1
Central Nervous
System Infection
(Infeksi
Susunan Saraf Pusat)
2
FOREWORD
• Central Nervous System Infections is a
serious Illness
• Late diagnosis and proper
Management leads to death or serious
disabilities
• Early diagnosis and treatment is
important
3
• CNS Infection may involve :
• The leptomeninges and CSF
space (meningitis)
• The gray and white matter of the
brain (encephalitis)
• The spinal cord (myelitis)
4
• Focus of bacterial infection of the brain
brain abcess or cerebritis in early stage
before a frank abcess is formed
• Pus located betwen the duramater and
the arachnoid membrane subdural
empyema
• Pus outside the dura is called an epidural
abcess.
5
Route Infection :
• Open Wound around cephalic
• Direct contiguous infection from otitis media,
sinus-sinus paranasal, skin infection around
cephalic and face.
• Septisemia/ bakteriemia
• Abses cerebri.
• Retrograde infection along nerve.
• Direct infection to CSF by non steril
lumbal punction.
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• Course :
• Acute :
• Purulent meningitis
Subacute :
• CNS listeriosis •Cerebral abcess
•Focal encephalitis
• Herpes simplex encephalitis
•Neuroborreliosis
•Neurosyphillis
•Tuberculous meningitis
•Actinomycosis
Chronic
•Nocardiosis
•Tuberculous meningitis
•Ricketsiosis
•Neuroborreliosis
•Neurobrucellosis
•Neurosyphillis
•Whipple encephalitis
•Creutzfeldt-Jacob disease
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DIAGNOSIS OF
MENINGO-ENCEPHALITIS
1. Presence of symptoms of an infection / fever
2. Presence of signs and symptoms of Central Nervous
System abnormalities:
• Lowering of consciousness
• Confusion
• Convulsions
• Neurological deficits
8
GENERAL LABORATORY
EXAMINATION
• Blood Leukocyte and differential
count
• Blood test for micro-organism :
• culture / staining
• serological
• staining
• PCR
9
TWO MOST IMPORTANT
EXAMINATION IN DIAGNOSIS
1. Cerebrospinal fluid (CSF) examinations
• Cell count / Differential cell count
• Glucose content, Protein quantitative
• Staining and Culture
• Serological test
• Polymerase Chain Reactions (PCR)
• CSF pressure, Color / Turbidity
• Qualitative protein test : Nonne / Pandy
2. Neuro-Imaging :
• CT-Scan
• MRI
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CSF EXAMINATION
In Viral infections:
• Cell count, Protein and Glucose content are not so
prominently altered.
In Bacterial and Fungal /Parasitic Meningitis:
• Cell count, protein content are much more
pronouncedly alleviated, and glucose content
lowered.
11
CSF ABNORMALITIES
Bacterial Serous Viral Meningitis/
Meningitis Meningitis Encephalitis
Appearance Purulent Turbid/Xanth Clear
Cell > 10,000 < 500 < 100
Diff count PMN >> MN >> MN >
Protein
Glucose -0 N
12
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POLYMERASE CHAIN
REACTION
Advantage:
Rapid diagnosis for certain diseases:
• Tb Meningitis
• Herpes Simplex encephalitis
Disadvantage:
• Not readily available.
• For certain specimen, contamination
is high
LUMBAR PUNCTURE
• Contraindications
• Infection in overlying skin
• Signs of intracranial mass lesion/ papil edema
• If an intracranial mass/hydrocephalus is suspected.
• NEURO IMAGING is indicated, before CSF examination
• Relative
• Coagulopathy
• Thrombocytopenia
• If delay is anticipated obtain blood cultures and GIVE
antibiotics
• You have 2 hours after ATB given before sensitivity is
effected
17
PLAIN X-RAY
• Indirectly to look for focus of Infections
• Chest x-ray is a must : present of pulmonary
infections
• Skull x-ray to look for focal infarction:
Mastioditis , Para nasal sinus infections ,
periodontal infection.
• In suspected Cysticercosis , calcified cyst in
the muscle.
18
NEURO -IMAGING
CT-Scan should be done with contrast
• In Brain Abscess - hyperintense ring
enhancement
• Intracranial mass lesions due to
Toxoplasmosis, Fungal infections,
cysticercosis
• In Tuberculous meningitis, hyperintense
visualization of the subarachnoidal
space will be seen
19
WHAT CAN BE SEEN IN NEURO-
IMAGING IN CNS INFECTIONS
• Presence of intra-cranial mass lesions
• Brain infarction of due to vasculitis ,or
hemorrhage due to vascular damage
• Hyper intensity of the CSF in Tb Meningitis
• Hydrocephalus due to CSF blockades
• Brain edema like in Herpes Encephalitis
20
OTHER LESIONS
• In congenital Toxoplasmosis, multiple
calcifications / hyperintense lesion
can be seen
• In Herpes simplex, hypo intense lesions
due to edema can be seen in the
temporal and frontal areas.
21
MAGNETIC RESONANCE
IMAGING
Advantage:
• More sensitive for certain lesions
• Can detect abnormalities in more earlier stage
than CT-Scan
Disadvantage:
• Good apparatus are more expensive
• Takes more time for examinations, difficult in
delirious patients
22
ETIOLOGY OF CNS
INFECTIONS
• In case of suspected CNS Infections, we
have to differentiate between:
• Bacterial : Specific /non-specific
• Parasites : Malaria / Toxoplasma
• Fungal : Cryptococcus/Aspergillus's
• Viral : Japanese Encephalitis HIV, Herpes
• Prion Disease : TSE , CJD
• Look for the possibility of MIXED infections
23
SPECIAL TO LOOK FOR
• Tuberculosis
• HIV / AIDS
• AIDS related opportunistic infections:
• Toxoplasma , Cryptococcus.
• Cysticercosis in endemic areas
• Malaria
• Typhoid
• New diseases ( Nipah E. , SARS )
24
CLINICAL SIGN AND
SYMPTOMS
• Neurological Deficits
• Sign of Increased Intracranial Pressure:
• Papil edema
• Severe headache
• With or without fever
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CLINICAL PRESENTATION
• Acute Meningo-Encephalitis
• Intracranial tumor Like : Brain abscess,
tuberculoma,Toxoplasma etc.
• First sign as Epilepsy : Cystecercosis
• Degenerative disease Like : SSPE,TSE
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CLINICAL PRESENTATION
OF INFECTIVE AGENTS
• Meningitis: Bacterial / viral / fungal
• Encephalitis: Viral
• Brain abscess: Bacterial, fungal, parasitic
• Sinus thrombosis: Bacterial
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HISTORY TAKING
• When does signs and symptoms begins
• History of past illnesses ( HIV , Tuberculosis )
• Economic status and occupation
• Habit : i.v. drug use ?
• Coming /traveling from Endemic areas ?
• Any recent outbreak of human or animal desease? (
West Nile , Nipah )
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PHYSICAL EXAMINATION,
NEUROLOGICAL
• Any sign of Infections ? Fever ,with headache, muscle
pain ?
• Lowering of Consciousness
• Alteration of Consciousness
• Cranial nerve palsies
• Neck stiffness/ meningeal signs
• Limb paralysis / hemiplegia
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PHYSICAL EXAMINATION,
INTERNAL
• Skin abnormalities , exanthema , bleedings.
• Body temperature ? Fever ?
• Vital signs ; Blood pressure ,pulse, respiration,
• Respiratory abnormalities : Dyspnoeic ?
• Abdomen : tenderness , stiffness . Liver /spleen
palpable ?
VIRAL MENINGITIS
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INFEKSI VIRAL
• Tergantung pada :
• Jumlah virus & virulensinya
• Daya tahan tubuh yang rendah seperti :
• Penyakit kronik
• Gangguan imunologik
• Reaksi alergi
• Demam, obat-obatan
• Radioterapi
• Adanya kerusakan ginjal, paru, hepar, jantung &
susunan eritropoetik
VIRAL MENIGITIS
• 85% secondary to
• Echo-
• Coxsackie
• Entero-
• Also consider HSV, and EBV
• Neutrophils may predominate in the CSF in the first 24
hours
• Consider starting ATB’s until cultures come back (-)
INFEKSI VIRAL
33
MENINGITIS VIRAL
Bersifat benigne , gejalanya kadang sangat ringan
Pada keadaan berat memberikan gejala:
• Sakit kepala
• Kaku kuduk
• LP : Pleiositosis limfositer . liquor jernih
• Penyebab : paling sering dari kelompok enterovirus :
• V. poliomyelitis
• V. coxsakie
• V. ECHO (Entero Cytophatic Human Orphan)
• Penetrasi melalui lintasan oral fecal / droplet spray
MENINGITIS
VIRAL 34
V. Coxsakie dikenal :
• Kelompok A :
• Menyebabkan meningitis
• Eksantema bersifat rubeliform dengan herpangina di
tangan, kaki, mulut
• Kelompok B
• Menyebabkan meningitis disertai keletihan otot hingga
paralysis.
• Rhinitis, laryngitis, bronchitis.
• Eksantema tidak dijumpai.
MENINGITIS
VIRAL 35
V. ECHO :
• Tersebar diseluruh dunia
• Lebih sering pada anak
• Anak sering rewel/ cengeng
• Sering timbul gejala eksantema yang lebih
menonjol
• Sakit kepala
• Muntah, nyeri otot anggota gerak
• ± 24 jam timbul bercak bercak merah mulai
dari muka hingga ke badan.
• Kaku kuduk & nyeri
EMPERIC ANTIVIRALS
• Concern of herpes
• Acyclovir 10mg/kg IV Q 8 hours
VIRAL
ENCEPHALITIS
VIRAL ENCEPHALITIS
• Infection of brain parenchyma
• Presents of neurological
abnormalities distinguish it from
meningitis
EPIDEMIOLOGY
• Incidence is 1/10 of bacterial meningitis
• HSV-1, zoster, EBV,CMV, rabies, arbo
• Arbo
• LAC (La Crosse)-diagnosed most frequently
• SEE(St Louis)-20% mortality in elderly
• WEE(Western)- causes seizures in 90% of infected
infants, permanent neuro deficits in 50%
• EEE(Eastern)- most devastating, mortality 70%
• WNV(West Nile)
ENSEPHALITIS VIRAL
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Virus DNA: ETIOLOGI
• Poxviridae : Poxvirus
• Herpetoviridae : Virus Herpes simpleks, Varicella Zoster,
dan Virus sitomegalik
• Virus RNA
• Paramiksoviridae : Virus parotitis, virus morbili
(rubeola).
• Picornaviridae : Enterovirus, Virus poliomielitis, Echovirus,
Coxsackie A, Coxsackie B.
• Rhabdoviridae : Virus rabies.
• Togaviridae : Virus ensevalitis alpha, Flavivirus ensefalitis
Jepang B, Virus demam kuning, Virus rubi.
• Bunyaviridae : Virus ensefalitis california.
• Arenaviridae : Khoromeningitis Limfositaria.
• Retroviridae : Virus HIV
PATHOPHYSIOLOGY
• Portals of entry
• Arbo-transmitted by mosquitoes, ticks
• Rabies-bite by infected animal
• Hematogenous dissemination v. travel backwards on
axons (HSV,HZV,rabies)
• Dysfunction & damage caused by disruption of neural
cell function & inflammation
PATHOPHYSIOLOGY
CONT.
• Gray matter predominately affected
• Cognitive/psychiatric signs, lethargy,
seizures
• White matter affected in post-infectious
encephalomyelitis
CLINICAL FEATURES
• New psych symptoms
• Cognitive deficit (aphasia, amnesia,
confusion)
• Seizure
• Movement d/o
DIAGNOSIS
• MRI-more sensitive than CT
• CT Scan
• EEG
• LP-findings consistent with aseptic
meningitis
DIFFERENTIAL
• Exclude the killers
• Bacterial meningitis & SAH
• More meningeal symptoms
• Lyme, TB, fungal, bacterial, viral, neoplastic
• More parenchymal symptoms
• Abscess, bacterial endocarditis, post-infectious
encephalomyelitis, toxic or metabolic encephalopathy
TREATMENT
• HSV: acyclovir 10mg/kg IV
• CMV: ganciclovir
• Rabies/EEE/HSVdevastating & usually
fatal or residual deficits
BACTERIAL
MENINGITIS
EPIDEMIOLOGY
• 400 per 100,000 in neonates
• 1-2 per 100,000 in adults
• S pneumoniae & N meningitidis m/c
• HIB vaccine has been very effective
• Mortality
• 5% in children beyond infancy
• 25% in neonates and in adults
PATHOPHYSIOLOGY
• S. pneumonia and N. meningitidis (and H.
influenzae) are encapsulated which
provides them with increased ability to
invade BBB
• Upper airway bloodstream
subarachnoid space subcapsular
constituents trigger inflammation fever,
meningimus, change in MS
brain/meningeal edema decreased CSF
drainage hydrocephalus increased
ICP ICP>CPP
50
CLINICAL FEATURES
• 25% of adult cases “classic”
• Rapid development of
• Fever
• Headache
• Stiff neck
• Photophobia
• Nonspecific signs/symptoms in very young/old
• 25% will develop seizures
MENINGITIS
BAKTERIAL AKUT 52
Pada neonatus , meningitis purulent
menunjukkan gejala :
• panas tinggi yang akut
• dyspnoe
• tidak mau menetek
• icterus, kesadaran menurun
• kejang & koma.
Sering disebabkan oleh :
• E Coli
• Streptokokus
• Stafilokokus
• Pneumokokus
MENINGITIS
BAKTERIAL AKUT 53
Pada bayi dan anak-anak yang lebih besar
menunjukkan gejala:
• tidak mau makan
• irritable
• confuse & letargy
• kejang & koma.
Sering disebabkan oleh :
• H. Infulenza
• Meningokokus
• Pneumokokus
• E Coli
• Streptokokus
MENINGITIS
BAKTERIAL AKUT 54
Pada orang dewasa sering disebabkan oleh :
• Pneumokokus
• Meningokokus
• Streptokokus
• Stafilokokus
• H. Infulenza
CLINICAL FEATURES
• History
• Living conditions
• College dorm/barracksN meningitidis
• Trauma
• Recent neurosurgeryStaph/gram(-) rod
• Immunocompetence
• Immunization hx
• NoneHiB
• Antibiotic use
CLINICAL FEATURES
• Physical Exam
• Brudzinski
• Passive neck flex hips & knees flex
• Kernig
• Flex hip, ext knee hamstrings contract
• Skin
• Purpura
• Petechiae/splinter hem, pustular lesionsmicroemboli
• Funduscopy
• Neurology Examination
DIAGNOSIS
• Parenchymal
• CT is the imaging of choice
• Brain abscess, encephalitis, toxoplasmosis
• Meningeal
• Lumbar puncture
• Neoplasm, CNS vasculitis, SAH
DIAGNOSIS
Parameter Bacterial Viral Neoplastic Fungal
(normal)
OP (<170 mm CSF) >300mm 200mm 200 300mm
WBC >1000 <1000 <500 <500
(<5mononuclear)
%PMN’s (0) >80% 1-50% 1-50% 1-50%
Glucose <40 >40 <40 <40
(>40mg/dL)
Protein (<50mg/dL) >200 <200 >200 >200
Gram stain (-) + _ - _
Cytology (-) _ _ + +
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TREATMENT
• First priority
• Antibiotics
• Second priority in some cases
• Anti-inflammatories
• Third priority
• Counter the adverse effects of increased ICP &
vasculopathy
EMPERIC ANTIBIOTICS
Age/Special Gram Stain Drug
18-50y/o Negative Ceftriaxone 2g IV +
vanco 1g IV or rifampin
>50 y/o Negative Ceftriaxone +
Ampicillin + vanco or rifampin
Recent penetrating head Negative Vanco 25mg/kg then 19mg/kg
injury/ surgery/shunt using Matzke nonogram +
ceftazidime
immunocompromised Negative ------------- Vanco+ amp+ ceftazidime
GPC ----------------- Ceftriaxone + vanco
GNC ----------------- Pen G
GPR ----------------- Amp + gent
GNR ---------------- Cetazidime + aminoglycoside
COMPLICATIONS
• Seizures
• Hyponatremia
• SIADH
• CVA
• Coagulopathies
• Cognitive deficits, epilepsy, hydrocephalus, hearing loss
affect 25% of survivors
MENINGITIS TUBERKULOSA
Berupa meningitis serosa akibat reaksi
peradangan yg disebabkan oleh
kuman tuberkulosa Terutama pada
anak
Penjalaran berasal dari :
– Paru – paru secara hematogen
– Infeksi TB di mastoid
– Spondilitis TB
63
MENINGITIS TUBERKULOSA
Pemeriksaan Fisik:
– Tanda-tanda rangsangan meningeal berupa kaku
kuduk, tanda Laseque dan Kernig
– Kelumpuhan saraf otak sering dijumpai
Pemeriksaan Penunjang :
– LCS :
• Pelikel (+)/Cobweb Appearance (+)
• Peliositosis 50 – 500/mm3, dominan sel mononuklear,
protein meningkat 100-200 mg%, glukosa menurun < 50-
60%, bakteriologis Ziehl Nielsen (+), kultur BTA (+)
– IgG anti TB atau PCR
– Thorax foto
– CT Scan Kepala atau MRI
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MENINGITIS TUBERKULOSA
Diagnosa Banding
– Meningoencephalitis karena Virus
– Meningitis bakterial yang pengobatannya tidak
sempurna.
– Meningitis oleh karena infeksi jamur/parasit
(Cryptococcus neoformans atau toxoplasma
gondii), sarcoid meningitis
– Tekanan selaput yang difus oleh sel ganas,
termasuk karsinoma, limfoma, leukemia, glioma,
melanoma dan medulablastoma.
65
MENINGITIS TUBERKULOSA
Tatalaksana :
– Umum
– Terapi kausal : kombinasi obat anti
tuberkulosa (OAT)
• INH
• Pyrazinamida
• Rifampisin
• etambutol
66
MENINGITIS TUBERKULOSA
Komplikasi :
– Hidrosefalus
– Kelumpuhan saraf kranial
– Iskemi dan infark pada otak dan mielum
– Epilepsi
– SIADH
– Retardasi mental
– Atrofi nervus optikus
Prognosis
– Sembuh lambat dan umumnya
meninggalkan sekuele neurologis
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Brain Abscess
Brain Abscess
Focal pyogenic infection
Pus-filled cavity ringed by
granulation tissue & outer fibrous
capsule surrounded by edematous
brain tissue
Epidemiology
Paranasal sinus focus
– 10-30 y/o
Otic
– Bimodal: <20 y/o & >40 y/o
Pathophysiology
Hematogenous spread
– 1/3 of cases
Contiguous (middle ear, sinus,
teeth)
– 1/3 of cases
– Otogenic (Bacteroides)temporal
lobe/cerebellum
– Sinogenic & odontogenic(anaerobic &
microaerophilic streptococci)frontal
lobe
Clinical Features
Classic triad
– Headache, fever, focal deficit <1/3 of
cases
– Toxic appearance is rare
– Seizures, vomiting, confusion,
obtundation possible
– Frontal lobe-hemiparesis
– Temporal lobe- homonymous superior
quadrant visual field deficit or aphasia
– Cerebellum-limb incoordination or
nystagmus
73
Diagnosis
CT with contrast
LP contraindicated
Biopsy or aspiration for
confirmation
Treatment
Presumed Primary Empiric Alternative Tx
Source Tx
Otogenic Cefotaxime 2g IV q8h Bactrim 5mg/kg IV q6h
+
Flagyl 1giv then 500mg
q6 or chloramphenicol
Sinogenic or Pen 24 million units/d IV Pen (same dose)
divided q4h +
odontogenic
+ Chloramphenicol
Flagyl 1g IV then 500mg 100mg/kg/d divided q6h
q6h
Penetrating trauma Nafcillin 2g IV q4h + Vanco 15mg/kg (max
Ceftazidime 2g IV q8h 1g)IV q6h + Ceftazidime
or neurosurgery 2g IV
Hematogenous Pen 24 million units/d Pen (same dose) +
divided q4h + Chloramphenicol
Flagyl 1g then 500mg q6h 100mg/kg/d divided q6h
No obvious source Cefotaxime 2g IV q6h + No recommendations
Flagyl 1g IV then 500mg
q6h
76
INFEKSI SPIROKHETAL
Disebabkan oleh kuman :
• Leptospira ikterohemoragika
• Treponema
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INFEKSI SPIROKHETAL
LEPTOSPIROSIS
• Penularan leptospirosis melalui air minum
yang terkontaminasi dengan kencing host
leptospira seperti tikus , kelinci, marmot.
• Penularan antar manusia tidak pernah
terjadi karena leptospira tidak dapat hidup
dalam urine manusia yang keasamannya
rendah.
78
INFEKSI SPIROKHETAL
LEPTOSPIROSIS
• Kuman masuk kedalam traktus digestivus
menyebar melalui pembuluh darah ke
organ organ tubuh terutama ke hati dan
ginjal kemudian menimbulkan reaksi
peradangan, oedema akhirnya terjadi
hepatic failure dengan ikterus obstruktif,
renal failure.
79
INFEKSI SPIROKHETAL
LEPTOSPIROSIS
• Gejala lain yang menyertainya : myalgia,
konjunctivitis perikorneal, uveitis,
hemorhagi, meningitis leptospirosis (paling
sering ± 50%), hemorhagi serebri.
• Meningitis leptospirosis menyerupai
meningitis serosa / meningitis aseptic.
80
INFEKSI SPIROKHETAL
SIFILIS
• Disebabkan oleh kuman Treponema
pallidum.
• Kuman ini tidak tahan terhadap panas,
mudah terbunuh oleh sabun, antiseptika,
pengeringan. Hanya bisa bertahan hidup
pada keadaan dingin.
• Penularan melalui kontak seksual.
81
INFEKSI SPIROKHETAL
SIFILIS
Gambaran penyakit :
• Menyerupai organic brain syndrome.
• Gejala prodromal berupa sakit kepala,
insomnia, cepat lupa, daya konsentrasi
menurun, badan letih. Pada tahap lanjut
timbul dementia dan perubahan watak
yang menyerupai psikosis.
82
INFEKSI FUNGAL
• Sering disebabkan oleh kriptokokus,
nokardia, mukomikosis, koksidiomikosis,
aktinomikosis, aspergillus.
• Penyebaran secara hematogen sering
berasal dari paru – paru.
• Meningitis oleh infeksi fungal ini menyerupai
meningitis serosa.
83
INFEKSI PROTOZOAL
Disebabkan oleh :
• Tripanosomiasis (tripanozoma gambiense)
• Malaria (Plasmodium Falciparum)
• Toksoplasmosis & amubiasis
INFEKSI PROTOZOAL
84
TOXOPLASMOSIS
Gejala Klinis :
• 80 – 90 % pasien tidak menimbulkan
gejala
• jika ada tersering limpadenopati
• Hidrosephalus
• Kalsifikasi serebral
• Khorioretinitis
ada binatang peliharaan kucing
INFEKSI PROTOZOAL 85
Liquor : TOXOPLASMOSIS
• kronik N
• Akut protein & limphosit meningkat
• EEG gelombang delta diselingi spike.
Pada keadaan kronis EEG normal
CT Scan :
• lesi multiple yang menyerap kontras
• bentruk bisa cincin atau noduler
• tumor di white matter
• dgn edema otak diffus
86
INFEKSI METAZOAL
• Disebabkan oleh :
• Nematoda : trikinela spiralis
• Trematoda : Skistosoma & paragonimus
• Sestoda :
• Tenia solium sistiserkosis
• Ekinokokus granularis
hidatidosis
• Mutiseps-mutiseps
INFEKSI METAZOAL
87
SCHISTOSOMIASIS
• Terbanyak di Cina, Philipina, Indonesia, Laos,
Thailand
• CT Scan : seperti granuloma lainnya
• EEG : gelombang lambat abnormal, fokal epilepsy
• LP : sel meningkat lymphositosis, bebrapa
eosinofil. Protein meningkat
• Gejala klinik : kejang umum & epilepsy Jakson.
INFEKSI METAZOAL
88
CEREBRAL
PARAGONIMIASIS
• Biasanya di lobus oksipitalis & parietal
• Bisa kena n II
• LP : protein meningkat, pleiocytosis
(eosinofil (+))
• CT Scan :
• biasanya selain ada kalsifikasi terdapat
banyak vascularisasi
INFEKSI METAZOAL
89
CYSTICERCOSIS
• Sering kena otak, mata (visual field terganggu) , otot
(pseudohipertropi)
• Kejang , hidrosephalus
• Gejala klinik : SOP
• CT Scan : single/multiple area hipodens didalam
jaringan otak
• Tidak dikelilingi cincin dan edema
• LP : tekanan meningkat, pleiositosis, Ig G meningkat,
glukosa menurun
90
MIELITIS TRANSVERSA
Yaitu radang medulla spinalis yang mengenai segmen
medulla spinalis (substansia alba & grisea).
Etiologi :
• Pasca infeksi atau parainfeksi : infeksi virus, rubeola,
varisella, variola, jarang pada rubella, mumps,
influenza.
• Pasca vaksinasi : anti rabies, varisella, pertusis, polio,
tetanus.
• Nekrotik atau degeneratif
• AIDS (Aquired Immuno Deficiency Syndrom)
• Dasar terjadinya mielitis oleh karena reaksi alergi
91
MIELITIS TRANSVERSA
GAMBARAN KLINIS :
• Pasca infeksi / pasca vaksinasi mulai timbul
deficit neurology setelah 5 – 10 hari
• Perjalanan penyakit akut
• ± 50% timbul dalam waktu 12 jam
• ± 75% timbul dalam waktu 24 jam
• Mula mula berupa demam, malaise, mialgia.
• Deficit neurologik berupa
• Kelemahan ekstremitas
• Gangguan sensibilitas
• Gangguan genitourinaria & defekasi
• Segmen medulla spinalis yang sering terkena
antara segmen thoracal 2 – thorakal 6.
92
MIELITIS TRANSVERSA
GEJALA NEUROLOGIK
AWAL :
• Parestesia anggota gerak bawah dan tubuh dengan
pola segmental
• Kadang nyeri punggung yang menjalar sepanjang
batas atas lesi medulla spinalis.
• Pada keadaan akut timbul fase syok spinal dengan
gejala paralysis flaksid ke 2 tungkai, retensio urine &
alvi, setelah 3 – 6 mg baru muncul paralysis spastic.
• Neuritis optika Devic disease.
93
MIELITIS TRANSVERSA
LABORATORIUM :
Liquor :
• Hambatan aliran liquor
• Pleiositosis moderat 20 – 200 sel/mm3 . limfosit lebih
banyak.
• Protein sedikit meningkat 50 – 120 mg/dl.
• Kadar glukosa normal.
94
TERIMA
KASIH