epilepsy an overview

Recent Advancements in Recent Advancements in EpilepsyEpilepsy

Dr. Helal Uddin AhmedDr. Helal Uddin AhmedAssistant RegistrarAssistant Registrar

National Institute of Mental HealthNational Institute of Mental Health

[email protected]

mailto:[email protected]

IntroductionIntroduction

Definition: The occurrence of transient paroxysms of excessive or uncontrolled discharges of neurons, which may be caused by a number of different etiologies, leading to epileptic seizures.

Synonyms: Seizure Disorder

Historical BackgroundHistorical BackgroundEpilepsy derived from a Greek term: Epilambanei -to posses, to take hold of, to grab or to seize.

Vedic period of 4500-1500BC :Vedic period of 4500-1500BC :Ancient Indian Medicine refined and Ancient Indian Medicine refined and developed the basic concept of developed the basic concept of epilepsyepilepsy

Charaka Samhita- The Ayurvedic Charaka Samhita- The Ayurvedic literature 400 BC: literature 400 BC: Describe Describe epilepsy as epilepsy as ‘‘Apasmara’Apasmara’ means loss means loss of consciousness.of consciousness.

Historical BackgroundHistorical Background contd contd

Hippocrates 400 BC:Hippocrates 400 BC: ‘This is not ‘This is not a sacred disease rather disorder of a sacred disease rather disorder of brain’brain’ . He described some . He described some physical treatment of epilepsy and physical treatment of epilepsy and stated it is an incurable chronic stated it is an incurable chronic illness.illness.

Ibn Sina 370 AH:Ibn Sina 370 AH: describe epilepsy as a describe epilepsy as a

brain disease.brain disease.


Europe and USA 1857: Europe and USA 1857: Bromide was used as Bromide was used as first anti-epileptic drugs.first anti-epileptic drugs.

1873 H. Jackson: 1873 H. Jackson: Neurologist of London-Neurologist of London-described relationship of electrochemical described relationship of electrochemical discharge of brain and seizure.discharge of brain and seizure.

1920 H. Berger:1920 H. Berger: German Psychiatrist developed German Psychiatrist developed EEG to measure brainwaves and its application in EEG to measure brainwaves and its application in the field of epilepsy.the field of epilepsy.


1909: Formation International league against epilepsy

(ILAE).

1912: Use Phenobarbitone as AED.

1938: Use Phenytoin as AED.

1950-1970: Developed many AED.

1981: ILAE classified epilepsy.

1997: ILAE, IBE and WHO jointly established Global

campaign against epilepsy.

Epilepsy synonyms in South East AsiaEpilepsy synonyms in South East Asia

India: Apasamra, Mirgee,Lata, Laran

Srilanka: Apasamra

Indonesia: Ayan

Thailand: Rake Lom Ba Mu, Role Lom Chak

Bangladesh: Khichuni, Mrigee, Batash (bad wind)

Epidemiology of EpilepsyEpidemiology of Epilepsy

Epilepsy knows no geographical, racial or social boundaries. About 50 million people in World have Epilepsy.It occurs in men and women and can begin at any age, but is most frequently diagnosed in infancy, childhood, adolescence and old age.Prevalence: Developed countries- 0.5% (0.4% - 1%)Developing countries- five times higherIncidence:After infancy annual incidence- 20-70/100000 in developed countries.Developing countries- Incidence is double. (100/100000)The life time risk of having a single seizure:About 5%.

Prevalence in South East Asian Countries

Bangladesh: 0.1% (in adult

population.)

India: 0.9% in Bangalore, 0.5% in

Mumbai, 0.4% in Delhi and 0.3% in

Kolkata.

Sri Lanka: 0.9% (In Kandy District)

Pakistan: 0.99%

Nepal: 0.73%

Thailand: 0.72%

Myanmar: 0.1%

Classification of Seizures ILAE Classification (1981)

I.I. Partial (Focal)seizures Partial (Focal)seizures A. Simple partial seizuresA. Simple partial seizures B. Complex Partial B. Complex Partial

SeizuresSeizures C. Partial Seizures C. Partial Seizures

evolving to secondary evolving to secondary generalized seizures generalized seizures (tonic-clonic, tonic or (tonic-clonic, tonic or clonic)clonic)

II. II. Generalized seizures Generalized seizures (Convulsive and non-convulsive)(Convulsive and non-convulsive)

A. Absence seizuresA. Absence seizures i) Typicali) Typical ii) Atypical ii) Atypical

B. Myoclonic seizuresB. Myoclonic seizuresC. Clonic seizuresC. Clonic seizuresD. Tonic seizuresD. Tonic seizuresE. Tonic-Clonic seizuresE. Tonic-Clonic seizuresF. Atonic seizuresF. Atonic seizures(Combinations may occur: myoclonic and atonic or myoclonic and tonic)

III.III. Unclassified epileptic Unclassified epileptic seizuresseizures

Causes of EpilepsyCauses of Epilepsy

In 28%In 28% cases cause can be determined. Rests (72%) are Idiopathic.Determined causes:Inherited genetic Acquired : trauma, Neuro surgery, Inflammatory, Metabolic,Infections, Tumor, Toxic disorders, drugs, etc. Congenital: inborn error of metabolism.Withdrawal of drugsthdrawal of drugs

AAlcohol,Benzodiazepine,Barbiturates, Other Anti-

Epileptics

Drugs That Induce SeizuresDrugs That Induce Seizures

Antibiotics:Antibiotics: Penicillin, INH, Cycloserin, Ciprofloxacin, Metronidazole.

Anti Diabetic:Anti Diabetic: Insulin,Phenformin.

HormonalHormonal: Prednisolone, OCP, Oxytocin

Cardiac:Cardiac: Lidocaine,Procaine, Disopiramide

Anesthetics:Anesthetics: Methohexital, Ketamin, Halothane,Propofol

Antimalarial:Antimalarial: Chroloquine, Mefloquine, Proguanil.

Anti Spastic:Anti Spastic: Baclofen

Stimulant:Stimulant: Aminophylline, Doxapram, Theophyline.

Radiographic contrast:Radiographic contrast: Meglumine derivatives, Metrizamide.

Drugs That Induce SeizuresDrugs That Induce SeizuresAntidepressant:Antidepressant: TCA- (Amitriptaline, Imipramine, TCA- (Amitriptaline, Imipramine,

Clomipramine), Dosulepin, Buproprion. Venlafaxine, Clomipramine), Dosulepin, Buproprion. Venlafaxine,

Duloxitine,ReboxetineDuloxitine,Reboxetine

Antipsychotics:Antipsychotics: Chlorpromazine, Zotepine, Chlorpromazine, Zotepine,

Loxapine,Depot Anti-psychotics,Clozapine Loxapine,Depot Anti-psychotics,Clozapine

Mood Stabilizer:Mood Stabilizer: Lithium Lithium

Psycho stimulant:Psycho stimulant: Amphetamine Amphetamine

Safe Psychiatric medication in EpilepsySafe Psychiatric medication in EpilepsyAntidepressant: Moclobemide, SSRI (with cautious)

Antipsychotics: Haloperidol, Trifluphenazine, Sulpiride

Pathophysiology of EpilepsyPathophysiology of EpilepsyIn normal brain inhibitory circuits limits synchronous discharge. GABA is particularly play this role.When GABA receptors blocked Rhythmic and repetitive hypersynchronus discharge of neurons seizuresExcitatory NT Ach , Aspartate and Glutamate also involved to develop seizuresIntracellular recording shows burst of rapid action potential firing with reduction of transmembrane potential. inhibitory system + excitation genesis of seizuresAbnormalities in Ion Channel(Na+, K+, Ca-) may cause seizures.(Prolongation of depolarization state)

Pathophysiology of Epilepsy Pathophysiology of Epilepsy contdcontd

Repeated subthreshhold of a neuron Repeated subthreshhold of a neuron generates an action potentials generates an action potentials seizuresseizuresIt has been suggested that chronic It has been suggested that chronic epileptic discharges may lead to epileptic discharges may lead to secondary epileptogenesis.secondary epileptogenesis.Short, uncomplicated seizures cause no Short, uncomplicated seizures cause no permanent/ progressive neorological permanent/ progressive neorological dysfunctions in human braindysfunctions in human brain

BUT BUTuncontrolled generalized tonic-clonic uncontrolled generalized tonic-clonic seizures or status epilepticus is seizures or status epilepticus is associated with high neurological associated with high neurological morbidity and permanent brain damage morbidity and permanent brain damage ( due to hypo perfusion, hypoxia, ( due to hypo perfusion, hypoxia, acidosis and other metabolic acidosis and other metabolic disturbance).disturbance).

Clinical PresentationsClinical Presentations((Partial Seizures)Partial Seizures)

Simple Partial Seizures:Simple Partial Seizures: Consciousness is fully preservedConsciousness is fully preserved Motor disturbance may involve any body part Motor disturbance may involve any body part Tingling , numbness, electrical shock like feelings Tingling , numbness, electrical shock like feelings Flashing light and colours, Flashing light and colours, Simple hallucinationsSimple hallucinations Changes in skin color, Blood pressure, Heart rate, Changes in skin color, Blood pressure, Heart rate,

Pupil size, Pupil size, Piloerection.Piloerection. Psychic manifestation: Dysphasic- when cortical Psychic manifestation: Dysphasic- when cortical speech speech area affected, Dysmnestic- disturbance of area affected, Dysmnestic- disturbance of

memory, memory, Cognitive symptoms- dreamy state, Cognitive symptoms- dreamy state, Affective Affective symptoms- fear, depression, anger, symptoms- fear, depression, anger, irritability, elation, irritability, elation, erotic erotic thoughts, Illusion of size, thoughts, Illusion of size, structured hallucinationstructured hallucination.

Clinical PresentationsClinical Presentations

Definition:

Clinical PresentationsClinical Presentations((Partial Seizures)Partial Seizures)

Clinical PresentationsClinical Presentations(Partial Seizures)(Partial Seizures)

Complex Partial Seizures Complex Partial Seizures (Psychomotor Seizures/Temporal lobe Epelepsy)(Psychomotor Seizures/Temporal lobe Epelepsy)

Always involved impairment of consciousness.Always involved impairment of consciousness.

Majority originate in Temporal lobe (60%); but Majority originate in Temporal lobe (60%); but

also also originate originate another lobe –another lobe – particularly particularly Frontal(30%). Frontal(30%).

May start as simple partial seizures then progress. May start as simple partial seizures then progress.

Aura may be present-short live (few seconds) Aura may be present-short live (few seconds)

Automatism: Oro-Alimentary, Mimicry, Gestural, Automatism: Oro-Alimentary, Mimicry, Gestural,

Ambulatory, Verbal, Responsive and Violent.Ambulatory, Verbal, Responsive and Violent.

Duration: < 3 minutes.

Clinical PresentationsClinical Presentations(Complex Partial Seizures)(Complex Partial Seizures)

Definition:

Clinical PresentationsClinical Presentations(Generalized Seizures)(Generalized Seizures)

Generalized Tonic-clonic (grand mal)ConvulsiveConvulsive seizuresNo Aura but have prodormal phase- general malaiseTonic phase:Tonic phase: stiff, crying out, tongue bite,

apnea,cyanosed, increase heart rate and blood pressure, fall, labored breathing, salivation.

Clonic phase:Clonic phase: intermittent clonic movements of muscles, followed by brief relaxations, involved four limbs.Incontinence at the end of clonic phase.Duration:Duration: few minutesPost ictal period:Post ictal period: drowsiness, confusion, headache, deep sleep

Generalized Tonic-clonic (grand mal)

Definition:

Clinical PresentationsClinical Presentations(Generalized Seizures)(Generalized Seizures)

Typical Absence Seizures (Petit mal):Typical Absence Seizures (Petit mal): Occur almost exclusively in

childhood or early adolescent. Sudden loss of consciousness and

cease all motor activities. Suddenly appears blank and stares, fluttering of the eyelids, swallowing, flopping of the head.

Attacks last only a few seconds (<10 sec) and often pass un- recognized. About 100-200 attacks may occur/day.

Characteristic EEG : 3 per sec generalized spike and wave

Attacks precipitate by fatigue, drowsiness, relaxation , photic stimulation or hyperventilation.

Clinical PresentationsClinical PresentationsTypical Absence Seizures (Petit mal)Typical Absence Seizures (Petit mal)

Clinical PresentationsClinical PresentationsMyoclonic seizuresMyoclonic seizures

Abrupt , very brief, involuntery flexion movements.Involve whole body or part of the bodyOccur most commonly at morning, shortly after walking.May occur in healthy people (physiological)

Atonic SeizuresAtonic SeizuresBrief loss of muscle tone.Heavy fall , with or without loss of consciousness.

Versive seizuresVersive seizuresA frontal epileptic foci may involve the frontal eye field.Force deviation of the eyes and turning head to the

opposite side.Status EpilepticusStatus Epilepticus

Series of recurrent Tonic-Clonic seizures occurs without Series of recurrent Tonic-Clonic seizures occurs without regaining consciousness over 30 min.regaining consciousness over 30 min.

Waist Syndrome:Waist Syndrome: Infantile spasm, hypsarrhythmic patterns of Infantile spasm, hypsarrhythmic patterns of EEG, severe encepalopathy with mental retardation.EEG, severe encepalopathy with mental retardation.

Clinical PresentationsClinical PresentationsInfantile Spasm: Infantile Spasm: Sudden brief seizures, typically tonic flexor Sudden brief seizures, typically tonic flexor spasm of waist, extremities and neck. 20% mortality, who spasm of waist, extremities and neck. 20% mortality, who survive 75% have mental retardation, 50% have life long survive 75% have mental retardation, 50% have life long seizures.seizures.Juvenile myoclonic epilepsyJuvenile myoclonic epilepsy: Inherited condition.Under : Inherited condition.Under recognized syndrome with myoclonic jerks, tonic-clonic or recognized syndrome with myoclonic jerks, tonic-clonic or clonic- tonic-clonic seizures or absence seizures. EEG shows clonic- tonic-clonic seizures or absence seizures. EEG shows spike and wave pattern of 3.5-6 Hz.spike and wave pattern of 3.5-6 Hz.Lennox-Gastaut syndromeLennox-Gastaut syndrome: Devastating disorder in children. : Devastating disorder in children. Mixed types of seizures and mental retardation. Usually Mixed types of seizures and mental retardation. Usually cognitive deficit present. EEG shows slow (<2.5 Hz ) spike cognitive deficit present. EEG shows slow (<2.5 Hz ) spike and wave patterns.and wave patterns.Catamenial epilepsy: Epileptic women experienced that their seizures worsen during menstruation; due to the imbalance between the proconvulsant estrogen and anticonvulsant progestogen.

Diagnosis of EpilepsyDiagnosis of EpilepsyThorough History taking :Thorough History taking :

From patientsFrom reliable valid informantsFrom observer (who observed seizures)

Physical Examination:Physical Examination:Specially neurological systemHigher Psychic function

Laboratory Investigation:Laboratory Investigation:S. Electrolytes, S. Prolactin, Blood sugar, CBC, TFT, LFT, RFT, CSF study

Imaging:Imaging:EEG, Video EEG telemetry, CT Scan of Brain, MRI

of Brain, MRS, PET, SPECT.

PolysomnographyPolysomnography

Differential DiagnosisDifferential Diagnosis

Condition mimicking Condition mimicking Seizures:Seizures:

1. Pseudoseizure2. Syncope3. Some sleep

disorders4. Hypoperfusion in

brain5. Cardiac Arrhythmia6. Emotional Outburst7. Dissociative fugue8. Drop Attacks9. Migraine10. Hypoglycaemia

True Seizure Vs PseudoseizureTrue Seizure Vs Pseudoseizure

Features & Lab findingsFeatures & Lab findings True SeizureTrue Seizure PseudoseizurePseudoseizure

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)

Management of EpilepsyManagement of EpilepsyMedical treatment:Immediate care of seizuresImmediate care of seizures

Move persons away from dangerRecovery position (semi prone)Ensure clear airwayDo not insert anything into mouthUrgent medical attention- (patent airway, O2 , anticonvulsant, investigate cause)Should not be left alone after recovery

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

Removal of epileptic focus (eg:mesial temporal sclerosis) Anterior Temporal LobectomyCorpus callostomySubpial transection

Vagus Nerve stimulationKetogenic diet

Guidelines for Anticonvulsant TherapyGuidelines for Anticonvulsant Therapy

Start with one first line drugsStart with one first line drugsStart with low dose: Gradually increase to effective dose or Start with low dose: Gradually increase to effective dose or until side effects. until side effects.Check complianceCheck complianceIf first drug fails due to side effects or continue seizures, If first drug fails due to side effects or continue seizures, start second line drugs whilst gradually withdrawing first.start second line drugs whilst gradually withdrawing first.Try Three AED singly before using combinationsTry Three AED singly before using combinationsBeware about drug interactionsBeware about drug interactionsDo not use more than two drugs in combination at any one Do not use more than two drugs in combination at any one timetimeIf above fails consider occult structural or metabolic lesion If above fails consider occult structural or metabolic lesion and whether seizures are truly epileptic.and whether seizures are truly epileptic.

Choice of Anti Epileptic DrugsChoice of Anti Epileptic Drugs

Epilepsy TypeEpilepsy Type First-LineFirst-Line Second-LineSecond-Line Third-LineThird-Line

Partial and /orPartial and /or

Secondary GTCSSecondary GTCS

CarbamazepineCarbamazepine

LamotrigineLamotrigineOxcarbazepineOxcarbazepine

TopiramateTopiramate S. Valporate S. Valporate(in (in children)children)

S. ValporateS. ValporateTiagabineTiagabineGabapentinGabapentin

ClobazumClobazumPhynytoinPhynytoinPhenobarbitalPhenobarbitalVigabatrinVigabatrinAcetazolamideAcetazolamide

Primary GTCSPrimary GTCS S. ValporateS. Valporate LamotrigineLamotrigineTopiramateTopiramateCarbamazepineCarbamazepine

PhynytoinPhynytoinGabapentinGabapentinPhenobarbitalPhenobarbitalTiagabineTiagabineAcetazolamideAcetazolamide

AbsenceAbsence S. ValporateS. Valporate

LamotrigineLamotrigine

EthosuximideEthosuximide ClonazepumClonazepum

AcetazolamideAcetazolamide

MyoclonicMyoclonic S. ValporateS. Valporate ClonazepumClonazepum PiracetamPiracetamLamotrigineLamotrigine Phenobarbital Phenobarbital

AED: Indications and DosageAED: Indications and DosageAEDAED Seizure typeSeizure type Dose Dose

range range

(mg/day)(mg/day)

DosesDosesper dayper day

TherapeuticTherapeutic

rangerange((μmol/L)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 50-150

AED: Side EffectsAED: Side EffectsAED AED SodiumSodium

ValporateValporateCarbamazepineCarbamazepine PhenobarbitalPhenobarbital TopiramateTopiramate PhenytoinPhenytoin

Side Effects Side Effects

NeurologicalNeurological Ataxia, Nystagmus,Diplopia, Tremor

Ataxia, Nystagmus,Diplopia

Ataxia, Nystagmus,DiplopiaNeuropathy

Ataxia Ataxia, Nystagmus,Diplopia, Tremor,Dystonia,AsterixisNeuropathy

Cognitive &Cognitive &behavioralbehavioral

Drowsiness Drowsiness Drowsiness ConfusionDrowsiness

Drowsiness

DermatologicalDermatological Rashes,Alopecia

Rashes, SJS, Rashes ---- Rashes,Hirsutism,Gum Hypertrophy,

HematologicalHematological Blood dyscrasias

Blood Dyscrasias,Thrombo--cytopenia

Megalobastic Anaemia,Osteomalacia

---- Blood dyscrasiasOsteomalacia

EndocrineEndocrine Pancreatitis ---- ---- ---- ----

Hepatology & Hepatology & KidneyKidney

Liver damage

---- ---- Nephro--lithiasis

Liver damage

OthersOthers Nausea,Weight Gain

Hyponatremia Foliate deficiency, Depression (adults), Excitement (Children), SLE

Nausea, depression,Taste alteration,Weight loss

SLEFacial Dysmorphism Foliate deficiency

Drug InteractionsDrug 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,CorticosteroidsThyroxine

Withdrawal of AED Withdrawal of AED

After complete control of seizures for 2-4 years, After complete control of seizures for 2-4 years, withdrawal of Anti Epileptic drugs may be withdrawal of Anti Epileptic drugs may be considered. But in case of special professional group considered. But in case of special professional group (car driver, machine man etc) withdraw the AED after (car driver, machine man etc) withdraw the AED after keen follow-up.keen follow-up.

AED should be tapered during the stopping of AED should be tapered during the stopping of medications. medications.

Slow reduction by increments over at least 6 months.Slow reduction by increments over at least 6 months.

If the patient is taking two AEDs one drug should be If the patient is taking two AEDs one drug should be slowly withdrawn before the second is tapered.slowly withdrawn before the second is tapered.

PrognosisPrognosis

Generalized seizures are more readily controlled than partial Generalized seizures are more readily controlled than partial seizures.seizures.Childhood onset epilepsy (particularly classical absence Childhood onset epilepsy (particularly classical absence seizures) carries the best prognosis for successful drug seizures) carries the best prognosis for successful drug withdrawal.withdrawal.The presence of a structural lesion makes complete control of The presence of a structural lesion makes complete control of epilepsy less likely.epilepsy less likely.Epilepsy outcome: After 20 yearsEpilepsy outcome: After 20 years50% seizure-free, without drugs, for last 5 years50% seizure-free, without drugs, for last 5 years20% seizure-free, continue to take medication, for last 5 years20% seizure-free, continue to take medication, for last 5 years30% seizures continue in spite of adequate dose of AEDs.30% seizures continue in spite of adequate dose of AEDs.Refractory epilepsy:Refractory epilepsy: When seizure control is not achieved When seizure control is not achieved with the with the first two appropriatefirst two appropriate and and well toleratedwell tolerated AED AED schedules taken as mono therapy or in combination.schedules taken as mono therapy or in combination.

Psychiatric comorbidities in EpilepsyMood variationMood variation: Nearly 1 in 3 patients of epilepsy report : Nearly 1 in 3 patients of epilepsy report significant concern about their mood.significant concern about their mood.

Depression:Depression: Upto 55% prevalent in patients with epilepsy. Upto 55% prevalent in patients with epilepsy.Suicide rate:Suicide rate: In In depressed patients with epilepsydepressed patients with epilepsy is 5 times is 5 times higher than that in the general population and 25 times higher higher than that in the general population and 25 times higher in patients with in patients with complex partial seizures of temporal lobe complex partial seizures of temporal lobe originorigin..Anxiety Anxiety : Upto 50% prevalent in patients with epilepsy.: Upto 50% prevalent in patients with epilepsy.PsychosisPsychosis: Incidence of Psychosis 3.3% in patients with : Incidence of Psychosis 3.3% in patients with idiopathic generalized epilepsy, 14% in Temporal lobe idiopathic generalized epilepsy, 14% in Temporal lobe epilepsy. In the concern of severity; Psychosis occurs in 0.6-epilepsy. In the concern of severity; Psychosis occurs in 0.6-0.7% patients with epilepsy in community and 19-27% of 0.7% patients with epilepsy in community and 19-27% of epilepsy patients who require hospitalization.epilepsy patients who require hospitalization.

Recent Research and AchievementsRecent Research and AchievementsDrug treatments: Drug treatments: Sodium valporate or Lamotrigin is chosen as Sodium valporate or Lamotrigin is chosen as

first line treatments for Absence seizures and partial first line treatments for Absence seizures and partial seizures. seizures. [BMJ vol 318 ][BMJ vol 318 ]

SANAD (SANAD (Standard and New Anti-epileptic DrugsStandard and New Anti-epileptic Drugs) study :) study : Valporate Valporate is significantly better than Topiramate and Lamotrigine in is significantly better than Topiramate and Lamotrigine in treatment of idiopathic generalized seizurestreatment of idiopathic generalized seizures .[Lancet vol 369 March .[Lancet vol 369 March 2007]2007]

Surgery:Surgery: In developing countries, in patients with Mesial TLE In developing countries, in patients with Mesial TLE are feasible by a knowledgeable team consisting epileptologist, are feasible by a knowledgeable team consisting epileptologist, neurosurgeon, and technicians with using MRI and EEG. neurosurgeon, and technicians with using MRI and EEG. [Epilepsia [Epilepsia 49(3):381-5.2008]49(3):381-5.2008]

In Benign Rolandic Epilepsy: In Benign Rolandic Epilepsy: Children with BRE demonstrated Children with BRE demonstrated specific recognition impairments due to cortical auditory specific recognition impairments due to cortical auditory dysfunction. dysfunction. [Epilepsia, 49(6):1018-1026.2008][Epilepsia, 49(6):1018-1026.2008]

Recent Research and AchievementsRecent Research and Achievements

Seizure after Stroke:Seizure after Stroke: Overall incidence of seizures within Overall incidence of seizures within 24 hours after stroke was 3.1%. Higher incidence seen in 24 hours after stroke was 3.1%. Higher incidence seen in hemorrhagic stroke (8.4%). Seizures after stroke had higher hemorrhagic stroke (8.4%). Seizures after stroke had higher mortality at 30 days after strokemortality at 30 days after stroke.[.[Epilepsia 49(6):974-981.2008]Epilepsia 49(6):974-981.2008]

Akershus StudyAkershus Study: Seizure free epilepsy patients on AED : Seizure free epilepsy patients on AED monotherapy improve neuropsychological performance after monotherapy improve neuropsychological performance after withdrawn the AED but a relative risk of seizures relapse withdrawn the AED but a relative risk of seizures relapse 2.46, compared to those continuing medications. 2.46, compared to those continuing medications. [Epilepsia [Epilepsia

49(3):455-463.200849(3):455-463.2008]

Famous Persons with Epilepsy

AristotleAristotleSocratesSocratesJulius CaesarJulius CaesarFyodor DostoyevskyFyodor DostoyevskyLord ByronLord ByronVincent Van GoghVincent Van GoghAlfred NobelAlfred NobelVlaldimir Illyich LeninVlaldimir Illyich LeninNaepoleon BonaparteNaepoleon BonaparteTony GreigTony Greig

Acknowledgements

Professor AH Mohammad FirozDirector-cum-Professor, NIMH

Professor Dr. Md. Enayet KarimProfessor, NIMH

All Respected Teachers of NIMHAll Doctors of NIMH

&Dr. Imtiaz Ahmed, Sanofi AventisMr. Subrata Kumar Saha, Sanofi Aventis.

THANK YOUTHANK YOU

epilepsy an overview

Health & Medicine