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EPILEPSYPresented by:

Post graduate studentsCourse: MD Phase A (Psychiatry)BSMMU, Dhaka18/8/2013

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Contents

•Introduction•Pathogenesis•Clinical features & Diagnostic approach•Management•Interphase & Summary

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IntroductionDr Towhidul Islam

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Past

•Oldest record SakikKu -babilonian medcal text 1067 B.C

•Aurvedic description as “Apasmara” 400 B.C

•“epilambanein” to be overwhelmed by surprise

•Falling sickness•Demonic possession

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Past

•“its cause lies in the brain”

•1920- Human EEG (Hans Berger)

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Basics

Seizure:

•Any clinical event•Abnormal brain discharge

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Basics

Epilepsy :

• Recurrence• Seizure attack

Pseudo seizure/PNES:

• Resemblance• Psychology• No abnormal brain discharge

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PNES

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Basics SEIZURE PSEUDO

SEIZURE SYNCOPE

• Sudden• Unconscious • Cyanosis• Injury• Sec to mints• Hand on

face• Post ictal

confusion• EEG,CPK,

Prolactin

• Gradual • Conscious • Thrusting• Mins to hr• Eye opening • Pupil-

Normal• Psycho

social• Suggestive

• Light headedness

• Standing• Preventive-

lying • Brief- lost

consciousness

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Current scenario

• 60 million people worldwide

• 85% people-inadequate/not at all

• Specialist care:LIC- 56%, HIC-89%

• AEDs: Govt priority, high cost , PB

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Current scenario

•Age: any age (childhood, old age)

•Prevalence: Single episode - 5%Repeated- 0.5 to 2.5%Our country- 2%Developing country- 5 times higher

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Classification

FOCAL (Partial)

GENERALIZED Unclassified-MAY BE Focal/Generalized/ Unclear

(Complex)With Dyscognitive features

(Simple) Without Dyscognitive features

AbsenceTonic ClonicAtonicMyoclonic

Epileptic spasmsFebrile convulsionInfeantile spasmLennox-Gastaut Sydrome

• Motor • Sensor

y• Versive• Visual

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Cause

•Family history 5 to 10% of all epilepsiesUsually- 10 GTCS, Febrile convulsion, Absence, Juvenile myoclonic epilepsy

•Primary generalized- 75% idiopathic

•Partial & 20 generalized- definite cause75% adult

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CauseNeonates<1 month

Infants < 12 years

Adolescents12-18 years

Young adult 18-35 years

Older >35 years

Perinatal hypoxia and ischemia

ICH

Ca++ , GlucoseBilirubin

Water intoxication

Inborn error of metabolismTrauma

Febrile seizures

CNS infection

Trauma

Developmental disorder

Inborn error of metabolism

Trauma

CNS infection

AVM

Infection

Congenital defect

Tumors

Trauma

CNS infection

Brain tumor

AVM

Drugs and alcohol

Drugs and alcoholTraumaTumor

CVD

Degenerative

CNS infection

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CauseGROUP Names

ALKYLATING AGENTS Busulfan, Chlorambucil

ANTIMALARIALS Chloroquine, mefloquine

ANTIMICROBIAL Beta lactam , Quinolones, Acyclovir, Isoniazid, Ganciclovir

ANESTHETICS, ANALGESICS

Meperidine, Tramadol, Local anaesthetics

DIETARY SUPPLEMENTS

Gingko, Ephedra

IMMUNOMODULATORY DRUGS

Cyclosporine, Tacrolimus, Interferron

PSYCHOTROPICS Antidepressants, Antipsychotics, Lithium

CONTRAST AGENTS Theophylline

SEDATIVE , HYPNOTIC (WITHDRAWL)

BZD, Barbiturates, Alcohol

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What happens inside?Dr Md Saleh Uddin

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Why & How?

•Shift of balance: Excitation & Inhibition(CNS)

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Why & How?

•Endogenous factor

Neuronal propensity to burst

Intrinsic : conductance to ion channel, receptor response, second messenger, translation etc.

Extrinsic : neuro transmitter, receptor, temporal /spatial property

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Why & How?

•Epileptogenesis

Transformation - normal to hyper excitable(structural change)

Lowered seizure thresholdLost inhibitionSprouting of surviving neurons

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Why & How?

•Precipitating factor

Sleep deprivationAlcoholRecreational drug misusePhysical and mental exhaustionFlickering lights Intercurrent infections and metabolic

disturbance

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What & How?

Seizure initiation and propagation

• Initiation: Bursts of action potentialHyper synchronization

• Propagation: Extracellular K+

Presynaptic Ca2+

Cortical connections& Commissural fibers

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Why & How?

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Updates

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Why & How?

Endogenous Factor

Precipitating Factor

Epileptogenic Factor

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Clinical features & Diagnostic approach

Dr Hosnea Ara

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GTCS/Grand mal

•Prodrome•Aura•Tonic phase•Clonic phase•Relaxation•Post ictal phase

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Absence Seizure

•Petit mal •Childhood•Frequency •Stops doing, vacant stares•Hyperventilation •No post ictal symptoms•EEG diagnostic

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Complex partial seizure

•Temporal lobe/psychomotor epilepsy•Never fall•Mood ,memory, perception•Features :

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Atonic seizure

•Brief loss of muscle tone•Heavy fall•Consciousness

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Simple partial

•Motor•Sensory•Versive•Visual

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Diagnostic approach

•History•Clinical exam•Lab enquiry•Differentials

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Diagnostic approach

•HISTORY

Age group Past history of illness Personal historyTriggering factorsEye witness description

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Diagnostic approach

•CLINICAL EXAM

General surveyVital signsCyanosis, JaundiceTongue bite mark

Systemic examNeurological, CVS, HBS, Resp

System

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Diagnostic approach

•LAB INQUIRY

Hematology BiochemistrySerologyCSF, Hormone, ECGImaging

• Late in onset • Partial / 2o

generalized• Refractory to drug• Focal neuro deficit• Status epilepticus• Suspected ICSOL• EEG shows focal

seizure

MRI/CT brain Indication

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Diagnostic approach

•LAB ENQUIRYEEG

Type of epilepsyDrug choice

Advanced lab testSphenoidal intra operative oval and

telemetric EEGAmbulatory EEG, VideotelemetryPET, SPET

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Diagnostic approach

•DIFFERENTIALS

SyncopeTIAMigraineDrop attackPanic attackHypoglycemiaCataplexy/NarcolepsyPseudoseizureCardiac arrhythmiaEpisodic confusion

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ManagementDr Mahjabeen Aftab Solaiman

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Management

•Immediate care•Medical treatment•Pregnancy•Status epilepticus•Surgical treatment

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Management

•Immediate Care:First Aid

MoveSemi proneAirwayDon’t insert

Immediately Patency of airwayO2, IV diazepam, blood

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Management

•Medical treatment

AEDs : Carbamazepine Na valproate PhenytoinPhenobarbitone

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Management

•Indication AEDs:

Single seizure( lesion , EEG, family history)

Unprovoked seizureAdult- > 1Child- > 2

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Management

•AEDs-

Single drug , Low dose, ComplianceSwitching3rd drug prior combinationTwo drugs at a timeResistant to drug- metabolic/structural

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Type First line Second line Third linePartial / Secondary GTCS

Carbamazepine LamotrigineNa ValproateTopiramaateTigabineGabapentin

ClobazamPhenytoinPrimidonePhenobarbitalOxcarbazepineLevetiracetamVigabatrinAcetazoalmide

Primary GTCS Na Valproate LamotrigineTopiramateCarbamazepine

PhenytoinGabapentinPrimidonePhenobarbital TigabineAcetazolamide

Absence Ethosuximide Na Valproate LamotirizineClonazepamAcetazolamide

Myoclonic Na Valproate Clonazepam PiracetamLamotrizinePhenobarbital

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Management

AEDs withdrawal :

Control 2 to 4 yearsGradually, 6-12 months

Prognosis: Primary generalized

Absence-BestOthers- Recurrence

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Management

Pregnancy

• AEDs: Enzyme inducerCongenital abnormalities(First

trimester)Number & risk %

• Folic acid supplement• Partial seizure-little risk• Vit K supplement

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Management

•Status epilepticusSeries of seizuresWithout regaining awareness30 minutes

Management: GeneralPharmacological

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Surgical treatment:

• 20-30% patients• Localization (video EEG, MRI, SPET,PET, Cortical

mapping at surgery)• Temporal lobectomy• Hemispherectomy • Corpus callosotomy • VNS

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Interphase & Summary

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Interphase

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Interphase

•Psychiatric disorders in epilepsy

50% patient with epilepsy.Ictal, peri-ictal , inter ictal (depression)

•Treatment related psychiatric problemDepression, psychosis etcAEDs (PB, Vigabatrin etc) “Forced normalization”

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Summary

History, Exam, Exclusion D/D

History of Epilepsy

Adequacy

Sub therapeutic

Level

Increase the dose

Therapeutic Level

Max dose, Alternative

drug

Lab features (biochemistry hematology)

Positive Treat the cause

No History of epilepsy

Lab features(Biochemistry, Hematology)

Positive Further work up

Drug

Normal Imaging

Treat cause Drug

Idiopathic Drug

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References• Davidson’s principal & practice of Medicine, 21st edition, elsevier

publisher, 2012• Harrison’s Principales of internal medicine, 18th edition. • Lecture Notes-Prof AKM Anwarullah• Epilepsia, 44(suppl 6): 12-143. 2003, Blackwell publishing Inc,

ILAE• History of epilepsy 1909-2009: The ILAE century• Recognition of psychogenic non epileptic seizure: acurable

neurophobia, S S O Sallivan et al, Journal of Neurosurg Psychiatry, 2013, 84: 228-231

• Why do some brain seize? Molecular ,cellular and network mechanism, Andrew Trevelyan, Jphysiol(editorial)591.4(2013) 751-752

• The treatment gap in epilepsy, A Neliga, J W Sander, Epileptology 1 (2013) 28-30

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“The sadness will last forever”(Vincent van Gogh)

Wheat field with crows (1890)

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Thank You