astatic epilepsy (Doose)
POST-TEST
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What medications are contraindicated in CAE?
What stage of sleep suppresses 3 Hz spike and wave activity?
What is the mechanism of action of felbamate?
Which AEDs are not metabolized by the liver?
Where are the spikes in panayiotopoulos syndrome?
What is the MRI hallmark feature of Aicardi syndrome?
 What does this EEG show?
POST-TEST
 What medications are contraindicated in CAE?
 The carbs- oxcarb, carb, esclicarb
 What stage of sleep suppresses 3 Hz spike and wave activity?
 REM
 What is the mechanism of action of felbamate?
 NMDA blocker, so helps GABA
 Which AEDs are not metabolized by the liver?
 Keppra, gabapentin
 Where are the spikes in panayiotopoulos syndrome?
 Occipital
 What is the MRI hallmark feature of Aicardi syndrome?
 Agenesis of the corpus callosum
 What does this EEG show?
 BRE/BECTs