Neuroinfeksi

Question 1

Pasien dengan gejala meningitis Dan tinta India positive. Diagnosis :

Answer 1

Cryptococcus

Question 2

Terdapat negri bodies pada PA

Diagnosis

Answer 2

Rabies

Question 3

Tatalaksana Pilihan CMV (Cytomegalovirus)

Answer 3

Fase induksi (3 minggu)

• foscarnet 60 mg/kgBN/8jam
• Ganciclovir 5 mg/kgBB 12 jam

Ganciclovir Merupakan analog 2-deoxyguanosine , yg merupakan obat antivirus yg memiliki efek Klinis pada virus CMV

Question 4

meningitis Listeria monocytogenes tatalaksana Pilihan adalah

Answer 4

Penicillin 6x2 g selama 3 minggu

Penicillin/ampicillin + gentamicin

Penicillin/ampicillin tidak bisa diberikan tunggal pada infeksi listeria.
Sefalosporin generasi 3 tidak aktif melawan listeria.

Question 5

Acute HIV aseptic meningitis

Answer 5

seroconversion syndrome (fase awal HIV).
Klinis :  febrile illness, headache, meningeal irritation. By definition, alertness and cognition are
preserved.
LCS : lymphocytic
pleocytosis (but usually less than 25 cells/μL) peningkatan protein level (less than 100 mg/dL), normal glucose levels.

Question 6

Lyme disease

Answer 6

Disebabkan Borrelia burgdorferi.
Klinis:
• Stage 1 (infeksi lokal):dalam 4 mg setelah digigit kutu, erythema chronicum migrans ( bull’s eye rash)
• Stage 2 (penyebaran infeksi) (beberapa Hari/minggu setelah merah):
systemic manifestations; fever, chills, migratory
musculoskeletal pain, arthralgias, fatigue,Cardiac involvement.After weeks
or months, lymphocytic meningitis,
neuropathies, including cranial and peripheral
neuropathies.
• Stage 3 (persistent infection) (months after the secondary
stage): Intermittent episodes of oligoarthritis,
encephalomyelitis,encephalopathy, and dementia. An axonal
polyneuropathy may also occur.

Question 7

mucormycosis

Answer 7

mucormycosis, which is a zygomycosis. This
fungus tends to enter through the respiratory tract, producing nasal
and sinus disease and pulmonary infections. In the presence of
predisposing factors and trauma, it may invade blood vessels and
gain entry into the CNS, where it can produce an acute necrotizing
reaction and vascular thrombosis, including venous sinus
thrombosis, especially affecting the cavernous sinus. Externally,
patients have a destructive inflammatory and necrotizing lesion
affecting the face, especially in the nasal and maxillary areas.
Diabetes mellitus and diabetic ketoacidosis are major and frequent
risk factors for this condition. Other predisposing conditions
include malignancies, high-dose steroids, organ transplantation,
immunosuppression, and iron chelation therapy (with
deferoxamine). The organisms causing this infection are mucor,
rhizopus, and rhizomucor, which are fungi and not acid-fast bacilli.
These fungi are seen as infrequently septated or nonseptated
hyphae on histopathologic specimens.

Question 8

HIV-associated neurocognitive disorder ( AIDS-dementia
complex)

Answer 8

Umumnya pada HIV stadium lanjut.
Spektrum terdiri atas :
- asymptomatic neurocognitive impairment (ANI)
- minor neurocognitive disorder (MND)
- HIV-associated dementia. (HAD). biasanya pada CD4<200 cells/mm3
The etiology of this
condition is the retrovirus itself rather than an opportunistic
infection. Progressive cognitive decline and prominent
psychomotor dysfunction are the main clinical manifestations.
These patients have significant difficulties with attention and
concentration, along with fine motor dysfunction, gait
incoordination, and tremors. However, focal neurologic deficits are
not common.
Pemeriksaan :
- MRI kepala : atropi difus, umumnya mengenai basal ganglia, white matter, regio cortical.

Question 9

Nile virus (WNV) encephalitis

Answer 9

West Nile virus (WNV) encephalitis, which is an
arboviral infection that spreads in the summer months, can occur in
epidemics, and is transmitted by mosquitoes of the genus Culex.
Most infected patients are asymptomatic, up to 20% may show
signs of a febrile viral illness, and less than 1% develop a severe
neurologic presentation. Patients with severe neurologic
presentation will have manifestations of encephalitis; however,
WNV can also invade the anterior horn cells leading to flaccid
weakness with arreflexia, similar to poliomyelitis. WNV infection
may also manifest with cranial neuropathies and tremors. Elderly
patients are particularly at risk for neurologic disease, especially
encephalitis, however, meningitis and flaccid paralysis may also
occur in young and middle-aged patients.
WNV encephalitis is diagnosed by serology and detection of
immunoglobulin M (IgM) antibodies in the CSF. CSF PCR is less
sensitive, but is diagnostic when positive. MRI is nondiagnostic.
Treatment is supportive

Question 10

Cryptococcal meningitis

Answer 10

Disebabkan Cryptococcus neoformans/gatii.
histopathologis : budding yeasts near blood
vessels and surrounded by an inflammatory infiltrat.
Umumnya pada immunocompromise dan opportunistic infeksi HIV
lanjut.
CSF : protein tinggi, pleositosis (pada immunocompromised tdk Ada reaksi inflamasi)
Sitologi : pseudohifa, jamur crypto

Question 11

Tatalaksana Cryptococcal meningitis

Answer 11

The initial treatment regimen is amphotericin plus flucytosine
for 2 to 3 weeks. These patients should be monitored closely, since
amphotericin is associated with renal failure, hypokalemia, and
hypomagnesemia; and flucytosine may cause hematologic
abnormalities. If the patient is doing well on amphotericin and
flucytosine, or the meningitis is mild, the treatment can be
switched to fluconazole 200 mg twice daily for 8 to 10 weeks.
Afterward, the patient should be kept on long-term maintenance
therapy with fluconazole 200 mg daily to prevent recurrences.
Highly active antiretroviral therapy, by promoting immune
reconstitution, plays a major role in the long-term treatment of
HIV patients with cryptococcal meningitis, after the acute infection
has cleared

Question 12

Toxoplasmosis

Answer 12

Infeksi oportunistik pd AIDS, terutama tanpa ARV adekuat. Pada immunosuppressive lanjut dgn CD4< 200/μL
Klinis : nyeri kepala, defisit Neurologis
Imaging : CT ; lesi hipodense menyangat kontras. Predileksi basal ganglia, Dan corticomedullary junction , kadang Di fossa posterior.
The organism is
usually acquired earlier in life and remains dormant until the
immune system declines and T. gondii becomes active.

Question 13

Tatalaksana Toxoplasmosis Encephalitis

Answer 13

Terapi induksi (6 minggu)
Pirimetamin loading 200 mg , dilanjutkan 50 mg (75 mg bila BB>50 kg)
+ Clindamycin 4x600 mg / sulfadiazine 4-8 gr per Hari
Terapi rumatan : setengah dosis terapi induksi, Atau cotrimoxazole 2x1 hingga CD4>200
Terapi perlu penambahan asam folat

Standard therapy is sulfadiazine plus pyrimethamine. Since both
agents affect the folate metabolism pathways, folinic acid should
be provided to avoid hematologic complications. An alternative
therapy is clindamycin, especially in patients who are allergic to
the sulfa components and cannot take sulfadiazine. Long-term
suppressive therapy is needed to prevent relapses. Highly active
antiretroviral therapy promotes immune reconstitution, and
patients whose CD4 counts rise above 200/μL may not need further
suppressive therapy. Trimethoprim-sulfamethoxazole is used for
prophylaxis. Patients with HIV and CD4 counts of less than 100/μL
with positive IgG antibodies to toxoplasma should be given
prophylaxis.

Question 14

primary CNS lymphoma (PCNSL) pada AIDS.

Answer 14

These patients usually present with focal neurologic
manifestations, which progress slowly over days to weeks. Since
PCNSL in AIDS patients is frequently associated with Epstein–Barr
virus, positive CSF PCR for this virus helps to make the diagnosis.
CSF findings usually demonstrate a lymphocytic pleocytosis,
elevated protein, and low to normal glucose levels. Cytology may
detect atypical cells; however, this test has low sensitivity. Flow
cytometry is helpful in making the diagnosis showing monoclonal
B lymphocytes. CT scan has poor sensitivity, and MRI is a better
tool, showing one or more lesions usually in the periventricular
and deep regions of the brain. These lesions may have contrast
enhancement, surrounding edema, and produce mass effect.
Definitive diagnosis is done with brain biopsy.
Corticosteroids are helpful in the treatment of edema and mass
effect, and the lesion itself tends to shrink with this treatment.
However, the use of steroids may alter the results and the
sensitivity of the brain biopsy. Whenever possible, their use should
be delayed until after the biopsy is obtained. The use of
chemotherapy is controversial in this setting, and may not be
optimal in patients with a baseline poor performance status related
to the underlying disease. Radiation therapy is used as palliative
treatment. The use of highly active antiretroviral therapy has
improved the overall prognosis in patients with AIDS and PCNSL

Question 15

progressive multifocal leukoencephalopathy

PML

Answer 15

progressive multifocal leukoencephalopathy
(PML), caused by JC virus, which is a polyomavirus. PML occurs in
patients with end-stage AIDS. A large percentage of the general
population has antibodies against this virus, certainly without
clinical manifestations; and therefore, the presence of serum
antibodies is not helpful for the diagnosis. Only those patients with
severe immunosuppression develop clinical manifestations; PML in
immunocompetent individuals is exceedingly rare but can occur.
PML is a demyelinating condition and presents with a gradually
progressive course of multiple focal neurologic manifestations,
with visual field deficits and visual agnosias being common, given
the predominant involvement of parieto-occipital regions.
Hemiparesis, sensory deficits, language disorders and ataxia may
occur.
The diagnosis can be suspected with the history and clinical
manifestations, supported with MRI findings and CSF JC virus DNA
PCR, and confirmed with brain biopsy (though brain biopsy is not
necessary in the setting of typical clinical, imaging, and CSF
findings).
MRI shows multiple white matter nonenhancing lesions that tend
to coalesce and predominate in the parieto-occipital regions. Brain
biopsy is the gold standard diagnostic test; neuropathologic
findings include myelin loss, giant astrocytes, and altered
oligodendrocytes, with enlarged nuclei and viral inclusions. On
electronic microscopy, the viral particles give a “spaghetti and
meatballs” appearance.

Question 16

HIV neuropathy

Answer 16

HIV neuropathy, which is a distal sensory
neuropathy seen in patients with HIV, more frequently as the CD4
count drops. This condition is a predominantly sensory, axonal
length-dependent symmetric polyneuropathy. It is thought to be
related to direct effects of the virus and cytokine upregulation.
These patients should continue antiretroviral therapy for virus
suppression, and the treatment is symptomatic for the neuropathic
pain.

Question 17

Bacterial meningitis penyebab:

Answer 17

Penyebab : *1 - 23 bln :Streptococcus pneumoniae, Neisseria meningitidis, Streptococcusagalactiae, Haemophilus influenzae, Escherichia coli.*2 - 50 th: Streptococcus pneumoniae, Neisseria meningitidis. *> 50 th : Listeria monocytogenes,Streptococcus pneumoniae, Neisseria meningitidis.* Riw Neurosurgical
: aerobic gram-negative
bacilli (including Pseudomonas aeruginosa), Staphylococcus aureus,
Staphylococcus coagulase negative (such as epidermidis).
*CNS instrumentation, these same agents and
Propionibacterium acnes should be considered. *Unlike in communityacquired meningitis, Streptococcus pneumoniae is not a common
cause of hospital-acquired meningitis.

Question 18

Meningitis bakterial pemeriksaan LCS

Answer 18

Pemeriksaan LCS rutin :
Peningkatan protein, penurunan glukosa, peningkatan neutrofil

Pemeriksaan gram :
90 % disebabkan Streptococcus
pneumoniae, 86% of those caused by Haemophilus influenzae, 75%
of those caused by Neisseria meningitidis, 50% of those caused by
gram-negative bacilli, and 33% of cases caused by Listeria
monocytogenes have positive Gram stain results.
Even though the yield of CSF Gram stain can be as low as 20% in
patients who have received antibiotics, this test is easy to do, is
rapid and inexpensive, and is recommended for all patients with
suspected bacterial meningitis.

Question 19

Tatalaksana meningitis bakterial

Answer 19

Neisseria meningitidis: cephalosporin (gen 3); ceftriaxone /cefotaxime, 7 days.
Streptococcus pneumoniae ;vancomycin and ceftriaxone, 10 - 14 days.
Listeria monocytogenes; ampicillin
+ gentamicin
for more than 21 days.
Haemophilus influenzae ;ampicillin if the organism is β-lactamase negative; however, if it is
β-lactamase positive, cephalosporin gen3. Pseudomonas aeruginosa :usually a hospital-acquired
infection and is typically resistant to ceftriaxone. Ceftazidime and
cefepime have been used to treat this infection, at least 21 days.

Question 20

Abses brain

Answer 20

brain abscesses. These lesions
originate from invasion of brain parenchyma by bacterial
organisms, commonly polymicrobial, with a combination of
streptococci, staphylococci, enterobacteria, and anaerobes. The
bacterial agents spread via hematogenous routes or from a
contiguous infected site, such as the sinuses, ears, or teeth. They
also can be encountered after open trauma or neurosurgical
interventions.
Patients may present with fever, headaches, neck stiffness, focal
neurologic findings, and altered mental status. The diagnosis is
made on the basis of clinical suspicion and the presence of risk
factors, along with clinical and radiologic findings, with the MRI
showing ring enhancing lesions with surrounding edema.
Lumbar puncture may be contraindicated in the presence of mass
effect, and therefore CSF may not be available. The presence of
atypical lymphocytes and monoclonal B cells in the CSF are seen in
lymphoproliferative disorders and not in brain abscesses.
Brain abscesses evolve through different stages, with initial
cerebritis in the first few days, then the formation of central
necrosis with surrounding vasogenic edema, and the subsequent
formation of a capsule. The abscess eventually matures, with the
development of collagenous tissue in the capsule and regression of
the vasogenic edema. Caseating granulomas are not seen in
cerebral bacterial abscesses.
Optimal treatment requires drainage of the abscess in
combination with intravenous antibiotics. Given that these lesions
are most commonly polymicrobial, the treatment of choice is a
combination of antibiotics, usually a third-generation cephalosporin
(for streptococci and gram-negative bacilli), metronidazole (for
anaerobes), and vancomycin (for staphylococci). The IV antibiotic
regimen is continued for 6 to 8 weeks, and subsequent continuous
oral antibiotics may be required beyond the initial treatment
period

Question 21

Tatalaksana brain abscesses

Answer 21

• drainage abses
• the treatment of choice is a
  combination of antibiotics, usually a third-generation cephalosporin
  (for streptococci and gram-negative bacilli), metronidazole (for
  anaerobes), and vancomycin (for staphylococci). The IV antibiotic
  regimen is continued for 6 to 8 weeks, and subsequent continuous
  oral antibiotics may be required beyond the initial treatment
  period.

Question 22

septic cavernous sinus thrombosis

Answer 22

septic cavernous sinus thrombosis, which can be a
complication of bacterial sinus infections, and manifests with
proptosis, compromise of the cranial nerves (CNs) traveling within
the sinus (CNs V1 and V2, III, IV, and VI), retinal vein
engorgement with retinal hemorrhages, and papilledema.
Patients with intracranial infections may also develop thrombosis
of other sinuses such as the superior sagittal or the transverse
sinuses. Diagnosis is based on clinical suspicion and radiologic
studies. Brain MRI, MRV and/or angiography with visualization of
the venous phase may be useful. Treatment involves antibiotic
therapy, covering gram-positive agents, staphylococci, gramnegative organisms, and anaerobes.

Question 23

Morbus Hansen / lepra

Answer 23

Hansen disease, or leprosy. This disease has a long
incubation period (from years to decades) and is caused by
Mycobacterium leprae, which is thought to spread through the
respiratory tract but does not typically produce a respiratory
illness. This mycobacterium has tropism toward peripheral nerves,
especially in cooler areas of the body.
Leprosy has two major variants, a lepromatous variant and a
tuberculoid variant, in addition to intermediate forms between the
two. The lepromatous variant occurs in patients with impaired cellmediated immunity, making it possible for the organism to spread
to the skin and peripheral nerves, causing a maculopapular rash,
nodules, and poorly demarcated skin lesions. The manifestations
can be systemic, and patients present with sensory loss
predominantly in the coolest regions of the body, such as the pinna
of the ear, tip of the nose, dorsal surfaces of the hands, forearms
and feet, and dorsolateral surface of the legs. The tuberculoid form
occurs in patients with good cellular immunity, in which the
disease is less disseminated, the skin lesions are better localized,
and the patient will also have asymmetric peripheral neuropathies
with thickened nerves. The ulnar nerve is commonly affected, and
the syndrome may resemble mononeuritis multiplex. Other
commonly involved nerves include the greater auricular, radial,
common peroneal, and sural nerves.
The diagnosis is suspected based on clinical and epidemiologic
data. Skin and/or nerve biopsies are often necessary,
demonstrating inflammatory granulomas with epithelioid and
mononuclear infiltrates and acid-fast organisms.

Question 24

Tatalaksana morbus Hansen

Answer 24

Chronic therapy is usually needed, using rifampin, dapsone, and
clofazimine.

Question 25

Meningitis Tuberculosis

Answer 25

TB meningitis is caused by Mycobacterium tuberculosis, which is
an aerobic mycobacterium that spreads via respiratory droplets
leading to a primary infection (usually pulmonary) and subsequent
reactivation (commonly in the setting of immunosuppression). TB
meningitis tends to affect the base of the brain and frequently
presents with fever, headache, neck stiffness, multiple cranial
neuropathies (due to involvement of the basal aspect of the brain)
and altered mental status. Focal neurologic manifestations and
seizures may also occur.
CSF demonstrates elevated protein level, low glucose level, and
lymphocytic pleocytosis. Opening pressure is usually elevated but
may be normal. Acid-fast bacillus (AFB) smear is diagnostic in 10%
to 30% of the cases, and CSF cultures may be positive in 45% to
70%; however, the results may take between 6 and 8 weeks to
become positive. PCR has higher sensitivity and may be helpful to
make a diagnosis earlier. Brain MRI may be normal or may
demonstrate meningeal enhancement, especially on the basal
surface. Pathologic specimens show caseating granulomas,
mononuclear inflammatory infiltrates, and multinucleated giant
cells as described in this case.

Question 26

Tatalaksana meningitis Tuberculosis

Answer 26

Combinations of multiple anti-TB agents are used to kill the
organisms and avoid inducing resistance. Commonly used
medications are isoniazid, rifampin, pyrazinamide, streptomycin,
and ethambutol. Usually, four drugs are initially administered for 2
months, after which the regimen can be reduced to two drugs that
can be continued for several months.
Mycobacterium tuberculosis can affect the spinal cord and the
brain parenchyma, where it can lead to the formation of
tuberculomas. These lesions behave like space-occupying lesions,
and the treatment is with anti-TB medications.

Question 27

lepromatous form

Answer 27

The lepromatous form is present in patients with poor cellmediated immunity with proliferation of the mycobacteria as they
invade the tissues. It is characterized by skin infiltration by the
mycobacteria, leading to diffuse cutaneous involvement in the
coolest regions such as the pinna of the ear, tip of the nose, and
dorsum of the hands and feet. Nerves may also be involved but
usually at later stages.

Question 28

Rabies, klinis , stadium

Answer 28

Disebabkan virus rabies family rhabdovilidae genus lyssa
Masa inkubasi 7 hari s/d bbrp tahun, rata-rata 1-2 bulan
Menyerang reseptor nicotinic dan asetylcolin di NMJ
Saat inkubasi, Dorman di otot area gigitan. Lalu menyebar secara retrograd melalui axon saraf tepi ke saraf pusat
Stadium
Prodromal: demam, lemas
Sensoris: hipersalivasi , hiperlakrimasi, dilatasi pupil
Eksitasi: aerofobia, hidrofobia, fotofobia
Paralitik

Symptoms begin with fever, malaise, headache, and
followed by psychomotor hyperactivity. Patients subsequently
experience dysarthria and dysphagia, with prominent spasms in the
pharyngeal, facial and neck muscles. These oropharyngeal spasms
may be triggered by attempts to swallow water, leading to
hydrophobia. The inability to swallow associated with salivation
may produce the described “frothing” in the mouth. Progression of
the disease is associated with increased attack frequency, agitation,
hallucinations, seizures, and coma. A paralytic form called “dumb”
rabies may progress from paresthesias and weakness of the bitten
limb, to quadriplegia. This paralytic form is more common from
bat rabies.

Question 29

Rabies histopathology

Answer 29

Neuropathologically, there are characteristic cytoplasmic
eosinophilic inclusions known as Negri bodies, which are found
mainly in Purkinje cells and pyramidal cells of the hippocampus,
but can also be seen in neurons in other parts of the brain and
spinal cord.

Question 30

Rabies Tatalaksana

Answer 30

Tx WHO : Dapat diberikan VAR 5 dosis ,dengan dosis 1/0,5 cc i.m , pada hari 0, dilanjutkan hari ke 3, 7, 14 Dan 21 otot deltoid (tidak boleh pd bokong)

• pada VAR 4 dosis, diberikan dua dosis pada Hari 0, lalu 1 dosis Hari 7, Dan 21
• (intradermal dosis 0.1 cc , pada Hari 0 pada dua area , lalu Hari 3,7,21)

Also they should receive
human rabies immunoglobulin (20 IU/kg) as soon as possible, at
least half of the dose around the wound and the rest
intramuscularly.
This condition is very serious, but some patients may survive if
they receive postexposure prophylaxis and adequate intensive
supportive care and mechanical ventilatory support.

Question 31

infective endocarditis

Answer 31

Patients with infective endocarditis can have a variety of
neurologic complications, most likely from embolization of
infected particles from the valvular vegetations. These neurologic
manifestations include ischemic and hemorrhagic strokes,
meningitis, encephalitis, abscesses, vasculitis, and mycotic
aneurysms, which can lead to subarachnoid hemorrhage if they
rupture. The exact mechanism of formation of mycotic aneurysms
is not well known, but it is likely that they form secondary to
septic emboli involving distal vessels, affecting their vasa vasorum,
with destruction and weakening of the arterial wall and subsequent
aneurysmal dilatation. These mycotic aneurysms are usually very
distal in the arterial tree, and commonly seen in distal bifurcations.
They are not typically seen in the proximal circle of Willis. The
subarachnoid hemorrhage resulting from rupture of these small
aneurysms is usually cortical and superficial, and is not generally
associated with vasospasm.

Question 32

Tatalaksana infective endocarditis

Answer 32

Patients with infective endocarditis should be properly treated
with early antibiotic therapy, which is mainstay of treatment.
Antibiotics not only treat the cardiac infection but also prevents
neurologic complications, and may potentially lead to resolution of
unruptured mycotic aneurysms.
Anticoagulants are generally contraindicated given the risk of
rupture of silent or known mycotic aneurysms, as well as potential
risk of hemorrhagic transformation of embolic strokes.
Patients who suffer subarachnoid hemorrhage in the setting of
infective endocarditis, should have a diagnostic cerebral angiogram
to evaluate for the presence of mycotic aneurysms (or other
potential cause of the subarachnoid hemorrhage). Some advocate
for cerebral angiogram in patients with endocarditis and ischemic
strokes or other signs of neurologic involvement, since mycotic
aneurysms may be silent, however, this practice is still not widely
recommended. Ruptured mycotic aneurysms should be treated
surgically or endovascularly.

Question 33

Sifilis, macam

Answer 33

Syphilis is caused by the spirochete
Treponema pallidum, which transmits vertically from mother to
child or via sexual contact. In infected adults, three phases with a
latent period and various neurologic complications are described:
• Primary syphilis is characterized by the development of a
painless chancre at the site of entry (genital region). There is
asymptomatic systemic spread of the organism, and the
chancre eventually disappears.
• Secondary syphilis develops approximately 2 to 12 weeks after
the exposure, with manifestations of systemic dissemination,
including constitutional symptoms, lymphadenopathy, and rash
(classically palms and soles). Syphilitic meningitis and cranial
neuropathies may occur in this second stage.
• Latent period is an asymptomatic phase with serologic evidence
of the disease, which may last for years.
• Tertiary syphilis is characterized by cardiovascular
complications (such as aortitis), gummatous complications, and
neurologic complications.

Question 34

Komplikasi Neurologis sifilis

Answer 34

Major neurologic complications include pure meningeal syphilis,
meningovascular syphilis, tabes dorsalis, and parenchymatous
neurosyphilis. Meningeal invasion of the treponemes can lead to
meningitis and meningovascular syphilis, in which there is
endarteritis obliterans and vasculitis, which can lead to strokes in
different arterial distributions; this can occur at any stage but often
occurs within the first 4 to 7 years of infection with syphilis. Tabes
dorsalis is the classical myelopathy with areflexia, lightning pains, sensory ataxia, loss of pain and temperature sensation, and
relatively preserved strength, leading to gait instability and the
development of Charcot joints. Parenchymatous syphilis (general
paresis) is the encephalitic form in which patients develop
progressive dementia, neuropsychiatric manifestations, speech
disturbance, and pupillary abnormalities. Argyll-Robertson pupils,
which accommodate but do not react to light, may be seen in
patients with neurosyphilis. Manifestations of neurosyphilis may
overlap in the same patient, usually presenting with a combination
of findings.

Question 35

tabes dorsalis

Answer 35

tabes dorsalis, which is caused by syphilis in its
tertiary phase, and occurs if syphilis in its primary stages is
untreated and the spirochete invades the CNS, in this case the
spinal cord. However, not all the cases of untreated syphilis
progress to the subsequent stages, and only a small percentage of
patients with untreated syphilis will develop symptomatic
neurosyphilis.
The diagnosis of syphilis is based on clinical manifestations along
with supportive laboratory evidence. There are treponemal and
nontreponemal tests. Nontreponemal tests are the Venereal Disease
Research Laboratory (VDRL) test and the Rapid Plasma Reagin
test. These tests are more sensitive but less specific than
treponemal tests and become negative sometime after treatment.
Treponemal antibodies remain positive for life and include the
fluorescent treponemal antibody and microhemagglutination assay
among others. For the diagnosis of neurosyphilis, CSF should be
analyzed, usually showing mononuclear pleocytosis with elevated
protein levels. CSF VDRL is very specific for neurosyphilis but may
be negative in as many as 25% of cases. Intrathecal antibody
production against Treponema pallidum, oligoclonal bands, and PCR
are also helpful for the diagnosis

Question 36

Tatalaksana neurosifilis

Answer 36

Treatment of neurosyphilis involves intravenous antibiotics, and
the first choice is penicillin G 4 million units every 4 hours for 14
days. Antibiotic therapy may clear the infection; however, it may
not reverse already established neurologic manifestations of
tertiary syphilis. Follow-up CSF analysis is recommended to assess response

Question 37

Encephalitis HSV

Answer 37

HSV encephalitis is predominantly caused by HSV-1, whereas meningitis is more often caused by HSV-2
it tends to
affect the orbitofrontal and temporal regions. Patients present with
fever, headaches, behavioral changes, altered mental status, focal
neurologic findings, and seizures.
CSF analysis demonstrates
pleocytosis with lymphocytic predominance (10 to 1,000 WBCs/
μL), moderately elevated protein and normal glucose levels.
Increased RBC count in the CSF or xanthochromia is seen
frequently; however, this finding is neither sensitive nor specific.
CSF HSV PCR has very high sensitivity and specificity for this
condition; however, there may be false-negative results if the CSF
is sampled in the first 24 hours of the illness. The MRI demonstrates FLAIR T2 hyperintensities and restricted
diffusion in the temporal regions—in this case, on the right side.

Abnormal EEG findings are common in patients with HSV
encephalitis. Periodic lateralized epileptiform discharges (PLEDs)
in the temporal regions are characteristic and support the
diagnosis. Diffuse slowing, which is nonspecific, can also be seen

Question 38

Tatalaksana encephalitis HSV

Answer 38

Treatment with intravenous acyclovir 10 mg/kg every 8 hours
should be started as soon as possible and continued for a minimum
of 14 days.

Question 39

Aspergillosis

Answer 39

aspergillosis, which is caused by the aspergillus
fungus. This organism is capable of causing various manifestations,
such as allergic syndromes, respiratory tract infections, and
sinusitis. However, it may also cause an invasive syndrome that
can spread to the CNS, especially in neutropenic patients,
immunocompromised patients, or those chronically on steroids.
Aspergillus fumigatus is the organism that causes most of the
invasive syndromes, invading blood vessels, causing stroke-like
syndromes, infarcts, and hemorrhagic transformation. A vasculitistype phenomenon occurs as the fungus invades the vessel walls and
may eventually progress to parenchymal disease, forming
granulomas, and abscesses. This fungus may invade multiple other
organs and cause systemic disease.
Histopathologically, invading hyphae are detected in blood
vessels, with the findings of necrosis, hemorrhage, and
inflammation. The specimen shown a Gomori
methenamine silver stain demonstrating septate hyphae that
branch at acute angles, which is consistent with aspergillus
infection. Aspergillosis does not typically present with meningitis.

Question 40

Neurocysticercosis

Answer 40

Neurocysticercosis is caused by the pork tapeworm
Taenia solium and has a worldwide disctribution, being endemic in
Latin America, Africa, India, and other parts of Asia.
Human ingestion of undercooked pork meat containing cysticerci
may lead to infection with the intestinal tapeworms but does not
cause the manifestations of neurocysticercosis, which occurs only
with infection at a specific stage of the tapeworm life cycle. When
the adult tapeworm resides in the small bowel of either the pig or
the human, proglottids are released and excreted in to the feces.
The eggs in these proglottids are infective to humans and animals.
After humans ingest these eggs, larvae are released which
penetrate the intestinal wall, migrating to various tissues, causing
cysticercosis and neurocysticercosis. Clinical manifestations may
occur years later, including seizures, focal neurologic symptoms, a
vasculitic-type syndrome with strokes, increased intracranial
pressure, headaches, hydrocephalus, and rarely coma.
Neuroimaging is helpful in the diagnosis of neurocysticercosis,
showing cystic lesions that may have contrast enhancement and
calcifications.
Taenia saginata is the beef tapeworm but does not cause
neurocysticercosis.

Question 41

Tatalaksana neurocysticercosis

Answer 41

The treatment of choice is albendazole. Praziquantel
is an alternative. Since patients commonly have seizures,
antiepileptic agents are often required.

Question 42

Amebic meningoencephalitis

Answer 42

Amebic meningoencephalitis is caused by free-living amebae,
such as Naegleria fowleri, Acanthamoeba, and Balamuthia mandrillaris.
Patients acquire the amebae by swimming in contaminated lakes or
ponds. The parasites enter the brain by passing through the
cribriform plate and along the olfactory nerve to enter the frontal
lobes and cause a necrotizing inflammation with destruction.
Acanthamoeba can also enter the CNS through hematogenous
dissemination and from a primary corneal infection acquired by
using contact lenses stored in contaminated solution.
Patients with amebic encephalitis present with headaches, fever,
neck stiffness, nausea, and vomiting and eventually develop focal
neurologic findings, seizures, and altered mental status. The
progression is rapid, and the disease is usually fatal.
CSF opening pressure is increased, and CSF analysis shows a
neutrophilic pleocytosis, increased protein, and decreased glucose
levels. Gram stain will not show the organism, but trophozoites
may be seen on a wet preparation of unspun spinal fluid.
Pathologically, there are findings consistent with purulent
meningitis, with microabscesses and necrotizing destruction of the
parenchyma. A polymorphonuclear inflammatory infiltrate and
trophozoites can be seen, such as in the histopathologic specimen

Question 43

VZV infeksi

Answer 43

VZV produces a variety of manifestations, and delayed neurologic
syndromes. Chickenpox is caused by VZV primary infection, and
after this, the virus remains latent in dorsal root ganglia,
autonomic ganglia, and cranial nerve ganglia

Question 44

Herpes zoster

Answer 44

Herpes zoster: Occurs more commonly in older patients, and in
those with some degree of immunodeficiency, but can occur in
anyone. Usually starts with hyperesthesia, tingling and burning
sensation in the involved dermatomes (usually one to three
dermatomes), followed by the zoster rash, which is a vesicular
rash in that same region. The rash gradually heals over several
days, but patients experience pain and sensory impairment that
can last weeks to months. The most commonly involved
dermatomes are in the mid-thoracic region.

Question 45

Ramsay–Hunt syndrome

Answer 45

Ramsay–Hunt syndrome: Characterized by facial palsy
combined with herpetic rash in the external auditory meatus,
sometimes with vertigo, tinnitus, and deafness. This syndrome
is secondary to geniculate ganglion involvement.

Question 46

VZV vasculopathy

Answer 46

VZV vasculopathy causing a stroke. VZV
vasculopathy is a multifocal disease and affects small and large
intracranial vessels. It can affect immunocompetent and
immunocompromised patients, manifesting with TIAs and strokes,
and less commonly with aneurysmal dilatation leading to
subarachnoid and intracranial hemorrhage. Typical angiographic
findings include multifocal segmental narrowing with poststenotic
dilatation. These findings can sometimes be seen on noninvasive
imaging such as CTA and MRA.
CSF may be abnormal, with mild mononuclear pleocytosis,
slightly elevated protein but normal glucose levels. Virologic
confirmation is required, and the value of detecting anti-VZV IgG
in the CSF has been demonstrated to be superior to the detection of
VZV DNA. Even though a positive VZV DNA in the CSF is helpful, a
negative PCR does not exclude the diagnosis.

Question 47

Tatalaksana VZV vasculopathy

Answer 47

Patients with VZV vasculopathy should be treated with acyclovir
10 to 15 mg/kg IV three times a day for at least 2 weeks. Steroids
may be required. Use of antiplatelet agents may be reasonable in
patients with intracranial stenosis and ischemic strokes or TIAs, but
should not be used alone without specific antiviral therapy in these
cases.

Question 48

Subacute sclerosing panencephalitis (SSPE)

Answer 48

Subacute sclerosing panencephalitis (SSPE) is a rare and late
complication of measles, which is not an arbovirus. Measles can
cause four major neurologic syndromes:
• Acute encephalitis.
• Postviral encephalomyelitis.
• Measles inclusion body encephalitis, which occurs in patients
with cell-mediated immunodeficiency, 1 to 6 months after
measles exposure. It is characterized by a rapidly progressive
dementing process with seizures, myoclonus, mental status
changes, and coma.
• SSPE, which is caused by defective measles virus maturation in
neural cells.
Children infected in the first 2 years of life are the ones at the
greatest risk for SSPE, which may develop 2 to 12 years after the
infection. It begins with behavioral and personality changes, later
causing seizures, myoclonus, spasticity, ataxia, choreoathetoid
movements, optic atrophy, quadriparesis, autonomic instability,
akinetic mutism, and eventually coma.
EEG shows periodic slow-wave complexes at regular intervals
and a background of depressed activity. MRI demonstrates T2 hyperintensity in the gray and subcortical white matter more in the
posterior regions. Neuropathologically, neurons contain nuclear
and cytoplasmic viral inclusion bodies, and levels of CSF and serum
antibodies are elevated.

Question 49

CJD

Answer 49

CJD is a prion disease, caused by conformational changes of the
prion protein from cellular prion protein (PrPC) to scrapie prion
protein (PrPSc), which has an increased β-sheet content. This leads
to physico-chemical changes in the protein, making it resistant to
proteinases, poorly soluble, and with a tendency to polymerize,
which eventually may lead to neuronal death. PrPSc has the ability
to bind to PrPC and induce its conformational change, therefore
making this agent infective. fatal familial insomnia,
which is a prion disorder characterized by progressive intractable
insomnia and symptoms of sympathetic hyperactivity such as
hypertension, tachycardia, hyperthermia, and hyperhidrosis.
Patients may also have cognitive impairment, tremor, ataxia,
hyperreflexia, and myoclonus.
CJD exists in different variants, including sporadic, familial,
iatrogenic, and new variant forms. (The sporadic form is the
typical form. The familial
variant is similar to the sporadic form; however, it may present
earlier, and the course is more protracted and insidious. The
iatrogenic form is very rare and has been described in the past in
patients who received cadaver-derived human growth hormone,
and after neurosurgical procedures or corneal transplants.

Question 50

Gerstmann–Straussler–Scheinker

Answer 50

Gerstmann–Straussler–Scheinker is an inherited prion disease that
progresses slowly over years. It is characterized by cerebellar
ataxia and dysarthria, sometimes extrapyramidal features followed
by dementia. The new variant CJD was first described in 1996 and
is believed to occur from infection through consumption of cattle
products contaminated with the agent of bovine spongiform
encephalopathy. In contrast to traditional forms of CJD, new
variant CJD affects younger patients (third to fourth decades of
life), and the duration is more protracted.

Question 51

Diagnosis CJD

Answer 51

CJD, which is a transmissible spongiform
encephalopathy. The MRI demonstrates
restricted diffusion of the cortex (cortical ribboning) and the head
of the caudate, which are findings not seen in the diagnoses
provided in the other options. Other MRI findings seen in some
CJD variants include bilateral signal hyperintensity in both thalami
(especially in the pulvinar region, known as the pulvinar sign) and
in the anterior portions of the putamen. The combination of
anterior putamen and caudate head hyperintensity is known as the
“hockey-stick” sign.
Patients with CJD present clinically with a rapidly progressive
dementia, neuropsychiatric symptoms, cerebellar ataxia, and
myoclonus. These patients deteriorate rapidly and inexorably die
within months. The diagnosis is suspected on the basis of clinical
features and supported by ancillary tests such as MRI, EEG, and
CSF studies. EEG shows a typical periodic pattern. The presence of
CSF 14-3-3 protein is helpful but not specific for this condition, as
it can be seen in many other causes of neuronal destruction. Other
potentially useful CSF biomarkers include total Tau, Neuronspecific enolase, and S100B. Neuropathologic evaluation may be
required in some cases and demonstrates significant spongiform
degeneration with neuronal loss, vacuolar changes, and
astrocytosis

Question 52

Gambaran LCS encephalitis HSV

Answer 52

CSF analysis demonstrates
pleocytosis with lymphocytic predominance (10 to 1,000 WBCs/
μL), moderately elevated protein and normal glucose levels.
Increased RBC count in the CSF or xanthochromia is seen
frequently; however, this finding is neither sensitive nor specific.
CSF HSV PCR has very high sensitivity and specificity for this
condition; however, there may be false-negative results if the CSF
is sampled in the first 24 hours of the illness.

Question 53

Karakteristik EEG encephalitis HSV

Answer 53

Abnormal EEG findings are common in patients with HSV
encephalitis. Periodic lateralized epileptiform discharges (PLEDs)
in the temporal regions are characteristic and support the
diagnosis. Diffuse slowing, which is nonspecific, can also be seen

Question 54

Struktur pembentuk blood brain barrier

Answer 54

• endotel kapiler
• astrocyt
• microglia
• Pericyte

Question 55

Transmembrane protein pada Blood Brain Barrier

Answer 55

transmembrane proteins such asoccludin,claudins,junctional adhesion molecule(JAM), or ESAM, for example

Question 56

Imunisasi rabies pre exposure

Answer 56

Diberikan 3 dosis Vaksin anti rabies 0.5 cc i.m pada Hari 0, 7, Dan 21/28
Atau intradermal (i.d.) vaccination  0.1cc

Question 57

Gambaran LCS meningitis Tuberculosis

Answer 57

1. Pleiositosis : 100 – 500 sel/ mm3
2. Protein 100 – 500 mg/dl atau hasil normal.
3. Glukosa rendah < 40 mg %
4. Hipokloremia.

Question 58

Human T cell lymphotropic virus type I (HTLV-I)–associated myelopathy (HAM)

Answer 58

Klinis : baal pada kaki, konstipasi dan inkontinensia urin sehingga harus memakai kursir roda selama 12 bulan. Pemeriksaan kulit menunjukkan lesi makulopapular multiple berwarna merah-coklat. Pemeriksaan neurologis menunjukkan penurunan sensasi pinprick, paraplegia, peningkatan tonus otot tungkai dan tanda babinski. Hasil tes serologis Lyme disease, sifilis dan HIV negatif.

Question 59

Ramsay Hunt syndrome

Answer 59

Lesi pada ganglion geniculate setelah infeksi virus herpes zoster.
Klinis :
Bell’s palsy ( movements of facial muscles, the touch sensation of a part of ear and ear canal, the taste function of the frontal two-thirds of the tongue, and the moisturization of the eyes and the mouth.)

Question 60

Pirimetamin Efek samping

Answer 60

Pyrimethamine is a folic acid antagonist. Increased doses of leucovorin (folinic acid) were administered in this case to abate hematologic toxicities known to be associated with pyrimethamine, including leukopenia and thrombocytopenia