Joint Session with ACOFP and Mayo Clinic So One of Your ... · PDF fileSo One of Your Patients...
Transcript of Joint Session with ACOFP and Mayo Clinic So One of Your ... · PDF fileSo One of Your Patients...
Joint Session with ACOFP and Mayo Clinic
So One of Your Patients has Seizures?
William Tatum IV, DO
9/30/2015
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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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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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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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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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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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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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• 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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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.