Pemicu 1 Blok Sistem Saraf &

Kejiwaan
Tidur atau Kejang
Lidya Oktaviani Siauw
405140006
Definisi & Klasifikasi Kejang

LO 1
 • Seizure:
– Transient occurrence of signs and/or symptoms due to abnormal excessive or
synchronous neuronal activity in brain (cortex)
– During seizure, large number of brain cells activated abnormally at a same
time (electrical storm in brain)
• A seizure is also referred to as a convulsion, fit, or attack.
– However, the words “convulsion” or “fit” are usually used to refer to
seizures with tonic-clonic muscle movements
• Nature of seizure depends on many factors:
– Sleep wake cycle
– Prior injuries to brain
– Genetic tendencies
– Medications
– Which circuits in brain involved
– etc

Robert S. Fisher MD, PhD, Patricia O. Shafer RN, MN, and Carol D’Souza MA Psych. 2017 Revised Classification of Seizures.12/2016. Available
from: http://www.epilepsy.com/article/2016/12/2017-revised-classification-seizures
 The New Basic Classification of
Seizures
• 3 key features:
– Where seizures begin in the brain
– Level of awareness during seizures
– Other features of seizures

Robert S. Fisher MD, PhD, Patricia O. Shafer RN, MN, and Carol D’Souza MA Psych. 2017 Revised Classification of Seizures.12/2016. Available
from: http://www.epilepsy.com/article/2016/12/2017-revised-classification-seizures
 Where seizure begins
• Focal seizures: prev. called partial seizures
– Starts in an area or network of cells on 1 side of
brain
• Generalized seizures: prev. called primary
generalized
– Involve networks on both sides of brain at onset
• Focal to bilateral seizure
– Starts in 1 side then spread to both sides
(secondary generalized seizures)

Robert S. Fisher MD, PhD, Patricia O. Shafer RN, MN, and Carol D’Souza MA Psych. 2017 Revised Classification of Seizures.12/2016. Available
from: http://www.epilepsy.com/article/2016/12/2017-revised-classification-seizures
 Awareness
• Focal aware: • Awareness unknown:
– Awareness remains intact – Sometimes it’s not possible
• even if the person is unable to to know if a person is aware
talk or respond during a or not
seizure, the seizure would be • for example if a person lives
called a focal aware seizure. alone or has seizures only at
– This replaces the term simple night.
partial. • Generalized seizures:
• Focal impaired awareness: – These are all presumed to
– Awareness is impaired or affect a person’s awareness
affected at any time during a or consciousness
seizure
• even if a person has a vague
idea of what happened, the
seizure would be called focal
impaired awareness.
– This replaces the term
complex partial seizure.

Robert S. Fisher MD, PhD, Patricia O. Shafer RN, MN, and Carol D’Souza MA Psych. 2017 Revised Classification of Seizures.12/2016. Available
from: http://www.epilepsy.com/article/2016/12/2017-revised-classification-seizures
 Motor and other symptoms in Focal
Seizures
• Focal motor seizure:
– Some type of movement occurs during the event.
• E.g: twitching, jerking, or stiffening movements of a
body part or automatisms (licking lips, rubbing hands,
walking, or running).
• Focal non-motor seizure:
– Other symptoms that occur first
• E.g. changes in sensation, emotions, thinking, or
experiences.

Robert S. Fisher MD, PhD, Patricia O. Shafer RN, MN, and Carol D’Souza MA Psych. 2017 Revised Classification of Seizures.12/2016. Available
from: http://www.epilepsy.com/article/2016/12/2017-revised-classification-seizures
 Generalized Onset Seizures
• Generalized motor • Generalized non-motor
seizure: seizure (Absence):
– Generalized tonic-clonic – Primarily absence
seizure: seizures with seizures
stiffening (tonic) and – “petit mal.”
jerking (clonic). – Involve brief changes in
– “grand mal.” awareness, staring, and
– Other forms of some may have
generalized motor automatic or repeated
seizures may happen. movements like
lipsmacking.

Robert S. Fisher MD, PhD, Patricia O. Shafer RN, MN, and Carol D’Souza MA Psych. 2017 Revised Classification of Seizures.12/2016. Available
from: http://www.epilepsy.com/article/2016/12/2017-revised-classification-seizures
Robert S. Fisher MD, PhD, Patricia O. Shafer RN, MN, and Carol D’Souza MA Psych. 2017 Revised Classification of Seizures.12/2016. Available
from: http://www.epilepsy.com/article/2016/12/2017-revised-classification-seizures
 Focal Motor Onset
distinction between clonic &
Atonic Focal loss of tone myoclonic:
• Clonic implies sustained,
Tonic Sustained focal stiffening regularly spaced
stereotypical jerks
Clonic Focal rhythmic jerking • myoclonus is less regular
and in briefer runs.
Myoclonic Irregular brief focal jerking
Epileptic Focal flexion or extension of arms & flexion of
Spasms trunk
Hyperkinetic Pedaling, thrashing activity
Automatism More or less coordinated, purposeless,
repetitive motor activity

Instruction manual for the ILAE 2017 operational classification of seizure types. Available from:
http://onlinelibrary.wiley.com/doi/10.1111/epi.13671/full
 Focal Non motor onset
Focal autonomic seizures: Focal cognitive seizures:
Behavior arrest: • gastrointestinal sensations, • patient reports or exhibits deficits in:
• Cessation of • a sense of heat or cold, • language,
movement and • flushing, • Thinking
unresponsiveness • higher cortical functions
• piloerection (goosebumps),
as predominant • during seizures
aspect of entire • palpitations,
• sexual arousal, • These symptoms outweigh other
seizure bcs this is
manifestations of the seizure.
common of many • respiratory changes,
seizures • Déjà vu, jamais vu, hallucinations,
• other autonomic effects.
illusions, and forced thinking are
examples of induced abnormal
cognitive phenomena.

Focal emotional seizures:

• emotional changes A focal sensory seizure:
• fear, anxiety, agitation, anger, paranoia, pleasure,
joy, ecstasy, laughing (gelastic), or crying
• somatosensory, olfactory,
(dacrystic). visual, auditory, gustatory, hot–
cold sense, or vestibular
• Some of these phenomena are subjective and
must be recalled and reported by the patient or sensations.
caregiver.
Instruction manual for the ILAE 2017 operational classification of seizure types. Available from:
http://onlinelibrary.wiley.com/doi/10.1111/epi.13671/full
 Generalized Motor Onset Seizures
Tonic–clonic “grand mal” seizure type
• The early movements of a tonic–clonic
seizure as being tonic.
• The clonic phase of a tonic–clonic seizure =
regularly decreasing frequency of jerks
over the course of the event.
• During a tonic–clonic seizure, awareness is
lost before or contemporaneously with the
stiffening and jerking movements.
Generalized Tonic seizures
• Bilateral limb stiffening or elevation, often
with neck stiffening.
• The tonic activity is not followed by clonic
movements.
• The tonic activity can be a sustained
abnormal posture,
• extension or flexion, sometimes + tremor
of the extremities.
tonic or tonic–clonic seizures more typically propel the
patient into a backward fall
Instruction manual for the ILAE 2017 operational classification of seizure types. Available from:
http://onlinelibrary.wiley.com/doi/10.1111/epi.13671/full
Generalized Clonic seizures
• Begin, progress, end with sustained
rhythmic jerking of limbs on both sides of
the body and often head, neck, face, and
trunk.
• << common than are tonic–clonic seizures,
• Usually occur in infants
• Should be distinguished from jitteriness
or shuddering attacks
Generalized myoclonic seizures
• can occur in +/- tonic or atonic
activity.
• Myoclonus differs from clonus by
being briefer and not regularly
repetitive.
 A myoclonic–atonic Atonic = without tone.
seizure • When leg tone is lost during a
generalized atonic seizure, the
• brief jerking of limbs or patient falls on the buttocks or
trunk  limp drop. sometimes forward onto the knees
and face.
• Recovery is usually within seconds.

Epileptic spasms previously were

referred to as infantile spasms
• the term “infantile spasms” remains suitable for
epileptic spasms occurring at infantile age.
• sudden flexion, extension, or mixed extension–
flexion of predominantly proximal and truncal
muscles.
• Most often during infancy.

Instruction manual for the ILAE 2017 operational classification of seizure types. Available from:
http://onlinelibrary.wiley.com/doi/10.1111/epi.13671/full
 Generalized non-motor seizure types

Typical Absence Seizures Atypical Absence Seizures

• Sudden onset of impaired • Less abrupt onset &
movement cessation
• Staring episodes of • More pronounced changes
“absence spells” in tone & longer duration
• + other motor, behavioural • Usually begins <5 yo
or autonomic phenomena • Assc w/ other generalized
• May interfere w. school fx seizure type & mental
and learning retardation

Pediatric Epilepsy; Diagnosis and Therapy; John M.Pellock, Blaise F.D.Burgeois

EEG In
TYPICAL ABSENCE SEIZURES
• Generalized 3Hz spike and wave complexes
ATYPICAL ABSENCE
• Slow spike and wave paroxysm classically 2,5 Hz
 • A myoclonic absence • Eyelid myoclonia
seizure – Myoclonic jerks of the eyelids
– Absence seizure with + upward deviation of the
rhythmic three-per-second eyes
myoclonic movements – Often precipitated by closing
– Abduction of the upper limbs the eyes or by light.
leading to progressive arm – Absence seizures with eyelid
elevation myoclonia, seizures, or EEG
– Associated with three-per- paroxysms induced by eye
second generalized spike- closure & photosensitivity
wave discharges. constitutes the triad of
– Duration is typically 10–60 s. Jeavons syndrome.
– Impairment of consciousness
may not be obvious.
– Myoclonic absence seizures
occur in a variety of genetic
conditions and also without
known associations.

ILAE Commission Report. Instruction manual for the ILAE 2017 operational classification of seizure types
 4 Components of Seizure
Prodromal phase Aura
• Begins few hrs or • Preceeds seizure by sec or few minutes
days before actual • Beginning of seizure & signals the focal onset of seizure
seizure • Symptom depends on location of focus
• Headache, • Often vague & indescribable leading to extreme fear
irritability, insomnia, • Strange epigastric sensations, dream like experiences,
bad temper, unpleasant smells etc
depression, • Patient remembers aura very well
increased activity • Happens before conciousness is lost

Post ictal phase

Seizure (ictus) • May be absent, brief or last sev hours
• Most seizure = loss of • Sometimes days
conciousness • Usually a deep sleep & waking up w/ headache, tiredness,
irritability, vomiting, confusion, muscular aches, ataxia
• Pts not able to give
• Transient paralysis of body parts (Todd’s paresis) may occur
info about actual ictus few hrs – day
• Depend on witnesses • Altered speech or aphasia may occur when dominant (left)
• No memory of seizure hemisphere involved
• Altered behaviour, emotional outbursts may occur

Epilepsy, A manual for Medical and Clinical Officers in Africa. WHO Geneva 2002. http://www.who.int/mental_health/media/en/639.pdf?ua=1
 Auras
• A detailed inquiry • Focal sensory or motor phenomena
should always be
Symptoms Origins
made about
Involuntary jerking of contralateral
prodromal and initial one hand, hemifacial frontoparietal cortex.
symptoms. paresthesias, forced
– A witness is critical. head turning
• Brief, symptoms Sensation of fear, temporal lobe.
(aura) at the onset olfactory or gustatory
hallucinations, or
of some seizures
visceral or déjà vu
may localize the CNS sensations
abnormality Progressive light- decreased cerebral
responsible for the headedness, dimming of blood flow from any
seizures vision, and faintness, cause (simple faints,
(more than one type of which indicate diffuse cardiac arrhythmias,
aura may occur) CNS dysfunction orthostatic hypotension)

ILAE Commission Report. Instruction manual for the ILAE 2017 operational classification of seizure types
Kejang berdasarkan etiologi

LO 2
 Epileptic vs Nonepileptic Seizure
Epileptic Nonepileptic
• Caused by >>, abnr • Not caused by electrocerebral
synchronized, localized or discharges
widely distributed neuronal • Sometimes divided into
– Organic nonepileptic:
electrical discharges • Atypical syncope
• Parasomnias (sleeping
disorders)
– Psychogenic nonepileptic
• Conversion symptoms
(showing psychological stress
in physical way)
• Dissociative states (breakdown
of awareness or memory)

Seizures and Epilepsy: Pathophysiology and Principles of Diagnosishttp://ww.w.turner-white.com/pdf/brm_EPI_V1P1.pdf

 Psychogenic/Pseudo-seizures
• Attacks that resembles seizures
• Manifestation of psychiatric disturbance
• Distinguished by clinical & EEG findings
• Resembles tonic-clonic attacks
• Usually no tonic phase, clonic phase w/ wild thrashing movement; patient
rarely comes to harm or incontinent
• Ictal eye closure common
• Abnormal movement of all extremities w/out loss of conciousness
• + shouting or obscene utterance during apparent loss of conciousness or
goal-directed behavior
• No post ictal confusion or abnr clinical signs following attack
• EEG doesn’t show organized seizure activity
• Post ictal slowing doesn’t occur
• Psychiatric referral may be helpful
Clinical Neurology. Lange. 7th edition
 Etiology of
Seizures
• Seizures can result
from either primary
CNS dysfunction or an
underlying metabolic
derangement or
systemic disease.
– This distinction is
critical! Therapy must
be directed at the
underlying disorder as
well as at seizure
control.
 Clinical Neurology. Lange. 7th edition

Epilepsy, A manual for Medical and Clinical Officers in Africa. WHO Geneva 2002.
http://www.who.int/mental_health/media/en/639.pdf?ua=1
 • Apart from the condition and maturation of the brain and the genetic
threshold, other factors may trigger a seizure.
• These factors may be different for each individual patient.
• Some patients learn which factors are important for them, and so they can
modify their behaviour or activities to try to avoid seizures

Epilepsy, A manual for Medical and Clinical Officers in Africa. WHO Geneva 2002. http://www.who.int/mental_health/media/en/639.pdf?ua=1
 Primary neurologic disorders
• Benign Febrile Convulsion of Childhood
– Seizures occur 2-4% children 3 mo – 5 yrs
– Usually in 1st day of febrile illness in absence of CNS infx
– May be a family hx of seizures
– Lasts ~ <10 – 15 minutes, lack focal features
– ~2/3 pts single seizures, < ~1/10 >3x seizures
– Seizures occurs during 1st hr of fever in children <18 mo or (+) family hx =
signif. risk for recurrence (90% occur w/in 2 yrs of initial eps)
– DD: meningitis, encephalitis, brain abscess
– Self limitid, th/ unnecessary
– Prolonged >15 min = ++ diazepam 0,3 mg/kg rectally (decrease risk of
recurrence)
– Probability dev chronic seizure 2-6%; high in pts w/ persistent neuro abnr,
prolonged, focal or multiple seizures or family hx of nonfebrile seizure

Clinical Neurology. Lange. 7th edition

 Idiopathic/cryptogenic
Head trauma Stroke
seizures
• 2/3 new onset • Common cause of • Affects cerebral
seizure in general epilepsy cortex  produces
population • Particularly occurs seizure 5-15%
• Age range broad 2nd perinatally or • Can occur following
– 7th decade associated w/ thrombotic or
• Risk of recurrence in depressed skull embolic infarction or
next 5 yrs 35% after fracture or intracerebral
1st unprovoked intracerebral or hemorrhage
seizure subdural hematoma • Even w/out
• 2nd seizure increased • Seizure occur w/in rupturing, vasc
risk of recurrence to 1st wk after malformations may
73% nonpenetrating be assc w/ seizures
• Most recur in 1st year head injuries = not (result of irritative
predictive of chronic effect on adjacent
seizure brain tissue)

Clinical Neurology. Lange. 7th edition

 Cortical dysgenesis &
Meningitis or
Mass lession neuronal migration
encephalitis
disorders
• Brain tumors or • Caused by bacterial: • Predispose to
abscess • e.g: H.influenza or epilepsy
• Glioblastomas, TB
astrocytomas, • Viral
meningiomas most • HSV
common tumor assc
• AIDS = often assc
w/ seizures
w/ AIDS dementia
complex,
toxoplasmosis or
cryptococcal
meningitis
• Fungal
• Parasitic
• Cysticercosis

Clinical Neurology. Lange. 7th edition

• Hypoglycemia & seizure
– Brain dependent on glucose as principal fuel 
interruption of supply due to systemic
hypoglycemia  dysfx of neurons & glia 
neurologic symptoms
• Hyponatremia & seizure
– Increased TBW, reduce urine output, Na+ loss,
inadeq Na+ intake  cerebral edema  seizures,
etc
 Meningitis
BACTERIAL MENINGITIS
• Leading cause of acute confusional state
• Early dx  improves outcome
• Predisposing condition:
– Systemic (esp respiratory) or parameningeal infx
– Head trauma
– Anatomic meningeal defects
– Prior neurosurgery
– Cancer
– Alcoholism
– Immunodef states
• Etiologic organisms varies w/ age & predisposing conditions

Clinical Neurology. Lange. 7th edition

 Bacteria typically
Pathophysiology of Bacterial
gain access to the Meningitis
CNS
1. local tissue Polysaccharide
• colonizing the mucous invasion, bacteria capsules,
membranes of the lipopolysaccharides,
nasopharynx 2. bacteremia,
outer membrane
• Spread to the meninges 3. hematogenous proteins contribute to
directly, through seeding of the the bacterial invasion
anatomic defects in the subarachnoid space. and virulence.
skull
• from parameningeal
sites: the paranasal
sinuses or middle ear

promote blood–brain
barrier permeability,
low levels of
vasogenic cerebral Inflammatory
antibody and
edema, response: release of
complement present
inflammatory
changes in cerebral in the subarachnoid
cytokines, IL 1, 6 and
blood flow, space inadequate to
TNF α
contain the infection.
and perhaps direct
neuronal toxicity
Clinical Neurology. Lange. 7th edition
https://clinicalgate.com/infections-of-the-central-nervous-system/

• At presentation, most
patients have had
symptoms of meningitis
for 1–7 days
– fever,
– confusion,
– vomiting,
– Headache,
– neck stiffness,
but the full syndrome is
often not present.
Clinical Neurology. Lange. 7th edition
S&S
• Physical examination:
– Fever
– signs of systemic or
parameningeal infection,
such as skin abscess or
otitis.
– A petechial rash is seen
in 50–60% of patients
with N. meningitidis
meningitis.
 • Signs of meningeal
irritation (~80% of cases)
• Often absent in the very
young and very old, or • The level of
with profoundly impaired consciousness, when
consciousness. altered, ranges from mild
confusion to coma.
• These signs include:
– neck stiffness on passive
• Focal neurologic signs,
flexion, seizures, and cranial
– thigh flexion upon flexion nerve palsies may occur
of the neck
– resistance to passive
extension of the knee with
the hip flexed (Kernig sign)

Clinical Neurology. Lange. 7th edition

MENINGEAL SIGNS
• The Kernig sign is performed
– patient lying supine and the hip and knee flexed
to 90 degrees.
– (+): extension of the knee from this position
elicits resistance or pain in the lower back or
posterior thigh.
• The classic Brudzinski sign
– spontaneous flexion of the knees and hips
during attempted passive flexion of the neck.
https://clinicalgate.com/infections-of-the-central-nervous-system/
• Nuchal rigidity or neck stiffness
– placing the examiner's hand under the patient's
head and gently trying to flex the neck.
– Undue resistance implies diffuse irritation of the
cervical nerve roots from meningeal
inflammation.
• Patients with severe meningeal irritation may
spontaneously assume the tripod position (also
called the Amoss sign or the Hoyne sign)
– knees and hips flexed, the back arched
lordotically, the neck extended, and the arms
brought back to support the thorax.

http://www.slremeducation.org/wp-content/uploads/2015/06/Chapter-171.-Meningitis-Encephalitis-and-Brain-Abscess.pdf
http://pdf.yassermetwally.com/ex.pdf
 Atypical presentations of ABM occur in infants, older
adults, and immunocompromised patients.
• Infants with bacterial meningitis:
– Fever or hypothermia
– hypoglycemia, poor feeding
– seizures, or irritability (excessive or abnormal crying).
• Examinations:
– findings of jaundice, ill appearance,
– a bulging fontanelle,
– meningeal irritation (including neck stiffness, the Kernig
sign, and the Brudzinski sign)
– fever higher than 40° C
– increased general body tone
predict bacterial meningitis.
http://www.slremeducation.org/wp-content/uploads/2015/06/Chapter-171.-Meningitis-Encephalitis-and-Brain-Abscess.pdf
 • Older and immunocompromised patients:
– higher rate of misdiagnosis that contributes to an
increase in the morbidity and mortality following
an episode of acute meningitis.
– lower proportion of fever, headache, and nausea
or vomiting
– Neck stiffness has a lower ensitivity and specificity
for meningitis in older patients.
– Finally, these populations may present to the
emergency department (ED) with altered mental
status and/or altered level of consciousness but
without a fever.
http://www.slremeducation.org/wp-content/uploads/2015/06/Chapter-171.-Meningitis-Encephalitis-and-Brain-Abscess.pdf
 Lab findings
• Peripheral blood may • Images of the chest,
reveal PMN sinuses, or mastoid
leukocytosis from bones may indicate a
systemic infection or primary site of
leukopenia due to infection.
immunosuppression. • A brain CT or MRI scan
• Causative organism can may show contrast
be cultured from the enhancement
blood in 40–90% of
meningitis

Clinical Neurology. Lange. 7th edition

 • Essential test in all cases of suspected meningitis = prompt
lumbar puncture & CSF examination.

• Gram-stained smears of CSF identify the causative organism in

70–80% of cases.
http://www.slremeducation.org/wp-content/uploads/2015/06/Chapter-171.-Meningitis-Encephalitis-and-Brain-Abscess.pdf
 Prevention
• Children should be routinely immunized against H. influenzae
by vaccination.
• A vaccine is also available for some strains of N. meningitidis
and is recommended for military recruits, college students,
and travelers to areas of ongoing epidemics.
• The risk of contracting H. influenzae or N. meningitidis
meningitis can be reduced in household & other close
contacts of affected patients
prophylactic administration of rifampin, 20 mg/kg/d orally,
– single daily dose for 4 days (H. influenzae)
– two divided doses for 2 days (N. meningitidis).

Clinical Neurology. Lange. 7th edition

Clinical Neurology. Lange. 7th edition
• Complications of bacterial
Complication &
meningitis:
– headache, seizures,
– hydrocephalus,
– syndrome of inappropriate secretion
of antidiuretic hormone (SIADH)
• A CT scan will confirm suspected
hydrocephalus and fluid and electrolyte
status should be carefully monitored to
detect SIADH.
– residual neurologic deficits (including
cognitive disturbances and cranial—
especially VIII—nerve abnormalities), • Factors that worsen prognosis
– death
– N. meningitidis infections may be
complicated by adrenal hemorrhage 
hypotension  death (Waterhouse–
Friderichsen syndrome).
Clinical Neurology. Lange. 7th edition
prognosis
• Morbidity and mortality from
bacterial meningitis are high.
• Fatalities occur in ~20% of
affected adults, more often with
some pathogens (e.g., S.
pneumoniae, gram-negative
bacilli) >> others (e.g., H.
influenzae, N. meningitidis).
include:
– extremes of age,
– delay in diagnosis and treatment,
– complicating illness,
– stupor or coma, seizures, and
focal neurologic signs.
 Aseptic
meningitis
• Aseptic meningitis
refers to a disorder
in which patients
have clinical and
laboratory
evidence of
meningeal
irritation with
negative results of
routine bacterial
cultures

http://www.slremeducation.org/wp-content/uploads/2015/06/Chapter-171.-Meningitis-Encephalitis-and-Brain-Abscess.pdf
 Viral Meningitis & Encephalitis
• Viral infections of the
meninges (meningitis)
• Brain parenchyma
(encephalitis)
• Often present as acute
confusional states.
• Children and young
adults are frequently
affected.
Clinical Neurology. Lange. 7th edition
• Viral meningitis most
often caused by enteric
viruses
• Viral encephalitis by
childhood exanthems,
arthropod borne
agents, HSV 1
Clinical Neurology. Lange. 7th edition
Clinical Neurology. Lange. 7th edition
Clinical Neurology. Lange. 7th edition
Clinical Neurology. Lange. 7th edition
 Pathophysiology

Viral infections can affect

the CNS in three ways:

Hematogenous
neuronal spread of the virus autoimmune postinfectious
dissemination of a systemic
by axonal transport (e.g., demyelination (e.g.,
viral infection (e.g.,
herpes simplex, rabies); varicella, influenza).
arthropod-borne viruses);

Clinical Neurology. Lange. 7th edition

 Clinical Findings
Clinical manifestations: Systemic viral infection may cause:
• skin rash, pharyngitis, lymphadenopathy,
• fever, headache, neck stiffness, pleuritis, carditis, jaundice,
photophobia, pain with eye organomegaly, diarrhea, or orchitis
movement, and mild impairment of • these findings may suggest a particular
consciousness. etiologic agent.
• Patients usually do not appear as ill
as those with bacterial meningitis.

Because viral encephalitis

When signs of meningeal
involves the brain directly
irritation and brain
 marked alterations of
dysfunction coexist, the
consciousness, seizures,
condition is termed
and focal neurologic signs
meningoencephalitis.
can occur.
Clinical Neurology. Lange. 7th edition
 Treatment
• Except for herpes simplex encephalitis, no specific therapy for
viral meningitis and encephalitis is available.
• Headache and fever can be treated with acetaminophen, but
aspirin should be avoided, especially in children and young
adults (association with Reye syndrome)
• Seizures usually respond to phenytoin or phenobarbital.
• Supportive measures in comatose patients = mechanical
ventilation and IV or NGT feeding.

Clinical Neurology. Lange. 7th edition

 Cerebral Malaria
• Malaria = by protozoan Plasmodium falciparum or other sp.transfereed by
human by female Anopheles mosquito
• Clinical features:
– Fever, chills, myalgia, nausea, vomiting, anemia, renal failure, hypoglycemia, pulmo
edema
• Plasmodia reach CNS in infected RBC  occlusion of cerebral capillaries 
neurologic involvement apparent wks after infection
• Cerebral malaria
– Acute confusional states
– Neurologic abnr
– Dx: plasmodia in RBC of Peripheral Blood smears
– CSF increased pressure, xanthochromia, mononuclear pleocytosis, mildly elevated
protein
• Severe P.falciparum malaria w/ coma (GCS <11); malaria + coma persist
>30 min after a seizure
• Cerebral malaria is not assc w/ signs of meningeal irritation but pts may be
opisthotonic

Clinical Neurology. Lange. 7th edition

Idro R. Pathogenesis, clinical features, and neurological outcomes of cerebral malaria. http://middleeast.thelancet.com/journals/laneur/article/PIIS1474-
4422(05)70247-7/fulltext
 Prophylaxis
Recommended for travelers to
areas endemic
• Chloroquine phosphate 500 mg
PO wkly
• 1-2 wks before travel, cont
until 4 wks after returning
Clinical Neurology. Lange. 7th edition
If exposure to chloroquine-
resistant strains expected, th/:
• Mefloquine 250 mg PO wkly for
4 wks
• Begin 1-2 wks before cont 4
wks after return
• Doxycycline 100 mg PO daily
• Begin 1-2 days before travel,
cont until 4 wks after return
• Atovaquone/proguanil 250/100
mg PO daily
• Begin 1-2 days before travel,
cont 1 wk after return
 Treatment
Chloroquine-sensitive cerebral malaria
• chloroquine, 10 mg base/kg by
continuous intravenous infusion over 8
hours  15 mg base/kg over 24 hours,
or
• 3.5 mg base/kg by the intramuscular or
• subcutaneous route every 6 hours to a
cumulative dose of 25 mg base/kg.
Clinical Neurology. Lange. 7th edition
Chloroquine-resistant cerebral malaria
• Quinidine, 10 mg base/kg IV infusion 1
hour followed by 0.02 mg base/kg/min,
or
• Quinine dihydrochloride 20 mg/kg IV
infusion 4 hours followed by 10 mg/kg
infused over 2–8 hours every 8 hours.
• Each of these regimens is continued
until oral therapy with chloroquine,
amodiaquine, or sulfadoxine and
pyrimethamine (for chloroquine-
sensitive malaria) or with mefloquine,
quinine, or quinidine (for chloroquine-
resistant malaria) can be substituted
 Tetanus
• disorder of neurotransmission associated with infection by
Clostridium tetani.
Organism
Gain access to
becomes
Skeletal muscle additional motor
established in a
nerves
wound

Toxin
Incubation
disseminated
Elaborate toxin period up to 3
through
wks
bloodstream

Motor nerve Trismus (lockjaw)

Transported
hyperactivity •Difficult swallowing
retrograde along •Spasm of facial muscles
(resting fire rate
motor nerves resembles contorted
alfa smile (risus sardonicus)

Interfere w/ release of Laryngospasm &

Painful muscular autonomic
Spinal cord or inhibitory
neurotransmitter spasms & rigidity instability = life-
brainstem (GABA) & disinhibit threatening
autonomic nerves • Opisthotonos
complications

Clinical Neurology. Lange. 7th edition

 Diagnosis
• Made on clinical grounds: presence of
continuous motor unit activity or absence of
the normal silent period in the masseter
muscle following elicitation of the jaw-jerk
reflex is a helpful electromyographic finding.
• Serum CK elevated + myoglobinuria may be
found

Clinical Neurology. Lange. 7th edition

 • Tetanus is preventable through immunization w/ TT
• Debridement of wounds = important preventive measure
• Open wound  + additional dose of TT if they have not received booster
dose w/in 10 yrs or if last booster dose >5 yrs ago & risk of infx w/ C.tetani
moderate  high

Moderate likehood of infx High – risk wound

• Wounds penetrate muscle • Acquired in barnyards
• Sustained on wood or pavement • Near sewers
• Human bites • Other source of waste material
• Nonabdominal bullet wounds • Abdominal bullet wounds

Moderate  high risk wounds = + tetanus Ig

(imunoglobulin)

Clinical Neurology. Lange. 7th edition

 Treatment
• Hospitalization in ICU  monitor respi & circulatory fx
• Tetanus Ig  neutralize toxin
• Penicillin or metronidazole  for infx itself
• Intrathecal administration of tetanus Ig assc w/ better clinical
progression > IM
• Diazepam 10-30 mg IV or IM every 4-6 hrs
• Chlorpromazine 25-50 mg IV or IM every 8 hrs = useful for th/
painful spasms & rigidity
• Baclofen has been used w/ intrathecal admn
• Neuromusc blockade w/ vecuronium or pancuronium req
when measures fail  ventilation (mechanical) must be used
Intrathecal: route of administration for drugs via an injection into the spinal
canal, or into the subarachnoid space so that it reaches the cerebrospinal fluid
Clinical Neurology. Lange. 7th edition (CSF)
 Tetanus Neonatorum
• Penyebab utama kematian neonatus
– Asfiksia
– Infeksi
• Tersering: sepsis & tetanus neonatorum (AK: >50%)
• Berhub dg aspek pelayanan kesehatan t/u pelayanan
persalinan (bersih & aman) khususnya perawatan tali
pusat
• Komplikasi yang ditakutkan: spasme otot diafragma
– BBLR

Pedoman pelayanan medis 2009. http://www.idai.or.id/downloads/PPM/Buku-PPM.pdf

 Diagnosis
Anamnesis PF
• Bayi sadar + spasme otot berulang
• Persalinan kurang higenis (t/u ditolong tenaga
non-medis tdk terlatih) • Mulut mencucu spt mulut ikan (carper
mouth)
• Perawatan tali pusat tdk higenis, +an zat pd
tali pusat • Trismus (mulut sukar dibuka)
• Bayi sadar, sering spasme/kaku, t/u bila • Perut teraba keras (perut papan)
terangsang/tersentuh • Opistotonus (ada sela punggung bayi dg alas
• Bayi malas minum saat ditidurkan)
• Tali pusat kotor & bau
• Anggota gerak spastik (boxing position)

PP
• Anamnesis + gejala cukup khas  tdk sering
perlu PP kecuali meragukan u/ membuat DD
• Px yg dpt dilakukan u/ bedakan tetanus
neonatorun & sepsis neonatal atau
meningitis:
• Pungsi lumbal
• Px darah rutin, preparat darah hapus atau
kultur dan sensitivitas

Pedoman pelayanan medis 2009. http://www.idai.or.id/downloads/PPM/Buku-PPM.pdf

 Tatalaksana
• Medikamentosa
– Pasang IV + cairan dosis rumatan
– + Diazepam 10mg/kg/hr IV 24 ham atau bolis IV tiap 3-6 jam (dosis
0,1-0,2 mg/kg/x pemberian)
• Max 40 mg/kg/hr
– Bila jalur IV tdk terpasang  pasang pipa lambung + diazepam mll
pipa atau rektum (dosis sama dg IV)
• Bila perlu + 10 mg/kg tiap 6 jam
– Bila freq nafas <30x/menit + tdk ada fasilitas tunjangan nafas
ventilator  hentikan obat meskipun bayi spasme
– Bila bayi henti nafas selama spasme atau sianosis sentral stlh spasme
 + O2 dg kecepatan aliran sedang  blm nafas  resusitasi  tdk
berhasil  rujuk ke RS dg NICU
– Stlh 5-7 hr dosis diazepam dikurangi bertahap 5-10 mg/hr via
orogastrik

Pedoman pelayanan medis 2009. http://www.idai.or.id/downloads/PPM/Buku-PPM.pdf

 Tatalaksana
Berikan Bayi Berikan ibu
• Human Tetanus Ig 500 U IM atau antitoxin • Imunisasi TT 0,5 mL
tetanus (equine serum) 5000 U IM
• Lakukan tes kulit terlebih dahulu TT 0,5 (lindungi ibu & bayi yg
mL IM pd tempat berbeda dg pemberian dikandung berikutnya)
antitoxin
• TT mgkn perlu ditunda hgg 4-6 mgg stlh • Minta datang kembali 1
(+) Tetanus Ig bulan kemudian u/ dosis
• Lini 1:
– Metronidazole 30 mg/kg/hr tiap 6 jam
kedua
(oral/parenteral) 7-10 hr atau
• Lini 2:
– Penisilin procain 100.000 U/kg IV dosis
tunggal 7-10 hr
– Jika hipersensitif thd penicillin  + tetra
50 mg/kg/hr (u/ >8th)

Pedoman pelayanan medis 2009. http://www.idai.or.id/downloads/PPM/Buku-PPM.pdf

 HIV/AIDS +/- complications
• AIDS is caused by infection with human immunodeficiency
virus type 1 (HIV-1)
• characterized by opportunistic infections, malignant
neoplasms (typically non-Hodgkin lymphoma or Kaposi
sarcoma), and a variety of neurologic disturbances.
• Transmission occurs through sexual activity or by transfer of
virus-contaminated blood or blood products.
• Individuals at particular risk of infection include those who
engage in unprotected sexual intercourse, intravenous drug
users who share needles, hemophiliacs who have received
factor VIII transfusions, and their sexual partners
• Neurologic complications of
HIV infection:
– Dementia
– Myelopathy
– Neuropathy
– Myopathy
– Stroke
• Patients with systemic HIV
infection are at increased
risk for direct HIV infection
of the nervous system, other
opportunistic infections, and
certain tumors
 Poliomyelitis
• Poliomyelitis is caused by wild poliovirus types 1, 2 and 3 or
by live vaccine derived poliovirus.
• Infection is established in the gastrointestinal tract.
• > 90% of infections are asymptomatic or involve non-specific
fever.
• Two phases of acute poliomyelitis can be distinguished:
– a nonspecific febrile illness (minor illness) followed, in a
small proportion of patients, by aseptic meningitis and/or
– paralytic disease (major illness).

VPD Surveillance Manual, 5th Edition, 2012

Poliomyelitis: Chapter 12-1
 the typical clinical
poliovirus exposure,
manifestations of
viral replication occurs poliomyelitis. Depending
cell destruction
in the oropharynx and on the site of infection &
the intestinal tract. paralysis
• Classified as:
• spinal,
Replication of • bulbar,
poliovirus in motor • spino-bulbar
Viremia neurons of the disease.
anterior horn and
brain stem

Progression to
virus attaches and maximum paralysis is
infection of central enters cells via a rapid (2– 4 days)
nervous system cells. specific poliovirus
• usually associated with
receptor. fever and muscle pain
• rarely progresses after
the temperature has
returned to normal.

VPD Surveillance Manual, 5th Edition, 2012

Poliomyelitis: Chapter 12-1
 • Spinal paralysis is typically asymmetric:
– severe proximally>>>distally
– deep tendon reflexes are absent or diminished.
– Bulbar paralysis may compromise respiration and
swallowing
• Infection with poliovirus results in lifelong, type
specific immunity.
• Following the acute episode, many patients
recover muscle functions at least partially, and
prognosis for recovery can usually be established
within six months after onset of paralytic
manifestations.

VPD Surveillance Manual, 5th Edition, 2012

Poliomyelitis: Chapter 12-1
 Diagnoses
• Laboratory confirmation requires isolation of poliovirus or
detection of poliovirus nucleic acid from a clinical specimen.
• Collect two faecal specimens at least 24 hours apart, 0–14
days after the onset of paralysis and send to the national
poliovirus reference laboratory (address below),
• Throat swab and cerebrospinal fluid samples may also be
collected if clinically indicated.

Communicable Disease Control Manual – Poliomyelitis May 2012.https://www.health.govt.nz/system/files/documents/publications/cd-manual-

poliomyelitis-may2012.pdf
 MANAGEMENT OF CONTACTS
• Laboratory investigation is needed for all household contacts
and for close social contacts who are in any of the following
situations:
– are under 12 years of age
– are at high risk of transmitting infection (for example, food handlers)
– work with susceptible groups (for example, young children,
immunocompromised, elderly).
Laboratory investigation of other contacts is not necessary

Th/: Conservative
Prophylaxis:
• it is recommended that unimmunised contacts be immunised
with IPV (inactivated polio vaccine)
Communicable Disease Control Manual – Poliomyelitis May 2012.https://www.health.govt.nz/system/files/documents/publications/cd-manual-
poliomyelitis-may2012.pdf
 Rabies
• Endemic in most African and
Asian countries
• Fatal zoonotic viral disease
• Transmitted to humans through
contact (mainly bites and
scratches) with infected animals,
both domestic and wild.
• There is no specific treatment for
rabies, which is a fatal disease.
(Supportive treatment alone has
been successful in one recently-
reported confirmed case of
human rabies in US)
http://www.who.int/rabies/epidemiology/Rabiessurveillance.pdf
• WHO promotes human rabies
prevention through:
– postexposure treatment: vaccine
types, antirabies
immunoglobulin;
– pre-exposure prophylaxis:
vaccine types for certain
professional groups at higher risk
and also if vaccines are easily
accessible, of children aged
under 15 in areas where rabies is
hyperendemic; increased access
of safe and effective rabies
vaccines.
– Dog rabies elimination through
mass vaccination of dogs and
dog-population management.
 • Causal agent: Lyssaviruses of the Rhabdoviridae
family.
• Main modes of transmission:
– Hosts are usually Canidae
• dogs (responsible for more than 99% of all human deaths from
rabies), foxes, coyotes, wolves and jackals;
• also cats, skunks, raccoons, mongooses, bats and other biting
animals.
– A bite or a scratch introduces virus-laden saliva from a
rabid animal.
– The incubation period ranges from a few days to several
years (most commonly 3-8 weeks).

http://www.who.int/rabies/epidemiology/Rabiessurveillance.pdf
 • Clinical description
– Paresis or paralysis, delirium, convulsions.
– Without medical attention, death in about 6 days, usually
caused by respiratory paralysis.
• Clinical case definition
– a person presenting with an acute neurological syndrome
(encephalitis) dominated by forms of hyperactivity (furious
rabies) or
– paralytic syndromes (dumb rabies) progressing towards
coma and death, usually by respiratory failure, within 7-10
days after the first symptom if no intensive care is
instituted.

http://www.who.int/rabies/epidemiology/Rabiessurveillance.pdf
• Dx: One or more of the following:
– Detection of rabies viral antigens
by direct fluorescent antibody
test (FAT) or by ELISA in clinical
specimens, preferably brain tissue
(collected post mortem).
– Detection by FAT on skin biopsy
(ante mortem).
– Detectable rabies-neutralizing
antibody titre in the serum or the
CSF of an unvaccinated person.
– Detection of viral nucleic acids by
PCR on tissue collected post
mortem or intra vitam in a clinical
specimen (brain tissue or skin,
cornea, urine or saliva).
http://www.bmj.com/content/350/bmj.g7827

http://www.who.int/rabies/epidemiology/Rabiessurveillance.pdf
Kejang demam

LO 3
 • Kejang demam = bangkitan kejang yang terjadi pada
kenaikan suhu tubuh (suhu rektal di atas 380C) yang
disebabkan oleh suatu proses ekstrakranium
• Tjd pd 2-4% anak usia 6 bln – 5 thn
• Tidak termasuk kejang demam:
– Anak pernah kejang tanpa demam kmdn kejang demam
kembali
– Kejang + demam pd bayi <1 bln
– Anak <6 bln atau > 5 tahun kejang didahului demam =
pikirkan infx SSP atau epilepsi kebetulan + demam

Konsensus Penatalaksanaan Kejang Demam IDAI 2006

http://www.idai.or.id/wp-content/uploads/2013/02/Kejang-Demam-Neurology-2012.pdf
 Klasifikasi Kejang Demam
Kejang demam sederhana Kejang demam kompleks
(Simple febrile seizures) (Complex febrile seizures)
• Berlgsg singkat • Lama
• <15 menit • >15 menit
• Berhenti sendiri
• Fokal atau parsial 1 sisi atau
• Tonik dan atau klonik tanpa
gerakan fokal kejang umum didahului
• Tdk berulang dlm wkt 24 jam parsial
• 80% seluruh kejang demam • Berulang >1x dlm 24 jam
• Kejang lama = kejang >15 menit atau kejang berulang >2x dan antara bangkitan kejang
anak tdk sadar (8% kejang demam)
• Kejang fokal = kejang parsial satu sisi atau kejang umum didahului parsial
• Kejang berulang = kejang 2x/>> dlm 1 hr, antara 2 bangkitan kejang anak sadar. (16%
kejang demam)
Konsensus Penatalaksanaan Kejang Demam IDAI 2006
http://www.idai.or.id/wp-content/uploads/2013/02/Kejang-Demam-Neurology-2012.pdf
 Patofisiologi: Etiologi
• Most febrile illnesses associated with febrile seizures
are due to common infections such as tonsillitis,
upper respiratory infections, and otitis media.
• Children of preschool age are subject to frequent
infections and accompanying high fevers, which in
combination with a relatively low seizure threshold,
allows for the common occurrence of febrile
seizures.

Debora Hirtz. Febrile Seizures. Available from: http://pedsinreview.aappublications.org/content/18/1/5

 Pemeriksaan penunjang
Pungsi Lumbal
Lab • Px CSF u/ menegakkan atau menyingkirkan
• Tdk rutin pd KD kemungkinan meningitis
• Bs untuk evaluasi sumber infx pybb demam • Risiko tjd meningitis bakterialis 0,6-6,7%
atau keadaan lain (mis:gastroenteritis
• Bayi kecil sering sulit menegakkan/menyingkirkan dx
dehidrasi + demam)
meningitis krn manifestasi klinis tdk jelas
• Dpt dikerjakan:
• Darah perifer • Krn itu pungsi dianjurkan untuk:
• Elektrolit • Bayi <12 bln sngt dianjurkan
• Gula darah • Antara 12-18 bln dianjurkan
• >18 bln tdk rutin
• Bila yakin bukan meningitis tdk perlu

Pencitraan
EEG
• X-Ray kepala & CT scan atau MRI
• Tdk dpt prediksi berulang kejang atau jarang dikerjakan, tdk rutin
perkiraan kemungkinan epilepsi ps KD • Indikasi:
• Tdk direkomendasikan • Kelainan neurologik fokal menetap
• Dilakukan pd keadaan KD tdk khas: KD (hemiparesis)
kompleks usia > 6 thn, KD fokal • Paresis nervus VI
• Papiledema
Konsensus Penatalaksanaan Kejang Demam IDAI 2006
http://www.idai.or.id/wp-content/uploads/2013/02/Kejang-Demam-Neurology-2012.pdf
 Prognosis
Kemungkinan kecacatan atau
kelainan neurologis Kemungkinan kematian
• Pada sebagian kecil kasus, • Tdk pernah dilaporkan
dan kelainan ini biasanya
terjadi pada kasus dengan
kejang lama atau kejang
berulang baik umum atau
fokal.

Konsensus Penatalaksanaan Kejang Demam IDAI 2006

http://www.idai.or.id/wp-content/uploads/2013/02/Kejang-Demam-Neurology-2012.pdf
 Kemungkinan berulang KD
• Faktor risiko berulangnya kejang
demam adalah :
– Riwayat kejang demam dalam
keluarga
– Usia <12 bln
– Temperatur yang rendah saat kejang
– Cepatnya kejang setelah demam
• Bila seluruh faktor di atas ada,
kemungkinan berulangnya kejang
demam adalah 80%
• Bila tidak terdapat faktor tersebut
kemungkinan berulangnya kejang
demam hanya 10%-15%.
• Kemungkinan berulangnya kejang
demam paling besar pada tahun
pertama.
Konsensus Penatalaksanaan Kejang Demam IDAI 2006
http://www.idai.or.id/wp-content/uploads/2013/02/Kejang-Demam-Neurology-2012.pdf
Faktor risiko tjdnya epilepsi
Faktor risiko menjadi epilepsi adalah
:
• Kelainan neurologis atau
perkembangan yang jelas
sebelum kejang demam pertama.
• Kejang demam kompleks
• Riwayat epilepsi pada orang tua
atau saudara kandung
Masing-masing faktor risiko
meningkatkan kemungkinan kejadian
epilepsi sampai 4%-6%, kombinasi
dari faktor risiko tersebut
meningkatkan kemungkinan epilepsi
menjadi 10%- 49%
Kemungkinan menjadi epilepsi tidak
dapat dicegah dengan pemberian
obat rumat pada kejang demam
 Penatalaksanaan saat kejang
• Datang dalam keadaan • Obat yang praktis dan
kejang obat yang paling dapat diberikan oleh
cepat untuk orang tua atau di rumah
menghentikan kejang = = diazepam rektal
diazepam IV – 0,5-0,75 mg/kg
– 0,3-0,5 mg/kg perlahan- – diazepam rektal 5 mg
lahan; kecepatan 1-2 untuk anak BB < 10 kg
mg/menit atau 3-5 – 10 mg untuk BB >10 kg
menit
– 5 mg u/ anak <3 tahun
– dosis maksimal 20 mg.
– 7,5 mg u/ anak >3 tahun

Konsensus Penatalaksanaan Kejang Demam IDAI 2006

http://www.idai.or.id/wp-content/uploads/2013/02/Kejang-Demam-Neurology-2012.pdf
 Bila setelah pemberian
diazepam rektal kejang belum
berhenti,
dapat diulang lagi dengan cara
dan dosis yang sama dengan
interval waktu 5 menit.

setelah 2 kali pemberian diazepam

rektal masih tetap kejang,
dianjurkan ke rumah sakit. Di
rumah sakit dapat diberikan
diazepam intravena dengan dosis
0,3-0,5 mg/kg.

Bila kejang telah berhenti,

pemberian obat
selanjutnya tergantung
dari jenis kejang demam
apakah kejang demam
sederhana
Konsensus Penatalaksanaan Kejang Demam IDAI 2006 atau kompleks dan faktor
http://www.idai.or.id/wp-content/uploads/2013/02/Kejang-Demam-Neurology-2012.pdf risikonya.
 Pemberian obat pada saat demam

Konsensus Penatalaksanaan Kejang Demam IDAI 2006

http://www.idai.or.id/wp-content/uploads/2013/02/Kejang-Demam-Neurology-2012.pdf
Pemberian obat rumat

Konsensus
Penatalaksanaan
Kejang Demam IDAI
2006
http://www.idai.or.id/
wp-
content/uploads/2013
/02/Kejang-Demam-
Neurology-2012.pdf
 Edukasi Orang tua
• Kejang selalu merupakan peristiwa yang menakutkan bagi orang tua.
• Pada saat kejang sebagian besar orang tua beranggapan bahwa anaknya
telah meninggal. Kecemasan ini harus dikurangi dengan cara yang
diantaranya:
– Menyakinkan bahwa kejang demam umumnya mempunyai prognosis
baik.
– Memberitahukan cara penanganan kejang
– Memberikan informasi mengenai kemungkinan kejang kembali
– Pemberian obat untuk mencegah rekurensi memang efektif tetapi
harus diingat adanya efek samping

Konsensus Penatalaksanaan Kejang Demam IDAI 2006

http://www.idai.or.id/wp-content/uploads/2013/02/Kejang-Demam-Neurology-2012.pdf
 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

Konsensus Penatalaksanaan Kejang Demam IDAI 2006

http://www.idai.or.id/wp-content/uploads/2013/02/Kejang-Demam-Neurology-2012.pdf
 Vaksinasi
• Tdk ada KI u/ vaksin pd anak KD
• Kejang stlh demam krn vaksinasi sgt jarang
• +diazepam oral atau rektal bila anak demam,
t/u stlh vaksin DPT atau MMR
• Bbrp merekomendasikan Parasetamol pd saat
vaksinasi hgg 3 hr kemudian

Konsensus Penatalaksanaan Kejang Demam IDAI 2006

http://www.idai.or.id/wp-content/uploads/2013/02/Kejang-Demam-Neurology-2012.pdf
Epilepsi & Status epilepticus

LO 4
 • Epilepsy is a condition in which persisting
cerebral dysfunction causes recurring epileptic
seizures w/out need for immediate insult to
provoke each seizure
• Epilepsy is a disorder characterized by two or
more unprovoked seizures occurring more
than 24 hours apart.
SEIZURE IS THE EVENT, EPILEPSY IS THE DISEASE
WITH RECURRING SEIZURES
• Exacerbants increase seizure freq in epilepsy
– Sleep deprivation
Robert S. Fisher, MD, PhD. The Definition of epilepsy. Available from: http://www.ilae.org/Visitors/Centre/Definition_Class.cfm
 • Epilepsy is now considered to be resolved*
for individuals who:
– had an age-dependent epilepsy syndrome but are
now past the applicable age OR
– who have remained seizure-free for the last 10
years, with no seizure medicines for the last 5
years.

* “Resolved” has the connotation of “no longer present,” but it

does not guarantee that epilepsy will never come back

Robert S. Fisher, MD, PhD. The Definition of epilepsy. Available from: http://www.ilae.org/Visitors/Centre/Definition_Class.cfm
 Acute Symptomatic Epilepsy
• Acute symptomatic seizures are events, occurring in
close temporal relationship with an acute CNS insult
• May be metabolic, toxic, structural, infectious, or due
to inflammation.
• The interval between the insult and seizure may vary
due to the underlying clinical condition.
• Acute symptomatic seizures have also been called:
• Reactive seizures
• Provoked seizures
• Situation-related seizures

Robert S. Fisher, MD, PhD. The Definition of epilepsy. Available from: http://www.ilae.org/Visitors/Centre/Definition_Class.cfm
 Framework for classification of the epilepsies.

Assumes that the clinician has already made a definite diagnosis of

an epileptic seizure and is not meant to be a diagnostic algorithm
to distinguish epileptic from nonepileptic events.

ILAE classification of the epilepsies: Position paper of the ILAE Commission for Classification and Terminology. Available from:
http://onlinelibrary.wiley.com/doi/10.1111/epi.13709/full
 Etiology of Epilepsy
• Abnr visible on structural neuroimaging
Structural • Acquired: stroke, trauma, infection, hypoxic ischemic encephalopathy
• Genetic: malformation of cortical dev

• Mutation in K+ channel genes KCNQ2,/3 in Benign familial neonatal

epilepsy
Genetic • Juvenile myoclonic or childhood absence epilepsy
• Mutation in SCN1A gene (Na+ channel)
• Most common etiology worldwide
• Common examples: neurocysticercosis, TB, HIV, cerebral malaria,
Infectious cerebral toxoplasmosis, congenital infections (CMV)
• May also refer to postinfx dev of epilepsi: viral encephalitis  seizures
• Known or presumed met disorder in which seizures are core symptom
• E.g: porphyria, uremia, aminoacidopathies, pyridoxine dependent
Metabolic seizures
• It is likely that most metabolic epilepsies have a genetic bases, some are
acquired such as cerebral folate deificiency
• Results directly from immune disorder in which seizure are a core
Immune symptom
• Autoimmune-mediated CNS inflammation

Unknown
ILAE classification of the epilepsies: Position paper of the ILAE Commission for Classification and Terminology. Available from:
http://onlinelibrary.wiley.com/doi/10.1111/epi.13709/full
 Types of Epilepsies
Combined
Generalized Epilepsy Focal Epilepsies: Generalized and “Unknown”
Focal Epilepsies
• Generalized spike- • Unifocal & • Patients have both • patient has
wave activity on multifocal generalized and Epilepsy but the
EEG. disorders as well as focal seizures. clinician is unable
• May have a range seizures involving • The interictal EEG to determine if the
of seizure types: one hemisphere. show both Epilepsy Type is
absence, • A range of seizure generalized spike- focal or generalized
myoclonic, atonic, types can be seen: wave & focal because there is
tonic, and tonic– • focal aware epileptiform insufficient
clonic seizures. seizures, discharges, information
• Epileptiform available.
• focal impaired
awareness activity is not • This may be for a
seizures, required for the variety of reasons:
• focal motor diagnosis. • no access to EEG
seizures, • Common examples • EEG studies may
• focal non-motor in which both types have been
seizures, of seizures occur = uninformative,
• Dravet syndrome for example,
• focal to bilateral
• Lennox-Gastaut normal.
tonic–clonic
seizures. syndrome.

ILAE classification of the epilepsies: Position paper of the ILAE Commission for Classification and Terminology. Available from:
http://onlinelibrary.wiley.com/doi/10.1111/epi.13709/full
 Epilepsy syndrome
• Cluster of features incorporating seizure types,
EEG, imaging features that tend to occur
together
• It may also have distinctive comorbids:
– Intellectual & psychriatric dysfx + specific EEG &
imaging findings

ILAE classification of the epilepsies: Position paper of the ILAE Commission for Classification and Terminology. Available from:
http://onlinelibrary.wiley.com/doi/10.1111/epi.13709/full
http://www.educatehealth.ca/physician/neurology/epilepsy-and-seizures/epilepsy-(seizure-disorder)-overview.aspx
http://www.educatehealth.ca/physician/neurology/epilepsy-and-seizures/epilepsy-(seizure-disorder)-overview.aspx
Epilepsy, A manual for Medical and Clinical Officers in Africa. WHO Geneva 2002. http://www.who.int/mental_health/media/en/639.pdf?ua=1
The Atkins diet & Ketogenic diet for epilepsy
MNT in Epilepsy
Atkins & KD: combat obesity

The ketogenic diet comprises of 80% fat, 15%

protein and 5% carbohydrate,

Atkins diet comprises of 60% fat, 30% protein

and 10% carbohydrate.

Published reports on the efficacy of Atkins

diet says that 45% of patients taking Atkins
diet have seizure reduction upto 50-90% and
28% patients have seizure reduction >90%
which is very much similar to that of
traditional ketogenic diet.

The Atkins diet have additional benefit of

being effective in both children as well as
adults and patients are more comfortable
with Atkins diet as compared to the
restrictions of KD Mechanism of anticonvulsant effect of Poly Unsaturated Fatty Acids (PUFAs).

https://www.researchgate.net/publication/259783835_Nutritional_therapy_for_epilepsy
• GABA = Gamma aminobutyric acid
– Primary inhibitory neurotransmitter in brain
– GABA + GABAergic rec on cell membranes of neurons 
hyperpolarize; unable to fire rapid sequential action
potentials (inh neuronal hyperexcitability)
– Deficiencies in the receptors  dev epilepsy
• The mitochondria
– during trauma or prolonged epileptic seizure the
production of ROS can overwhelm the endogenous
antioxidant defense systems  cause damage to lipids,
proteins, and DNA resulting in cellular dysfunction and
subsequent neuronal loss (Suggesting that oxidative
damage is the result of prolonged seizure activity)
 Diagnostic of Seizure & Epilepsy
• The diagnosis of seizures is based on
clinical recognition of one of the
seizure types
• The EEG can be a helpful
confirmatory test in distinguishing
seizures from other causes of loss of
consciousness
• However, a normal or nonspecifically
abnormal EEG never excludes the
diagnosis of seizures.
• Specific EEG features that suggest
epilepsy
Metabolic and toxic disorders should be
– E.g. abnormal spikes, polyspike excluded  do not require anticonvulsants.
discharges, and spike-wave
complexes

http://ww.w.turner-white.com/pdf/brm_EPI_V1P1.pdf
Katzung Trevors Pharmacology examination and board review 10th ed
Katzung Trevors Pharmacology examination and board review 10th ed
Katzung Trevors Pharmacology examination and board review 10th ed
 Status Epilepticus
• Condition characterized by an epileptic seizure prolonged or
repeated at sufficiently brief intervals so as to produce an
unvarying & enduring epileptic condition
• Seizure duration 30 min
– Rationale behing the definition: irreversible neuronal injury occur after
30 min ongoing seizure activity
• Condition results either from:
– failure of mechanism for seizure termination
– initiation of mechanism leading to abnr prolonged seizures
• Long term consequence: neuronal death, injury, alter
neuronal networks; carries a risk of serious neurologic
sequelae ("epileptic encephalopathy")

A definition and classification of status epilepticus . http://onlinelibrary.wiley.com/doi/10.1111/epi.13121/full

A definition and classification of status epilepticus . http://onlinelibrary.wiley.com/doi/10.1111/epi.13121/full
 Approach to The Treatment of SE in adults
Initial assessment
• Ensure adeq ventilation, Oxygenation, BP Immediate Initiation or reloading
• Intubate if necessary (based on low O2 suppression of w/ anticonvulsant
saturation & labored breathing) convulsions • Phenytoin 15-20 mg/kg
• Insert IV line
• Lorazepam or IV at 25-50 mg/min in
• + glucose & tiamine (in appropriate
circumstances) diazepam 2-4 mg/min normal saline or
• Send toxic screen IV (total dose 10-15 • Fosphenytoin 50-75
• Assess quickly for cranial & cervical injury if mg) + BP monitor when mg/min
onset of seizures unwitnessed higher rate/dose used

Further th/ if convulsion or electrographic seizures persist

after sev hours General anesthetic
• + valproate or phenobarbital 10 mg/min to total dose 20 mg/kg as
doses of meds for
additional anticonvulsant IV or persistent SE
• Carbamazepin or levetiracetam by NGT if gastric & bowel Activiry (+) • Midazolam 0.2 mg/kg
• Consider neuromusc paralysis w/ EEG monitoring if convulsion loading + infusion 0.1-
persist 0.4 mg/kg/hr or
• Phenobarbital 10 mg/kg/hr
• Propofol 2 mg/kg/hr
• Inhalation anesthetics (isoflurane)

Adams and Victors Principles of Neurology