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Epilepsy
‘Sacred illness’
• ‘Sacred illness’: 600 BC
• Hippocrates 400 BC: It is thus with regard to the disease called
sacred: it appears to me to be in no way more divine nor more
sacred than other diseases [...].
The brain is the cause of this affliction [...].
Alexander the Great Julius Caesar Napoleon F. Dostoyevsky
Epileptic seizure
 Abnormal synchronous
discharge of the cortex
leading to transient
dysfunction of the brain
 A seizure can be evoked
by any pathology
affecting the brain,
transient or permanent
 Epileptic seizure =
symptom
Acute symptomatic seizure versus
epilepsy disease
 Acute symptomatic seizure: symptom of a
transient pathological state of the brain
 Withdrawal of alcohol, drugs
 Hypoglycemia
 Fever etc.
 Epilepsy disease: lasting epileptic dysfunction
of the brain → spontaneous seizures
Types of seizures
Generalised seizures
 Tonic - clonic
 Tonic
 Clonic
 Atonic
 Absence
 Myoclonus
Focal (partial)
seizures
 Simplex partial
 Complex partial
 Partial onset with
secondary
generalisation
Seizures of undetermined type
Generalised tonic-clonic seizure
(grand mal)
 The most common seizure
 Acute symptomatic seizures are
generalised tonic-clonic seizures
 Course:
 Cry, loss of consciousness, fall
 Tonic phase- generalised muscle
contraction, apnoea
 Clonic phase- rhythmic
contraction of muscles, tongue
bite, foaming, enuresis
 Terminal sleep and gradual
regaining of consciousness
(transient confusion)
Absence
 Cognitive dysfunction with a
sudden onset and end,
lasting 5-10 seconds
 Stare, expressionless face;
arrest of ongoing activity;
generally no motor
phenomena
 EEG: generalised 3 Hz spike
and wave activity
 Occurs in genetic (idiopathic)
epilepsies, mostly in children
Myoclonic seizure
 Sudden, quick, arrhythmic
muscle contraction, twitch
of a limb; no loss of
consciousness
 EEG: generalised
polyspike and wave activity
 Occurs in genetic (idiopathic)
epilepsies
 Not only an epileptic
phenomenon- it can be the
sign of diffuse
encephalopathies
Simplex partial seizures
 No loss of consciousness
 Symptoms depend on area
of brain involved:
 Motor
 Sensory
 Autonomic
 Psychosensory
 It can be the introductory
phase of a complex partial
or generalised tonic-clonic
seizure (‘aura’)
Complex partial seizures
 Origin is most often in the temporal
lobe
 A common seizure type in
adulthood
 Can be introduced by a simplex
partial psychosensory seizure:
 olfactory hallucination
 déjà vu, jamais vu
 feeling of alienation
 Loss of consciousness: stare,
‘going blank’
 Automatisms:
 oral automatisms
 fiddling with the hands
Causes of epilepsy / epileptic
syndromes
Idiopathic / genetic
epilepsies
 Localisation related:
 Benign centrotemporal epilepsy
 Benign occipital epilepsy
 Autosom dominant nocturnal
frontal lobe epilepsy
 Idiopathic generalised
epilepsy:
 Childhood and juvenile absence
 Juvenile myoclonic epilepsy
 Grand mal seizures on
awakening
Symptomatic epilepsies
 Localisation related :
 Temporal lobe
epilepsy
 Frontal lobe epilepsies
 Parietal, occipital lobe
epilepsies
 Symptomatic generalised
epilepsies:
 West- syndrome
 Lennox-Gastaut syndrome
 Cryptogenic epilepsies
Genetics
 Risk of a non-provoked
seizure in offsprings of a
parent with epilepsy: 6%
 Idiopathic generalised
epilepsies: 9-12%
 Over 140 single gene
diseases are accompanied by
epilepsy
 Inborn metabolic, storage
diseases
 Mitochondrial diseases
 Neurocutaneous diseases
 Chromosomal diseases
Tuberous sclerosis
Benign centrotemporal epilepsy
 Age of onset: 3-15 years
 Seizure types: facial, oro-bucco-
pharyngeal motor and sensory
simplex partial seizures; speech
arrest
 Nocturnal seizures
 Mild disease, therapy not always
needed
 No neurological or mental
alterations
 EEG: centrotemporal spike
waves
 Spontaneous remission by
puberty
Childhood absence epilepsy
 Age of onset: 3-10 years
 Seizure types: absence; often in clusters; hyperventillation and
fotostimulation are provoking
 No neurological or mental alterations
 EEG: generalised 3 Hz spike and wave activity
 Good response to treatment
 Spontaneous remission by puberty
Juvenile myoclonic epilepsy
 Most common form of idiopathic
generalised epilepsy
 Family history positive in 40%
 Age of onset: 15-18 years
 Seizure types:
 myoclonic
 generalised tonic-clonic
 absence
 EEG: generalised 3-4 Hz spike
and wave, polyspike and wave,
hyperventillation and
fotostimulation are provoking
 Good response to treatment, but
needs life-long treatment
Common causes of symptomatic
epilepsies
 Head injury
 Tumors
 Infarcts, hemorrhages
 Blood vessel malformations
 Infections
 Cortical dysgenesis
Cause of newly diagnosed
epilepsies is unknown in 60-
65% (cryptogenic).
Temporal lobe epilepsy
 Most common epilepsy in adulthood;
can be heralded by a few seizures in
childhood, but typical age of onset is
20-22 years
 Seizure types:
 olfactory hallucination (simplex
partial)
 psychosensory seizures (simplex
partial)
 complex partial
 generalised tonic-clonic
 Febrile convulsions in childhood
 Hippocampal sclerosis
 Often refractory to therapy
 Characteropathy, memory
dysfunction
West syndrome
 Age of onset: 3-5 months
 Seizure types: infantile spasms
 Causes: inborn metabolic, storage diseases, perinatal
hipoxic brain damage
 Cryptogenic in 40-50%
 Neurological symptoms, mental retardation; bad
prognosis; can transform into Lennox-Gastaut
syndrome
 EEG: hypsarrhythmia
Lennox-Gastaut syndrome
 Age of onset: 1-8 years
 Seizure types: atonic, axial
tonic, myoclonic, atypical
absence, tonic-clonic
 Injuries are common
 Causes: same as in West
syndrome; can develop from
West syndrome
 Neurological symptoms,
mental retardation
 Unfavourable prognosis,
refractory to treatment
Diagnosis / differential diagnosis
Is it an epileptic
seizure? ?
Yes No
1. Seizure type?
2. Acute symptomatic
seizure or epilepsy?
Epilepsy
Idiopathic or
symptomatic?
Acute symptomatic seizure
Cause?
Symptomatic epilepsy
Cause?
Syncope?
TIA?
Psychogenic?
Epileptic seizure versus syncope
Syncope Tonic-clonic seizure
Position Upright Any
Facial colour Paleness Cyanosis
Onset Gradual; introduced by
dizziness, blurring of vision
Sudden; can start by ‘aura’
(simplex partial seizure)
Twitchings Rarely (‘convulsive syncope’) Always
Enuresis Rarely Often
Tongue bite No Often
Duration 10-20 seconds Few minutes
Postictal confusion No Yes
Perspiration Pronounced Not typical
Diagnostic steps
 History
 EEG
 Negative EEG does not
exclude epilepsy
 Pozitive EEG without clinical
signs does not prove
epilepsy
 EEG after sleep withdrawal or
during sleep
 Long-term EEG / video
monitoring
 CT, MRI
Epilepsy is a clinical diagnosis.
Medical treatment of epilepsy
 When do we start antiepileptic medication
(AED)?
 Which AED to choose?
 When and how do we switch AEDs?
 When is polytherapy needed?
 When can AEDs be discontinued?
 Pregnancy
 Driver’s licence
When do we start treatment?
 More than one non-provoked, well-documented
seizure
 AEDs are usually not started after the first seizure
(needs individual assessment)
 Preventive treatment is not justified
AEDs
Old
 Primidon
 Phenobarbital
 Phenytoin
 Clobazam
 Clonazepam
 Ethosuximid
 Valproate
 Carbamazepine
New
 Lamotrigine
 Oxcarbazepine
 Topiramate
 Gabapentin
 Felbamate
 Vigabatrin
 Levatiracetam
 Zonisamide
 Tiagabin
Mechanism of action of AEDs
Inhibition of voltage gated Na,
Ca channels
Na: phenytoin, carbamazepine,
oxcarbazepine, lamotrigine,
topiramate, felbamate, zonisamide
Ca: ethosuximid, valproate?
lamotrigine, topiramate,
zonisamide
Potentiaton of GABA mediated
inhibition
phenobarbital, benzodiazepins,
vigabatrin, tiagabine, topiramate,
valproate, gabapentin, felbamate
Decrease of glutamate mediated
excitation
felbamate, topiramate
Efficacy of AEDs
All seizure types: absence,
myoclonic, generalised tonic-
clonic seizures, partial seizures
valproate, lamotrigine, topiramate
clobazam, clonazepam
phenobarbital, primidon
felbamate
levatiracetam, zonisamide
Partial seizures, generalised
tonic-clonic seizures
carbamazepine, oxcarbazepine
gabapentin, vigabatrin, tiagabine
phenytoin
Absence ethosuximid
Pharmacology of AEDs I.
Hepatic metabolism valproate, carbamazepine,
oxcarbazepine, lamotrigine,
topiramate, clobazam, clonazepam,
phenobarbital, primidon, phenytoin,
ethosuximid, felbamate, tiagabin
No metabolism gabapentin, vigabatrin
(topiramate, levatiracetam)
Hepatic enzyme induction carbamazepine, phenytoin,
phenobarbital, primidon
(oxcarbazepine)
Hepatic enzyme inhibition valproate, felbamate
Pharmacology of AEDs II.
Phenytoin 7-20 days
Phenobarbital 10-30
Primidon 2-5
Valproate 2-5
Carbamazepine 3-5
Ethosuximid 7-12
Clobazam 4-5
Lamotrigine 3-10
Topiramate 3-6
Gabapentin 2-5
Vigabatrin 2-5
Steady state Binding to plasma proteins
Pronounced
(>90%) binding
phenytoin
valproate
Moderate (30-80%)
binding
carbamazepine
clobazam
lamotrigine
No or minimal
(<20%) binding
gabapentin
vigabatrin
topiramate
ethosuximid
Side effects of AEDs
 Allergy
 Central nervous system side
effects (dose dependent)
 drowsiness, headache
 dizziness, dysequilibrium
 cognitive dysfunction (memory)
 Idiosynchratic reactions / chronic
side effects
 bone marrow suppression
 hepatic failure
 rash
 weight gain, weight loss
 tremor
 polycystic ovary syndrome
 visual field defect
Selection of AEDs
 Selection of AED is based on:
 Seizure type / epilepsy syndrome
 Other: side effects, pharmacology, drug interactions,
comorbidities
 As there are no major differences among first-line AEDs, safety
and tolerability must be of paramount consideration in choosing
AED.
 Matching drugs to patients (holistic approach):
 Side effects
 Work
 Sleep
 Mood
 Well being
Selection of AEDs
Idiopathic generalised epilepsies valproate, topiramate, lamotrigine,
levatiracetam
Localisation related epilepsies (eg.
temporale lobe epilepsy)
carbamazepine, oxcarbazepine,
valproate, lamotrigine, topiramate,
gabapentin, levatiracetam
Symptomatic generalised epilepsies
West-syndrome
Lennox-Gastaut syndrome vigabatrin
felbamate, lamotrigine, valproate
Therapeutic principles
 Aim: maximal seizure control, minimal side
effects
 Monotherapy
 Usually gradual introduction of AED
 Assessment of AED effect (seizure frequency)
 After AED has reached steady state
 Depends on the average time interval of seizures
before treatment
Possible causes of AED inefficacy
 Inadequate dose → dose escalation
 Lack of compliance → measure blood AED levels
 False diagnosis: the patient doesn’t have epilepsy
 ‘Pseudoseizures’ → precise description of seizure, EEG
/ video monitoring
 Inadequate selection of AED
 True inefficacy of AED → AED switch
 Other AED on monotherapy
 AED combination
AED combinations
 Rules of AED combination:
 Establish optimal dose of baseline AED
 Avoid combining similar modes of action
 Add drug with multiple mechanisms
 Titrate new drug slowly
 Be prepared to reduce dose of original drug
 Replace either drug if response is poor
 Some effective combinations:
 valproate-lamotrigine
 valproate-carbamazepine/oxcarbazepine
 valproate-topiramate
 etc.
Drug interactions
Enzyme inductors
carbamazepine, phenytoin
phenobarbital, primidon
Increase of metabolism / decrease
of efficacy
valproate, lamotrigine, topiramate,
carbamazepine
oral contraception
oral anticoagulation
Enzyme inhibitors
valproate
Decrease of metabolism /
increase in efficacy - toxicity
lamotrigine, carbamazepine,
phenytoin
Does not cause interaction
lamotrigine, gabapentin, topiramate,
vigabatrin, tiagabin


Therapeutic success- remission rates
Partial epilepsies
First AED in monotherapy: 43%
Second AED in monotherapy: 7%
Other monotherapies: 2%
AED combination: 5%
Total in remission: 57%
Juvenile myoclonic
epilepsy
First AED (valproate) in
monotherapy: 85%
Altogether 65-70% of patients with epilepsy
respond well to AED treatment.
Discontinuation of AED
 After 3-5 seizure free years
 A decision of both the doctor and patient
 AED should be very slowly tapered, lasting weeks-
months.
 Discontinuation of AED is not recommended:
 Earlier unsuccessful AED withdrawal
 Earlier refractoriness to treatment
 Known brain lesion
 Juvenile myoclonic epilepsy
Epilepsy and pregnancy
 Teratogenic risk
 In normal population: 2-3%
 In women on AEDs: 4-9%
 Teratogenic risk is increased
 High AED dose
 Fluctuating plasma levels
 Polytherapy
 Occurrence of spina bifida in the family
 Folic acid deficiency
Epilepsy and pregnancy: what to do?
 Before conception:
 Attain the best possible seizure control with the lowest possible
AED dose, preferably in monotherapy
 Folic acid profilaction 4 mg/day
 During pregnancy:
 During first trimester supplement folic acid 4 mg/nap
 Change medication only if seizure control worsens
 Screening of fetal malformations (ultrasound on week 16 and
20, AFP)
 In case of enzyme inductor AEDs, give vitamin K in the third
trimester
Epilepsy and breast feeding
 Breast feeding is not contraindicated with
women on AEDs.
 Sleep deprivation can provoke seizures.
Epilepsy and driving
 Driving is prohibited for one year after a seizure
with loss of consciousness
 Driving is permitted:
 2-3 years of seizure free interval with patients on
AEDs
 2-3 years of seizure free interval after withdrawal of
AEDs

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Epilepsy

  • 2. ‘Sacred illness’ • ‘Sacred illness’: 600 BC • Hippocrates 400 BC: It is thus with regard to the disease called sacred: it appears to me to be in no way more divine nor more sacred than other diseases [...]. The brain is the cause of this affliction [...]. Alexander the Great Julius Caesar Napoleon F. Dostoyevsky
  • 3. Epileptic seizure  Abnormal synchronous discharge of the cortex leading to transient dysfunction of the brain  A seizure can be evoked by any pathology affecting the brain, transient or permanent  Epileptic seizure = symptom
  • 4. Acute symptomatic seizure versus epilepsy disease  Acute symptomatic seizure: symptom of a transient pathological state of the brain  Withdrawal of alcohol, drugs  Hypoglycemia  Fever etc.  Epilepsy disease: lasting epileptic dysfunction of the brain → spontaneous seizures
  • 5. Types of seizures Generalised seizures  Tonic - clonic  Tonic  Clonic  Atonic  Absence  Myoclonus Focal (partial) seizures  Simplex partial  Complex partial  Partial onset with secondary generalisation Seizures of undetermined type
  • 6. Generalised tonic-clonic seizure (grand mal)  The most common seizure  Acute symptomatic seizures are generalised tonic-clonic seizures  Course:  Cry, loss of consciousness, fall  Tonic phase- generalised muscle contraction, apnoea  Clonic phase- rhythmic contraction of muscles, tongue bite, foaming, enuresis  Terminal sleep and gradual regaining of consciousness (transient confusion)
  • 7. Absence  Cognitive dysfunction with a sudden onset and end, lasting 5-10 seconds  Stare, expressionless face; arrest of ongoing activity; generally no motor phenomena  EEG: generalised 3 Hz spike and wave activity  Occurs in genetic (idiopathic) epilepsies, mostly in children
  • 8. Myoclonic seizure  Sudden, quick, arrhythmic muscle contraction, twitch of a limb; no loss of consciousness  EEG: generalised polyspike and wave activity  Occurs in genetic (idiopathic) epilepsies  Not only an epileptic phenomenon- it can be the sign of diffuse encephalopathies
  • 9. Simplex partial seizures  No loss of consciousness  Symptoms depend on area of brain involved:  Motor  Sensory  Autonomic  Psychosensory  It can be the introductory phase of a complex partial or generalised tonic-clonic seizure (‘aura’)
  • 10. Complex partial seizures  Origin is most often in the temporal lobe  A common seizure type in adulthood  Can be introduced by a simplex partial psychosensory seizure:  olfactory hallucination  déjà vu, jamais vu  feeling of alienation  Loss of consciousness: stare, ‘going blank’  Automatisms:  oral automatisms  fiddling with the hands
  • 11. Causes of epilepsy / epileptic syndromes Idiopathic / genetic epilepsies  Localisation related:  Benign centrotemporal epilepsy  Benign occipital epilepsy  Autosom dominant nocturnal frontal lobe epilepsy  Idiopathic generalised epilepsy:  Childhood and juvenile absence  Juvenile myoclonic epilepsy  Grand mal seizures on awakening Symptomatic epilepsies  Localisation related :  Temporal lobe epilepsy  Frontal lobe epilepsies  Parietal, occipital lobe epilepsies  Symptomatic generalised epilepsies:  West- syndrome  Lennox-Gastaut syndrome  Cryptogenic epilepsies
  • 12. Genetics  Risk of a non-provoked seizure in offsprings of a parent with epilepsy: 6%  Idiopathic generalised epilepsies: 9-12%  Over 140 single gene diseases are accompanied by epilepsy  Inborn metabolic, storage diseases  Mitochondrial diseases  Neurocutaneous diseases  Chromosomal diseases Tuberous sclerosis
  • 13. Benign centrotemporal epilepsy  Age of onset: 3-15 years  Seizure types: facial, oro-bucco- pharyngeal motor and sensory simplex partial seizures; speech arrest  Nocturnal seizures  Mild disease, therapy not always needed  No neurological or mental alterations  EEG: centrotemporal spike waves  Spontaneous remission by puberty
  • 14. Childhood absence epilepsy  Age of onset: 3-10 years  Seizure types: absence; often in clusters; hyperventillation and fotostimulation are provoking  No neurological or mental alterations  EEG: generalised 3 Hz spike and wave activity  Good response to treatment  Spontaneous remission by puberty
  • 15. Juvenile myoclonic epilepsy  Most common form of idiopathic generalised epilepsy  Family history positive in 40%  Age of onset: 15-18 years  Seizure types:  myoclonic  generalised tonic-clonic  absence  EEG: generalised 3-4 Hz spike and wave, polyspike and wave, hyperventillation and fotostimulation are provoking  Good response to treatment, but needs life-long treatment
  • 16. Common causes of symptomatic epilepsies  Head injury  Tumors  Infarcts, hemorrhages  Blood vessel malformations  Infections  Cortical dysgenesis Cause of newly diagnosed epilepsies is unknown in 60- 65% (cryptogenic).
  • 17. Temporal lobe epilepsy  Most common epilepsy in adulthood; can be heralded by a few seizures in childhood, but typical age of onset is 20-22 years  Seizure types:  olfactory hallucination (simplex partial)  psychosensory seizures (simplex partial)  complex partial  generalised tonic-clonic  Febrile convulsions in childhood  Hippocampal sclerosis  Often refractory to therapy  Characteropathy, memory dysfunction
  • 18. West syndrome  Age of onset: 3-5 months  Seizure types: infantile spasms  Causes: inborn metabolic, storage diseases, perinatal hipoxic brain damage  Cryptogenic in 40-50%  Neurological symptoms, mental retardation; bad prognosis; can transform into Lennox-Gastaut syndrome  EEG: hypsarrhythmia
  • 19. Lennox-Gastaut syndrome  Age of onset: 1-8 years  Seizure types: atonic, axial tonic, myoclonic, atypical absence, tonic-clonic  Injuries are common  Causes: same as in West syndrome; can develop from West syndrome  Neurological symptoms, mental retardation  Unfavourable prognosis, refractory to treatment
  • 20. Diagnosis / differential diagnosis Is it an epileptic seizure? ? Yes No 1. Seizure type? 2. Acute symptomatic seizure or epilepsy? Epilepsy Idiopathic or symptomatic? Acute symptomatic seizure Cause? Symptomatic epilepsy Cause? Syncope? TIA? Psychogenic?
  • 21. Epileptic seizure versus syncope Syncope Tonic-clonic seizure Position Upright Any Facial colour Paleness Cyanosis Onset Gradual; introduced by dizziness, blurring of vision Sudden; can start by ‘aura’ (simplex partial seizure) Twitchings Rarely (‘convulsive syncope’) Always Enuresis Rarely Often Tongue bite No Often Duration 10-20 seconds Few minutes Postictal confusion No Yes Perspiration Pronounced Not typical
  • 22. Diagnostic steps  History  EEG  Negative EEG does not exclude epilepsy  Pozitive EEG without clinical signs does not prove epilepsy  EEG after sleep withdrawal or during sleep  Long-term EEG / video monitoring  CT, MRI Epilepsy is a clinical diagnosis.
  • 23. Medical treatment of epilepsy  When do we start antiepileptic medication (AED)?  Which AED to choose?  When and how do we switch AEDs?  When is polytherapy needed?  When can AEDs be discontinued?  Pregnancy  Driver’s licence
  • 24. When do we start treatment?  More than one non-provoked, well-documented seizure  AEDs are usually not started after the first seizure (needs individual assessment)  Preventive treatment is not justified
  • 25. AEDs Old  Primidon  Phenobarbital  Phenytoin  Clobazam  Clonazepam  Ethosuximid  Valproate  Carbamazepine New  Lamotrigine  Oxcarbazepine  Topiramate  Gabapentin  Felbamate  Vigabatrin  Levatiracetam  Zonisamide  Tiagabin
  • 26. Mechanism of action of AEDs Inhibition of voltage gated Na, Ca channels Na: phenytoin, carbamazepine, oxcarbazepine, lamotrigine, topiramate, felbamate, zonisamide Ca: ethosuximid, valproate? lamotrigine, topiramate, zonisamide Potentiaton of GABA mediated inhibition phenobarbital, benzodiazepins, vigabatrin, tiagabine, topiramate, valproate, gabapentin, felbamate Decrease of glutamate mediated excitation felbamate, topiramate
  • 27. Efficacy of AEDs All seizure types: absence, myoclonic, generalised tonic- clonic seizures, partial seizures valproate, lamotrigine, topiramate clobazam, clonazepam phenobarbital, primidon felbamate levatiracetam, zonisamide Partial seizures, generalised tonic-clonic seizures carbamazepine, oxcarbazepine gabapentin, vigabatrin, tiagabine phenytoin Absence ethosuximid
  • 28. Pharmacology of AEDs I. Hepatic metabolism valproate, carbamazepine, oxcarbazepine, lamotrigine, topiramate, clobazam, clonazepam, phenobarbital, primidon, phenytoin, ethosuximid, felbamate, tiagabin No metabolism gabapentin, vigabatrin (topiramate, levatiracetam) Hepatic enzyme induction carbamazepine, phenytoin, phenobarbital, primidon (oxcarbazepine) Hepatic enzyme inhibition valproate, felbamate
  • 29. Pharmacology of AEDs II. Phenytoin 7-20 days Phenobarbital 10-30 Primidon 2-5 Valproate 2-5 Carbamazepine 3-5 Ethosuximid 7-12 Clobazam 4-5 Lamotrigine 3-10 Topiramate 3-6 Gabapentin 2-5 Vigabatrin 2-5 Steady state Binding to plasma proteins Pronounced (>90%) binding phenytoin valproate Moderate (30-80%) binding carbamazepine clobazam lamotrigine No or minimal (<20%) binding gabapentin vigabatrin topiramate ethosuximid
  • 30. Side effects of AEDs  Allergy  Central nervous system side effects (dose dependent)  drowsiness, headache  dizziness, dysequilibrium  cognitive dysfunction (memory)  Idiosynchratic reactions / chronic side effects  bone marrow suppression  hepatic failure  rash  weight gain, weight loss  tremor  polycystic ovary syndrome  visual field defect
  • 31. Selection of AEDs  Selection of AED is based on:  Seizure type / epilepsy syndrome  Other: side effects, pharmacology, drug interactions, comorbidities  As there are no major differences among first-line AEDs, safety and tolerability must be of paramount consideration in choosing AED.  Matching drugs to patients (holistic approach):  Side effects  Work  Sleep  Mood  Well being
  • 32. Selection of AEDs Idiopathic generalised epilepsies valproate, topiramate, lamotrigine, levatiracetam Localisation related epilepsies (eg. temporale lobe epilepsy) carbamazepine, oxcarbazepine, valproate, lamotrigine, topiramate, gabapentin, levatiracetam Symptomatic generalised epilepsies West-syndrome Lennox-Gastaut syndrome vigabatrin felbamate, lamotrigine, valproate
  • 33. Therapeutic principles  Aim: maximal seizure control, minimal side effects  Monotherapy  Usually gradual introduction of AED  Assessment of AED effect (seizure frequency)  After AED has reached steady state  Depends on the average time interval of seizures before treatment
  • 34. Possible causes of AED inefficacy  Inadequate dose → dose escalation  Lack of compliance → measure blood AED levels  False diagnosis: the patient doesn’t have epilepsy  ‘Pseudoseizures’ → precise description of seizure, EEG / video monitoring  Inadequate selection of AED  True inefficacy of AED → AED switch  Other AED on monotherapy  AED combination
  • 35. AED combinations  Rules of AED combination:  Establish optimal dose of baseline AED  Avoid combining similar modes of action  Add drug with multiple mechanisms  Titrate new drug slowly  Be prepared to reduce dose of original drug  Replace either drug if response is poor  Some effective combinations:  valproate-lamotrigine  valproate-carbamazepine/oxcarbazepine  valproate-topiramate  etc.
  • 36. Drug interactions Enzyme inductors carbamazepine, phenytoin phenobarbital, primidon Increase of metabolism / decrease of efficacy valproate, lamotrigine, topiramate, carbamazepine oral contraception oral anticoagulation Enzyme inhibitors valproate Decrease of metabolism / increase in efficacy - toxicity lamotrigine, carbamazepine, phenytoin Does not cause interaction lamotrigine, gabapentin, topiramate, vigabatrin, tiagabin  
  • 37. Therapeutic success- remission rates Partial epilepsies First AED in monotherapy: 43% Second AED in monotherapy: 7% Other monotherapies: 2% AED combination: 5% Total in remission: 57% Juvenile myoclonic epilepsy First AED (valproate) in monotherapy: 85% Altogether 65-70% of patients with epilepsy respond well to AED treatment.
  • 38. Discontinuation of AED  After 3-5 seizure free years  A decision of both the doctor and patient  AED should be very slowly tapered, lasting weeks- months.  Discontinuation of AED is not recommended:  Earlier unsuccessful AED withdrawal  Earlier refractoriness to treatment  Known brain lesion  Juvenile myoclonic epilepsy
  • 39. Epilepsy and pregnancy  Teratogenic risk  In normal population: 2-3%  In women on AEDs: 4-9%  Teratogenic risk is increased  High AED dose  Fluctuating plasma levels  Polytherapy  Occurrence of spina bifida in the family  Folic acid deficiency
  • 40. Epilepsy and pregnancy: what to do?  Before conception:  Attain the best possible seizure control with the lowest possible AED dose, preferably in monotherapy  Folic acid profilaction 4 mg/day  During pregnancy:  During first trimester supplement folic acid 4 mg/nap  Change medication only if seizure control worsens  Screening of fetal malformations (ultrasound on week 16 and 20, AFP)  In case of enzyme inductor AEDs, give vitamin K in the third trimester
  • 41. Epilepsy and breast feeding  Breast feeding is not contraindicated with women on AEDs.  Sleep deprivation can provoke seizures.
  • 42. Epilepsy and driving  Driving is prohibited for one year after a seizure with loss of consciousness  Driving is permitted:  2-3 years of seizure free interval with patients on AEDs  2-3 years of seizure free interval after withdrawal of AEDs