EPILEPSY - PowerPoint Presentation

Slide1

EPILEPSY

DEPARTMENT OF GENERAL MEDICINE

MADURAI MEDICAL COLLEGESlide2

DEFINITION

CLASSIFICATION

ETIOLOGY

MECHANISM OF SEIZURES

STAGES IN EVOLUTION GTCS

SYMPTOMS OF INDIVIDUAL SEIZURE TYPES

INVESTIGATION

MANAGEMENT

SPECIAL CONSIDERATION

REFRACTORY / INTRACTABLE SEIZURE

IN PREGNANCY AND WOMEN

STATUS EPILEPTICUS

PSEUDO SEIZURES

WHEN TO STOP ANTIEPILEPTICSSlide3

A

seizure

is a paroxysmal event due to abnormal excessive or

synchronous neuronal activity in the brain.

Epilepsy

is condition in which a person has recurrent seizures

due to chronic underlying proces

s.

Convulsion

.

An intense paroxysm of involuntary repetitive muscular contractions

.

Seizure (is a generic term)

Convulsive seizure or motor seizure.

Non convulsive seizure

sensory seizure.

Psychic seizure.

Autonomic seizure.

All seizures are not convulsions.

Not all

convulsions

are

seizure.Slide4

Classification of Seizures

ILAE Classification (1981)

I. Partial (Focal)seizures

A. Simple partial seizures

B. Complex Partial Seizures C. Partial Seizures evolving to secondary generalized seizures (tonic-clonic, tonic or clonic)

II. Generalized seizures

(Convulsive and non-convulsive)

A. Absence seizures

i

) Typical ii) Atypical

B. Myoclonic seizures

C.

Clonic

seizures

D. Tonic seizures

E. Tonic-

Clonic

seizures

F. Atonic seizures

(Combinations may occur: myoclonic and atonic or myoclonic and tonic)

III. Unclassified epileptic seizuresSlide5

A

natomical site

Cortex

Temporal

Frontal

ParietalOccipitalGeneralised (diencephalon) Multifocal Pathological causeGenetic Developmental Tumours Trauma Vascular Infections Inflammation Metabolic Drugs, alcohol and toxins Degenerative Slide6

Idiopathic

Benign

Rolandic

epilepsy of childhood •

Benign occipital epilepsy of childhood •

Focal structural lesionsGeneticTuberous sclerosis von Hippel–Lindau disease Neurofibromatosis Cerebral migration abnormalitiesinfantile hemiplegiaDysembryonic

Cortical

dysgenesis

Sturge–Weber syndrome Mesial temporal sclerosis(associated with febrile convulsions

Cerebrovascular diseaseIntracerebral haemorrhage Cerebral infarction Arteriovenous malformation Cavernous haemangioma Tumours(primary and secondary)Trauma(including neurosurgery)InfectiveCerebral abscess (pyogenic)Toxoplasmosis Cysticercosis Tuberculoma Subdural empyema Encephalitis Human immunodeficiency virus (HIV)InflammatorySarcoidosis • Vasculitis •

Causes of partial seizuresSlide7

Genetic

Inborn errors of metabolism

Storage diseases

Phakomatoses (e.g. tuberous sclerosis,)Cerebral birth injuryHydrocephalusCerebral anoxiaDrugsAntibiotics: penicillin, isoniazid, metronidazole • Antimalarials: chloroquine

,

mefloquine

Ciclosporin • Cardiac anti-arrhythmics: lidocaine,

disopyramide • Psychotropic agents: phenothiazines, tricyclic antidepressants, lithiumAmphetamines (withdrawal)Alcohol (especially withdrawal)ToxinsHeavy metals (lead, tin) • Organophosphates (sarin) • Metabolic diseaseHypocalcaemia • Hypoglycaemia • Hyponatraemia • Renal failure • Hypomagnesaemia • Liver failure InfectiveMeningitis Post-infectious encephalopathy Inflammatory

Multiple sclerosis (uncommon)

SLE

Diffuse degenerative diseasesAlzheimer’s disease (uncommonly) Creutzfeldt–Jakob disease (rarely) s

Causes of partial seizuresSlide8

The Causes of Seizures and Epilepsy

Seizures are a result of a

shift in the normal balance of excitation and inhibition

within the CNS

The normal brain is capable of having a seizure under the appropriate circumstances, and there are

differences between individuals in the susceptibility or threshold for seizures. seizures may be induced by high fevers in children who are otherwise normal and who never develop other neurologic problems, including epilepsy.Normal development also plays an important role, since the brain appears to have different seizure thresholds at different maturational stagesSlide9

There are a variety of conditions that have an extremely high likelihood of resulting in a chronic seizure disorder

.

severe, penetrating head

trauma

long-lasting

pathologic change in the CNS that transforms a presumably normal neural network into one that is abnormally hyperexcitable. This process is known as epileptogenesis,

epileptogenic

factors

.

stroke, infections, and abnormalities of CNS development.

Slide10

Seizures are episodic

.

completely

normal for months or even years between seizures.

important

provocative or precipitating factors that induce seizures in patients with epilepsy. Precipitants psychological physical stress sleep deprivation

hormonal

changes associated with the menstrual cycle.

exposure

to toxic substances and certain medications.Slide11

These observations emphasize the concept that the many causes of seizures and epilepsy result from a

dynamic interplay between

endogenous factors,

epileptogenic factors, and

precipitating factors. Slide12

Mechanisms of Seizure Initiation and Propagation

seizure initiation

phase

The initiation phase is characterized by

two concurrent events in an aggregate of neurons: (1) high-frequency bursts of action potentials and (2) hypersynchronization. The bursting activity is caused by a relatively long-lasting depolarization of the neuronal membrane due to influx of extracellular calcium (Ca2+), which leads to the opening of voltage-dependent sodium (Na

+

) channels, influx of Na

+

, and generation of repetitive action potentials. This is followed by a hyperpolarizing afterpotential

mediated by ℽ -aminobutyric acid (GABA) receptors or potassium (K+) channels, depending on the cell type. Slide13
Slide14

seizure propagation

phase

.

Normally

, the

spread of bursting activity is prevented by intact hyperpolarization and a region of "surround" inhibition created by inhibitory neurons. With sufficient activation there is a recruitment of surrounding neurons via a number of synaptic and nonsynaptic mechanisms, including: an increase in extracellular K+, which blunts

hyperpolarization

and depolarizes neighboring neurons;

(2) accumulation of Ca

2+ in presynaptic terminals, leading to enhanced neurotransmitter release; and (3) depolarization-induced activation of the N

-methyl-D-aspartate (NMDA) subtype of the excitatory amino acid receptor, which causes additional Ca2+ influx and neuronal activation; (4) ephaptic interactions related to changes in tissue osmolarity and cell swelling. The recruitment of a sufficient number of neurons leads to the propagation of seizure activity into contiguous areas via local cortical connections, and to more distant areas via long commissural pathways such as the corpus callosumSlide15

Mechanisms

intrinsic

to the neuron include changes

in the conductance of ion channels,

response characteristics of membrane receptors, cytoplasmic buffering, second-messenger systems, and protein expression as determined by gene transcription, translation, and posttranslational modification. Mechanisms extrinsic to the neuron include changes in the amount or type of neurotransmitters present at the synapse, modulation of receptors by extracellular ions and other molecules, and temporal and spatial properties of synaptic and

non synaptic

input.

Nonneural

cells such as astrocytes and oligodendrocytes, have an important role in many of these mechanisms as well.

The basic mechanisms of other precipitating factors of seizures such as sleep deprivation, fever, alcohol withdrawal, hypoxia, and infection, are not as well understood but presumably involve analogous perturbations in neuronal excitabilitySlide16

Mechanisms of Action of Antiepileptic

Drugs

Antiepileptic

drugs appear to act primarily by

blocking the initiation or spread of seizures.

inhibition of Na+-dependent action potentials in a frequency-dependent manner (e.g., phenytoin, carbamazepine, lamotrigine, topiramate, zonisamide, lacosamide

,

rufinamide

inhibition of voltage-gated Ca2+ channels (phenytoin

, gabapentin, pregabalin), attenuation of glutamate activity (lamotrigine, topiramate, felbamate), potentiation of GABA receptor function (benzodiazepines and barbiturates), increase in the availability of GABA (valproic acid, gabapentin, tiagabine), and modulation of release of synaptic vesicles (levetiracetam). The two most effective drugs for absence seizures, ethosuximide

and

valproic

acid, probably act by inhibiting T-type Ca2+ channels in thalamic neurons.Slide17

SIMPLE PARTIAL SEIZURESSlide18

Simplex partial seizures

No loss of consciousness

Symptoms depend on area of brain involved:

Motor

Sensory

AutonomicPsychosensoryIt can be the introductory phase of a complex partial or generalised tonic-clonic seizure (‘aura’)Slide19

COMPLEX PARTIAL SEIZURESSlide20

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 vufeeling of alienationLoss of consciousness: stare, ‘going blank’Automatisms:oral automatismsfiddling with the handsSlide21

Additional features of partial motor seizures.

JACKSONIAN SEIZURE

Motor seizure begins in a restricted region such as the fingers and gradually progresses over seconds to minutes to include a larger portion of the extremity

.Slide22

TODDS PARALYSIS.

Patients may experience paresis of the involved limb for minutes to many hours following the seizure

.Slide23

EPILEPSIA PARTIALIS CONTINUA.

Rarely the seizure may continue for hours to days when it is called

epilepsia

partialis

continua.Often refractory to treatment.Slide24

VERSIVE SEIZURES

A frontal epileptic focus may involve the frontal eye field causing forced deviation of the eyes and sometimes turning of the head to the opposite side.

Such seizures often become

generalised

to a tonic

clonic seizure.Slide25

PARTIAL SENSORY SEIZURES

Somatosensory seizures.

Special sensory seizures.Slide26

Somatosensory seizures

Focus in the contralateral post

rolandic

convolution.

Sensory seizures described as

NumbnessTinglingPins and needles feelingSensation of crawling (formication)Electric sensation,Sensation of movement of the part.Pain and thermal sensations occur occasionally.Slide27

Special sensory seizures

Visual seizures.

Rare.

Occur as sensation of darkness or flashes of light which may be stationary or moving.

May appear

colourless or coloured.There may be twinkling or pulsating lights.Visual hallucinations may occur with involvement of occipito-temporal or antero-medial temporal areas.Slide28

Auditory hallucinations.

Rare.

There may be sensation of buzzing or roaring in the ears or sensation of human voice repeating

unrecognisable

words.

Vertiginous sensations.occur with supero posterior temporal region or parieto temporal region involvement.Slide29

Olfactory hallucinations.

assoc

with lesions of inferior and medial parts of temporal lobe usually in the region of

parahippocampal

convolution or

uncus and hence the term uncinate seizures.patient perceives a foul smellSlide30

Gustatory hallucinations.

in temporal lobe disease.

salivation and sensation of thirst is present.

Vague and often indefinable visceral sensations arising in the thorax, epigastrium and abdomen may occur with temporal lobe focus.Slide31
Slide32

COMPLEX PARTIAL SEIZURES OR PSYCHOMOTOR SEIZURES OR TEMPORAL LOBE SEIZURES

.

These patients have

Aura- in the form of a simple focal seizure or a hallucination or illusion suggestive of a temporal lobe origin.

have a period of altered behavior, altered consciousness and amnesia to the event

.Psychic experiences which occur in complex partial seizures.Sensory illusions and distortions Micropsia and macropsia- objects and persons in the environment appear to shrink or recede into distance or may enlargeSlide33

Hallucinations.

visual and auditory common.

Olfactory and gustatory rare

.

Dyscognitive

states.Dejavu- feelings of increased familiarity.Jamais vu- feelings of strangeness or unfamiliarity.Feeling of depersonalisation.Sudden interruption in memory.Fragments of old memories and scenes appear in patients mind and recur with striking clarity.Slide34

Emotional experiences.

Less commonly observed.

sadness,loneliness,anger,happiness,sexual

excitement.

Fear and anxiety-most common affective experiences.

Sense of rage and intense anger.Dyscognitive states.Dejavu- feelings of increased familiarity.Jamais vu- feelings of strangeness or unfamiliarity.Feeling of depersonalisation

.

Sudden interruption in memory.

Fragments of old memories and scenes appear in patients mind and recur with striking clarity.Slide35

AUTOMATISMS - occur in the form of

Lipsmacking

Chewing

Swallowing

Fumbling of handsShuffling of feetInappropriate acts.OTHER AUTOMATISMS.Gelastic epilepsy — laughter may be the most striking feature of an automatism.Volvular epilepsy—patient may walk repititively

in small circles.

Epilepsia

procursiva—runs repititively.Poriomania—wanders aimlessly as an

ictal or postictal phenomenon.Slide36

During the episode, patient is not in contact with his surroundings.

Patient is typically confused following the seizure.

May take seconds to an hour for full recovery of consciousness.

Postictally

patient may show anterograde amnesia or aphasia (if dominant hemisphere

)Interictal EEG is often normal or may show brief epileptiform spikes or sharo waves.Since CP seizures can arise from the medial temporal lobe or inferior lobe which are distant from the scalp, EEG during seizure may be non localising but detected using

sphenoidal

or surgically placed intracranial electrodesSlide37

CP seizures can occur at any age.

Usually seen in adolescence and adults.

H/o febrile seizures in childhood is often present.

2/3rds of CP seizure

pts

have GTC seizures.Cp seizure pts may show - features of Depressive illnessPsychotic symptomsParanoid delusional state and Abnormalities of behaviour and

Personality during

interictal

period.Slide38

TONIC-CLONIC SEIZURESSlide39

Generalised tonic-clonic seizure

(grand mal)

The most common seizure

Acute symptomatic seizures are generalised tonic-clonic seizures

Course:

Cry, loss of consciousness, fallTonic phase- generalised muscle contraction, apnoeaClonic phase- rhythmic contraction of muscles, tongue bite, foaming, enuresisTerminal sleep and gradual regaining of consciousness (transient confusion)Slide40

ABSENCE SEIZURESSlide41

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 childrenSlide42

Absence seizures may be accompanied by rapid blinking movements, chewing, or

clonic

movements of the hands.

Begin in childhood (4-8

yrs

age) or early adolescence.Main seizure type in 15-20% of children with epilepsy.May occur 100 times a day (pykno epilepsy)May manifest as unexplained day dreaming or poor performance.EEG-typically reveals characteristic generalised 3 -Hz/sec spike and wave discharges.Respond well to treatment.About 60—70% usually have a spontaneous remission during adolesence.

May be associated with GTC seizures.Slide43

ATYPICAL ABSENCE SEIZURES

LOC may be longer.

Focal motor signs may be present.

EEG not characteristic and may show

generalised

slow spike and wave pattern with a frequency of about 2.5Hz/sec.Often associated with diffuse structural abnormalities of the brain and patients may have neurologic dysfunction like mental retardation.Less responsive to treatment.Slide44

ATONIC SEIZURESlide45

ATONIC SEIZURES

Sudden loss of muscle tone lasting 1—2

secs

Brief impairment of consciousness.

No post ictal confusion.

EEG reveals brief generalised spike and wave discharges followed immediately by diffuse slow waves that correlate with loss of muscle tone.Usually seen in association with known epileptic syndromes.Slide46

MYCLONIC SEIZURES Slide47

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 encephalopathiesSlide48

Clinical Presentations

Myoclonic seizures

Abrupt , very brief,

involuntery

flexion movements.

Involve whole body or part of the body Occur most commonly at morning, shortly after walking. May occur in healthy people (physiological)Atonic Seizures

Brief loss of muscle tone.

Heavy fall , with or without loss of consciousness.

Versive

seizures A frontal epileptic foci may involve the frontal eye field.

Force deviation of the eyes and turning head to the opposite side.Status Epilepticus Series of recurrent Tonic-Clonic seizures occurs without regaining consciousness over 30 min. Catamenial epilepsy: Epileptic women experienced that their seizures worsen during menstruation; due to the imbalance between the proconvulsant estrogen and anticonvulsant progestogenSlide49

Differential Diagnosis

Condition mimicking Seizures:

Pseudoseizure

Syncope

Some sleep disorders

Hypoperfusion in brainCardiac ArrhythmiaEmotional OutburstDissociative fugueDrop Attacks

Migraine

Hypoglycaemia

True Seizure

Vs Pseudoseizure

Features & Lab findingsTrue Seizure

Pseudoseizure

Resemble known seizure types

Yes

No

Tongue bite

Yes

No

Duration

Short

Long

Post-

Ictal

Phenomena

Present

Absent

Injury

Yes

No

Occurs during sleep

Yes

No

Can be precipitated by suggestion

No

Yes

EEG during attack

Abnormal

No Change

EEG after attack

Slowing pattern

No Change

Serum prolactin (after attack)

Raised

No change

Anti Epileptic drug usage

Suppress seizures

No Change (may worsen)Slide50

Epileptic seizure versus syncope

Syncope

Tonic-clonic seizure

Position

Upright

Any

Facial colour

Paleness

Cyanosis

Onset

Gradual; introduced by dizziness, blurring of visionSudden; 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 typicalSlide51

Diagnosis of Epilepsy

Thorough History taking :

From patients

From reliable valid informants

From observer (who observed seizures)Physical Examination: Specially neurological system Higher Psychic functionLaboratory Investigation: S. Electrolytes, S. Prolactin, Blood sugar, CBC, TFT, LFT, RFT, CSF studyImaging: EEG, Video EEG telemetry, CT Scan of Brain, MRI of Brain, MRS, PET, SPECT.PolysomnographySlide52

Management of Epilepsy

Medical treatment:

Immediate care of seizures

Move persons away from danger

Recovery position (semi prone)

Ensure clear airway Do not insert anything into mouth Urgent medical attention- (patent airway, O2

,

anticonvulsant, investigate cause)

Should not be left alone after recovery

Consider about regular AEDSurgical treatment:Indicated when seizures shown to be intractable to medical treatment.

Removal of epileptic focus (eg:mesial temporal sclerosis) Anterior Temporal Lobectomy Corpus callostomy Subpial transectionVagus Nerve stimulationKetogenic diet Slide53

Guidelines for Anticonvulsant Therapy

Start with one first line drugs

Start with low dose: Gradually increase to effective dose or until side effects.

Check compliance

If first drug fails due to side effects or continue seizures, start second line drugs whilst gradually withdrawing first.

Try Three AED singly before using combinationsBeware about drug interactionsDo not use more than two drugs in combination at any one timeIf above fails consider occult structural or metabolic lesion and whether seizures are truly epileptic

.Slide54

Choice of Anti Epileptic Drugs

Epilepsy Type

First-Line

Second-Line

Third-Line

Partial and /or

Secondary GTCS

Carbamazepine

Lamotrigine

Oxcarbazepine

Topiramate

S. Valporate

(in children)

S. Valporate

Tiagabine

Gabapentin

Clobazum

Phynytoin

Phenobarbital

Vigabatrin

Acetazolamide

Primary GTCS

S. Valporate

Lamotrigine

Topiramate

Carbamazepine

Phynytoin

Gabapentin

Phenobarbital

Tiagabine

Acetazolamide

Absence

S. Valporate

Lamotrigine

Ethosuximide

Clonazepum

Acetazolamide

Myoclonic

S. Valporate

Clonazepum

Piracetam

Lamotrigine

PhenobarbitalSlide55

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

ethosuximidSlide56

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?PregnancyDriver’s licenceSlide57

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 justifiedSlide58

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, topiramateSlide59

Efficacy of AEDs

All seizure types: absence, myoclonic, generalised tonic-clonic seizures, partial seizures

valproate, lamotrigine, topiramate

clobazam, clonazepam

phenobarbital, primidon

felbamatelevatiracetam, zonisamide

Partial seizures, generalised tonic-clonic seizures

carbamazepine, oxcarbazepine

gabapentin, vigabatrin, tiagabine

phenytoin

AbsenceethosuximidSlide60

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, felbamateSlide61

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 monitoringInadequate selection of AEDTrue inefficacy of AED → AED switchOther AED on monotherapyAED combinationSlide62

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 epilepsyFirst AED (valproate) in monotherapy: 85%

Altogether 65-70% of patients with epilepsy

respond well to AED treatment.Slide63

Epilepsy and pregnancy

Teratogenic risk

In normal population: 2-3%

In women on AEDs: 4-9%

Teratogenic risk is increased

High AED doseFluctuating plasma levelsPolytherapyOccurrence of spina bifida in the familyFolic acid deficiencySlide64

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/napChange medication only if seizure control worsensScreening of fetal malformations (ultrasound on week 16 and 20, AFP)In case of enzyme inductor AEDs, give vitamin K in the third trimesterSlide65

Epilepsy and breast feeding

Breast feeding is not contraindicated with women on AEDs.

Sleep deprivation can provoke seizures. Slide66

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 AEDsSlide67

AED: Indications and Dosage

AED

Seizure type

Dose range

(mg/day)

Doses

per day

Therapeutic

range

(

μmol

/L)

Carbamazepine

Partial,Secondary GTCS,

250-2000

2-3

30-50

Sodium

Valporate

Primary & Secondary GTCS,

Absence, Myoclonus

400-2500

1-2

NA

Phenytoin

Partial, Secondary GTCS

150-350

1

40-80

Lamotrigine

Partial, secondary GTCS

25-500

1-2

NA

Lorazepum

Status Epilepticus

4 i.v.

--

NA

Clonazepum

Partial (adjunctive),

Myoclonus

1-8

2-4

NA

Ethosuximide

Childhood Abssence

500-1500

2

200-700

Topiramate

Partial, secondary GTCS

200-600

1-2

NA

Phenobarbital

Partial, secondary GTCS

60-100

1

50-150Slide68

AED: Side Effects

AED



Sodium

Valporate

Carbamazepine

Phenobarbital

Topiramate

Phenytoin

Side Effects



Neurological

Ataxia,

Nystagmus,

Diplopia,

Tremor

Ataxia,

Nystagmus,

Diplopia

Ataxia,

Nystagmus,

Diplopia

Neuropathy

Ataxia

Ataxia,

Nystagmus,

Diplopia,

Tremor,

Dystonia,

Asterixis

Neuropathy

Cognitive &

behavioral

Drowsiness

Drowsiness

Drowsiness

Confusion

Drowsiness

Drowsiness

Dermatological

Rashes,

Alopecia

Rashes, SJS,

Rashes

----

Rashes,

Hirsutism,

Gum Hypertrophy,

Hematological

Blood

dyscrasias

Blood

Dyscrasias,

Thrombo-

-cytopenia

Megalobastic Anaemia,

Osteomalacia

----

Blood

dyscrasias

Osteomalacia

Endocrine

Pancreatitis

----

----

----

----

Hepatology

&

Kidney

Liver

damage

----

----

Nephro-

-lithiasis

Liver damage

Others

Nausea,

Weight Gain

Hyponatremia

Foliate deficiency,

Depression (adults),

Excitement (Children),

SLE

Nausea, depression,

Taste alteration,

Weight loss

SLE

Facial Dysmorphism Foliate deficiency

Drug Interactions

Other AEDs,

Antimalarials

Other AEDs,

OCP,

Antimalarials,

Corticosteroids

Other AEDs,

CCB,OCP,

Digoxin,

Antidepressant,

Antimalarials

Other AEDs, OCP

Other AEDs,

OCP, Anti Arrythmic,

Antimalarials,

Corticosteroids

ThyroxineSlide69

Withdrawal of AED

After complete control of seizures for 2-4 years, withdrawal of Anti Epileptic drugs may be considered. But in case of special professional group (car driver, machine man

etc

) withdraw the AED after keen follow-up.

AED should be tapered during the stopping of medications.

Slow reduction by increments over at least 6 months.If the patient is taking two AEDs one drug should be slowly withdrawn before the second is tapered.Slide70

Prognosis

Generalized seizures are more readily controlled than partial seizures.

Childhood onset epilepsy (particularly classical absence seizures) carries the best prognosis for successful drug withdrawal.

The presence of a structural lesion makes complete control of epilepsy less likely.

Epilepsy outcome: After 20 years

50% seizure-free, without drugs, for last 5 years 20% seizure-free, continue to take medication, for last 5 years 30% seizures continue in spite of adequate dose of AEDs.Refractory epilepsy:

When seizure control is not achieved with the

first two appropriate

and well tolerated AED schedules taken as mono therapy or in combination.Slide71

Psychiatric comorbidities in Epilepsy

Mood variation

: Nearly 1 in 3 patients of epilepsy report significant concern about their mood.

Depression:

Upto 55% prevalent in patients with epilepsy.Suicide rate: In

depressed patients with epilepsy

is 5 times higher than that in the general population and 25 times higher in patients with

complex partial seizures of temporal lobe origin

.Anxiety :

Upto 50% prevalent in patients with epilepsy.Psychosis: Incidence of Psychosis 3.3% in patients with idiopathic generalized epilepsy, 14% in Temporal lobe epilepsy. In the concern of severity; Psychosis occurs in 0.6-0.7% patients with epilepsy in community and 19-27% of epilepsy patients who require hospitalization.