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Joint Session with ACOFP and Mayo Clinic So One of Your Patients has Seizures? William Tatum IV, DO

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Page 1: Joint Session with ACOFP and Mayo Clinic So One of Your ... · PDF fileSo One of Your Patients has Seizures? William Tatum IV, DO. ... – Refractory seizures – Severe EEG abnormalities

Joint Session with ACOFP and Mayo Clinic

So One of Your Patients has Seizures?

William Tatum IV, DO

Page 2: Joint Session with ACOFP and Mayo Clinic So One of Your ... · PDF fileSo One of Your Patients has Seizures? William Tatum IV, DO. ... – Refractory seizures – Severe EEG abnormalities
Page 3: Joint Session with ACOFP and Mayo Clinic So One of Your ... · PDF fileSo One of Your Patients has Seizures? William Tatum IV, DO. ... – Refractory seizures – Severe EEG abnormalities

9/30/2015

1

So Someone You Know HasEpilepsy?

William O. Tatum IV, DO, FAAN, FACNSProfessor of Neurology

Mayo College of Medicine

Senior Consultant

Mayo Clinic in Florida

Director, Epilepsy Monitoring Unit

Jacksonville, Florida USA

Faculty Disclosure

• Financial Involvement– National Board Affiliations (Neurophysiology)

• ABCN, ACNS

– Consultant/speaker’s bureau/honoraria

• Demos Publishers, Springer Publishers

– Research support• Brain Sentinel

• Significant Financial Involvement creating a conflict of interest– None

• Off label discussion– None

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KH is a 24 year old female with a prior Oligodendroglioma presents tothe ED after 3 witnessed “grand mal” seizures. She is taking Buspar 10

mg PO TID, Xanax 1 mg PO TID, and Tegretol XR 400 mg PO BID with weekly attacks failing LTG and GBP....

Does this patient have epilepsy?

Epilepsy

• Definition: Epilepsy exists after a single unprovoked seizure when the risk of a recurrence is >60%.1

– Nearly 3 million people in U.S (50 million worldwide)

– One epileptic seizure/life-time occurs in 1/10 people

• Approximately 70% of adults with new-onsetepilepsy have focal seizures.

• The cause is unknown in 62%.– In the rest, stroke in 9%, trauma 9%, alcohol 6%, neurodegenerative dz

4%, static encephalopathy 3.5%, brain tumor 3%, and infection in 2%.

– An age-related predisposition exists that reflects cause.

1. Fisher R et al. Epilepsia 2014; DOI: 10.1111/epi.12550

2. French JA, Pedley TA. N Engl J Med 2008;359:166-76.

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3

Seizures are a Symptom

Annegers JF. The Epidemiology of Epilepsy. In: Wyllie E, ed. The treatment of epilepsy: principles & practice.

3rd edition. Philadelphia: Lippincott Williams & Wilkins, 2001:165-72.

• Brain malformations and infection during childhood

• Trauma and brain tumor in mid-life

• Stroke and dementia in later life

EEG

• Sensitivity: (Low-moderate)– First recording is “+” IEDs in 29-55%.

– Recovery is related to brain location (temporal v frontal).

– Increases to 85% with repeated study, sleep deprivation, < 24 hrs.

• Specificity: (Very high)– IEDs are rare in non-epileptic people (1-2%).

– More common in kids (1.9-3.5%) than adults (0.2-0.5%).

• Video-EEG: definitive means of diagnosis,classification, and characterization2.

1.

2.

Pillai J, Sperling MR. Epilepsia 2006;47(suppl 1):14-22.

Tatum WO. J Clin Neurophys 2001;18(5):442-455.

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A 58 y/o M awoke with a feeling “everything was spinning” worsened by head movement with concomitant nausea and

sweating. No LOC was noted and he was A & O x3.

EEG with bilateral myogenic artifact created by movement of the muscles of mastication (presumed chewing). Note brief “spikes” and polyphasic

artifact followed by an apparent “slow wave” at 1.5-2Hz. Parameters: longitudinal bipolar montage; sensitivity 7 uv; filters 1-70 Hz.

Tatum WO. www.epilepsy.com Clinical Corner September 2011.

Tatum WO. Artifact-related epilepsy. Neurology 2012 (in press).

ED= Vertigo

EEG:

Generalized

Spike-waves

Told no

Driving.

Diagnosis:

“Seizure D/O”.

Couldn’t

get to work.

“Sick”from CBZ

A Treatment Plan

Newly

Diagnosed

Drug

Resistant

1st

Monotherapy

2nd

Monotherapy

3rd Mono or

Polytherapy

Epilepsy

Surgery

ASDs (Polytherapy)

Neurostimulation

Ketogenic Diet

(children)

Seizure freedom

No Side effects

Seizure reduction

Minimize AED side effects

Optimize quality of life

Video-EEG

MonitoringNo

Adapted from Wheless JW. Neurostimulation Therapy for Epilepsy. In: Wheless JW, Willmore LJ, Brumback RA,

eds. Advanced Therapy in Epilepsy. Hamilton, Ontario: BC Decker, Inc. 2008.

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5

Treatments

• Medical1

– Seizure reduction

– SE reduction

• Non-medical2

– Neurostimulation3

– Ketogenic Diet4

1.Kwan P, Brodie MJ. Neurology 2003;60(Suppl 4):S2-S12.

2.Wiebe S et al. NEJM 2001;345:311-318.

3.Cascino GD. Epilepsia 2008;49(Suppl 9):79-84.

4.Sirven J et al. Epilepsia 1999;40:1721-1726.

The First Seizure as Epilepsy

• ASD treatment renders 65-

85% seizure free.1

• Recurrence greatest in the

1st 2 years (21-45%).

– Response to the first

ASD predicts control.1

– + risk factors double the

likelihood & tx halves it.

• Prior brain insult (level A)

• Epileptiform EEG (level A)

• Abnormal MRI (level B)

• SE in 7-31% (level B)

High Risk for Seizure: No

Treatment

Brodie MJ et al. Neurology 2012;78:1548–1554.

Krumholz A et al. Neurology 2015;84:1705–1713.

Hakami T, et al. Neurology 2013;81(10):920-7.

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6

Anti-Seizure Drugs

• None alter the course of the disease process (“AEDs”).

• All current ASDs provide symptomatic treatment.

– Effective in focal seizures 2/3rds of the time.

– Effective in generalized seizures 80-85% of the time.

– Response to treatment has been stable over time.

• All ASDs potentially have adverse events and none treat

the non-seizure symptoms (neurocognitive/psychosocial).

• No ASDs are truly prophylactic for prevention of epilepsy

(due to trauma, stroke, brain tumor etc.).

Mohanraj R, Brodie MJ. Eur J Neurol 2006;13:277–282.

Kwan P, Schachter SC, Brodie MJ. N Engl J Med 2011;369:919–926.

Choose the Most Effective ASD

• The mainstay of treatment in >90% of patients.

• Choices1

– Conventional: PB, PHT, CBZ, VPA

– Newer: LTG, TPM, GBP/PGB, OXC, LEV, ZNS, LCS, RUF,CLB, GVG, EZO, PER, ESLI [FBM, TGB]

– Choice based on seizure type and epilepsy syndrome• Focal Epilepsy: Essentially all ASDs

• Generalized Epilepsy: VPA, LTG, TPM, ETH (absence only)

• Advantages of the newer ASDs include tolerability and the advantages of conventional ASDs is cost.

1. Marson A et al. The Lancet 2007;369:1000-1026.

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Consider Safety

• Steven-Johnson Syndrome– Most of the ASDs

• Aplastic Anemia– Carbamazepine, oxcarbazepine, felbamate

• Organ Failure (e.g. hepatic)– Valproate, felbamate

• Depression– Phenobarbital, perampanel, leviteracetam, zonisamide

topiramate, lacosamide

• Nephrolithiasis– Topiramate, zonisamide

• Visual loss– Vigabatrin, ezogabine

• Weight Loss– Felbamate, topiramate, zonisamide

• Weight Gain– Gabapentin, pregabalin, perampanel, vigabatrin, valproate

• Teratogenesis– All ASDs

• Childbearing potential 12-44 years old

• Contraception

• Pregnancy

• Vitamin supplementation

• Precautions

Harden CL, Hopp J, Ting TY, et al. Practice parameter update: management issues for women with epilepsy: focus on pregnancy (an

evidence-based review): obstetrical complications and change in seizure frequency: report of the Quality Standards

Subcommittee and Therapeutics and Technology Assessment Subcommittee of the American Academy of Neurology and

American Epilepsy Society. Neurology 2009;73:126-132.

Women of Childbearing Potential

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8

How Many Drugs Do You See?

• The brand of ASD should remain stable.

• Seizures or clinical toxicity may occur in some1.– Little data exists to justify safety.

– Discrepancy exists with FDA position

• FDA considers a “generic” drug “equivalent” to abrand with same amount of active ingredient.– Identity, purity, quality, strength, dose

– Drug concentration time curve and maximum concentration within 80-125% of reference Rx

• “Generic AEDs should not be substituted for brand AEDs without knowledge of the patient and the attending physician.2”

1. Lowe K et al. AAN Position Statement. Neurology 2007;68:1249-1250.

Spectrum of Use

Tatum WO. Current Treatment Neurology 2013

French JA, et al. Neurology. 2003;60:1631-1637.

*New AEDs used as adjunctive therapy in patients refractory to standardAEDs in RCTs.

TGB1

LTG1

TPM1 LVT

ZN

mg)

on (minus placebo)

OXC

S 25%

PGB5

35%

tsneti GPB1

Dose (

a P

50% seizure reducti

0%

10%

5%

ts

15%

Pa

20%ti

en

30%

40%

Slide courtesy of Jacqueline French, MD

Focal Generalized Focal and

Generalized

Spectrum Not

Established

Carbamazepine Ethosuximide Levetiracetam Lacosamide

Oxcarbazepine Rufinamide Lamotrigine Ezogabine

Gabapentin Zonisamide Perampanel

Pregabalin Valproic acid

Tiagabine Topiramate

Vigabatrin

(+Spasms)

Felbamate

Eslicarbazepine Phenytoin

Phenobarbital

Clobazam

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9

Genetic Generalized Epilepsy

• Absence, myoclonic,(clonic)-tonic-clonic

• Genetic influence

• Common in children

• Normal neuroimagingand intelligence

• Treatment responsive– ETH for CAE1,3

– VPA1,3 (JAE, JME, GTC)

– LEV, LTG, TPM, ZNS

Nadkarni S et al. Neurology 2005;64(suppl3):S2-S11.

Nicolson A et al. JNNP 2004;75:75-79.

Karceski S et al. Epilepsy & Behavior 2005;7:S1-S64.

1.

2.

3.

Juvenile Myoclonic Epilepsy

• A 21 year old female has been out late at night with her friends in college. She has been active in sports and is a cheerleader at University of Florida. She may have had someone slip something into her drink at the party. She recalls that she felt like she had been struck several times with a lightening bolt and then “blacked out”. Her friends later noted that she had a “grand mal seizure” and suggested that she see you.

• What is her diagnosis?

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10

• Mental Health issues

– Select: LTG, VPA, OXC, PGB

– Avoid: PB, TPM, LEV, ZNS, PER

• Pain– Select: GBP, PGB, TPM, CBZ

• Eating disorder: avoid drugs that impact weight

– Weight gain: VPA, GBP, PGB, CBZ, OXC, EZO

– Weight loss: TPM, ZNS, FBM

• Hyponatremia (elderly, on diuretics)

– Avoid: CBZ, OXC, ESLI (CBZ derivatives)

• Cardiovascular risks (e.g. high cholesterol)

– Avoid: CBZ, PHT (“inducers)

Consider Co-morbidities Encephalopathic Epilepsy

• Clinical features– Cognitive impairment

– Refractory seizures

– Severe EEG abnormalities

• Seizures– Mixed seizure types

– Generalized motor

– Tonic and atonic

• Refractory to treatmentoften with recurrent injury– Broad spectrum ASDs

– Surgical procedures

Winesett P, Tatum WO. The Treatment of Epilepsy,6th edition, Chapter 21. In: Wyllie, E, ed.Baltimore, Lippincott. 2016 (in press).

• Quality of Life

• Limit ASDs

• Side effect reduction

• Minimize injury

• Limit ED visitation

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Lennox-Gastaut Syndrome

• A 28 year old mentally retarded hispanic male experienced episodes of “flinching” at 8 months old. Development had global delay of milestone in development. Seizures occurred multiple times daily and was given a “steroid”. At 2 years old he began to manifest multiple seizure types including “grand mal”, “petit mal”, “dropping”, “falls”, and “jerks”. He has failed 11 ASDs.

• What are his options?

More than 30 ASDs Exist Globally

1850 1870 1890 1910 1930 1950

Year of introduction

1970 1990 20100

5

10

15

20

25

30

35

40

Bromide

Phenobarbital

Borax

Ethosuximide Ethotoin Methsuximide

Primidone Phensuximide

Phenacemide Corticosteroids/ACTH Paramethadione Mephenytoin Trimethadione

Acetazolamide Phenytoin

Mephobarbital

Valproate Carbamazepine

Diazepam Sulthiame

Chlordiazepoxide

Clobazam Clonazepam

Progabide

Eslicarbazepine acetate LacosamideRufinamideStiripentol

PregabalinLevetiracetam

Tiagabine Topiramate Gabapentin Felbamate

Oxcarbazepine Lamotrigine ZonisamideVigabatrin

First generation

Second generation

Third generation

Nu

mb

er

of

AE

Ds

AES 2013 Page B. Pennell

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Vagus Nerve Stimulation• VNS has efficacy equal to new ASDs in RCTs.1

• Guideline Subcommittee of the AAN.2

– Recommendation: VNS may be considered for seizures in children, for LGS-

associated seizures, and for improving mood in adults with epilepsy (Level C).

– VNS may be considered to have improved efficacy over time (Level C).

• Long Term Effectiveness Trial3

– Improvement in HRQoL compared with BMP.

• VNS reduced cardiac electrical instability.4

– T-wave alternans (biomarker for SUDEP) was reduced.

Fisher RS, Handforth A. Neurology 1999;53:666-669.

Morris GL et al. Neurology 2013;81(16):1453-1459.

Ryvlin P et al. Epilepsia 2014;DOI: 10.1111/epi.12611.

Schomer AC et al. Epilepsia 2014;55(12):1996-2002.

Focal Epilepsy

• Most common type in adults– > 60% of epilepsies

– Focal seizures with and without impaired consciousness

– Focal evolving to convulsion

• Due to focal CNS “lesion”

• EEG may clarify seizure classification.

• Treatment– *Initial: CBZ, LTG, OXC

– Alternate: LEV

*Karceski S et al. Epilepsy & Behavior 2005;7:S1-S64.

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Focal Epilepsy

• A 58 year old female is seen for a seizure disorder. She has HTN, DM, osteoporosis, DJD, and hypercholesterolemia on Coumadin for a PE. She has not had a “grand mal” seizure since she was 19 years old.

• She thinks she is having 1-2 “mini-mal” seizures per month.She is on multiple medications and has been followed by her PCP for 40 years on Dilantin® 400 mg PO daily. She see Neurologyadds CBZ 800 mg po qD added but levels are low (PHT= 7 ug/dl and CBZ 3.6 ug/dl); seizures increased.

• What do you do?

What About Driving?

• State-specific driving

laws exist (3 mos- 1 yr.).

• Epilepsy increases the

risk of MVAs (up to 7x).1

• Fatalities rare (<0.2%).2

• Most patients with

epilepsy are controlled

with ASDs and drive.

Lings S. Neurology 2001;57(3):435-9. Sheth

S et al. Neurology 2004;63(6):1002-7.

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Drug Induction

• Reasons

– Non-compliance

– “Fast metabolizer” (20% of AA for 2C9 drugs).

– Reciprocal induction: both ASDs together lead to

combined reduction in serum concentrations.

• Solution

– Transition to CBZ monotherapy (3A4, 2C9)

– Substitute a different ASD to PHT (2C9)

A 24 year old male comes to clinic with his girlfriend. She describes starring spells followed by erratic behavior. The patient denies a problem and states that his girlfriend is making things up to

get back at him for getting her pregnant. MRI brain and EEG is normal.

• Treatment depends on seizure frequency.

• In-patient VEM:•

39-49% of seizures were recognized.1,2

30% of people denied all seizures

23% of people were aware of all their seizures.1

• Out-patient CAA-EEG:• 62% of seizures were recognized.3

• Left temporal and bitemporal Sz a predictor4

1. Blum D et al. Neurology 1996;47:260-4.2. Kerling F et al. Epilepsy & Behav 2006;9:281-5.3. Tatum WO. J Clin Neurophysiol 2001;18:14-9.4. Langston ME, Tatum WO. Epilepsy Res 2015;109:163-168.

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15

What about Epilepsy and Pregnancy?

• Globally 15 million WWE = child-bearing age.

• Seizures may increase in 25%

– Uncontrolled GTC Sz can have devastatingconsequences (> 5 associated with lower IQ).

– 10-fold increase in SUDEP in pregnant WWE.

• MCM in 4-8%

• VPA impairs cognitive development

– 6 years post-partum

– Lower IQ (~ 10 IQ points)

– Dose-dependence > 800 mg/day

Baker GA et al. IQ after in utero exposure to AEDs: a controlled cohort study. Neurology 2015;84:382-390.

Meador KJ et al. NEAD Sutdy Group. A prospective observational study. Lancet Neurol 2013;12:244-252.

Adab N et al. The long term outcome of children born to mothers with epilepsy. JNNP 2004;75:1575-1583.

ASDs-Hormonal Contraception

Pregnancy Potential

• Carbamazepine, OXC, Esli• Phenobarbital• Phenytoin• Primidone• Topiramate*• Rufinamide• Clobazam• Eslicarbazepine• Perampanel*Potential inactivation at 200 mg/day

Tatum WO et al. Arch Intern Med 2004;5(1):137-45.

Montouris G. Curr Med Res Opin. 2005;21:693-701.

Safe

• Divalproex• Ethosuximide• Gabapentin• Lamotrigine^• Levetiracetam• Zonisamide• Tiagabine• Lacosamide• Vigabatrin• Ezogabine^HC interaction with LTG reduction

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Prevalence of Major Malformations

North American Pregnancy Registry Fall 2014

General Population: 1.1%

What about Pharmacogenomics?

Scheffer I, Epilepsy Currents 2011.

Chung, JAMA 2014

Influence on management (e.g. SCN1A, GLUT-1 def, GRIN2A)

Influence on ASD treatment consequences.

Asians are at risk for TEN/SJS on CBZ when found to have a HLA-B 1502* allele.

CYP2C genes (10q23.33) associated with PHT-related severe cutaneous reactions.

HLA-B 1502* testing recommended in all Asians prior to starting CBZ and OXC.

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What’s Next in Line for “AEDs”?

• Treating chronic epilepsy is different than treating

developing hyperexcitable networks in animal models.

• Drugs that treat recurrent seizures may be ineffective

in preventing the development of a first seizure.

• Trials in patients with brain lesions (e.g. tumors and

trauma) do not support the concept of prophylaxis.

• Questions remain whether ASD alternatives (e.g. anti-

inflammatories, anti-oxidants, neuroprotectants or

inhibitors of neural sprouting can prevent epilepsy.

What About Weed?

• Schedule 1, illegal, ? harmful & no evidence for efficacy.

• Activates Endocannabinoid systems with receptors 1 (G-

proteins) & 2 expressed in neocortex and hippocampus.– Animal models have shown benefit from canabidiol (CBD): No Controlled trials in humans yet.

– Anectdote: Charlotte Figi (Charlotte’s Web): extract high in cannabidiol/low in THC

• Adverse Events– Early use associated with poor cognitive development and younger first-episode psychosis.

– Synthetics: “Spice” or “K-2” with MS changes, seizures, cardiotoxicity; JWH-018 with stroke.

• Drugs– Sativex® approved for spasticity/neuropathic pain in MS/cancer outside USA

– 2013 FDA granted orphan drug status of CBD for Dravet syndrome (expanded access).

– Safety/tolerability open-label trial with Epidiolex (plant liquid CBD multi-center Int’l peds study).

Collins T. Special Report: What Neurologists are doing about medical marijuana. Neurology Today 2014;14(8):28-33.

Wilner AN. Medscape Neurology/ Epilepsy Notes. March 25, 2014.

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Drug ResistanceThe Reasons

• Wrong Diagnosis– Psychogenic (physiologic) NEA

– Bizarre or another seizure type

• Wrong Drug– for seizure type

– Drug interactions prevent use

• Wrong Dose– Too low (ie status)

– Side-effects limit use

• Wrong Lifestyle– Poor compliance

– Inappropriate lifestyle

Kwan P, Leung H. In:Therapeutic Strategies in Epilepsy. French J, Delanty N, eds. 2009:136.

Confirm theDiagnosis

• A 17 y/o boy grew up in a

dysfunctional home environment.

• He had a right craniotomy at 12

years for a parietal lesion (DNET)

with subsequent CDH.

• Grand mal seizures began at age

13 years and he failed 5 ASDs.

• He is taking LEV, TPM, KLN and

PB when he presents in serial

seizures/status epilepticus.

• What is the next step?

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Avoid Wrong Drugs

• An 19 y/o male with migraine

experienced his first “grand mal”

seizure. He was partying the PM

before. In the ED he was given IV

PHT and maintained on PHT 200

mg po BID (15 ug/dl). He

experience an increase in the

“dropsies”.

• In follow-up, VPA 250 mg po bid is

added to PHT. VPA is increased to

1000 mg po q hs. He complains of

dizziness, blurry vision and

difficulty walking. Levels are

“normal”.

• What is going on?

Inhibitor + Inducer

• Reason

– VPA and PHT are both highly protein bound ASDs and

compete for the carrier protein albumin.

– PHT free fractions rise (bioactive) with toxicity!

– The ASD with the higher concentration usually

predominates (VPA > PHT).

• Solution

– Taper PHT

– Substitute an alternative ASD (e.g. LEV)

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A 25 year old male developed jerks at age 12 years. GTC started at 14 years. Diagnosed with JME he remained refractory to ASDs despite VPA, LTG, LEV, and LCS. GTCs were monthly and he presented to clinic with a

smartphone video.

• SUDEP (24 x > gen. populus)

• 1.1-3.8/1000 person years

– Young people 20-40 years

– Males: females 7:4

– Substance abuse

– Epilepsy > 10 years

– GTC seizures

– Unattended/prone position

– MR/Symptomatic epilepsy

(1/100)

Shorvon S, Tomson T. SUDEP. The Lancet 2011;378(9808), 2028-2038.

Compliance

“Drugs don’t work if you don’t take them.”

C. Everett Koop

Compliance

• Non-compliance is common.

• 37% reported changing theirbehavior because of SUDEPdisclosure.– Included improved adherence

to medication

– potentially mitigating risk of SUDEP.

• Most participants did notreport long-term anxietyfollowing disclosure.

http://www.epilepsyscotland.org.uk

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Drug-Resistance

• Surgery Candidates1

– Disabled by seizures*

– Drug-resistant

– Localized/surgically

accessible.

– Healthy/motivated for surgery.

• Selection1-3.– Surgical techniques vary

among centers.

– Patient selection and

evaluations varies over time.

1.Engel J Jr et al. Neurology 2003;60:538-547.

2.Vlooswijk MCG et al. Neurology 2010;75:395-402.

3.Kobayashi E et al. Epilespia 2009;50(12):2549-2556.

8.

N= 3895 patients-Temporal

Seizure free rates

Results > 5 years

Pooled data if > 2 studies

Seizure free rates1

(defined by the authors; follow-up ≥ 5 years;

70% 66% results pooled if > 2 studies)

61%59%

60%

50% 46% 46%

stn 40%i 35% 34%etpa

% 30% 27%

20% 16%

10%

0%

TL HEMI TL+EXTRA PAR OCCI CALLO* EXTRA TL FRONT MST

TL: temporal lobe

HEMI: hemispherectomy

TL+EXTRA: grouped temporal and extratemporal lobe

PAR: parietal lobe; OCCI: occipital lobe

CALLO: callosotomy – freedom from drop attacks

EXTRA TL: grouped extratemporal lobe

FRONT: frontal lobe

MST: multiple subpial transection

Téllez-Zenteno JF, et al. Brain 2005;128:1188-9

©2011 MFMER | slide-41

Phase 1 Evaluation

• Structural (pathology)

– Brain MRI• High resolution

• Epilepsy protocol

• Functional (physiology)

– EEG (neuron)– MEG (neuron)

– Tractography (axons)

– PET (metabolism)

– MRS (neurochemistry)

– SPECT/SISCOM (rCBF)

– fMRI (vascular)

– Neuropsychological testing/Wada (function)

1. Sperling MR et al. Neurology

1992;;42(2):416. 2.Quarato PP et al. JNNP

2005;76:815-824.

3.Cascino GD et al. MRI based volume studies. Ann Neurol 1991;30:31-36.

©2011 MFMER | slide-42

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Phase 2 Evaluation

Slide Courtesy of Greg Cascino MD

Minimally Invasive Surgery

©2011 MFMER | slide-44

• Minimally invasive

approaches may achieve

seizure freedom yet

minimize adverse effects.

• It may be more attractive to

patients (13/17 chose

SLAH v open resection).1

• 80% were DC in < 24 hrs.2

1. Willie JT et al. Neurosurgery 74:569–585, 2014

2. Petito G, Tatum WO. Epilepsia 2015A.

• 2-5 treatments/patients (mean= 3) in

mean of 9.6 minutes (+/- 6.4).

• Workstation thermometry monitors

target/collateral tissue.

• Rapid irreversible brain ablation at 60

C (range 40-90 C) with localized heating

of tissue with sharp boundaries.

• Optical fibers and laser energy are MR

compatible to enable real-time feedback

control of laser and tissue ablation.

LaserApplicator

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Intracranial RNS for DRLRE

• Delivers stimulation in response to seizures.

• 18 years old

• 1-2 epileptogenic foci

• Drug-resistant

• Frequent disabling seizures

Heck, C et al. Epilepsia 2014; 22 FEB 2014; DOI: 10.1111/epi.12534

Quality Indicators in Epilepsy

1. Seizure frequency and seizure intervention specified

each encounter.

2. Etiology, seizure type and epilepsy syndrome

specified each visit.

3. Ask about side-effects to ASDs each visit.

4. Personalize safety issues/education yearly.

5. Screen for psychiatric health each visit.

6. Counsel women of childbearing yearly.

7. Refer drug-resistant patients to a CEC q 2 years.

Fountain NB et al. Quality Improvement in Neurology: Epilepsy Update Quality Measurement Set. Neurology 2015;84(14):1483-1487.

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Conclusions

• The treatment of epilepsy requires a definitive diagnosis

and classification of seizure/epilepsy type.

• Management is individualized and a shift toward the

new ASDs has been based upon Pks and tolerability.

• Drug-resistance is a real problem and non-medical

therapies should be considered as a standard of care.

• The future promises better diagnosis and treatment for

patients with epilepsy.

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