e p i l e p s i by dr. poppy

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7/21/2019 e p i l e p s i by Dr. Poppy

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E P I L E P S I

dr. Poppy Chandra Dewi, Sp.S, M.Sc

Fakultas Kedokteran

Universitas Islam e!eri "akarta

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Tujuan belajar

•Memahami epilepsi secara garis besar,meliputi:

- definisi epilepsi

- klasifikasi epilepsi

- epileptogenesis

- etiologi epilepsi

- jenis serangan epilepsi- manajemen epilepsi

- jenis-jenis obat anti-epilepsi

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DEFINISI EPILEPSI

Suatu gangguan kronik yang ditandai denganadanya bangkitan epileptik berulang akibatgangguan fungsi otak secara intermiten yang terjadioleh lepas muatan listrik abnormal neuronneuronsecara paroksismal! akibat berbagai etiologi

"L#SIFI"#SI EPILEPSI

"lasi$kasi IL#E %&'% untuk tipe serangan

epilpsi"lasi$kasi IL#E %&'& untuk sindroma epilpsi

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(#N)"I*#N EPILEPSI

#dalah manifestasi klinis dari bangkitan serupa+stereotipik, yg berlebihan dan abnormal! ber langsung

secara mendadak dan sementara! dg atau tanpaperubahan kesadaran! disebabkan oleh hiperakti-itaslistrik sekelompok neuron di otak yg bukan disebabkanoleh suatu penyakit otak akut +unpro-oked,

SIND./0# EPILEPSI

#dalah sekumpulan gejala atau tanda klinisepilepsi yg terjadi bersamasama meliputi berbagaietiologi! umur onset! jenis serangan! faktor pencetus!

kronisitas1

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Anatomi dan fisiologi otak Otak memiliki > 15 miliar neuron ang

membangun substansia alba dan grisea

Otak merupakan organ ang sangat kompleksdan sensitif 

Otak berfungsi sebagai pengendali danpengatur akti!itas: motorik, sensasi, berpikir,dan emosi

Otak merupakan tempat kedudukan memori

dan pengatur akti!itas in!oluntar atau otonom

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 "alam keadaan normal: otak secara konstanmenghasilkan listrik secara teratur danberirama

#eurotransmite merangsang ataumenghambat cetusan listrik 

#euron seperti sistem telepon di dalam otak:mengirim cetusan listrik dari satu titik ketitik lainna

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$el-sel otak bekerja bersama-sama,berkomunikasi melalui signal-signal listrik 

%adang-kadang dapat terjadi cetusan listrikang berlebihan dan tidak teratur padasekelompok sel ang kemudian menghasilkan

serangan atau sei&ure

$istem limbik merupakan bagian otak angpaling sensitif terhadap serangan

'kspresi akti!itas otak secara abnormal dapatberupa gangguan motorik, sensorik, kognitif,psikis, otonom dan(atau gangguan fungsi luhur

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E*I/L/)I EPILEPSI Idiopatik

"riptogenik Simtomatik

IDI/P#*I"2 biasanya berupa epilepsi dg bangkitankejang umum! penyebab tak diketahui! umumnyagenetik1

".IP*/)ENI"2 dianggap simtomatik tetapi

penyebabnya blm diketahui! tmsk disini sindr1 3est!sindr1 Lenno4 )estaut dan Epilepsi 0ioklonik1 "linisberupa ensefalopati difus1

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SI0*/0#*I"2 *rauma! Infeksi! "elainan kongenital! S/P! Stroke! *o4ic +alcohol! obat,! 0etabolik! "elainan Neurodegenerati-

DI#)N/SIS

%1 #namnesis51 Pemeriksaan +$sik umum! neurologik,

61 EE)

71 8* Scann! 0.I

91 Laboratorium

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Cere#ral lesions,

 $iochemical disorders,

Cere#ral trauma,

%arious sei&ure disorders

'((ected neurons more permea#le

and reactive to hyperthermia,

hypo)ia, hypo!lycemia,

 hyponatremia,or 

repeated sensory stimulus *repeatedly depolari&e with

Increasin! amplitude * (re+uency

Clinical manifestations of seizure

'

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Cere#ral lesions,

#iochemical disorders,

cere#ral trauma, *

various sei&ure disorders

'((ected neurons more permea#le

and reactive to hyperthermia,hypo)ia, hypo!lycemia,

hyponatremia, or 

repeated sensory stimulus *

repeatedly depolari&e with

increasin! amplitude * (re+uency

Prodroma - a mani(estation that

may occur hours to days prior to

the actual sei&ure

'ura - a partial sei&ure or 

sensory warnin! that

precedes !enerali&ed sei&ure

activity

Clinical manifestations of seizure

hat is the pathophysiolo!y o( the aura

'

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P r o d r o m a

 During the prodromal phase slightalterations in neurological function may

or may not be detected.Often the patient might report a moodchange or you might observe a

behavior change.What come next?

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Depolari&ation spreads throu!h ad/acent normal neurons via

corticocortical synapses

Depolari&ation spreads throu!h

intrahemispheric tracts to

contralateral corte), #asal !an!lia,thalamus * #rainstem

'ura - a partial sei&ure or sensory warnin! that

precedes !enerali&ed

sei&ure activity

hat is the clinical mani(estation o( this ne)t step

$

C

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A u r a

•Many times the patient will report the auraas a peculiar smell, taste, feeling, or sound.

•Sometimes patients will experience sudden

onset of dizziness, headache, “spots beforetheir eyes”, or even cry out.

•Once the patient experiences this aura,more pronounced seizure activity is soon to

follow.•What happens next?

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Depolari&ation spreads throu!h

intrahemispheric tracts to

contralateral corte), #asal !an!lia, thalamus * #rainstem

Impaired or loss o( 

 consciousness

Spread o(

depolari&ation

throu!h

spinal cord

0onic phase o( muscle

contraction as

impulse reaches

motor units

C

1 2 3

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Loss of consciousness

•A loss of consciousness does occurbefore more generalized manifestations

begin.

•Let’s look at what happens next…..

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Depolari&ation spreads throu!h

Intrahemispheric tracts tocontralateral corte), #asal !an!lia,

thalamus * #rainstem

Spread o( depola4

ri&ation throu!h

spinal cord

Inhi#itory neurons in corte),

anterior thalamus * #asal

!an!lia #e!in to inhi#it

cortical e)citation

Increased cere#ral #lood

(low and o)y!en5!lucose

consumption

hat are these three symptoms

C

1

2

3

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)nhibitor neurons in corte*, anterior

thalamus, and basal ganglia begin to

inhibit cortical e*citation

2

+lonic phase of muscle contracting(

rela*ing as sporadic impulses are lessened

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'

$

C

1 2 3

Cere#ral hypo!lycemia

Cere#ral hypo)ia

Meta#olic acidosis

Status epilepticusDeath

ith prolon!ed sei&ure

activity, these may

#ecome critical

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1 2 3

eurons reset to

normal restin!

state

Intermittent clonic

#ursts #ecome less

(re+uent until cessation

Consciousness returns

6 7

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Spread o( 

depolari&ation

throu!h spinal

cord

Inhi#itory neurons in corte),

anterior thalamus * #asal

 !an!lia #e!in to inhi#it

Cortical e)citation

Increased cere#ral

#lood (low * o)y!en5

!lucose consumption

eurons reset to

ormal restin! state

Cere#ral #lood (low

* meta#olism returns

to pre4sei&ure level

Intermittent clonic #ursts

#ecome less (re+uent until

cessation

Consciousness returns

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+erebral lesions,

 biochemical disorders,

cerebral trauma,

!arious sei&ure disorders

Affected neurons more permeable

and reacti!e to hperthermia,

hpo*ia, hpoglcemia,

hponatremia, or repeated sensor

stimulus repeatedl depolari&e ith

increasing amplitude fre.uenc

"epolari&ation spreads

 through adjacent normal

neurons !ia

 corticocortical snapses

+linical manifestations of sei&ure

/rodroma 0 a manifestationthat ma occur hours to das

prior to the actual sei&ure

Aura 0 a partial sei&ure or

sensor arning that preceeds

generali&ed sei&ure acti!it

1

2

3

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"epolari&ation spreads

through intrahemispheric

tracts to contralateral corte*,

basal ganglia, thalamus,

brainstem

3

)mpaired or loss of 

consciousness

$pread of depolari&ation

through spinal cord

)nhibitor neurons in

corte*, anterior thalamus,

basal ganglia begin to

inhibit cortical e*citation

)ncreased cerebral blood

flo o*gen(glucose

consumption

a

b

c

Tonic phase of muscle

contraction as impulse

reaches motor units

+lonic phase of muscle

 contraction(rela*ing as

 sporadic impulses are

lessened b inhibitoractions

5a

5b

3

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)ncreased cerebral blood

 flo and o*gen(glucoseconsumption

+erebral hpoglcemia

+erebral hpo*ia

Metabolic acidosis

+erebral blood flo

metabolism returns to

pre-sei&ure le!el

#euron resets to normal resting state

5a 5b

)ntermittent clonic bursts

become less fr.uent

until cessation

+onsciousness returns

$tatus epilepticus

" e a t h2

3

4

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$erangan 6sei&ure7

#euron mencetuskan listrik secara salah:cetusan listrik muncul pada saat tidakdiperlukan, dan sebaliknya tidak

mencetuskan listrik pada saat diperlukan

8asilna: aktivitas listrik abnormal di otak

 yang bersifat mendadak dan tidak terkontrol 

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$erangan 6seizure7

$erangan berupa efek fisik dari energilistrik abnormal di otak 

$ignal ang terganggu diteruskan keseluruh tubuh melalui jalur saraf 

9enis serangan bergantung pada jumlahneuron ang terlibat dan area otak angterkena: gangguan kesadaran, perilaku,motorik, sensorik, otonom, in!oluntar

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Ambang serangan 6seizure threshold 7

Ambang serangan adalah batas tingkatrangsang 6stimulus7 ang memungkinkan

otak mengalami serangan atau tidak 

/enderita epilepsi memiliki ambangserangan ang lebih rendah daripada orang

normal : hana denga sedikit rangsangan6dibandingkan dengan orang normal7 makaserangan dapat terjadi

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Ambang serangan

$ebagian besar ambang serangandiariskan secara genetik 

mur muda 6; 5 tahun7 mempunaiambang serangan ang lebih rendah

"emam menurunkan ambang serangan

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/earisan ambang serangan

o $etiap indi!idu mearisi ambang

serangan ang menentukan seberapa jauh tingkat kerentanan indi!idu

terhadap serangan

o Apakah indi!idu mengalami serangan

atau tidak: masalah lain

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/earisan ambang serangan

o <akta: sebagian besar kasus epilepsi tanpalatar belakang riaat epilepsi

o /opulasi normal: insidensi epilepsi 1-=

o Orang tua ang mengalami epilepsi: 2keturunanna mengalami epilepsi

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o )nstabilitas neuron diariskan, terutamapada epilepsi umum 6 generalized epilepsy)

o Mekanisme instabilitas neuron masih dalam

penelitian mendalam

o Abnormalitas terletak pada struktur

membran neuron bagian luar angmemudahkan terjadina instabilitas aruslistrik 

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'pileptogenesis 617

• #eurotransmiter eksitatorik: asamglutamat, asam aspartat, asetilkolin

• #eurotransmiter inhibitorik: ?A@A,glisin, noradrenalin, dopamin, serotonin

• %edua kelompok neurotransmiter taditermasuk neurotransmiter ang bekerjacepat: berpengaruh langsung terhadappembukaan saluran ion 6ion channel7

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'pileptogenesis 6=7

•/eran neurotransmiter dalam epilepsi

diduga meliputi:

- pembentukan kondisi epileptik 

- permulaan serangan

- lamana serangan- penghentian serangan

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'pileptogenesis 67

•'pileptogenesis primer:

- ?elombang paku 6spikes7 berulang angmenetap di dalam neuron

- Terjadi depolarisasi ang cukup lama,disebabkan oleh penurunan inhibisisi6?A@A7, perubahan eksitatori 6reseptor

#M"A dan glutamat7, perubahan potensialmembran dan aktupenutupan(pembukaan saluran #aB, +aBB,dan %B

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'pileptogenesis 67

•'pileptogenesis sekunder:

- Terjadina fokus cetusan listrik abnormalsebagai tanggapan atas adanaabnormalitas di area otak tertentu

- Terjadi perubahan morfologi dalam halinhibisi, eksitasi berulang, dan transmisi

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'tiologi epilepsi

Merupakan kombinasi antara ambangserangan 6genetik7, abnormalitas jaringanotak 6predisposisi7, dan faktor lingkungan6presipitasi7/enebab ang spesifik: belum diketahui

62C7

)diopatik: tak diketahui penebabna$imtomatik: diketahui penebabna%riptogenik: penebabna tersembuni

6sulit diidentifikasi7

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'tiologi epilepsi

•%husus pada neonatus:

-'nsefalopati hipoksik-iskemik 

-infeksi $$/

-perdarahan intrakranial

-infark otak 

-malformasi otak 

-hipoglikemia-hiokalsemia

-ketergantungan terhadap piridoksin

-inborn errors of metabolism

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/encetus serangan epilepsi

o %urang tiduro $tres emosionalo %elelahan fisik 

o )nfeksio "emamo Alkoholo Dangsangan cahaa

o Obat tertentuo /erubahan hormonalo Dangsangan suara

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'kspresi serangan epilepsi

•Motorik:- %ejang- ?erakan abnormal, aneh

•$ensorik:

- #eri- /arestesi

•<ungsi luhur:- ?angguan kesadaran- Afasia

•<ungsi otonom:- #gompol- Eomitus- @erkeringat- 'pistaksis

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)nternational +lassification of

 Epileptic Seizures 61417

)F/artial sei&ures 6sei&ures beginning locall7:AF $imple partial sei&ures 6consciousness not impaired7:

1FGith motor smptoms=FGith somatosensor or special sensor

smptoms

FGith autonomic smptomsFGith pschic smptoms

@F +omple* partial sei&ures 6ith impairment ofconsciousness7

1F@eginning as simple partial sei&ures and

progressing to impairment of consciousness:aFGith no other featuresbFGith features as AF1-cFGith automatisms

+F /artial sei&ures secondaril generali&ed

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)nternationalH6=7

))F ?enerali&ed sei&ures 6bilaterall smmetricaland ithout local onset7:AF 1F Absence sei&ures

=F Atpical absence sei&ures

@F Moclonic sei&ures+F +lonic sei&ures"F Tonic sei&ures'F Tonic-clonic sei&ures

"F Atonic sei&ures

)))F nclassified epileptic sei&ures 6inade.uateor incomplete data7

) i l +l ifi i f ' il i

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)nternational +lassification of 'pilepsies

and Epileptic syndromes 6147

1FIocali&ation-related 6focal, local, partial7: Idiopathic (primary7:

-@enign childhood epileps ith centro-temporal spike

-+hildhood epileps ith occipital paro*sms

-/rimar reading epileps

Cryptogenic (secondary)

-Temporal lobe epileps

-<rontal lobe epileps

-/arietal lobe epileps

-Occipital lobe epileps-+hronic progressi!e epilepsia partialis continua of

childhood

-$ndrome characteri&ed b sei&ures ith specific

modes of precipitation

) t ti l 6=7

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)nternationalH6=7=F ?enerali&ed

 Idiopathic:-@enign neonatal familial con!ulsions

-@enign neonatal con!ulsions-@enign moclonic epileps in infanc-+hildhood absence epileps 6pknoleps7-9u!enile absence epileps-9u!enile moclonic epileps-'pilepsies ith grand mal sei&ures on aakening-Other idiopathic generali&ed epilepsies-'pilepsies ith sei&ures precipitated b specific modes of

acti!ationCryptogenic or symptomatic:

-Gest sndrome-Ienno*-?astaut sndrome-'pileps ith moclonic-astatic sei&ures

-'pileps ith moclonic sei&ures onspecific etiology:!'arl moclonic encephalopath-'arl infantile epileptic encephalopath ith suppression bursts-Other smptomatic generali&ed epilepsies

 Specific syndromes:-'pileptic sei&ures ma complicate man disease states

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)nternational H67F ndetermined epilepsies

-Gith both generali&ed and focal sei&ures-#eonatal sei&ures-$e!ere moclonic epileps in infanc-'pileps ith continuous spike-a!es during slo

a!e sleep

-Ac.uired epileptic aphasia 6Iandau-%effnersndrome7-Other undetermined epilepsies-Githout une.ui!ocal generali&ed or focal features

F $ituation-related sei&ures 6?elegenheitsanfalle7:-<ebrile con!ulsions-)solated sei&ure or isolated status epilepticus-$ei&ures occuring onl hen there is an acute or to*ic

e!ent due to factors such as alcohol, drugs, eclampsia,nonketotic hperglcemia

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$erangan umum tonik-klonik Mendadak berteriak, kemudian jatuh, tak sadar

$eluruh tubuh kaku 6tonik7, kemudian menentak-nentak 6klonik7

@ola mata terputar ke atas, mulut berbuih

%ulit kebiruan, napas dangkal atau terhentiIidah dapat tergigit

%adang-kadang ngompol

$erangan berlangsung beberapa menit

%etika serangan reda: napas menjadi teraturkembali, kesadaran pulih secara bertahap, penderitatampak bingung

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$erangan umum absence•/enderita menghentikan akti!itasna secaramendadak 

•Mata terbuka, seolah-olah melihat jauh ataumelamun

•@erlangsung selama beberapa detik 

•/enderita kemudian melanjutkan akti!itasnakembali, seolah-olah tak terjadi apa-apa

•/enderita tidak sampai terjatuh

•%adang-kadang disertai mata berkedip-kedipsecara cepat, mulut komat-kamit

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/emeriksaan klinis 617•Anamnesis:

- apakah serangan-serangan memiliki pola ang samaJ- apakah munculna serangan berkaitan dengansituasi(kondisi tertentuJ- apakah serangan muncul pada saat tidur atau tidakJ- apakah serangan terjadi di sembarang tempatJ

- apakah serangan melibatkan fungsi motorik, sensorik,otonom, fungsi luhur, atau kombinasiJ- apakah ada saksi mataJ- berapa kali serangan dalam satu hari, minggu, atau

bulanJ

- setiap kali serangan: berapa lamaJ- apakah ada faktor pencetusnaJ- apakah ada riaat ang sama di keluarganaJ- apakah sebelumna mengalami penakit tertentuJ- apakah ada gejala-gejala lainnaJ

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/emeriksaan klinis 6=7

•/emeriksaan fisik:

- inspeksi

- palpasi

- perkusi

- auskultasi- fungsi motorik, sensorik, dan otonom

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/emeriksaan penunjang

•'lektroensefalografi

•Iaboratorium:

- bergantung umur, hasil anamnesis dan

pemeriksaan fisik 

• euroimaging:

- bergantung hasil pemeriksaan fisik 

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"iagnosis

"iagnosis epilepsi didasarkan atas buktiklinisK ''? membantu penentuan jenisepilepsi

9enis serangan perlu dideskripsikan:untuk keperluan terapi

"iupaakan agar mencapai diagnosisetiologik 

/enampaian diagnosis kepada penderitamemerlukan penjelasan ang cukupsekaligus disertai rencana terapi

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T e r a p i 617

•/emilihan OA':

- sesuai dengan jenis serangan

- monoterapi(monofarmasi

- dosis tunggal, mulai dengan

minimal

- pertimbangan harga

- pertimbangan efek samping

- pertimbangan kondisi(penakitlain

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Terapi 6=7:Mekanisme aksi OA':

Meningkatkan inhibisi neuronal 6?A@Aergictransmission7:

-meningkatkan aksi ?A@A pada reseptor ?A@AA

-menghambat pemecahan ?A@A di sinapsis-blokade ambilan ?A@A di terminal presinaptik 

Menurunkan eksitasi neuronal 6glutaminergictransmission7:

-menurunkan pelepasan glutamat-blokade aksi glutamat di #M"A(AM/A(reseptorkainat

@lokade terhadap !oltage-gated #a channels

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Terapi 67

• Obati(atasi serangan epileptik, bukan ''?L

• Mulailah dengan dosis rendah dan bilaperlu dosis dinaikkan secara bertahap

• #aikkan dosis OA' sampai mencapai efekklinis, atau toksik 

• Monitor kadar OA' dalam serum

• 8entikan OA' secara bertahap

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T e r a p i 67

•Monitor(e!aluasi:

- apakah OA' efektif atau tidak efektif 

- apakah ada efek samping

- apakah ada rasa bosan minum obat

- perubahan berat badan

- perubahan jenis serangan

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/ertolongan aktu serangan

9angan panik 

@iarkan serangan berlalu karena seranganakan berhenti dengan sendirina

Amankan penderita dari lingkungan angmembahaakan penderita

Ionggarkan pakaian ang ketat

/osisi kepala dimiringkan 6bila kejang sudahberhenti7

@ila serangan berkepanjangan: kirim ke D$

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<aktor psikososial

+enderung dikucilkan dari lingkungan

+enderung ditolak untuk sekolah

$ulit mencari pekerjaan

Merupakan aib bagi keluarga

Menurunkan rasa percaa diri

Iebih mudah mengalami cedera

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%esempatan bekerja

• /ada dasarna tidak ada larangan untukbekerja bagi penderita epilepsi

• /ekerjaan disesuaikan dengan jenis

serangan• /enderita harus paham tentang penakit

ang dideritana

• "ukungan positip dari keluarga danlingkungan kerja

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%esempatan untuk sekolah

o Tidak larangan untuk sekolah

o @ila perlu guru dan orang tua penderitaberkonsultasi dengan dokter ang

meraatnao Antara orang tua dan guru diperlukan sifat

terbuka dan saling mengerti

o Masalah ang ada pada penderita bukansekedar cerdas atau bodoh

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%esempatan untuk menikah

• Menikah adalah hak a&asi manusia

• /erhatian lebih khusus pada penderitaperempuan 6menstruasi, hamil, melahirkan,

menusui7

•$uami-isteri harus selaras

• %eputusan pahit: jangan hamil

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Mengemudi kendaraan bermotor

#anti duluL

Ada prasarat ang harus dipenuhi

penderita$ifatna sangat terbatas

Iebih aman apabila penderita tidak

mengemudi kendaraan 6bermotor7/enderita harus memahami kondisina

sendiri secara jujur

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S*#*:S EPILEP*I":S +SE,

De$nisi SEBangkitan epilepsi yang berlangsung terus menerusatau tanpa pemulihan kesadaran selama 30 menitatau lebih.

"lasi$kasi SE

•Konvulsive

•Non konvulsive

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13.A 21-year-old cocaine-abusing man developsseizures that persist for more than 30 min before

emergency medical attention is available. Whenexamined nearly 1 h later, he is still exhibiting tonic-clonic movements and has never recoveredconsciousness. (SELECT 1 SEIZURE TYPE)

 a. Generalized tonic-clonic

b. Generalized absence

c. Complex partial

d. Tonic-clonic status epilepticus

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Thank You

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