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Management of Disorders > Neurological Treatment of Epilepsy > Flashcards

Neurological Treatment of Epilepsy Flashcards

1
Q

What is epilepsy?

A

The tendency to have recurrent epileptic seizures (not one disease process)

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2
Q

What are epileptic seizures?

A

Abnormal, synchronous firing of a large number of cortical neurons, causing symptoms

(Fundamentally abnormal as most actions use spare coding = strong activation from small set of neurons)

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3
Q

What poorer outcomes are associated with epilepsy?

A

▪️ Education
▪️ Employment
▪️ Mental health
▪️ Stigma
▪️ Injury and mortality
▪️ Unplanned hospital admissions

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4
Q

What are the eight steps of the NICE neurological management pathway for epilepsy?

A
  1. Patient presents with suspected seizure(s)
  2. History, examination, and investigations
  3. Diagnosis and classification
  4. Explanation, discussion, provision of info
  5. Decision to treat
  6. Ongoing treatment
  7. Possible referral to tertiary service depending on response/outcome
  8. Stopping treatment
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5
Q

What usually happens after an individual presents to their GP/A&E with suspected seizure(s)?

A

They are referred to a specialist for diagnosis and decision to start treatment, ideally within 2 weeks

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6
Q

Why is the aim to get patients with suspected seizure(s) seen by a specialist within 2 weeks?

A

This follows the cancer pathway due to the possibility of a tumour

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7
Q

What investigations might be ordered by an epilepsy specialist?

A

▪️ EEG
▪️ ECG
▪️ Neuroimaging
▪️ Neuropsychological assessment
▪️ Blood test

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8
Q

What information does the NICE guidelines say should be provided to people with epilepsy?

A

▪️ Epilepsy in general (incl. treatment options, types and triggers, SUDEP, status epilepticus)
▪️ Risk management
▪️ Psychological issues
▪️ Education and employment
▪️ Road safety and driving
▪️ Lifestyle (incl. alcohol, sleep deprivation)
▪️ Issues relevant to women
▪️ Voluntary organisations

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9
Q

What should drug treatment for epilepsy be individualised to?

A

▪️ Seizure type
▪️ Epilepsy syndrome
▪️ Co-medication
▪️ Co-morbidity
▪️ Lifestyle
▪️ Preferences

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10
Q

What should be tried if a single AED is not successful in controlling seizures?

A

Another drug should be tried as monotherapy

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11
Q

When should combination therapy (polytherapy) be considered?

A

When monotherapy with more than one AED has not resulted in seizure freedom

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12
Q

What risk should be considered when prescribing sodium valproate to a woman?

A

Risk of malformation and neurodevelopmental impairments in an unborn child

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13
Q

When is SUDEP most likely to occur and why?

A

During sleep likely due to suppression of brain stem autonomic processes (e.g., decreased HR and breathing)

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14
Q

How many antiepileptic drugs are currently available in the UK?

A

25

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15
Q

What are the main issues with the evidence base for which AED to prescribe?

A

▪️ Only “newer” drugs have gone through RCTs in comparison to placebos
▪️ Trials mostly in difficult-to-treat, chronic patients in addition to current therapy
▪️ Very few comparative trials, mostly in new-onset treatment naïve epilepsy
▪️ Very little evidence for polytherapy

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16
Q

What did Kwan and Brodie (2000) find when comparing monotherapy to polytherapy?

A

▪️ Most people become seizure free with monotherapy, usually with the first drug tried
▪️ No evidence that any particular drug was preferable
▪️ Outcome predicted by “idiopathic” aetiology and fewer seizures before treatment

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17
Q

What was the SANAD trial?

A

A large RCT investigating the effectiveness of standard and new epileptic drugs in partial (focal-onset) seizures and generalised/unclassifiable seizures

(Sodium valproate vs topiramate, lamotrigine, carbamazepine, and gabapentin)

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18
Q

What did the SANAD trial find in regards to generalised or unclassifiable seizures?

A

▪️ Valproate was better tolerated than topiramate and more efficacious than lamotrigine
▪️ BUT must not adverse effects in pregnancy

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19
Q

What did the SANAD trial find in regards to patial (focal) seizures?

A

▪️ Lamotrigine = better tolerated than carbamazepine and equally efficacious
▪️ Lamotrigine = better tolerated than topiramate but both better than gabapentin

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20
Q

What were the two arms of the SANAD II trial?

A

A) Lamotrigine vs levetiracetam vs zonisamide in untreated focal onset seizures
B) Levetiracetam vs valproate in untreated generalised onset/unclassifiable seizures

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21
Q

What did Arm B of the SANAD II trial conclude?

A

Valproate = best 12 months remission for generalised onset seizures (and cheaper)

22
Q

What did Arm A of the SANAD II trial conclude?

A

Lamotrigine = best 12 month remission for focal onset seizures (and cheaper)

23
Q

What did Nevitt et al., (2017) find when comparing ‘time to withdrawal of allocated treatment’ of different AEDs for partial seizures?

A

▪️ Best = levetiracetam (best combination of efficacy and tolerability)
▪️ Second best = lamotrigine
▪️ Third best = carbamazepine

24
Q

What did Nevitt et al., (2017) find when comparing ‘time to withdrawal of allocated treatment’ of different AEDs for generalised seizures?

A

Sodium valproate was better than all others

25
Q

What did Nevitt et al., (2017) find was the best AED for achieving 12-month remission?

A

Phenobarbital and phenytoin

BUT not the best adherence, which is more important?

26
Q

What is the best medication for treating partial (focal) seizures?

A

▪️ Levetiracetam (no interactions and well tolerated)
▪️ Lamotrigine or carbamazepine

27
Q

What is the best medication for treating generalised seizures in men?

A

▪️ Sodium valproate
▪️ Lamotrigine or levetiracetam

28
Q

What is the best medication for treating generalised seizures in women?

A

Lamotrigine or levetiracetam

29
Q

What could be considered for frequent absence seizures that are uncontrolled by the usual drugs?

A

Ethosuximide

30
Q

How might topiramate be used for epilepsy?

A

Start at very low dose and escalate slowly, aiming for low continuing dose is better tolerated despite the contrary evidence

31
Q

What is rational polytherapy?

A

Combining drugs known to have different mechanisms of action

32
Q

What is the evidence for polytherapy in epilepsy?

A

▪️ Weak
▪️ Kwan & Brodie - 3% seizure free
▪️ Some anecdotal evidence for rational polytherapy

33
Q

What do the NICE guidelines say about continuing pharmacological treatment in epilepsy?

A

▪️ Monitor for adverse effects
▪️ Continuation should be planned by the specialist
▪️ If straightforward, can be prescribed in primary care

34
Q

How can we optimise adherence to treatment in epilepsy?

A

▪️ Information on their condition and rationale of treatment
▪️ Reduced stigma
▪️ Simple medication regimens
▪️ Positive relationships with healthcare professionals

35
Q

Should regular blood tests be carried out in adults taking AEDs?

A

Not necessarily

36
Q

When might regular blood tests be necessary for adults taking AEDs?

A

▪️ Detection of non-adherence
▪️ Suspected toxicity
▪️ Adjustment of phenytoin dose
▪️ Management of drug interactions
▪️ Clinical conditions such as status epilepticus, organ failure, or pregnancy

37
Q

How can we tell if epilepsy has stopped and treatment can be discontinued?

A

▪️ Just have to stop medication and see
▪️ Not test, can still see abnormalities on EEG when seizure-free

38
Q

According to the MRC Antiepileptic Drug Withdrawal Study Group (1991), what percentage of people withdrawn from treatment remained seizure-free 2 years later?

A

59% (compared to 78% continuing treatment)

The difference decreased after this

39
Q

In the recent meta-analysis by Lamberink (2017), what percentage of people relapsed after AED withdrawal?

A

46%

40
Q

What predictors are associated with increased risk of seizure recurrence following withdrawal of AEDs?

A

▪️ Longer epilepsy duration before remission
▪️ Shorter seizure-free interval before withdrawal
▪️ Younger age at onset
▪️ History of febrile seizures
▪️ Higher number of seizures before remission
▪️ Absence of self-limiting syndrome
▪️ Developmental delay
▪️ Epileptiform abnormality on EEG before withdrawal
▪️ >1 AED
▪️ History tonic-clonic seizures

41
Q

What can be used for the emergency treatment of seizure clusters or prolonged seizures (status epilepticus)?

A

Benzodiazepines:
▪️ Rectal diazepam (in US)
▪️ Intranasal midazolam and diazepam
▪️ Buccal midazolam (in EU)
▪️ Sublingual or intranasal lorazepam
▪️ Oral benzos (e.g., clobazam) (but lack evidence)

42
Q

How does levetiracetam work?

A

SV2A modulation, preventing release of NT such as glutamate from presynaptic vesicles

(synaptic vesicle protein, regulating neurotransmitters)

43
Q

How do lamotrigine, carbamazepine, and oxcarbazepine work?

A

Na+ channel blocker, preventing depolarisation

44
Q

How does sodium valproate work?

A

▪️ GABA potentiation
▪️ Glutamate (NMDA) inhibition
▪️ Na+ and calcium channel blockade

45
Q

What are the main mechanisms of action of AEDs?

A

▪️ GABA potentiation (reduce rate of GABA removal, enhance inhibition)
▪️ Na+ channel blockade (prevent depolarisation)
▪️ T-type Ca2+ channel blockade (prevent NT release)
▪️ Glutamate (NMDA/AMPA) inhibition
▪️ SV2A modulation

Anything that stops synchronous and excessive neuronal transmission/firing!

46
Q

How does phenobarbital work?

A

GABA potentiation

47
Q

How does phenytoin work?

A

Na+ channel blockade

48
Q

What medication is recommended for absence seizures and how does it work?

A

Ethosuximide - Ca2+ channel blocker

49
Q

What is the main mechanism of action of benzodiazepines?

A

Hold open GABA receptors for longer, reducing the likelihood of excitatory synapse firing, and increasing likelihood of GABA action

50
Q

When might a tertiary referral for epilepsy be considered?

A

▪️ Child under 2 years old
▪️ Epilepsy is not controlled with meds within 2 years and/or after two drugs
▪️ Diagnostic doubt
▪️ Unacceptable side effects
▪️ Psychological/psychiatric co-morbidity
▪️ Unilateral structural lesion
▪️ Specific rare syndromes

Management of Disorders (28 decks)

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