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AC- CNS lectures > Module 4.1.2 (Management of Epilepsy) > Flashcards

Module 4.1.2 (Management of Epilepsy) Flashcards

1
Q

What are some non-pharmacological treatment options for epilepsy?

A

Lifestyle medications

  • Avoid stress, sleep deprivation, triggers

Seek and try to remove precipitants

  • Medication, alcohol

Counselling

  • Complianece with medications
  • Benefits of treatment
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2
Q

When is pharmacological treatment started in epilepsy? What factors to consider after first and after second seizure?

A

Start antiepileptic treatment when the impact of further seizures outweighs the risks of treatment

After first seizure

  • Factors to consider when deciding to treat include:

> symptomatology (previous seizures may have been unrecognised, eg in complex focal (partial) seizures)

> signs (an abnormal EEG or neurological abnormalities may indicate an increased risk of recurrence)

> seizure type or epilepsy syndrome (some are more likely to be recurrent, eg focal (partial) seizures, juvenile myoclonic epilepsy)

> seizure severity

> age (elderly people are at higher risk of recurrence)

> the person’s wishes.

After second seizure

  • Treatment is usually indicated when 2 or more seizures have occurred within 6–12 months (about 80% of people will have recurrent seizures after 2 seizures), except when there is a clear avoidable precipitant or with some types of seizures (eg benign childhood epilepsy with centrotemporal spikes).
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3
Q

What are lowest reccurent rates for a seizure associated with?

A

Associated with a normal EEG and no identifiable cause for seizures or when there is a clear avoidable precipitant (eg sleep deprivation, drugs)

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4
Q

What are the anti-epileptic drugs (AEDs) used?

A

Barbiturates

  • Phenobarbital, primidone

BZDs

  • Clobazam, clonazepam, diazepam, midazolam

Acetazolamide n

Brivaracetam, levetiracetam n

Carbamazepine, oxcarbazepine n

Ethosuxamide n

Gabapentin, pregabalin n

Lacosamide n

Lamotrigine n

Perampanel n

Phenytoin n

Sulthiame n

Tiagabine n

Topiramate n

Valproate n

Vigabatrin n

Zonisamide

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5
Q

What are the goals of pharmacological management?

A
  • Prevent seizures
  • Minimise effects on cognitive function and development
  • Minimise side effects

> Monotherapy preferable to polytherapy

> Non-sedating preferable to sedating anticonvulsants

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6
Q

What does drug selection depend on?

A
  • Accurate diagnosis and classification of seizure type
  • Efficacy and toxicity of each drug
  • Potential for drug interactions
  • Patient preference
  • Age of patient
  • Childbearing potential
  • Co-morbidities
  • Formulations avaliable
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7
Q

How to start pharmacological treatment? What to do if first line medication cant be used?

A

1. Start with ONE first-line medication only

> Increase the dose gradually (esp carbamazepine and lamotrigine)

> Can start phenytoin at target dose (can also use loading dose)

> treatment failure, then check compliance (TDM) and dose

> ~50% symptom free with manageable AE’s with 1st AED

2. Replace with an alternate first-line or second line drug if

  • Maximal tolerated dose of above medication does not give control
  • Side effects from the above medication
  • Cross-taper (introduce 2nd drug gradually; once maintenance dose is established, first drug should be tapered down and withdrawn

> consider fitness to drive

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8
Q

What is the third option for treatment if previous 2 options failed?

A

Polytherapy (>1 drug) only if above

  • Combined drugs with different modes of action
  • Reconsider dx if still not successful
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9
Q

What are some factors affecting AED choice?

A

Efficacy in treating syndrome

Certainty of syndrome diagnosis

> If unsure consider drugs that are effective in both focal and generalised = sodium valproate, levetiracetam, lamotrigine, topiramate

Pregnancy

> avoid sodium valporate is possible

Adverse effects

  • Impaired cognition (phenobarb and topiramate worsen)
  • Body weight changes (valproate and pregabalin↑, topiramate↓)
  • Cosmetic changes

phenytoin –> hirsutism, coarsened facial features, gingival hyperplasia,

valproate –> hair loss

  • Hypersensitivity (pts of some Asian origins –> increased risk of severe skin reactions with carbamazepine and phenytoin)

Age (valproate hepatotoxicity ↑likely in infants)

Cost

Ease of use

Need for TDM

Pharmacokinetics

Drug interactions (eg with COC or warfarin)

Time to achieve therapeutic dose

> Phenytoin can be started at therapeutic dose

> Lamotrigine, perampanel and topiramate need to be started slowly

Preparations available (IV, liquid, scored tab etc)

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10
Q

What to use for focal seziure?

A

Carbamezapine

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11
Q

What to use for generalized seizure or if unsure?

A

Sodium valproate

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12
Q

What is first line for:

A) focal (partial) seizures?

B) generalised tonic-clonic seziures

C) absence seizures

D) myoclonic seizures

E) infantile spasms

A

A)

Carbamazepine

B)

Valproate

C)

Valproate or ethosuximide

D)

Valproate

E)

Prednisolone, tetracosactide

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13
Q

What is second line for:

A) focal (partial) seizures?

B) generalised tonic-clonic seziures

C) absence seizures

D) myoclonic seizures

E) infantile spasms

A
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14
Q

What are some adverse reactions associated with AED’s?

A

Serious adverse reactions usually occur suddenly

  • Hepatic failure with valproate
  • Agranulocytosis with carbamazepine
  • Baseline blood tests but no evidence routine monitoring helps px

Serious skin reactions – SJS, TENS, DRESS

  • Pharmacogenetics – genes with predisposition to cutaneous reactions
  • HLA-B*1502 allele – check in Asian pts (not Japanese)

> Before starting carbamazepine

> May also have increased risk SJS/TEN with lamotrigine and phenytoin

> Be aware of potential for cross-reactivity for skin AE’s

Vitamin D

  • Monitor 25(OH)D in patients on long-term AED’s

> Esp if on enzyme inducers

> Risk factors for osteoporosis (↓BMD)

> High falls risk

Dizziness, drowsiness and diplopia common adverse effects

association between some antiepileptics and an increased risk of suicidal thoughts and behaviour –> benefits will usually outweigh the risks in epilepsy

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15
Q

For phenobarbital, primidone (barbiturates)

A) Precautions

B) watch for

A

A)

  • Hypersensitivity syndrome with carbamazepine, phenytoin or phenobarbital—avoid use
  • Allergy or rash with other antiepileptics—may increase risk of rash with phenobarbital or primidone.
  • Respiratory disease—risk of respiratory depression (esp if IV)

B)

  • Drowsiness
  • Tolerance

> Withdraw treatment very slowly

  • Drug interactions
  • Vitamin D and Ca
  • Very toxic in overdose

TDM: 10-40 mg/L

Contains ethanol 10% = be careful in children on oral liquid

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16
Q

For clobazam, clonazepam, diazepam, midazolam (BZD)

A) indications

B) why not suitable for long term tx

A

A)

  • Acute treatment of seizures and status epilepticus
  • Adjunctive treatment of refractory epilepsy

B)

  • sedation
  • tolerance –> withdraw treatment very slowly
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17
Q

What is Acetazolamide used for? AE?

A

Used in menstrual related epilepsy

AE’s – paraesthesia, metallic taste, black faeces, ↓K, ↓Na, SJS, blood dyscrasias

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18
Q

What is Brivaracetam, levetiracetam associated with?

A

Levetiracetam associated with behavioural AE’s (depression, emotional lability, hostility, aggression, agitation and anxiety)

  • SJS, TENS, multi-organ sensitivity (rare)
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19
Q

For carbamazepine, oxcarbazepinem: explain in detail about hypersensitivity and skin reactions. TDM?

A

Cross-sensitivity with phenytoin and phenobarbitone

  • HLA-B*1502 allele – significantly increases risk
  • HLA-A*3101 allele – may increase risk
  • May also occur as part of multi-organ hypersensitivity (DRESS)
  • Blood dyscrasias – check FBC, ↓ Na

Enzyme inducer (and autoinduction)

  • BMD, Vitamin D and Calcium

> TDM = 4-12mg/L Css trough level

Oxcarbazine – fewer CNS AE’s and fewer DI’s (watch ↓Na)

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20
Q

AE of Ethosuxamide

A

GI upset and weight loss n

SJS, multi-organ hypersensitivity and blood dyscrasias (rare)

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21
Q

Gabapentin and pregabalin for epilepsy?

A

Not used often for epilepsy

Renally cleared

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22
Q

What can lacosamide cause?

A

Can cause bradycardia and AV block.

SJS, multi-organ hypersensitivity (rare)

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23
Q

AE of lamotrigine? When is there increased risk of AE?

A

Risk of severe skin reactions – eg SJS

  • Increased risk with rapid dose escalation, combination with valproate (use lower doses with valproate)
  • If treatment interrupted and restarted may need to re-do dose titration
  • Stop immediately if rash occurs
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24
Q

What cuation with perampanel?

A

Caution if substance misuse – can –> euphoria

  • Can cause serious psychiatric adverse effects (including homicidal ideation)
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25
Q

AE of phenytoin? What is the issue with enteral feeds? Why may IV phenytoin be preferred?

A

AE

  • Cross –reactivity with phenobarb and carbamazepine hypersensitivity syndrome
  • Asian ancestry – increased risk of skin reactions
  • IV – risk of ventricular arrhythmias and purple glove syndrome
  • Blood dyscrasias, SJS, TENS
  • Coarsened faces, hirsutism, gingival hyperplasia
  • TDM available

Enteral feeds

  • Can significantly ↓ phenytoin absorption
  • Stop feed 2 hours before and after and flush well

IV phenytoin may be preferred

> Slow IV with inline filter (risk of precipitation)

> BP, ECG, respiratory monitoring

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26
Q

Dose equivalence of phenytoin?

A

Check level and adjust dose if converting from phenytoin to phenytoin sodium product

  • Dose equivalence -100 mg phenytoin sodium ~ 92 mg phenytoin

> Capsules and injection contain phenytoin sodium

> Tablets and oral liquid contain phenytoin.

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27
Q

What are some AEs of sulthiame?

A

AE’s – hyperventilation, dyspnoea, psych adverse effects, paraesthesia

> carbonic anyhdrase inhibitor

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28
Q

What happens when dose is increased for Tigabine?

A

Can cause NCSE on dose increase

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29
Q

What are some AE of topiramate?

A
  • Psychiatric AE’s (emotional lability, agitation, suicidal ideation)
  • Decreased sweating and hyperthermia –keep up fluids
  • Metabolic acidosis (↓HCO3) – monitor
  • Kidney stones
  • Acute myopia with secondary acute angle-closure crisis
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30
Q

What is there a risk of with valproate?

A

Risk of hepatic failure (usually in 1st 6mths – can be fatal)

  • Increased risk in young children, congenital disease, organic brain disease, on multiple AED’s
  • Contraindicated in mitochondrial disorders with mutation of POLG gene

Hyperammonaemic encephalopathy - ↑risk with topiramate, phenobarb, carbamazepine and phenytoin

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31
Q

Which patients to avoid valproate in?

A

Avoid in women of child-bearing age

  • Risk of birth defects and developmental delay in child
32
Q

What are some AE of valproate? TDM?

A

Weight gain, PCO, hyperandrogenism in females, hair loss

Blood dyscrasias (esp thrombocytopenia) – FBC before tx

BMD, calcium and vitamin D

Multi-organ hypersensitivity

TDM = 40-100mg/L (up to 150mg/L in some people) Css trough level (3-5d)

33
Q

What are some AE of vigabatrin?

A

Visual field defect, in particular visual field constriction, occurs in 20– 40% of patients; it may be asymptomatic and is usually irreversible

  • Psychiatric adverse effects
34
Q

Wht are some AE of zonisamide?

A

Psychiatric adverse effects (including psychosis and suicidal ideation)

Nephrolithiasis – keep up fluids n Decreased sweating and hyperthermia

Metabolic acidosis (HCO3 at baseline and periodically)

SJS, TENS, multi-organ hypersensitivity

35
Q

What are some other options for the treatment of epilepsy?

A
  • Lifestyle
  • Medication
  • Surgery –> intractable focal epilepsy
  • Nerve stimulation
  • Ketogenic diet

> Intractable childhood epilepsy

> >50% ↓ in seizures in 38-60% of patients

> >90% ↓ in ~30% of patients

36
Q

Drug efficacy for epilepsy is measured by clinical response to the antiepileptic drug rather than its serum concentration. The serum concentration of an AED may be used to?

A
  • Check compliance
  • Help diagnose that symptoms or signs are due to toxicity. If low levels = syndrome. If high levels = medication.
  • Guide the dosage of phenytoin (IV –> nasogastric –> oral)
  • Adjust the dosage of lamotrigine/other AED’s in pregnancy
37
Q

Phenytoin has non-linear kinetics, small dose changes result in large changes of Css level. What is the therapeutic reange? When is free phenytoin used?

A

TR: Total phenytoin 10–20 mg/L (40–80 micromol/L)

  • If level <5mg/L can increase by 100mg daily
  • If level >5mg/L only increase by 30mg daily

Free phenytoin 1–2 mg/L (4–8 micromol/L)

> Free phenytoin (not bound to albumin) is recommended in CRF or low albumin

38
Q

Many drugs used in the treatment of epilepsy reduce the efficacy of hormonal contraception by inducing hepatic enzymes. What are examples of these drugs? How long do these effects of last for?

A

Carbamazepine

Oxcarbazepine

Perampanel (at doses >12mg)

Phenobarbitone

Phenytoin

Primidone

Topiramate (at doses >200mg)

  • The effectiveness of these contraceptives may be reduced during therapy with, and for at least 4 weeks after stopping, enzyme-inducing antiepileptic drugs
39
Q

What contraception is effective in epilepsy with women of childbearing age?

A

Effective contraception is provided by depot medroxyprogesterone acetate, progestin-releasing intrauterine contraceptive devices (eg Mirena) or copper intrauterine contraceptive devices.

40
Q

What are contraceptives that may be ineffective in females taking enzyme-inducing antiepileptic drugs?

A

Oral contraceptive pill

Progestin only pill

Vaginal ring

SC etenogestrel implant

Levonorgestrel emergency

Ulipristal emergency

41
Q

Most teratogenic effects probably occur before pregnancy is confirmed

Neurodevelopmental effects probably depend on exposure throughout pregnancy

Is this true regarding taking AED medications when trying to get pregnant?

A

YES ITS TRUE BIG FACTS

42
Q

Principles for treating epilepsy in females planning a pregnancy?

A

Only continue treatment if needed to prevent seizures.

Use monotherapy if possible.

Minimise the dose of antiepileptic drug. In practice, the minimal effective dose can only be established by lowering the dose sufficiently to cause a seizure. If dose particularly high, try and reduce

Avoid sodium valproate if possible

> If sodium valproate is essential, use 600 mg or less daily if possible

43
Q

What pre natal screening to do for epilepsy in women of childbearing age?

A

Alpha-fetoprotein measurement and ultrasound

Folic acid 5mg daily

?Vitamin K in neonate

44
Q

What is the issue with using valproate for Epilepsy in women of childbearing age? When may valproate have to be used regardless?

A
  • Increases risk of spina bifida up to 10 fold (0.2-2%)
  • Associated with other severe malformations

> Orofacial clefts, cardiac, urogenital and limb defects

  • Dose-related decrease in intelligence and increased learning difficulties
  • Some data suggest association with autism spectrum disorder

> <600mg/day effects are similar to other AED’s

> Avoid doses >600mg/day

Often valproate the only suitable medication in genetic generalised epilepsies (incl juvenile myoclonic epilepsy)

  • Risk of seizures if valproate withdrawn. Use lowest possible dose
45
Q

Explain the effects of following AED in women of childbearing age

A) phenytoin

B) lamotrigine and carbamazepine

C) topiramate

D) newer antiepileptic drugs

A

A)

  • Risk of seizures if valproate withdrawn. Use lowest possible dose

B)

  • Slight and dose-related increase in congenital abnormalities

C)

  • May increase the risk of congenital malformations

D)

  • Limited data available for levetiracetam suggest it has a low risk of teratogenicity
46
Q

What happens to some AEDs during pregnancy? Which ones do this?

A

Serum concentrations of some AED’s fall during pregnancy

> Compliance may be a problem

  • Lamotrigine –> dose may need to be increased, check baseline level before/early pregnancy. Measure q2mths and adjust dose to ensure level remains stable. After birth the kinetics return to normal in 2-3 weeks
  • Phenytoin and carbamazepine –> levels may decrease, need to check levels and adjust dose if necessary
  • Levetiracetam –> levels may decrease but measurement not widely available
47
Q

Treatment withdrawal of AED. This may be attempted after 2–3 years without seizures. Good prognostic signs for remaining seizure-free at the time of withdrawal are? What are the benefits and risks?

A
  • History of few seizures
  • Absence seizures only
  • Younger age when seizure control achieved
  • Normal EEG
  • Normal neurological examination
  • Absence of brain lesions.

Benefits: Adverse effects, teratogenicity risk, D/Is, QoL

Risks: Social and medical implications, injury, death. Seizures recur in 50%.

48
Q

What are some points for advice for treatment withdrawal?

A
  • Patient must stop driving during any dose reduction and for 3 months after the last dose (many patients continue tx indefinitely)
  • Do not stop antiepileptic treatment abruptly; increased seizures and status epilepticus may occur
  • When withdrawing treatment, reduce the dosage of antiepileptic drug over several weeks to months (up to 6 months or longer for benzodiazepines or barbiturates)
  • Withdraw one drug at a time.
  • Juvenile myoclonic epilepsy has such a high recurrence rate that it is best not to withdraw therapy, at least not until many years without seizures of any type (including jerks)
49
Q

Approximately one-third of patients with epilepsy do not achieve complete seizure control. Reasons include?

A
  • poor concordance with antiepileptic drug therapy or lifestyle advice
  • wrong diagnosis of epilepsy (eg psychogenic nonepileptic events, convulsive syncope)
  • wrong diagnosis of epilepsy syndrome (focal seizures mistaken for generalised seizures, or vice versa)
  • suboptimal choice or use of antiepileptic drug
  • drug-resistant epilepsy
50
Q

For uncontrolled epilepsy, the patients who have video-electroencephalogram (EEG) monitoring get diagnosed with?

A
  • up to 30% are diagnosed with psychogenic nonepileptic seizures (pseudoseizures)
  • more than 50% have the diagnosis of epilepsy or the type of epilepsy syndrome changed.

> Patients referred to an epilepsy centre who have drug-resistant epilepsy may be considered for surgery. If surgery is not suitable, a vagus nerve stimulator may be implanted

> For a child with refractory epilepsy, a ketogenic diet should be considered, under the guidance of a specialist dietitian.

51
Q

How to classify epileptic syndrome? FOUR main types.

A

Generalised epilepsies

  • Idiopathic generalised

> childhood absence epilepsy

> juvenile absence epilepsy

> juvenile mycoclonic epilepsy

> epilpesy with tonic-clonic seizures on awakening

  • symptomatic generalised

> lennox-gastaut syndrome

Focus (partial) epilepsies

> self-limited (benign childhood epilepsy with centrotemporal spikes)

> symptomatic (mesial temporal lobe epilepsy)

Epilepsies that can be focused or generalised

> neonatal seizures

> west syndrome (infantile spasms)

Special syndromes

> febrile seizures

> isolated seizure or status epilepticus

> metabolic and toxin-induced seizures

52
Q

What to do for Childhood and juvenile absence epilepsies (general)? treatment, avoid?

A

Genetic (idiopathic) generalised epilepsy

  • Usual age of onset 4-15 years

Treatment

  • Ethosuxamide (NB does not protect against tonic-clonic)
  • Sodium valproate

Avoid

  • Carbamazepine, oxcarbazepine and phenytoin
  • Can worsen absence seizures
53
Q

What to do for Juvenile myoclonic epilepsy (general)? treatment, avoid?

A

Most common form of genetic, generalised epilepsy in adults

  • Onset late adolescence
  • Usually presents with tonic-clonic seizure and hx of myoclonic jerks

Treatment

  • Sodium valproate
  • Avoid sleep deprivation and excess alcohol
  • Long-term treatment usually required

Avoid

  • Carbamazepine, oxcarbazepine and phenytoin – may aggravate
54
Q

What to do for Lennox-Gastaut syndrome and other symptomatic generalised epilepsies? first and second line treatment?

> Symptomatic (structural, metabolic, immune, infectious) generalised epilepsies occur in patients with generalised or multifocal brain disorders

A

First line treatment

  • Sodium valproate

Second line treatment

  • Valproate PLUS lamotrigine (watch for DI e.g. rash)
  • Clobazam and topiramate also used
  • ?Cannabidiol (medicinal cannabis)
55
Q

What is the causes of focal (partial) epilepsy? how to treat?

A

Causes

  • Mesial temporal lobe epilepsy due to hippocampal sclerosis
  • Tumours
  • Head injuries
  • Congenital brain anomalies and perinatal brain injury

Treatment

> First line

  • Carbamazepine
  • First sign of dose-limiting toxicity = diplopia (30-60 mins post-dose)
  • Serum concentrations of limited benefit in determining dose

> Second line (see attached image)

  • surgery may be of benefit
56
Q

What treatment for Benign childhood epilepsy with centrotemporal spikes?

> Typically starts mid-childhood ( Seizures usually occur during sleep and begin in the face or mouth, producing a typical glugging sound)

> Focal (partial) seizure may –> secondary generalisation

A
  • Carbamazepine
  • Sodium valproate
  • Sulthiame
57
Q

What treatment for Tonic-clonic seizures where onset is unclear? What to avoid?

A

If unclear if focal or generalised onset

  • Use “broad spectrum antiepileptic” effective against both types

> Eg sodium valproate, levetiracetam, lamotrigine, topiramate, clobazam

> First line – sodium valproate or levetiracetam (women of childbearing potential)

Avoid

  • Carbamazepine (for focal seizures) and phenytoin

> less likely to be effective

> may exacerbate epilepsy if seizures are generalised onset

58
Q

What treatment options for west syndrome (Infantile spasms)? –> focal or generalised.

> Sudden brief contractions of the head, neck and trunk, usually in flexion but sometimes in extension

> Last a few minutes

> Usual age of onset 4-12 months

A

Treatment

  • Prednisolone
  • Tetracosactrin depot 0.5mg IM
  • Vigabatrin (risk visual field defects)
  • Clonazepam/nitrazepam
59
Q

What treatment for neonatal seizures? –> focal or generalised

> causes: hypoxic-ischaemic encephalopathy, intracranial haemorrhage, perinatal ischaemic stroke, meningitis, hypoglycaemia, hypocalcaemia, electrolyte disturbances and metabolic conditions

> some neonatals seizures are familial and benign –> check family hx

A

Treatment –> aim to stop seizures asap

first line: Phenobarbitone

rare syndrome: Pyridoxine dependent seizures (lifelong pyridoxine treatment)

60
Q

What to use for acute treatment and prevention of simple febrile seizures? –> special syndrome

> Simple febrile seizures (brief, generalised, occurring only once in 24 hours and associated with a fever from a source outside the CNS)

A

Acute treatment: use diazepam (IV or rectal) or midazolam (IV, IM, intranasal, buccal) for the treatment of prolonged seizures

Prevention: rarely necessary;

  • Diazepam (oral or rectal) at the onset of fever for children at high risk of severe or complicated seizures. Rarely phenobarb or valproate
61
Q

What to do for isolated seizures (most seizures are brief and do not need treatment)

A
  • Position on left side, protect airway, O2
  • BGL, IV access, FBC, UEC, TDM, VBG
  • After the seizure:

> CT, UDS (urine/drug scan), lumbar puncture (?infection)

62
Q

What is status epilepticus? How long does seizure have to last for it to to be se?

A

Status epilepticus refers to continuous seizure activity or repeated seizures without full recovery of consciousness between attacks.

  • The minimum duration of continuous seizure activity required for the diagnosis of status epilepticus is traditionally agreed to be 30 minutes

> However, drug treatment for a seizure should start after 5 minutes of continuous seizure activity

63
Q

Status epilepticus is a special syndrome and medical emergency, what are the types and what are the goals of managing status epilepticus?

A

May be convulsive or nonconvulsive

Convulsive

  • Usually tonic-clonic but may be tonic (rhabdomyolysis, lactic acidosis)

Non-convulsive

  • May be generalised (absence status epilepticus) or
  • Focal (partial) (impaired awareness [complex partial] or
  • Aware [simple partial] status epilepticus)

The goals of managing status epilepticus are to:

  • Resuscitate the patient
  • Stop the seizures
  • Diagnose the cause of the seizures and treat it when possible
  • Find and treat complications of the seizures.
64
Q

Treatment advice for status epilepticus?

A

> The treatment of nonconvulsive status epilepticus is less urgent and the risks of therapy, particularly respiratory depression, must be weighed against the risks of continuing nonconvulsive seizures

  • Most patients need to be intubated
  • IV midazolam/diazepam/clonazepam –> can give IM/IN/buccal midazolam
  • If seizure stopped and cause reversed – no further tx.

In all other patients prevent further seizures with:

  • IV phenytoin or IV sodium valproate
  • OR can use other agents especially if they are already on AED’s

> Eg levetiracetam, phenobarb)

Transfer to ICU:

  • Thiopental, propofol
65
Q

What are complications of seizures?

A

Check for complications of seizures and treat if needed. Complications include

  • aspiration
  • trauma (eg posterior shoulder dislocation).

When seizures are prolonged, complications include:

  • central nervous system injury
  • noncardiogenic pulmonary oedema
  • rhabdomyolysis, acidosis and kidney failure
  • hyperthermia
66
Q

Acute symptomatic seizures (see attached image) are caused by a transient systemic or central nervous system insult, what to do to manage?

A
  • For seizures caused by a known toxin or drug, see specific treatment guidelines –> mostly BZDs
  • If alcohol withdrawal cannot be excluded as the cause of a seizure, give intravenous thiamine to help wernicks encepholathy
  • Resolution of the cause usually stops the seizure
  • Seizures will recur if:

> The cause recurs (eg BZD withdrawal)

> The illness has caused permanent brain injury (eg gliosis caused by herpes encephalitis)

  • Sometime antiepileptic treatment is indicated if the cause is not immediately reversible

> Eg eclampsia, bacterial meningitis

67
Q

Counselling patients with epilepsy

A
  • Keep a seizure diary
  • Warn patients that abruptly stopping antiepileptic drugs can provoke status epilepticus

Seizures can be provoked by:

  • Sleep deprivation
  • Excess alcohol intake n
  • Illicit drugs n
  • Psychological stress n
  • Other medication

Avoid situations where seizures may be dangerous

  • Operating machinery/driving
  • Swimming/bathing alone

Advise licencing authorities

Have a management plan

Counsel on contraception and pregnancy if appropriate

68
Q

Treatment of epilepsy summary

A
69
Q

Antiepileptic drug summary

A
70
Q

Pharmacological treatment summary

A
71
Q

adverse reaction of AED summary

A

Dizziness, drowsiness and diplopia n

Hepatic failure and hyperammonaemic encephalopathy with valproate n

Agranulocytosis and ↓Na with carbamazepine n

Serious skin reactions SJS/TENS/DRESS – esp carbamazepine, lamotrigine, phenobarb, phenytoin, valproate n

Osteoporosis – phenobarb, phenytoin, carbamazepine, valproate n

Cosmetic changes with valproate and phenytoin n

Impaired cognition (esp phenobarb + topiramate) n

Suicidal ideation with AED’s n

Behavioural changes – levetiracetam, topiramate, perampanel, zonisamide n

Decreased sweating, hyperthermia – topiramate, zonisamide n

Metabolic acidosis and kidney stones – topiramate, zonisamide

72
Q

TDM and other considerations summary

A

Drug efficacy for epilepsy is measured by clinical response to the antiepileptic drug rather than its serum concentration.

73
Q

Epilepsy in women of childbearing age summary

A
74
Q

Treatment withdrawal summary

A

This may be attempted after 2–3 years without seizures

Decision requires careful assessment

Benefits: Adverse effects, teratogenicity risk, D/Is, QoL n

Risks: Social and medical implications, injury, death and seizures recur in 50%

75
Q

Epileptic syndrome classification summary

A

AC- CNS lectures (28 decks)

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