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Epilepsy Flashcards

1
Q

What is a seizure?

A

Burst of electrical activity

Can originate in one spot (focal onset) or can occur in a broad, bilateral network (generalised onset)

Can originate focally and spread bilaterally and impair awareness

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2
Q

How to categorise seizures?

A

Focal

Focal to generalised

Generalised

Aware or impaired awareness

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3
Q

What is epilepsy?

A

2 or more provoked seizures that are more than 24h apart (can’t be more than 2 years apart)

OR

Single unprovoked seizure and a probability of further seizures if >60%

OR

Single seizure or other characteristics of an epilepsy syndrome

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4
Q

What is the chance of having a second seizure after 1st unprovoked seizure?

A

50% by 5 years (unchanged by medication)

> 60% if x2 or more seizure (medication does improve seizure recurrence)

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5
Q

What is an acute symptomatic seizure?

A

Provoked seizures that aren’t epilepsy

Febrile seizures (0.5-6 years old)
ETOH withdrawal seizures
Metabolic seizures (sodium, calcium, magnesium, glucose, oxygen)
Toxic seizures (drug reactions or withdrawal, renal failure)

Don’t need medication
Just remove the insult

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6
Q

How do you assess the probability of another seizure occuring?

A

EEG abnormalities
Abnormal neuro exam including intellectual disability
Structural abnormality presumed to have caused seizure

Consider AED

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7
Q

DDx of seizures

A 
Syncope
Migraine
Sleep disorder
Movement disorder
TIA
PNES
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8
Q

Tests to consider in seizures

A

1) EEG
- Only detects epilpetiform discharges up to 30%. Slightly increased in sleep deprived, and dramatically increased in prolonged study
- Can’t rule out epilepsy

2) MRI
- Structural abnormality. Look at the hippocampus for hippocampal sclerosis
- CT is good for looking at gross abnormality but won’t see subtle things

3) Genetics
- Not routinely done
- Constellation of symptoms including intellectual disability, dysmorphic features
- They might fit a syndrome

4) Functional imaging (brain PET, SPECT, CT perfusion, functional MRI)
- Not routinely done
- more specialist testing, to try localise a lesion and when considering surgery

5) Neuropsych

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9
Q

Juvenile myoclonic epilepsy

1) Age
2) Presentation
3) Trigger
4) EEG

A

Most common genetic epilepsy
Accounts for 10% of all epilepsy cases
Onset in adolescence (12-18 years)
Myoclonus usually in AM (can cause people to fall over or drop things; often people don’t realise) + GTCS +/- absence seizures

Combination of myoclonus and GTCS should make you think of this

Photosensitivity in up to 40% (triggers seizures)

Atypical spike wave discharges (4-6Hz)

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10
Q

Juvenile absence epilepsy

1) Age
2) Presentation
3) EEG

A

Onset in adolescence (10-12 years old)
Absence seizures + often GTCS
3Hz spike wave discharges typical; often activated by hyperventilation

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11
Q

Most common area of onset of focal epilepsy

A

Temporal lobe

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12
Q

How do focal temporal lobe focal epilepsy present?

A 
1) Aura
Rising epigastric sensation 
Fear/anxiety DDx panic attacks
Deja vu/jamais vu 
Autonomic symptoms
Olfactory or gustatory symptoms

2) Often followed by behavioural arrest/impaired awareness
Automatisms (lip smacking, repetitive hand movements)
Motor features

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13
Q

Management of seizures

A
  • Avoid risk factors - sleep deprivation, ETOH (seizure typically the following day), stress, missing medications, specific triggers (light, bright sunshine)
  • Seizure safety - around water, heights, heavy machinery
  • Driving (Austroads guidelines) - usually need 6 month seizure free period in first seizure
  • Medication
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14
Q

What do AEDs do?

2 main mechanisms

A

1) Block excitation (glutamate)
2) potentiate inhibition (GABA)

In reality, AEDs work on many targets

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15
Q

List broad spectrum AEDs

A 
Valproate
BZA
Keppra
Topiramate
Phenytoin
Lamotrigine
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16
Q

List AEDs for focal seizures

A 
Carbamazepine
Oxcarbamazepine
Lacosamide
Lamotrigine
gabapentin
Phenytoin
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17
Q

List AED for absence seizure

A

Ethosuxamide

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18
Q

What to use in juvenile myoclonic epilepsy?

A

Very responsive to valproate

Keppra + Lamotrigine can be used in first line rather than valproate in female (but teratogenic)

Lamotrigine may worsen myoclonus so avoid if prominent feature

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19
Q

When is someone with epilepsy considered to be in remission?

A

Seizure-free for the last 10 years, with no seizure medication for last 5 years

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20
Q

Contraception in epilepsy

A

Long-acting reversible contraceptive rather than OCP due to drug interactions

Choose less teratogenic AED even prior to fertility planning

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21
Q

Which AEDs are safe in pregnancy?

A

Safer to not safe

Lamotrigine, levetiraectam (still increased risk of clef palate)

Carbamazpine, oxcarbamazepine, zonisamide

Phenytoin, phenobarbitone, topiramate

Valproate (high teratogenicity, probably a dose dependent effect)

Use lowest dose possible

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22
Q

How to monitor seizures/AED use in pregnancy?

A

Continue at lowest dose required to control seizures
Clearance of drugs (LTG/LEV) increases in 3rd trimester
Monitor levels weekly and titrate accordingly

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23
Q

How effective are AEDs in reducing further seizures?

A

Adding 1 agent reduces seizures by 50%, adding 2nd agent reduces it by a further 20%… not much use adding 3rd agent

So if still having seizures after 2 agents, need specialist referral

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24
Q

Which AED to use in people with concurrent behaviour/psych problems?

A

Sodium valproate, lamotrigine

Avoid Levetiracetam, (can cause sedation especially in the elderly)

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25
Q

Which AED to use in people with concurrent migraine?

A

Topiramate, valproate

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26
Q

Risk of SJS/hypersensitivity reaction in Asian population with ….

A

CBZ (can test HLA B1502)

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27
Q

… can cause weight gain. Caution in metabolic syndrome and PCOS

A

Sodium valproate

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28
Q

… can cause arrhythmias especially IV

A

Phenytoin

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29
Q

Beware of CYP450 inducers - can reduce levels of other AED or contraception or DOAC

Examples?

A

CBZ, phenytoin, phenobarbitone

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30
Q

Beware of CYP450 enhancers - will increase levels of other AEDs; particularly LTG - can work synergistically

Example?

A

Valproate

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31
Q

GTCS features

A
  • 2 phases - tonic and clonic
  • Apnoea during and after
  • Typically 1-4 minutes
  • Impaired consciousness
  • No recollection until ambulance or ED
  • Tongue biting, shoulder dislocation
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32
Q

Absence seizures features

A
  • Children and teenagers
  • Brief impaired awareness
  • 2-10 seconds
  • Don’t lose postural tone. Continue to sit upright
  • May get some facial twitching
  • Immediate offset
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33
Q

Myoclonic seizures

A
  • Subtype of generalised seizures
  • Sudden, involuntary muscle twitch/jerks usually with preserved consciousness
  • Common in sleep especially in falling asleep, metabolic encephalopathy (e.g. ETOH, CO2), opioid use
  • Usually posture/action related (when they have their arms up or when they’re standing up)
  • May appear as prodrome to GTCS
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34
Q

What are the 2 types of focal seizures?

A

Simple focal (without impaired awareness)

Focal seizure with impaired awareness

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35
Q

How do the following common patterns of focal seizures present?

1) Temporal lobe
2) Frontal lobe
3) Parietal lobe
4) Occipital lobe

A

1) Chemical noxious smell, deja vu, copper taste, helicopter noise, ringing, whistling, distorted noise

2)
Localised tonic jerking (particularly in face, hand due to large cortical representation)

Hypermotor activity such as paddling or cycling, pelvic thrusting, commonly during sleep or on waking

3) Somatosensory
4) Evolving coloured shapes (funny colourful shapes, lights, not usually in any identifiable form), usually in one hemisphere and can potential spread, can last hours

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36
Q

How do you differentiate between focal seizure with impaired awareness and absence seizures?

A
  • Fewer of them 1-2/month vs 200/day
  • Longer
  • Much more gradual offset
  • Preceding focal seizure symptoms may be experienced/recollected

Other features

  • Staring/motor arrest
  • Automatism - chewing, lip smacking, repetiive hand movements
  • Depth of impaired consciousness variable - may still follow commands, or respond, or drive (familial motor tasks)
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37
Q

What’s secondary GTCS?

A

Focal onset –> GTCS

E.g. starts with noxious smell or deja vu before convulsive episode

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38
Q

What features during an attack would favour seizures?

A 
Tongue biting
Head turning
Unusual posturing
Urinary incontinence 
Cyanosis
Post-ictal confusion, headache
No recollection of events just prior to seizure
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39
Q

What’s a reasonable AED to try in someone with first focal seizure and high risk of recurring seizure?

A

Carbamazepine

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40
Q

What’s a reasonable AED to try in someone with a first generalised seizure and high risk of recurring seizure?

A

Sodium valproate (but avoid in females of childbearing potential)

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41
Q

… is most likely to cause cosmetic changes

A

Phenytoin
Hirsutism, gingival hyperplasia, coarser facial features

Sodium valproate can cause hair loss

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42
Q

What is Todd’s paresis?

A

When you get lateralised or localised weakness of limbs mimicking an acute stroke following an unwitnessed seizure

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43
Q

How to differentiate between myoclonic and clonic seizures?

A

Clonic seizures are repetitive jerking movements

Repetitiveness differentiates from myoclonic seizures

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44
Q

Describe tonic seizures

A

Co-contraction of agonist and antagonist musculature
<15 seconds
With or without vocalisation
Falls

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45
Q

Describe atonic seizures

A

Loss of muscle tone and falls

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46
Q

List AEDs that are sodium channel blockers

A 
Lamotrigine
Carbamazepine
Oxcarbamazepine
Phenytoin
Lacosamide 
Topiramate
Zonisamide
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47
Q

List AEDs that are GABA enhancers

A

PB
Clobazam/clonazepam
VPA
Topiramate

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48
Q

List AEDs for generalised seizures

A

Valproate
Levetiracetam
Lamotrigine

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49
Q

Avoid … in hepatic disease

A

Sodium valproate

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50
Q

Avoid … in renal disease

A

Pregabalin
Gabapentin
Levetiracetam
Renally excreted

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51
Q

Which AED to avoid in those with insomnia?

A

Lamotrigine

If it can’t be avoided, take it mane

52
Q

Which AED to use in those with concurrent movement disorders?

A

Avoid valproate in those with tremors

Use CBZ in those with chorea

53
Q

Which AEDs to avoid in those with cognitive isuses?

A

Topiramate

Phenobarbitone

54
Q

Which AEDs to avoid in those with concurrent haematological issues?

A

Avoid VPA - can cause thrombocytopenia

Avoid carbamazepine - agranulocytosis. Also hypoNa+

55
Q

List 2 AED combinations that should be avoided

A

1) Phenytoin + CBZ = induce metabolism of each other
2) PB + VPA = lead to increased levels of PB and PB toxicity; PB can also induce metabolism of VPA and reduce its efficacy

56
Q

Which AED combination is synergistic?

A

LTG + VPA

Can use less dose of either

57
Q

List AED that has synaptic vesicle 2A action

A

Levetiracetam

58
Q

Which AED doesn’t need titration?

A

Phenytoin

59
Q

Which 2 AEDs have non-linear kinetics?

A

Linear kinetics = as you increase the dose, the serum drug conc also increases

Phenytoin = as you increase the dose, it saturates its own metabolism, so any increase beyond 300mg will cause disproportionate rise in serum –> toxicity

Gabepentin = as you increase the dose, it saturates the absorption mechanism in the gut –> serum conc falls

60
Q

What happens when you have high serum conc of phenytoin >30mg/L?

A

Paradoxical increase in seizures

Non-linear kinetics

61
Q

How long do most seizures last?

A

3-5 minutes

62
Q

What is considered status epilepticus?

A

> 5 minutes
less likely to end without intervention

Prognosis worsens with increasing duration. Time is brain!

63
Q

What’s generalised vs focal seizures?

A

Generalised - originate at some point but rapidly spreads to bilateral networks

Focal - comes from a specific area, limits to one hemisphere, can spread to widespread networks –> can transition to bilateral tonic clonic

64
Q

What’s atonic seizures?

A

Drops to the ground and lose tone

Usually kids

65
Q

What’s an absence seizure?

A 
Generalised seizure
3Hz on EEG
A very specific seizure type 
5-10sec
The longer it goes, the more automatism there is e.g. lip smacking etc
66
Q

Where in the tongue do people bite during seizure?

A

Side of the tongue

Due to the force of the clench during a seizure

67
Q

Is incontinence common in seizure?

A

Yes but not specific, can happen in syncope

Faecal incontinence is very rare but more likely in syncope

68
Q

What’s an acute symptomatic seizure?

A

Provoked

  • Can be structural or metabolic
  • E.g. SAH, stroke, TBI, meningitis
  • E.g. ETOH withdrawal, hypoglycaemia, hypoNa+, uraemic encephalopathy, chronic liver disease
69
Q

DO you treat acute symptomatic seizure?

A

Rx: Reverse cause. May not require AED.

Consider AED if likely to have ongoing seizures

70
Q

Juvenile absence epilepsy

A
  • Genetic epilepsy
  • Onset 8-12 years
  • Children with normal development
  • Absence seizures and occasional GTCS
  • Ceased in the late teens
  • Rx: valproate
71
Q

Juvenile myoclonic epilpesy

A
  • Genetic epilepsy
  • ICK gene identified
  • Onset 12-18 years
  • Children with normal development
  • Myoclonus is a predominant features on waking (clumsy, dropping their cereal bowls) + 90% GTCS + 30% absence seizures
  • Worse with sleep deprivation + ETOH (think college students)
  • EEG 3Hz spikes/polyspike-wave discharges
72
Q

EEG for juvenile myoclonic epilepsy

A
  • EEG 3Hz spikes/polyspike-wave discharges (increased with photic stimulation and hyperventilation)
73
Q

Rx juvenile myoclonic epilepsy

A

Valproate 1st line
Lamotrigine (women of child bearing age)

Can have very good control

Can’t come off medications. High relapse rate

74
Q

Risk factors for Mesial temporal lobe epilepsy with hippocampal sclerosis

A

Risk factors: prolonged febrile convulsions, CNS infection

Single most common form of epilepsy

75
Q

EEG can help demonstrate

A

Encephalopathy

Seizures - focal vs generalised

76
Q

MRI findings for Mesial temporal lobe epilepsy with hippocampal sclerosis

A
  • MRI: unilateral or rarely bilateral hippocamapl atrophy and T2 signal increase
77
Q

Presentation for Mesial temporal lobe epilepsy with hippocampal sclerosis

A
  • Typical auras, focal seizure with impaired awareness +/- automatism
  • Dreamy states with deja vu/jamais vu, gustatory or olfactory hallucinations, epigastric rising sensation
  • Can evolve to bilateral TC seizures
78
Q

Rx Mesial temporal lobe epilepsy with hippocampal sclerosis

A

Rx surgery for medically refractory in 60-90%

79
Q

Most common form of epilepsy

A

Mesial temporal lobe epilepsy with hippocampal sclerosis

80
Q

When to start AED?

A
  • After 2 seizures (>24h or <2 years apart)
  • After 1 seizure at >60% of having a second seizure
  • If further seizures are expected to be severe or in a vulnerable population (fragile elderly patients)
81
Q

Rx focal seizures

A

Carbamazpine is 1st line
- lots of AE, especially bad for elderly
Lamotrigine (not PBS)
- Takes time to push dose up

82
Q

Rx generalised seizures

A

Valproate

Lamotrigine (first line for women of child-bearing age)

Other - Keppra

83
Q

Rx absence seizure

A

Valproate
Ethosuximide

Other - Keppra

84
Q

Rx if unknown seizure semiology

A

Valproate

85
Q

Asians and carbamazpine. What’s the problem?

A

100% of those exposed and with SJS are HLAB*1502 positive

Must do genotyping in people from Asia before starting

86
Q

Rash on carbamazepine

A

Stop it

Likely to get a rash with phenytoin, oxcarbamazepine, phenobarbitone, lamotrigine

87
Q

Which AEDs can you load?

A

You want to load in those that have recurrent seizures in a short time

Phenytoin, levetiracetam, valproate

Otherwise, start low, go slow in other cases. Aim seizure free with the lowest dose possible.

88
Q

When do you check AED serum levels?

A

Most people can be seizure free at a “subtherapeutic” level. Do not titrate dose based on level.

Take a level when someone is seizure free - this level is specific to the patient and will act as the goal.
In the future, if their pharmacodynamics change e.g. pregnancy, you can measure the level again to aim this level.

Take the level to check toxicity.

Take the level to check drug compliance.

89
Q

Carbamazpine and HLA A*3101

A

Hypersensitivity reaction in European

Not as severe as HLAB*1502 in Asians

90
Q

When do you check AED serum level?

A

At steady state
4-5 t/12 after starting dose (especially with carbamazpine that autoinduces itself - need to wait until it reaches SS)

Take trough level (just before next oral dose)

91
Q

When someone fails their AED, what do you do?

A

Check compliance and that you have the right dx
Reach optimal dose
Gradually switch to another monotherapy (downtitrate one, while uptitrating another)
May go to dual
- Don’t combine drugs from the same class
- Lamotrigine + valproate is synergistic

92
Q

What’s drug resistant epilepsy?

A

When you have after adequate trials of at least 2 appropriate AEDs, given alone or in combination

Refer to an epilepsy unit (live there for 7 days and they monitor you)
Consider surgery?

93
Q

Contraception and AED

A

Most AEDs are inducers that lead to rapid clearance of normal contraception
Lamotrigine is the only exception - levels are lowered by hormonal contraception

Consider IUD or progestin implant

94
Q

Do you get less seizures during pregnancy?

A

No change in seizure frequency during pregnancy and post-partum

Most pregnancy women require dose changes of AED

95
Q

Is monotherapy better in pregnancy?

A

Yes
Polytherapy is much worse

Lamotrigine and carbamazepine and keppra are safe monotherapy

96
Q

Dose change in pregnancy

1) Lamotrigine
2) Keppra
3) Carbamazepine

A

1) Increased clearance –> must increase dose
2) Increased clearance –> must increase dose
3) Nothing

97
Q

SUDEP (sudden death)

A
  • Usually affects young people with convulsive seizures
  • Death occurs at night (80% unwitnessed)
  • Risk factors
    > GTCS >2 years
    > Nocturnal seizures
    > Treatment resistant seizures
    > Long duration of epilepsy and early age of onset
    > Dravet syndrome - Na+ channel gene mutation
98
Q

Epilepsy and psychosis when does it happen?

A

Can be inter-ictal, intra-inctal (very rare) and post-ictal

Inter-ictal

  • Looks like schizophrenia
  • RF: temporal lobe epilepsy (bilateral), early age of onset, refractory course
  • Responds to antipsychotics

Post-ictal

  • Focal epilpesy with impaired awareness, sometimes with bilateral TC seizures. Cluster of seizures. Completely return to baseline then 12-72h later, you develop psychosis
  • May last up to weeks
99
Q

Status epilepticus and mortality

A

> 30 minutes are unlikely to terminate spontaneously and have increased mortality +++

More status epilepticus –> more brain damage –> more seizures

100
Q

How long is considered status epilepticus?

A

> 5 minutes or 2 or more seizures between which there is incomplete recovery of consciousness

101
Q

Rx status epilepticus

A

1st line
IV lorazepam 2-4mg (fasting acting and superior) or IM midazolam 10mg
Repeat if needed
BZD terminates the seizure

2nd line
Phenytoin or
Sodium valproate or
Keppra or
Phenobarbitone or
Propofol

3rd line
intubate
Midazolam infusion
Propofol

4th line
Pentobarbital

Airway management and oxygenation
Intubation
Check BSLs and electrolytes
Thiamine if suggestive history and give glucose

102
Q

Non-convulsive status epilepticus

Presentation

A

Can happen after convulsive seizure or independent of one
Drowsy, behavioural/cognitive change, and never back to baseline

Not life threatening but prolonged can lead to neuronal damage and should be treated quickly

103
Q

Non-convulsive status epilepticus

Increased risk if?

A

Increased risk if

  • Known history of epilpesy
  • Stroke/structural abnormality
  • BZD withdrawal
104
Q

How to pick up Non-convulsive status epilepticus?

A

Only way to pick this up on EEG

105
Q

Rx non-convulsive status epilepticus

A

Rx
BZD and AED
Don’t need to treat aggressively. Try to avoid intubation.

106
Q

Lateral tongue biting vs tip of tongue biting

Seizure or syncope?

A

Lateral: seizure

Tip of tongue: syncope

107
Q

How good is EEG?

A

40% yield

72h EEG - 85-90% yield

108
Q

General mechanism of AEDs

A

Fast and slow Na+ open –> Ca2+ comes in to presynaptic region –> synaptic vesicle binds to dock –> lets NT out on synapse –> acts on post synaptic receptor

GABA acts on GABA receptor = inhibitory
Glutamate acts on NDMA/AMPA receptors = excitatory

109
Q

Enzyme inducer P450 AEDs

A 
PHT
PB
Primodone
CBZ
OXC
TPM

Make OCP not work!

110
Q

Enzyme inhibitor P450 AEDs

A

VPA

111
Q

Bad AED combinations

A

Lacosamine (slow Na+ channel blocker)
AND
LTG/CBG/PHT (fast Na+ channel blocker)

Neurotoxicity

112
Q

Good AED combinations

A

VPA + LTG (synergistic)

113
Q

1st line focal epilepsy

A

CBZ

P450 enzyme inhibitor
Can accelerate bone loss

114
Q

1st line generalised epilepsy

A

VPA

Avoid in young women

115
Q

Perampanel MOA (new drug)

A

MOA: non-competitive antagonist at one of the glutamate receptors. By binding to the post-synaptic AMPA-glutamate receptor, perampanel is thought to reduce glutamate-induced neurotransmission.

AE: treatment emergent dizziness (take it before you go to bed)

116
Q

Lacosamine MOA and AE

A

Enhances slow Na+ channels

AE: PR prolongation (do ECG first)

117
Q

Clobazam - how does it compare to other BZD?

A

Less anxiolytic effect and drowsiness

Good add on for sleep onset epilesy

118
Q

Brivaracetam - how does it work?

A

Works on SVTA protein but with 30% greater affinity than levetiracetam
Less psychiatric side effects

119
Q

Epilepsy surgery?

A

NNT = 2
Works very well if you have the right candidate
Refer early! Early workup is associated with better outcome, rather than trying multiple lines of therapy

Temporal lobe epilepsy, hippocampal sclerosis and drug resistant

120
Q

Sudden unexpected death in epilepsy (SUDEP)
Who gets it?
How common?

A

Affects young people 18-45

More likely to occur in people that have had seizures for a long time, but can happen after 1-2 seizures

More likely in GTCS

Unknown MOA
?Respiratory dysfunction
?Cardiac arrhythmia
?Central depression of both resp and cardiac dysfunction (prolonged slowing after seizure)

1 in 1000 adults every year
1in 4500 children every year

121
Q

Teratogenic effects of AEDs are dose dependent

True or false

A

True
Use the lowest dose possible
Utilise synergy if valproate really required - valproate (small dose) + lamotrigine (large dose)

122
Q

Topiramate is teratogenic. True or false

A

True
Moderate effect
Causes cleft palate

123
Q

What should pregnant women also be on if they’re on AEDs?

A

Folic acid 5mg

124
Q

Which 2 drugs levels need to be monitored in pregnancy?

A

Lamotrigine
Levetiracetam

Estrogen induces metabolism of lamotrigine in 2nd/3rd trimester –> lamotrigine levels drop

Levetiracetam is renally cleared. As blood volume increases during pregnancy, GFR also increases, levetiracetam levels drop.

125
Q

How do OCP and lamotrigine interact?

A

OCP can reduce the level of lamotrigine

Do a level before starting the OCP… increase dose of lamotrigine accordingly

126
Q

How to distinguish between convulsive syncope vs seizure?

A

Convulsive syncope - flaccid then twitch, much quicker recovery, tongue tip biting

Seizure - tonic clonic, slower recovery, side tongue biting

Neuro (9 decks)

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