Pemicu 2 saraf&kejiwaan

Christabella Monica
405090013
Kejang
Definition
 Seizures are disorders characterized by temporary neurologic signs or
symptoms resulting from abnormal, paroxysmal, hypersynchronous
electrical neuronal activity in the cerebral cortex.
 A seizure is a transient disturbance of cerebral function caused by an
abnormal neuronal discharge. Epilepsy, a group of disorders
characterized by recurrent seizures, is a common cause of episodic
loss of consciousness; the incidence of epilepsy in the general
population is 45/100 000, prevalence is 0.5%, and the lifetime
probability of a seizure is approximately 3%.
 An actively convulsing patient or a reported seizure in a known
epileptic usually poses no diagnostic difficulty. Because most seizures
occur outside the hospital unobserved by medical personnel, the
diagnosis often must be established retrospectively.
Kriteria Kejang
Kejang pada BBL Kejang pada bayi usia 0-28 hari

Kejang pada suhu >38oC o.k proses

Kejang Demam ekstrakranial

Kejang lama Kejang >15 menit

Kejang berulang Berulang 3x/lebih dalam 24 jam

Kejang epileptikus Kejang >30 mnt tanpa sadar

Epilepsi Kejang tanpa provokasi > 2x

Etiology
 Seizures can result from either primary CNS dysfunction or an
underlying metabolic derangement or systemic disease. This
distinction is critical, since therapy must be directed at the
underlying disorder as well as at seizure control. A list of common
neurologic and systemic disorders that induce seizures is
presented in Table 8-1. The age of the patient may help in
establishing the cause of seizures (Figure 8-1). The genetic
contribution to epilepsy and the response of epilepsy to
treatment is complex. A homogenous epileptic syndrome (juvenal
myoclonic epilepsy) can result from varying genetic causes and a
single gene mutation can cause varying epilepsy phenotypes.
SCN1A, encoding a neuronal sodium channel α subunit has been
shown to have multiple mutations resulting in multiple clinical
syndromes.
Causes of seizures as a function of age at onset.

Bars show the range of ages at which seizures from a given cause typically begin;
darker shading indicates peak incidence
Common causes of seizures of new onset
Primary neurologic disorders Systemic disorders
 Benign febrile convulsions of  Hypoglycemia
childhood  Hyponatremia
 Idiopathic/cryptogenic seizures  Hyperosmolar states
 Cerebral dysgenesis  Hypocalcemia
 Symptomatic epilepsy  Uremia
 Head trauma  Hepatic encephalopathy
 Stroke or vascular malformations  Porphyria
 Mass lesions  Drug toxicity
 CNS infections  Drug withdrawal
 Encephalitis  Global cerebral ischemia
 Meningitis  Hypertensive encephalopathy
 Cysticercosis  Eclampsia
 HIV encephalopathy  Hyperthermia
Major categories of drugs reported to cause
seizures.
 Antibiotics (quinolones, penicillins, isoniazid)
 Anticholinesterases (organophosphates, physostigmine)
 Antidepressants (tricyclic,monocyclic, heterocyclic; selective serotonin reuptake inhibitors)
 Antihistamines
 Antipsychotics (phenothiazines, butyrophenones, clozapine)
 Chemotherapeutics (etoposide, ifosfamide, cisplatinum)
 Cyclosporine, FK 506
 Hypoglycemic agents (including insulin)
 Hypoosmolar parenteral solutions
 Lithium
 Local anesthetics (bupivacaine, lidocaine, procaine, etidocaine)
 Methylxanthines (theophylline, aminophylline)
 Narcotic analgesics (fentanyl, meperidine, pentazocine, propoxyphene)
 Phencyclidine
 Sympathomimetics (amphetamines, cocaine, ephedrine, MDMA1 “ecstasy,”
phenylpropanolamine, terbutaline)

Methylenedioxymethamphetamine.
International Classification of Epileptic Seizures
I. Generalized seizures (bilaterally symmetrical and without local onset)
A. Tonic, clonic, or tonic-clonic (grand mal)
B. Absence (petit mal)
1. With loss of consciousness only
2. Complex—with brief tonic, clonic, or automatic movements
C. Lennox-Gastaut syndrome
D. Juvenile myoclonic epilepsy
E. Infantile spasms (West syndrome)
F. Atonic (astatic, akinetic) seizures (sometimes with myoclonic jerks)
II. Partial, or focal, seizures (seizures beginning locally)
A. Simple (without loss of consciousness or alteration in psychic function)
1. Motor–frontal lobe origin (tonic, clonic, tonic-clonic; jacksonian; benign childhood epilepsy; epilepsia
partialis continua)
2. Somatosensory or special sensory (visual, auditory, olfactory, gustatory, vertiginous)
3. Autonomic
4. Pure psychic
B. Complex (with impaired consciousness)
1. Beginning as simple partial seizures and progressing to impairment of consciousness
2. With impairment of consciousness at onset
International Classification of Epileptic Seizures
III. Special epileptic syndromes
A. Myoclonus and myoclonic seizures
B. Reflex epilepsy
C. Acquired aphasia with convulsive disorder
D. Febrile and other seizures of infancy and childhood
E. Hysterical seizures
 Common Partial Seizure Patterns
Clinical type Localization
Somatic motor
Jacksonian (focal motor) Prerolandic gyrus
Masticatory, salivation, speech arrest Amygdaloid nuclei, opercular
Simple contraversive Frontal
Head and eye turning associated with arm movement or athetoid-dystonic postures Supplementary motor cortex
Somatic and special sensory (auras)
Somatosensory Contralateral postrolandic
Unformed images, lights, patterns Occipital
Auditory Heschl gyri
Vertiginous Superior temporal
Olfactory Mesial temporal
Gustatory Insula
Visceral: autonomic Insular-orbital-frontal cortex
Complex partial seizures
Formed hallucinations Temporal neocortex or amygdaloid–
hippocampal complex
Illusions —
Dyscognitive experiences (déjà vu, dreamy states, depersonalization) —
Affective states (fear, depression, or elation) Temporal
Automatism (ictal and postictal) Temporal and frontal
Absence Frontal cortex, amygdaloid–hippocampal
complex, reticular–cortical system
The distribution of the main types of epilepsy
by age
Causes of Recurrent Seizures in Different Age
Groups
Age of onset Probable causea
Neonatal Congenital maldevelopment, birth injury, anoxia, metabolic disorders (hypo-
calcemia, hypoglycemia, vitamin B6 deficiency, biotinidase deficiency,
phenylketonuria, and others)
Infancy As above; infantile spasms (West syndrome)
(1–6 mos)
Early childhood Infantile spasms, febrile convulsions, birth injury and anoxia, infections, trauma,
(6 mos–3 yrs) metabolic disorders, cortical dysgenesis, accidental drug poisoning
Childhood Perinatal anoxia, injury at birth or later, infections, thrombosis of cerebral
(3–10 yrs) arteries or veins, metabolic disorders, cortical malformations, Lennox-Gastaut
syndrome, "idiopathic," probably inherited, epilepsy (Rolandic epilepsy)
Adolescence Idiopathic epilepsy, including genetically transmitted types, juvenile myoclonic
(10–18 yrs) epilepsy, trauma, drugs
Early adulthood Idiopathic epilepsy, trauma, neoplasm, withdrawal from alcohol or other
(18–25 yrs) sedative drugs
Middle age Trauma, neoplasm, vascular disease, alcohol or other drug withdrawal
(35–60 yrs)
Late life Vascular disease (usually postinfarction), tumor, abscess, degenerative disease,
(>60 years) trauma
Distribution of the main causes of seizures at
different ages
Classification & clinical findings
Seizures are classified as follows:
 Generalized Seizures
 Tonic-clonic (grand mal)
 Absence (petit mal)
 Other types (tonic, clonic, myoclonic-Juvenile myoclonic
epilepsy, and others)
 Partial Seizures
 Simple partial
 Complex partial (temporal lobe, psychomotor)
 Partial seizures with secondary generalization
PATOFISIOLOGI

 Patofisiologi tingkat seluler berhubungan dengan

terjadinya paroxysmal depolarization shift (PDS)
 PDS=depolarisasi potensial pasca sinap yang
berlangsung lama
 PDSlepasnya muatan listrik berlebihan pd neuron-
neuronmerangsang sel neuron lain
PATOFISIOLOGI
 Terdapat hambatan GABAergik
 Eksitasi neurotransmiter asam amino (glutamat,
aspartat) dapat menghasilkan eksitasi neuron yang
mengakibatkan kejang
 Kejang juga dapat berasal dari kematian neuron yang
mengakibatkan meningkatnya perkembangan sinaps
hipereksitabel.
PATOFISIOLOGI
 Otak yang kurang berkembang (terutama substansia
abu-abu) lebih rentan terhadap kejang.
 Subtanstia nigra pars reticulata sensitif terhadap GABA
yang memainkan peran terhadap pencegahan kejang.
GEJALA-GEJALA BERGANTUNG LETAK LESI PADA
OTAK
Evaluation of a new seizure disorder in a stable
patient
 History (including medications or drug exposure)
 General physical examination
 Complete neurologic examination
 Blood studies
 Fasting glucose
 Serum calcium
 Serum FTA-ABS
 Serum electrolytes
 Complete blood count
 Renal function studies
 Hepatic function studies
 EEG (positive in 20-59% of first EEGs; 59-92% with repeated EEGs)
 Brain MRI (especially with abnormal examination, progressive disorder,
or onset of seizures after 25 years of age)
Penatalaksanaan Kejang

Airway  pembersihan jalan napas

Breathing  oksigenasi & nilai frekuensi

napas
Circulation  nilai frekuensi jantung
 Pengawasan jalan napas bersih & terbuka, Beri O2
↓
Jalur infus IV & beri cairan
↓
Tangani hipoglikemia  dekstrosa 10% dlm air (2-4 mL IV) + 6-8 mg/kgBB/menit
(continous infusion)
↓
Injeksi fenobarbital 20 mg/kgBB (IV); pelan2 slama 5 menit) dlm keadaan kejang
atau kejang dlm beberapa jam
↓
IV belum tpasang  20 mg/kg dosis tunggal (IM) atau di↑ 10-15% dosis IV
↓
# stop dlm 30 menit  fenobarbital 10mg/kgBB (IV atau IM); ulangi 30 menit
kemudian (bila perlu); dosis max 40 mg/kgBB/hari
↓
Lanjut atau berulang  injeksi fenitoin 20 mg/kg, dgn phatikan :
 Harus IV
 Hanya boleh dicampur garam fisiologis 15 mL dgn kecepatan 0,5 mL/menit
 Monitor denyut jantung
SELECTION OF THERAPY
 Therapy should be directed toward the cause of the
seizures, if known. Seizures associated with metabolic
and systemic disorders usually respond poorly to
anticonvulsants but cease with correction of the
underlying abnormality. Acute withdrawal from alcohol
and other sedative drugs produces self-limited seizures
that, in general, require no anticonvulsant drug therapy.
Acute head trauma and other structural brain lesions that
result in seizures must be rapidly diagnosed and treated,
and the associated seizures controlled by anticonvulsant
drug therapy. Idiopathic epilepsy is treated with
anticonvulsant medications.
 Anticonvulsant Drug Treatment
 Commonly used anticonvulsant drugs and their dosages and methods of
administration are listed in Table 8-4. There are four key principles of
management:
 Establish the diagnosis of epilepsy before starting drug therapy. Therapeutic trials
of anticonvulsant drugs intended to establish or reject a diagnosis of epilepsy may
yield incorrect diagnoses.
 Choose the right drug for the seizure type. Absence seizures, for example, do not
respond to most drugs used for complex partial or generalized tonic-clonic
seizures.
 Treat the seizures, rather than the serum drug levels. Control of seizures is
achieved at different drug levels in different patients.
 Evaluate one drug at a time. In most cases, seizures can be controlled with a single
drug. Therefore, beginning therapy with multiple drugs may expose patients to
increased drug toxicity without added therapeutic benefit.
 Most patients with epilepsy fall into one of the following treatment categories.
 A. NEW SEIZURES
 Most epileptologists do not recommend chronic anticonvulsant drug treatment following a single seizure
unless an underlying cause is found that is not correctable and is likely to produce recurrent seizures (e.g.,
brain tumor). However, recurrent seizures do require anticonvulsant treatment, and if such therapy is to
be administered, the oral loading schedules presented in Table 8-4 can be used. Note that starting a drug
at its daily maintenance dose produces stable serum drug levels only after approximately five half-lives
have elapsed. Therefore, loading doses should be given to achieve therapeutic drug levels promptly in
patients with frequent seizures. Phenytoin and carbamazepine or lamotrigine are appropriate drugs of
first choice for treating partial or secondarily generalized tonic-clonic seizures. Valproic acid is preferred
for all types of primary generalized seizures. Phenobarbital is also very effective in treating generalized
tonic-clonic seizures in adults, but it is less helpful for treatment of complex partial seizures. Absence
attacks of the petit mal variety are treated with valproic acid or ethosuximide (Table 8-4). The former has
the advantage of also providing protection against tonic-clonic seizures but has caused fatalities from
hepatic damage in children younger than 10 (usually younger than 2) years of age.
 Myoclonic seizures are treated with valproic acid, levetiracetam, zonisamide, or clonazepam (seeTable 8-
4).
 As experience is gained with newer anticonvulsants (gabapentin, levetiracetam, pregabalin, vigabatrin,
topiramate, tiagabine, zonisamide), some will find indications as effective monotherapy for epilepsy.
Levetiracetam, topiramate, and zonisamide have broad spectrum against both partial and generalized
epilepsies. Oxcarbazepine can be used in monotherapy for partial and secondarily generalized tonic-clonic
seizures. Gabapentin, tiagabine, and pregabalin should be avoided in patients with generalized seizures.
 B. RECURRENT SEIZURES ON DRUG THERAPY
 1. Determining serum levels of drugs—Blood levels of the anticonvulsant drugs the patient has been taking should be measured in
samples taken just prior to a scheduled dose. For a single seizure, no acute change in medication is mandated even if there has been no
interruption of drug therapy and anticonvulsant drug levels are in the therapeutic range, but a slight increase in prescribed dose may be
considered. If the history or serum drug levels suggest that treatment has been interrupted, the prescribed drug should be started again
as for new seizures.
 2. Changing to a second drug—A second anticonvulsant should be introduced only if seizures continue to occur after maximum
therapeutic benefit has been achieved with the initial drug. This means that blood levels of the drug are in the therapeutic range or that
drug toxicity precludes further dosage increments. An anticonvulsant that has failed to alter seizure frequency should be discontinued
gradually once therapeutic levels of the second drug have been achieved. Transition to a second drug used in monotherapy is
recommended before trials of two-drug combination therapy.
 3. Treating refractory seizures—In some patients, disabling seizures persist despite trials of all major anticonvulsants, alone and in
combination, and at the highest doses the patient can tolerate. When no treatable cause can be found, seizures are not due to a
progressive neurodegenerative disease, and medical treatment has been unsuccessful for at least 2 years, evaluation for possible
surgical therapy should be considered. Presurgical evaluation begins with a detailed history and neurologic examination to explore the
cause of seizures and their site of origin within the brain and to document the adequacy of prior attempts at medical treatment. MRI
and electrophysiologic studies are performed to identify the epileptogenic zone within the brain. Several electrophysiologic techniques
can be used: EEG, in which cerebral electrical activity is recorded noninvasively from the scalp; intracranial or invasive EEG, in which
activity is recorded from electrodes inserted (depth electrodes) into the brain or placed over the brain surface (subdural electrodes); and
electrocorticography, which involves intraoperative recording from the surface of the brain. When an epileptogenic zone can be
identified in this manner and its removal is not expected to produce undue neurologic impairment, surgical excision may be indicated.
Patients with complex partial seizures arising from a single temporal lobe are the most frequent surgical candidates; unilateral anterior
temporal lobectomy abolishes seizures and auras in approximately 50% of these patients and significantly reduces their frequency in
another 25%. Hemispherectomy and corpus callosum section are also sometimes used to treat intractable epilepsy. Left vagal nerve
stimulation has been shown to reduce seizure frequency by as much as 50% in adults and children with refractory epilepsy. The
mechanism of action is unknown. Afferent responses from the vagus are received in N. tractus solitarius in the medulla and project
widely. Transcranial magnetic stimulation and deep brain stimulation are evolving experimental treatments.
 C. MULTIPLE SEIZURES OR STATUS EPILEPTICUS
 1. Early management
 a. Immediate attention should be given to ensure that the airway is patent and the patient positioned to prevent aspiration of
stomach contents.
 b. The laboratory studies listed in Table 8-5 should be ordered without delay.
 c. Dextrose, 50 mL of 50% solution, should be given intravenously.
 d. If fever or meningeal signs are present, immediate lumbar puncture is mandatory, and a gram-stained smear of spinal fluid should
be examined to exclude bacterial meningitis. Patients without these signs should also undergo lumbar puncture if the cause of the
seizures has not been determined (e.g., by their cessation upon administration of dextrose), unless signs of increased intracranial
pressure or of focal brain dysfunction are present. It should be noted that postictal pleocytosis is detectable in cerebrospinal fluid
(CSF) in approximately 2% of patients with single generalized tonic-clonic seizures (and approximately 15% of those with status
epilepticus) in the absence of infection. The white blood cell count may be as high as 80/mm3, with either polymorphonuclear or
mononuclear predominance. Serum protein content may be slightly elevated, but glucose concentration is normal, and Gram stain is
negative. The postictal pleocytosis resolves in 2-5 days.
 2. Drug therapy to control seizures—Every effort must be made to establish a precise etiologic diagnosis so that treatment of the
underlying disorder can be started. Because generalized seizure activity per se damages the brain if it persists for more than 30
minutes, drug therapy to terminate seizures should be instituted immediately. An outline for rapid pharmacologic control of acute
multiple seizures is presented in Table 8-6.
 3. Management of hyperthermia—The metabolic consequences of status epilepticus are related to increased motor activity and high
levels of circulating catecholamines; they include hyperthermia (temperature elevation to 42-43°C [108-109°F]), lactic acidosis
(temperature elevation to pH <7.00), and peripheral blood leukocytosis (temperature elevation to 60 000 cells/mm3). These
derangements typically resolve over a few hours after cessation of the seizures. Only hyperthermia, which is known to increase the
risk of brain damage from status epilepticus, requires specific attention.
 Severe hyperthermia must be treated with a cooling blanket and, if necessary, the induction of motor paralysis with a neuromuscular
blocking agents. Mild or moderate hyperthermia (101-102°F), not requiring specific intervention, may persist for 24-48 hours. Lactic
acidosis resolves spontaneously over 1 hour and should not be treated. Infection should, of course, be excluded.
 Discontinuance of Anticonvulsants
 Patients (usually children) with epilepsy who are seizurefree on
medication for 2-5 years may wish to discontinue
anticonvulsant drugs. In patients with normal intelligence and
a normal neurologic examination, the risk of seizure recurrence
may be as low as 25%. Risk factors for recurrence include
slowing or spikes (maximum risk with both present) on EEG.
When anticonvulsants are to be withdrawn, one drug is
eliminated at a time by tapering the dose slowly over 6 weeks.
Recurrence of seizures has been reported in approximately
20% of children and 40% of adults following medication
withdrawal, in which case prior medication should be
reinstituted at the previously effective levels.
 FASE AKUT
DIAZEPAM (iv) atau DIAZEPAM (rektal)
0,3 – 0,5 mg/kg IV (MAKS. 20 mg) 5 mg (BB<10kg)
(MIDAZOLAM) 10 mg (BB>10 kg)

BILA KEJANG TIDAK BERHENTI

DIULANGI 5 MENIT KEMUDIAN : DIAZEPAM iv/rektal

Kejang berhenti
Stop obat
Kejang tidak berhenti
FENITOIN ( 15 – 20 mg/kg IV) Kecepatan < 50mg/mnt

Kejang tak berhenti Kejang berhenti

FENOBARBITAL : 12 jam kemudian

(10-20 mg/kg im) Rumatan sampai panas turun
( 5 – 7 mg/kg/hr )

Kejang tidak berhenti : PICU Kejang berhenti : 12 jam kemudian Rumatan : 3-4 mg/kg im
MIDAZOLAM
Summary of anticonvulsant drug therapy.

Serum Half-Life
(Normal Renal
Usual Loading or Maintenance and Hepatic Therapeutic
Drug Preparation Initial Dose Dose Function) Serum Levels Indications1
Phenytoin (Dilantin) 100-mg capsule. Oral loading: 1000 300-400 mg/day in a Oral: 18-24 hours 10-20 µg/ml P, G, S
Also 30-mg capsule, mg in two to four single dose or Intravenous: 12
50-mg tablet divided doses over divided doses hours (kinetics are
12-24 hours dose dependent and
Intravenous loading: may vary widely)
1000-1500 mg (15-18
mg/kg) not
exceeding 50
mg/min
Fosphenytoin is
prodrug form for
intramuscular or
intravenous use

Carbamazepine 200, 300 mg XR: 100, 100 mg twice a day; 400-1600 mg/day in 12-18 hours 4-12 µg/mL P, S
(Tegretol) 200, 400 mg increase by 200 three or four doses, monotherapy
mg/day to or in two doses if XR
maintenance dose form

Oxcarbazepine 150, 300, 600 mg 300 mg twice a day 600-2400 mg/day in 8-10 hours 12-30 µg/mL* P, S
(Trileptal) two divided doses
Phenobarbital 15, 30, 60, 100 mg Oral loading: 180 mg 90-180 mg/day in a 3-5 days 20-40 µg/mL P, G, S
(Luminal) twice a day for 3 single dose
days or same as
maintenance

Valproic acid 250 mg Same as 750-3000 mg/day in 6-18 hours 50-150 µg/mL G, M, A, P, S
(Depakote, maintenance dose two or three doses
Depakene)
Ethosuximide 250-mg capsules 15 mg/kg/day, then 15-40 mg/kg/day in 24-36 hours 40-100 µg/mL A
(Zarontin) increase by 25 two or three doses (children); 60 hours
mg/day at weekly (adult)
intervals to
maintenance dose
Summary of anticonvulsant drug therapy.

Serum Half-Life
(Normal Renal
Usual Loading or Maintenance and Hepatic Therapeutic
Drug Preparation Initial Dose Dose Function) Serum Levels Indications1
Clonazepam 0.5,1,2 mg Children: 0.01-0.03 Children: 0.01-0.02 20-40 hours 0.02-0.10 µg/mL P, G
(Klonopin) mg/kg/day in two or mg/kg/day Adults:
three divided doses 1.5-2.0 mg/day; in
Adults:0.5 mg/day two or three divided
doses

Gabapentin 100, 300, 400 mg 300 mg three times 900-4800 mg/day in 5-7 hours Not established P, S
(Neurontin) a day three divided doses
Lamotrigine 50,100,200 mg 25 mg twice a day 200-500 mg/day 24 hours 12-60 5-15 ug/mL* G, P, S, A
(Lamictal) then slow increase1 100-700 in two hours1
doses 1

Levetiracetam 250, 500, 750 mg 250-500 twice a day 1000-3000 mg/day 8-10 hours 10-40 ug/mL* G, P, M
(Keppra) in two divided doses
Vigabatrin2 (Sabril) 500 mg 500 mg twice a day; 2-4 g/day in two 5-8 hours Not established P
increase by 500 mg divided doses
every week
Topiramate 25,100,200 mg 25 mg/day; increase 100-400 mg/day in 16-30 hours 4-12 mg/mL* G, P, S
(Topamax) by 25-50 mg every 2 two divided doses
weeks
Tiagabine (Gabatril) 4,12,16,20 mg 4 mg/day; increase 12-56 mg/day in 5-13 hours Not established P, S
by 4-8 mg every three divided doses
week
Zonisamide 100 mg 100 mg/day 300-600 mg/day in 52-69 hours 10-40 mg/mL* G, P, S, M
(Zonegran) one to two doses
Pregabalin (Lyrica) 25, 50, 75, 100, 150, 100-150 mg/day in 150-600 mg/day 6 hour Not established
200, 225, and 300 two divided doses
mg

A, absence; G, generalized tonic-clonic; M,myoclonic; P, partial; S, secondarily generalized tonic-clonic;

*
, provisional.
1
Varies depending on interaction with coadministered anticonvulsant drugs; 25 mg every other day for 2 weeks when taking valproic acid; see
Table 8-8.
2
Not approved in the United States.
Common Antiepileptic Drugs
Generic name Usual dosage Principal therapeutic indications Serum half- Effective
Children, mg/kg Adults, mg/d life, h blood level,a
mg/mL

Major anticonvulsants used as monotherapy

Valproic acid 30–60 1,000–3,000 Generalized tonic-clonic, partial, absence, 6–15 50–100
myoclonic
Phenytoin 4–7 300–400 Generalized tonic-clonic, partial, absence, 12–36 10–20
myoclonic
Carbamazepine 20–30 600–1,200b Generalized tonic-clonic, partial 14–25 4–12

Oxcarbazepine 10–40 900–2,400 Partial 1–5 —

Phenobarbital 3–5 (8 for infants) 90–200 Generalized tonic-clonic, partial 40–120 15–40
Lamotrigine 0.5 300–500 Generalized, partial 15–60 2–7
Levetiracetam 20–60 500–3,000b Partial, myoclonic 6–8 —
Common Antiepileptic Drugs
Generic name Usual dosage Principal therapeutic indications Serum half- Effective
Children, mg/kg Adults, mg/d life, h blood level,a
mg/mL

Adjuvant and special-use anticonvulsants

Topiramate — 400 Generalized tonic-clonic, atypical absence, 20–30 —
myoclonic, partial
Tiagabine — 30–60 Partial and secondary generalized 7–9 —
Gabapentin 30–60 900–1,800b Partial and secondary generalized 5–7 —

Primidone 10–25 750–1,500b Generalized tonic-clonic, partial 6–18 5–12

Ethosuximide 20–40 750–1,500 Absence 20–60 50–100

Methsuximide 10–20 500–1,000 Absence 28–50 40–100
ACTH 40–60 Units daily — Infantile spasms — —
Clonazepam 0.01–0.2 2–10 Absence, myoclonus 18–50 0.01–0.07
Anticonvulsants for status epilepticus (initial loading or continuous infusion doses shown) —phenytoin and phenobarbital used in
c

doses higher than shown above

Diazepam 0.15–2 2–20 Status epilepticus — —
Lorazepam 0.03–0.22 2–20 Status epilepticus — —
Midazolam — 0.1–0.4 mg/kg/h Status epilepticus — —
Propofol 2.5–3.5 2–8 mg/kg/h Status epilepticus — —
Fosphenytoin 30–50 mg 1,000–1,500 Status epilepticus — 10–20
Choices of Antiepileptic Drugs by Type of Adult
Seizure Disorder
Seizure type Initial choice Second line
Tonic-clonic Carbamazepine, valproate, Lamotrigine, oxcarbazepine
phenytoin
Myoclonic Valproate Topiramate, levetiracetam, zonisamide
Partial Carbamazepine, phenytoin Valporate, lamotrigine, oxcarbazine,
levetiracetam
Absence Valproate Ethosuximide, lamotrigine
Unclassifiable Valproate Lamotrigine
Choices of Antiepileptic Drugs in Childhood
Seizure Disorders
Seizure type Initial choice Second Third
Tonic-clonic Valproate, Lamotrigine, Phenytoin
carbamazepine oxcarbazine
Myoclonic Valproate Lamotrigine Phenobarbital,
clobazam
Absence Valproate Topiramate, Lamotrigine
levetiracetam,
ethosuximide
Partial Carbamazepine, Valproate, Lamotrigine,
phenytoin levetiracetam, vigabatrin,
gabapentin, topiramate
oxcarbazine
Infantle spasms Vigabatrin, Valproate Lamotrigine
corticosteroids
Lennox-Gastaut Valproate Topiramate, Felbamate
lamotrigine
Combination Antiepileptic Regimens for
Refractory Seizures
Combination Indication
Valproate and lamotrigine or levetiracetam Partial or generalized seizures
Valproate and ethosuximide Generalized absence
Carbamazepine and valproate Complex partial seizures
Levetiracetam and lamotrigine or Partial seizures
tiagabine
Topiramate and lamotrigine or Numerous types
levetiracetam
COMPLICATIONS OF EPILEPSY &
ANTICONVULSANT THERAPY
 Complications of Epilepsy
 When the diagnosis of epilepsy is made, the patient
should be warned against working around moving
machinery or at heights and reminded of the risks of
swimming alone. The issue of driving must also be
addressed. Many state governments have notification
requirements when a diagnosis of epilepsy is made.
 Side Effects of Anticonvulsant Drugs
 The side effects of anticonvulsant drug therapy are summarized in Table 8-7.
All anticonvulsant drugs may lead to blood dyscrasias, but carbamazepine
and valproic acid have been associated with the highest incidence of
hematologic—and hepatic—toxicity. For this reason, a complete blood count
and liver function tests should be obtained before initiating administration of
these drugs and at intervals during the course of treatment. The authors
recommend performing these tests twice in the first weeks/months and every
6 to 12 months thereafter. Carbamazepine should be discontinued if the total
neutrophil count falls below 1500/mL or if aplastic anemia is suspected.
Valproic acid should be terminated if symptoms of hepatotoxicity, such as
nausea, vomiting, anorexia, or jaundice occur. Lamotrigine has a 1:1000
incidence of Stevens-Johnson syndrome in the first 8 weeks.
 Most anticonvulsant drugs (especially barbiturates) affect cognitive function
to some degree, even in therapeutic doses.
Table 8-7. Side effects of anticonvulsant drugs.

Drug Dose Related Idiosyncratic

Phenytoin Diplopia Skin rash
Ataxia Fever
Hirsutism Lymphoid hyperplasia
Coarse facial features Hepatic dysfunction
Polyneuropathy Blood dyscrasia
Osteoporosis Stevens-Johnson syndrome
Megaloblastic anemia
Sedation Gingival hyperplasia
Carbamazepine Diplopia Skin rash
Ataxia Blood dyscrasia
Osteoporosis Hepatic dysfunction
Hyponatremia Stevens-Johnson syndrome
Oxcarbazepine Hyponatremia Skin rash
Phenobarbital Sedation Skin rash
Insomnia
Behavioral disturbance Stevens-Johnson syndrome
Diplopia
Ataxia
Valproic acid Gastrointestinal distress Hepatic dysfunction
Tremor Peripheral edema
Sedation weight gain Pancreatitis
Hair loss
Thrombocytopenia
Ethosuximide Gastrointestinal distress Skin rash
Sedation Blood dyscrasia
Ataxia
Headache
Table 8-7. Side effects of anticonvulsant
drugs.

Drug Dose Related Idiosyncratic

Clonazepam Sedation
Diplopia
Ataxia
Behavioral disturbance
Hypersalivation
Drowsiness
Gabapentin and pregabalin Fatigue
Drugged sensation weight gain
Lamotrigine Dizziness
Ataxia Skin rash in 1-2% (frequency increased by
concomitant valproic acid therapy and
Insomnia reduced by gradual build-up of dose)
Diplopia Stevens-Johnson syndrome
Vigabatrin Sedation
Vertigo Peripheral visual constriction
Psychosis (irreversible)
Topiramate Anorexia Renal stones
Mental slowing Glaucoma
Parasthesia
Anxiety
Tiagabine Dizziness Rash
Sedation
Nausea
Zonisamide Drowsiness Nephrolithiasis
Anorexia Skin rash
Drug Interactions
 A variety of drugs alter the absorption or metabolism of
anticonvulsants when given concomitantly. The changes
in anticonvulsant levels are summarized in Table 8-8.
Some anticonvulsants (carbamazepine, primidone,
phenytoin, phenobarbital, topiramate, felbamate, and
oxcarbazepine) induce the cytochrome P450 system
which may lead to reduced effectiveness of oral
contraceptives.
Table 8-8. Some major anticonvulsant drug interactions.
Levels Levels
Drug Increased by Decreased by
Phenytoin Benzodiazepines Chloramphenicol Carbamazepine Phenobarbital
Disulfiram Ethanol Isoniazid Pyridoxine Vigabatrin
Phenylbutazone Sulfonamides
Topiramate Trimethoprim Warfarin
Zonisamide

Carbamazepine Erythromycin Felbamate1 Isoniazid Phenobarbital Phenytoin

Propoxyphene Valproic acid Oxcarbazapine Zonisamide
Phenobarbital Primidone Valproic acid —
Valproic acid — Topiramate Tiagabrin Lamotrigine
Phenytoin Carbamazepine

Ethosuximide Valproic acid —

Clonazepam — —
Gabapentin — —
Lamotrigine Valproic acid Carbamazepine Phenobarbital
Phenytoin
Vigabatrin — —
Topiramate — Carbamazepine Phenytoin Valproic
acid
Tiagabine — Carbamazepine Phenytoin
Phenobarbital
Zonisamide Lamotrigine Carbamazepine Phenytoin
1
Levels of the parent compound are diminished, but levels of active metabolite increase.
Epilepsy & Anticonvulsant Therapy in
Pregnancy
 The incidence of stillbirth, microcephaly, mental retardation, and seizure disorders is increased
in children born to epileptic mothers. Anticonvulsant therapy during pregnancy, however, is also
associated with a greater than normal frequency of congenital malformations— especially cleft
palate, cleft lip, and cardiac anomalies. Such malformations are about twice as common in the
offspring of medicated than of unmedicated epileptic mothers, but because patients with more
severe epilepsy are more likely to be treated, it is difficult to know whether epilepsy or its
treatment is the more important risk factor. Folic acid supplementation (1 mg/d) should be
provided for all women of childbearing age who take antiepileptic drugs.
 Among commonly used anticonvulsants, valproic acid and to some degree carbamazepine are
associated with an increased incidence of neural tube defects (2% and 0.5%, respectively).
Phenobarbital and phenytoin pose some teratogenic risk, but the extent of the risk is
controversial. The fetal risks of the newer anticonvulsants are not known.
 When an epileptic patient who has been seizure free for several years is contemplating
pregnancy, an attempt should be made to assess whether anticonvulsant drugs can be safely
withdrawn prior to conception. In contrast to generalized tonic-clonic seizures, partial and
absence seizures present little risk to the fetus, and it may be possible to tolerate imperfect
control of these seizures during pregnancy to avoid fetal drug exposure. In general, it is best to
maintain treatment with a single drug that has been shown effective for the patient's seizures,
using a dose that avoids clinical toxicity. Status epilepticus is treated as described above for
nonpregnant patients.
 Plasma levels of anticonvulsant drugs may decrease during pregnancy because of the patient's
enhanced drug metabolism, and higher doses may be required to maintain control of seizures. It
is therefore important to monitor drug levels closely in this setting.
PROGNOSIS
 After a single unprovoked seizure, only one-third to
onehalf of patients will have a recurrence (develop
epilepsy). If a second seizure occurs, however, the
recurrence rate approaches 75% and anticonvulsants
therefore should be started. With appropriate
anticonvulsant drug treatment, seizures can be well
controlled, although not always eliminated, in most
epileptic patients. At the onset of treatment patients
should be seen every few months to monitor seizure
frequency and make dose adjustments.
Komplikasi
 Kerusakan otak akibat hipoksia
 Retardasi mental
 Dapat timbul depresi dan keadaan cemas
PSEUDOSEIZURES
 Attacks that resemble seizures (psychogenic seizures, or pseudoseizures) may be manifestations of a
psychiatric disturbance such as conversion disorder, somatization disorder, factitious disorder with
physical symptoms, or malingering. In conversion or somatization disorder, the patient is unaware of
the psychogenic nature of symptoms and the motivation for their production. In factitious disorder,
the patient recognizes that the spells are self-induced, but not the reason for doing so. In
malingering, there is conscious awareness of both the production of symptoms and the underlying
motivation.
 Pseudoseizures usually can be distinguished both clinically and by the EEG findings. In patients with
pseudoseizures resembling tonic-clonic attacks, there may be warning and preparation before the
attack; there is usually no tonic phase, and the clonic phase consists of wild thrashing movements
during which the patient rarely comes to harm or is incontinent. Ictal eye closure is common. In some
instances, there are abnormal movements of all extremities without loss of consciousness; in others,
there is shouting or obscene utterances during apparent loss of consciousness or goal-directed
behavior. There is no postictal confusion or abnormal clinical signs following the attack. The EEG
recorded during the episode does not show organized seizure activity, and postictal slowing does not
occur. The differential diagnosis should include frontal lobe seizures, which may be marked by
unusual midline movements (pelvic thrusting, bicycling) and by very brief postictal states. Ictal EEG
abnormalities may escape detection as well.
 It is important to appreciate that some patients with pseudoseizures also have genuine epileptic
attacks that require anticonvulsant medications, but these should be prescribed at an empirically
appropriate dose. Psychiatric referral may be helpful.
 PERBEDAAN ANTARA KEJANG & SERANGAN yg MENYERUPAI KEJANG
KEADAAN KEJANG MENYERUPAI KEJANG
Onset Tiba2 Mungkin gradual

Lama serangan Detik atau menit Beberapa menit

Kesadaran Sering terganggu Jarang terganggu

Sianosis Sering Jarang

Gerakan ekstremitas Sinkron Asinkron

Stereotipik gerakan Selalu Jarang

Lidah tergigit atau luka lain Sering Sangat jarang

Gerakan abnormal bola mata Selalu Jarang

Fleksi pasif ekstremitas Gerakan tetap ada Gerakan hilang

Dapat diprovokasi Jarang Hampir selalu

Tahanan thp gerakan pasif Jarang Selalu

Bingung paska serangan Hampir selalu Tidak pernah

Iktal EEG abnormal Selalu Hampir tidak pernah

Paska iktal EEG abnormal Selalu Jarang

KEJANG DEMAM
DEFINISI
 Bangkitan kejang yang terjadi pada kenaikan suhu tubuh
(suhu rektal >38°C) yang disebabkan oleh suatu proses
ekstrakranial.
 terjadi pada 2-5% anak antara usia 6 bulan sampai 5
tahun
 Kejang disertai demam pada bayi berumur kurang dari 1
bulan tidak termasuk dalam kejang demam.
EPIDEMIOLOGI
 KD terjadi pd 2-4% populasi 6 bl - 4 th
 KDS 80 %, KDK 20 %
 Kejang > 15 mnt ± 8 %
 Berulang dlm waktu 24 jam ± 16 %
 Resiko menjadi epilepsi 2% - 50%
ETIOLOGI
 Intrakranial
 Asfiksia : Ensefolopati hipoksik – iskemik
 Trauma (perdarahan) : perdarahan subaraknoid, subdural, atau intra
ventrikular
 Infeksi : Bakteri, virus, parasit
 Kelainan bawaan : disgenesis korteks serebri, sindrom zelluarge,
Sindrom Smith – Lemli – Opitz.
 Ekstra kranial
 Gangguan metabolik : Hipoglikemia, hipokalsemia, hipomognesemia,
gangguan elektrolit (Na dan K)
 Toksik : Intoksikasi anestesi lokal, sindrom putus obat.
 Kelainan yang diturunkan : gangguan metabolisme asam amino,
ketergantungan dan kekurangan produksi kernikterus.
 Idiopatik
 Kejang neonatus fanciliel benigna, kejang hari ke-5 (the fifth day fits)
FAKTOR RESIKO BERULANGNYA KEJANG
1. Riwayat KD dlm keluarga (org tua – sdr)
2. Usia < 12 bulan
3. Tingginya suhu badan sebelum kejang. (makin rendah
 makin mudah berulang)
4. Lamanya demam sebelum kejang  >16 jam 
lebih mudah berulang.
Bila sel. Faktor ada  80% berulang, jika (-)  10 – 15%,
berulang t.u pd tahun I.
FAKTOR RESIKO MENJADI EPILEPSI
1. KELAINAN NEUROLOGIS
2. KEJANG DEMAM KOMPLEKS
3. RIWAYAT EPILEPSI DLM KELUARGA.
- Tiap faktor resiko  epilpepsi↑ 4 – 6 %
- Kombinasi dari faktor tsb diatas  10–50 %
- Kemungkinan menjadi Epilepsi tidak dapat dicegah
dengan obat rumat pd KD.
KLASIFIKASI

Sederhana

Kejang
demam
Kompleks
KEJANG DEMAM SEDERHANA
 Kejang bersifat umum
 Lama kejang < 15 menit
 Usia waktu KD pertama < 6 tahun
 Frekwensi serangan 1-4 x dlm 1 th
 EEG normal.
KEJANG DEMAM KOMPLEKS
( ILAE 1993)
Adalah KD dg salah satu gejala sbb:
 Kejang berlangsung lama, ≥ 15 menit.
 Kejang fokal atau parsial satu sisi, atau kejang umum
didahului kejang parsial.
 Kejang berulang 2 kali atau lebih dlm 24 jm
MEMBEDAKAN KEJANG DEMAM DENGAN
EPILEPSI DAN INFEKSI SSP
PATOFISIOLOGI KEJANG
DEMAM  EPILEPSI
Manifestasi klinis
1. Suhu anak tinggi
2. Tampak apatis
3. Mata terbelalak ke atas
4. Gerakan sentakan berulang tanpa didahului kekakuan atau hanya
sentakan atau kekakuan fokal
5. Umumnya berlangsung singkat (beberapa menit)
6. Sering berhenti sendiri
KRITERIA DIAGNOSA
 Kriteria diagnosis kejang demam:
 Kejang didahului oleh demam.
 Pasca-kejang anak sadar kecuali kejang lebih dari 15 menit.
 Pemeriksaan cairan serebrospinalis dalam batas normal.
 Diagnosis
Diagnosis didasarkan atas gejala dan tanda menurut kriteria
Livingstone sebagai berikut :
1. Umur anak kejang pertama antara 6 bulan sampai 4 tahun
2. Kejang terjadi dalam 16 jam pertama setelah mulai panas
3. Kejang bersifat umum
4. Kejang berlangsung tidak lebih dari 15 menit
5. Frekuensi bangkitan tidak lebih dari 4x dalam setahun
6. Pemeriksaan EEG yang dibuat 10-14 hari setelah bebas
panas tidak menunjukkan kelainan
7. Tidak didapatkan kelainan neurologis
DIAGNOSIS
 Anamnesis
 Adanya kejang, jenis kejang, kesadaran, lama kejang, suhu
sebelum/saat kejang, frekuensi, interval, pasca kejang,
penyebab kejang di luar SSP.
 Tidak ada riwayat kejang tanpa demam sebelumnya.
 Riwayat kelahiran, perkembangan, kejang demam dalam
keluarga, epilepsi dalam keluarga (kakak-adik, orangtua).
 Singkirkan dengan anamnesis penyebab kejang yang lain.
DIAGNOSIS
 Pemeriksaan fisik dan neurologis
 Kesadaran, suhu tubuh, tanda rangsang
meningeal, tanda peningkatan tekanan
intrakranial, dan tanda infeksi di luar SSP.
 Pada umumnya tidak dijumpai adanya kelainan
neurologis, termasuk tidak ada kelumpuhan nervi
kranialis.
DIAGNOSIS
 Pemeriksaan penunjang
 Darah tepi lengkap  penyebab demam
 Elektrolit, glukosa darah  diare, muntah, hal lain yg dpt
mengganggu kesimbangan elektrolit atau gula darah.
 L P  curiga meningitis, umur 12 bl sangat dianjurkan, 12-18
bl dianjurkan.
 EEG  tdk dpt memprediksi berulangnya kejang/ menjadi
epilepsi  tidak perlu.
DIAGNOSIS
 Pemeriksaan penunjang
 PCR  HHV-6, HHV-7 dan virus influenza
 Kadar TNF alfa, IL-1 alfa & IL-6 pada CSS  meningkat 
Ensefalitis akut / Ensefalopati.
 CTscan atau MRI tidak dilakukan pd KDS
 Vaksinasi bukan merupakan kontra indikasi
 Diagnosis Banding Kejang Demam
klinis Ensefalitis herpes Meningitis Meningitis serosa Meningitis serosa Kejang demam
simpleks bakterial/purulenta tuberkulosa virus lama

Awitan Akut Akut Kronik Akut Akut

Demam < 7 hari < 7 hari 7 hari < 7 hari < 7 hari

Tipe kejang Fokal/umum Umum Umum Umum Umum/fokal

Singkat / lama Singkat Singkat Singkat Lama > 15 menit

Kesadaran Sopor-koma Apatis-som Som-sopor Sadar-apatis Somnolen

Pemulihan Lama Cepat Lama Cepat Cepat

Tanda rangsang -- ++/-- ++/-- +/-- --

meningeal

Tekanan
intrakranial N N
  

Paresis --- ---

+++/-- +/- +++

Pungi lumbal Jernih Jernih

Jernih Keruh Jernih

Etiologi Virus Di luar SSP

Virus HS Bakteri M.tuberkulosis

terapi simptomatik Penyakit dasar

antivirus antibiotik Anti TBC
 Penatalaksanaan
1. Penanganan Pada Saat Kejang

• Terapi suportif : stabilisasi ABCD

• Menghentikan kejang : Diazepam

• Dosis awal 0,3-0,5 mg/KgBB/dosis IV (perlahan-lahan) atau
0,4-0,6mg/KgBB/dosis REKTAL SUPPOSITORIA
• Bila kejang masih belum teratasi dapat diulang dengan dosis yang sama
20 menit kemudian

• Turunkan demam:
• Antipiretika:
– Paracetamol 10 mg/KgBB/dosis PO atau Ibuprofen 5-10
mg/KgBB/dosis PO, keduanya diberikan 3-4 kali perhari
• Kompres

• Terapi kausatif : antibiotika sesuai indikasi dan etiologi

PENGOBATAN dlm kead. KEJANG
 DIAZEPAM*
 REKTAL ( 5 mg – BB < 10 kg , 10 mg – BB > 10 kg ) , atau
 PARENTERAL ( 0,3 – 0,5 mg/ kgBB/ kali ).
 Pemberian dpt diulangi setelah 5 menit  2 kali I.V / 2 kali Rektal + 1
kali I.V.
 MASIH KEJANG  FENITOIN ( 10-14 mg/ kgBB – 50 mg/ mnt )
 BELUM TERATASI  I C U

*dosis maksimal 20mg

OBAT YG DIGUNAKAN
 PHENOBARBITAL 4-6 mg/kgBB/hr – 2X
 Efek samping:
 Gangguan perilaku
 Kesulitan belajar
 ASAM VALPROAT  20-40 mg/ kgBB/ Hr
 diberikan 2 – 3 kali
 Efek samping: gangguan fungsi hati
 LAMA PEMBERIAN  1 tahun
 TIDAK EFEKTIF MENCEGAH EPILEPSI
 Penatalaksanaan

2. Pencegahan Kejang
• Pencegahan berkala (intermiten) untuk kejang demam
sederhana
Diazepam 0,3 mg/KgBB/dosis PO dan antipiretika pada saat anak
menderita penyakit yang disertai demam

• Pencegahan kontinu untuk kejang demam komplikata

Asam Valproat 15-40 mg/KgBB/hari PO dibagi dalam 2-3 dosis
PROGNOSIS
 Kejang demam sederhana tidak berbahaya.
 Tidak ada bukti bahwa mereka menyebabkan
kematian, kerusakan otak, epilepsi, keterbelakangan
mental, penurunan iq, atau kesulitan belajar.
 Sekitar sepertiga anak yang pernah kejang demam
akan mengalami kejang demam ke dua.
 Dari orang-orang yang memiliki serangan kedua,
sekitar setengah akan memiliki kejang ketiga.
KOMPLIKASI
 Menggigit diri
 Masuknya cairan ke paru-paru melalui pernapasan
 Meningitis
 Luka dari jatuh atau menabrak benda
 Luka dari kejang yang lama
 kejang yang tidak disebabkan oleh demam
Epilepsi
EPILEPSI
 Cetusan listrik lokal pada substansia grisea otak yang
terjadi sewaktu-waktu, mendadak, dan sangat cepat
 Gangguan paroksismal dimana cetusan neuron korteks
serebri mengakibatkan serangan penurunan kesadaran,
perubahan fungsi motorik atau sensorik, perilaku atau
emosional yang intermiten dan stereotipik
Profil EEG pada penderita epilepsi
EPIDEMIOLOGI

 Agak sulit mengestimasi jumlah kasus epilepsy  pada

kondisi tanpa serangan, pasien terlihat normal dan
semua data lab juga normal, selain itu ada stigma
tertentu pada penderita epilepsy  malu/enggan
mengakui
 Insiden paling tinggi pada umur 20 tahun pertama,
menurun sampai umur 50 th, dan meningkat lagi
setelahnya terkait dg kemungkinan terjadinya penyakit
cerebrovaskular
 Pada 75% pasien, epilepsy terjadi sebelum umur 18 th
 KLASIFIKASI EPILEPSI

 Berdasarkan tanda klinik

dan data EEG, kejang dibagi
menjadi :
 kejang umum (generalized
seizure)  jika aktivasi terjadi
pd kedua hemisfere otak
secara bersama-sama
 kejang parsial/focal  jika
dimulai dari daerah tertentu
dari otak
ETIOLOGI
 Epilepsi mungkin disebabkan oleh:
 aktivitas saraf abnormal akibat proses patologis yang
mempengaruhi otak
 gangguan biokimia atau metabolik dan lesi mikroskopik di otak
akibat trauma otak pada saat lahir atau cedera lain
 pada bayi  penyebab paling sering adalah asfiksi atau hipoksia
waktu lahir, trauma intrakranial waktu lahir, gangguan metabolik,
malformasi congenital pada otak, atau infeksi
 pada anak-anak dan remaja  mayoritas adalah epilepsy
idiopatik, pada umur 5-6 tahun  disebabkan karena febril
 pada usia dewasa penyebab lebih bervariasi  idiopatik,
karena birth trauma, cedera kepala, tumor otak (usia 30-50 th),
penyakit serebro vaskuler (> 50 th)
PATOGENESIS
 Kejang disebabkan karena ada
ketidakseimbangan antara
pengaruh inhibisi dan eksitatori
pada otak
 Ketidakseimbangan bisa terjadi
karena :
 Kurangnya transmisi inhibitori
 Meningkatnya aksi eksitatori
 meningkatnya aksi glutamat
atau aspartat
DIAGNOSIS
 Pasien didiagnosis epilepsi jika mengalami serangan kejang
secara berulang
 Untuk menentukan jenis epilepsinya, selain dari gejala,
diperlukan berbagai alat diagnostik :
 EEG
 CT-scan
 MRI
 Lain-lain

A CT or CAT scan (computed

tomography) is a much more
sensitive imaging technique than X-
ray, allowing high definition not only
of the bony structures, but of the soft
tissues.
 ALGORITMA Diagnosa positif
TATALAKSANA
EPILEPSI Mulai pengobatan dg satu AED
Pilih berdasar klasifikasi kejang
dan efek samping

Ya Sembuh ? Tidak

Efek samping dapat ditoleransi ? Efek samping dapat ditoleransi ?

Ya Tidak Ya Tidak

Tingkatkan dosis Turunkan dosis

Kualitas hidup Turunkan dosis Tambah AED 2
optimal ?

Pertimbangkan,
Sembuh?
Ya Tidak Hentikan AED1
Atasi dg tepat Tetap gunakan Ya Tidak
AED2
Lanjutkan
terapi
lanjut
lanjut
 lanjutan

Lanjutkan Tidak sembuh

terapi
Efek samping dapat ditoleransi ?
Tidak kambuh
Selama > 2 th ? Tidak Ya

ya tidak Hentikan AED yang tdk efektif, Tingkatkan dosis

Tambahkan AED2 yang lain AED2, cek
interaksi,
Hentikan Kembali ke Cek kepatuhan
pengobatan Assesment Sembuh ?
awal
Ya Tidak

Lanjutkan terapi Rekonfirmasi diagnosis,

Pertimbangkan pembedahan
Atau AED lain
 OBAT ANTI EPILEPSI
 Obat-obat yang meningkatkan inaktivasi kanal Na +:
 Fenitoin, karbamazepin, lamotrigin,
okskarbazepin, valproat
 Obat-obat yang meningkatkan transmisi inhibitori
GABAergik:
 Benzodiazepin, barbiturat, Vigabatrin, Tiagabin,
Gabapentin
 Pemilihan obat : Tergantung pada jenis epilepsinya

Kejang Umum (generalized seizures)

Kejang
parsial
Tonic-clonic Abscense Myoclonic,
atonic

Drug of Karbamazepin Valproat Etosuksimid Valproat

choice Fenitoin Karbamazepin Valproat
Valproat Fenitoin

Alternatives Lamotrigin Lamotrigin Clonazepam Klonazepam

Gabapentin Topiramat Lamotrigin Lamotrigin
Topiramat Primidon Topiramat
Tiagabin Fenobarbital Felbamat
Primidon
Fenobarbital
OBAT ANTI EPILEPSI

OBAT DOSIS CARA

Dextrose 25 2-4 mg/kg/BB IV cepat
Pyridoxine 50 mg IV cepat
Calcium Gluconate 10% Sampai 10cc IV lambat 10 menit
MgSO4 3% Sampai 3 cc IV lambat 10 menit
*Phenobarbital 10-20mg/kg/BB IV lambat 5 menit
*Phenytoin 10-15 mg/kg/BB IV 25 mg/menit
*Diazepam Sampai 3mg IV lambat 5 menit
PROGNOSIS
 Prognosis umumnya baik, 70 – 80% pasien yang mengalami
epilepsy akan sembuh, dan kurang lebih separo pasien akan bisa
lepas obat
 20 - 30% mungkin akan berkembang menjadi epilepsi kronis 
pengobatan semakin sulit  5 % di antaranya akan tergantung
pada orang lain dalam kehidupan sehari-hari
 Pasien dg lebih dari satu jenis epilepsi, mengalami retardasi
mental, dan gangguan psikiatri dan neurologik  prognosis
jelek
 Penderita epilepsi memiliki tingkat kematian yg lebih tinggi
daripada populasi umum
PROGNOSIS
Penyebab kematian pada epilepsi :
 Penyakit yg mendasarinya dimana gejalanya berupa
epilepsi misal : tumor otak, stroke
 Penyakit yg tidak jelas kaitannya dg epilepsi yg ada
misal : pneumonia
 Akibat langsung dari epilepsi : status epileptikus,
kecelakaan sebagai akibat bangkitan epilepsi dan sudden
un-expected death
Status epileptikus
Definisi
 Aktivitas bangkitan terus menerus yg berlangsung slama
30menit/lebih.
 Aktivitas bangkitan hilang timbul yg berlangsung slama
30menit/lebih, dan selama waktu tsb tdk tdpt pemulihan
kesadaran.
Etiologi
 Riwayat epilepsi sblmnya
 Riwayat lesi otak (stroke, tumor, hematoma subdural)
 Stroke baru
 a/hipoksia otak
 G3an metabolik
 Putus obat etilalkohol
Etiologi
 Lesi primer neurologik
 Neurovaskular (stroke, malformasi A-V, perdarahan)
 Tumor (primer, metastasis)
 Infeksi SSP (abses, meningitis, ensefalitis)
 Penyakit inflamasi (vaskulitis, acute disseminated encephalomyelitis)
 Trauma kapitis (kontusio, perdarahan)
 Epilepsi primer
 Lesi non-primer nerologik
 Hipoksia/iskemia
 Toksisitas obat/zat (AB, antidepressan, antipsikotik, bronkodilator, anestesi
lokal, obat imunosupresif, kokain, amfetamin)
 Putus obat/zat (barbiturat, benzodiazepin, opioid, alkohol)
 Demam infeksi (febrile seizures)
 G3an metabolik (hiponatremia, hipofosfatemia, hipoglikemia, g3an
ginjal/hati, kraniotomi)
Klasifikasi
SE konvulsif SE non-konvulsif
SE umum Tonik-klonik Lena
Tonik Atipikal lena
Mioklonik Kejang atonik
SE parsial Kejang motorik parsial Afasia
(epilepsy partialis Nonmotorik parsial
continua) sederhana
Parsial kompleks
SE parsial -> umum Kejang parsial dg Subtle/comma
(secondary generalized) generalisasi sekunder
SS

SE konvulsif SE nonkonvulsif
 Hilangnya kesadaran  pe↓an ksadaran
 Aktivitas tonik-klonik otot  Agitasi
 Mulut berbusa  Afasia
 Lidah tergigit  nistagmus
 Mata yg menatap ke atas
 Inkontinensia urin
Diagnosis
 Anamnesis
 Riw penyakit dulu
 Faktor penyebab : penggantian obatantikonvulsan, putus obat
alkohol, overdosis obat, stroke, infeksi SSP,
 Deskripsi kekjang, keadaan preiktal, iktal, postiktal.
 Deviasi gaze, kelojotan, automatisme, g3an kesadaran
 Lama kejang konvulsi&postiktal / kejang nonkonvulsi
 Riw penyakit epilepsi
 Fk resiko epilepsi (riw cedera kepala +hilangnya ksadaran,
meningitis/ensefalitis, kejang demam)
 Riw hipoglikemi pd diabetes
 Riw lesi struktural otak (tumor, stroke, perdarahan subdural)
 Jk ps epilepsi -> jenis obat & kepatuhan minum obat
 Penyalahgunaan obat2
Diagnosis
 PF
 Status neurologis lengkap
 GCS
 Pupil
 Tnd rangsang meningeal
 Gjl2 lain
 Gjl negatif (koma, letargi, konfusi, afasia, amnesia)
 Gjl positif (automatisme, mengedip, agitasi)
 Defisit neurologik fokal
Diagnosis
 PP
 EEG continue 24jam
 Pencitraan -> ssuai indikasi : jk tdpt proses fokal pd otak
 Lumbal pungsi -> ssuai indikasi : jk tdk ditrmukan pe↑an TIK
DD
 Status epileptikus konvulsi atau status epileptikus non-
konvulsi.
 Postictal state (jk pe↓an ksadaran menetap stlh 30-60menit
stlh berakhirnya konvulsi, perlu dipikirkan adanya NCSE).
 G3an pergerakan : mioklonus, tremor, korea, tics, distonia
 Herniasi
 Limb-shaking TIA
 G3an psikiatri : psychogenic nonepileptic seizure, g3an
konversi, psikotik akut, katatonia.
 Kondisi lain yg menyebabkan pe↓an ksadaran, g3an tidur,
sinkop.
Emergency evaluation of serial seizures or status
epilepticus.
 Treatment with anticonvulsants should be instituted immediately (Table 8-6), while the following measures are taken.
 Vital signs:
 Blood pressure: exclude hypertensive encephalopathy and shock
 Temperature: exclude hyperthermia
 Pulse: exclude life-threatening cardiac arrhythmia
 Draw venous blood for serum glucose, calcium, electrolytes, hepatic and renal function blood studies, complete blood
count, erythrocyte sedimentation rate, and toxicology
 Insert intravenous line
 Administer glucose (50 mL of 50% dextrose) intravenously
 Obtain any available history
 Rapid physical examination, especially for:
 Signs of trauma
 Signs of meningeal irritation or systemic infection
 Papilledema
 Focal neurologic signs
 Evidence of metastatic, hepatic, or renal disease
 Arterial blood gases
 Lumbar puncture, unless the cause of seizures has already been determined or signs of increased intracranial pressure of
focal neurologic signs are present
 ECG
 Calculate serum osmolality: 2 (serum sodium concentration) + serum glucose/20 + serum urea nitrogen/3 (normal range: 270-
290)
 Urine sample for toxicology, if indicated
Approach to the Treatment of Status Epilepticus in
Adults
Initial assessment
Ensure adequate ventilation, oxygenation, blood pressure
Intubate if necessary, based on low oxygen saturation and labored breathing
Insert intravenous line
Administer glucose and thiamine in appropriate cirumstances
Send toxic screen
Assess quickly for cranial and cervical injury if onset of seizures is unwitnessed
Immediate suppression of convulsions
Lorazepam or diazepam, 2 to 4 mg/min IV to a total dose of 10 to 15 mg with blood pressure monitoring when
higher rates or doses are used
Initiation or reloading with anticonvulsants
Phenytoin 15–20 mg/kg IV at 25–50 mg/min in normal saline or fosphenytoin at 50 to 75 mg/min
General anesthetic doses of medication for persistent status epilepticus
Midazolam 0.2 mg/kg loading dose followed by infusion at 0.1 to 0.4 mg/kg/h or propofol 2 mg/kg/h
Further treatment if convulsions or electrographic seizures persist after several hours
May add valproate or phenobarbital 10 mg/min to total dose of 20 mg/kg as additional anticonvulsants
intravenously, or carbamazepine or levetiracetam by nasogastric tube if there is gastric and bowel activity
Consider neuromuscular paralysis with EEG monitoring if convulsions persist
Pentobarbital 10 mg/kg/h
Inhalational anesthetics (isoflurane)
Algoritma tatalaksana pada status epileptikus
Thankyou <3