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Patient Semester 2 > Epilepsy > Flashcards

Epilepsy Flashcards

1
Q

Incidence/prevalence of epilepsy?

A

50 per 100,000 diagnosed each year
approx 1 in 100 people in the UK have it

most commonly presents in children and the elderly

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2
Q

Prognosis of epilespy?

A

up to 70% can become seizure free
50% can withdraw medicatiom
20-30% will continue to have seizures despite treatment

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3
Q

Mortality of epilepsy?

A

2-3x higher than general population
can be due to accidents not just the disease (indirect)
sudden unexpected death in epilepsy (more common in generalised tonic clonic and poor seizure control)

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4
Q

How many different types of epilepsy?

A

over 40

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5
Q

Definition of a seizure?

A

episode of neurological dysfunction of abnormal firing of neurones manifesting as changes in motor control

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6
Q

Definition of epilepsy?

A

Condition of recurrent, spontaneous seizures arising from abnormal, synchronus and sustained electrical activity in the brain

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7
Q

Aetiology of epilepsy?

A
  • idiopathic epilepsy: genetic cause
  • symptomatic epilepsy: e.g. head injury or stroke
  • up to 50% have no apparent cause
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8
Q

What is the first step of epilepsy diagnosis?

A

establish if paroxysmal event was actually a seizure

acute symptomatic seizure? e.g. head injury, infection, imbalance etc

Non-epileptic attack from syncope, encephalitis, migraine?

witnesses are very helpful

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9
Q

Updated NICE guidelines on diagnosis of epilepsy?

A

must be made by a specialist (i.e. neurologist) as other doctors had an even worse misdiagnosis rate

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10
Q

What is the clinical decision of epilepsy diagnosis based on?

A
  • desrcription of attack (footage, witness)
  • family history (genetic cause)
  • blood tests
  • ECG (cardiac cause/syncope?)
  • Medication history - illegal drugs can cause seizures, overdose of some drugs can cause seizures, many commonly prescribed drugs can lower seizure threshold)
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11
Q

Tongue biting pattern of seizures?

A

tonic clonic seizures - patients tend to bite the sides of their tongue

tip of tongue - generally non-epileptic attack disorder

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12
Q

Which drugs can lower seizure threshold?

A

SSRIs, tricyclics, quinolones, tramadol

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13
Q

Importance of imaging in epilepsy diagnosis?

A

MRI preferrred to CT - can see structural abnormalities

important in <2s and adults who develop seizures (see a treatable cause)
should be performed within 4 weeks

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14
Q

Role of EEGs in epilepsy diagnosis?

A

should never be used in isolation
main use is to classify the epilepsy for correct treatment

however: 10% epileptics have normal EEGs, and 2-4% healthy people have abnormal EEGs

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15
Q

Principles of classification of seizures?

A
  • depend on the location and focus on the pathway involved
  • patients can have more than one type of seizures
  • failure to classify correctly can lead to inappropriate treatment and therefore treatment failure
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16
Q

Two main types of seizures?

A

Partial and generalised seizures

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17
Q

Types of partial seizures?

A
  • simple partial seizures (maintain consciousness)
  • complex partial seizures (lose consciousness)
  • with secondary generalisation
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18
Q

Types of generalised seizures?

A
  • tonic/clonic (muscles spasm in tonic, then limb shaking in clonic)
  • absence
  • myoclonic
  • atonic
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19
Q

Common seizure triggers?

A

fatique, lack of sleep, stress, excess alcohol, flashing lights, excitement, menstruation, missing meals, some medications

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20
Q

NICE guidelines for treatment of epilepsy?

A
  • always intiated by a specialist after diagnosis
  • monotherapy to start (low and slow)
  • adjunctive treamtent only if monotherapy has failed
  • AEDs are not usually started after first seizure
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21
Q

Ideal epilepsy therapy aim?

A

Single drug
lowest possible dose
minimum side effects

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22
Q

Patient factors that contribute to choice of drug for epilepsy?

A
  • epilepsy syndrome
  • seizure type
  • co-morbidity
  • lifestyle
  • gender, age
  • preferences of individual/carers
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23
Q

Drug factors that contribute to choice of drug epilepsy?

A
  • side effect profile
  • dose
  • formulation
  • treatment schedule
  • interactions
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24
Q

First line drugs for tonic-clonic seizures?

A

carbamazepine, lamotrigine, sodium valproate, oxcarbazepine

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25
Q

Adjunctive drugs for tonic-clonic seizures?

A

Clobazam, lamotrigine, levetiracetam, sodium valproate, topiramate

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26
Q

Drugs that may worsen tonic-clonic seizures?

A

Carbamazepine, gabapentin, oxcarbazepine, phenytoin, pregabalin

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27
Q

First line drugs for tonic or atonic seizures?

A

Sodium valproate

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28
Q

Adjunctive drugs for tonic or atonic seizures?

A

Lamotrigine

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29
Q

Drugs that may worsen tonic or atonic seizures?

A

Carbamazepine, gabapentin, oxcarbazepine, pregabalin

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30
Q

First line drugs for absence seizures?

A

Ethosuximide, lamotrigine, sodium valproate

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31
Q

Adjunctive drugs for absence seizures?

A

Ethosuximide, lamotrigine, sodium valproate

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32
Q

Drugs that may worsen absence seizures?

A

Carbamazepine, gabapentin, oxcarbazepine, phenytoin, pregabalin

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33
Q

First line drugs for myoclonic seizures?

A

Levetiracetem, sodium valproate, topiramate

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34
Q

Adjunctive drugs for myoclonic seizures?

A

Levetiracetem, sodium valproate, topiramate

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35
Q

Drugs that may worsen myoclonic seizures?

A

Carbamazepine, gabapentin, oxcarbazepine, phenytoin, pregabalin

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36
Q

First line drugs for partial seizures?

A

carbamazepine, lamotrigine, sodium valproate, oxcarbazepine, levetiracetem

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37
Q

Adjunctive drugs for partial seizures?

A

carbamazepine, lamotrigine, sodium valproate, oxcarbazepine, levetiracetem, clobazam, gabapentin, topiramate

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38
Q

Dosing info for sodium valproate?

A

600mg/day in 1-2 divided doses gradually increased every 3 days

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39
Q

Dosage forms of sodium valproate?

A

EC tablets, MR tablets, liquid, granules, IV

IV is equivalent to oral doses

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40
Q

Monitoring requirements for sodium valproate?

A

signs of liver, blood and pancreatic disorders

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41
Q

Side effects of sodium valproate?

A

nausea, gastric irritation, diarrhoea, weight gain, hair loss

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42
Q

Who is sodium valproate not suitable for?

A

Women of childbearing age, risk of serious neurodevelopment effects

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43
Q

Dosing info for carbamazepine?

A

Initially 100-200mg 1-2 times daily, increased slowly every 2 weeks

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44
Q

Monitoring requirements for carbamazepine?

A

blood liver and skin disorders

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45
Q

Dosage forms of carbamazapine?

A

oral and PR

125 suppository is equiv to 100mg orally

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46
Q

How is carbemazepine metabolised?

A

CYP3A4 - so susceptible to DDIs. potent inducer

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47
Q

Side effects of carbamazepine?

A

Headache, nausea/vomiting, drowsiness, dizziness, rash, ataxia, hyponatraemia

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48
Q

How can the side effects of carbamazepine be managed?

A

They are dose related and can be dose limiting

can be reduced using MR tabs

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49
Q

Dosing info for lamotrigine?

A

Initially, 25mg/day and slowly titrated every 2 weeks

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50
Q

Side effects of lamotrigine?

A

Nausea/vomiting, diarrhoea, dry mouth, skin reactions

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51
Q

How to manage the skin reactions with lamotrigine?

A

more common in the first 8 weeks or when also on valproate

increase dose slowly

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52
Q

Use of lamotrigine in pregnancy?

A

Considered the safest AED for pregnancy

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53
Q

Dosage forms of lamotrigine?

A

Oral only

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54
Q

Dosing info for levetiracetam?

A

250mg/day, increased every 1-2 weeks to max 1.5g BD

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55
Q

How is levetiracetam metabolised?

A

very little, so no CYP450 interaction

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56
Q

Dosage forms of levetiracetam?

A

oral and IV

good oral bioavailability, so no dose adjustment required between the two

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57
Q

Side effects of levetiracetam?

A

Nasopharyngitis, somnolence, fatigue, dizziness, headache

Low mood, irritability, depression are common reasons for discontinuation

58
Q

Dosing info for phenytoin?

A

Initially 3-4mg/kg/day (usual dose 200-500mg/day)

Dose adjusted according to levels and effect

59
Q

Place of phenytoin in epilepsy treatment?

A

Not recommended by NICE for first line

60
Q

Pharmacokinetics of phenytoin?

A
  • Narrow therapeutic index with saturable kinetics
  • Half life 4-72 hours (depends on dose)
  • Steady state reached after 7-10days
  • Extensive hepatic metabolism
  • Strong inducer of CYP450 - interactions
  • Highly protein bound – albumin
  • Interactions with enteral feeding
61
Q

Phenytoin dosage forms and how to interchange?

A

Capsules and IV - phenytoin sodium
Liquid and chewable tablets - phenytoin base

92mg phenytoin = 100mg phenytoin sodium

62
Q

Side effects of phenytoin?

A

N+V, constipation, drowsiness, parasthesia, gingival hyperplasia, acne, hirsuitism, coarsening of facial features

63
Q

Signs of phenytoin overdose?

A

Nystagmus (involuntary eye movements), ataxia, diplopia (double vision), slurred speech, confusion, hyperglycaemia

64
Q

What is the desired phenytoin plasma concentration?

A

10-20mg/L

65
Q

MHRA categories for antiepileptics for supply - category 1?

A

Includes phenytoin, carbamazepine, phenobarbital,

Specific measures are necessary to ensure consistent supply of a particular product

66
Q

MHRA categories for antiepileptics for supply - category 2?

A

Includes sodium valproate, lamotrigine, oxcarbazepine

The need for continued supply based on clinical judgement

67
Q

MHRA categories for antiepileptics for supply - category 3?

A

Includes levetiracetam, lacosamide, gabapentin

No specific measures required

68
Q

Important points when giving antiepileptics to women?

A
  • Antiepileptics interact with hormonal medications
    Can reduce effectiveness as enzyme inducers
    E.g. Carbamazepine, phenytoin
    Oral contraceptives and EHC can reduce effectiveness of lamotrigine.
    May need to increase dose of lamotrigine
  • Some AEDs are teratogens/can cause birth/developmental defects
  • These drugs are to be avoided in women of childbearing potential and pregnant women
  • Pharmacokinetics can be altered in pregnancy
  • All women on AEDs should be offered folic acid 5mg OD before any possibility of pregnancy
  • Some women have increased seizure frequency around menstruation
  • Side effects of some AEDs may be undesirable
69
Q

Risks when giving antiepileptics to the elderly?

A

Pharmacokinetic and pharmacodynamic issues

  • Polypharmacy
  • Co-morbidity

Consider using lower doses of AEDs

If on carbamazepine, this should be modified release

70
Q

What is status epilepticus?

A

Medical emergency associated with significant morbidity and mortality

Generalised Convulsive Status Epilepticus is defined as a tonic clonic seizure which lasts longer than 30 minutes or repeated tonic clonic seizures within 30 minutes with little or no recovery in between

71
Q

Treatment aims for status epilepticus?

A

Efficient and effective treatment is key

Aim of treatment is seizure termination

72
Q

Treatment for status epilepticus?

A
  • IV Lorazepam 0.1mg/kg (usually 4mg), repeated once after 10-20 minutes if seizure continues
  • Give usual AEDs if already on treatment
  • Alternatives to lorazepam are IV diazepam or buccal midazolam
  • then Phenytoin IV 20mg/kg over 20 minutes (or phenobarbital if already on phenytoin) if still no success

last resort - general anaesthesia

73
Q

What to check if treatment is failing?

A
  • compliance
  • change in brand/formulation?
  • diagnosis - wrong drug for their epilepsy type
  • brain tumour?
  • alcohol/drug misuse
74
Q

How to change drug in case of treatment failure?

A
  • change to second line therapy
  • initiate new drug, titrate up, then wean off old drug
  • never abruptly stop AEDs, risk of rebound seizures
75
Q

What to do if combination therapy doesn’t work?

A

revert to the regimen that provided the best balance of tolerability and efficacy (could me mono or combination therapy)

76
Q

What are the issues with combination therapy in epilepsy?

A
  • drug interactions (many are potent inducers)
  • increased toxicity
  • identifying ADRs
  • non-compliance (increased pill burden and side effects)
77
Q

When is treatment withdrawal suitable?

A
  • seizure free for at least two years

- joint decision by patient, carers and under guidance of specialist

78
Q

How is treatment withdrawal carried out?

A
  • slowly over months
  • one drug at a time if combination therapy
  • plan in place if seizures recur: reverse last dose reduction and seek specialist help
79
Q

What counselling points are important to patients on epilepsy treatment?

A
  • Importance of compliance explained – even when seizure free
  • Dosing schedule and dose titration
  • Signs and symptoms of adverse effects (Blood disorders, Liver dysfunction, Skin disorders)
  • Brands and formulations
80
Q

What are some of the social impacts of epilepsy?

A
  • Employment: cannot be refused but must consider health and safety
  • Driving: must be one year seizure free to drive (also consider side effects)
  • Alcohol: interaction with drugs, can trigger seizures
81
Q

How is childhood epilepsy diagnosed?

A

Same as adults

  • history (description, video, witness)
  • exclusion of other causes (cardiac, structural, metabolic)
82
Q

Non-epileptic causes of childhood seizures?

A
  • febrile seizures
  • trauma
  • metabolic
83
Q

Epileptic causes of childhood seizures?

A
  • primary idiopathic (genetic)
  • secondary (tumour, structural abnormality)
  • neurodegenerative disorders
84
Q

What are paroxysms?

A

‘fully turns’

  • anoxic tonic-clonic seizures
  • breath holding attacks, dramatic tantrums

reflex anoxic seizures arise from cold food, trauma or fright

85
Q

What are febrile seizures?

A

NOT EPILEPSY

  • often a strong family history
  • high incidence (3% of 3 months to 5 years)
  • generalise tonic-clonic
  • short lived, self resolving, associated with high body temperature
86
Q

How to treat febrile seizures?

A
  • reassure and comfort parents
  • cool the child (remove clothing, bedding, reduce heaitng)
  • antipyretics don’t prevent them, cold swabbing no longer recommended
  • maintenance AEDs are not appropriate as will resolve by age 5
  • management of prolonged seizures should follow status epilepticus pathway
87
Q

What is Dravets Syndrome?

A

80% have a mutation in SCN1A gene

88
Q

Characteristics of Dravets Syndrome?

A
  • Intractable seizures
  • developmental delay
  • failure to thrive
  • dysregulated autonomic nervous system (thermoregulation, sweating)

15-20% mortality - as it doesn’t respond to any AEDs

89
Q

Management of Dravets Syndrome?

A
  • Sodium valproate, plus clobazam, plus stiripentol if the first two doesn’t work
90
Q

Treatment goals for Dravets Syndrome?

A

Reduce frequency and severity of seizures

Reduce doses of valproate and clobazam

91
Q

What must we do to valproate and clobazam if steripentol is initiated?

A

Reduce dose - potent inhibitors of CYP2C19, 2D6 and 3A4

92
Q

Mode of action of Stiripentol?

A
  • increase amount of GABA, inhibit metabolism of other AEDs
93
Q

Who is stiripentol licensed in?

A

> 3 years with Dravets Syndrome

94
Q

Formulations fo stiripentol?

A

Oral suspension (sachet) and capsule

sachet has greater bioavailability, so not bioequivalent

95
Q

Starting dose for stiripentol?

A

10mg/kg BD for a week

then 15mg/kg BD for a week

96
Q

Max dose for stiripentol <6 years?

A

increase over three weeks to max 25mg/kg BD

97
Q

Max dose for stiripentol 6-12 years?

A

increase over four weeks to max 25mg/kg BD

98
Q

Max dose for stiripentol >12 years?

A

increase slowly to maximum tolerated dose

99
Q

Why can we increase stiripentol dose quicker in under 6s than 6-12s?

A

Different pharmacokinetics in children

100
Q

How does drug absorption vary between children and adults, and relate to AEDs?

A
  • children have higher gastric pH (5-6 vs 2-3)
  • lower bioavailability of phenytoin than adults (<75% vs 95%)
  • slower gastric motility (reduced peak levels of phenobarbitone, which is rapidly absorbed through the GI tract - increase dose). also slower time to reach peak levels of carbemazepine
  • milk based diets react with AEDs (phenytoin absorption reduced by 35% if administered with enteral feed)
101
Q

How does drug metabolism vary between children and adults, and relate to AEDs?

A
  • Hepatic extraction ratio is much higher - liver surface area is larger relative to their size
  • increased first pass metabolism
  • higher mg/kg dose for carbemazepine and sodium valproate required compared to adults
  • higher expression of 1A2, 2C9 and 3A4 so lower F of substrates of these
102
Q

Results of varying pharmacokinetics on dosing in children of AEDs?

A

Usually higher doses mg/kg than adults

103
Q

Child vs adult dose of valproate?

A

10mg/kg for BD childen

300mg BD for adults - approx 3.8mg/kg

104
Q

Child vs adult dose of clobazam?

A

5mg/kg daily for child

100mg BD for adult - approx 1.3mg/kg

105
Q

Child vs adult dose of phenytoin?

A

5mg/kg/day child

3mg/kg/day adult

106
Q

What is Lennox-Gastaut syndrome?

A
  • most common form of intractable epilepsy
  • characterised by ‘drop attacks’ - generalised absense seizures, atypical focal absence seizures (floppy and unresponsive), tonic seizures (jerking)
  • developmental delays
107
Q

Why does epilepsy cause development delays?

A

large amount of calorie expenditure on seizures

108
Q

Treatment options for Lennox-Gastaut syndrome?

A

1st line: valproate
2nd line: lamotrigine, topiramate, clobazam, phenytoin

corticosteroids to reduce inflammation and neuronal damage
surgery to remove the affected area of the brain

109
Q

Properties of valproate?

A

short chain fatty acid that inhibits uptake of GABA in the CNS

110
Q

Why is valproate so commonly used in epilepsy?

A
  • broad spectrum
  • well tolerated
  • cheap
  • range of formulations
111
Q

Toxicity profile of valproate?

A
  1. Liver (monitor LFTs, bilirubin, ALT etc) - fatty liver
  2. Pancreatitis (10% of patients)
  3. Haemotological (pancytopaenia, thrombocytopoenia)
  4. Metabolic derangement (urea cycle disorders)
112
Q

Pharmacokinetics of valproate?

A
  • half life 4-8 hours (8-20 hours in adults)
  • 90% protein bound
  • 65% renally cleared
  • therapeutic level 40-100mg/L
    concentration not correlated with therapeutic efficacy, only useful if concerned about toxicity
113
Q

Valproate and teratogenicity?

A
  • should not be used in women of childbearing age
  • 1 in 10 risk of birth defects
  • 4 in 10 risk of developmental delays (memory impairment, lower IQ, delay in walking/talking)
114
Q

Why is valproate still on the market despite the risks?

A

Patient centred assessment, risk vs benefit

115
Q

Counselling for children on valproate

A

Make parents/carers aware of risk of valproate and epilepsy in pregnancy
At a suitable time for the patient, discuss suitable contraception
When the child reaches child bearing age, review valproate and consider a change

116
Q

What to do in unplanned pregnancy whilst taking valproate?

A
  • review treatment and risk assess
  • remind her to continue therapy until a decision is made
  • use smallest dose possible, consider prolonged release formulation
  • check understanding of risks and consider further counselling
  • refer to specialist obstetrician for specialist guidance
117
Q

Mode of action of carbemazepine?

A
  • dose dependent voltage gated sodium channel antagonist: prevents repetitive action potentials, downregulates seizureactivity at the nerve
  • also a GABA agonist
118
Q

When is carbemazepine contraindicated?

A

Epilepsy seizures with sodium channel involvement, as it makes them worse

  • Dravets Syndrome
  • Myoclonic seizure disorders
119
Q

Pharmacokinetic information on carbamazepine?

A
  • half life 30 hours after a single dose (15 hours after repeated dosing) (2-12 hours if with phenytoin)
  • 65% protein bound
  • hepatically metabolised by CYP3A4
  • therapeutic level 4-12mg/L - seldom correlates with efficacy
120
Q

Mode of action of lamotrigine?

A

Direct effect on voltage gated sodium channels
- interacts with other AEDs (valproate, increased level. carbemazepine, decreased level)
-

121
Q

Uses for lamotrigine?

A

1st line for focal seizures

1st line for generalised tonic clonics (good alternative to valproate)

122
Q

What is the dynamic target of seizure control?

A

Balance between factors that influence excitatory and inhibitory post synaptic potentials

123
Q

What factors influence excitatory post synaptic potential?

A
  • sodium influx
  • calcium influx
  • paroxysmal depolarisation
124
Q

What factors influence inhibitory post synaptic potential?

A
  • potassium efflux
  • chloride influx
  • low pH
125
Q

At what levels does physiological protection against repetitive firing occur?

A

cellular (e.g. sodium channel inactivation)

network (e.g. GABA mediated inhibition)

126
Q

What are the main categories of anticonvulsants?

A
  1. drugs that inhibit sodium channels
  2. drugs that inhibit calcium channels
  3. drugs that enhance GABA mediated inhibition
  4. drugs that inhibit glutamate
127
Q

How do the drugs that inhibit the sodium channels work?

A

prevent the return of these channels to active state by stabilising them in the inactive state

128
Q

How do the drugs that inihibit the calcium channels work?

A

inhibit T-calcium channels (particularly useful in absence seizures)
high voltage activated channels - involved in neurotransmitter release

129
Q

How is GABA synthesised?

A

mediated by glutamic acid decarboxylase (GAD)

130
Q

How is GABA stored?

A

GABA is packaged into presynaptic vesicles by a transporter (VGAT)

131
Q

How is GABA released?

A

In response to an action potential and the presynaptic elevation of intracellular Ca2+, GABA is released into the synaptic cleft by fusion of GABA-containing vesicles with the presynaptic membrane

132
Q

Reuptake of GABA?

A

Neurons and glia take up GABA via specific GABA transporters (GATs). Four GATs have been identified, GAT-1, GAT-2, GAT-3 and GAT-4, each with a characteristic distribution in the CNS

133
Q

How is GABA broken down?

A

widely distributed mitochondrial enzyme GABA-transaminase (GABA-T) metabolises GABA

134
Q

Types of drugs that enhance GABA mediated inhibition?

A

GABA receptor agonists, GABA reuptake inhibitors, GABA-transaminase inhibitors

135
Q

What do glutamate receptors do?

A

glutamate is a major excitatory neurotransmitter in the brain

136
Q

What are the sites on ionotropic glutamate receptors?

A

AMPA, kainate, NMDA

137
Q

How do AMPA and Kainate receptor sites regulate glutamate response?

A

oopen a channel that allows small amounts of sodium and calcium ions through

138
Q

How do NMDA receptor sites regulate glutamate response?

A

open a channel that allows large amounts of calcium to enter alongside the sodium

139
Q

What facilitates the opening of the NMDA rececptor channel?

A

Glycine

140
Q

What mediates and regulates the metaobtropic receptors?

A

Regulated by complex reactions and response mediated by second messengers

141
Q

Why do NMDA receptor agonists have limited use?

A

produce psychosis and hallucinations

can also impair learning and memory

Patient Semester 2 (10 decks)

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