Definition / meaning

• Epilepsi :
- Disruption SSP be marked with
occurrence generation (seizure, fit,
attack, spell) which is spontaneous
(unprovoked) and periodic
- Event convulsions that occur recur
(recurrent)
• convulsions : manifestation clinic
from activity neurons exaggerated
in in cortices cerebral
• Manifestation clinic convulsions
very varies dependent from area
brain functional that involved
 Epidemiology
• Rather difficult to estimate the number of cases of
epilepsy  on the condition without an attack, the
patient looks normal and all lab data is also normal,
but it is a certain stigma in people with epilepsy 
shy / reluctant to admit
• Highest incidence at the age of 20 the first year,
decreasing to the age of 50 years, and increased again
later related to some possibility of cerebrovascular
disease
• In 75% of patients, epilepsy occur before age 18 years
 The impact of disease
• Aspect psychosocial (problem medical, psychological,
social, and economy
• Aspect medical : increasing cost care, the need
power trained that skilled, amenities technique and
availability drug antiepileptic (OAE)
• Aspect economy : limited field work, increasing
unemployment
• Aspect psychological : flavor anxious, loss trust self
• Aspect social : stigma negative about disease and
patient
 prognosis
• prognosis generally well, 70-80% patient that experience
epilepsy will recover, and less more half patient will can
free drug
• 20-30% maybe will flourish Becomes epilepsy chronic 
treatment more and more difficult  5% in among will
dependent on other people in life daily
• Patient dg more from one type epilepsy, experience
retardation mental, and disruption psychiatry and
neurologic  prognosis ugly
• patient epilepsy have level Dead reply more high of the
population general
 Continued prognosis ...
Cause of death in epilepsy:
• That the underlying disease in which symptoms of
epilepsy eg, brain tumors, stroke
• Diseases which are not clearly related dg existing
epilepsy eg pneumonia
• As a direct result of epilepsy: status epilepticus,
accidents as a result of epileptic seizures and sudden
un-expected death
 Etiology
• Epilepsy may be caused by:
– activity nerve abnormal result process pathological that
influence brain
– disruption biochemistry or metabolic and lesions
microscopic in brain result trauma brain on time born or
injury other
– on baby  cause most often is asphyxiation or hypoxia
time born, trauma intracranial time born, disruption
metabolic, malformation congenital on brain, or infection
– on children and juvenile  majority is epilepsy idiopathic,
on age 5-6 year  caused because febrile
– on age adult cause more varies  idiopathic, because
birth trauma, injury head, tumor brain (age 30-50 th)
disease serebro vascular (> 50 th)
 pathogenesis
Seizures are caused because there
imbalance between inhibitory
and excitatory influences on the
brain
Imbalance can occur due to:
• The lack of inhibitory
transmission
– Example: after administration of
GABA antagonists, or during the
discontinuance of GABA agonists
(alcohol, benzodiazepines)
• Increased excitatory action 
increasing the action of
glutamate or aspartate
 diagnosis
• Patient diagnosed epilepsy if experience attack
convulsions in recur
• For determine type epilepsy, apart from symptom, be
required various tool diagnostic :
– EEG
– CT-scan
– MRI
– Etc

A CT or CAT scan (computed

tomography) is a much more
sensitive imaging technique than X-
rays, allowing high definition not only
of the bony structures, but of the soft
tissues.
 Classification epilepsy

• Based on clinical signs and

EEG data, seizures are
divided into:
– generalized seizures
(Generalized seizures)  if
activation occurs both
hemisfere brain pd together
– Partial seizures / focal  if
starting from a specific area
of ​the brain
Generalized seizures are divided into:
• Tonic-clonic grand mal convulsion =
– is the most common form
– the patient suddenly falls, seizures, shortness of breath, salivation
– could cyanosis, bedwetting, or biting the tongue
– occurred a few minutes, followed by weakness, confusion,
headache or sleep
• Abscense attacks = petit mal
– rare species
– generally only occurs in childhood or early adolescence
– patient suddenly bulging, or eye blinking, head drooping
– it happened just a few seconds, and even often unrecognized
• myoclonic seizures
– tjd usually in the morning, after waking up
– patients experienced a sudden jolt
– the same type (but non-epileptic) can occur in patients with normal
• atonic seizures
– rarely happening
– patient suddenly lost
muscle strength  fall, but could
soon recovered

Petit mal
Partial seizures are divided into:
• Simple partial seizures
– the patient does not lose consciousness
– the spasms occur in certain parts of the body
• Complex partial seizures
– the patient performs uncontrollable movements: chewing
movements, grimacing, etc. without awareness

convulsions Partial
 Therapeutic targets
So that no seizure control and minimize
adverse effect of drug

Therapeutic
strategies
 prevent or lower the loss load electricity
nerve that exaggerated  through
change on canal ion or set availability
neurotransmitter
The general principle of epilepsy
therapy:
– monotherapy more well  decrease potency adverse effect,
Upgrade obedience patient, no proven that polytherapy more
well from monotherapy and usually less effective because
interaction inter- drug precisely will disturb effectiveness and
accumulation effect side dg polytherapy
– avoid or minimize use antiepileptic sedative  tolerance, effect
on intelligence, memory, ability motor can stay During treatment
– if maybe, start therapy with one antiepileptic non-sedative, if
failed new be given sedative or polytherapy
– provide therapy in accordance with the type of epilepsy
– pay attention risk-benefit ratio therapy
– Use drug should sparingly maybe and wherever maybe in
period time short
– start with dose The smallest and could upgraded
corresponding dg condition clinical patient  urgent :
obedience patient
– there is variation individual to responses drug
antiepileptic  need monitoring strict and adaptation
dose
– if something drug failed reach therapy that be
expected  slowly terminated and be replaced with
drug other (jgn polytherapy)
– do monitoring content drug in blood  if maybe, do
adaptation dose with look too condition clinical patient
 monitoring content drug in serum (TDM = Therapeutic Drug Monitoring )

Purpose :
• For evaluate obedience patient
• Rate factor pharmacokinetics and pharmacodynamics drug 
excursions possibility if occur failure therapy
• identifying content drug reply effective For recognize
perubahan2 reply maybe retrievable inflict
convulsions/generation or effect side
• Determine drug What reply possibility retrievable inflict effect
toxic if be used more from one kind drug
Obstacles :
Amenities & cost examination laboratory
 monotherapy approach
• The main purpose: to control epileptic seizures dg one drug
• Drugs that have adl medicine; the best or most correspond to a particular
generation and patients themselves
• If the first drug shown to tdk jelas2 effective, the second type of drug
should be administered
• The first sudden withdrawal of the drug is not recommended because it
will cause repeated seizures, a dose reduction is recommended 20% of the
total dose 5 times daily every half time drug
• In practice monotherapy approach may not be applied consistently given
the necessary professionals, laboratory facilities that support and that
good cooperation between the patient and the family
 Procedures therapy
• Non pharmacology:
– observe factor triggers
– Avoid factor triggers (if there is) for example :
Stress, OR, consumption coffee or alcohol, change
schedule sleep, late eat, etc,
• Pharmacology : use medicines antiepileptic
 Drug selection: Depending on the type of epilepsy

General Seizures (generalized

convulsions seizures)
Partial Tonic- abscense Myoclonic,
clonic atonic

Drug of carbamaze valproate Ethosuxim valproate

choice pine carbamaz ide
phenytoin epine valproate
valproate phenytoin
Alternati lamotrigine lamotrigin clonazepa clonazepa
ves gabapentin e m m
Topiramate Topiramat lamotrigin lamotrigin
Tiagabine e e e
primidone primidone Topiramat
phenobarbi phenobar e
tal bital Felbamat
 Status epilepticus

• = convulsions general that occur During 5 minute or

more or event convulsions 2 times or more without
recovery awareness in Among two event mentioned
• constitute condition emergency reply need
treatment that right for minimize damage neurologic
permanent nor Dead
 Etiology
Type 1 Type 2
(no there is lesions ( There is lesions
structural) structural)
• Infection • anoxia/hypoxia
• Infection CNS • CNS tumors
• disruption metabolic • CVA
• fall AED level • overdose drug
• Alcohol • hemorrhage
• idiopathic • trauma
 Therapy ?
• Non-pharmacological:
– Vital signs are monitored
– Maintain ventilation
– Give oxygen
– For check blood gas monitor respiratory or metabolic
acidosis
– Occasional hypoglycemic  give glucose

• Pharmacology: with medicines

Algorithms in the treatment of status epilepticus
 profile drug
• Carbamazepine (carbamazepin)
Metabolized in the liver carbamazepin - 10, 11 -
epoxide (active metabolite) 
anticonvulsants
 neurotoxicity ES: nausea, confusion, drowsiness,
blurred vision, ataxia
ES rare: agranulocytosis
Kons serum increased linearly dose dg (dg depending
phenytoin)
• phenytoin
hydroxylated The liver mell system saturation
enzyme,
kec Metab varies inter- individual
be required to 20 day u reach content levels stable
after Perub dose SHG need prevented ↑ dose in
gradual or to tjd sign gangg cerebral (nystagmus,
ataxia, movement involuntar)
Need monitoring KONS serum scr strict  ↑ dose
small produce content toxic drug dlm serum
Other ES: hypertrophy gum, pimple, skin fatty, picture
advance Rough and hirsutism
• lamotrigine
Could be used dlm BTK single, spt phenytoin dg
ES <
ES: view hazy, confused, sleepy
Reaction skin seriously especially pd child
small
• phenobarbital
Kmk same effective dg carbamazepine & phenytoin pd
treatment convulsions tonic-clonic and Partial, ttp
ICE sedative >
Tolerance tjd pd usage period long and withdrawl scr
tiba2 reply retrievable spark status epilepticus,
ES: simptom cerebral (sedation, ataxia, nystagmus)
sleepy (pd DWS) and hyperkinesia pd anak2
primidone dimetab mjd metabolite active
anticonvulsants, false only adl phenobarbital
• vigabatrin, Gabapentin, and topiramate
be used as "Add-on" drugs pd patient epilepsy reply
morbidly reach effect well dg drug antiepileptic
other
vigabatrin a little / rarely be used krn retrievable
decrease area view (Visual fields) to 1/3 patient
gabapentin & carbamazepine too be used For treat
painful neuropathic (Shooting and stabbing) reply
aprox responds thdp analgesic conventional
• Ethosuximide
Only effective pd treatment convulsions
myoclonic (without effect loss awareness)
• valproate
profit : risk sedative <, spectrum activity large &
ES nausea, enhancement BB, bleeding & hair
fall out relatively small
Loss main : kdg2 responses idiosyncratic cause
toxicity hepatic severe / fatal
• benzodiazepines : Clonazepam
anticonvulsants potent, effective pd absences,
tonic-clonic seizures & myoclonic seizures
Characteristically sedative and tolerance strong
Where tjd on administration oral reply long
If therapy pharmacology failed, How ?
• Operative therapy should be considered (mainly for
epilepsy refractory / recurrent)
• The most safe and effective: resection of the anterior
portion of the temporal lobe, which is another kind:
resection of the cerebral cortex, hemisferektomi,
corpus callosum surgery, resection multilobar in
infants
• Approximately 70-80% of patients who undergo
surgery free of seizures, even if some of them should
continue to take