childhood seizure and its management

CHILDHOOD SEIZURE AND ITS MANAGEMENT

Dr. TAUHID IQBALI

MBBS (JIPMER)

MD PEAD Jr.II ( PMCH Patna )

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

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.

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

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

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

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

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

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

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

GENERALIZED SEIZURE

GENERALIZED SEIZURE TONIC-CLONIC SEIZURE

GENERALIZED SEIZURE

CLONIC SEIZURE Repetitive

jerking movements

GENERALIZED SEIZURE

TONIC SEIZURE Muscle stiffness

Rigidity

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

GENERALIZED SEIZURE

MYOCLONIC SEIZURE

These are brief jerks of the extremities and/or axial trunk muscles

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

PARTIAL SEIZURE

ANTIEPILEPTIC DRUGS

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

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

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

• P-Phenytoin

• V-Valproate

• R-Rufinamide

• T-Topiramate

• F-Felbamate

• C-Carbamazepine

• Zinger chicken -zonisamide

• Le-Lamotrigine

• Lo-Lacosamide

Ca++

Ca++ Ethosuximide Valproate

Reduced current through T type Calcium channels

Zonisamide

GABA Enhancers

Tiagabine Gabapentin

Valproate

Barbiturate BZD

Vigabatrine

Glutamate blockers

Metabotrophic Under research

AMPA Blocker Topiramate

NMDA Blockers

Felbamate

Levetiracetam

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

AED Adverse effects

Cerebellar Phenytoin

Carbamazepine

Valproic acid

Lamotrigine

Ethosuximide

Gabapentin

Lacosamide

Rufinamide

Psychomotor slowing

Language problems Topiramate

Tiagabine

Mood changes Felbamate

Levetiracetam

Zonisamide

Cardiac conduction Lacosamide

Rufinamide

Hepatotoxicity Valproate

Benzodiapine

Felbamate

BM Suppression Carbamazepine

Ethosuximide

Levetiracitam

Valproate

Felbamate

Skin rash Lamotrigine

Phenytoin

Carbamazepine

Phenobarbitone

Phenytoin

Gum hyperplasia

Hirsutism

Osteomalacia

CBZ

Hyponatremia

VPA

Increase NH3

Weight gain

Topiramate

Renal stones

Weight loss

Glaucoma

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

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

AED AND ATT INTERACTIONS

INH increase

PHT and CBZ level

INH and Rifampicin increase

Carbamazepine level

Rifampicin reduces

Phenytoin and valproate level

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

APPROACH TO THE CHILD WITH A SUSPECTED SEIZURE DISORDER

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

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

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

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

• 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

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.

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%

Febrile Seizures- Trigger

Febrile seizures often occur in the context of: Otitis media

Roseola

Human herpesvirus 6 (HHV6)

Shigella Infection

Febrile Seizures- Recurrence risk factors

(Low fever)

Febrile Seizures- Predictors of epilepsy

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

MANAGEMENT OF STATUS EPILEPTICUS

Approach to a child with suspected febrile seizures

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

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.

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

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

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

CHOICE OF DRUG ACCORDING TO SEIZURE TYPE AND EPILEPSY SYNDROME

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.

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

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

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)

Monotherapy is the rule!!

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.

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.

If the second drug fails monotherapy

with a third drug or dual (combination) therapy is considered.

Additional Treatment

Non-pharmacological options

• Ketogenic diet

• Vagal nerve stimulation

• Resective surgery

• Repetitive transcranial

magnetic stimulation

• ECT

• Mild hypothermia

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

Intermittent programmed electrical stimulation of left Vagus nerve

50% reduction of seizures can be

expected in up to 30–40% of patients

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

Additional Treatment

pharmacological options:NonAEDs

Steroids ACTH Prednisone Intravenous gamma globulin (IVIG)

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.

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

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.

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

Therapeutic range (In micro gm/mL)

Phenytoin 10-20

CBZ 6-12

VPA 50-125

Phenobarbital 10-40

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

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

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

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

THANK YOU