Evelline Priscillia P 405140047 Pemicu 1 Neuro

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Pemicu 1
Evelline Priscillia Pebriyanto 405140047
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Tujuan pembelajaran/Learning objectives
MM
1. Klasifikasi, definisi, etiologi kejang secara

klinis
2. Patofisiologi kejang
3. Tanda & gejala kejang
4. Diagnosis banding kejang
5. Pemeriksaan penunjang (imaging dan lab)
6. Tatalaksana (farmako & non farmako (gizi/KIE)
7. Prognosis & komplikasi

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LO 1
Klasifikasi, definisi, etiologi
kejang secara klinis
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Klasifikasi Kejang
 Seizures  Purely tonic, purely clonic,
generalized clonic-tonic-clonic
 Etiology  Non-convulsive seizures
 Idiopathic (primary)
 brief lapse of consciousness or
 Symptomatic (secondary) absence (petit mal)
 Site of origin  minor motor phenomena (brief
 Clinical form myoclonic, atonic, or tonic
seizures)
 Generalized
 Focal  Partial / focal seizures
 Frequency  Simple
 Isolated  consciousness is undisturbed
 Cyclic  Complex
 Repetitive  consciousness is altered
 Electrophysiologic correlates
 Generalized seizures
 Convulsive seizures Harrisons Principles of Internl Medicine, 18th Ed. 2012
 Tonic-clonic (grand mal)

seizures
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Klasifikasi Kejang
Harrisons Principles of Internl Medicine, 18th Ed. 2012

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Klasifikasi Kejang
http://www.epilepsy.com/sites/core/files/upload/image/ilae-2017-classification-basic.png
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Klasifikasi Kejang
http://www.epilepsy.com/sites/core/files/upload/image/ilae-2017-classification-expanded.png
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Klasifikasi Kejang
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Generalized seizure
 Grand mal seizure (tonic-clonic seizure)
 Petit mal seizure (Idiopathic Nonconvulsive Seizures)
 Myoclonic seizure

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Grand mal seizure
 Patient sometimes senses the approach of a seizure by one of
several subjective phenomena (a prodrome)
 Apathetic, depressed, irritable, or, the opposite (very rarely) 
some hours
 Myoclonic jerks of the trunk or limbs
 Turning of the head and eyes or whole body or intermittent
jerking of a limb (few seconds before consciousness is lost)
 Abdominal pains or cramps
 A sinking, rising, or gripping feeling in the epigastrium
 Pallor or redness of the face
 Throbbing headache
 Constipation, or diarrhea

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Grand mal seizure
 Initial motor signs
 Brief flexion of the trunk
 An opening of the mouth and eyelid
 Upward deviation of the eyes
 Arms are elevated and abducted
 Elbows semiflexed
 Hands pronated
  followed by a more protracted extension (tonic) phase  10-20s
 First the back and neck, arms and legs
 Piercing cry as the whole musculature piercing cry as the whole
musculature closed vocal cords
 Respiratory muscles are caught up in tonic spasm  breathing
suspended  skin and mucous membranes may become
cyanotic (few seconds)
 Dilated pupil (unresponsive to light)

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Grand mal seizure
 Transition from the tonic to the clonic phase of convulsion 
30s
 Mild generalized tremor (repetitive relaxation of the tonic
contraction)
 Violent flexor spasms that come in rhythmic salvos and agitate
the entire body
 Face becomes violaceous and contorted by a series of grimaces
 Often the tongue is bitten
 Autonomic signs are prominent
 Pulse is rapid
 Blood pressure is elevated
 Pupils are dilated
 Salivation & sweating are abudant

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Grand mal seizure
 Terminal phase of the seizure
 All movements have ended
 The patient lies still and limp
 Deep coma
 Pupils equal / unequal  begin to contract with light
 Breathing may be quiet / stertorous
 Several minutes later
 Patient may open his eyes, confused and may be quite agitated,
speak and later not remember anything that he said  drowsy
and falls asleep

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Grand mal seizure
 When the patients fully recovered
 No memory of any part of the spell
 Pulsatile headache
 Sore, bitten tongue and aching muscles
 If violent enough 
 crush a vertebral body
 Fracture
 periorbital hemorrhage
 subdural hematoma

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Grand mal seizure
 EEG pattern
 Repetitive spikes or spike-wave discharges lasting a few seconds,
followed by an approximately 10-s period of 10-Hz spikes
 spikes become mixed with slow waves  EEG slowly assumes a
polyspike-and-wave pattern (clonic phase)
 When all movement have ceased  EEG tracing is nearly flat, the
brain waves resume their preseizure pattern
 Other clinical state that simulate grand mal seizure

 Clonic jerking of extended limbs that occurs with vasodepressor
syncope or a Stokes-Adams attack
 basilar artery occlusion (Ropper)  ischemia of the corticospinal
tracts in the pons
 Limb-shaking TIA  clonic movements of one limb or one side of
the body during an episode of cerebral ischemia
 Hysterical (nonepileptogenic, “psychogenic”) seizureHarrisons Principles of Internl Medicine, 18th Ed. 2012
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Petit mal seizure
 Paucity of motor activity  patients themselves are sometimes not
aware
 Resemble a moment of absentmindedness / daydreaming
 The attack coming without warning
 Sudden interruption of consciousness
 Patient stares and briefly stops talking or ceases to respond
 Burst of fine clonic movements

 Eyelids, facial muscles, fingers or synchronous movements of both arms
 Minor automatisms
 Lip-smacking, chewing, and fumbling movements of the fingers
 Postural tone may be slightly decreased or increased
 Patients do not fall

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Petit mal seizure
 After 2 to 10 s, occasionally longer  patient re-establishes
full contact with the environment and resumes preseizure
activity
 Typical absence seizures constitute the most characteristic

epilepsy of childhood
 EEG pattern
 Generalized three-per-second spike and wave pattern
 Other type of seizure that simulate petit mal

 Atypical petit mal
 long runs of slow spike-and-wave activity, usually with no
apparent loss of consciousness
 External stimuli (asking the patient to answer a question) 
interrupt the run of abnormal EEG activity Harrisons Principles of Internl Medicine, 18th Ed. 2012
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Petit mal seizure
 Juvenile myoclonic epilepsy
 a common and relatively benign variety of myoclonic seizure
occurs in late childhood and adolescence
 display symmetrical or asymmetrical myoclonic jerks without
loss of consciousness
 Lennox-Gastaut syndrome
 onset between 2 and 6 years of age
 atonic, or astatic seizures (i.e., falling attacks), often succeeded
by various combinations of minor motor, tonic-clonic, and
partial seizures and by progressive intellectual impairment
 distinctive, slow (1- to 2-Hz) spike-and-wave EEG pattern
 West syndrome
 infantile spasms
 EEG picture (3-Hz “hypsarrhythmia”)
 arrest in mental development Harrisons Principles of Internl Medicine, 18th Ed. 2012
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Myoclonic seizure
 Brusque, brief, muscular contraction
 Some myoclonic jerks are so small as to involve only one

muscle or part of a muscle
 May occur intermittently and unpredictably or present as a

single jerk or a brief salvo
 Signs
 Outbreak of several small, rhythmic myoclonic jerks may appear
with varying frequency as part of absence seizures
 As isolated events in patients with generalized clonic-tonic-clonic
or tonic-clonic seizures
 Quite benign & respond well to medication

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Myoclonic seizure
 Disseminated myoclonus (polymyoclonus) 
 Childhood
 acute viral encephalitis
 the myoclonus-opsoclonus-ataxia syndrome of Kinsbourne
 Lithium or other drug toxicity
 If lasting for few weeks  subacute sclerosing panencephalitis
 Chronic progressive polymyoclonus + dementia 
 group of juvenile lipidosis, Lafora type familial myoclonic
epilepsy
 progressive dementia, myoclonus, and episode of generalized
seizure
 certain mitochondrial disorders
 other chronic familial degenerative diseases of undefined type
(paramyoclonus multiplex of Friedreich, dyssynergia
cerebellaris myoclonica of Ramsay Hunt)
 middle and late adult years, disseminated myoclonus + dementia 
Creutzfeldt-Jakob disease; alzheimer disease (rare)

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Myoclonic seizure
 Juvenile Myoclonic Epilepsy
 most common form of idiopathic generalized epilepsy in older
children and young adults
 begins in adolescence (15 yo)
 Clinical signs
 generalized seizure often upon awakening
 myoclonic jerks in the morning that involve the entire body
 occasional myoclonic jerks of the arm and upper trunk that
become prominent with fatigue, during early stages of sleep, or
after alcohol ingestion
 EEG pattern
 bursts of 4- to 6-Hz irregular polyspike activity
 Th/ valproic acid

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Partial seizure
 Frontal lobe partial seizure (focal & jacksonian)
 Somatosensory, Visual, and Other Types of Sensory Seizures
 Complex Partial Seizures (Psychomotor Seizures, Temporal

Lobe Seizures)

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Partial / focal seizure
 Partial / focal seizure
 Often the product of a demonstrable focal lesion or EEG
abnormality
 In some part of the cerebral cortex
 Simple
 Consciousness retained
 arise from foci in the sensorimotor cortex
 Complex
 focus in the temporal lobe on one side or the other, but a

frontal localization is also well known

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Frontal Lobe Partial Seizures
(Focal Motor and Jacksonian Seizures)
 Focal motor seizure
 E/  discharging lesion of the opposite frontal lobe
 Most common type  originating in the supplementary motor
area
 Movement of the head and eyes to the side opposite the irritative
focus often associated with a tonic contraction of the trunk and
limbs on that side
  entire seizure / generalized clonic movements, before or
with loss of unconsciousness
 Clinical sign
 Forceful, sustained deviation of the head and eyes, and
sometimes of the entire body (versive / adversive)  opposite
side (contraversive); same side (ipsiversive)
 Seizures of temporal lobe origin  head turning ipsilaterally
followed by forceful contraversive head (and body) turning
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 Jacksonian motor seizure
 Tonic contraction of the fingers of one hand, the face on one side,
or the muscles of one foot  clonic movements
 Localized movement / spread movement (“march” from the part
first affected to other muscles on the same side of the body)
 Classic jacksonian form 
 Seizure spreads from the hand, up the arm, to the face, and
down the leg;
 If the first movement is in the foot, the seizure marches up the
leg, down the arm, and to the face (uncommon)
 One-sided seizure activity  turning of the head and eyes to the
convulsing side  generalized seizure with loss of consciousness
 Consciousness is not lost if the sensorimotor symptoms remain
confined to one side

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 May be a transient paralysis of the affected limbs persists for minutes
or at times for hours after seizure (Todd’s paralysis)
 If there are continued focal paralysis  presence of a focal brain
lesion
 Focus of excitation is usually in or near the rolandic (motor) cortex 
onset of focal motor epilepsy in the hand
 High medial frontal lesions (area 8 and supplementary motor
complex) 
 Tonic elevation and extension of the contralateral arm (“fencer’s
posture”) and choreoathetotic and dystonic postures have been
 Complex, bizarre, and flailing movements of a contralateral limb
(hysterical seizure)
 Seizure discharges arising from the cortical language areas  brief
aphasic disturbance (ictal aphasia) and ejaculation of a word, or, more
frequently, a vocal arrest
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Somatosensory, Visual, and
Other Types of Sensory Seizures
 Somatosensory seizures
 E/  a focus in or near the postrolandic convolution of the
opposite cerebral hemisphere
 Numbness, tingling, or a “pins-and-needles” feeling and
occasionally as a sensation of crawling, electricity, or movement
of the part
 In the lips, fingers, or toes, and the spread to adjacent parts of
the body follows a pattern determined by sensory
arrangements in the postcentral convolution of the parietal lobe

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 Visual seizures
 E/  Lesions in or near the striate cortex of the occipital lobe
  elemental visual sensations of darkness or sparks and
flashes of light, which may be stationary or moving and
colorless / colored
 Seizure arising in one occipital lobe  momentary blindness in
both fields
 Temporal half of a homonymous field defect
 Lesions on the lateral surface of the occipital lobe  sensation of
twinkling or pulsating lights
 Focus in the posterior part of the temporal lobe near its junction
with occipital lobe  visual hallucinations & auditory
hallucinations

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 Auditory hallucinations
 Infrequent
 E/  focus in one superior temporal convolution
  buzzing or roaring in the ears
 Human voice  sometimes repeating unrecognizable words /
the sounds of music
 Vertiginous sensations
 E/  lesion in the superoposterior temporal region (junction
between parietal and temporal lobes)
  sensation of vertigo
 With a temporal focus  vertigo is followed by an auditory
sensation
 Giddiness, or light-headedness, is a frequent prelude of seizure

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 Olfactory hallucinations
 E/  disease of the inferior and medial parts of the temporal lobe
 Perceived odor is exteriorized (disagreeable or foul,
unidentifiable)
 Gustatory hallucinations
 E/  lesions of the insula and parietal operculum
 Salivation and a sensation of thirst may be associated

+ Complex Partial Seizures
(Psychomotor Seizures, Temporal Lobe Seizures)
 Signs
 The aura
  focal seizure of simple type / hallucination (visual and
auditory) / perceptual illusion  indicating temporal lobe
origin
 Objects or persons in the environment may shrink / enlarge in
the distance (micropsia/macropsia); perseverate as the head is
moved (palinopsia)
 Dyscognitive state (déjà vu & jamais vu)
 Certain old memories or scenes may insert / abrupt
interruption of memory
 Emotional experiences (sadness, loneliness, anger, happiness)
 Period of altered behavior and consciousness, the patient is later
found to be amnesic
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 Motor activity to seizure
 automatisms such as lip-smacking, chewing or swallowing
movements, salivation, fumbling of the hands, shuffling of the feet
 walk around in a daze or act inappropriately
 Certain complex acts that were initiated before consciousness is
lost (walking, chewing food, turning the pages of a book, or
driving)
 patients are obviously out of contact with their surroundings /
partially responsive patients  seizure originate at right temporal
lobe

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 Psychomotor triad by Lennox for patient with temporal lobe
seizure
 Motor changes
 Automatic behavior
 Alterations in psychic function
 Postictal behavior
 Global and nonfluent aphasia (left sided origin)
 Prolonged disorientation for time and place (right sided origin)
 Postictal nose wiping is carried out by the hand ipsilateral to the
seizure focus

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 Other manifestation
 Amnesic seizure
 Rarely, brief, recurrent attacks of transient amnesia
(manifestations of temporal lobe epilepsy)
 Behavioural & psychiatric seizure
 Post ictal state  protracted paranoid-delusional or amnesic
psychosis lasting for days or weeks
 Epileptic personality disorder
 exhibit a number of abnormalities of behavior and personality
during the interictal period (slow and rigid in their thinking,
verbose, circumstantial and tedious in conversation, inclined to
mysticism, preoccupied with rather naive religious and
philosophical ideas)

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Definisi Kejang
 A seizure (from the Latin sacire, “to take possession of”) is a
paroxysmal event due to abnormal excessive or synchronous
neuronal activity in the brain.
 Epilepsy describes a condition in which a person has

recurrent seizures due to a chronic, underlying process.

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Etiologi Kejang

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Etiologi Kejang

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LO 2
Patofisiologi kejang
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Patofisiologi Kejang
 MECHANISMS OF SEIZURE INITIATION AND PROPAGATION
 Focal seizure, there is a seizure initiation phase and a seizure
propagation phase. The initiation phase: (1) high-frequency bursts
of action potentials and (2) hypersyn- chronization.
 The bursting activity is caused by a relatively long- lasting
depolarization of the neuronal membrane due to influx of
extracellular calcium (Ca2+), which leads to the opening of
voltage- dependent sodium (Na+) channels, influx of Na+, and
generation of repetitive action potentials. This is followed by a
hyperpolarizing afterpotential mediated by γ-aminobutyric acid
(GABA) receptors or potassium (K+) channels, depending on the
cell type. The synchronized bursts from a sufficient number of
neurons result in a so-called spike discharge on the EEG.
 With sufficient activation there is a recruitment of surrounding
neurons via a number of synaptic and nonsynaptic mechanisms,
including:
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 (1) an increase in extracellular K+, which blunts
hyperpolarization and depolarizes neighboring neurons;
 (2) accumulation of Ca2+ in presynaptic terminals, leading to
enhanced neurotransmitter release; and
 (3) depolarization-induced activation of the N-methyl-D-
aspartate (NMDA) subtype of the excitatory amino acid
receptor, which causes additional Ca2+ influx and neuronal
activation; and
 (4) ephaptic interactions related to changes in tissue osmolarity
and cell swelling.
 The recruitment of a sufficient number of neurons leads to the
propagation of seizure activity into contiguous areas via local
cortical connections, and to more distant areas via long
commissural pathways such as the corpus callosum.

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 MECHANISMS OF EPILEPTOGENESIS
 Epileptogenesis refers to the transformation of a normal neuronal
network into one that is chronically hyperexcitable.
 There is often a delay of months to years between an initial CNS
injury such as trauma, stroke, or infection and the first seizure.
 The injury appears to initiate a process that gradually lowers the
seizure threshold in the affected region until a spontaneous
seizure occurs. In many genetic and idiopathic forms of epilepsy,
epileptogenesis is presumably determined by developmentally
regulated events.
 Thus, an initial injury such as head injury may lead to a very focal,
confined region of structural change that causes local
hyperexcitability.
 The local hyperexcitability leads to further structural changes that
evolve over time until the focal lesion produces clinically evident
seizures. Harrisons Principles of Internl Medicine, 18th Ed. 2012
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 MECHANISMS OF ACTION OF ANTIEPILEPTIC DRUGS
 Antiepileptic drugs appear to act primarily by blocking the
initiation or spread of seizures.
 The mechanisms include inhibition of Na+-dependent action
potentials in a frequency-dependent manner (e.g., phenytoin,
carbamazepine, lamotrigine, topiramate, zonisamide, lacosamide,
rufinamide), inhibition of voltage-gated Ca2+ channels
(phenytoin, gabapentin, pregabalin), attenuation of glutamate
activity (lamotrigine, topiramate, felbamate), potentiation of
GABA receptor function (benzodiazepines and barbiturates),
increase in the availability of GABA (valproic acid, gabapentin,
tiagabine), and modulation of release of synaptic vesicles
(levetiracetam).
 The two most effective drugs for absence seizures, ethosuximide
and valproic acid, probably act by inhibiting T-type Ca2+
channels in thalamic neurons.
 In contrast to the relatively large number of antiepileptic drugs
that can attenuate seizure activity, there are currently no drugs
known to prevent the formation of a seizure focus following CNS
injury. Harrisons Principles of Internl Medicine, 18th Ed. 2012
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LO 3
Tanda & gejala kejang
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Tanda & Gejala Kejang

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Tanda & Gejala Kejang
 Trigers of Seizures
 Missed medicine
 Lack of sleep and epilepsy
 Stress and epilepsy
 Alcohol
 Drug Abuse
 Menstruation
 Photosensivity and epilepsy
 Other triggers of seizures
 Nutritional deficiencies
 OTC medications
http://www.epilepsy.com/learn/triggers-seizures
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LO 4
Diagnosis Banding
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Diagnosis Banding

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LO 5
Pemeriksaan penunjang (imaging
& lab)
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Pemeriksaan Penunjang
 Clinical approach
 Is it indeed a seizure?
 How’s the clinical & EEG pattern & other characteristics?
 What’s the underlying cause?
 In the diagnosis of epilepsy  history is the key
 The examination in children & infant  greater value
 Finding of dysmorphic & cutaneus abnormalities  highly
characteristic cerebral disease that give rise to epilepsy
 Some lab studies (CBC, blood chemistries, liver & thyroid function
tests, EEG, imaging studies of brain: MRI, CT for emergency &
very young children)

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 History and Examination
 An in-depth history is essential, for in many cases the diagnosis of
a seizure is based solely on clinical grounds—the examination and
laboratory studies are often normal.
 Questions should focus on the symptoms before, during, and after
the episode in order to differentiate a seizure from other
paroxysmal events.
 The history should also focus on risk factors and predisposing
events.
 Clues for a predisposition to seizures include a history of febrile
seizures, earlier auras or brief seizures not recognized as such,
and a family history of seizures.
 Epileptogenic factors such as prior head trauma, stroke, tumor, or
infection of the nervous system should be identified. In children, a
careful assessment of developmental milestones may provide
evidence for underlying CNS disease.
 Precipitating factors such as sleep deprivation, systemic diseases,
electrolyte or metabolic derangements, acute infection, drugs
that lower the seizure threshold, or alcohol or illicit drug use
should also be identified. Harrisons Principles of Internl Medicine, 18th Ed. 2012
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 Careful examination of the skin may reveal signs of
neurocutaneous disorders such as tuberous sclerosis or
neurofibromatosis, or chronic liver or renal disease.
 A finding of organomegaly may indicate a metabolic storage
disease, and limb asymmetry may provide a clue to brain injury
early in development.
 Signs of head trauma and use of alcohol or illicit drugs should be
sought.
 Auscultation of the heart and carotid arteries may identify an
abnormality that predisposes to cerebrovascular disease.
 All patients require a complete neurologic examination, with
particular emphasis on eliciting signs of cerebral hemispheric
disease.
 Careful assessment of mental status (including memory, language
function, and abstract thinking) may suggest lesions in the anterior
frontal, parietal, or temporal lobes.
 Testing of visual fields will help screen for lesions in the optic pathways
and occipital lobes.
 Screening tests of motor function such as pronator drift, deep tendon
reflexes, gait, and coordination may suggest lesions in motor (frontal)
cortex, and cortical sensory testing (e.g., double simultaneous
stimulation) may detect lesions in the parietal cortex. Harrisons Principles of Internl Medicine, 18th Ed. 2012
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 Laboratory Studies
 Routine blood studies are indicated to identify the more common
metabolic causes of seizures such as abnormalities in electrolytes,
glucose, calcium, or magnesium, and hepatic or renal disease.
 A screen for toxins in blood and urine should also be obtained
from all patients in appropriate risk groups, especially when no
clear precipitating factor has been identified.
 A lumbar puncture is indicated if there is any suspicion of
meningitis or encephalitis, and it is mandatory in all patients
infected with HIV, even in the absence of symptoms or signs
suggesting infection.

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 Electrophysiologic Studies
 All patients who have a possible seizure disorder should be
evaluated with an EEG as soon as possible.
 The absence of electrographic seizure activity does not exclude a
seizure disorder, however, because focal seizures may originate
from a region of the cortex that cannot be detected by standard
scalp electrodes.
 The EEG is always abnormal during generalized tonic-clonic
seizures. Since seizures are typically infrequent and
unpredictable, it is often not possible to obtain the EEG during a
clinical event.
 In particular, video-EEG telemetry is now a routine approach for
the accurate diagnosis of epilepsy in patients with poorly
characterized events or seizures that are difficult to control.
 The EEG is also used for classifying seizure disorders and aid-
ing in the selection of anticonvulsant medications.
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In general, a normal EEG implies a
better prognosis than otherwise,
whereas an abnormal background or
profuse epileptiform activity suggests
a poor outlook.
The EEG findings are sometimes used
to determine whether anticonvulsant
medication can be discontinued in
epileptic patients who have been
seizure-free for several years, but the
findings provide only a general guide
to prognosis.

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 Brain Imaging
 MRI has been shown to be superior to CT for the detection of
cerebral lesions associated with epilepsy.
 In some cases MRI will identify lesions such as tumors, vascular
malformations, or other pathologies that need immediate therapy.
 The use of newer MRI methods such as 3-Tesla scanners,
multichannel head coils, three-dimensional structural imaging at
submillimeter resolution, and new pulse sequences including
fluid-attenuated inversion recovery (FLAIR), has increased the
sensitivity for detection of abnormalities of cortical architecture,
including hippocampal atrophy associated with mesial temporal
sclerosis, as well as abnormalities of cortical neuronal migration.
 In the patient with a suspected CNS infection or mass lesion, CT
scanning should be performed emergently when MRI is not
immediately available.
 Functional imaging procedures such as positron emission
tomography (PET) and single photon emission computed
tomography (SPECT) are also used to evaluate certain patients
with medically refractory seizures. Harrisons Principles of Internl Medicine, 18th Ed. 2012
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LO 6
Tatalaksana farmako & non
farmako (gizi, KIE)
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Tatalaksana

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Tatalaksana

+ Tatalaksana Harrisons Principles of Internl Medicine, 18th Ed. 2012
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Tatalaksana
 TREATMENT OF UNDERLYING CONDITIONS
 If the sole cause of a seizure is a metabolic disturbance such as an
abnormality of serum electrolytes or glucose, then treatment is
aimed at reversing the metabolic problem and preventing its
recurrence.
 If the apparent cause of a seizure was a medication (e.g.,
theophylline) or illicit drug use (e.g., cocaine), then appropriate
therapy is avoidance of the drug
 Seizures caused by a structural CNS lesion such as a brain tumor,
vascular malformation, or brain abscess may not recur after
appropriate treatment of the underlying lesion. However, despite
removal of the structural lesion, there is a risk that the seizure
focus will remain in the surrounding tissue or develop de novo as
a result of gliosis and other processes induced by surgery,
radiation, or other therapies

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Tatalaksana
 AVOIDANCE OF PRECIPITATING FACTORS
 ANTIEPILEPTIC DRUG THERAPY

 Antiepileptic drug therapy is the mainstay of treatment for most
patients with epilepsy.
 The overall goal is to completely prevent seizures without causing
any untoward side effects, preferably with a single medication
and a dosing schedule that is easy for the patient to follow.
 Seizure classification is an important element in designing the
treatment plan, since some antiepileptic drugs have different
activities against various seizure types

+
Tatalaksana
 SURGICAL TREATMENT OF REFRACTORY EPILEPSY
 Understanding the potential value of surgery is especially
important when a patient’s seizures are not controlled with initial
treatment, as such patients often fail to respond to subsequent
medication trials.
 Rather than submitting the patient to years of unsuccessful
medical therapy and the psychosocial trauma and increased
mortality associated with ongoing seizures, the patient should
have an efficient but relatively brief attempt at medical therapy
and then be referred for surgical evaluation.
 The most common surgical procedure for patients with temporal
lobe epilepsy involves resection of the anteromedial temporal
lobe (temporal lobectomy) or a more limited removal of the
underlying hippocampus and amygdala (amygdalohippocampec-
tomy).

+
Tatalaksana
 Focal seizures arising from extratemporal regions may be
abolished by a focal neocortical resection with precise removal of
an identified lesion (lesionectomy).
 When the cortical region cannot be removed, multiple subpial
transection, which disrupts intracortical connections, is
sometimes used to prevent seizure spread.
 Hemispherectomy or multilobar resection is useful for some
patients with severe seizures due to hemispheric abnormalities
such as hemimegalencephaly or other dysplastic abnormalities,
and corpus callosotomy has been shown to be effective for
disabling tonic or atonic seizures, usually when they are part of a
mixed-seizure syndrome (e.g., Lennox-Gastaut syndrome).

+
Tatalaksana
+
LO 7
Prognosis & Komplikasi
+
Prognosis dan Komplikasi
Prognosis
 A normal EEG implies a better prognosis than otherwise,

whereas an abnormal background or profuse epileptiform
activity suggests a poor outlook.
Complications
 Cognitive and behavioral complications
 Injuries
 Accidents
 Status epilepticus
 Sudden unexplained death in epilepsy Harrisons Principles of Internl Medicine, 18th Ed. 2012
http://www.livestrong.com/article/74926-complications-seizures/
+
Daftar Putaka
 Harrisons Principles of Internl Medicine, 18th Ed.

2012
 http://www.livestrong.com/article/74926-
complications-seizures/
 http://www.epilepsy.com/learn/triggers-seizures
+
Tambahan LO
- Kejang ekstracranial (metabolik)
- Kejang intracranial (trauma, tumor, stroke, infeksi,
eklampsia)
- Beda kejang dengan epilepsi
- Kejang demam
- Rabies
- Malaria cerebral
+
Tumor Intrakranial
DEFINISI
 Massa intrakranial -- baik primer maupun sekunder -- yang
memberikan gambaran klinis proses desak ruang dan atau gejala
fokal neurologis
KRITERIA DIAGNOSIS
 Gejala tekanan intrakranial yang meningkat
 Sakit kepala kronik, tidak berkurang dengan obat analgesic
 Muntah tanpa penyebab gastrointestinal
 Papil edema (sembab papil = choked disc)
 Kesadaran menurun / berubah
 Gejala fokal
 True location sign
 False location sign
 Neighbouring sign
 Tidak ada tanda-tanda radang sebelumnya.
 Pemeriksaan neuroimaging terdapat kelainan yang menunjukkan
adanya massa (SOL)
Perhimpunan Dokter Spesialis Saraf Indonesia. Standar Pelayanan Medik (SPM). 2013
+
Tumor Intrakranial
PEMERIKSAAN PENUNJANG
 Foto polos tengkorak
 Neurofisiologi : EEG, BAEP
 CT Scanning / MRI kepala + kontras
DIAGNOSIS BANDING
 Abses serebri
 Subdural hematom
 Tuberkuloma
 Pseudotumor serebri
+
Tumor Intrakranial
TATALAKSANA
 Kausal
 • Operatif
 • Radioterapi
 • Kemoterapi
 Obat-obat dan tindakan untuk menurunkan tekanan intrakranial
 • Deksamethason
 • Manitol
 • Posisi kepala ditinggikan 20 – 300
 Simptomatik (bila diperlukan dapat dibicarakan) :
 • Antikonvulsan
 • Analgetik / anti peretik
 • Sedativa
 • Antidepresan bila perlu
 Rehabilitasi medik
+
Stroke
DEFINISI
 Suatu keadaan hilangnya sebagian atau seluruh fungsi neurologis
(defisit neurologik fokal atau global) yang terjadi secara
mendadak, berlangsung lebih dari 24 jam atau menyebabkan
kematian, yang semata-mata disebabkan oleh gangguan
peredaran darah otak karena berkurangnya suplai darah (stroke
iskemik) atau pecahnya pembuluh darah secara spontan (stroke
perdarahan)
PEMBAGIAN STROKE
1. Etiologis
 Infark: aterotrombotik, kardioembolik, lakunar
 Perdarahan: Perdarahan Intra Serebral, Perdarahan Subarahnoid,
Perdarahan Intrakranial et causa AVM
2. Lokasi
 Sistem Karotis
 Sistem Vertebrobasiler
+
Stroke
DASAR DIAGNOSIS
1. Anamnesa dari pasien keluarga atau pembawa pasien
2. Pemeriksaan fisik
 Keadaan umum, kesadaran (Glasgow Coma Scale/ kwantitas/
kwalitas), tanda vital, status generalis, status neurologist.
3. Alat Bantu scoring (skala)
 Siriraj Stroke Score (SSS ), Algoritme Stroke Gajah Mada
(ASGM)
4. Pemeriksaan penunjang
 Pungsi lumbal (bila neuroimejing tidak tersedia)
 Neuroimejing : CT Scan, MRI, MRA, Angiografi, DSA
+
Stroke
KRITERIA DIAGNOSIS Pemeriksaan penunjang
 Tergantung gejala dan tanda,
Anamnesis usia, kondisi pre dan paska
 Defisit neurologis yang terjadi stroke, resiko pemeriksaan,
secara tiba-tiba, saat aktifitas/ biaya, kenyamanan
istirahat, kesadaran baik/ pemeriksaan penunjang
terganggu, nyeri kepala/  Tujuan  membantu
tidak, muntah/ tidak, riwayat menentukan diagnosa,
hipertensi (faktor risiko strok diagnosa banding, faktor
lainnya), lamanya (onset), risiko, komplikasi, prognosa
serangan pertama/ulang dan pengobatan
Pemeriksaan Fisik (Neurologis

dan Umum)
 Ada defisit neurologis,
hipertensi / hipotensi /
normotensi Perhimpunan Dokter Spesialis Saraf Indonesia. Standar Pelayanan Medik (SPM). 2013
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Stroke
PEMERIKSAAN LABORATORIUM
 Dilakukan pemeriksaan Darah Perifer Lengkap (DPL), Gula
Darah Sewaktu (GDS), Fungsi Ginjal
 (Ureum, Kreatinin dan Asam Urat), Fungsi Hati (SGOT dan SGPT),
Protein darah (Albumin, Globulin), Hemostasis, Profil Lipid
(Kolesterol, Trigliserida, HDL, LDL), Homosistein, Analisa Gas
Darah dan Elektrolit.
 Jika perlu pemeriksaan cairan serebrospinal
RADIOLOGIS
 Pemeriksaan Rontgen dada untuk melihat ada tidaknya infeksi
maupun kelainan jantung
 Brain CT-Scan tanpa kontras (Golden Standard)
 MRI kepala
+
Stroke
TATALAKSANA
Penatalaksanaan Umum
 Umum  ditujukan terhadap fungsi vital: paru-paru, jantung, ginjal,
keseimbangan elektrolit dan cairan, gizi, higiene
 Khusus  pencegahan dan pengobatan komplikasi, rehabilitasi,
pencegahan stroke : tindakan promotif, primer dan sekunder
Penatalaksanaan Khusus
 Stroke iskemik / infark
 Anti agregasi platelet: Aspirin, tiklopidin, klopidogrel, dipiridamol,
cilostazol
 Trombolitik : rt-PA (harus memenuhi kriteria inklusi)
 Antikoagulan : heparin, LMWH, heparinoid (untuk stroke emboli)
 Neuroprotektan
 Perdarahan subarakhnoid
 Antivasospasme: Nimodipin
 Neuroprotektan
+
Stroke
TATALAKSANA
 Perdarahan intraserebral
 Konservatif:
 Memperbaiki faal hemostasis (bila ada gangguan faal
hemostasis)
 Mencegah / mengatasi vasospasme otak akibat perdarahan :
Nimodipine
 Neuroprotektan
 Operatif: Dilakukan pada kasus yang indikatif/memungkinkan:
 Volume perdarahan lebih dari 30 cc atau diameter > 3 cm
pada fossa posterior
 Letak lobar dan kortikal dengan tanda-tanda peninggian TIK
akut dan ancaman herniasi otak
 Perdarahan serebellum
 Hidrosefalus akibat perdarahan intraventrikel atau serebellum
 GCS > 7
+
Tetanus
DEFINISI
 Penyakit sistem saraf yang perlangsungannya akut dengan
karakteristik spasme tonik persisten dan eksaserbasi singkat
KRITERIA DIAGNOSIS
 Hipertoni dan spasme otot
 Trismus, risus sardonikus, otot leher kaku dan nyeri, opistotonus,
dinding perut tegang, anggota gerak spastik
 Lain-lain : Kesukaran menelan, asfiksia dan sianosis, nyeri pada otot-otot
di sekitar luka
 Kejang tonik dengan kesadaran tidak terganggu
 Umumnya ada luka/ riwayat luka
 Retensi urine dan hiperpireksia
 Tetanus lokal
+
Tetanus
 Bila memungkinkan, periksa bakteriologik untuk menemukan C. tetani.
 EKG bila ada tanda-tanda gangguan jantung
 Foto toraks bila ada tanda-tanda komplikasi paru-paru
DIAGNOSIS BANDING
 Kejang karena hipokalsemia
 Reaksi distonia
 Rabies
 Meningitis
 Abses retrofaringeal, abses gigi, sulbluksasi mandibula
 Sindrom hiperventilasi/ reaksi histeri
 Epilepsi/ kejang tonik klonik umum
+
Tetanus
TATALAKSANA  Ampisilin dengan dosis 1 gr/8
jam i.v. (TES KULIT
 IVFD dekstrose 5% : RL = 1 : 1 SEBELUMNYA)
/ 6 jam  Bila alergi terhadap Penilisin
 Kausal: dapat diberikan :
 Eritromisin 500 mg/6 jam/oral.
 Antitoksin tetanus: ATAU
 Serum antitetanus (ATS)  Tetrasiklin 500mg/6 jam/oral.
diberikan dengan dosis 20.000
 Penanganan luka:
IU/hari/i.m. selama 3-5 hari TES
KULIT SEBELUMNYA. ATAU  Dilakukan cross incision dan
 Human Tetanus lmmunoglobulin irigasi menggunakan H2O2
(HTlG). Dosis 500-3.000 lU/IM
tergantung beratnya penyakit.
Diberikan SINGLE DOSE
 Antibiotik:
 Metronidazole 500 mg/ 8 jam
drips i.v.
+
Tetanus
TATALAKSANA  Nutrisi
 Diberikan TKTP dalam bentuk
 Simtomatis dan supportif lunak, saring, atau cair. Bila
perlu, diberikan melalui pipa
 Diazepam nasogastrik
 Setelah masuk rumah sakit,  Menghindari tindakan/
segera diberikan diazepam
dengan dosis 10 mg Iiv perlahan perbuatan yang bersifat
2-3 menit. Dapat diulangi bila merangsang, termasuk
diperlukan rangsangan suara dan cahaya
 Dosis maintenance : 10 ampul = yang intensitasnya bersifat
100 mg/500 ml cairan infus (10- intermitten.
12 mg/KgBB/hari) diberikan  Mempertahankan/
secara drips (syringe pump) membebaskan jalan nafas:
 Setiap kejang diberikan bolus pengisapan lendir oro/
diazepam 1 ampul / IV perlahan nasofaring secara berkala
selama 3-5 menit,
 Posisi / letak penderita
diubah-ubah secara periodik.
 Pemasangan kateter bila
teriadi retensi urin.
+
Tetanus Neonatorum
 Penyebab utama kematian neonatus adalah asifikasia

neonatorum, infeksi (sepsis dan tetanus neonatorum), dan
BBLR
 Kejadian penyakit ini sangat berhubungan dgn aspek

pelayanan kesehatan neonatal, terutama pelayanan
persalinan (persalinan yg bersih dan aman), khusunya
perawatan tali pusat
 Komplikasi yg ditakutkan adalah spasme otot diafragma
Ikatan Dokter Anak Indonesia, Pedoman pelayanan medis edisi 2. 2011.

+
Tetanus Neonatorum
ANAMNESIS
 Persalinan yg kurang higienis terutama yg ditolong oleh tenaga
nonmedis yg tidak terlatih
 Perawatan tali pusat yg tidak higienis, pemberian dan
penambahan suatu zat pada tali pusat
 Bayi sadar, sering mengalami kekakuan (spasme) terutama bila
terangsang atau tersentuh
 Bayi malas minum
PEMERIKSAAN FISIK
 Bayi sadar, terjadi spasme otot berulang
 Mulut mencucu seperti mulut ikan (carper mouth)
 Trismus (mulut sukat dibuka)
 Perut teraba keras (perut papan)
 Opistotonus (ada sela antara punggung bayi dengan alas, saat bayi
ditidurkan)
 Tali pusat biasanya kotor atau berbau
 Anggota gerak spastik (boxing position)
+
Tetanus Neonatorum
Pemeriksaan yg dpt dilakukan untuk membedakan anatara tetanus
neonatorum dgn sepsi nenoatal / meningitis:
 Pungsi lumbal
 Pemeriksaan darah rutin, preparat darah hapus atau kultur dan
sensitivitas
TATALAKSANA
Medikamentosa
 Pasang jalur IV dan beri cairan dgn dosis rumatan
 Berikan diazepam 10mg/kg/hari secara IV dalam 24 jam atau dgn
bolus IV setiap 3-6 jam (0.1-0.2 mg/kg per kali pemberian)
maksimum 40 mg/kg/hari
 Bila bayi mengalami henti napas selama spasme atau sianosis sentral
setelah spasme, berikan oksigen dgn kecepatan aliran sedang, bila
belum bernapas lakukan resusitasi
 Setelah 5-7 hari, dosis diazepam dapat dikurangi secara bertahap 5-10
mg/hari dan diberikan melalui rute oroastrik
+
Tetanus Neonatorum
TATALAKSANA
Berikan bayi:
 Human tetanus immunoglobulin 500 U IM atau antitoksin tetanus 5000
U IM  pada pemberian antitoksin tetanus, sebelumnya dilakukan ts
kulit tetanus toksoid 0.5 mL IM pada tempat yg berbeda dgn
pemberian antitoksin
 Bila terjadi kemerahan dan atau pembengkakan pada kulit sekitar
pangkal tali pusat atau keluar nanah dai permukaan tali pusat, beirkan
pengobatan untuk infeksi lokal tali pusat
 Lini 1 Metronidazol 30 mg/kg/hari setiap 6 jam (oral / parenteral)
selama 7-10 hari
 Lini 2  penisilin procain 100.000 U/kg IV dosis tunggal selama 7-10
hari
Berikan ibu:
 Imunisasi tetanus toksoid 0.5 ml (untuk melindungi ibu dan bayi yg
dikandung berikutnya) dan minta utk datang kembali satu bulan
kemudian untuk pemberian dosis kedua
+
Tetanus Neonatorum
PEMANTAUAN
Perawatan lanjut bayi tetanus neonatorum
 Rawat bayi di ruang yg tenang dan gelap utk mengurangi rangsangan
yg tidak perlu
 Lanjutkan pemberian cairan IV dgn dosis rumatan
 Nilai kemampuan minum dua kali sehari dan dianjurkan untuk
menyusu ASI secepatnya begitu terlihat bayi siap utk mengisap
 Bila sudah tidak terjadi spasme selama 2 hari, bayi dapat minum baik
makan bayi dapat dipulangkan
Tumbuh kembang
 Meskipun angkan kematian tetanus neonatorum masih tinggi (50%
atau lebih), tetapi bila bayi bisa bertahan hidup tidak akan
mempunyai dampak penyakit di masa datang
Preventif
 Pelaksanaan pelayanan neonatal esensial terutama pemotongan tali
pusat dgn alat steril
 Perawatan pasca neonatal, tidak mengoles atau menabus sesuatu yg
tidak higienis pada tali pusat
+
Eclamptic Seizures
ECLAMPSIA
 The development of grand mal seizures in a woman with
gestational HT or PE, which are not attributable to another cause.
May occur in the antepartum or postpartum period
ISSUES TO CONSIDER
 Magnesium sulphate (MgSO4) is the anticonvulsant of choice for
the treatment of eclamptic seizures
 Rapid infusion of MgSO4 requires ECG monitoring, call MET
 Rapid infusion can lead to hypotension, facial flushing, drowsiness, CNS
depression, nausea and decreased foetal heart variability
 Caution in patients with impaired renal function or electrolyte
imbalance, heart block, or myocardial damage.
 Make sure you have Calcium Gluconate 10 mls 10% solution
(antidote)
Ballarat Health Services. Clinical pratice guideline eclamptic seizures. 2008

+
Eclamptic Seizures
PROCEDURE
 When a woman has an eclamptic seizure the first priority is stabilisation of the
mother, once this is achieved assessment of foetal wellbeing should be
undertaken
 Call for assistance
 Place patient in left lateral position if able and apply oxygen  6-8 L O2 via
mask
 Gain IV access, take bloods at same time
 Once seizure has finished undertake maternal vital signs. If able to do, take
foetal heart rate. (Seizures are usually self limiting)
 Administer loading bolus of Magnesium Sulphate (MgSO4)
 8ml of 50% solution of MgSO over five minutes (= 4gm loading dose)
4
 Check patella reflexes after bolus dose

 Cardiac monitoring MUST be in place during bolus
 Alternatively if MgSO is unavailable give Midazolam 5mg IV or rectally
4
 If unable to get IV access or midazolam unavailable then administer 4ml

MgSO into each buttock (8ml total)
4
Ballarat Health Services. Clinical pratice guideline eclamptic seizures. 2008

+
Eclamptic Seizures
PROCEDURE
Treat recurrent seizures with a further 4ml MgSO4 bolus (2gm)
 Consider an increase in the infusion rate
Have resuscitation and ventilatory support available during and after
loading of MgSO4 dose.
Stabilise patient
 Treat hypertension with Hydralazine
 Hydralazine 1mg stat as test dose
 If BP okay then 5mg over 1 min
 Repeat 15 minutely if required (up to culmative dose of 20mg)
 Must be given by medical staff
 Monitor BP minutely for 5 minutes after hydralazine then every 15 minutes
 Only bolus doses can be given on the maternity unit – patients requiring
hydralazine infusions should be transferred to ICU.
If BP remains elevated consider sublingual GTN or GTN infusion.
If appropriate arrange for urgent delivery. (Patient’s condition will dictate
method). Ballarat Health Services. Clinical pratice guideline eclamptic seizures. 2008
+
Kejang Demam pada anak
 Bangkitan kejang yang terjadi pada kenaikan suhu tubuh

(suhu rektal di atas 380C) yang disebabkan oleh suatu proses
ekstrakranium
 2 – 4% → anak usia 6 bulan – 5 tahun
 KLASIFIKASI
 Kejang demam kompleks
 Kejang lama > 15 menit
 Kejang fokal atau parsial satu sisi, atau kejang umum didahului kejang
parsial
 Berulang atau lebih dari 1 kali dalam 24 jam
 Kejang demam sederhana
 Kurang dari 15 menit, umumnya akan berhenti sendiri
 Kejang berbentuk umum tonik dan atau klonik, tanpa gerakan fokal
 Kejang tidak berulang dalam waktu 24 jam
Pusponegoro HD, widodo DP, ismael S, editors. Konsensus penatalaksanaan kejang demam.
Jakarta: unit kerja koordinasi neurologi ikatan dokter anak indonesia; 2006.
+
ETIOLOGI
 Lepasnya sitokin inflamasi (IL-1 beta) atau hiperventilasi  alkalosis dan
meningkatkan pH otak  kejang
 Diturunkan secara genetik  eksitasi neuron tjd lebih mudah (keterkaitan
kromosom 19p dan 8q13-21)
 Kejang berasal dari proses ekstrakranial, paling sering disebabkan karena
ISPA, otitis media akut, roseola, ISK, infeksi saluran cerna
DIAGNOSIS BANDING
 Infeksi intrakranial  demam tjd bersamaan atau setelah kejang
 Meningitis  bayi tampak letargi, ubun-ubun besar mmebonjol, pemerikasaan
darah tepi adanya leukositosis
 Darah perifer lengkap, gula darah dan elektrolit  jika dicurigai hipoglikemi,
ketidakseimbangan elektrolit, infeksi
 Pungsi lumbal  singkirkan diagnosis meningitis
 EEG
 X-ray, CT-Scan, MRI
Kapita Selekta Kedokteran Jilid I. Edisi 4. Jakarta: Meida Aesculapius. 2014
+
FAKTOR RISIKO BERULANGNYA KEJANG DEMAM
 Riwayat kejang demam dalam keluarga
 Usia kurang dari 12 bulan
 Temperatur yang rendah saat kejang
 Cepatnya kejang setelah demam
+
Kementrian Kesehatan RI. Buku Saku Pelayanan Kesehatan Ibu di Fasilitas

Kesehatan Dasar dan Rujukan Pedoman Bagi Tenaga Kesehatan. Edisi pertama.
Jakarta: Kementrian Kesehatan RI, 2013
+
BEBERAPA HAL YANG HARUS DIKERJAKAN BILA
KEMBALI KEJANG
 Tetap tenang dan tidak panik
 Kendorkan pakaian yang ketat terutama disekitar leher
 Bila tidak sadar, posisikan anak terlentang dengan kepala miring.
Bersihkan muntahan atau lendir di mulut atau hidung. Walaupun
kemungkinan lidah tergigit, jangan memasukkan sesuatu
kedalam mulut
 Ukur suhu, observasi dan catat lama dan bentuk kejang
 Tetap bersama pasien selama kejang
 Berikan diazepam rektal. Dan jangan diberikan bila kejang telah
berhenti
 Bawa kedokter atau rumah sakit bila kejang berlangsung 5 menit
atau lebih
+
Rabies
DEFINISI
 Penyakit peradangan akut SSP oleh virus rabies, bermanifestasi
sebagai kelainan neurologi yang umumnya berakhir dengan
kematian
ANAMNESIS
Penderita mempunyai riwayat tergigit, tercakar dengan anjing,
kucing atau binatang lainnya yang :
 Positif rabies (hasil pemeriksaan otak hewan tersangka)
 Mati dalam waktu 10 hari sejak menggigit (bukan dibunuh)
 Tak dapat diobservasi setelah menggigit (dibunuh, lari,
sebagainya)
 Tersangka rabies (hewan berubah sifat, malas makan dll)
+
Rabies
GAMBARAN KLINIK
 Stadium prodromal (2-10 hari)
 Sakit dan rasa kesemutan di sekitar luka gigitan (tanda awal rabies),
sakit kepala, lemah, anoreksia, demam, rasa takut, cemas, agitasi
 Stadium kelainan neurologis (2-7 hari)

 Bentuk spastik  peka terhadap rangsangan ringan, kontraksi otot
faring dan esofagus, kejang, aerofobia, hidrofobia, kaku kuduk,
delirium, semikoma, meninggal setelah 3-5 hari
 Bentuk demensia
 Kepekaan terhadap rangsangan bertambah, gila mendadak, dapat
melakukan tindakan kekerasan, koma, mati
 Bentuk paralitik (7-10 hari)
 Gejala tidak khas, penderita meninggal sebelum diagnosis

tegak, terdapat monoplegi atau paraplegi flaksid, gejala bulbar;
kematian karena kelumpuhan otot napas
+
Rabies
PEMERIKSAAN MENUNJANG DIAGNOSIS
PENUNJANG BILA DITEMUKAN
 Pemeriksaan laboratorium  Darah
 Lekosit, hematokrit, Hb,  Lekosit : 8.000-13.000/mm3
Albumin urine, dan Lekosit  Hematokrit : berkurang
urine, Likuor Serebrospinal  Hb : berkurang
bila perlu
 Urine
 Pemeriksaan radiologik
 Albuminuria
 Dapat dilakukan
 Sedikit lekosit
pemeriksaan CT Scan
kepala untuk menyingkirkan  CSF
kausa lain  Protein normal atau sedikit
meninggi
+
Rabies
TATALAKSANA
Perhimpunan Dokter Spesialis Saraf Indonesia. Standar

Pelayanan Medik (SPM). 2013
+
Rabies
TATALAKSANA
Perhimpunan Dokter Spesialis Saraf Indonesia. Standar

Pelayanan Medik (SPM). 2013
+
Malaria
 Malaria merupakan penyakit infeksi akut hingga kronik yg
disebabkan oleh satu atau lebih spesies Plasmodium,
ditandai dgn panas tinggi bersifat intermiten, anemia, dan
hepato-splenomegali
 Malaria dapat ditularkan melalui alamiah (natural infection)

melalui gigitan nyamuk anophelles dan penularan bukan
alamiah yaitu malaria bawaan (kongenital) dan penularan
secara mekanik melalui transfusi darah atau jarum suntik
 Masa inkubasi
 Masa inkubasi 9-30 hari tergantung pada spesies parasit, paling
pendek pada P. falciparum dan paling panjang pada P. malariae
 Masa inkubasi pada penularan secara alamiah bagi masing-
masing spesies parasit untuk P. falciparum 12 hari, P. vivax dan P.
ovale 13-17 hari, P. malariae 28-30 hari

+
Malaria Serebral
KRITERIA DIAGNOSIS
 Merupakan komplikasi dari malaria. Paling sering disebabkan
oleh P. falciparum. Diagnosis ditegakkan pada penderita malaria
(terbukti dari pemeriksaan apus darah) yang mengalami
penurunan kesadaran (GCS < 7) disertai gejala lain gangguan
serebral (ensefalopati)
 Pemeriksaan apus darah tebal : ditemukan parasit malaria
DIAGNOSIS BANDING
 Penurunan kesadaran sebab lain: Hipoglikemi, asidosis berat,
syok karena hipotensi
+
Malaria Serebral
TERAPI
 Antimalaria : Kinin dihidroklorida lV
 Terapi suportif : antikonvulsan, antipirektika, penanganan
hipoglikemia, menjaga keseimbangan cairan dan elektrolit
 Pencegahan : Anti malaria oral sejak dua minggu sebelum
perjalanan ke daerah endemis
PENYULIT
 Hipoglikemia, Asidosis, Edema paru, Syok hemodinamik, Gagal
ginjal
PROGNOSIS
 Sequele jangka panjang : Ataksia, buta kortikal, kejang,
hemiparesis
+

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1. Klasifikasi, definisi, etiologi kejang secara

3. Tanda & gejala kejang

4. Diagnosis banding kejang

5. Pemeriksaan penunjang (imaging dan lab)

6. Tatalaksana (farmako & non farmako (gizi/KIE)

7. Prognosis & komplikasi

 Tonic-clonic (grand mal)

Harrisons Principles of Internl Medicine, 18th Ed. 2012

 Petit mal seizure (Idiopathic Nonconvulsive Seizures)

Harrisons Principles of Internl Medicine, 18th Ed. 2012

Harrisons Principles of Internl Medicine, 18th Ed. 2012

Harrisons Principles of Internl Medicine, 18th Ed. 2012

Harrisons Principles of Internl Medicine, 18th Ed. 2012

Harrisons Principles of Internl Medicine, 18th Ed. 2012

Harrisons Principles of Internl Medicine, 18th Ed. 2012

 Other clinical state that simulate grand mal seizure

 Resemble a moment of absentmindedness / daydreaming

 The attack coming without warning

 Sudden interruption of consciousness

 Patient stares and briefly stops talking or ceases to respond

 Burst of fine clonic movements

 Postural tone may be slightly decreased or increased

 Patients do not fall

 Typical absence seizures constitute the most characteristic

 Other type of seizure that simulate petit mal

 Some myoclonic jerks are so small as to involve only one

 May occur intermittently and unpredictably or present as a

Harrisons Principles of Internl Medicine, 18th Ed. 2012

Harrisons Principles of Internl Medicine, 18th Ed. 2012

Harrisons Principles of Internl Medicine, 18th Ed. 2012

 Somatosensory, Visual, and Other Types of Sensory Seizures

 Complex Partial Seizures (Psychomotor Seizures, Temporal

Harrisons Principles of Internl Medicine, 18th Ed. 2012

 focus in the temporal lobe on one side or the other, but a

Harrisons Principles of Internl Medicine, 18th Ed. 2012

Harrisons Principles of Internl Medicine, 18th Ed. 2012

Harrisons Principles of Internl Medicine, 18th Ed. 2012

Harrisons Principles of Internl Medicine, 18th Ed. 2012

Harrisons Principles of Internl Medicine, 18th Ed. 2012

Harrisons Principles of Internl Medicine, 18th Ed. 2012

Harrisons Principles of Internl Medicine, 18th Ed. 2012

Harrisons Principles of Internl Medicine, 18th Ed. 2012

Harrisons Principles of Internl Medicine, 18th Ed. 2012

 Epilepsy describes a condition in which a person has

Harrisons Principles of Internl Medicine, 18th Ed. 2012

Harrisons Principles of Internl Medicine, 18th Ed. 2012

Harrisons Principles of Internl Medicine, 18th Ed. 2012

Harrisons Principles of Internl Medicine, 18th Ed. 2012

Harrisons Principles of Internl Medicine, 18th Ed. 2012

Harrisons Principles of Internl Medicine, 18th Ed. 2012

Harrisons Principles of Internl Medicine, 18th Ed. 2012

Harrisons Principles of Internl Medicine, 18th Ed. 2012

Harrisons Principles of Internl Medicine, 18th Ed. 2012

Harrisons Principles of Internl Medicine, 18th Ed. 2012

Harrisons Principles of Internl Medicine, 18th Ed. 2012

Harrisons Principles of Internl Medicine, 18th Ed. 2012

 ANTIEPILEPTIC DRUG THERAPY

Harrisons Principles of Internl Medicine, 18th Ed. 2012