Epilep

sy
(Once Sacred Disease)
World Epilepsy Day
(26th March)
Introduction & Epidemiology
 History

Epilepsy has existed for thousands of years but only in past

hundreds years or so has it begun to Understood.

In past, believed that disorders was also caused by presence

of demons in a person & if person breathed On or touched
another the demon would spread to another person unless that
person split immediately.
•The first person actually credited
with the electrical theory was John
Hughlings Jackson in 1873.

•It was held that epilepsy was the

result of erratic electrical discharges
throughout the entire body
In the 1930’s the 1st method for testing the electrical
hypothesis for epilepsy was discovered by HANS BERGER
when he invented the EEG

HANS BERGER , German Neurologist

1873 - 1943
 IS EPILEPSY..??
Epilepsy is a condition in which a person has recurrent SEIZURES with
disturbance of consciousness, with or without characteristic body
movements (CONVULSIONS)

So…WHAT IS SEIZURE?
Paroxysmal event due to abnormal, excessive, hypersynchronous
discharge from aggregate of CNS neurons.

CONVULSIONS..
Manifestation of seizures by uncontrolled body movements…..
EPIDEMIOLOGY
 EPILEPSY IN WORLD

•Incidence of epilepsy is around 0.3-0.5%

in different Population of world.

•The prevalence of epilepsy has been

estimated at 5-10 person per 1000.
Epilepsy is one of the commonest
neurological disorder …

Injury or Death can result from poorly

treated or Untreated Epilepsy…
Epilepsy Incidence Rates by Age*

1000
Incidence per 100,000

All Epilepsy Types

100

10
0 10 20 30 40 50 60 70 80

Age (years) *Data from Rochester, MN (1975-84)

Hauser WA et al. Epilepsia. 1991;32:429-445.
 MORTALITY OF EPILEPSY

Patient with Epilepsy Have risk of death is roughly 2 or 3

times Greater than normal people without epilepsy

 Significant number of patient die because of Accident ,

Status Epilepticus and a syndrome Known as SUDEP
( Sudden Unexpected Death in Epileptic Patient )
 PATHOPHYSIOLOGY

•Exact cause of Epilepsy is not Known..

•According to Some researches ……

Epilepsy occurs due to Iron Channels Mutation

Congenital
Imbalance of

Neurotransmitter Etc…..
GABA receptor mediates inhibition responsible for normal
termination of a seizure

NMDA (Glutamate) receptor activation required for

propagation of seizure activity

NMDA Receptor Reduced GABA

Seizure
Activation Receptor function
ETIOLOGY
CNS
– Head trauma
• Seizure in 1 week of injury not predictive of epilepsy
– Stroke
– Vascular malformations
– Mass (tumor/abscess)
– Meningitis/encephalitis
– Congenital malformations/ cortical dysplasias
– Idiopathic
SYSTEMIC
– Hypo/hyperglycemia
– Hypo/hypernatremia
– Hypocalcemia
– Uremia
– Hepatic encephalopathy
– Hypoxia
– Hyperthermia
– Drug overdose or withdrawal
 DUE TO SOME DRUGs…

ANTI MICROBIALS & ANTIVIRAL :- Acyclovir , Isoniazid

ANESTHETICS & ANALGESIC :- meperidine , Tramadol , Local

Anesthetic

PSYCOTROPIC :- Lithium , Antipsychotic , Antidepressent

ANTI MALERIAL :- Chloroquine , Mefloquine

DRUG OF ABUSE :- Amphetamine , Cocaine , Phencyclidine

 EXPERIMENTAL MODELS

•Maximal Electroshock Seizures

•Pentylenetetrazol (PTZ) Clonic Seizures

•Chronic Focal Seizures

•Kindled Seizures
Classification of SEIZURES
CLASSIFICATION OF SEIZURES

The International League Against Epilepsy

(ILAE) published a modified version of the
International classification of epileptic seizures
in 1981

Based on clinical features & electroencephalic

findings rather than underlying etiology or
cellular substrate.
 Classification of Seizures

Focal Generalized Unclassified

(partial)
epileptic
Absence
Simple partial
Neonatal
Myoclonic

Infantile
Complex Clonic
partial

Toni
Partial c
seizures
evolving to Tonic-
secondary Clonic
generalized
Atonic
 Seizures

Partial Generalized

– Electrical discharges in – Diffuse abnormal

a relatively small electrical discharges
group of dysfunctional from both hemispheres
neurones in one cerebral – Symmetrically
hemisphere involved
– Structural abnormalities – Cellular, biochemical or
– Aura may reflect site of structural
origin abnormalities
– + / - LOC – No warning
– Always LOC
What is
AURA..???
When the effects of a partial
seizure appear as a ‘warning sign’
before a larger seizure, they are
known as an Aura.
 Partial Seizures (Focal
Onset)
Simple partial (Relatively w/o
impaired consciousness)
Complex partial
(impaired consciousness)
Partial Seizures evolving to
Secondarily Generalized
Seizures
Simple Partial (Relatively
w/o impaired Consciousness)
 Motor symptoms (focal motor seizure)
 Involves motor strip
 Manifested by abnormal movement of an extremity
 Jacksonian march- spread to involve contiguous regions
 Todd’s paralysis- post ictal transient hemibody weakness
 Epilepsia partialis continua-rare instance, seizures continue
for hours & days

 Somatosensory symptoms
 Autonomic symptoms
 Psychic symptoms
Complex partial
(impaired consciousness)

 Typically frontal or temporal lobe onset

 Often stereotyped for the individual patient

 Average duration 1-3 minutes

 Frequently seen in adult onset epilepsy

 Automatisms: coordinated involuntary

 Partial Seizures evolving to
Secondarily Generalized Seizures

 Simple Partial Seizures to Generalised Seizures

 Complex Partial Seizures to Generalised Seizures

 Simple Partial Seizures to Complex Partial Seizures to

Generalised Seizures
 Absence
 Myoclonic
 Clonic
 Tonic
 Tonic-
clonic
 Atonic
Absence Seizure(Petit Mal Epilepsy)
 Sudden onset
 Interruption of ongoing activities
 Blank stare
 Brief upward rotation of eyes
 Duration: a few seconds to 1/2 minute
 Evaporates as rapidly as it started
 Usually begin in childhood(Ages 4-8) or
early adolescence
Tonic-clonic seizures
(Grand mal/Epileptic fit)
10-20 s
Tonic Phase Clonic Phase
Sudden sharp tonic Superimposition of periods of
contraction of muscles muscle relaxation on the
throughout the body tonic muscle contraction
respiratory muscle: tridor /  Small gusts of grunting
s respiration
moan /ictal cry on Frothing of saliva
 Respiratory inhibiti
Deep respiration
cyanosis
Remains unconscious
Tongue
 Urinary biting
incontinence
Goes into deep p
slee re,
headachesfeeling so
Awakens
Clonic seizures
•Myoclonus
•Regularly repeating at a rate of 2-3 per sec

Myoclonic seizures
•Extremely brief (<0.1 sec) Muscle
contraction
•Jerky muscle movements

Atonic seizures
•Loss of muscle tone
•Patient may fall to ground
•Drop attacks
 Pseudoseizures
 Non-epileptic seizures

 May be manifestation of conversion disorder, factitious

disorder or malingering

 Features that may distinguish from epileptic seizures

• Pre-attack preparation, absence of post-ictal confusion
• “Disorganized” movements, pelvic thrusting, thrashing
• Bilateral convulsions without loss of consciousness
• Violent or goal-directed behavior, obscene language

 Video EEG may help to diagnose

 Epilepsy Syndromes

They are disorder in which epilepsy is a

predominant feature & there is sufficient evidence
(clinical, EEG,radiological or genetic observations)
to suggest a common underlying mechanism

 Juvenile Myoclonic Epilepsy

 Lennox-Gastaut Syndrome
 Mesial Temporal Lobe Epilepsy Syndrome
 Epidemiology by Seizure Types

Generalized TC
(23%)
Complex Partial
(36%)

Simple Partial
(14%)

Unclassified (3%)
Myoclonic (3%)
Other Generalized
Absence (6%)
(8%) Partial Unknown
(7%)
Reproduced with permission from Hauser WA. Epilepsia. 1992;33(suppl 4):S10.
Diagnosis & Investigations
 Epilepsy Differential Diagnosis

 The following should be considered in

the differential diagnosis of epilepsy:

 Syncope attacks (when pt. is standing; results

from global reduction of cerebral blood flow;
prodromal pallor, nausea, sweating; jerks!)

 Cardiac arrythmias (e.g. Adams-Stokes attacks).

Prolonged arrest of cardiac rate will
progressively lead to loss of consciousness –
 Migraine. (Basilar migraine may lead to loss
of consciousness!)

 Hypoglycemia – seizures or intermittent

behavioral disturbances may occur.

 Narcolepsy – inappropriate sudden sleep episodes

 Panic attacks

 PSEUDOSEIZURES – psychosomatic
and personality disorders
I. LABORATORY ANALYSIS :
Haematological: CBP( complete Blood Picture)

Biochemical: Calcium, glucose

Radiological: CT head

Microbiological: Lumbar Puncture

(Always used with justification)
Cont……..

 II. Confirmation of epilepsy:

◦ Dynamic investigations : result changes with attacks
 E.g. EEG
◦ Static investigations : result same between and during attacks
 E.g. Brain scan
WHAT IS EEG……?????

A record of the electrical

activity of large numbers of
neurons in the brain, recorded with
electrodes applied to the surface of
the scalp.
• EEG indicated whenever epilepsy suspected

• Uses of EEG in epilepsy

– Diagnostic: support diagnosis, classify seizure, localize
focus, quantify
– Prognostic: adjust anti-epileptic treatment
• Note:
– Normal in 10-20% of epileptic patients
– Background slowed by:
• diffuse cerebral process, postictal state
– Artifact from:
• Eye rolling, tremor, other movement, electrodes
• Interpreted in the light of proximity to
seizure
Normal EEG
EEG in Grand Mal Epilepsy
Classification
:

Barbiturate Phenobarbitone Deoxybarbiturate: Primidone

Phenytoin Carbamazepine

Hydantoin Iminostilbene

Fosphenytoin Oxcarbazepine

Valproic Acid
Aliphatic
Succinimide Ethosuximide Carboxylic
Acid
D
Cont…

Diazepam Phenyltriazine Lamotrigne

Lorazepam

Benzodiazepines

Clobazam
Gabapentine
Cyclic GABA
Analogues
Clonazepam
Pregabalin
 Phenytoin

Mechanism of Action:-
 At Therapeutic Dose:
•Prolonging The Inactivation State of Voltage Sensitive
Neuronal Na+Channal
 At High Dose:
• ↓Ca++ Influx
• Inhibition of Glutamate
• Facilitation of GABA Response
Therapeutic Plasma Conc. Is 10-20
µg/ml

Use:
•GTCS and partial seizures.
•Digitalis induce Arrhythmia

Dose:
•100mg BD
•In Children 5-8mg/kg/day
ADRs …..(Phenytoin)
•Gingival hyperplasia

•Hirsutism

•Hypersensitivity

•Megaloblastic Anemia

•Foetal Hydantoin Syndrome

•Osteomalacia

•Lymphedenopathy
Other:
•Ataxia
•Vertigo
•Hyperglycemia
•Diplopia
•Epigastric Pain
•Nausea
•Vomiting
•Thrombophlebitis
 Carbamazepine

Mechanism of Action:-
•Prolongation of Na+ Channel Inactivation
Therapeutic Plasma Conc. Is 5-10
µg/ml

Use:-
•DOC for Partial Seizures & GTCS
•DOC for Trigeminal Neuralgia

Dose:-
200-400mg TDS
In Children 15-30mg/kg/day
ADRs….(Carbamazepine)

•Dizziness
•Headache
•Ataxia
•Vertigo
•Diplopia
•Photosensitivity
•Leucopenia
•Aplastic Anemia
•Hepatotoxicity
•In Elderly Water Retention and Hyponetramia
 Valproic acid(Sodium Valproate)
 Broad Spectrum Anti Seizure
Drug

Mechanism of Action:-
•Prolongation of Na+ channel inactivation
•Inhibition of T type Ca+2 current
•Increased activity of GABA
•Decrease release of Glutamate
 Therapeutic Plasma Conc. Is 40-100
µg/ml

Uses:-
•DOC in Absence, Myoclonic, Atonic
Seizure
•Alternative Drug in GTCS, Partial Seizure

Dose:-
•200mg TDS
•In Children 15-30mg/kg/day
ADRs………(Valproic Acid)
•Anorexia
•Vomiting
•Loose motion
•Weight gain
•Curling of Hair
•Hypersensitivity Reaction

 In Pregnancy:-
•Neural Tube Defects
•Spina Bifida

 In Young Girls:-
•Polycystic ovarian Disease
•Menstrual Irregularity
 Diazepam
•First line Drug in emergency

Use:-
•In Children Febrile Convulsion( Rectal
instillation of Diazepam)

Dose:-
•0.2-0.5 mg/kg slow i.v. inj.
ADRs…

•Thrombophlebitis
•Fall in BP
•Respiratory depression
 Lorazepam

Use:-
•During Emergency & Status Epilepticus

Dose:-
•0.1 mg/kg inj. i.v.

ADR:-
•Local Thrombophlebitis
 Newer DRUGS
•Topiramate

•Zonisamide

•Levetiracetam

•Vigabatrin

•Tiagabine

•Lacosamide
Treatment & General Management
 Seizure Treatment

• Acute Management
– 90% of seizures stop without treatment in under 5
minutes
– Can give lorazepam or diazepam for seizures
>5min
– Monitor ABCDs, avoid injury and aspiration
– Treat underlying medical conditions
Cont…

• Long Term Management

– Decide if therapy needed
• Seizures due to secondary causes (metabolic d/o, EtOH
withdrawal, immediately following head trauma/stroke)
may not need longterm Rx.
• Single generalized tonic-clonic seizure recurs in about 50%
– Anti-epileptic medications
• Try single therapy
• Add second medication if: Seizures not controlled with
single drug and maximal levels/side effects are achieved
• Treat the seizures, not drug levels
TREATMENT OF EPILEPSY…
 General management

At personal level…….

•Identity card

•No. of nears & dears

•Visiting card of Dr

•Drugs in pocket advanced for 15 days

•Maintain seizure diary ( onset, duration etc)

•Adequate sleep

•Avoid fasting

•Avoid working near moving

machines

•Avoid swimming

•Avoid driving
 Instruction for nears n dears…

•Ensure airway protection/ position to prevent aspiration

•Do not place anything in the mouth except when to suction

•DO NOT try to force suction/airway through clenched teeth

•When the patient stops convulsing, place patient in lateral

decubitus

•Assess safety of patient

•Ensure lights in room are on

•Remove any object within reach of patient that could cause

injury

•Loosen clothing

•Side rails should be up if patient is in bed

•Do not try to “hold the patient down

 EPILEPSY IN PREGNANCY…
•Control the Seizures

•Same Drugs Should be Continued

•Valproate + Folic acid

•Phenytoin + Vit K

•Regular Ultrasound(USG) & other

Assessments
•Planning to become Pregnant – minimum
drugs

•NEWER Drugs-less Teratogenicity

DOC:-Among older drugs-Carbamazepine

Lamotrigine-Preferred Drug
Topiraamate-also used C/I Typical
Absence Seizure
 Status Epilepticus

Definition:-
• Continuous seizure lasting greater
than 30 minutes

• Two or more sequential seizures

without recovery of full consciousness
lasting >30 minutes
 Status Epilepticus

• Lorazepam 4 mg (0.1 mg/kg children) IV push at rate of 2 mg/min

(can be given IM)

• Diazepam 10 mg (0.2-0.3 mg/kg) IV push at rate of 2 mg/min

• Fosphenytoin 150 mg/min (20 mg/kg) IV up to(can be given IM)

 Phenytoin sod.20 mg/kg IV no faster than 50 mg/min
 Consider Phenobarbitone sod. 50-100 mg (20 mg/kg)
IV
• If Seizure continues: Intubation required

• General Anesthesia – Titrate to burst Suppression (Continuous

EEG monitoring required)

– Pentobarbital (5 mg/kg load, 0.5-3 mg/kg/hr maint.)

– Propofol (1-2 mg/kg load over 5 min, 2-10 mg/kg/hr
maint.)
– Midazolam(0.2 mg/kg slow IV bolus, 0.05-0.5 mg/kg/hr
maint.)
PATIENT EDUCATION

•3 Years medication

•Do Not change brand of drugs

1. 22nd February
2. 21st March
3. 18th April
4. 26th March
High Performance Liquid
Chromatography
Who discovered 1st method for testing
electrical hypothesis of epilepsy?

1. John Hughlings Jackson

2. Robert Koch
3. Hans Berger
4. None of above
1. Absence seizures
2. Clonic seizures
3. Tonic-clonic seizures
4. Atonic seizures
1. Shock
2. Hypoglycemia
3. Pseudoseizures
4. Narcolepsy
1. Phenytoin
2. Sodium Valproate
3. Carbamazepine
4. Fosphenytoin
1. Lorazepam
2. Diazepam
3. Phenytoin
4. Fosphenytoin
1. Clonazepam
2. Diazepam
3. Lorazepam
4. Clobazam
1. 6 months
2. 1 year
3. 3 years
4. 18 months