INFECTIONS OF THE

CENTRAL NERVOUS SYSTEM

RADANG I

DR. dr. Kiking Ritarwan, SpS (K), MKT

Departement of Neurology Medical

Faculty of University of Sumatera Utara
2016
 CNS INFECTION
MENINGITIS: TBM, Bacterial, Viral, Jamur
- Inflamation of the meningeal covering of
Brain and spinal cord.
- LEPTOMENINGITIS (arachnoid + pia)
PACHYMENINGITIS (duramater)
- TYPE OF MENINGITIS : Bacterial, TB, Viral,
fungal.
ENCEPHALITIS VIRAL
MYELITIS
ABSCESS CEREBRI
 Acute Pyogenic Meningitis
= Bacterial meningitis
Is an inflamatory response to bacterial infections
involving the pia and arachnoid membrane covering
the brain and spinal cord.

Many org. can produce pyogenic meningitis

It can be categorised into:

a. Spontaneous community acquired meningitis
b. Post traumatic meningitis following neurosur-
gery or fx of the skull.
c. Device associated meningitis particularly in assoc.
With CSF Shunts and drain.
The causative org. of meningitis can be
predicted based on the patient’s age, exposure
to an epidemic, vacc. Against common agents
(eg. H. Influenza, Streptococcus pneumonie, N.
meningitidis) and Immune state.

Pathology is characterized by inflammation of

the meninges and cortical blood vessels.
 Etiology of Bacterial meningitis
Age Microorg.
- Neonate ( 0-2 bln) Streptococ group B, E coli, list.
Stap. Aureus, Enterobacter,
Pseudomonas, Haemofilus
- Child S. pneumonie, N. meningitidis,
H. influenzae.
- Youth ( 6-20th) N. meningitidis, S. pneumonie,H. infl.
- Adult ( > 20 thn) S. pneu, N. meningi, Streptococ,Staph.
 Clinical Picture Bacterial Meningitis
The conditions occurs equally in both sexes
Children aged 6 month to 1 year are at the greatest
risk and children under 15 years of age comprise 75%
of all cases. Patients aged 60 and older may be
atypical.
Symptoms and signs
I. early infection: fever, headache, malaise,vomite
II. Higher ICP: vomite, headache, seizure, alteration of
consciousness, papiledema
III. Meningeal irritation: nuchal rigidity, Kernig and
Brudzinski +
IV. CSF:neutrophilic pleocytosis, low glucose level,
elevated protein concentration
 CSF Findings
CSF Parameter Bacterial meningitis
• WBC Count > 2000/ ul, >60% PMN
• Glucose < 40 mg/ dl
• Protein > 200 mg/ dl
• Gram stain + 80%
• Culture + > 90%
 Diagnostic Prosedure
Lumbal Puncture
Blood should be drawn for blood culture before
administration of antibiotic.
Bacterial antigen
Chest, skull mastoid and paranasal sinus x rays
MRI or CT
Neuroimaging shoul be performed before LP in
the following settings:60 yo or older, Depressed
LOC, Focal neurologic signs, papilledema,
Patients is immunocompromised.
Lumbal Puncture
Peralatan Lumbal Pungsi
Peralatan yang diperlukan untuk
tindakan lumbal pungsi adalah
sebagai berikut.
1. Sarung tangan steril
2. Iodine solusio
3. Alkohol
4. Kassa steril
5. Duk
6. Lidocaine (1%)
7. Syringe 5 ml
8. Jarum spinal (22G)
9. Manometer
10. Tabung LCS
11. Reagen Nonne dan Pandy
12. Plester
 Treatment
1.Antibiotic therapy should be administrated. A minimum of 2
weeks of therapy is recommended.
Age Antibiotic
0 – 4 mgg Cefotaxim + Ampi
4-12 mgg Gen III. Cephalos+ Ampi
3 bln- 18 thn Gen III. Ceph + Ampi atau
Ampi + chloramph.
18 thn – 50 thn Gen III. Ceph + Ampi
50 thn Gen III. Ceph + ampi.

2. When possible etiologies for meningitis include H. Influenza or

S Pneumoniae in child, or S Pneumoniae in adults, give
dexamethasone 0,15 mg/kg (IV) every 6 hours for 2-4 days in
child and 10 mg IV every 6 hours for 4 days in adults.
Complication Bacterial meningitis
Cerebral abscess
Empyema subdural
Convulsie
Shock septic
Cerebral edema
Infarck serebral
Herniation
Sequele bacterial meningitis
Mental retardation
Hydrocephalus
Convulsie, psikose
Parese, deafness, blind.
 HYDROCEPHALUS
Complication or manifestation of Bacterial and
TB Meningitis.
Definition: Hydrocephalus is an excessive
accumulation of CSF within the cranial cavity.
Two main functional subdivisions of
Hydrocephalus:
1. Obstructive
2. Communicating
 Etiology
Hydrocephalus may occur under the following
conditions:
1. Cerebral malformation
2. Increased production of CSF
3. Obstruction of CSF circulation
a. Tumor of the lateral ventricles
b. Obstruction of the third ventricles by
tumors, colloid cysts, or parasitic cyst.
c. Pressure on the third ventricles
 Etiology …..
3.d. Aqueductal narrowing by congenital stenosis
e. Obstruction in the fourth ventricle by tumors or
parasityc cyst
f. Occlusions of the foramina of Luscha and
Magendie by cerebellopontine angle tumors by
fibrosis following meningitis or subarachnoid
hemorrhage.
g. Impaired circulation of CSF in the subarachnoid
space, ex SAH, chronic meningitis, brain injury,
intramedullary spinal cord
 Etiology….
4. Reduced absorption of the CSF.
ex: meningitis, SAH, Thrombosis of the
mayor venous sinuses may also decrease
CSF absorption.
5. Compensation for cerebral atrophy 
Hydrocephalus ex vacuo.
 HASIL FOTO HEAD CT
SCAN HYDROCEPHALUS
 SIGN AND SYMPTOMS
In young children In older child/ adults
1. Cranium enlarges at a 1. Increased ICP
rate > facial growth - Headache
2. Irritability - nausea
3. Fontanella full and - vomiting
bulging - visual impairement
4. Enlargement and
- Ataxia
engorgement of scalp
veins; due to reversal of - papil edema
the flow from the
intracerebral sinuses
due to increased ICP
 Oedema serebri
Def: increasing of intra/extra brain cellulair
cause by local or diffuse brain process
Type
Vasogenic
Citotoxic
Osmotic
hydrostatic

Kiking Ritarwan 21
 Edema cerebri

Vasogenic : Tr capitis, stroke, meningitis,

encephalitis, SOL, malignant hypertension,
convulsion
Sitotoxic: asphyxia, cardiac arrest, toxic subst
Osmotic: water intoxication, hemodyalisis
Hydrostatic: hydrocephalus

Kiking ritarwan 22
 Diagnostic Procedure
1. MRI and CT Scan

2. LP : should be delayed or avoided

 Treatment of Hydrocephalus
Tumor or cyst causing hydrocehalus shoud be
removed surgically if possible
Ventriculostomy and ventricular drainage may
be required in emergency situations
In less emergent situations, a ventricular
peritoneal shunts:
- most commonly
- lateral ventricle is the usual proximal location
- intraperitoneal pressure, normal is near
atmospheric
 Tuberculous meningitis
The first clinical description of tuberculous meningitis
in the late 18th Century is credited to the Scottish physiologist
Sir Robert Whytt , even before Robert Koch isolated
mycobacterium tuberculosis in 1882.
Almost 40 years later, Rich and McCordock demonstrate the
presence of minute caseous tubercles known as “Rich-foci”
within the brain or meninges, which formed the basis for
understanding the pathogenesis of CNS tuberculosis.

Tuberculosis of the central nervous system (CNS) is the most

serious complication of tuberculosis, especially in children.

TB hematogenous spread infection to the brain

parenchyma or meninges.
 TB meningitis (TBM)
Definition:
TBM is an infection of the meninges caused by
the acid-fast bacillus Mycobacterium
tuberculosis.
 In the west country,the first make not much
difference again, but lately incident mount
drastically in all the world.
 TBM happened at all of age.
 Before important HIV factor in prevalens is age
+ 1,7 milyar people ( 1/3 worldwide
people)  Mycobacterium tuberculosa
infected.
Reported CDC 2002 was 5,36 cases per
100.000 people, but worldwide the
infection rate is much higher.
TB in Indonesian occupy 3rd rank from 22
high burden countries.
 3% of All Deaths in Developed
Countries Are Due to Tuberculosis
Tuberculosis Malaria
Diarrheal disease
Perinatal causes
2%
3% 3%
Chronic obstructive 4%
pulmonary disease 5%
Other
HIV/AIDS 5% 27%

Respiratory tract
infection 7%

Coronary heart
Injury
disease
9%
Cancer 13%
Stroke 12%
10%

HIV/AIDS = human immunodeficiency virus/acquired immunodeficiency syndrome.

Adapted with permission from MacKay J, Mensah GA. The Atlas of Heart Disease and Stroke.
Available at: http://www.who.int/cardiovascular_diseases/en/cvd_atlas_16_death_from_stroke.pdf
Accessed February 27, 2006.
Etiologi
Mycobacterium tuberculosis
gol ordo Actinomycetales, famili
Mycobacteriaceae, genus
Mycobacterium
Sifat : aerob, spora (-), motil (-),
berkembang biak lambat
Mati dgn pemanasan & sinar UV
Bakteri batang tahan asam dgn
pewarnaan Ziehl–Neelsen
/Auramin  leading to nickname
“ red snapper”.
Size :0,3-,0,6 to 1-4 um
Shape: Rods, straight or
slightly curved, occurring
singly or in occasional
threads
Temperature: 33-39o C
pH 6,6-6,8
 PATHOLOGY

Aerosol transmission of Tuberculosis

Tuberculosis is spread by droplet nuclei which are expelled when a person with
infectious TB coughs, sneezes, speaks, or sings
 Pathology
TBM is always secondary to TB elsewhere in the
body. The primary focus of infection is usually in the
lungs but may be in the lymph glands, bones, nasal
sinuses, GIT, or any organ in the body.
The bacilli usually enter the body by inhalation.
Transmission through the skin or by ingestion are rare
cause of infection.
The organisms undergo multiflication and
hematogenous dissemination and it is during this
stage that the meninges are most likely to become
involved.
Cell mediated immunity with migration of
macrophages at the site of infection leads
to the development of tubercles.
When the immune response fails, the
subarachnoid space is infected by rupture
of meningel tubercles followed by release
of bacilli and the development of
meningitis.
The presence of bacilli in the subarachnoid space is
followed by an intense granulomatous inflamation of
the leptomeninges and subjacent cortex.

A thick, heavy fibrous and necrotic exudate is

produced, which tends to collect at the base of the
brain.

The arteries at the base of the brain are involved, and

there is inflamation of the adventitia and media, with
narrowing and thrombosis of the lumen.
CN II and III, occasionally CN VII, VIII, are subject to
compression by the heavy exudate.
 Classification of neurotuberculosis
• Intracranial
- Tuberculous meningitis
- Tuberculoma
- Tuberculous abscess
- Tuberculous encephalopathy
- Tuberculous vasculopathy

• Spinal
- Pott’s spine and Pott’s paraplegia
- Tuberculous arachnoiditis
- Spinal tuberculoma
- Spinal meningitis
 Clinical features TBM
The disease occurs in all ages, but the incidence
is higher in infants, young children, and the
aged. It is more common amomg the
undernourished and in those areas of the world
characterized by poor hygiene and
overcrowding.
History of contact with an infected individual or a
history previous active tuberculosis in 30 to 50
percent of patients.
Clinical staging of patients with
TBM

(terminus/ advance)
The course of the illness depends:
- on the extend of meningeal involvement,
- the immune response of the host,
- the virulence of the organism,
- and the stage at which treatment is
administered.
 Diagnosis Meningitis TB
Kepastian diagnosis sulit
Algoritme diagnostik
Pada anak
Pada orang dewasa
Sistem skoring klinik

Kategori diagnostik (definite atau bukan)

– Menggunakan pola klinis, adanya abnormalitas
LCS dan adanya TB ekstraneural (nodus
lymph,sumsum tulang, hati, pleura).
 Diagnosis Meningitis TB
Algoritme diagnostik
– Pasien anak
Hal yang berhubungan dengan diagnosis MTB:
– Riwayat sakit > 7 hari
– Atrofi papil
– Defisit neurologi fokal
– Gangguan gerak ekstrapiramidal
– Persentase netrofil di CSS < 50%
Sensitivitas 98%, spesifisitas 98% (jika didapatkan
> 3 kriteria)

Kumar et al., Arch. Dis. Child. 1999; 81; 221-4

 Diagnosis Meningitis TB
Algoritme diagnostik
– Pasien dewasa
Hal yang berhubungan dengan diagnosis MTB:
– Usia < 36 tahun
– Leukosit darah perifer < 15.000
– Riwayat sakit > 6 hari
– Leukosit di CSS < 760
– Netrofil di CSS < 75%
Sensitivitas 86%, spesifisitas 79%

Thwaites 2002, Lancet; 360: 1287-92)

 Sistem Skoring Klinik
 Sensitivitas untuk
diagnosis TBM 99%
 Belum diujikan terhadap
kelompok HIV+
 Diagnosis Meningitis TB
Kategori diagnostik
– Thwaites
MTB definite:
– Gejala klinis meningitis
dan
– Gambaran LCS abnormal
dan
– BTA di LCS (mikroskopi) dan/atau kultur TB positif
(PCR?)
 Diagnosis Meningitis TB
Kategori diagnostik
– Thwaites
MTB probable:
– Gejala klinis meningitis
dan
– Gambaran LCS abnormal
dan
– Didapatkan setidaknya satu dari 2 hal berikut:
Kecurigaan TB paru aktif (thorax foto)
Didapatkan BTA dari sampel lain selain LCS
 Diagnosis Meningitis TB
Kategori diagnostik
– Thwaites
MTB possible:
– Gejala klinis meningitis
dan
– Gambaran LCS abnormal
dan
– Didapatkan setidaknya 4 dari 7 hal berikut:
Riwayat menderita TB
Predominansi MN di LCS
Lama sakit > 5 hari
Rasio glukosa LCS: darah < 0.5
Penurunan kesadaran
Warna LCS kuning / xanthochrom
Didapatkan defisit neurologi fokal
 Kategori diagnosis Ogawa
Definite
- bila kultur positi
- otopsi positip, atau keduanya
Probable
- likuor pleiositosis (>5/mm3), kultur bak-
teri dan jamur negatip + salah satu:
1. test tuberkulin positip
2. TB diluar SSP atau TB aktip sebelumnya
3. glukosa likuor < 40 mg/dl
4. protein likuor > 60 mg/dl
Grading Meningitis TB (MIRC)
Grade I
– Sadar penuh, tanpa defisit neurologis fokal
Grade II
– Grade 2a: GCS 15 dengan defisit neurologi
fokal
– Grade 2b: GCS 10 – 14 dengan atau tanpa
defisit
Grade III
– GCS < 10 dengan atau tanpa defisit neuro
fokal
 Complication
Arteritis  thrombosis of a major artery
cerebral infarction.
Hydrocephalus
Seizures
Focal motor deficits and impaired cognitive
Hypopituitarism in childhood.
 Differential DX
Viral encephalitis
Partially treated pyogenic meningitis
Fungal infection
Other inflammatory disorders
The presence of active TB elsewhere, and
the results of CSF examination are usually
sufficient to establish the dx.
 Diagnostic Prosedures
 1. Lumbal Puncture
CSF Parameter TB meningitis
• WBC Count < 500/ ul, MN
• Gluco moderate or marked decrease
• Protein marke increse
• Gram stain + +.-
• CSF lactic acid > 35 mg/dl.
 Diagnostic Prosedure…..
 2. Laju endap Darah
 3. Radiologic
3a. Chest x ray: detect pulmonary involvement
3b. Head CT scan  enhancement of the
basal cistern.
3b. MRI are more sensitive than CT
sans in detecting basal meningitis
infarction owing to arteritis hydrocephalus
and parenchymal tuberculomas often in
combination in AIDS patient.
 4.Mikrobiologi: BTA + KULTUR
 5. Arteriografi
Images of CT Scans
Contrast-enhanced
computed tomography (CT)
scan in a patient with
tuberculous meningitis
demonstrating marked
enhancement in the basal
cistern and meninges, with
dilatation of the ventricles.
 Investigations TBM
CSF examination
CSF Smear examination:
Gram’s
CSF culture on solid media:
Adjunctive tests
Molecular diagnosis :
Zeihl Nelson’s,
and India Ink stain.
Egg or agar based
BACTEC systems.
CSF tuberculostearic acid,
adenosine deaminase,
radiolabelled bromide
partition test.
Nucleic acid amplification,
DNA finger printing, PCR.
 Petechial hemorrhages in
the subcortical white
matter of the brain as a
result of tuberculous
meningitis–associated
vasculitis.
 Extensive infarcts of the
right basal ganglia and
internal capsule after the
appearance of vasculitis in
the thalamoperforating
arteries in a child treated for
tuberculous meningitis.
 Treatment
1. Combination of antituberculous drug
Therapy WHO GILROY ATS
- Initial INH+R+PZA+E INH+R+PZA INH+R+PZA atau S
atau R+ PZA+S

-2MO - 2 MO - 2 MO
- Continued INH+R INH+R INH+R
-7 MO - 9 MO - 9 MO
Pyridoxine 50 mg/ hr
2. Spinal arachnoiditis and arteritis may show
improvement when terated with corticosteroid.
3. Seizure  anticonvulsant
4. ventriculoperitoneal shunt.
 Adjunctive steroid therapy

• A recent Cochrane review and meta-analysis of 7

randomised controlled trials involving 1140 participants
(with 411 deaths) concluded that corticosteroids improved
outcome in HIV-negative children and adults with TBM, but
the benefit in HIV infected individuals remains uncertain.

Prasad K, Singh MB. Corticosteroids for managing tuberculous meningitis.

Cochrane Database Syst Rev 2008;(1):CD002244.
Differentiated Corticosteroid
Regimen in TBM

Thwaites et al, J Infect 2009; 59: 167-187

 ATD….
CSF Consentration of certain
antituberculosis drugs
DRUGS Daily Serum Normal Inflammated
Dose Ug/dl Meningens menigens
Mg/ kg Ug/ms ug/ms
Isoniazid 5 - 10 3-5 0,6- 1,6 2,0 – 3,2
Rifampicine 10 - 20 0,4 – 1,2 0 0,4-1,0
Ethambutol 15 - 25 1,0 -7,7 0 0,5-2,5
Pyrazinamide 25 - 30 15 - 50 10 30 – 50
Streptomycine 15 - 40 25 – 50 trace 2.0 – 9.0

Misra ,UK. Tuberculous meningitis. XVII World Congress of neurology, London,(2001)

 PRINCIPLES THERAPHY
Good penetration in CSF Treatment:
Isoniazid,
Rifampicine,Pyrazinamide,prothianamide/ethi
onamide and cycloserine.
Only in the presence of meningeal
inflamation: kanamycin, amikacin and
capreomycin
Poor or no penetration: PAS and ethambutol
 Prognosis
Mortality 10 & 20%
The prognosis is poor in infants, the elderly,
when treatment is delayed, and in patients with
poor nutrition or debilation from HIV infection or
other chronic disease.
The outcome is clearly associated with the stage
of the disease at dx and the introduction of early
treatment. Those who are conscious and without
neurological deficits have a good prognosis;
those in coma at the beginning of treatment
have 20% mortality and only 20 oercent make
complete recovery.
 Viral meningitis
Viral meningitis shares clinical features with
bacterial meningitis, but patients appear less ill
and the disease follows a more benign course.
Headache, often meningismus and photophobia,
is often the presenting symptoms.
The most pathogens include herpes simplex-1
(HSV1), mumps, enterovirus, herpes zoster,
adenoviruses and Epstein barr virus.
 Infeksi Varicella Zoster
• Transmisi melalui saluran napas
• Skin erruption muncul setelah 4-6 hari.
• Infeksius 4 hari sebelum dan 5 hari
setelah munculnya lesi kulit.
• Kematian 30.9 / 100,000
Komplikasi
– Pneumonia
– Reyes syndrome: encephalitis,
hepatitis with aspirin use.
– Thrombocytopenia
– Purpura Fulminans
virus dorman di dalam
ganglion radiks dorsal
Reaktivasi  Herpes
Zoster  kerusakan
ganglion, primary
afferent nerve dan kulit
 Herpes Zoster
Reactivasi infeksi virus dari ganglion radiks
dorsalis
– Lesi kulit muncul 1-5 hari
– Sepanjang Dematom (sesuai lesi kulit pada varicella)
– Nyeri dan gatal
Durasi lesi bergantung pada
– Usia. Muda = 2-3minggu, geriatri = 5-6 minggu
– Tingkat keparahan
– Immunosuppression
Insiden meningkat dengan bertambahnya umur
dan imunosupresan
 Pain
Intractable
Konstan
Feeling of heat
Burning, shooting, twisting, lancinating,
pressure, and gripping
Membaik saat tidur
 Reaktivasi virus

Transkripsi Virus

Axonal transport
ke semua neuron sensori

Necrosis sel kulit, nerve, root, ganglion

Excess electrical activity Pain

Mechanism of pain and itc caused by Herpes Zoster (shingles). The Journal of Pain 208
 Dx procedure Viral meningitis
Lumbal Puncture
Cells Glucose Protein Smear CSF lactic
< 500 Normal Mild incr No org < 35 mg/dl
MN /mm3
 PCR
 MRI  predominant temporal lobe and insular
changes in HSE-1 and basal ganglia lesion in
japanese encephalitis.
 Treatment
Aciclovir 10 mg/ kg iv every 8 hours for 10-
14 days.
 FUNGAL MENINGITIS
ETIOLOGY
Fungi invade of CNS producing meningitis in a small fraction of
patients with systemic fungal infection (mycoses)

 The most pathogens are Cryptococcus neoformans,

Coccidiodes immitis, Candida albicans, Aspergillus, H.
Capsulatum, Blastomyces, and Mucor

 Mucormycosis and aspergillosis usually spreads to the CNS

from infected sinuses and generally cause local inflamation and
necrosis rather than a diffuse meningitis
Fungi can cause infection in patients with:
1. Cancer
2. Receiving corticosteroids
3. Other immunosuppressive drugs
(Diabetes, malignancy, immunosuppressive
th., or AIDS)
4. IV drug abuse.

Route of entry
A. Haematogenous: from the heart, lung, GIT and skin
B. Direct: from the orbit and paranasal sinuses.
 Clinical Picture of Fungal Meningitis

Symptoms progress over days, sometimes

weeks, with headache, nausea, vomiting and
mild encephalopathy.
Neurologic examination:
1. meningeal irritation (+) 5, Visual loss
2. papilledema 6. Confusional state
3. Cranial nerve palsies 7. Focal paralysis
4. Ptosis
 Investigations
Lab investigations:
1. Blood culture
2. Serum glucose
3.Arterial blood gases
4. Electrolyte
5. Liver function test
6. Urinalysis
CSF Examinations:
Imaging
 Invest…..
CSF Exam:
- Pressure: Increased
- Appearance: varies with organism
- White Blood cells: 50 – 10.000 (mixed or
lymphocytic).
- Glucose :Normal
- Protein: increased
- Cryptoccal antigen is more sensitive
- Fungal culture of CSF(+)
 Invest….
Chest X-ray : Hilar lymphadenopathy,
cavitation, effusion.
CT or MRI: mass lesion (Cryptococcus)
 Treatment
Amphotericin B
- Protocol, starting with 1 mg/ day
- doubling the dose daily until reaching 16
mg per day, than increasing at increments
of 10 mg until reaching full therapeutic
dose of 0,5 to 1,5 mg/ kg per day IV.
 Myelitis

Inflamation of the spinal cord

I. Transverse Myelitis, II. Disseminata, III.
Difussa
Transverse myelitis (MYELOPATHY) is a
syndrome characterized by acute spinal cord
dysfunction both halves the cord in transverse
section.
Myelitis transversalis
– inflamasi akut atau sub akut
– mengenai suatu area fokal di medula spinalis
– karakteristik klinis disfungsi neurologis pada
saraf motorik, sensorik dan otonom dan
traktus saraf di medula spinalis
 MYELITIS
Gray matter…… Poliomyelitis.
White matter …. Leukomyelitis.
The whole crossectional are…Tranversemyelitis.
Lesions are multiple and wide spreadOver a long vertical extent…..
DiffuseOr Disseminated.
Combined meninges and spinal cord…Meningomyelitis.
Combined meninges and root--- meningpradiculitis.
Inflammatory disease limited to the spinal dura…. Pachymeningitis.
Infected material collects in the epidural or subdural space… Epidural
spinal Or subdural spinal abcess or Granulomatous.

CLASSIFICATION OF INFLAMMATORY DISEASE

OF THE SPINAL CORD … SEE TRANSPARANTS
 ACUTE TRANSVERSE
MYELITIS
IS USUALLY BILATERAL AND TENDS
TO CAUSE MORE SEVERE WEAKNESS
THAN THE TYPICAL ATTACKS OF
PARTIAL MYELITIS.
The condition may be peri infectious or
postinfectious process and has been
associated with many viral infection,
including poliovirus, echovirus and
coxsackieviruses.
Etiologie Transverse myelitis
1. Congenital – vascular malformation
2. Infectious – viral infection
3. Autoimune- peri or post infection or vaccinial myelitis.
4. Multiple sclerosis
5. Neoplastic
6. Toxic- secondary to heroin injection
7. Vascular
8. Degenerative- irradiation
9. Idiopathic.
 PATOLOGI
JHTMC (John Hopkins Transverse Myelitis Center) 
kondisi inflamasi yang berhubungan dengan mekanisme
immune-mediated

Pasien myelitis transversalis perubahan inflamasi

pada medula spinalisnya

Abnormalitas patologi ( bervariasi )

– infiltrasi lokal oleh limfosit dan monosit dalam segmen medula
spinalis dan daerah perivaskuler
– adanya aktifitas yang bervariasi dari mikroglia dan astroglia
Besar dan luasnya gambaran inflamasi
 faktor etiologi dan profile perubahan
myelopati :
– Myelitis post infeksius  perubahan white
matter, demielinasi, gangguan aksonal
– myelitis transversalis  gambaran yang
melibatkan keduanya secara bersamaan
baik white maupun grey matter
Viral causes of acute myelitis
Herpesvirus: HSV2, Varicella Zoster,
HSV1, Epstein barr, Cytomegalo, human
herpes6.
Enterovirus: Poliovirus, Enterovirus 70,
Echovirus, Coxsackievirus.
Arbovirus: west nile virus
Other: Mumps, HIV, Dengue.
 Affinities virus in myelitis
Enterovirus anterior horn or nuclei of the
brain stem
Herpes zoster dorsal root ganglion
 Clinical manifestation
Acute paraplegic or Quadriplegic.
Urinary retention.
Sensory disturbances
 Diagnostic prosedure
CSF examination:
- mild to moderate lymphocytic pleocytosis (10-1000
cell/mm3), elevated protein (100-500 mg/dl), and normal
or mildly depressed glucose level.
• PCR- virus spesific PCR and antibody titer should be
performed.
• MRI-T2 weighted shows increased signal intensity
involving gray matter and surronding white matter.
DIAGNOSIS BANDING :

Multiple sclerosis
Penyakit sistemik (SLE, Sjorgen disease)
Venous infarct
Malformasi vaskuler (fistula AV, AVM, angioma
kavernosa)
Fibrocartilagenous embolism
Myelopati radiasi
 Treatment Viral myelitis
Antiviral treatment:
Glucocorticoid
Spasticity: baclofen (lioresal) 10 mg q6h,
benzodiazepin and tizanidine.
 BRAIN ABSCESS Definition

Brain abscess is a focal intracerebral

infection that begin as a localized area of
cerebritis and develops into a collection of
pus surrounded by a weil-vascularized
capsule.
Parenchymal brain infection can arise from
hematogenous delivery of infected material,
which often results in multiple abscess.
Especially at risk are patients with congenital
heart disease or valve infection.
Pathogenesis: abscess begin with local
cerebritis, causing necrosis and surronding
edema.
Epidemiology: 0,3 – 1,3 per 100.000 / tahun
Male to female ratio of 2:1 to 3:1
 Common etiologic factors
Common etiologic factors Distingushing
characteristics
Ear inf: temporal lobe abscess, sinus inf:
Middle ear,paranasal sinus, frontal lobe abscess, mastoid inf: cerebellar
or mastoid infection abscess

Metastatic embolic from lung, pulmonary

abscess, bronchietasis, or chronic
empyema
Head trauma or Neurosurg.
Multiple abscess
Gunshot wounds are the most common
head trauma assc. With abscess

Endocarditis Drug abuser

Rare cause: dental procedures, Metastatic
emboli from abdominal inf. Or PID,
-
osteomyelitis of skull
Common etiologic factors Microorgnism involved
Aerobes Anaerob
Streptococci, Streptococci
Middle ear,paranasal Staph aureus Bacteriodes
sinus, or mastoid
infection
Metastatic embolic from lung, Staph aureus, Klebsiela Streptococci,
pulmonary abscess, bronchietasis, or S.Pneumoniae Fusobacteria
chronic empyema
Staph aureus, streptococci
Head trauma or
Pseudomonas
Neurosurg.
Endocarditis Staph aureus -
Rare cause: dental procedures,
Metastatic emboli from abdominal inf.
-
Or PID, osteomyelitis of skull
 Neuropatologi (4 stages)
1. Early cerebritis ( days 1-3)
infection of the brain with surronding white matter edema.
2. Late cerebritis ( days 4-9)
The core of the cerebritis becomes necrotic and enlarges and
capsular fibroblasts begin to form.
3. Early capsule formation ( days10-13)
The capsule is well developed, with proliferation of fibroblasts, a
surronding astrocytic proliferation, and edema
4. Late capsule formation (days 14 or more).
A mature, thick capsule surronds the central cavity containing
debris and PMN cells. There is usually marked cerebral edema in
the surronding brain tissue in the presence of a mature abscess.
 Gejala dan tanda klinis:
Sakit kepala (70-90%)
Muntah (25-50%)
Kejang(30-50%)
Gejala pusing, vertigo, ataksia ( pd abses cerebelli)
Ggn bicara (19,6%), hemianopsia (31%), unilateral
midriasis (20,5%)
Gejala fokal (61%) pd penderita abses supratentorial.
 Pemeriksaan utk Diagnosa:
Glasgow coma scale : utk kesadaran penderita
Rontgen foto kepala, sinus, mastoid, thoraks.
EEG
CT Scan/ MRI
Angiografi : utk menentulan lokasi abses (24%).
Lab: jlh leukosit 10.000-20.000/ cm3 (60-70%)
LED meningkat 45 mm/jam (75-90%).
 Head Ct San

A B

A. Multiple brain abscesses associated with bacterial endocarditis (Staphylococcus aureus) in a

55-year-old man. The large abscess in the left hemisphere shows a characteristic ring enhancement.
B. Contrastenhanced
CT scan 4 months after institution of antibiotic treatment. The abscesses have resolved.
 Komplikasi Abses Otak
Robeknya kapsul abses kedalam ventrikel atau
keruangan subarakhnoid.
Penyumbatan cairan serebrospinal 
hidrosefalus
Edema otak
Herniasi tentorial oleh massa abses otak.
 Pengobatan abses otak
Konservatif:
- Pemberian AB yg tepat : 6-8 mgg mengecilkan abses.
- Prinsip pemberian AB: bakterisid thdp organisme hasil kultur, dapat
melewati BBB.
- Pemberian kortikosteroid:
dewasa : loading dose 10-12 mg secara IV
maintenance dose 4 mg secara IV setiap 6 jam
anak : loading dose 10-12 mg/kg diberikan satu kali IV
maintenance dose 1-1,5 mg/kg/hari IV
- Pemberian antikonvulsan
Operatif: Aspirasi dan eksisi. konsul Bedah Saraf , jika terapi
konservatif gagal.

102
 Antibiotic treatment for brain
abscess
Ear, Streptococcal Metronidazole
mastoid, species, Ps 7.5 mg IV
sinus anaerobes, every 6 h +
Enterobaceteriacea Cefepime 2 gr
IV every 6 h or
meropenem
2gr IV every 8
h
Lung S. pneumoniae Same as
above
 AB treatment
Teeth, mouth Anaerobic Metro 7,5
streptococci, mg/kg IV every
Eikenella, 12 h + PNC G
Prevotella, 4million units IV
Actinomyces every 4 h or
ceftizoxime 3 gr
IV every 6 h
Post operative Staphiloc Cefepime 2 gr
infection, IV every 8 h, or
furuncles or Nafcillin or
decubiti oxacillin 2 g IV
every 4 h
 Defenition Viral encephalitis
Is an acute febrile illness with evidence of
damage to the parenchymal tissue of the CNS,
producing alteration of consciousness, focal
neurological signs and seizures.
Etiology:viral infection of the nervous system,
– Herpes simpleks
– Eastern equine
– Venezuela St Louis
– Japanese – B
– Russian tick-borne
– Rabies
 Etiology viral encephalitis
 Viral is the most common cause
 The commonest is HSV type I in adults
and type 2 in neonates.
 It may occur sporadically or in epidemics
 50-70% mortality if untreated
 So establishment of on early specific
diagnosis and early initiation of antiviral
chemotherapy is of great importance
 2/3 of cases involve patients over 40 yo.
Patogenesis.
Bila virus patogen masuk kedalam tubuh
pada SSP dapat terjadi:
Radang akut
Radang kronis
Neoplasma
Virus hidup dalam keadaan laten
Cara penyebaran ke SSP:
Cara penyebaran Contoh virus
Hematogen herpes simplex
sitomegalovirus
Epstein-Barr
Coxsackie
HIV
Morbilli
Echovirus
khoriomeningitis limfositik
paravirus
Neurogen Herpes simpleks
B-virus
Varisela-Zoster
Rabies
Gambaran klinik:
Tanda dan gejala bervariasi tergantung
virus penyebab.
Umumnya: demam akut disertai tanda rang-
sang meningeal, sakit kepala, mual, fotofobi,
muntah, ggn kesadaran, defisit neurologik
fokal dan kejang2.
Mortalitas bervariasi dari tinggi (eastern
equine encephalitis) sampai rendah (Vene-
zuelan equine encephalitis).
Gejala sisa termasuk kejang2
Komplikasi : - perubahan kepribadian
- ggn ekstrapiramidal
- demensia
- ggn motorik - sensorik
 Kriteria diagnosis ensefalitis viral
1. Bentuk asimptomatik  analisis LP
2. Bentuk abortif : Nyeri kepala, demam yg tdk
tinggi, kaku kuduk. ISPA/ Infeksi GIT
3. Bentuk fulminan: Berlangsung bbrp jam
sampai dengan beberapa hari yg berakhir
dengan kematian.
4. Bentuk khas ensefalitis: NK, demam,
keasadaran menurun, kejang fokal atau
umum, hemiparesis, ggn koordinasi,
disorientasi, ggn bicara, ggn mental
Prosedur diagnostik.
LP : CSF jernih, tekanan normal atau
meningkat, Pleositosis limfositik < 1000/ul,
glukosa dan klorida nornal, protein normal
atau sedikit meninggi ( 80-200 mg/dl
MRI atau CT scan  SOL (?)
EEG
Liquor  virus DNA dg “polymerase chain
reaction” (prosedur cepat, sensitif, akurat)
Virus kadang2 dikultur dari
liquor,feces,urine nasofaring atau darah.
Titer antibodi thd virus tertentu.
Pengobatan Viral encephalitis.
Tidak bisa diidentifikasi  dianggap
sebagai ensefalitis herpes simpleks dan
terapi dgn. Acyclovir atau ganciclovir
Jalan nafas diawasi
Keseimbangan cairan dan elektrolit dijaga
Atasi kejang
Atasi peninggian ICP