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Epilepsy Board Study > Epilepsy Treatment > Flashcards

Epilepsy Treatment Flashcards

1
Q

Ketogenic Diet Mechanism

A

Uses long chain fatty acids > break down to acetyl-CoA –> ketone bodies (specifically acetoacetate) -> acetone + beta hydroxybutyrate
Ketone bodies cross BBB –> used for energy instead of glucose

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2
Q

Ratios of Ketogenic diet

A

3:1 or 4:1 (fat:protein +carb)

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3
Q

Medium Chain Triglyceride (MCT) diet

A

Uses MCT oil as source of MC FA
More effiecient in generating ketones
Can consume more protein and carbs

Cons: GI side effects, diarrhea, vomiting, and abdominal pain

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4
Q

Modified Atkins Diet

A

0.9:1 ratio
60-65% of calories from fat
30% from protein
10% carbs

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5
Q

Low Glycemic Index

A

allows high carbohydrates, but limits carbs to low glycemic index (foods that have lower postprandial index)
All carbs glycemic index <50

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6
Q

Indications for diet therapy

A

Strongly consider:
Failed 2-3 anticonvulsants
Symptomatic generalized epilepsies

Probable benefit:
MAE, Dravet sydnrome, TS, Retts, infantile sapasm

Possibly beneficial: LKS, Lafora body disease, SSPE, mitochondrial respiratory chain complex disorders, phosphofructokinase def, FIRES, LGS, HIE, focal malformations

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7
Q

Conditions where Keto diet is treatment of choice

A

GLUT1 deficiency

Pyruvate dehydrogenase deficiency (b/c pyruvate cannot be metabolized to acetyl-coA(

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8
Q

Contraindications for Keto Diet

A

Disorders of FA metabolism defects:

  • Primary carnitine deficiency
  • Carnitine translocase deficiency
  • Beta oxidation defects (MCAD, LCAD, SCAD)
  • Pyruvate Caroxylase deficiency

Relative contraindications: FTT, if surgical focus, noncompliance, lack of parental readiness

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9
Q

Labs to screen for contraindications for KD

A

CBC, Lytes, Mg, Phos, Zinc, Selenium, LFTs, UA, UCa/Cr, UOA, SAA, ACP

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10
Q

Duration of KD

A

Range of benefit 1 - 65 days, typically within 2 weeks
KD for 3 months
If seizure free x 2 years, can consider discontinuing
,

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11
Q

Complications of KD

A

Short term: vomiting, dehydration, hypoglycemia, and excessive acidosis
Long term: growth limitations, kidney stones, dyslipidemia, GERD

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12
Q

Monitoring labs evert 3 months:

A 
Check weight/height
Fasting Lipid Panel
BMP, Ca, Mg, Phos, 
CBC, Free/total carnitine
Zinc
Selenium 
Vit D
Urine Ketones, 
BHOB
Bone density scan if on for >2 years
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13
Q

Efficacy for diet therapy:

A

KD: 38% experience 50% reduction rate at 3 months

MAD:

  • 45-65% had at least >50% reduction of seizurse, 35-36% with >90% seizure reduction
  • 45% with 50-90% seizure reduction, 28% with >90% seizure reduction

LGIT:
38% of pts >50% decreased seizures
-24% with >90% seizure decreased

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14
Q

Meds with extended release formulations

A 
Gabapentin
Lamotrigine
Topiramate
Levetiracetam
Oxcarbazepine
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15
Q

Brivaracetam

A

Sodium blocking mechanism + SV2A binding

Similar SE profile, but higher potency

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16
Q

Cannabidiol

A

Indication for Dravet, LGS

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17
Q

Two main animal models in screening AED candidates:

A
  1. Maximal electroshock model (MES)

2. Subcutaneous pentylenetetrazole

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18
Q

Maximal electroshock model (MES)

A

Electrical stimulation applied through the cornea –> elicits hind limb extension

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19
Q

Subcutaneous Pentyenetetrazole Model

Description

A

PTZ is injected subcut at a dose to induce at least 5 s of clonic seizures activity in 97% animals.
-Predictive of efficacy against generalized tonic-clonic activity and absences seizures

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20
Q

Genetic mice model DBA/2

A

Model for audiogenic seizures

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21
Q

GAERS mice models

A

Genetic model for absence seizures

22
Q

6Hz psychomotor seizure model

A

6Hz pulse of 0.2ms duration through the cornia for 3 sec results in limbic seizures

23
Q

Metylazoxymethanol acetate (MAM) model

A

Cortical dysplasia mouse model
MAM exposed in utero –> cortical dysplastic type lesions
Seizures inducted by kainate are drug resistant

Model for pharmacoresistant epilepsy

24
Q

Catamenial Epilepsy

A

C1 = increased seizures just prior to menses
-> Responds to progesterone 200mg TID on days 14-28
C2 = increased seizures during ovulation
C3 = increased seizures with anovulatory cycles

25
Q

Hormones in Catamenial Epilepsy

A

Estrogen –> proconvulsant
Progesterone –> Anticonvulsant

Seizures more likely to occur when ratio of progesterone to estrogen decreases (usually during menstruation or at ovulation)

26
Q

ACTH used in treatment for

A

Infantile Spasm
Lennox Gastaut Syndrome
Landau Kleffner Sydnrome

27
Q

IVIG/Steroids

Used in treatment for

A

Rassmussens
Limbic encephalitis
Faciobrachial dystonic seizures
Anti-LGI1 encephalitis (VGKC), anti GAD, anti thyroid, anti-NMDA

28
Q

AED that REDUCE levels of OCPs

A

Phenytoin
Carbamazepine
Phenobarbital
Primidone

*Use alternative methods of contraception

29
Q

AED that are affected by OCPs

A

Lamotrigine –> Estrogen reduces lamotrigine level

30
Q

Teratogenicity and AED

A

Increased risk for major congenital malformations, 2-3x higher

Risk for lower IQ

VPA avoided in monotherapy or polytherapy in first trimester

31
Q

Safest medications in Pregnancy

A 
lamtorigine
levetiracetam
oxcarbazepine
zonisamide 
Gabapentin

Less: CBZ, PHT

32
Q

VNS Approval Indications

A
  1. Adjunctive therapy for pts >/= 12 years with refractory focal onset epilepsy
  2. Adjunctive therapy in pateints >/= 18 years with chronic or recurrent major depression episodes refractory to >4 adequate antidepressant
33
Q

AED success rates in patients

A

Focal epilepsy 50%

Primary Generalized epilepsy 80%

34
Q

Definition for refractory Epilepsy

A

Failure of adequate trials of two appropriate and tolerated doses of two appropriate and tolerated AED at maximum possible doses (in monotherapy or combination) for enough time

Enough time = f/u period of 3x longest interseizure interval

35
Q

Clinical Indications for VNS

A 
Refractory focal seizures not eligible for brain surgery
Multifocal epilepsy
Unclear seizure focus
Overlapping eloquent cortex
Opposed to surgery
36
Q

Efficacy of VNS

A

18.75% of patients had >/= 50% reduction in in seizure frequency

37
Q

VNS Lead placement

A

Lead must be placed below where the superior and inferior cervical cardiac branches separate from the Left vagus nerve.
- Stim of these nerves may cause bradycardia and/or asystole
Main vagus nerve is the largest of the three nerves

38
Q

VNS electrode polarity

A

Bipolar lead transmit stim from the generator to the left vagus nerve

Lead consists of a pin that connects to the generator on one end and helices contain the stimulation and electrodes and anchor tether on the other end

39
Q

VNS clinical trial

A

High group - signficant seizure reduction compared with baseline and LOW group

In High group - 31% of pts had >50% seizure reduction
In low group - 13% of pts had >50%

40
Q

Side effects of VNS

A

In order of most common:

  1. Hoarseness -> due to device malfunction, nerve constriction, nerve fatigue
  2. Dyphagia/cough
  3. Dyspnea -esp with COPD/asthma
  4. OSA - esp during stim
  5. Nerve damage/pain
  6. Laryngeal irritation
  7. Lead break
  8. Trauma to VN
  9. SUDEP = not any difference than population
    10: Twiddler syndrome - damage or disconnect
41
Q

VNS parameters

A

Output current
Signal frequency
Pulse width
ON/OFF time

42
Q

What VNS settings can cause degeneratve damage

A

High frequency (>50Hz) + ON time&raquo_space; OFF time

43
Q

Recommended starting parameters for VNS

A

Output current 0.25mA
On time 30s Off time 5min
Signal frequencies 20-30 Hz
Pulse width 250-500u

44
Q

How do you optimize VNS?

A

Increase output current

Modifying on or off time

45
Q

How do you manage side effects?

A

Decreasing signal frequencies 30 ->20 Hz
Decreasing output current (by 0.25mA)
If this doesnt achieve tolerability, lowering the pulse width 500 > 250uS.

46
Q

MRI and VNS

A

VNS is MRI compatible
Before going to MRI –> need to set outptu current and magnet current to 0mA.
When MRI is done –> need to reprogram

47
Q

Mechanism of Action of VNS

A

Unknown, but possibly

  • Affect heart rated and respiratory rate
  • Vagus-initiated activity in the brain has been localsed through fos1 immunoreactivity
  • Regional brain glucose metabolism
48
Q

Investigational neurostimulators

A

DBS and RNS

49
Q

RNS

A

Responsive neurostimulation
-short trains of electrical stim can stop after discharges

Candidates:

  1. Focal seizures in eloquent cortex
  2. bilateral MTS
50
Q

RNS Efficacy

A

Trials
12 weeks after: 37.9% had seizure reduction (compared to sham 17.3%
5 months postimplantation - 41.5% seizure reduction (compared 9.4%)

Open label:
50% responder rate seen in 55% of patients
44% responders at 1 year
53% at 2 years

51
Q

SANTE Trial for DBS

A

DBS in focal epilepsy patients (with baseline 19.5 sz/month)
Implantation in the anterior nucleus of the thalamus
3months - 1/2 received stim vs no stim
Last month, simulated group had 29% greater seizure reduction compared to control

Epilepsy Board Study (8 decks)

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