CASE OBJECTIVES

After completing this case, the students should be able to:

1.       To know epidemiology of human cysticercosis especially in developing countries.

2.       To know clinical manifestations made on the basis of a combination of clinical presentation,
radiographic studies, serologic tests, and exposure history.

3.       To know diagnostic criteria for human cysticercosis included absolute, major, minor and
epidemiologic criteria.

4.       To know the laboratory findings, complication, prevention and treatment of cysticercosis.

5.       To describe the life cycle of taenia solium; pathogenesis of taenia infection in human

6.       To understand how to prevent taenia infection in human

Page 1

Mr. Ali 35-year-old man was admitted to Siloam Hospital because of an apparent seizure 5 days ago.
He was talking to his assistant when he suddenly stared, turned his head to right, began smacking his
lips and then had a generalized tonic-clonic seizure. The seizure lasted 2 to 3 minutes. Mr. Ali does
not recall anything immediately prior to or during the event and was still confused 20 minutes later. 
Three days ago he had twice recurrent seizure. After episode of seizure he got back his consciousness.
The patient had been in excellent health recently, there was no history of head trauma. 

QUESTIONS

1.       What are Mr. Ali’s problems?

 seizure 2-3 menit

 turned his head to right, smacking his lips

 generalized tonic-clonic seizure

 does not recall anything, confused 20 minutes later

 3 hari lalu, twice recurrent seizure

 No history of head trauma

2.       What are the possible causes which make Mr. Ali get seizure?

 Vascular :
  Infection : bakteri, viral, fungal, parasit  brain infection

 Trauma : -

 Autoimun :

 Metabolic : electrolyte imbalance Na, K, Cl

 Idiopatik

 Neoplasm : metastasis/brain tumor

 Degenerative : -

3.       What possible mechanism might explain his problem?

Page 2

Eighteen months before admission, he had participated in a field study in Papua for 6 months. During
his stay in Papua he often consumed a variety of meats, which included under-cooked pork. He had
been accompanied in Papua by his wife, who remained well.

QUESTIONS

1. Does this information help your hypotheses?

Under-cooked pork : infeksi parasit

2.       What is your possible diagnosis now?

Neuro sistiserkosis

3.       What further information do you need?

 Anamnesis : RPD, tentang istri, travel history

 Lab : CBC, eosinofil, feses, urin
 PF : neurology examination, reflex
 Brain imaging : CT head
Manifestasi : abdominal cramp, weight loss
Page 3

Physical examination revealed the blood pressure was 130/80 mm Hg, pulse was 60 times/min, the respirations
rate was 18 and temperature was 36.3°C. Other physical, neurologic, and ophthalmologic examinations
revealed no abnormalities. Laboratory tests were performed.

Hematologic Laboratory Values

Hb                      : 13,9 gr/dl                            ( 12 – 15 gr/dl)

Ht                       :  42,6%                           (35 – 43%)

WBC                  : 8000 mm/2                           (5000 – 10.000/mm3)

Differential Count (%)

             Neutrophils                     61

             Lymphocytes                  30

Monocytes                      2

Eosinophils                     7

Platelet              : 289.000 /mL                           (150.000 – 400.000/mL)

             ESR                   : 8 mm/hour                           (<10 mm/h)

RBG                  : 98 mg/dL                           ( <200 mg/dL)

             SGOT                : 18                                 (<30 u/L)

SGPT                : 20                                 (<30 u/L)

Ureum               : 21

Creatinin            : 0,7

Natrium              : 137 mg/dL                          (135-145mg/dL)             

Kalium               : 3, 6 mg/dL                          (3,5- 5,5 mg/dL)          

The urine was normal. Microscopically examination of urine and stool specimens disclosed no ova or parasites.

QUESTIONS

1.       What is your interpretation these finding?

 - eosinophilia

Dd metabolik bisa disingkirkan

2.       What more information do you want?

- radiografi
- ELISA

Page 4 

A magnetic resonance imaging (MRI) study of the brain with contrast revealed a small cystic enhancing mass in
the left frontal lobe as illustrated below. Radiographs of the chest showed no abnormalities.

QUESTIONS

1.       Interpret the findings of imaging.

 Small cyst di left frontal lobe (LO)

2.       What is the differential diagnosis?

 LO

3.       How Mr. Ali get this condition?

 Undercooked pork

4.       Where else in the body does this cause neurological problems?

 CNS, spinal cord, subarachnoid, intramedula

5.        What are the treatment options for this disease?

- antiparasitic
- steroid
- antiepileptic
Page 5
 
Mr. Ali was prescribed Albendazole (15 mg/kg per day for 28 days). He also was given oral phenytoin
100 mg, three times daily to control his seizure.
 
QUESTIONS
 
1.       What is the side effect of this treatment?

 Albendazole : mual, muntah, abdominal pain, headache

 Alopecia, increased liver enzyme
 
2.       What is the impact of this condition on patient’s health, social and economic?
 Health : epilepsy, defisit neurologis
 Sosial : menjauh dr lingkungan sekitar, stress, ketakutan
 Economic : defisit ekonomi negara krn penyakit ini sendiri, loss of work days
3.       What can Mr. Ali do to prevent this disease?
 Improve sanitization pasien (cuci tangan) & lingkungan (pencegahan kontaminasi dari
makanan, air)
 Pencegahan mekanik dari cara masak
 Penyimpanan freeze dibawah -5 perlu 4 hari, -15 derajat perlu 3 hari, -24 perlu 1 hari
 Edukasi pasien
 Identifikasi pasien yang sudah terinfeksi
 Rutin pemeriksaan serologi

Epilogue
Page 6
 
After the treatment Mr. Ali got better and during the care only had minimal seizures. Evaluation brain
MRI on 2 months later showed decreased size of lesion and he has continued taking phenytoin. For
convenience, this was changed to 300 mg at bed time.
 1. Vaskular, autoimun, metabolik yang related ke seizure
Seizure : transient disturbance dr fungsi serebral disebabkan krn abnormal neuronal
discharge
Epilepsy : kumpulan disorder, dikarakteristik o/ recurrent seizures

Etiologi  bisa tjd akibat primary CNS dysfunction atau underlying metabolic
derrangement/sistemik
- Benign febrile convulsions of childhood
- Vaskular : stroke, vascular malformations (AVM), infarction, hemorrhage
(intraserebral, subarachnoid, subdural, epidural), venous thrombosis, cavernosus
angioma
- Infeksi : CNS infections, ensefalitis, meningitis, sistiserkosis, HIV encephalopathy
- Trauma : head
- Autoimun : RA, Grave’s disease, Hashimoto’s thyroiditis, Crohn’s disease,
ulcerative colitis, SLE
- Metabolik : hypoglycemia, hyponatremia, hyperosmolar state, hypocalcemia
- Idiopatik : cryptogenic seizures

- Other systemic disorders : uremia, hepatic encephalopathy, porphyria, drug

toxicity, drug withdrawal, cerebral ischemia, hypertensive encephalopathy,
eclampsia, hyperthermia
 2. Causes of seizure based on age

USIA ETIOLOGI
0-3 tahun (<1 bulan) perinatal hypoxia, metabolic disturbances, intracranial
hemorrhage, brain malformations, maternal drug use
3-12 tahun Febrile seizures, genetik, developmental disorders, infeksi CNS,
idiopatik
12-20 tahun Infeksi, trauma, genetik, brain tumor, kongenital (neurofibromatosis,
down’s syndrome, angelman’s syndrome)
20-60 tahun Trauma, alcohol withdrawal, illicit drug use, brain tumor
>60 tahun Cerebrovascular disease, brain tumor, alcohol withdrawal, metabolic
disorders (liver failure, uremia, hypo/hyperglycemia) , degenerative
(alzheimer’s disease), trauma

3. Why is the epidemiology of epilepsy important in tropical countries ?

Epilepsy di tropical countries paling sering disebabkan krn malaria
Malaria = world’s most common fatal parasitic disease & is endemic in Africa, Asia,
tropical America, subtropicalareas of eastern Mediterranean. Hampir setengah populasi
dunia ± 3,2 miliar beresiko thd malaria
Cerebral malaria/CM = acute, non traumatic encephalopathy krn komplikasi infeksi P.
falciparum
- Malaria penyebab dr 69% kasus kejang di anak-anak yg dibawa ke RS
- Frekuensi seizures akibat malaria 22% di Asia Selatan & Tenggara - 80% di Afrika
- Seizure biasanya fase akut dr malaria  acute symptomatic seizures : focal,
repetitive, prolonged w/ or w/o secondary generalization
- Epilepsy adalah neurological sequelae dr CM
RF : hipertermia, presence of acute seizures, FH of epilepsy

Negara tropis punya global burden of epilepsy,terbukti dgn insidensi & mortalitas
epilepsy tertinggi di negara tropis. Epidemiologi dr epilepsi semakin rumit krn adanya
cultural beliefs, lack of medical records, lack of expertise in diagnosis epilepsy

Hal ini bisa tjd krn di negara tropis terdapat daerah endemik spt malaria,
neurocysticercosis, adanya insidensi kejadian kecelakaan traffic, birth-related injuries,
dll

Beberapa agents penyebab epilepsy in tropical countries :

- Malaria
 - HIV infection
- Neurocysticercosis
- Zika virus
- Tuberculous meningitis
- Others : japanese encephalitis, West Nile virus, dengue, nipah virus , enterovirus,

4. Common symptoms of parasite infections

- Demam, body aches, headache
- Diare, abdominal cramping
- Bloating, gas, mual, fatigue, weight loss

5. All about taenia solium & cysticercosis

TAPEWORM
 Terdiri dari : scolex/head, neck, tail
1. Scolex : punya 2 suckers & ada rostellum atau small hooks (yg nempel ke
host’s intestine)
 Scolex dihubungkan oleh short neck ke bagian bawah tapeworm, disebut
strobila (rantai spt pita yg terhubung)  segmen ini disebut proglottids
 Proglottids : punya male & female sex organs (HEMAFRODIT)  u/
produksi parasite’s eggs
Muncul berkembang di neck region dan mature + pindah ke strobila
Proglottid hemafrodit jadi subur dan keluar dr tapeworm  muncul di
stool, keluarin telur
Bbrp kasus, yg masuk ke stool adalah strobila = artinya even eggs di stool
tinggi levelnya, deteksi parasite eggs bisa sporadik, jadi butuh multiple
stool samples, rectal swabs, visual exam od stool nya
2. Jika telur dikeluarkan dari parasite sudah berkembang parsial = embryonated
Ingested  keluar di intermediate host intestine  oncosphere  masuk gut
mucosa  masuk organ” dan mjd cyst, cysticercoid/cysticercus/alveolar
cyst/hydatid cyst  dimakan definitive host  mature tapeworm di definitive
intestine
3. Jika telur embrio blm diferensiasi = nonembryonated  perkembangan tjd di
luar badan, di dlm air
Telur menetas dan keluar as free-swimming coracidium larva  dimakan
small crustacean (copepod)  mjd procercoid larva di copepod’s tissue 
copepod dimakan ikan/intermediate lain, menginfeksi musculature 
plecercoid cyst/sparganum  dimakan manisa (definitive host) 
mature/intraluminal fish tapeworm
Proglottid T.
solium

Scolex T.
solium
Taenia spp.
eggs
 TAENIA SOLIUM
= penyebab utama seziures di most of the world
 T. solium ± 2-8 m, survive 10-20 tahun, lebih kecil dr saginata
Scolex solium sgt beda : dipersenjatai o/ 2 barus curved hooklets
Proglottids T. solium not motile & not migrate
 Manusia = definitive hosts
Babi = intermediate hosts
 Manusia terinfeksi dr konsumsi undercooked pork mengandung cysticerci dan
msk ke intestinal tract
 Manusia bisa alamin autoinfection  reverse peristalsis shg taenia eggs travel dr
usus balik ke lambung
 Infeksi T. solium biasanya asimtomatik, didiagnosis dgn deteksi telur slm stool
examProglottids T. solium not motile & not migrate
Pathology
- Ingested eggs diaktivasi o/ gastric duodenal environment  mengeluarkan
invasive larvae di usus halus, oncospheres
- Oncosphere mlwti intestinal wall dan dibawa oleh bloodstream ke bbrp tmpt u/
maturasi mjd cysticerci (butuh waktu smpe sini sktr 2 bulan)
- Cysticerci bisa dmn aja, paling sering di : CNS, eye ; jarang di : subkutan, otot
- Appearance cysticerci di otak : cyst dikeliling o/ jaringan yg terkompresi dan
dikeliling inflammatory infiltrate
- Cyst yg udah mati, terkalsifikasi, / terhialinisasi dikelilingi o/ host-derived capsule
 CYSTICERCOSIS
= infeksi jaringan disebabkan larva cysts cestoda, terjadi akibat konsumsi T. solium
eggs dr fecal-oral transmission

a. WO no 1 : epidemiology of human cysticercosis in developing countries

- CC endemik di undeveloped countries
- Di developed countries, immigrants account for major proportion of cases
- Prevalensi tinggi di Meksiko, Amerika pusat, amerika selatan, filipina, Asia
tenggara, Afrika, China, India, Amerika latin
- WHO estimasi kematian >50.000/tahun dr neurocysticercosis
- Faktor risiko : usia, konsumsi daging babi, poor hygiene
- 0.02-12,6% exposure to causative agents : Vietnam, China, Korea, india

b. WO no 2 : manifestasi klinis
- Morbiditas sistiserkosis paling sering krn CNS & okular
- Di lokasi endemik T. solium, 30-50% pasien punya antibodi thd T. solium
- Cardiac cysticercosis : heart failure/conduction abnormalities
- Muscle : aching, altered function

NEUROCYSTICERCOSIS
= terjadi di seluruh bagian dr CNS, seringkali asimtomatik
MOST COMMON : kejang (70%), intracranial hypertension
Gejala lain : focal weakness, extrapyramidal disorders, perubahan status mental,
gangguan kognitif, penyakit psikiatrik, chronic meningitis (skt kepala, perubahan fungsi
serebral gn abnormal CSF), spinal cord syndromes (paraplegia progresif)

Dibedakan menjadi 2 grup besar :

1. Extraparenchymal NCC : intracranial HTN, progresif & significant mortality
2. Intraparenchymal NCC : seizure, good prognosis, menunjukkan viable
degenerating/calcified cysts yg ada fluid-filled vesicles

Gejala berdasarkan lokasi :

1. Lesi intraserebral (most often)
Mass effects, kejang, atau keduanya
2. Kista intraventrikular & basilar  cause symptoms krn obstruksi CSF flow/local
meningeal irritation yg leads to injury local BV, cranial nerves, brain stem =
hidrosefalus
 Basilar neurocysticercosis agresif = racemose cysticercosis  dmn kista proliferasi
di base of brain shg mental deterioration, coma, death
3. Lesi subarachnoid
Meningitis kronik
4. Lesi spinal cord
Cord compression syndrome / meningitis
5. Kista intraparenchymal cerebral
Membesar lama-lama, menyebabkan gejala minimal, dan kista nya mulai mati. Di
titik ini, kista kehilangan osmoregulasi nya dan makin membengkak. Selain itu,
bisa juga mengeluarkan antigenic material yg memicu inflammatory response =
cerebritis & meningitis  dua ini kontribusi ke focal/generalized seizures,
sensorimotor deficits, intellectual impairment, psychiatric disorders, gejala
hidrosefalus
6. Intraparenchymal spinal cord lesions
Simtomatik krn direct local pressure effects
Selain lokasi, juga dipengaruhi o/ jumlah, ukuran, evolutive stage, degree of host
inflammation

Gejala berdasarkan radiology o/ CT :

1. Extraparenchymal : ada kecembungan dr hemisphere, Sylvian fissure, basal
subarachnoid cisterns, atau didlm ventrikel
2. Intraparenchymal : kista disini cenderung lebih tumbuh & infiltrasi, block CSF
criculation shg menyebabkan hidrosefalus & intracranial HTN

OCULAR CYSTICERCOSIS
= terlihat di mata, kista paling sering di
subretinal
Gejala : altered vision & blindness
Penting u/ rule out intraocular dlu di
cysticercosis sblm dikasi antiparasitic
krn inflammatory reaction nya bisa
rusak mata

c. WO no 3 : diagnosis

1. Absolute : histologik dgn

observasi jaringan, funduscopic
 visualization of parasite (lihat bagian anterior chamber, vitreous, subretinal
spaces), neuroimaging
2. Major
a. Neuroradiologic : cystic lesions dgn/tnp enhancement, ≥1 nodular calcifications
atau focal enhancing lesions
- Cysticerci di parenkim otak 5-20 mm diameter dan bulat
- Cystic lesions di subarachnoid / fissure up to 6 cm diameter dan lobulated
(dinding tipis, fluid isodense dgn CSF)
- CT lebih sensitif u/ kalsifikasi // MRI lebih bgs buat liat lesi cyst, scolices,
enhancement
b. Deteksi antibodi thd cysticerci  immunoblot assay
- Assay memakai lentil lectin purified glycoproteins >99% spesifik & highly
senstive

Confirmed diagnosis : either 1 absolute atau kombinasi 2 kriteria major, 1 minor,

& 1 epidemiologik
Probable diagnosis : disupport dgn fulfillment (1) satu kriteria major + dua minor; (2)
satu major + satu minor & satu epidemiologik; atau (3) tiga minor + satu
epidemiologik
 Kista subkutan : palpasi  klo masi janggal : histologik
 Cysts di otot lurik paling susah dan lebih cpt kalsifikasi = spindle-shaped
calcifications on radiography

a. Imaging (CT/MRI)
 u/ diagnosis ketika ada gejala yg mirip tumor = CT/MRI  multiple enhancing
& nonenhancing unilocular cysts
- Cerebral cysts : multiple (7-10)
 CT/MRI bisa memperlihatkan degenerating cysts, calcifications,
intraventricular lesions, atau cisternal cysts/membranes (cari tau jumlah,
lokasi, size, degree inflamasi di sekitar lesi)
 MRI bisa liatin posterior fossa & spinal lesions, superior u/ imaging ventricular
cysts, poor buat cari kalsifikasi
 Viable cysts on Degenerating cysts enhancing after contrast (MRI, T1)
MRI

Multiple parenchymal brain calcifications on CT Basal subarachnoid cysticercosis

b. Serological diagnosis
 Memperlihatkan exposure to T. solium antigens, circulating antibodies
 Antigen diekstraksi dr kista T. solium. Glikoprotein diekstraksi dr cyst fluid dan
mrpkn indikator determinan
c. Others
 CSF examination : hasilnya lymphocytic / eosinophilic pleocytosis ,
hypoglycorrhachia, elevated protein levels
High CSF protein persistem tanda poor prognosis, ada progression ke
hidrosefalus shg konsekuensi nya demensia & kebutaan
d. Pemeriksaan feses u/ parasite eggs/proglottids
Cara :
 Makroskopik : konsistensi (watery/loose lebih ke protozoa)
Kalo ada motile segment = T saginata
 Mikroskopik : teknik wet mounts
- Menggunakan physiologic saline u/ identifikasi helminths & protoza
(trofozoit, cysts, ova, larvae)
- Iodine solution u/ protozoal cysts & ova
- Sensitivitas egg detection dapat dibantu dgn formyl ethyl acetate dgn
prosedur sedimentasi (krn cestode eggs relatif berat
**prosedur lainnya zinc sulfate flotation
- Prosedur fiksasi dan staining (Ziehl-Neelsen) : kalo ada intact proglottids di
stool
e. Proglottids T. solium = 11x15 mm, w/ lateral genital pore & 7-13 branches di
either side of central uterine canal
T. saginata similar tp branches nya 15-20

d. WO no 4 : lab findings, komplikasi, prevention, treatment of cysticercosis

Lab findings
1. Stool examination
2. Wet mounts
3. Staining
4. Nonspecific tests
 Eosinophilia (>500 uL)  tjd krn muscle encystation & saat cysticerci di CSF
w/ neurocysticercosis

Komplikasi
- Cerebrovascular : hidrosefalus, brain edema, chronic meningitis, vaskulitis,
seizures, stroke
- Spinal cord syndromes : paraplegia, paralysis
- Psychology : mental status changes, intellectual impairment
- Okular : blindness
- Coma, death

Treatment
NON MEDIKAMENTOSA
 u/ symptomatic cysts diluar CNS = surgical resection
  Intraventricular cysts = surgical excision

 MEDIKAMENTOSA
Bisa dicapai dgn praziquantel / niclosamide  punya efek lsg parasiticidal di
intraluminal cestode
1. Niclosamide
= poorly absorbed, narrow-spectrum anthelmintic
 Dosis  dewasa 2 g (4 tablet) single dose; anak >34 kg 1,5 g (3 tablet), 11-34 kg
1 g (2 tablet)
 Cara minum : dikunyah sblm ditelan
 Efek samping mild : malaise, mild abdominal pain, nausea
 Autoinfection saat terapi  diberi mild laxative 1-2 jam stlh niclosamide masuk
2. Praziquantel
= broad-spectrum anthelmintic, bisa treat trematoda & cestoda, well-absorbed di
GI & bisa masuk ASI
 Dosis : 50 mg/kg dailu for 15 days
 Follow up stool screening 1&3 bulan pengobatan
 Efek samping mild (10-50%) : transient dizziness, headache, malaise, abdominal
pain, nausea
 Efek samping moderate (<10%) : sedation, vomit, diare, urticaria, rash, fever, mild
transaminitis
 Krn bisa masuk ASI, ibu breast-feed ga boleh nurse dlm 24h stlh treatment
3. Albendazole
 Dosis : 15 mg/kg daily for 30 days

 Alternatif  nitazoxanide
 Efek samping : damage inflicted on cysticerci & consequent acute inflammatory
response = cerebral edema, raised ICP, severe headache
 sebelum, selama, atau setelah drug therapy, seizures bisa dikontrol dgn pemberian
antiepileptik
 hidrosefalus simtomatik diobati dgn shunting
 CNS inflammation = corticosteroids (dexamethasone) 0,1 mg/kg per hari

KONTROL
Cara kontrolnya dicapai dgn interruption dr life cycle, jaga sanitasi, formal pig raising
Di negara berkembang, babi dipelihara deket sm manusianya sehingga babi pny akses
ke human faeces
Contohnya : di pedesaan
Solusi = memperkenalkan sanitasi baik, sosialisasi praktik modern dlm merawat babi
(peternakan)

Cara lain u/ kontrol adalah dgn mass chemotherapy u/ kurangi tapeworm carriage

Prevention
 Adequate cooking; temperatur minimal 56 C selama 5 menit u/ destroy cysticerci
 Disimpan di kulkas /salting /di freezer at 10 C selama 9 hari u/ kills cysticerci
 Meminimalkan kesempatan konsumsi fecally derived eggs dengan good hygiene,
effective fecal disposal, treatment+prevention intestinal infections
 Vaksin u/ prevent porcine cysticercosis (under development)

e. WO no 5 : taenia dimana babinya, life cycle and pathogenesis

Pathology
 - Ingested eggs diaktivasi o/ gastric duodenal environment  mengeluarkan
invasive larvae di usus halus, oncospheres
- Oncosphere mlwti intestinal wall dan dibawa oleh bloodstream ke bbrp tmpt u/
maturasi mjd cysticerci (butuh waktu smpe sini sktr 2 bulan) = masih di pig
- Cysticerci bisa dmn aja, paling sering di : CNS, eye ; jarang di : subkutan, otot
- Appearance cysticerci di otak : cyst dikeliling o/ jaringan yg terkompresi dan
dikeliling inflammatory infiltrate
- Cyst yg udah mati, terkalsifikasi, / terhialinisasi dikelilingi o/ host-derived capsule

6. WO no 6 : how to prevent taenia infection in human

Transmisi tapeworm bisa diturunkan dgn memperhatikan sanitasi :

1. Pembuangan kotoran manusia punya aliran yang baik u/ limit spread of parasite
eggs
2. Jangan kontak bare skin dgn larva infektif
3. Pembatasan area pakan ternak & pakai safe feed u/ binatang spt sapi, babi yg
bisa jadi intermediate hosts
4. Inspeksi daging sblm dijual u/ sortir cyst-infested
5. Prolonged freezing (<18 C), daging dimasak >50 C u/ kill cyst
6. Sering cuci tangan & general hygiene
7. Health education campaign u/ self-recognition of human tapeworm carriers
8. Screening for immigrants di daerah endemik Taenia spp.
9. Prevention for global : via pemerintah, international agencies, NGO, philanthropic
institutions, industri

7. Page 3 no 1,2 : MRI bedanya malignancy, intracerebral mass, scolex, died cyst, dll

a) MRI neurocysticercosis based on location :

1. Subarachnoid/intraventricular
 Scolex ga keliatan
 Kalau di basal cisterns, bentunya grape-like (racemose)
 Kista diameter 1-2 cm
 Similar signal intensity to CSF
 Cyst di 4th ventricle : signal intensity cyst udah sedikit beda dgn CSF,
hidrosefalus
 Subarahcnoid NCC : cyst pny signal intensity similar to CSF, ga enhance
stlh gadolinium masuk, ada mass effect = subarachnoid enlargement
 2. Parenchymal (most common)
 Involve grey-white matter junction
 Viable is characterized by vesicular
lesions = ada contrast enhancement
&/ surrounding edema
 Scolex keliatan di high-definition
imaging
 Single small enhancing cystic or
nodular enhancing lesion <2 cm =
degenerasi parasit dgn inflamasi &
cyst fluid
 Non viable form = nodular
calcifications <20 mm diameter w/
or w/o edema &/ contrast
enhancement (calcified granuloma
w/ or w/o inflammation &/ gliosis

nonenhanced CT = multiple calcified lesions

MRI based on stage :
- Vesicular :
cysticercus is
viable, few
inflammatory
changes di
surrounding
tissue. Kista
pny dinding
tipis, cyst fluid
pny signal
intensity yg
similar ke CSF
*in viable cyst :
scolex terlihat
dgn bentuk
mural nodular
- Colloid
vesicular :
inflammatory
reaction disekitar cysticercus, dinding menebal & vesicular fluid membentuk
aspek koloid spt agar”, intensitas signal cystic fluid mulai beda dgn CSF. Scolex
nya mulai alami
degenerasi, ada
gradual decrease dr
size of lesion. Dibantu
contrast, peripheral &
perilesional edema
udah mulai terlihat
- Granular nodular :
parasit udah mati, lesi
mulai termineralisasi,
mulai semisolid
digantikan jaringan
granuloma, ada
nodular/ring
enhancement di lesi,
edema makin meluas
 - Nodular calcified : lesi termineralisasi sempurna, lesi berbentuk small nodules
dgn hipointensitas T2W, lebih bgs dideteksi di CT. Ada calcified lesions di
persistent contrast enhancement di MRI, no edema

**Scolex : presence of cystic lesions demonstrating scolex

Karakteristik : bright nodule within cyst, producing so-called “hole-with-dot”
-->kalau ada scolex = ABSOLUTE criteria

b) Brain metastases
T1
 Iso to hypointense
 Kalau hemorrhagic, ada intrinsic high signal
 Non hemorrhagic melanoma metastases bisa ada intrinsic high signal krn
paramagnetic properties of melanin
T1C+
 Enhancement bisa uniform, punctate, ring-enhancing, biasanya intense
 Delayed sequences krn additional lesions
T2
 Hyperintense
FLAIR
 Hyperintense
 Hyperintense peri-tumoral edema of variable amounts

c) Cerebral abscess
T1
 central low intensity
(hyperintense to CSF)
 peripheral low intensity
(vasogenic edema) 
 ring enhancement 
 ventriculitis may be
present, in which case
hydrocephalus will
commonly also be seen
T2/FLAIR
 central high intensity (hypointense to CSF, does not attenuate on FLAIR)
 peripheral high intensity (vasogenic edema)
 the abscess capsule may be visible as an intermediate to slightly low signal thin rim 

8. Sebutan kejadian inflamasi akibat died cyst

Blood-brain barrier (BBB) break (di CNS)

Dying cysticerci menginisiasi pro-inflammatory response menginduksi disrupsi blood-

brain barrier, diikuti infiltrasi sel imun di site infeksi

Immunohistochemical di granuloma sekitar dying cyst  ada infiltrasi makrofag,

limfosit B T, sel plasma, sel mast. Sel” ini semua produksi immune mediators spt sitokin.
Selain itu, granuloma disktr kista juga produksi high level sitokin Th1 (IFN-γ, IL-18, TGF-
β) & low amount sitokin Th2 (IL-44, IL-13, IL-10). Mixed cytokine response ini terjadi di
NCC stage kronik.

Ketika cysticerci menginfeksi parenkim, inflammatory response terlimitasi di

surrounding cysticerci nya aja, CSF masih normal = infeksi benign
Kalo cysticerci menginfeksi ventrikel & subarachnoid, menyebabkan increased CSF
cellularity dan perparah inflammatory process = hidrosefalus/vaskulitis

Severe NCC juga disertai eosinophilic infiltration di CSF dan produksi mixed Th1/Th2
cytokines (IL-5, IL-6, IL-10). Selain itu, pasien dgn multiple cyst memiliki high expression
dr IL-5 IL-6. Selain itu, di pasien dgn subarachnoid cyst ada peningkatan ekspresi IgG,
IgM, IgE, IL-1β, IL-6, TNF-α.

Respon imun perifer

Ketika cysticerci ada di CNS, respon imun trigger sekresi antigen. Antigen ini bisa
sampai peripheral blood dr brain krn ada BBB break = systemic immune response

Trdpt produksi Th2 & Th1 sitokin & low plasma levels dr IgG subclasses di pasien
asimtomatik. Sdgkan pasien simtomatik, trdpt penurunan cellular immune response
dan peningkatan all IgG subclasses.
Inflammatory response akibat dying cyst dapat menyebabkan : vaskulitis, mass effect,
cerebral edema

9. What is the role of imaging to diagnose neurocysticercosis ? Kenapa lebih ke MRI?

Findings in neuroimaging :
- Cystic lesions w/ or w/o enhancement
- ≥1 nodular calcifications
- Focal enhancing lesions, or
- Multilobulated cystic lesions in subarachnoid space
- Cysticerci di parenkim otak = 5-20 mm, bulat
Cystic lesions di subarachnoid / fisura = bisa membesar sampai 6 cm, lobulated

NCC adalah kondisi adanya parasit di CNS. Saat di CNS, larva seringkali di dlm
parenkim otak. Tp bisa juga masuk di ventrikel & subarachnoid, atau keduanya. Jadi =
lokasi lesi penting dlm symptom development nya  ini dibantu dgn imaging CT &
MRI. Imaging fungsinya u/ cari lokasi & jumlah lesi, stages, degree of inflammatory
response krn parasitnya

MRI = imaging modality di neurocysticercosis, khususnya u/ evaluasi intraventricular &

cisternal/subarachnoidal cysts
Teknik --> noninvasive magnetic resonance cisternography (MRC), fluid-attenuated
inversion recovery (FLAIR) sblm & sesudah inhalasi 100& oksigen provide hasil lebih
bgs, khususnya buat deteksi racemose cisternal cyst

Guideline treatment NCC juga hrs mempertimbangkan number&location lesi nya. Hal
ini dicover semuanya oleh MRI. Lokasi paling sering di parenkim otak. Kedua tersering
di 4th ventricle  sangat susah dideteksi di CT, even MRI bisa salah. Di 4 th ventricle,
signal intensity dr cyst nya udah dikit beda dr CSF even tnp enhancement, ada
hidrosefalus krn obstruksi CSF flow

Stages in MRI imaging :

- Vesicular : cysticercus is viable, few inflammatory changes di surrounding tissue.
Kista pny dinding tipis, cyst fluid pny signal intensity yg similar ke CSF
*in viable cyst : scolex terlihat dgn bentuk mural nodular
- Colloid vesicular : inflammatory reaction disekitar cysticercus, dinding menebal &
vesicular fluid membentuk aspek koloid spt agar”, intensitas signal cystic fluid
mulai beda dgn CSF. Scolex nya mulai alami degenerasi, ada gradual decrease dr
 size of lesion. Dibantu contrast, peripheral & perilesional edema udah mulai
terlihat
- Granular nodular : parasit udah mati, lesi mulai termineralisasi, mulai semisolid
digantikan jaringan granuloma, ada nodular/ring enhancement di lesi, edema
makin meluas
- Nodular calcified : lesi termineralisasi sempurna, lesi berbentuk small nodules
dgn hipointensitas T2W, lebih bgs dideteksi di CT. Ada calcified lesions di
persistent contrast enhancement di MRI, no edema

Kalau CT lebih sensitif cari kalsifikasi, tp overall lebih akurat MRI di NCC

10. Side effect of antiparasitic treatment

 Allergic dermatitis, peripheral neuropathy, leukopenia,

thrombocytopenia

 Nausea, vomiting, abdominal discomfort

 Mebendazole = transient abdominal pain, diare

 Albendazole = LF abnormality & BM toxicity (prolonged use), damage

inflicted on cysticerci & consequent acute inflammatory response

 Niclosamide, efek samping mild : malaise, mild abdominal pain, nausea

 Praziquantel = Efek samping mild (10-50%) : transient dizziness,

headache, malaise, abdominal pain, nausea
Efek samping moderate (<10%) : sedation, vomit, diare, urticaria, rash,
fever, mild transaminitis

11. What is impact of this condition on the patient’s health & socioeconomic status?

Impact on human health : cysticercosis, neurocysticercosis

 NCC penyebab 30% kasus epilepsi di seluruh dunia dmn parasit ini endemik
(WHO)

 CC/NCC adalah focal disease dan biasanya menyerang daerah endemik dgn low-
middle economic area. Jika terinfeksi, dpt tjd ignorance dr diseasenya sendiri atau
tidak tersedianya faskes & infrastruktur memadai di areanya shg akses ke
 pengobatan kurang. WHO catat 75% pasien dunia CC/NCC mendapatkan
pengobatan yg buruk

Impact on socioeconomic

 Menurunkan market value penjualan babi, orang jadi waspada makan

daging babi = economic losses to pig industry

 30% pasien CC/NCC tidak bisa hidup normal, terutama karena epilepsi
nya sehingga lead to poverty

 Krn pengobatan yg buruk spt yg disebut diatas, berefek pada kinerja

dan mata pencaharian. Pasien alami kesulitan bekerja khususnya bagi
simtomatik

12. Pasien dikasi phenytoin, berapa lama u/ maintenance di pasien ini ?

Phenytoin = anticonvulsants drugs  dipakai di pasien kejang / high risk seizures

Pasien cysticerci aktif yg lesi nya sembuh tanpa adanya kalsifikasi, diberikan
antikonvulsan sampai free of seizures minimal 1 tahun & hasil neuroimaging normal =
antikonvulsan boleh tappering down

Pasien recurrent seizures : long-term anticonvulsant

 Phenytoin
 Carbamazepine : dipakai klo phenytoin ga tersedia
 Phenobarbital : dipakai klo phenytoin ga tersedia