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EPILEPSY
DR.MALIHA
DEFINATION
Term epilepsy is derived from the Greek word
Epilepsia” which means ‘to be seized’, ‘to be taken
hold of’, or ‘to be attacked’
Epilepsy: A condition in which a person has
recurrent seizures due to chronic, underlying process
Characterized by,
 Recurrent seizures –
 Loss of consciousness
 With or without body movements
CLINICAL DEFINITION
 Epilepsy – a predisposition to having 2 or
more unprovoked seizures in 24 hours
 Seizure; Sudden, involuntary, usually time-
limited alteration in behavior, including motor
activity, autonomic function, consciousness, or
sensation.
 Caused by abnormal electrical discharges of
neuronal circuits
MECHANISM OF SEIZURE
1. Mutation ; in voltage gated channels, ligand gated
channels and other proteins.
2. Epileptogenesis ; mechanism through which
brain or part of brain become epileptic.
3. Paroxysmal depolarization shift
Sudden Depolarization series of AP After-
Hyperpolarization(K ,GABA)
Cl- channel open disrupted sufficient neuron
inhibitory neuron lost and excitatory neuron fires at same
time seizure
CAUSES
 Idiopathic (70 – 80%) – cause unknown but presumed
genetic
 Secondary
 Cerebral dysgenesis /malformation
 Cerebral vascular occlusion
 Cerebral damage
-Antenatal: Congenital infections, drugs, alcohol
. -Natal: HIE, birth trauma
- Postnatal: IVH in prematurity, CNS infections,
kernicterus, trauma.
 Cerebral tumors
 Neurodegenerative disorders
 Neurocutaneous syndrome
CLASSIFICATION
TONIC- CLONIC SEIZURES(GRAND MAL
EPILEPSY)
1.Aural stage; which may be sensory or motor
2.Tonic stage;
 Onset is abrupt with tonic spasm
 Pt loses consciousness and may fall on ground
 Facial pallor ,up rolling of eye ,pupil dilated ,conjunctiva
become insensitive, tongue biting , muscles become
stiff. This stage lasts for 10-20 seconds
3.Clonic stage; is characterize by shaking of trunk and
extremities and frothing in mouth. phase lasts for 30 sec
4.Postictal stage; Pt exhausted and confused going to
sleep for many hours
 Transient paralysis may occur (Todd's paralysis)
CLINICAL AND EEG FINDING
ABSENCE SEIZURE( PETIT MAL EPILEPSY)
1.Typical absence seizure start at 5-8 year of age
and disappear after puberty.
 Do not have an aura.
 Seizure consist of transient loss of consciousness ,
vacant stares, up rolling of eye, blinking and nodding of
head . Followed by resumption of work as before
seizure.
 EEG as generalized 3 per sec . spike & wave pattern.
2.Atypical absence seizure consist of myoclonic
components and tone changes of head and body
 Associated with 1-2 Hz spike and slow discharge
3.Juvenile absence seizure similar to typical seizure
but 4-5 Hz spike
CLINICAL AND EEG FINDING
MYOCLONIC EPILEPSY
 It is characterize by frequent recurrence of brief minor
seizure , brief muscle contraction and atonia resulting in
multiple falls.
 It is associated with mental retardation and is resistance
to drug . Having several forms;
 Benign myoclonus of infancy ;having myoclonic
movements confine to neck , trunk and extremities .
EEG is normal
 Typical myoclonic epilepsy of early childhood;
 Mean age is 2-4 years .1/3 children have +ve family
history . EEG shows fast spike wave complexes>2.5Hz
.Prognosis is good.
 Progressive myoclonic epilepsy; progressive
dementia and myoclonus.
 Prognosis is poor.
MYOCLONIC……..
 Complex myoclonic epilepsy;
 1/3 have delayed developmental milestone .
 Hx of HIE may present.
 Generalized upper motor and extrapyramidal sign with
microcephaly .
 Prognosis is poor.
 Juvenile myoclonic epilepsy(Janz syndrome)
 It occur at12-16 years.
 Child experience frequent myoclonic jerks on
awakening. After some years early morning generalized
tonic- clonic seizures develop in association with
myoclonus.
 Neurological examination is normal.
1.SIMPLE PARTIAL SEIZURE
 Focal seizure without impairment of consciousness
 Specific nature which gives clue of location of
seizure.
 Brief motor seizure include focal tonic , clonic or
atonic seizure.
2.Complex Partial Seizure
 Focal seizure with impairment of consciousness
 It usually last 1-2 min and are preceded by aura .
SIMPLE PARTIAL SEIZURES
COMPLEX PARTIAL SEIZURES
INFANTILE SPASMS
 3 to 9 month of age.
 Brief symmetrical contractions of neck, trunk ,
extremities , sudden dropping of head & flexion of
arms - ‘Salaam fit’
 EEG- Hypsarrhythmic pattern – diffuse high voltage
slow spike and chaotic activity
INFANTILE SPASM …….
1. Cryptogenic -10-20% cases - Normal birth Hx -
Normal development - Neurologic exam, CT,MRI
head normal - No risk factors
2. Symptomatic- 80-90% cases Related to brain
damage from prenatal insult ,HIE, cong infections,
inborn errors of metabolism, , Cong anomalies of
brain Post natal insult, infections, head Trauma, 80-
90% MR
LENNOX –GASTAUT SYNDROME
 Onset –late infancy or childhood
 Mixed seizure- myoclonic, atypical absence
,generalized tonic-clonic, partial
 Prognosis unsatisfactory
Triad;
1.Atypical absences, axial tonic seizures, drop
attacks
2. Typical EEG pattern - Slow spike and waves on
awake EEG & 10Hz bursts during sleep
3.Psychomotor retardation
APPROACH TO THE PATIENT
 History and physical - emphasis on seizure event is
most valuable tool
 Lab tests - CBC, metabolic profile.
 Electroencephalogram(EEG) –
To correlate with seizure activity and electrical discharges
in the brain
 Spinal tap for CSF analysis
 Brain imaging studies – CT and MRI
 PET and SPECT; To detect areas of hypometabolism in
epileptogenic lesions.
 Genetic studies.
TREATMENT
1. Deciding of long term therapy
2. Counseling
PRINCIPLES OF ANTICONVULSANT
THERAPY
 Treatment recommended if ≥ 2 episodes→ recurrence
risk 80%
 Attempt to classify the seizure type & epileptic
syndrome
 Monotherapy as far as possible → most appropriate
drug → increase dose gradually till epilepsy controlled,
maximum dose reached .
 Alternative monotherapy (Add on the 2nd drug if 1st
drug failed. Optimize 2nd drug, then try to withdraw 1st
drug.
 Rational combination therapy (usually 2 or maximum 3
drugs )
 Combines drugs with different mechanism of action &
consider their spectrum of efficacy, drug interactions &
adverse affects.
 Monitor drug levels to check compliance → if
seizures not well controlled/in situations of
combination therapy where drug interaction is
suspected.
 When withdrawal of medication is planned →
seizure free for 2 years . Then attempting slow
withdrawal of medication over 3-6 months .
 If seizures recur → last dose reduction is
reversed & medical advice sought.
ADVICE FOR PATIENTS/PARENTS
 Educate and counsel on epilepsy.
 Emphasize compliance if on anticonvulsant.
 Don’t stop the medication by themselves . this may
precipitate breakthrough seizures.
 In photosensitive seizures-watch TV in brightly lit
room . avoid sleep deprivation.
 Use a shower with bathroom door unlocked.
 No cycling in traffic , climbing sports or swimming
alone.
 Know emergency treatment for seizure.
 Inform teachers and school about the condition.
CHOICE OF DRUG
 Drug of first choice
 Focal seizure ; oxcarbazepine and carbamazepine
 Absence seizure; ethosuximide
 Juvenile myoclonic epilepsy; Valporate nd
lemotrigene
 Lennox- Gastaut syndrome ; clobazam , valporate ,
topiramate , lamotrigine, and rufinamide
 Infantile spasm ;adrenocorticotropic hormone
(ACTH)
ADJUNCTIVE T WHEN S POORLY
CONTROLLED
 Gabapentine , clobazam , lamotrigine, topiramate
, vigabatrin
Surgical Rx -Resection of corpus callosum,
 Focal resection of parts of cerebral cortex involved
as epileptic foci.
 Recommended
for refractory
seizure
 Ketosis raises
the seizure
threshold
 Diet consist of
3:1 or 4:1
INTRACTABLE /REFRACTORY EPILEPSY
Re- evaluate the following possibilities
 Is it a seizure /non epileptic event ?
 Anticonvulsant dose not optimized.
 Poor compliance to anticonvulsant
 Wrong classification of epilepsy syndrome →
wrong anticonvulsant .
 Anticonvulsant aggravating seizures.
 Lesional epilepsy, hence a potential epilepsy
surgery candidate .
 Progressive epilepsy or neurodegenerative
disorder.
Epilepsy
Epilepsy

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Epilepsy

  • 2. DEFINATION Term epilepsy is derived from the Greek word Epilepsia” which means ‘to be seized’, ‘to be taken hold of’, or ‘to be attacked’ Epilepsy: A condition in which a person has recurrent seizures due to chronic, underlying process Characterized by,  Recurrent seizures –  Loss of consciousness  With or without body movements
  • 3. CLINICAL DEFINITION  Epilepsy – a predisposition to having 2 or more unprovoked seizures in 24 hours  Seizure; Sudden, involuntary, usually time- limited alteration in behavior, including motor activity, autonomic function, consciousness, or sensation.  Caused by abnormal electrical discharges of neuronal circuits
  • 4. MECHANISM OF SEIZURE 1. Mutation ; in voltage gated channels, ligand gated channels and other proteins. 2. Epileptogenesis ; mechanism through which brain or part of brain become epileptic. 3. Paroxysmal depolarization shift Sudden Depolarization series of AP After- Hyperpolarization(K ,GABA) Cl- channel open disrupted sufficient neuron inhibitory neuron lost and excitatory neuron fires at same time seizure
  • 5. CAUSES  Idiopathic (70 – 80%) – cause unknown but presumed genetic  Secondary  Cerebral dysgenesis /malformation  Cerebral vascular occlusion  Cerebral damage -Antenatal: Congenital infections, drugs, alcohol . -Natal: HIE, birth trauma - Postnatal: IVH in prematurity, CNS infections, kernicterus, trauma.  Cerebral tumors  Neurodegenerative disorders  Neurocutaneous syndrome
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  • 9. TONIC- CLONIC SEIZURES(GRAND MAL EPILEPSY) 1.Aural stage; which may be sensory or motor 2.Tonic stage;  Onset is abrupt with tonic spasm  Pt loses consciousness and may fall on ground  Facial pallor ,up rolling of eye ,pupil dilated ,conjunctiva become insensitive, tongue biting , muscles become stiff. This stage lasts for 10-20 seconds 3.Clonic stage; is characterize by shaking of trunk and extremities and frothing in mouth. phase lasts for 30 sec 4.Postictal stage; Pt exhausted and confused going to sleep for many hours  Transient paralysis may occur (Todd's paralysis)
  • 10. CLINICAL AND EEG FINDING
  • 11. ABSENCE SEIZURE( PETIT MAL EPILEPSY) 1.Typical absence seizure start at 5-8 year of age and disappear after puberty.  Do not have an aura.  Seizure consist of transient loss of consciousness , vacant stares, up rolling of eye, blinking and nodding of head . Followed by resumption of work as before seizure.  EEG as generalized 3 per sec . spike & wave pattern. 2.Atypical absence seizure consist of myoclonic components and tone changes of head and body  Associated with 1-2 Hz spike and slow discharge 3.Juvenile absence seizure similar to typical seizure but 4-5 Hz spike
  • 12. CLINICAL AND EEG FINDING
  • 13. MYOCLONIC EPILEPSY  It is characterize by frequent recurrence of brief minor seizure , brief muscle contraction and atonia resulting in multiple falls.  It is associated with mental retardation and is resistance to drug . Having several forms;  Benign myoclonus of infancy ;having myoclonic movements confine to neck , trunk and extremities . EEG is normal  Typical myoclonic epilepsy of early childhood;  Mean age is 2-4 years .1/3 children have +ve family history . EEG shows fast spike wave complexes>2.5Hz .Prognosis is good.  Progressive myoclonic epilepsy; progressive dementia and myoclonus.  Prognosis is poor.
  • 14. MYOCLONIC……..  Complex myoclonic epilepsy;  1/3 have delayed developmental milestone .  Hx of HIE may present.  Generalized upper motor and extrapyramidal sign with microcephaly .  Prognosis is poor.  Juvenile myoclonic epilepsy(Janz syndrome)  It occur at12-16 years.  Child experience frequent myoclonic jerks on awakening. After some years early morning generalized tonic- clonic seizures develop in association with myoclonus.  Neurological examination is normal.
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  • 16. 1.SIMPLE PARTIAL SEIZURE  Focal seizure without impairment of consciousness  Specific nature which gives clue of location of seizure.  Brief motor seizure include focal tonic , clonic or atonic seizure. 2.Complex Partial Seizure  Focal seizure with impairment of consciousness  It usually last 1-2 min and are preceded by aura .
  • 19. INFANTILE SPASMS  3 to 9 month of age.  Brief symmetrical contractions of neck, trunk , extremities , sudden dropping of head & flexion of arms - ‘Salaam fit’  EEG- Hypsarrhythmic pattern – diffuse high voltage slow spike and chaotic activity
  • 20. INFANTILE SPASM ……. 1. Cryptogenic -10-20% cases - Normal birth Hx - Normal development - Neurologic exam, CT,MRI head normal - No risk factors 2. Symptomatic- 80-90% cases Related to brain damage from prenatal insult ,HIE, cong infections, inborn errors of metabolism, , Cong anomalies of brain Post natal insult, infections, head Trauma, 80- 90% MR
  • 21. LENNOX –GASTAUT SYNDROME  Onset –late infancy or childhood  Mixed seizure- myoclonic, atypical absence ,generalized tonic-clonic, partial  Prognosis unsatisfactory Triad; 1.Atypical absences, axial tonic seizures, drop attacks 2. Typical EEG pattern - Slow spike and waves on awake EEG & 10Hz bursts during sleep 3.Psychomotor retardation
  • 22. APPROACH TO THE PATIENT  History and physical - emphasis on seizure event is most valuable tool  Lab tests - CBC, metabolic profile.  Electroencephalogram(EEG) – To correlate with seizure activity and electrical discharges in the brain  Spinal tap for CSF analysis  Brain imaging studies – CT and MRI  PET and SPECT; To detect areas of hypometabolism in epileptogenic lesions.  Genetic studies.
  • 23. TREATMENT 1. Deciding of long term therapy 2. Counseling
  • 24. PRINCIPLES OF ANTICONVULSANT THERAPY  Treatment recommended if ≥ 2 episodes→ recurrence risk 80%  Attempt to classify the seizure type & epileptic syndrome  Monotherapy as far as possible → most appropriate drug → increase dose gradually till epilepsy controlled, maximum dose reached .  Alternative monotherapy (Add on the 2nd drug if 1st drug failed. Optimize 2nd drug, then try to withdraw 1st drug.  Rational combination therapy (usually 2 or maximum 3 drugs )  Combines drugs with different mechanism of action & consider their spectrum of efficacy, drug interactions & adverse affects.
  • 25.  Monitor drug levels to check compliance → if seizures not well controlled/in situations of combination therapy where drug interaction is suspected.  When withdrawal of medication is planned → seizure free for 2 years . Then attempting slow withdrawal of medication over 3-6 months .  If seizures recur → last dose reduction is reversed & medical advice sought.
  • 26. ADVICE FOR PATIENTS/PARENTS  Educate and counsel on epilepsy.  Emphasize compliance if on anticonvulsant.  Don’t stop the medication by themselves . this may precipitate breakthrough seizures.  In photosensitive seizures-watch TV in brightly lit room . avoid sleep deprivation.  Use a shower with bathroom door unlocked.  No cycling in traffic , climbing sports or swimming alone.  Know emergency treatment for seizure.  Inform teachers and school about the condition.
  • 27. CHOICE OF DRUG  Drug of first choice  Focal seizure ; oxcarbazepine and carbamazepine  Absence seizure; ethosuximide  Juvenile myoclonic epilepsy; Valporate nd lemotrigene  Lennox- Gastaut syndrome ; clobazam , valporate , topiramate , lamotrigine, and rufinamide  Infantile spasm ;adrenocorticotropic hormone (ACTH)
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  • 30. ADJUNCTIVE T WHEN S POORLY CONTROLLED  Gabapentine , clobazam , lamotrigine, topiramate , vigabatrin Surgical Rx -Resection of corpus callosum,  Focal resection of parts of cerebral cortex involved as epileptic foci.
  • 31.  Recommended for refractory seizure  Ketosis raises the seizure threshold  Diet consist of 3:1 or 4:1
  • 32. INTRACTABLE /REFRACTORY EPILEPSY Re- evaluate the following possibilities  Is it a seizure /non epileptic event ?  Anticonvulsant dose not optimized.  Poor compliance to anticonvulsant  Wrong classification of epilepsy syndrome → wrong anticonvulsant .  Anticonvulsant aggravating seizures.  Lesional epilepsy, hence a potential epilepsy surgery candidate .  Progressive epilepsy or neurodegenerative disorder.