1. Febrile seizures are seizures that occur in children between 6 months and 5 years of age associated with a fever over 38°C but without an underlying infection or metabolic imbalance. They are classified as simple or complex based on duration and recurrence. 2. The underlying pathophysiology of febrile seizures is unknown but likely involves a genetic predisposition. Risk factors include a family history of febrile seizures and developmental delays. 3. Management of febrile seizures focuses on treating the underlying cause of fever. For recurrent or prolonged seizures, antiepileptic drugs may be considered.

1. CHILDHOOD SEIZURE AND ITS MANAGEMENT
Dr. TAUHID IQBALI
MBBS (JIPMER)
MD PEAD Jr.II ( PMCH Patna )

2. Learning Objectives
Define what we mean by seizures and related terminology
Understand the different types of seizures
Understand the pathophysiology of seizures
Understand AED mechanism of actions and common side effects
Approach to the child with a suspected seizure disorder
Know the emergency and long term management of seizure

3. SEIZURE
WHAT IS IT?
A Seizure is a transient occurrence of signs and/or symptoms
resulting from abnormal excessive or synchronous neuronal
activity in the brain.

4. RELATED TERMINOLOGIES
Symptomatic epilepsy
Epilepsy is called ‘symptomatic’ when it has a known cause
• Acute symptomatic seizure
• Remote symptomatic seizure
Idiopathic epilepsy
Epilepsy is called ‘idiopathic’ when it is thought to be due to a genetic tendency
(which could have been inherited from one or both parents) or due to a
change that happens in the person's genes before they are born.
Cryptogenic epilepsy( presumed symptomatic epilepsy)
This is when the cause for a person's epilepsy has not yet been found, despite
investigations but there is presumed underlying brain disorder.
Epilepsy
≥ 2 unprovoked seizures occur in a time frame of > 24 hr
secondary to a distant brain injury such as a old stroke.
secondary to an acute problem affecting brain excitability such as electrolyte
imbalance or meningitis etc.
Brain disorder with an enduring predisposition to generate epileptic seizure

5. RELATED TERMINOLOGIES
Epileptic encephalopathy
Epilepsy syndrome in which the severe EEG abnormality is thought to result in
cognitive and other impairments in the patient.
Febrile seizure
• Seizures that occur between the age of 6 and 60 months
• With a temperature of 38 ° C or higher
• That are not the result of central nervous system infection or any metabolic imbalance
• And that occur in the absence of a history of prior afebrile seizures
Status Epilepticus
Two or more seizures without recovery of consciousness in between
Single seizure >30 min (operationally >5 min)
Epileptic syndrome
Seizure disorder that manifests one or more specific seizure types and has
a specific age of onset and a specific prognosis

6. SEIZURE- PATHOPHYSIOLOGY
PATHOPHYSIOLOGY OF GENESIS OF SEIZURES CONSIST OF CONSIST OF:
- 4 DISTINCT
- OFTEN SEQUENTIAL( But not always)
AND THESE ARE:
1. UNDERLYING ETIOLOGY
2. EPILEPTOGENESIS
3. PDS AFTERHYPERPOLARIZATION DISRUPTION
4. SEIZURE RELATED NEURONAL INJURY
MECHANISTIC PROCESS

7. SEIZURE- PATHOPHYSIOLOGY
UNDERLYING ETIOLOGY
(ANY PROCESS THAT CAN DISRUPT NEURONAL FUNCTION AND CONNECTIVITY)
LEADS TO PROCESS OF MAKING THE BRAIN EPILEPTIC
EPILEPTOGENESIS
(MECHANISM DURING WHICH BRAIN TURNS EPILEPTIC)
PDS AFTERHYPERPOLARIZATION DISRUPTION
LEADS TO
SEIZURE FOCUS
SEIZURE
SEIZURE RELATED NEURONAL INJURY
APOPTOSIS AND NECROSIS OF NEURONS
FURTHER SEIZURE

8. SEIZURE- PATHOPHYSIOLOGY
MECHANISM OF EPILEPTOGENESIS
REPETATIVE STIMULATION
ACTIVATES
METABOTROPIC AND IONOTROPIC GLUTAMATE
RECEPTORS AS WELL TrKB AND NT-4 RECEPTORS
INCREASES INTRANEURAL CALCIUM
ACTIVATES
CaMKII AND CALCINEURIN
Ca DEPENDENT EPILEPTOGENIC GENE
EXPRESSION (eg c-fos)
PROMOTE MOSSY FIBRE SPROUTING
INCREASED EXCITABILITY
EXCITATORY INTERNEURON INHIBITORY INTERNEURON
NO SEIZURE

9. SEIZURE- PATHOPHYSIOLOGY
PDS (PAROXYSMAL DEPOLARIZATION SHIFT)
STEREOTYPIC SYNCHRONIZED RESPONSE OF EACH NEURON IN A SEIZURE
FOCUS
IT CONSIST OF :
• DEPOLARIZATION PHASE
• AFTERHYPERPOLARIZATION PHASE
DEPOLARIZATION PHASE
IT OCCUR DUE TO GLUTAMATE AND CALCIUM CHANNEL ACTIVATION RESULTING IN
SERIES OF ACTION POTENTIALS
AFTERHYPERPOLARIZATION PHASE
IT OCCUR DUE TO ACTIVATION OF POTASSIUM CHANNELS AND GABA RECEPTORS RESULTING
IN INHIBITION OF ACTION POTENTIALS
SO WHEN PDS AFTERHYPERPOLARIZATION IS DISRUPTED, THE INHIBITORY SURROUND IS LOST AND THE
NEURONS FIRES CONTINIOUSLY RESULTING IN SEIZURE FOCUS

10. Types of seizures
Absence Myoclonic Tonic-Clonic Tonic Atonic
Partial Generalised
Seizures
Simple Complex
specific area in one
cerebral hemisphere
both cerebral hemispheres
no loss of
conciousness
conciousness impaired Secondary
generalized
seizure

14. GENERALIZED SEIZURE

15. GENERALIZED SEIZURE
TONIC-CLONIC SEIZURE

16. GENERALIZED SEIZURE
CLONIC SEIZURE
Repetitive
jerking movements

17. GENERALIZED SEIZURE
TONIC SEIZURE
Muscle stiffness
Rigidity

18. GENERALIZED SEIZURE
ATONIC SEIZURE
The ictal phenomenon in
these seizures is a sudden
generalized loss of tone.
This may manifest as a head
drop or if the patient is
standing as a forward fall

19. GENERALIZED SEIZURE
MYOCLONIC SEIZURE
These are brief jerks of the extremities and/or
axial trunk muscles

20. GENERALIZED SEIZURE
ABSENCE SEIZURE
Typical
• Behavioral and mental arrest for a few seconds
• The patient typically resumes their activity as if nothing had happened
Atypical
• Behavioral arrest may be longer
• More difficult to ascertain the arrest as such, compared to the patient’s
behavior at baseline

21. PARTIAL SEIZURE

22. ANTIEPILEPTIC DRUGS

23. Old drugs (Before 1993)
Carbamazepine
Clonazepam
Ethosuximide
Phenobarbital
Phenytoin
Primidone
Valproic acid
New drugs (Since 1993)
Felbamate
Gabapentin
Lamotrigine
Levetiracetam
Lacosamide
Oxcarbazepine
Pregabalin
Tiagabine
Topiramate
Vigabatrine
Zonisamide
Ezogabine
Rufinamide
Eslicarbazepine

24. Mechanism of Action of AED
Seizure!!! Control
EPSPs
Na+ Influx
Ca++ Currents
Paroxysmal Depolarization
IPSPs
K+ Efflux(GABA mediated)
Cl- Influx(GABA mediated)
Channel(Glutamate mediated)
Low pH

26. Enhanced Sodium channel inactivation
Na
+
Na
+
Valproate
Carbamazepine
Phenytoin
Lamotrigine
Topiramate
Zonisamide
Activation gate
Inactivation gate
Felbamate
Rufinamide Lacosamide
Resting state
Active state
Inactive state

27. • P-Phenytoin
• V-Valproate
• R-Rufinamide
• T-Topiramate
• F-Felbamate
• C-Carbamazepine
• Zinger chicken -zonisamide
• Le-Lamotrigine
• Lo-Lacosamide

28. Ca++
Ca++
Ethosuximide Valproate
Reduced current through T type Calcium channels
Zonisamide

29. GABA Enhancers
TiagabineGabapentin
Valproate
BarbiturateBZD
Vigabatrine

30. Glutamate blockers
Metabotrophic
Under research
AMPA Blocker
Topiramate
NMDA Blockers
Felbamate
Levetiracetam

31. Carbonic anhydrase inhibitors
Inhibition of the enzyme carbonic anhydrase
Concentration of hydrogen ions intra cellularly and decreases the pH
Potassium ions shift (efflux) to the extracellular compartment to buffer the acid-base status
Hyperpolarization
Increase seizure threshold

32. AED Adverse effects

33. Cerebellar
Phenytoin
Carbamazepine
Valproic acid
Lamotrigine
Ethosuximide
Gabapentin
Lacosamide
Rufinamide
Psychomotor slowing
Language problems
Topiramate
Tiagabine
Mood changes
Felbamate
Levetiracetam
Zonisamide

34. Cardiac conduction
Lacosamide
Rufinamide
Hepatotoxicity
Valproate
Benzodiapine
Felbamate
BM Suppression
Carbamazepine
Ethosuximide
Levetiracitam
Valproate
Felbamate
Skin rash
Lamotrigine
Phenytoin
Carbamazepine
Phenobarbitone

35. Phenytoin
Gum hyperplasia
Hirsutism
Osteomalacia
CBZ
Hyponatremia
VPA
Increase NH3
Weight gain
Topiramate
Renal stones
Weight loss
Glaucoma

36. AED-DRUG INTERACTIONS
ENZYME INDUCERS
Phenobarbital
Carbamazepine
Phenytoin
Primidone
ENZYME INHIBITOR
Valporate
Reduces levels of:
Valporate
Lamotrigine
Topiramate
Zosnisamide
Inhibits metabolism and
increases levels of:
Phenobarbital
Lamotrigine
Felbamate

37. AED- INTERACTIONS
VALPORATE DISPLACES PROTEIN BOUND PHENYTOIN FROM PROTEIN
BINDING SITE THUS INCREASING FREE FRACTION OF PHENYTOIN - SO WHEN
BOTH ARE BEING USED FREE FRACTION OF PHENYTOIN SHOULD BE
CHECKED.
MEDICATION EXCLUSIVELY EXCREATED BY KIDNEY
LEVETIRACETAM
GABAPENTIN LESS INTERACTION WITH OTHER DRUGS

38. AED AND ATT INTERACTIONS
INH increase
PHT and CBZ level
INH and Rifampicin increase
Carbamazepine level
Rifampicin reduces
Phenytoin and valproate level

39. AED AND ART INTERACTIONS
With Phenytoin -- ↑Dose of Ritonavir & Lopinavir
With Valproate -- ↓ Dose of Zidovudine
With Ritonavir / Atazanavir --↑Dose of Lamotrigine
Avoid enzyme inducing AED with PI/NNRTI

40. APPROACH TO THE CHILD WITH A SUSPECTED SEIZURE DISORDER

41. APPROACH TO THE CHILD WITH A SUSPECTED SEIZURE DISORDER
DID THE CHILD HAVE A SEIZURE?
NO YES
BENIGN PAROXYSMAL VERTIGO
SYNCOPE
FAMILIAL CHOREOATHETOSIS
HEREDITARY CHIN TREMBLING
SHUDDERING ATTACKS
NARCOLEPSY
NIGHT TERROR
PSEUDOSEIZURES
NIGHT TERROR
RAGE ATTACK
BENIGN MYOCLONUS OF INFANCY
TICS
INITIAL SEIZURE
RBS
SERUM CALCIUM
MAGNESIUM
POTASSIUM
SODIUM
EEG?
CT BRAIN?
MRI BRAIN?
CSF EXAMINATION?
RECURRENT SEIZURES
DRUG COMPLIANCE?
IMPROPER DOSE?
INCORRECT DRUG?
METABOLIC DISORDER?
UNDERLYING STRUCTURAL LESION?
DRUG INTERACTION?
CNS DEGENERATIVE DISEASE?
INTRACTABLE SEIZURE?
STUDIES AND EXAMINATION
ABNORMAL
SYMPTOMATIC SEIZURE
TREAT UNDERLYING CAUSE
AED IF NECESSARY
NORMAL
ISOLATED FIRST SEIZURE
WITH NORMAL EEG
NEGATIVE FAMILY HISTORY
NO CONTINUOUS DRUG RX
CLOSE OBSERVATION
PRESCRIBE RESCUE MEDICATIONS
FOR SEIZURE
NORMAL( EXCEPT EEG)
CONSIDER DRUG THERAPY
FOLLOW UP

42. APPROACH TO THE CHILD WITH A SUSPECTED SEIZURE DISORDER
FOLLOW UP
GOOD CONROL
REGULAR FOLLOW –UP
AED DRUG LEVELS
MONITOR TOXICITY(CBC,LFT,
BEHAVIOUR, LEARNING)
EEG AS INDICATED
POOR CONTROL
CONSIDER HOSPITALIZATION
PROLONGED EEG RECORDING AND
VIDEO MONITORING FOR
POSSIBLE EPILEPSY
READJUST MEDICATION
CONSIDER UNDERLYING PATHOLOGY
AND REINVETIGATE WITH CT OR MRI
FREQUENT FOLLOW UP

43. Febrile Seizures-Criteria
Seizures that occur between the age of 6 and 60 months
With a temperature of 38 ° C or higher
That are not the result of central nervous system infection or any metabolic
imbalance
And that occur in the absence of a history of prior afebrile seizures

44. Febrile Seizures-Types
Simple febrile seizure (all of the following) 70-75%
Duration of less than 15 minutes
Generalized
No previous neurologic problems
Occur once in 24 hours
Complex febrile seizure (any of the following) 20-25%
More prolonged ( > 15 min)
Focal
And/or recurs within 24 hr.
Febrile status epilepticus
Febrile seizure lasting > 30 min.
Symptomatic febrile seizure 5%
Age and fever are the same as for simple febrile seizure
The child has a preexisting neurologic abnormality or acute illness

45. • The underlying pathophysiology is unknown.
• But genetic predisposition clearly contributes to the occurrence of this disorder.
• Although clear evidence exists for a genetic basis of febrile seizures, the mode of
inheritance is unclear.
• While polygenic inheritance is likely, a small number of families are identified
with an autosomal dominant pattern of inheritance of febrile seizures, leading to
the description of a "febrile seizure susceptibility trait" with an autosomal
dominant pattern of inheritance with reduced penetrance.
Mutations have been found in genes encoding the sodium channel and the
gamma amino-butyric acid A receptor.
Febrile Seizures-Pathophysiology

46. Febrile Seizures-Epidemiology
Frequency:
United States
Between 2% and 5% of children have febrile seizures by their fifth birthday
India
between 5% and 10%
Mortality:
simple febrile seizures- No risk of mortality
Complex febrile seizure- 2-fold increased risk of mortality
Morbidity:
2-7% of children who experience febrile seizures proceed to develop epilepsy later in life
Race:
Febrile seizures occur in all races.
Sex:
Some studies demonstrate a slight male predominance.
Age:
By definition, febrile seizures occur in children aged 6months to 5 years.

47. Febrile Seizures-Risk factor
Risk factors for developing febrile seizures are as follows:
• Family history of febrile seizures
• High temperature
• Parental report of developmental delay
• Neonatal discharge at an age greater than 28 days (suggesting perinatal illness
requiring hospitalization)
• Daycare attendance
Maternal alcohol intake and smoking during pregnancy - Two-fold increased risk
Presence of 2 of these risk factors - Increases the probability of a first febrile seizure
to about 30%

48. Febrile Seizures- Trigger
Febrile seizures often occur in the context of:
Otitis media
Roseola
Human herpesvirus 6 (HHV6)
Shigella Infection

49. Febrile Seizures- Recurrence risk
factors
(Low fever)

50. Febrile Seizures- Predictors of epilepsy

51. 10 first aid steps (when someone has a convulsive seizure)
• Stay calm
• Look around
• Note the time
• Stay with them
• Cushion their head
• Don't hold them down
• Don't put anything in their mouth
• Check the time again. If a convulsive seizure doesn't stop after 5 minutes
or they have another seizure without recovering fully from the first seizure
(status epilepticus)
• After the seizure has stopped, put them into the recovery position
• Stay with them until they are fully recovered.
Emergency management of seizure

52. MANAGEMENT OF STATUS EPILEPTICUS

54. Approach to a child with suspected febrile seizures

55. Work-up
• No specific studies are indicated for a simple febrile seizure
• Focus should be on diagnosing the cause of fever
Blood Studies
recommendations:
• Blood studies (serum electrolytes, calcium, phosphorus,
magnesium, and complete blood count [CBC]) are not routinely
recommended in the work-up of a child with a first simple febrile seizure
• Blood glucose should be determined only in children with prolonged
postictal obtundation or those with poor oral intake

56. Lumbar Puncture-Indication in FS
RECOMMENDATIONS:
• Strongly consider Lumbar puncture in children younger than 12 months,
because the signs and symptoms of bacterial meningitis may be minimal
or absent in this age group.
• Lumbar puncture should be considered in children aged 12-18 months,
because clinical signs and symptoms of bacterial meningitis may be subtle
in this age group.
• In children older than 18 months, the decision to perform lumbar
puncture rests on the clinical suspicion of meningitis.

57. Neuroimaging in FS
RECOMMENDATIONS:
According to the AAP practice parameter, a CT or MRI is not recommended in
evaluating the child after a first simple febrile seizure
INDICATION:
Complex febrile seizure (4%)
Febrile status epilepticus
Intermediate or high risk of recurrence of FS

58. Electroencephalogram in FS
RECOMMENDATIONS:
If the child is presenting with his or her first simple febrile seizure and is otherwise
neurologically healthy, an EEG need not normally be performed as part of the
evaluation.
If at all an EEG is indicated, it is delayed until or repeated after > 2 wk have passed
INDICATIONS OF EEG:
• If epilepsy is highly suspected
An EEG would not predict the future recurrence of febrile seizures or epilepsy
even if the result is abnormal
• Distinction between ongoing seizure activity and a prolonged postictal period
• Intermediate or high risk of recurrence of FS

59. TREATMENT-FS
RECOMENDARTIONS:
An antiepileptic therapy continuous or intermittent is not recommended for
children with one or more simple febrile seizures
If the seizure lasts for > 5 min
Then acute treatment with diazepam lorazepam or midazolam is needed
Rectal diazepam is often prescribed to be given at the time of recurrence of
febrile seizure lasting > 5 min
Alternatively buccal or intranasal midazolam may be used
Antipyretics do not reduce the risk of having a recurrent febrile seizure

60. CHOICE OF DRUG ACCORDING TO SEIZURE TYPE
AND EPILEPSY SYNDROME

61. CHOICE OF DRUG: OTHER CONSIDERATIONS
 Comparative effectiveness and potential for paradoxical seizure aggravation by
some AEDs
precipitation of absence seizures and myoclonic seizures by carbamazepine and
tiagabine
 Comparative tolerability:
Increased risk of liver toxicity for valproate therapy in children< 2 yr of age, on
polytherapy, and or with metabolic disorders
The choice of an AED can also be influenced by the likelihood of occurrence of
nuisance side effects such as:
• Weight gain (valproate, carbamazepine)
• Gingival hyperplasia(phenytoin)
• Alopecia (valproate)
• Hyperactivity (benzodiazepines,barbiturates, valproate, gabapentin)
• Children with behavior problems and/or with attention deficit disorder can
become particularly hyperactive with GABAergic drugs such as benzodiazepines and
barbiturates or even valproate.

62. CHOICE OF DRUG: OTHER CONSIDERATIONS
 Cost and availability:
• Cost of the newer AEDs often precludes their use, particularly in developing
countries where costis a major issue.
• Generic substitution is generally best avoided if a brand name drug has already
proved efficacious.
 Ease of initiation of the AED:
• AEDs that are started very gradually may not be chosen in situations when there is
a need to achieve a therapeutic level quickly- lamotrigine and topiramate
• AEDs that have intravenous preparations or that can be started and titrated more
quickly may be chosen- valproate, phenytoin, or levetiracetam
 Drug interactions:
 The presence of comorbid conditions:
Avoid : VPA, PB and BZD
Safe : OXC,LEV and GBP

63. CHOICE OF DRUG: OTHER CONSIDERATIONS
Phenytoin, Lamotrigine and Valproate are safer
Avoid:Levetiracetam
Avoid- Valporate
Use-Topiramate
Adolescent girls of child-bearing potential
• Enzyme-inducing AEDs should be avoided because they can interfere with birth control pills
• Some AEDs, particularly valproate, can increase risks for fetal malformations so need to be avoided

64. CHOICE OF DRUG: OTHER CONSIDERATIONS
 Coexisting seizures:
• In Absence and generalized tonic-clonic seizures broad spectrum AEDs could be used-
lamotrigine or valproate
• Rather than medications that have a narrow spectrum of efficacy- phenyton
 History of prior response to specific AEDs:
 Mechanism of drug actions:
• avoid combining medications that have similar mechanisms of action-phenytoin and
carbamazepine(both work on sodium channel)
Lamotrigine and valproate
Topiramate and lamotrigine
 Ease of use:
 Ability to monitor the medication and adjust the dose:
 Patient ’s and family ’s preferences:
 Genetics and genetic testing:
• There strong association between the human leukocyte antigen HLA-B * 1502 allele
and severe cutaneous reactions induced by carbamazepine, phenytoin, or lamotrigine
in Chinese patients
• Mutations of the SCN1A sodium channel gene indicating Dravet syndrome can lead to a
seizures exacerbation if lamotrigine is used
 Teratogenic profiles:
synergistic effects ( different mechanisms of action)

65. Monotherapy is the rule!!

66. The principles of monotherapy
indicate that a second medication
needs to be considered after the first
either is pushed as high as
tolerated and still does not control
the seizures or results in intolerable
adverse effects.

67. In those cases, a second drug is
started and the first is tapered and
then discontinued. The second drug is
then again pushed to the dose that
controls the seizure or that results in
intolerable side effects.

68. If the second drug fails monotherapy
with a third drug or dual
(combination) therapy is considered.

69. Additional Treatment
Non-pharmacological options
• Ketogenic diet
• Vagal nerve stimulation
• Resective surgery
• Repetitive transcranial
magnetic stimulation
• ECT
• Mild hypothermia

70. KETOGENIC DIET
• Low carbohydrate, low protein, high
fat after fasting to initiate ketosis
• Anti-seizure effect of ketosis, acidosis
• Main experience with children,
especially with multiple seizure types
• Long-term effects unknown

71. Intermittent programmed electrical
stimulation of left Vagus nerve
50% reduction of seizures can be
expected in up to 30–40% of
patients

72. Focal resection
Hemispherectomy
Multiple subpial transection
Corpus callosotomy
Focal resection and hemispherectomy result in
a high rate (50-80%) of seizure freedom.
Corpus callosotomy result in lower rates
(5-10%) of seizure freedom

73. Additional Treatment
pharmacological options:NonAEDs
Steroids
ACTH
Prednisone
Intravenous gamma globulin (IVIG)

74. A prospective, single-blind study
demonstrated no difference in effectiveness
between high-dose long-duration
corticotropin (150 U/m2/day for 3 wk,
tapering over 9 wk) and low-dose short-
duration corticotropin (20-30 U/day for 2-6
wk, tapering over 1 wk) with respect to
spasm cessation and improvement in the
patient's EEG.
Hypertension was more common with larger
doses.

75. One double-blind, placebo-controlled,
crossover study demonstrated no difference
between low-dose ACTH (20-30 U/day) and
prednisone (2 mg/kg/day) in suppressing
clinical spasms and hypsarrhythmic EEG in
infants with infantile spasms

76. Prospective, randomized, single-blinded
study demonstrated high-dose ACTH at 150
U/m2/day to be superior to prednisone (2
mg/kg/day) in suppressing clinical spasms
and hypsarrhythmic EEG in infants with
infantile spasms.

77. MONITORING AND FOLLOW-UP
CBC, LFT & RFT
before Starting
treatment and every
3-6 month
Ca2+,ALP and
Vit-D every year
First follow-up
within 2-4 weeks
Subsequent
follow-ups every
3-6 months
Seizure diary
Routine
Monitoring not
recommended
Suspected AED toxicity
Managing drug
interactions
Liver or renal disease and
pregnancy
Routine
laboratory tests
Follow-up
AED level
monitoring

78. Therapeutic range
(In micro gm/mL)
Phenytoin 10-20
CBZ 6-12
VPA 50-125
Phenobarbital 10-40

80. DISCONTINUATION OF AED THERAPY
Usual indication of withdrawal:
Seizure free >=2 years
Normal EEG when AED withdrawal is attempted
In benign epilepsy syndrome the duration of therapy can often be as short as 6 months
Prolonged period of seizure freedom on treatment is often warranted
before AEDs are withdrawn, if withdrawal is attempted at all in the following:
•Temporal lobe epilepsy secondary to mesial temporal sclerosis
•Lennox-Gastaut syndrome
•Severe myoclonic epilepsy
Following AEDs withdrawal most relapses occur within the first 6 months

81. DISCONTINUATION OF AED THERAPY
Risk factors which help predicting prognosis after AEDs
withdrawal (risk factor for seizure relapse):
• Abnormal EEG before medication is discontinued
• Remote symptomatic epilepsy
• Absences seizure
• Those treated with valproate for primary generalized epilepsy
• Old age of epilepsy onset
• Long duration of epilepsy
• Presence of multiple seizure type
• Need to use > 2 AEDs

82. DISCONTINUATION OF AED THERAPY
How to discontinue ADEs?
AED therapy should be discontinued gradually often over a period of 3-6 months
Abrupt discontinuation leads to:
• Withdrawal seizure
• Status epilepticus
Withdrawal seizure is common with:
• Phenobarbital
• Benzodiazepines
Seizures that occur > 2 to 3 mo after AEDs are completely discontinued indicate relapse-
Resume treatment
A prescription for rectal diazepam to be given at the time of seizures that might occur
during and after tapering is warranted

83. DISCONTINUATION OF AED THERAPY
• In meningitis:
• In NCC:
Acute symptomatic seizures due to active lesions (cystic lesions, granulomas) till such
time that they disappear or become inactive (no edema, no enhancement, calcified) – usually
for a period of 6 months
Remote symptomatic due to inactive calcified lesions presenting with seizures either
denovo or as relapses should be treated till a 2 year seizure free period is achieved.
Relationship of convulsion with fever Action
Before 72 hrs of fever Stop AEDs before discharge
After 72 hrs of fever Continue AEDs for 2-3 months

84. THANK
YOU