INFECTIONS OF THE

CENTRAL NERVOUS SYSTEM

Dr. Kiking Ritarwan, SpS(K), MKT

Departement of Neurology Medical
Faculty of University of Sumatera Utara
CNS INFECTION
MENINGITIS
- 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
CEREBRAL MALARIA
NCC
ANATOMI MENINGS
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 patients 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 ( 6-20
th
) N. meningitidis, S. pneumonie,H. infl.
- Adult ( > 20 thn) S. pneu, N. meningi, Streptococ,Staph.


Clinical Picture
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.
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.
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 3
rd
rank from 22
high burden countries.
Indonesia
22 High Burden Countries
1. India
2. China
3. Indonesia
4. Bangladesh
5. Nigeria
6. Pakistan
7. South Africa
8. Philippines
9. Russia
10. Ethiopia
11. Kenya
12. DR Congo
13. Viet Nam
14. UR Tanzania
15. Brazil
16. Thailand
17. Zimbabwe
18. Cambodia
19. Myanmar
20. Uganda
21. Afghanistan
22. Mozambique
Indonesia 10%
Bangladesh 4%
China
15%
India
30%
Other
28%
Philippines 3%
Pakistan 4%
Nigeria 3%
South Africa 2%
Russia 1%
3% of All Deaths in Developed
Countries Are Due to Tuberculosis
HIV/AIDS = human immunodeficiency virus/acquired immunodeficiency syndrome.
Other
27%
Cancer
12%
Stroke
10%
Injury
9%
Respiratory tract
infection 7%
HIV/AIDS 5%
Chronic obstructive
pulmonary disease 5%
Perinatal causes
Diarrheal disease
Tuberculosis
3%
3%
4%
2%
Malaria
Coronary heart
disease
13%
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 ZiehlNeelsen
/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: 33-39
o
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.
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.
Kategori diagnosis Ogawa
Definite
- bila kultur positi
- otopsi positip, atau keduanya
Probable
- likuor pleiositosis (>5/mm
3
), 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
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.

2. Laju endap Darah
3. Radiologic
3a. Chest x ray: detect pulmonary involvement
3b. CT scan8 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. Arteriografi
Images of CT Scans
file 1: 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.
file 2: Petechial
hemorrhages in the
subcortical white matter of
the brain as a result of
tuberculous meningitis
associated vasculitis.
file 3: 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.
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.
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
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 areTranversemyelitis.
Lesions are multiple and wide spreadOver a long vertical extent..
DiffuseOr Disseminated.
Combined meninges and spinal cordMeningomyelitis.
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.
Abscess of the brain has been known for
over 200 years, and surgical treatment
started with MacEwen in 1893 [published:
pyogenic infective disease of the Brain].
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
Middle ear,paranasal sinus,
or mastoid infection
Ear inf: temporal lobe abscess, sinus inf:
frontal lobe abscess, mastoid inf: cerebellar
abscess
Metastatic embolic from lung, pulmonary
abscess, bronchietasis, or chronic
empyema
Multiple abscess
Head trauma or Neurosurg.
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
Middle ear,paranasal
sinus, or mastoid
infection
Streptococci, Streptococci
Staph aureus Bacteriodes
Metastatic embolic from lung,
pulmonary abscess, bronchietasis, or
chronic empyema
Staph aureus, Klebsiela Streptococci,
S.Pneumoniae Fusobacteria
Head trauma or
Neurosurg.
Staph aureus, streptococci
Pseudomonas
Endocarditis Staph aureus -
Rare cause: dental procedures,
Metastatic emboli from abdominal inf.
Or PID, osteomyelitis of skull
-
RISK FACTORS AND PATHOGENESIS
CEREBRAL ABSCESS
Directly from the paranasal sinuses, mastoid, middle
ear or via hematogenous spread e.g. colonic diverticulae,
pulmonary infection, periodontal infection, bacterial
endocarditis, except rabies (infiltration along peripheral nerve),
Naegleria and herpes via the olfactory bulbs
Bacterial caused by aerobic and anaerobic gram
negative/positive
The source of inoculation of CNS remain unknown in
up to one-third
Head trauma : CSF leak, reoperation, delay in care or
basilar skull fracture
Implantation of a foreign body : shunt, high-grade
glioma, irradiation
Immunocompromised : transplant, cancer, chemotherapy,
retroviral infection
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
Cerebritis results in a non homogeneous mass with
irregular margins and diffuse enhancement
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. 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.
A B
TEMPORAL LOBE ABSCESS
CT scan showing ring enhancement in temporal sinistra
(hyperdense capsule differentiated from central low density
(pus) and marked surronding edema)
Komplikasi Abses Otak
Robeknya kapsul abses kedalam ventrikel atau
keruangan subarakhnoid.
Penyumbatan cairan serebrospinal
hidrosefalus
Edema otak
Herniasi tentorial oleh massa abses otak.
72
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.
SURGICAL MANAGEMENT CEREBRAL ABSCESS
Stereotactic aspiration
Advantages :
Avoidance of general anesthesia
Access to multiple lesions without an increase in surgical
complexity
Ability to decompress lesions in eloquent areas such as the
thalamus and basal ganglia
Simple cystic structure ; size <1.5 cm ; deep gray matter ; no
air/fluid level ; no fistula
Complication : intracerebral hematoma 0.4% to 1.6%
Mortality less than 0.2% ; morbidity 1-4%

Open craniotomy with or without excision of the capsule
Posterior fossa masses indicate for open craniectomy ; encapsulated
; silent cortex or white matter
Multiloculated abscesses, which are difficult to fully
decompress stereotactically, should open ; size >2.5 cm ;
air/fluid level in abscess ; fistula
Mortality 1% to 11% ; morbidity 4% to 30%

The goal treatment in brain abscesses :

Reduce mass effect
Decrease intracranial pressure
Prevent herniation or intraventricular
rupture and ventriculitis
Identify the causative microorganism
Establish antibiotic sensitivities
Antibiotic treatment for brain abscess
Rational Administration :Timing of initial therapy, Choice of agents,
Penetration of various agents into the brain, Duration of therapy


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
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
NEUROLOGICAL SEQUELAE
Most likely due to :
Delayed diagnosis
Poor initial neurological conditions
Larger size
Common neurological sequelae are cognitive
defisits, hemiparesis, and seizures
Infants and children have a worse outcome than
adults ,IQ lower than 80, 70% children had
difficulties with school performance, 38% had
severe hemiparesis
Adult : 87% were able to continue their normal
work and none had severe hemiparesis

Seizure disorders
3 to 4 years after treatment (15% to 92%)
Children are more likely than adults
Most common lesion at frontal and temporal
lobes ; occipital lobe are unusual ; cerebellar
do not predispose to seizures
Anticonvulsant for at least 6 months
Rates of recurrence 10% to 50%
PROGNOSIS Cerebral Abscess
Mortality > 60% if sign of brain herniation are
present
Mortality rate <29% among alert patients
90% among comatose patients
Mortality rate 12.5% in posttrauma without signs of
herniation
Mortality rate 4.3% since CT became a routine
diagnotic test
Sex and ethnic origin is no evidence for mortality
High mortality rate in :
Patients related to immaturity
Virulence of the gram-negative organisms
Coexistent systemic disease
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.
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
Spektrum NeuroAIDS
Primary complication (non-
opportunistic disease)
HIV-Dementia
HIV-Sensory neuropathy
Secondary complication
(opportunistic disease)
Cerebral Toxoplasmosis
TB Meningitis / tuberculoma
Cryptococcal meningitis
Other opportunistic diseases....
Komplikasi neurologi HIV
Brain Predominantly nonfocal
AIDS dementia complex
Acute HIV-related encephalitis
Cytomegalovirus encephalitis
Varicella-zoster virus encephalitis
Herpes simplex virus encephalitis
Metabolic encephalopathies
Predominantly focal
Cerebral toxoplasmosis
Primary CNS lymphoma
Progressive multifocal leukoencephalopathy
Cryptococcoma
Brain abcess / tuberculoma
Neurosyphilis (meningovascular)
Vascular disorders
Spinal cord
Vacuolar myelopathy
Herpes simplex or zoster myelitis
Meninges
Aseptic meningitis (HIV)
Cryptococcal meningitis
Tuberculous meningitis
Syphilitic meningitis
Metastatic lymphomatous meningitis
Peripheral nerve and root and root
infectious
herpes zoster
cytomegalovirus lumbar polyradiculopathy
Virus or immune-related
acute and chronic inflammatory HIV poly-
neuritis
mononeuritis multiplex
sensorimotor demyelinating polyneuropathy
distal painful sensory polyneuritis
Muscle
polymyositis and other myopathies
Perjalanan penyakit infeksi HIV
Infeksi virus (2-3 minggu) sindroma
retro- viral akut (2-3 minggu) gejala
menghilang + serokonversi infeksi
kronis HIV asimpto matik (rata2 8 thn)
infeksi HIV / AIDS simptomatik (rata2 1,3
thn) kematian.
Window period masa dimana
pemeriksa- an test serologis utk antibodi
HIV masih negatif, tapi virus sdh ada dlm
darah (sudah mampu menularkan kpd
orang lain)
HIV dementia (AIDS
Dementia Complex)
This progressive dementia occurs in AIDS,
owing to a direct primary HIV infection of
neurons or an indirect neurotoxicity
induced by presence of the virus in the
brain
Pathology: the virus may be transported
into the brain by infected peripheral
monocytes (Trojan horse theory).

Manifestasi klinis demensia HIV:

Cognititive disorders
Gangguan kognitif, kesulitan konsentrasi,
forgetfullness, cognitive slowing. Kadang2 agitasi,
mania.
Pd std awal sulit membedakan dgn keluhan psikiatri.
Motor abnormalities: ataksia, hiperreflels. Babinski
refleks srg muncul. Pada std lanjut : paraparese dgn
inkontinansia urin et alvii
Behavioural dysfunction : Apathy, altered personality,
disorientasi. Std akhir Mutism
CEREBRAL TOXOPLASMOSIS
Reactivation of latent infection
Toxo seroprevalence 12-46% (SA)
IgG indicates past infection (FN <3-6%)


CD4 > 200 virtually excludes Toxo
Over 80% have CD4 < 100

Typically multiple ring enhancing lesions on CT/MRI
27-43% have single lesions
Up to 10% may have diffuse encephalitis without any
visible focal lesions


The course of HIV/AIDS
Notes:
Normal
MRI
CT Scan
Atrofi Meningeal
enhancement
hidrosefalus SOL
Evaluasi LCS Shunt
(kalau perlu)
Positif Negatif
Terapi sesuai
etiologi
Observasi
Lesi massa(-) Lesi massa (+)
Skema 2
Keluhan intrakranial
Skema-1. Algoritme Penatalaksanaan Keluhan Intraserebral bagi
Penderita HIV-AIDS

normal
Terapi toksoplasmosis
Seumur hidup
Terapi sesuai
etiologi
Dekompresi dan
biopsi terbuka
Lesi massa intrakranial
Alert-lethargic
stabil
Steroid ? Stupor-koma
Perburukan cepat, massa besar
Dengan resiko herniasi
Lesi multipel Lesi tunggal

Serologi
toksoplasma
Negatif Positif
Obat antitoksoplasmosis
Perbaikan
Ya Tidak Biopsi stereotaktik
Ancaman herniasi
Skema-2. Algoritme Penatalaksanaan Lesi massa Intrakranial pada penderita HIV-AIDS

Toxoplasmosis Clinical Features
Usually subacute over weeks

Headache 50%
Fever 45%
Behaviour changes 40%
Confusion 15-52%
Focal signs
Seizures 24-29%
TREATMENT
Acute treatment : 3-6 weeks.
Induction : pyrimethamine 200 mg
First line :
Pyrimethamin 75-100 mg/day + sulfadiazine +
folinic acid or
Pyrimethamin + clindamycin + folinic acid.
Second line :
Azithromycin, clarithromycin, or atovaquone can
substitute for sulfadiazine.
Glucocorticoid life threatening condition.
TREATMENT
Maintenance :
Until the immune system has sufficiently
reconstituted.
Pyrimethamine and sulfadiazine or
Pyrimethamine and clindamycin.
Stop :
Asymptomatik.
CD4+ > 200/cmm until 6 months.
Fase akut (3-6
minggu)
Pemeliharaan/rum
atan

Pilihan pertama



Pilihan kedua




Pilihan ketiga

Pyrimethamine oral 200 mg hari pertama,
selanjutnya 50-75 mg/hr + leucovorin oral
10-20 mg/hr + sulfadiazine oral 1000-1500
mg/hr

Pyrimethamine + leucovorin (dosis di atas) +
clindamycin oral atau IV 4 x 600 mg


Pyrimethamine + leucovorin (dosis di atas) +
salah satu :
Atovaquone oral 2 x 1500 mg
Azithromycin oral 1 x 900 1200 mg
Clarithromycin oral 2 x 500 mg
Dapson oral 1 x 100 mg
Minocyclin oral 2 x 150-200 mg

Pyrimethamine oral 25-50 mg/hr +
leucovorin oral 10-20 mg/hr +
sulfadiazine oral 500-1000 mg/hr.


Pyrimethamine + leucovorin (dosis di
atas) + clindamycin oral 4 x 300 mg
450 mg

Pyrimethamine + leucovorin (dosis di
atas) + salah satu antibiotika tersebut
dosis sama.
107
CT - Multiple ring enhancing lesions
Toxo more likely

Tuberculomas still
possible


Differential Diagnosis
Toxoplasmosis P CNS L
Location Basal ganglia.
Gray-white junction
Periventricular
Number of lesion Multiple Solitary>multiple
Enhancement pattern Ring Heterogeneous or
homogeneous.
Edema Moderate to marked Variable
T2-weighted image
(lesion relative to
white matter)
Hyperintense Isointense to
hyperintense.
Diffusion-weighted
image
Usually hypointense Often hyperintense
(positive)
Differential Diagnosis
Toxoplasmosis P CNS L
MR perfusion Decreased Increased
MR spectroscopy Markedly elevated
lactate.
Markedly elevated
choline
SPECT thallium
(lesion relative to
white matter)
Cold-no thallium
uptake
Hot-increased
thallium uptake.
Other Toxoplasma IgG Ab
(+) (90% of patients)
EBV DNA amplified
by PCR in CSF
(most patients)
Malaria Serebral (MS)
MS adalah malaria dengan penurunan
kesadaran ( dewasa GCS < 9 dan anak
Blantyre coma score < 3) atau koma lebih dari
30 menit setelah serangan kejang yg tidak
disebabkan oleh penyakit lain.
MS komplikasi dari malaria falcifarum berat,
dijumpai st ensefalopati difus dengan penurunan
kesadaran dan berhubungan dengan
sequestrasi mikrovaskuler serebral.
Blantyre coma scale(0-7)
Oculer response
- Follow mothers facial reaction 1
- non reaction 0
Verbal response
- Normal crying 2
- Whimpering 1
- no sound .. 0
Motoric response
- Localize pain 2
- rettraction of limb ..1
- non reaction 0
Plasmodium falcifarum
morphology in stained preparation
Ring form: vary in
shape; double
chromatin, double
infection, accole

Trophozoit: rare in
peripheral blood
after half grown
Plasmodium falciparum
Morphology of all stadiums
Patogenese
Ada 3 teori:
1. Teori mekanis :
tjdnya penyumbatan pemb drh otak akibat
tjdnya sitoadherens, sekuester, rosetting dan
faktor rheologi.
2. Teori Toksik menghasilkan TNF
3. Teori Permeabilitas: tjdnya adhesi parasit pd
endothel, vasculer serta banyak faktor toksik yg
lepas serta radikal bebas terutama Nitric oxide
(NO).

Diagnosa Malaria Serebral
Gjl Klinik : Trias malaria ( demam, menggigil, dan
berkeringat), Sakit kepala, ggn mental, nyeri tengkuk,
kaku otot dan kejang umum
Sering dijumpai splenomegali dan hepatomegali
Ggn kesadaran atau koma ( biasanya 24-72 jam)
Pemr darah (thin/thick smear) dijumpai bentuk aseksual
P. Falcifarum
Tidak ditemukan infeksi lain
Lain-lain:hipoglicaemia, hiponatremia, hipofosfatemia,
pleocytosis sampai 80 cel/ micron kubik, limfosit
sampai 15 cel/ mikron kubik
CT/ MRI: edema serebri.
Laboratorium
Pemeriksaan dengan mikroskop
- sediaan darah tebal dan tipis
Test diagnostik lain
- Metode immunokromatografi
- Analisa cairan Serebrospinal pd
Malaria serebral didapti peningkatan
limfosit > 15/ul.
- CT dan MRI: edema serebral
Comparison of diagnosis method
Clinical
diagnosis
Microscopic RDTs
Sensitivity 60-75% 60-95% 44-100%
Specificity 30-40% 75-95%
95% (only for Pf
or Pv or Pan)
Infrastructure
needed
Minimal High Moderate
Skill needed Minimal High Moderate
Cost Cheap Moderate Expensive
Pengobatan Malaria Tanpa Komplikasi
Malaria Falsiparum
Lini pertama = Artesunat + Amodiakuin + Primakuin
Lini kedua = Kina + Doksisiklin atau Tetrasiklin + Primakuin
Pengobatan lini kedua diberikan jika pengobatan
lini pertama tidak efektif, dimana 28 hari setelah
pemberian obat :
Gejala klinis memburuk dan parasit aseksual positif, atau
Gejala klinis tidak memburuk tetapi parasit aseksual tidak
berkurang (persisten) atau timbul kembali (rekurensi)
Neurocisticercosis (NCC)
Def: cysticercosis cellulosa is the larval
stage of development of the cestode
Taenia solium (pork tapeworm).
More than 60 million people are infected
with T. saginata world wide and about 4
million are infected with T. solium

In Indonesia
North Sumatra
Lampung
Jakarta
Bali
Flores
East Timor
Irian Jaya
North Sulawesi West Kalimantan
Fig. I. Geographic distribution of in Indonesia until 1995. Areas endemic with taeniasis are indicated in colour.
( Modified from the unpublished report CDC & EH. Ministry of Health, Indonesia, 1983 1996 )
Pathology :3 Form cysticercosis in CNS
1. A cystic form involving the ventricles and
brain parenchyma
2. A racemose form involving the meninges
3. A miliary form that is common in children

PATOGENESIS
Human NCC : ingest food contaminated
with T.solium egg
Parasite survive over period of year
It secretes protease inhibitor, taeniastatin
that inhibit complement activation,
neutrophyl, lymphocyte and cytokine
production.
Minimal inflammation around viable cyst
Inflammatory respons attacks the
parasite, leads to degeneration and
calcification

CLINICAL MANIFESTATION

Number of the cysts
Location (parenchimal/spinal)
Parasite activity
Immune respons of the host



DIAGNOSIS
Definitive
Present of the scolex on
histologic examination or on CT
scan/MRI


MRI
More sensitif for detect
parenchymal cyst,
intraventricular and
subarachnoid cyst


MANAGEMENT NCC


Anti parasitic drug
Symptomatic and anti-
inflamatory
Surgery




ANTI PARASITIC DRUG
Praziquantel :
50mg/kg/day, two weeks.
Albendazol :
15mg/kg/day, one month.



SYMPTOMATIC/
ANTIINFLAMMATION

Corticosteroid :
Dexamethasone 4,5 12 mg/day, or
Prednisone 1mg/kg/day.
Decrease neurological symptoms
due to the death of the parasite.
Manitol 2g/kg/day, for acute intracranial
hypertension.
First line antiepileptic
SURGERY
For excision of large cysts or cyst
in the ventricles