INFECTIONS OF THE CENTRAL NERVOUS SYSTEM

1. INFECTIONS OF THE CENTRAL
NERVOUS SYSTEM
RADANG I
Prof.DR. dr. Kiking Ritarwan, SpS (K), MKT
Departement of Neurology Medical
Faculty
University of Sumatera Utara
2021
Email:kikingritarwan@gmail.com

2. 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

3. ANATOMY OF MENINGES

4. ANATOMY OF MENINGES
DURAMATER PACHYMENIX Dura mater otak digambarkan terdiri dari dua
lapis, yaitu lapisan endosteal dan lapisan
meningeal. Lapisan tersebut bersatu dengan
erat, kecuali pada garis-garis tertentu, tempat
mereka berpisah untuk membentuk sinus
venosus.
ARACHNOID LEPTOMENINX Arachnoidea mater merupakan membran yang halus
dan bersifat impermeabel, yang menutupi otak dan
medulla spinalis dan terletak di antara pia mater di
bagian dalamnya dan dura mater di bagian luar.
Arachnoidea mater dipisahkan dari dura mater oleh
ruang potensial (ruang subdural) yang terisi oleh
selapis cairan; dipisahkan dari pia mater oleh ruang
subarachnoid yang berisi cairan serebrospinal.
PIAMATER LEPTOMENINX Pia mater adalah membran vaskular yang diliputi oleh
sel-sel mesotelial yang gepeng. Struktur ini melekat
erat pada otak dan medulla spinalis.

5. 1. Type of Meningitis
Bacterial Meningitis
(ICD X: G00.9)
• 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 neurosurgery or fx of
the skull.
c. Device associated meningitis
particularly in assoc.
With CSF Shunts and drain.
Tuberculous Meningitis
(ICD X: A17.0).
• 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.
• TBM is an infection of the
meninges caused by the acid-
fast bacillus Mycobacterium
tuberculosis.

6. Type of Meningitis
1.1. Bacterial Meningitis
• 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
1.2. TBM
• 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”.

7. 1.1.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.

8. 1.1.Empiric antimicrobial Therapy
for Bacterial Meningitis
AGE GROUP ANTIMICROBIAL AGENTS
Neonates Ampicillin + Cefotaxime or cefipime
Infants and Children Ceftriaxone, cefotaxime or cefipime plus vancomycin
Adults (15-50 yo)
Community acquired Ceftriaxone, cefotaxime or cefipime + Vancomycin
Postneurosurg. Ceftazideime + Vancomycin
Immunocompromised Ceftazidime + Ampicilin
Other adults Ceftriaxone, cefotaxime or cefepime +Vancomycin + Ampicillin
Roos, K.L. Tormoehlen L.M. Central
Nervous System Infection in Practical
Neurology

9. 1.1.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(PMN) pleocytosis, low glucose level (<
40 mg/dl), elevated protein concentration

10. MENINGEAL SIGN
1. NECK STIFFNESS
2. BRUDZINSKI I
3. KERNIG SIGN ( N > 1350 )

11. MENINGEAL SIGN
4. BRUDZINSKI II
Resistance to neck flexion causes of the
nuchal rigidity most commonly
 Inflammation (Meningitis )
 Subarachnoid hemorrhage
POSITIVE Meningeal sign

12. PEMERIKSAAN TANDA PERANGSANGAN MENINGEAL
Pemeriksaan Kaku Kuduk (Nuchal/ Neck Rigidity)
1. Letakkan tangan kiri pemeriksa di bawah kepala pasien yang sedang berbaring. Rotasikan kepala ke kanan dan ke kiri untuk menyingkirkan adanya
proses lokal.
2. Fleksikan kepala pasien dan diusahakan agar dagu dapat menyentuh dada.
3. Perhatikan ada / tidaknya tahanan
Pemeriksaan Brudzinski I
1. Letakkan tangan kiri pemeriksa di bawah kepala pasien yang sedang berbaring.
2. Fleksikan kepala pasien dan diusahakan agar dagu dapat menyentuh dada.
3, Perhatikan ada / tidaknya fleksi kedua tungkai. Dikatakan positif , jika terjadi fleksi kedua tungkai.
Pemeriksaan Brudzinski II
1. Penderita disuruh berbaring, dengan kedua tungkai ekstensi.
2. Fleksikan salah satu sendi panggul sampai membuat sudut 900, sementara sendi lutut difleksikan maksimal.
3. Ekstensikan sendi lutut hingga mencapai 1350 antara tungkai bawah dan tungkai atas
4. Perhatikan ada / tidaknya fleksi tungkai kontralateral. Dikatakan positif, jika terjadi fleksi tungkai kontralateral.

13. 1.1. CSF Findings
CSF Parameter Bacterial meningitis NORMAL
• WBC Count > 1000/ ul, < 5
• Cell types >60% PMN
• Glucose < 40 mg/ dl 45 - 60
• Protein > 200 mg/ dl 20 - 45
• Gram stain + 80%
• Culture + > 90%

14. 1.1.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.

15. 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

16. 1.1. Treatment
1.Antibiotic therapy should be administrated. A minimum of 2 weeks of
therapy is recommended.
Age Antibiotic
0 – 4 mgg Cefotaxim + Ampicillin
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 (adults) Gen III. Cephalosporin+ ampicillin
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.

17. 1.1.Complication Bacterial meningitis
• Cerebral abscess
• Empyema subdural
• Convulsie
• Shock septic
• Cerebral edema
• Infarck serebral
• Herniation

18. 1.1.Sequele bacterial meningitis
• Mental retardation
• Hydrocephalus
• Convulsie, psikose
• Parese, deafness, blind.

19. 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

20. 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

21. 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

22. 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.

23. Cerebrospinal Fluid (CSF)
• Sebagian besar CSS (dua pertiga atau lebih) diproduksi di pleksus choroideus
ventrikel serebri (utamanya ventrikel lateralis). Sejumlah kecil dibentuk oleh sel
ependim yang membatasi ventrikel dan membran arakhnoid dan sejumlah kecil
terbentuk dari cairan yang bocor ke ruangan perivaskuler disekitar pembuluh
darah otak (kebocoran sawar darah otak).
• Pada orang dewasa, produksi total CSS yang normal adalah sekitar 21 mL/jam
(500 mL/ hari), volume CSS total hanya sekitar 150 mL.
• CSS mengalir dari ventrikel lateralis melalui foramen intraventrikular (foramen
Monroe) ke venrikel ketiga, lalu melewati cerebral aquaductus (aquaductus sylvii)
ke venrikel keempat, dan melalui apertura medialis (foramen Magendi) dan
apertura lateral (foramen Luschka) menuju ke sisterna cerebelomedular (sisterna
magna). Dari sisterna cerebelomedular, CSS memasuki ruang subarakhnoid,
bersirkulasi disekitar otak dan medula spinalis sebelum diabsorpsi pada granulasi
arachnoid yang terdapat pada hemisfer serebri

26. HASIL FOTO HEAD CT SCAN
HYDROCEPHALUS

27. SIGN AND SYMPTOMS
In young children
1. Cranium enlarges at a rate
> facial growth
2. Irritability
3. Fontanella full and bulging
4. Enlargement and
engorgement of scalp
veins; due to reversal of
the flow from the
intracerebral sinuses due
to increased ICP
In older child/ adults
1. Increased ICP
- Headache
- nausea
- vomiting
- visual impairement
- Ataxia
- papil edema

28. Oedema serebri
• Def: increasing of intra/extra brain cellulair
cause by local or diffuse brain process
• Type
• Vasogenic
• Citotoxic
• Osmotic
• hydrostatic
28
Kiking Ritarwan

29. Edema cerebri
29
Kiking ritarwan
Types of Edema Neurology in clinical practice
Vasogenic edema
= It is an extracellular edema which mainly
affects the white matter via leakage of fluid from
capillaries.
Tr capitis, stroke, meningitis, encephalitis,
SOL, malignant hypertension
Cytotoxic edema
=Imaging wise cytotoxic edema seen as
hypodensity involving cortical grey matter as well
as white matter result in loss of normal grey
white matter interphase. Cytotoxic edema is
seen with various intoxications and early
ischemia.
asphyxia, cardiac arrest, toxic subst
Osmotic edema water intoxication, hemodyalisis
Hydrostatic edema Hydrocephalus
Available from : www. Neuroradiologycases.com/2011

30. Diagnostic Procedure
1. MRI and CT Scan
2. LP : should be delayed or avoided

31. Treatment of Hydrocephalus
• Tumor or cyst causing hydrocephalus 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

32. 1.2. PATHOLOGY TBM
Aerosol transmission of Tuberculosis
Tuberculosis is spread by droplet nuclei which are expelled when a person with
infectious TB coughs, sneezes, speaks, or sings

33. 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

34. 1.2.Clinical staging of patients with TBM
(terminus/ advance)

35. 1.2.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).

36. 1.2.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

37. 1.2.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)

38. 1.2.Sistem Skoring Klinik
 Sensitivitas untuk
diagnosis TBM 99%
 Belum diujikan terhadap
kelompok HIV+

39. 1.2.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?)

40. 1.2.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

41. 1.2.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

42. 1.2.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

43. 1.2.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

44. Complication TBM
• Arteritis  thrombosis of a major artery
cerebral infarction.
• Hydrocephalus
• Seizures
• Focal motor deficits and impaired cognitive
• Hypopituitarism in childhood.

45. 1.2. Differential DX TBM
• 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.

46. 1.2. Diagnostic Prosedures TBM
1. Lumbal Puncture
CSF Parameter TB meningitis
• WBC Count < 500/ ul, MN
• Gluco moderate or marked decrease
• Protein marked increase
• Gram stain + +.-
• CSF lactic acid > 35 mg/dl.

47. 1.2. Diagnostic Prosedure TBM
 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
scans in detecting basal meningitis
infarction owing to arteritis hydrocephalus
and parenchymal tuberculomas often in
combination in AIDS patient.
 4.Mikrobiologi: BTA + KULTUR
 5. Arteriografi

48. 1.2. 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.

49. 1.2. Investigations TBM
• CSF examination
• CSF Smear examination: Zeihl Nelson’s, Gram’s
and India Ink stain.
• CSF culture on solid media: Egg or agar based
BACTEC systems.
• Adjunctive tests CSF tuberculostearic acid,
adenosine deaminase,
radiolabelled bromide partition test.
• Molecular diagnosis : Nucleic acid amplification,
DNA finger printing, PCR.

50. • Petechial hemorrhages in the
subcortical white matter of the
brain as a result of tuberculous
meningitis–associated
vasculitis.

51. • 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.

52. 1.2.Treatment TBM
• 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.

53. 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.

54. Differentiated Corticosteroid Regimen
in TBM
Thwaites et al, J Infect 2009; 59: 167-187

57. • CSF Consentration of certain antituberculosis
drugs
Anti Tuberculosis Drug
DRUGS Daily Dose
Mg/ kg
Serum
Ug/dl
Normal
Meningens
Ug/ms
Inflammated
menigens
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)

58. • Good penetration in CSF Treatment: Isoniazid,
Rifampicine,Pyrazinamide,prothianamide/ethion
amide and cycloserine.
• Only in the presence of meningeal inflamation:
kanamycin, amikacin and capreomycin
• Poor or no penetration: PAS and ethambutol
PRINCIPLES THERAPHY TBM

59. Prognosis TBM
• 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.

60. 1.3. 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.

61. 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

62. 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.

63. Treatment
1. Antiviral Activity. Acyclovir 10 mg/ kg iv every
8 hours for 10-14 days. Intravenous Acyclovir
can cause transient renal insufficiency
secondary or crystallization of the drug in
renal epithelial cells.
2. Anticonvulsant therapy
3. Therapy for increased ICP.

64. 1.4.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

65. • 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.

66. Clinical Picture of Fungal Meningitis
• Symptoms progress over days, sometimes 2-4
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

67. 1.4. Investigations
• Lab investigations:
1. Blood culture
2. Serum glucose
3.Arterial blood gases
4. Electrolyte
5. Liver function test
6. Urinalysis
• CSF Examinations: LCS tinta India dan kultur
• Imaging: CT brain dengan kontras

68. 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(+)

69. Invest….
• Chest X-ray : Hilar lymphadenopathy,
cavitation, effusion.
• CT or MRI: mass lesion (Cryptococcus)

70. 1.4.Treatment Meningitis
Cyptococcus
• Amphotericin B
- Protocol, starting with 0,7-1 mg/ Body weight
/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.
* Fluconazole: 800-1200mg/ hari (PO) selama 2
minggu.

71. HASIL LUMBAL PUNKSI
MENINGITIS

72. 2. 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.

73. • 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

74. 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.

75. 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.

76. 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

77. • 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

78. 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.

79. Affinities virus in myelitis
• Enterovirus anterior horn or nuclei of the
brain stem
• Herpes zoster dorsal root ganglion

80. Clinical manifestation
• Acute paraplegic or Quadriplegic.
• Urinary retention.
• Sensory disturbances

81. 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.

82. DIAGNOSIS BANDING :
• Multiple sclerosis
• Penyakit sistemik (SLE, Sjorgen disease)
• Venous infarct
• Malformasi vaskuler (fistula AV, AVM, angioma kavernosa)
• Fibrocartilagenous embolism
• Myelopati radiasi

83. Treatment Viral myelitis
• Antiviral treatment:
• Glucocorticoid
• Spasticity: baclofen (lioresal) 10 mg q6h,
benzodiazepin and tizanidine.

84. 3. BRAIN ABSCESS (ICD X: G06.0)
• 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.
• Multiple brain abscesses most frequently in : CHD,
lung abscess, empyema, bronchiectasis, bacterial
endocarditis, and immunocompromised states.

85. Mekanisme kuman masuk ke otak
Perluasan langsung dari kontak fokus infeksi
HHematogen
Post Trauma Kepala/ Operasi Bedah Saraf
HKriptogenik
25 – 50 %
30 %
30 %

86. 4 tahap proses evolusi
Serebritis awal
(day 1-3)
Serebritis lanjut (day 4-9)
Pembentukan kapsus awal
(day 10-13)
Pembentukan
kapsul akhir (day
14)

87. SEREBRITIS AWAL
Hari ke 1 – 3
 Infeksi serebri
 Terisi sel-sel radang
 Edema substansia alba,
batas belum jelas
PEMBENTUKAN KAPSUL
AWAL
Hari ke 10 - 13
 Resolusi daerah
serebritis
 Peningkatan makrofag
dan fibroblas
 Pembentukan kapsul dan
edema
PEMBENTUKAN KAPSUL
AKHIR
> Hari ke 14
 Kapsul yang matang
mengelilingi daerah
inflamasi berisi debris dan
sel PMN
 Edema serebri semakin
meluas
SEREBRITIS LANJUT
Hari ke 4 - 9
 Jaringan pusat
nekrotik
 Fibroblas
 Neovaskular tepi
daerah nekrotik

88. etiologi
Infeksi
Otoge
nik
Endokar
ditis
Bakterial
Sinus
Paranasal
Infeksi
Odonto
genik
Infeksi
Pulmon
al
Shunt
kanan
ke kiri
Post
Operasi
AIDS

89. Manifestasi klinis
Sistemik
• Demam
subfebril
Serebral
umum
• Nyeri kepala
kronis
progresif
• Mual,
muntah
• Penurunan
kesadaran
• Papil edema
Serebral fokal
• Kejang,
sering
general
• Perubahan
status
mental
• Defisit
neurologi
fokal,
motorik,
sensorik, n.
kranialis

90. Diagnosis Brain Abscess
 Anamnesis: dental sources, otogenic, sinus sources, penetrating
injury, cardiac disease
 Pemeriksaan Neurologi
 Head CT Scan  gold standard showing ring enhancing
lesion

91. Head ct scan BRAIN ABSCESS
Brain absces CT with contrast showing Ring
enhancing lesion

92. Tatalaksana BRAIN ABSCESS
Antibiotika
Drainase atau Eksisi
Atasi Edema Serebri
Pengobatan Infeksi Primer Lokal

93. Indikasi Operasi ABSES CEREBRI
Lesi diameter > 2,5 cm
Terdapat efek massa yang signifikan
Lesi dekat dengan ventrikel
Kondisi neurologik memburuk
Setelah terapi 2 minggu abses membesar
Setelah terapi 4 minggu ukuran abses tidak mengecil

94. TERAPI MEDIKA MENTOSA SAJA
DIPERTIMBANGKAN PADA KONDISI:
 Abses tunggal, ukuran < 2 cm
Abses multipel atau yang lokasi sulit
dijangkau
Keadaan kritis

95. komplikasi
Herniasi unkal / Tonsilar
Abses ruptur ke dalam
ventrikel atau ruang
subarakhnoid
Sekuele neurologis
jangka lama
Abses berulang

96. Antibiotic treatment for brain abscess
Ear,
mastoid,
sinus
Streptococcal
species, Ps
anaerobes,
Enterobaceteriacea
Metronidazole 7.5
mg IV every 6 h +
Cefepime 2 gr IV
every 6 h or
meropenem 2gr IV
every 8 h
Lung S. pneumoniae Same as above

97. AB treatment
Teeth, mouth Anaerobic
streptococci,
Eikenella,
Prevotella,
Actinomyces
Metro 7,5
mg/kg IV every
12 h + PNC G
4million units IV
every 4 h or
ceftizoxime 3 gr
IV every 6 h
Post operative
infection,
furuncles or
decubiti
Staphiloc Cefepime 2 gr
IV every 8 h, or
Nafcillin or
oxacillin 2 g IV
every 4 h

98. 4. Definition 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

99. 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.

100. Patogenesis.
Bila virus patogen masuk kedalam tubuh
pada SSP dapat terjadi:
• Radang akut
• Radang kronis
• Neoplasma
• Virus hidup dalam keadaan laten

101. Cara penyebaran ke SSP:
Cara penyebaran Contoh virus
• Hematogen herpes simplex
sitomegalovirus
Epstein-Barr
Coxsackie
HIV
Morbilli
Echovirus
khoriomeningitis limfositik
paravirus

102. • Neurogen Herpes simpleks
B-virus
Varisela-Zoster
Rabies

103. 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).

104. • Gejala sisa termasuk kejang2
• Komplikasi : - perubahan kepribadian
- ggn ekstrapiramidal
- demensia
- ggn motorik - sensorik

105. 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

106. 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.

107. 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