Your Epi Fellows EEG/EPILEPSY: HIGH YIELD RITE REVIEW.

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Your Epi Fellows EEG/EPILEPSY: HIGH YIELD RITE REVIEW

Transcript of Your Epi Fellows EEG/EPILEPSY: HIGH YIELD RITE REVIEW.

Page 1: Your Epi Fellows EEG/EPILEPSY: HIGH YIELD RITE REVIEW.

Your Epi Fellows

EEG/EPILEPSY: HIGH YIELD RITE REVIEW

Page 2: Your Epi Fellows EEG/EPILEPSY: HIGH YIELD RITE REVIEW.

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?

PRE-TEST

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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?

A. TopiramateB. ZonisamideC. LamotrigineD. PhenobarbitalE. Phenytoin withdrawal

QUESTION 1

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~10% patient develop erythema and maculopapular rash.

Develops during the fi rst 2-8 weeks of therapySerious rashes—SJS, TEN, angioedema in 1% of cases.

LAMOTRIGINE

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22 yo man evaluated for seizures. Head CT shows widespread rounded lesions:

What is the treatment?A. AcyclovirB. SteroidsC. AspirinD. InterferonE. Albendazole

QUESTION 2

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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. DrowsinessB. Dizziness and ambulatory difficultyC. Pancreatic dysfunctionD. Aplastic anemiaE. QRS prolongation and heart block

QUESTION 3

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NMDA blocker; potentiates GABAPartial seizures, approved in 1993

Bad side effects: fulminant liver failure and aplastic anemia

Other side effects: mild drowsiness, ataxia, nystagmus, tachycardia, N/V [anorexia]

FELBAMATE

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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

QUESTION 4

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If it’s a choice, it’s usually the answerNo drug interactionsOkay in pregnancy [as is lamotrigine]What is not okay in pregnancy???

LEVETIRACETAM

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Valproic acid

Phenytoin

Topiramate

Phenobarbital

Spinal cord issues

Fetal hydantoin syndrome

Oral/cleft lip/palate

Low IQ

AEDS BAD IN PREGNANCY

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Valproic acid

Phenytoin

Topiramate

Phenobarbital

Spinal cord issues

Fetal hydantoin syndrome

Oral/cleft lip/palate

Low IQ

AEDS BAD IN PREGNANCY

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Metabolized p450TopiramateTiagabinePhenobarbital

Liver: beta-oxidation/glucuronidationValproic acid

P450 inhibitorsValproic acid

P450 inducerPhenobarbital

METABOLISM

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Metabolized p450TopiramateTiagabinePhenobarbital

Liver: beta-oxidation/glucuronidationValproic acid

P450 inhibitorsValproic acid

P450 inducerPhenobarbital

METABOLISM

Non liver AEDs: - Gabapentin- Keppra

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55 yo woman here for f/u after being started on carbamazepine for localization-related epilepsy. She initially had no seizures for the fi rst 2 months, but then started having seizures 2 weeks ago.

QUESTION 5

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.

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Auto-induces itselfTypically occurs 15-30 days after onset of treatmentPlasma clearance doublesPearl: Don’t restart someone’s carbamazepine at the

same dose when it was held Doesn’t apply to oxcarb or esclicarb

CARBAMAZEPINE

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QUESTION 6

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Treat with ethosuximideLess effi cacious are lamotrigine and valproic acid Induced by hyperventilationWas asked about 5 times on my boardsWhat meds are contraindicated?

CHILDHOOD ABSENCE EPILEPSY (CAE)

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Treat with ethosuximideLess effi cacious are lamotrigine and valproic acid Induced by hyperventilationWas asked about 5 times on my boardsWhat meds are contraindicated?

Carbamazepine, oxcarb, tiagabine, vigabatrin

CHILDHOOD ABSENCE EPILEPSY (CAE)

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Treat with ethosuximideLess effi cacious are lamotrigine and valproic acid Induced by hyperventilationWas asked about 5 times on my boardsWhat meds are contraindicated?

Carbamazepine, oxcarb, tiagabine, vigabatrin

CHILDHOOD ABSENCE EPILEPSY (CAE)

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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?

A. PsychiatryB. Sleep studyC. Brain MRID. ReassuranceE. 24-EEG monitor

QUESTION 7

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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 diff erent syndrome/phenotype

BENIGN CHILDHOOD EPILEPSY WITH CENTROTEMPORAL SPIKES: BECTS/BRE

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Landau-Kleffner

Panayiotopoulos

BRE/BCECTS

Generalized + regression: CSWS

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A 3 yo girl presents to the ED with her fi fth 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.

QUESTION 8

What is the next step in management? 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

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Simple febrile sz: <15 minutes, does not recur within 24 hours, no focality

Complex: does not fi t above criteriaStill low risk of developing epilepsy (2%)Though related to sodium channel mutations,

typically not tested at this point and would not change management

FEBRILE SEIZURES

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Which of the following suppressed 3 Hz spike and wave activity on EEG?

A. AlkalosisB. HyperventilationC. HypoglycemiaD. DrowsinessE. REM sleep

QUESTION 9

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Which of the following suppressed 3 Hz spike and wave activity on EEG?

A. AlkalosisB. HyperventilationC. HypoglycemiaD. DrowsinessE. REM sleep [all of the above increase 3 Hz

EEG activity]

QUESTION 9

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A. Brain deathB. The electrode box is disconnected.C. This patient is on benzosD. This person likely has focal seizures.E. There is some residual cortical activity, although

the prognosis is poor.

QUESTION 10

A 10 yo child suff ered 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 deathB. The electrode box is disconnected.C. This patient is on benzosD. This person likely has focal seizures.E. There is some residual cortical activity, although

the prognosis is poor.

QUESTION 10

A 10 yo child suff ered 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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Phenobarbital Phenytoin ACTH Carbamezepin

e Lamotrigine

QUESTION 11:WHAT IS THE TREATMENT FOR

THIS?

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Regarding the pharmacokinetics of phyntoin, which of the following is correct?

A. It is renally metabolizedB. It is exclusively metabolized in the liverC. It has zero-order (nonlinear) kineticsD. It is a hepatic enzyme inhibitorE. It has fi rst-order kinetics

QUESTION 12

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Regarding the pharmacokinetics of phyntoin, which of the following is correct?

A. It is renally metabolizedB. It is exclusively metabolized in the liverC. It has zero-order (nonlinear) kineticsD. It is a hepatic enzyme inhibitorE. It has fi rst-order kinetics

QUESTION 12

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What is the MOA for benzos?

A. Chloride channel antagonismB. Chloride channel agonismC. GABAa antagD. GABAa agonistE. GABAb agonism

QUESTION 13

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What is the MOA for benzos?

A. Chloride channel antagonismB. Chloride channel agonismC. GABAa antagD. GABAa agonistE. GABAb agonism

QUESTION 13

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Where does the figure 4 localize?

A. Mesial temporal lobe B. Occipital lobe C. Motor cortex D. Supplementary motor cortex E. Frontal lobe

QUESTION 14

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Where does the figure 4 localize?

A. Mesial temporal lobe B. Occipital lobe C. Motor cortex D. Supplementary motor cortex E. Orbitofrontal lobe

QUESTION 14

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In a patient with CSF-positive HSV encephalitis, what would you find on their EEG?

A. Triphasic wavesB. Wicket spikesC. Periodic lateralized epileptiform discharges (PLEDs)D. PolyspikesE. Fast spike-wave complexes

QUESTION 15

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In a patient with CSF-positive HSV encephalitis, what would you find on their EEG?

A. Triphasic wavesB. Wicket spikesC. Periodic lateralized epileptiform discharges

(PLEDs)D. PolyspikesE. Fast spike-wave complexes

QUESTION 15

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In a patient with CSF-positive HSV encephalitis, what would you find on their EEG?

A. Triphasic wavesB. Wicket spikesC. Periodic lateralized epileptiform discharges

(PLEDs)D. PolyspikesE. Fast spike-wave complexes

QUESTION 15

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Myoclonic seizuresGTCsTx “life long”: Keppra, VPA, Lamotrigine

JME

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12 yo boy with frequent falls, clumsiness, drops objects and has frequent GTCs. Has a history of infantile spasms.

A. Landau-Kleff nerB. Lennox-GastautC. Myoclonic epilepsyD. Doose syndromeE. JME

QUESTION 16

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12 yo boy with frequent falls, clumsiness, drops objects and has frequent GTCs. Has a history of infantile spasms.

A. Landau-Kleff nerB. Lennox-GastautC. Myoclonic epilepsyD. Doose syndromeE. JME

QUESTION 16

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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

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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

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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?

A. West syndromeB. Ohtahara syndromeC. Severe myoclonic epilepsy of infancy (Dravet)D. Aicardi syndromeE. Myoclonic-astatic epilepsy (Doose)

QUESTION 18

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A 2 month old girl has blindness, infantile spasms, and an abnormal retinal examination. Her brain is below. What is the most likely cause?

A. West syndromeB. Ohtahara syndromeC. Severe myoclonic epilepsy of infancy (Dravet)D. Aicardi syndromeE. Myoclonic-astatic epilepsy (Doose)

QUESTION 18

Page 46: Your Epi Fellows EEG/EPILEPSY: HIGH YIELD RITE REVIEW.

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

Page 47: Your Epi Fellows EEG/EPILEPSY: HIGH YIELD RITE REVIEW.

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

POST-TEST