saraf 070830 dr epilepsi
TRANSCRIPT
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EPILEPSI
Blok Sistem Saraf
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• Epilepsi: gangguan kronik ditandai bangkitan epileptik berulang akibat gangguan fungsi otak secara intermiten yang terjadi oleh lepas muatan listrik abnormal neuron -neuron secara paroksismal akibat berbagai etiologi
(Perdossi, 2003)
• Seizure: manifestasi klinis dari eksitasi yang abnormal dan berlebihan dari neuron kortikal
• Epileptogenesis: rangkaian kejadian yang mengubah jaringan neuronal normal menjadi jaringan hipereksitabel.
• Sindrome Epilepsi: kelompok gejala dan tanda yang menggambarkan kondisi epilepsi khusus
Sumber: ILAE Report on Classification and Terminology, 2003
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• Idiopathic epilepsy Syndrome: suatu sindrome epilepsi tanpa lesi struktural yang mendasarinya dan tanpa tanda dan gejala neurologis lain.
• Generalized Seizures: melibatkan 2 hemisfer otak, dengan masifestasi bilateral
• Partial Seizures: melibatkan 1 hemisfer otak, dengan manifestasi asimetrik/ bangkitan menjadi general.
• Typical IGE: CAE, JAE, JME, atau sindrom bangkitan tonik–klonik saja dengan umur onser 3-20 thn
• Atypical IGE: meliputi pasien dengan atypical absence dan epilepsi mioklonik dan bangkitan tonik-klonik saja, diluar umur onset yang sesuai
Sumber: ILAE Report on Classification and Terminology, 2003
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Epilepsi
• Bangkitan paroksismal berulang akibat abnormalitas aktivitas listrik di otak
(WHO,2001)
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Bangkitan epilepsi
Manifestasi klinis dari bangkitan serupa (stereotipik) yang berlebihan dan abnormal, berlangsung secara mendadak dan sementara dengan atau tanpa perubahan kesadaran, disebabkan oleh hiperaktifitas listrik sekelompok sel saraf di otak yang bukan disebabkan oleh suatu penyakit otak akut (unprovoked)
Pedoman Tatlaksana EpilepsiPokdi Epilepsi Perdossi
2003
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Seizure: manifestasi klinis dari eksitasi yang abnormal dan berlebihan dari neuron kortikal
Epileptogenesis: rangkaian kejadian yang mengubah jaringan neuronal normal menjadi jaringan hipereksitabel.
Sindrome Epilepsi: kelompok gejala dan tanda yang menggambarkan kondisi epilepsi khusus
ILAE Report on Classification and Terminology, 2003
Epilepsi
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Serangan (seizure) Serangan berupa efek fisik dari
energi listrik abnormal di otak
Signal yang terganggu diteruskan ke seluruh tubuh melalui jalur saraf
Jenis serangan bergantung pada jumlah neuron yang terlibat dan area otak yang terkena: gangguan kesadaran, perilaku, motorik, sensorik, otonom, involuntar
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Ambang serangan (seizure threshold)
Ambang serangan adalah batas tingkat rangsang (stimulus) yang memungkinkan otak mengalami serangan atau tidak
Penderita epilepsi memiliki ambang serangan yang lebih rendah daripada orang normal : hanya denga sedikit rangsangan (dibandingkan dengan orang normal) maka serangan dapat terjadi
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Ambang serangan
Sebagian besar ambang serangan diwariskan secara genetik
Umur muda (< 5 tahun) mempunyai ambang serangan yang lebih rendah
Demam menurunkan ambang serangan
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Pencetus serangan epilepsi
o Kurang tiduro Stres emosionalo Kelelahan fisiko Infeksio Demamo Alkoholo Rangsangan cahayao Obat tertentuo Perubahan hormonalo Rangsangan suara
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Table 2-1 International Classification of Epileptic Seizures
I. Partial (focal, local) seizures
A. Simple partial seizures (consciousness not impaired)
1. With motor sign
2. With sensory symptoms
3. With autonomic symptoms or signs
4. With psychic symptoms
B. Complex partial seizures (temporal lobe or psychomotor seizures; consciousness impaired)
1. Simple partial onset, followed by impairment
a. With simple partial features (A.1-A.4), followed by impaired consciousness
b. With automatisms
2. With impairment of consciousness at onset
a. With impairment of consciousness only
b. With automatisms
C. Partial seizures evolving to secondarily generalized seizures (tonic-clonic, tonic or clonic)
1. Simple partial seizures (A) evolving to generalized seizures
2. Complex partial seizures (B) evolving to generalized seizured
3. Simple partial seizures evolving to complex partial seizures, evolving to generalized seizures
II. Generalized seizures (convulsive or nonconvulsive)
A. Absence (petit mal) seizures
B. Myoclonic seizures
C. Tonic seizures
D. Atonic seizures
E. Clonic seizures
F. Tonic-clonic (grand mal) seizures
III. Unclassified epileptic seizures (caused by incomplete data)
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International Classification of Epilepsies and Epileptic syndromes
(1989)1. Localization-related (focal, local, partial):
Idiopathic (primary):-Benign childhood epilepsy with centro-temporal spike-Childhood epilepsy with occipital paroxysms-Primary reading epilepsy
Cryptogenic (secondary)-Temporal lobe epilepsy-Frontal lobe epilepsy-Parietal lobe epilepsy-Occipital lobe epilepsy-Chronic progressive epilepsia partialis continua of childhood-Syndrome characterized by seizures with specific
modes of precipitation
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International…(2)2. Generalized
Idiopathic:-Benign neonatal familial convulsions-Benign neonatal convulsions-Benign myoclonic epilepsy in infancy-Childhood absence epilepsy (pyknolepsy)-Juvenile absence epilepsy-Juvenile myoclonic epilepsy-Epilepsies with grand mal seizures on awakening-Other idiopathic generalized epilepsies-Epilepsies with seizures precipitated by specific modes of activation
Cryptogenic or symptomatic:-West syndrome-Lennox-Gastaut syndrome-Epilepsy with myoclonic-astatic seizures-Epilepsy with myoclonic seizures
Nonspecific etiology:-Early myoclonic encephalopathy-Early infantile epileptic encephalopathy with suppression
bursts-Other symptomatic generalized epilepsies
Specific syndromes:-Epileptic seizures may complicate many disease states
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International …(3)3. Undetermined epilepsies
-With both generalized and focal seizures-Neonatal seizures-Severe myoclonic epilepsy in infancy-Epilepsy with continuous spike-waves during slow wave sleep-Acquired epileptic aphasia (Landau-Keffner syndrome)-Other undetermined epilepsies-Without unequivocal generalized or focal features
4. Situation-related seizures (Gelegenheitsanfalle):-Febrile convulsions-Isolated seizure or isolated status epilepticus-Seizures occuring only when there is an acute or toxic event due to factors such as alcohol, drugs, eclampsia, nonketotic hyperglycemia
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P r o d r o m a
During the prodromal phase slight alterations in neurological function may or may not be detected.
Often the patient might report a mood change or you might observe a behavior change.
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A u r a
• Many times the patient will report the aura as a peculiar smell, taste, feeling, or sound.
• Sometimes patients will experience sudden onset of dizziness, headache, “spots before their eyes”, or even cry out.
• Once the patient experiences this aura, more pronounced seizure activity is soon to follow.
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Spread ofdepolarizationthrough spinal
cord
Inhibitory neurons in cortex,anterior thalamus & basal ganglia begin to inhibit
Cortical excitation
Increased cerebralblood flow & oxygen/glucose consumption
Neurons reset toNormal resting state
Cerebral blood flow& metabolism returns
to pre-seizure level
Intermittent clonic burstsbecome less frequent until
cessation
Consciousness returns
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Cerebral lesions, biochemical disorders,
cerebral trauma, &various seizure disorders
Affected neurons more permeableand reactive to hyperthermia,
hypoxia, hypoglycemia, hyponatremia, or repeated sensory
stimulus & repeatedly depolarize withincreasing amplitude & frequency
Depolarization spreads through adjacent normal
neurons via corticocortical synapses
Clinical manifestations of seizure
Prodroma – a manifestationthat may occur hours to days
prior to the actual seizure
Aura – a partial seizure orsensory warning that preceeds
generalized seizure activity
1
2
3
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Depolarization spreads through intrahemispheric
tracts to contralateral cortex,basal ganglia, thalamus,
& brainstem
3
Impaired or loss ofconsciousness
Spread of depolarizationthrough spinal cord
Inhibitory neurons in cortex, anterior thalamus,& basal ganglia begin toinhibit cortical excitation
Increased cerebral bloodflow & oxygen/glucose
consumption
4a
4b
4c
Tonic phase of muscle contraction as impulse
reaches motor units
Clonic phase of muscle contraction/relaxing as sporadic impulses are lessened by inhibitory
actions
5a
5b
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Increased cerebral blood flow and oxygen/glucose
consumption
Cerebral hypoglycemia
Cerebral hypoxia
Metabolic acidosis
Cerebral blood flow &metabolism returns to
pre-seizure level
Neuron resets to normal resting state
5a 5b
Intermittent clonic burstsbecome less frquent
until cessation
Consciousness returns
Status epilepticus
D e a t h6
7
8
9
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Serangan umum absence• Penderita menghentikan aktivitasnya secara
mendadak
• Mata terbuka, seolah-olah melihat jauh atau melamun
• Berlangsung selama beberapa detik
• Penderita kemudian melanjutkan aktivitasnya kembali, seolah-olah tak terjadi apa-apa
• Penderita tidak sampai terjatuh
• Kadang-kadang disertai mata berkedip-kedip secara cepat, mulut komat-kamit
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Serangan umum tonik-klonik
Mendadak berteriak, kemudian jatuh, tak sadar
Seluruh tubuh kaku (tonik), kemudian menyentak-nyentak (klonik)
Bola mata terputar ke atas, mulut berbuih
Kulit kebiruan, napas dangkal atau terhenti
Lidah dapat tergigit
Kadang-kadang ngompol
Serangan berlangsung beberapa menit
Ketika serangan reda: napas menjadi teratur kembali, kesadaran pulih secara bertahap, penderita tampak bingung
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Precipitating Factors
• Trauma/ illness/ fever• Hiperventilation• Lack of sleep• Photosensitivity• Increase emotional stress• Hormonal changes• Fluid& electrolyte imbalance• Alcohol/ drugs
Handbook of epilepsy, Browne&Holmes
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Etiologi epilepsi
Merupakan kombinasi antara ambang serangan (genetik), abnormalitas jaringan otak (predisposisi), dan faktor lingkungan (presipitasi)
Penyebab yang spesifik: belum diketahui (60%)
Idiopatik: tak diketahui penyebabnya Simtomatik: diketahui penyebabnya Kriptogenik: penyebabnya
tersembunyi (sulit diidentifikasi)
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ETIOLOGI EPILEPSI
1. Epilepsi Idiopatik
2. Epilepsi Simptomatik:
a. Usia 0 – 6 bl:- intra uterin
-selama persalinan
-kongenital
-metabolik
-defisiensi piridoksin
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ETIOLOGI EPILEPSI
2 Epilepsi Simptomatik: b.usia 6 bl-3 th:-kejang demam
-trauma kepalac.anak-remaja: - infeksid.usia muda: -trauma kepala
-tumor - infeksi
e. usia lanjut: -GPDO -tumor -trauma kepala - degenerasi
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Causes of Epilepsy
Symptomatic E Cryptogenic E Idiopathic E
(Etiologic unkn) = Residual Process 30% of Epilepsy Genetic E
- Idiopathic" epilepsy = unknown cause- "Cryptogenic" epilepsy = presumed to be due to an unidentified structural abnormality- "Symptomatic" epilepsy = due to know structural abnormality
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Etiological Newly Dx Epilepsy ( National General Practice Study of
Epilepsy ) • Cryptogenic/ Idiopathic: 61% (
83%: 0-9 yr ; 38%: > 60 yr )• Symptomatic
~ Vascular disease : 15%
~ Alcohol : 6%
~ Cerebral Trauma : 6%
~ Trauma : 3%
~ Infection : 2%
~ Other : 7%
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Causes of Seizure
Kim BG, 2000, Interdisciplinary Neuroscience, Epilepsy
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Penyebab atau faktor resiko epilepsi
1. Idiopatic - terutama kelompok umur 5 – 20 tahun
- tidak didapatkan kelainan neurologis- sering ada riwayat epilepsi pada keluarga
2. Metabolik : DM, ggn. Elektrolit, uremia, alkohol,obat3. Trauma kepala : PTS, terjadi 2 tahun pasca trauma4. Tumor otak5. Kardiovasculer : stroke6. Infeksi : Ensefalitis, meningitis, abces otak7. Penyakit degenerativ :Demensia Alzheimer
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Sumber: Molecular genetics of human epilepsies, 1999
EPILEPSY
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1. Partial Simplex2. Partial Complex
Modified: Crank, 2003
Patofisiologi
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Clinical Simposia, no I 1994
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Basic Mechanism of Epilepsy
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Basic Mechanisms Underlying Seizures and Epilepsy
Ionic channel Na+, Ca++, K+, Cl-
Lignad-gated Channel excitatory - Glutamate inhibitory - GABA
Excitatory postsynaptic potentialInhibitory postsynaptic potentialAction potentialExcessive discharge
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Neuronal Excitation
• Action Potential
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Mechanism: Increase Inhibition
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MEKANISME SELULER TIMBULNYA EPILEPTOGENESIS
DARAH hemolisis Fe++ atau Fe+++
Hidrogen Peroksida (H2O2)Radikal Hidroksil (OH-)Radikal Superoksid (O2-)
Radikal Bebas
Peroksidasi Lipid
Aktivasi asam arakhidonat
Asam arakhidonik fosfitate (IP3)
Osilasi kalsiumPada sel glia
Ca++ intrasel
Kerusakan eksitotoksik
Kematian neuron/jar. Parut sel glia
AKTIVITAS EPILEPTIFORM
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Basic Mechanism of Epilepsy
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Fungsi EEG
• Mendukung diagnosa klinik epilepsi
• Membedakan tipe general dari partial
• Identifikasi sydroma epilepsi
• Menentukan prognosis pada kasus tertentu
• Pertimbangan dalam penghentian OAE
• Membantu dalam menentukan letak fokus
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Gelombang EEG normal :
• Alpha : 8 – 13 cps
• Beta : > 13 cps
• Theta : 4 – 7 cps
• Delta : < 4 cps
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EEG Abnormal :
• Gel. Lambat (slow wave)
• Gel. Paroksismal : spike/ sharp wave
• Amplitudo abnormal.
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Gelombang EEG
Beta :
- Banyak terlihat pd pemakaian barbiturat
- Dominan di daerah frontal
Delta :
- Normal semua umur dlm keadaan tidur
- Abnormal dewasa muda dlm keadaan bangun
Theta :
- Fisiologi dijumpai pd neonatus
- Sering pd dewasa muda dan usia > 50 th
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531 second
Beta activity: > 13 Hz
Alpha activity: 8-13 Hz
Theta activity: 4-7.5 Hz
Delta activity: < 4 Hz
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COMMON DIAGNOSTIC INDICATIONS FOR EEG
• Clinical seizures• Definite epilepsy• Headache• Syncope• Learning disabilities• Movement disorders• Patients with altered mental status and coma• Attention-deficit hyperactivity disorder (ADHD)
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Indikasi Neuroimejing
• Kasus bangkitan pertama yg diduga ada kelainan struktural
• Perubahan bentuk bangkitan
• Terdapat defisit neurologik fokal
• Epilepsi bangkitan parsial
• Bangkitan pertama diatas usia 25 tahun
• Untuk persiapan operasi epilepsi
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Diagnosis
Diagnosis epilepsi didasarkan atas bukti klinis; EEG membantu penentuan jenis epilepsi
Jenis serangan perlu dideskripsikan: untuk keperluan terapi
Diupayakan agar mencapai diagnosis etiologik
Penyampaian diagnosis kepada penderita memerlukan penjelasan yang cukup sekaligus disertai rencana terapi
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Dx Epilepsi
• Ax– Pola/ bentuk serangan– Lama serangan– Gejala sebelum, selama, dan paska serangan– Frekuensi serangan– Faktor pencetus – Ada/ tdk penyakit lain yg diderita sekarang– Usia saat terjadi serangan pertama– Riw kwhamilan, persalinan, dan perkembangan– Riw peny, penyebab, atau tx sebelumnya
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Dx Epilepsi
• Px fisik– Melihat tanda dari gangguan yg berhub dg
epilepsi spt trauma kepala, infeksi sinus, gangg kongenital, defisit neurologi fokal atau difus, alkohol, obat terlarang, kanker
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Dx Epilepsi
• Px Penunjang– EEG– Neuroimejing– Lab
Pedoman Tatlaksana Epilepsi
Pokdi Epilepsi Perdossi
2003
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Dx Pasti Epilepsi
• Gejala dan tanda klinis bangkitan
• Gambaran epileptiform pada eeg
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Algoritma diagnosis epilepsi
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Prinsip terapi
• Min 2x bangkitan dlm setahun• Dx tegak, informasi u/ pasien dan keluarga• Tepat obat• Sebaiknya monoterapi• Dimulai dari dosis rendah dianikkan sampai efektif• Dimulai dg obat lini pertama, bila perlu penggantian obat
pertama diturunkan bertahap, obat kedua dinaikkan bertahap
• Bila gagal monoterapi, kombinasi• Bila mungkin pantau kadar obat
Pedoman Tatlaksana EpilepsiPokdi Epilepsi Perdossi
2003
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Serangan pertama diterapi
• Dijumpai fokus epilepsi yang jelas pada EEG• Pada CT/ MRI otak dijumpai lesi yg berkorelasi dg
bangkitan• Ada kelainan neurologis mengarah pada kerusakan otak• Ada riw epilepsi pada orang tua dan saudara kandung
kec kejang demam sederhana• Ada riw infeksi otak atau trauma kapitis disertai
penurunan kesadaran• Serangan pertama berupa status epileptikus
Pedoman Tatlaksana EpilepsiPokdi Epilepsi Perdossi
2003
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Tx Epilepsi
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Terapi (2):Mekanisme aksi OAE:
Meningkatkan inhibisi neuronal (GABAergic transmission):-meningkatkan aksi GABA pada reseptor GABAA
-menghambat pemecahan GABA di sinapsis-blokade ambilan GABA di terminal presinaptik
Menurunkan eksitasi neuronal (glutaminergic transmission):-menurunkan pelepasan glutamat-blokade aksi glutamat di NMDA/AMPA/reseptor kainat
Blokade terhadap voltage-gated Na channels
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Terapi (3)
• Obati/atasi serangan epileptik, bukan EEG!
• Mulailah dengan dosis rendah dan bila perlu dosis dinaikkan secara bertahap
• Naikkan dosis OAE sampai mencapai efek klinis, atau toksik
• Monitor kadar OAE dalam serum• Hentikan OAE secara bertahap
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T e r a p i (4)
• Monitor/evaluasi:
- apakah OAE efektif atau tidak efektif
- apakah ada efek samping
- apakah ada rasa bosan minum obat
- perubahan berat badan
- perubahan jenis serangan
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Classification of AnticonvulsantsAction on Ion
ChannelsEnhance GABA
Transmission
Inhibit EAA
TransmissionNa+:
Phenytoin, Carbamazepine, Lamotrigine
Topiramate
Valproic acid
Ca++:
Ethosuximide
Valproic acid
Benzodiazepines
(diazepam, clonazepam) Barbiturates (Fenobarbital)
Valproic acid
Gabapentin
Vigabatrin
Topiramate
Felbamate
Felbamate
Topiramate
Na+:
For general tonic-clonic and partial seizures
Ca++:
For Absence seizures
Most effective in myoclonic but also in tonic-clonic and partial
Clonazepam: for Absence
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Classification of AnticonvulsantsClassical
• Phenytoin• Phenobarbital• Primidone• Carbamazepine• Ethosuximide• Valproic Acid• Trimethadione
Newer• Lamotrigine• Felbamate• Topiramate• Gabapentin• Tiagabine• Vigabatrin• Oxycarbazepine• Levetiracetam• Fosphenytoin• Others
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• May act in motor cortex, inhibit spread of seizure activity. • Activity of brainstem centers inhibittonic phase of grand mal
seizures• Irritation administer with or immediately after meals.• Rapid injection or direct IV injection severe hypotension or CNS
depression IV rate not to exceed 50 mg/min; in elderlyIV rate not to exceed 25 mg/min; in childrenIV at rate not to exceed 0.5-1 mg/kg/min and do not exceed 50 mg/min; in infants, do not give via scalp veins.
Adult Dose• IV loading dose for patients who have not received phenytoin in
preceding 7 days: 10-15 mg/kgMaintenance dose: 4-7 mg/kg/d PO/IV
Pediatric Dose• IV loading dose: 15-18 mg/kg
Maintenance dose: 5 mg/kg/d PO/IV divided bid• If the patient has not experienced a seizure, phenitoin should be
discontinued after 7 to 10 days
PHENYTOIN
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PHENYTOIN (Cont’)
Contraindications• Reduce dose in hepatic impairment; sino-atrial block; Adams-Stokes
syndrome; second- or third-degree AV block Pregnancy• C - Safety has not been established. Precautions• Rapid IV infusion may result in death from cardiac arrest, marked by
QRS widening Has narrow therapeutic index monitoring of plasma levels Perform blood counts and urinalyses when therapy is begun and at monthly intervals for several months thereafter to monitor for blood dyscrasias; discontinue use if skin rash : exfoliative, bullous, or purpuric; caution in acute intermittent porphyria and diabetes (may elevate bloodglucose); discontinue use if hepatic dysfunction occurs
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MEDIKAMENTOSA: Sodium valproate As adjunctive therapy: 10-15 mg/kg/d. May increase by 5-10 mg/kg/wk to
achieve optimal clinical response. Ordinarily, optimal clinical response achieved at daily doses <60 mg/kg/d.
Adult Dose• 600 mg/d PO divided bid, preferably after food; increase by 200 mg/d at 3-d
intervals; not to exceed 2.5 g/d (20-30 mg/kg/d) Pediatric Dose• <2 years: Not recommended because of risk of fatal hepatotoxicity
>2 years: 20 mg/kg/d initially in divided doses; can be increased, not to exceed 35 mg/kg/d
Contraindications• hypersensitivity; active liver disease; porphyria; family history of hepatic
dysfunction Pregnancy• D - Unsafe in pregnancy Precautions• Thrombocytopenia and abnormal coagulation parameters have occurred;
Monitor for hepatotoxicity (perform LFTs periodically)Hyperammonemia malaise, weakness, facial edema, anorexia, jaundice, and vomiting; may cause drowsiness
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• Indicated for complex partial seizures. • Adult Dose• 100-200 mg PO qd/bid; slowly increase to usual dose of 0.8-1.2 g/d in
divided doses; not to exceed 1.6-2 g/d • Pediatric Dose• <1 year: 100-200 mg/d PO in divided doses
1-5 years: 200-400 mg/d PO in divided doses10-15 years: 0.6-1g/d PO in divided doses
• Contraindications• Documented hypersensitivity; AV conduction abnormalities (unless
paced); porphyria; history of bone marrow depression; concurrent MAOIs
• Pregnancy• C - Safety has not been established. • Precautions• In first trimester, risk of teratogenesis, Risk of neonatal bleeding; • Counseling, and folate supplements advised
Increased intraocular pressure; obtain complete blood cell counts and serum iron level prior to treatment, during first 2 months, and yearly or every other year thereafter; can cause drowsiness, dizziness, and blurred vision;
Carbamazepine
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TERAPI ANTIOKSIDAN
DARAH hemolisis Fe++ atau Fe+++Hidrogen Peroksida (H2O2)Radikal Hidroksil (OH-)Radikal Superoksid (O2-)
Radikal Bebas
Peroksidasi Lipid
Aktivasi asam arakhidonat
Asam arakhidonik fosfitate (IP3)
Ca++ intrasel
Kerusakan eksitotoksik
Kematian neuraon/jar. Parut sel glia
AKTIFITAS EPILEPTIFORM
Tokoferol 2 mg/kg bb
Selenium
Peroksidase/ katalase
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Dosis obat antiepilepsi
Phenytoin 100-200mg/h 5 mg/kgBB
Fenobarbital 30 mg/hari 3-4 mg/hari
Carbamazepin 100 mg 10-40 mg/kg/hr
Clonazepam 0,25 mg/hari
Sod.Valproat 400-500mg/h 20 mg/kgBB/hr
Gabapentin 300 mg/hari 15-30 mg/kg/hr
Okskarbazepin 600mg/hari
Lamotrigin 12,5-25mg/hr 0,5 mg/kg/hr
Topiramat 25-50mg/hr 0,5-1 mg/kg/hr
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GUIDELINES FOR DOSES OF 1ST LINE AEDS IN Adults (Brodie 1996, Browne 2001)
Drug Indication Starting
dose
Most Common
Daily Dose
Standard maintenance dose(range) mg/kg/day
No of
Doses / day
Target plasma
drug concentr. (range) g/ml
CBZ
PHT
VPA
BAR
PMD
ETX
CNP
Partial & GTCS
Partial & GTCS /SE
Partial & GTCS
Partial & GTCS
Neonatal seizure/SE
Partial & GTCS
Generalized absense seizure
Myoclonic epilepsi, L Gestaut Syndrome infantile spasm / SE
400
300
500-1000
60-90
100-125
500
1
600
300
1000
120
500
1000
4
600-1200
300-500
1000-3000
90-120
250-1500
1000-2000
2-8
2-3
1
2
1
3
2
1 or 2
4-12
10-20
50-150
10-40
5-12
40-120
none
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GUIDELINES FOR DOSES OF 2nd LINE AEDS IN Adults (Brodie 1996, Browne 2001)
Drug Indication Starting
Dose
Maintenance dose
Plasma Half Life(hrs)
Plasma Binding
(%)
Gabapetin
Lamotrigine
Felbamat
Clobazam
Oxcarbazpn
Tiagabin
Topiramat
Vigabatrin
Zonisamide
Partial & SGTCS
(Adults)
Partial & SGTCS
(Adults)
Partial & SGTCS
(Adults)
L-G Syndrome
Partial & GTCS
Partial & GTCS
Partial & SGTCS
Partial & SGTCS
Partial & SGTCS
Possibly inf Spasm
Partial & SGTCS
300mg/d; 300 mg/d q1-3d
25-50mg/d; 50mg q1-2wk or25mgq2d with VP
2-3x 400mg/d; with dose by 400-600mg/d q2wk
3-4x 15mg/kg/d
15mg/kg/d/q1-2wk
10mg qb or
2 x 10mg/d
2x300mg/d
Not available
100 mg/d
100mg/d/q1wk
2x500 mg/d
100-200 mg/d
1200-2400mg/d
Up to 700mg/d
(100-150mg/d with VP)
1800-4800mg/d
Up to 45mg/kg/d
20-30mg/d
Up to 60 mg/d
1200-2400mg/d
32-56mg/d
400-100mg/d
Up to 3g/d
400-600mg/d
6
25(12-24 with enzyme inducing drug; 60 with VP
20-23
30-46
8-24
6-8
20-24
4-8(effect last 3 d)
30-68(27-38 with enzyme inducing drug)
0
54
22-25
85
40
96
10-20
Minimal
38-40
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AEDS CHOICE BASED ON SEIZURE TYPE (Jarrar 2003)
Seizure type & subtype
First choice drug
Other options
Generalized
• infantile spasm
• absence
•Atonic
•Tonic
•Myoclonic
•Tonic-clonic
Partial
• with and without secondary generalization
corticotropin
Ethosuximide
Valproic acid
Valproic acid
Valproic acid
Valproic acid
Carbamazepin
Topiramate, lamotrigine, zonisamide,
Valproic acid, felbamat
Lamotrige, zonisamide, VPA
Topiramate, lamotrigine, phenytoin,
Phenobarbital, zonisamide, felbamat
Topiramate, lamotrigine, phenytoin,
Phenobarbital, zonisamide, felbamat Topiramate, lamotrigine, phenytoin,
Phenobarbital, zonisamide, felbamat Topiramate, lamotrigine, phenytoin,
Phenobarbital, zonisamide, felbamat
Oxcarbazepin lamotrigine, topiramate, phenytoin, levetiracetam, zonisamide, tiagabine, gabapentin, VPA, phenobarbital, felbamat
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Determining a Loading Dose of an AED
Dose (mg) =
Weight (kg) x VD (L/kg) x Change in concentration
VD= Volume of distribution
Change in concentration = Desired AED level Current AED level
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Mechanisms of ActionAntiepileptic Drugs
• Sodium channel effects
• Potassium channels and GABA release
• GABAergic effects– Precursors, mimicry, and transporters
• Glutamate regulation-neuroprotection
• Calcium channels and transmitter release
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FIG. 4. Schematic diagram of an inhibitory synapse in the central bervous system, and the putative major sites of actions of various antiepileptic drugs (AEDs). GABA, -aminobutryc acid; GABA-T, GABA transaminase; GAD, glutamic acid decarboxylase.
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FIG. 5. Schematic diagram of an excitatory synapse in the central nervous system, and the putative major sites of actions of various antiepileptic drugs (AEDs). NMDA, N-methyl-D-asparate; AMPA, -amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid.
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Pertolongan waktu serangan
Jangan panik Biarkan serangan berlalu karena serangan
akan berhenti dengan sendirinya Amankan penderita dari lingkungan yang
membahayakan penderita Longgarkan pakaian yang ketat Posisi kepala dimiringkan (bila kejang sudah
berhenti) Bila serangan berkepanjangan: kirim ke RS
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Faktor psikososial
Cenderung dikucilkan dari lingkungan
Cenderung ditolak untuk sekolah Sulit mencari pekerjaan Merupakan aib bagi keluarga Menurunkan rasa percaya diri Lebih mudah mengalami cedera
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Kesempatan bekerja
• Pada dasarnya tidak ada larangan untuk bekerja bagi penderita epilepsi
• Pekerjaan disesuaikan dengan jenis serangan
• Penderita harus paham tentang penyakit yang dideritanya
• Dukungan positip dari keluarga dan lingkungan kerja
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Kesempatan untuk sekolah
o Tidak larangan untuk sekolaho Bila perlu guru dan orang tua penderita
berkonsultasi dengan dokter yang merawatnya
o Antara orang tua dan guru diperlukan sifat terbuka dan saling mengerti
o Masalah yang ada pada penderita bukan sekedar cerdas atau bodoh
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Spells
Seizure Other
Non-Epileptic Epileptic Syncope, Panic attack, migraine, TIA, Movement disorder, sleep disorder
Psychogenic Pseudosizure
Syncope with anoxic seizure
Recurent seizures Febrile seizure
Single Seizure (unprovoked)
Acute seizure(s)
Epilepsy Recurent Febrile seizures
Metabolic, head trauma, stroke, drugs, alcohol withdrawl, etc
Seizure type (s) Etiology
No syndromeSyndromeGeneralized, Partial, Partial secundary generalization, unclassified
Localization related Not localization related
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Epilepsi Pasien Kejang
Psikogenik 1. Pencetus Biasanya tidak ada Tidak ada Faktor emosi
2. Suasana Biasa waktu tidur dan sendirian
Santai, sedikit orang Jarang waktu tidur, lingkungan banyak orang
3. Prodroma Jarang Biasa
4. Awal Biasa mendadak, mungkin ada aura
Mendadak, ada aura Berangsur dg meningkatnya emosi
5. Jeritan pada awal Biasa terjadi Tidak ada Tidak biasa
6. Fenomena motorik Stereotipe Stereotipe Bervariasi
7. Lidah tergigit Biasa terjadi Jarang terjadi
8. Kesadaran Dapat terjadi penurunan kesadaran
Tidak sadar Tidak terjadi
9. Pengekangan Tidak berpengaruh Tidak berpengaruh Dapat melawan, kdg menghentikan
10. Lama/durasi Biasanya pendek 3 – 5 menit Dapat memanjang
11. Henti serangan Biasanya pendek, kdg memanjang bila dg autisme. Biasanya bingung, menmgantuk atau tidur
Badan lemah dan agak bingung
Dapat berangsur, serig dg penampakan emosi: bingung, mengantu atau tidur tidak biasa terjadi
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PNEs (Psychogenic Nonepileptic seizures)
Sinonim : Pseudoseizure, pseudoepileptic seizure, hysteroepilepsi, Psychogenic seizure, psychogenic nonepileptic seizures, nonelectrical seizure, non epileptic pseudoseizure
Insidensi ; 5 – 20 % populasi umum Definisi adalah kejadian paroksimal dimana terjadi
perubahan fungsi neurologis yang menghasilkan tanda motorik, sensorik, autonom atau gejala psikis yang mirip dengan kejadian selama serangan epilepsi
Merupakan maifestasi penyebab fisiologik dan psikologik
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Psichogenic nonepileptic seizure
Definisi ; Serangan yang berupa gangguan tingkah laku mirip serangan eoilepsi tetapi tidak berhubungan dengan kelainan elektrofisiologi otak seperti pada epilepsi
Gejala : perubahan tingkah laku, kesadaran dan atau kejang
Serangan timbul bila ada beberapa orang disekitarnya, kejang berhenti tanpa disertai bingung
Manifestasi ; kejang extremitas yang tidak sinkron, gemetar, gerakan pinggul, kepala, epistotonus, bicara keras
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Promoting Control factors
• Adequate amount of AED in blood
• Adequate sleep and rest
• Correct AED
• Good Nutrition
• Alcohol Abstinence
• Fluid& electrolyte balance
• Low anxiety levelHandbook of epilepsy, Browne&Holmes
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Glu
Glu
Glu
Ca2+
Ca2+
NM
DA
VS
CC
Na+
Ca2+
Na+
AMPANa+C
Na+
G l u
Inflammatorymediators
Depolari- zation
Celldistension
Membranedegradation
Free radicals
Enzymeinduction
Mitochondrialinjury
DNA injury
Apoptosis
Neuronal injury cascadeNeuronal injury cascadeDirnagl et al. Trends Neurosci 22:391-397
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Glu
Glu
Glu
Ca2+
Ca2+
NM
DA
VS
CC
Na+
Ca2+
Na+
AMPA
Na+
G l u
Depolari-zation
Celldistension
Membranedegradation
Free radicals
Enzymeinduction
Na+C
Neuronal injury cascade / Action of AEDsNeuronal injury cascade / Action of AEDs
TopiramatePhenytoin
CarbamazepineValproic acidLamotrigine
Na+ channel blockers:
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Glu
Glu
Glu
Ca2+
Ca2+
NM
DA
Na+
Ca2+
Na+
AMPA
Na+
G l u
Depolari- zation
Celldistension
Membranedegradation
Free radicals
Enzymeinduction
Na+C
VS
CC
Neuronal injury cascade / Action of AEDsNeuronal injury cascade / Action of AEDs
FelbamateMK801
Ketamine
NMDA antagonists
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Glu
Glu
Glu
Ca2+
Ca2+
NM
DA
Na+
Ca2+
Na+
AMPA
Na+
G l u
Depolari-zation
Celldistension
Membranedegradation
Free radicals
Enzymeinduction
Na+C
VS
CC
Neuronal injury cascade / Action of AEDsNeuronal injury cascade / Action of AEDs
TopiramatePhenobarbital
AMPA antagonists
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Mechanism of antiepileptic Drug – associated Bone Disease
• Hepatic induction of the citochrome P450 enzyme system leading to increased catabolism of vitD is the principal mechanism. (Allison M.Pack, 2003)
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Mechanism of antiepileptic Drug – associated Bone Disease
• AED that induced cytochrome P450 enzymes may cause increased conversion of vitD to polar inactive metabolism in the liver microsomes, reducing bioavailable vitD. Decreased biologically active vitD leads to decreased absorption of calcium in the gut, resulting in hypocalcemia and an increase in circulating PTH. PTH then increases the mobilization of bone calcium stores and subsequent boMne turnover
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• AED may interfere with intestinal absorption of calcium. Impaired absorption would lead to hypocalcemia and feedback hypersecretion of PTH – increase mobilization bone calcium store and bone turnover
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