5. Neurocysticercosis
• Most common parasitic infection of CNS
• Most common cause of acquired epilepsy in
• Incidence 4% in some areas.
• Incubation period within 7 years from exposure (83%).
• Spinal cord and peripheral nerve involvement is rare.
• Occurs from ingesting the parasite’s eggs, not from eating infested
meat
• T. solium can infect a person in two different ways: as the adult
worm or as the larva.
6.
7. Commonly involved sites
● brain: involved in 60–92% of cases of
cysticercosis.
Latency from ingestion of eggs to symptomatic
neurocysticercosis: 2–5 years
● skeletal muscle
● eye: immunologically privileged, like brain
● subcutaneous tissue
● heart
8. • Many larvae die naturally within 5–7 yrs or
with cysticidal therapy producing an
inflammatory reaction with collapse of the
cyst (granular nodular stage); these
sometimes calcify (nodular calcified stage).
9. Giant cysts
• Cyst with diameter > 50 mm.
• Two types of cysts tend to develop in the brain:
1. cysticercus cellulosae: in the parenchyma or
narrow subarachnoid spaces. It contains a scolex
(head), is usually static, and produces only mild
inflammation during the active phase
2. cysticercus racemosus: larger (4–12 cm), grows
actively producing grape-like clusters in the basal
subarachnoid spaces & fourth ventricle
and produces intense inflammation.
10. 4 Location of the cysts
1. Meningeal: found in 27–56% of cases with neural
involvement.
2. Parenchymal: found in 30–63%; focal or generalized
seizures occurs in ≈ 50% of cases (up to 92%
in some series)
3. Ventricular: found in 12–18%, possibly gaining access
via the choroid plexus.
Intermittent intracranial hypertension (Brun
syndrome).
4. Mixed lesions: found in ≈ 23%
11.
12. DX
Laboratory evaluation
• Mild peripheral eosinophilia
• CSF
• Stool: less than 33% of cases have T. solium ova in the stool.
• Serology
Most centers use enzyme-linked immunoelectrotransfer
blot (EITB) against glycoprotein antigens
(western blot), which is ≈ 100% specific and 98% sensitive,
although sensitivity is less (70%) in cases with a solitary
cyst.
16. Treatment
Medical
1. Anthelmintic : antiparasitic and/or cysticidal : Praziquantel vs Albendazole
vs Niclosamide
NB: Needed even following surgery.
2. Antiepileptics:
3. Steroids: must precede (3 doses) anthelmintic in incresed ICP
No Rx needed: HCP, calcified, high burden
Surgical :
A) Establish DX: stereotactic vs open biopsy
B) Spinal cysts and for intraventricular cysts
C) Ventricular CSF diversionary procedures
D) Giant cysts when intracranial hypertension does not respond to steroids
E) Mesial temporal lobe epilepsy with hippocampal sclerosis caused by NCC
F) Hydrocephalus secondary to cysticercotic arachnoiditis
17. Echinococcosis (hydatid cyst)
• Caused by encysted larvae of the dog tapeworm
Echinococcus granulosa in endemic areas.
• The dog is the primary definitive host of the
adult worm.
• Intermediate hosts for the larval stage include
sheep and man.
• Man is infected either by eating food
contaminated with ova, or by direct contact with
infected dogs
18.
19.
20. • CNS involvement occurs in only ≈ 3% (less in spinal
cord)
• Confined to the white matter.
• Most commonly located supratentorially, parietal lobe
commonest; MCA territory
• The cyst enlarges slowly (rates of ≈1 cm per year,
higher in children)
• contains germinating parasitic particles called “hydatid
sand” containing ≈ 400,000 scoleces/ml
• Primary cysts are usually solitary vs secondary cysts
• Intracranial hydatidosis is rare and more affects
pediatric age group.
• CT density of the cyst is similar to CSF.
23. Treatment
• Surgical removal of the intact cyst: Dowling
technique
• Avoid cysts ruptur during removal,
• Scoleces may contaminate the adjacent tissues
with possible
• Recurrence of multiple cysts or
• Allergic reaction.
• Adjunctive medical treatment with albendazole
for 28 days
24. Role of medical Rx for small or
inoperable brain cysts
• Medical therapy has shown promising effects
but surgery remains the golden treatment and
results in a complete cure.
• Chemotherapy is indicated for inoperable
patients with primary liver/lung
echinococcosis and for patients with multiple
cysts in two or more organs.
25. Amebic infections of the CNS
• Rare
• The ameba lives in fresh water and soil
• Naegleria fowleri: the only ameba known to
cause CNS infection in humans → primary
amebic meningoencephalitis (PAM): diffuse
encephalitis with hemorrhagic necrosis and
purulent meningitis… ICP
• Rapid progression
• More prominent in the frontal lobes.
27. Lab ix
• CSF: cloudy and often hemorrhagic, ↑
leukocytes, ↑ protein, normal or ↓ glucose,
• Gram stain negative (no bacteria or fungi), wet
prep → motile trophozoites (may be confused
with WBCs).
• Fatal in ≈ 95% of cases, usually within 1 week.
28. Diagnosis
• Neuroimaging studies usually show multiple
ring-enhancing lesions in patients infected
with Acanthamoeba spp., E. histolytica and B.
mandrillaris and diffuse edema in those
infected with N. fowleri.
• Examination of fresh CSF may reveal mobile
trophozoites in patients with N. fowleri
encephalitis
29. Treatment
• Medical: 6-week course of amphotericin B,
rifampicin, and chloramphenicol
• Surgical intervention:
1. drainage of a brain abscess
2. ventriculostomy with CSF
30. CNS toxoplasmosis
• Occurs late in the course of HIV infection, usually
when CD4 counts are < 200 cells/mm3.
• Present as:
1. Mass lesion (toxoplasmosis abscess): the most
common lesion-causing mass effect in AIDS
patients (70–80% of cerebral mass lesions in
AIDS)
2. Meningoencephalitis
3. Encephalopathy
31. CT/MRI findings in toxoplasma abscess
1. most common findings: large area (low density on CT) with mild to
moderate edema, ring enhancement with IV contrast in 68%
compatible with abscess (of those that did not ring-enhance,
many showed hypodense areas with less mass effect, with slight
enhancement adjacent to lesion), well circumscribed margins51
2. most commonly located in basal ganglia , are also often subcortical
3. often multiple (typically > 5 lesions) and bilateral
4. usually with little to moderate mass effect (in BG, may compress
third ventricle and Sylvian aqueduct, causing obstructive
hydrocephalus)
5. most patients with toxoplasmosis had evidence of cerebral atrophy
32. Treatment
• Pyrimethamine + sulfadiazine + Folinic acid
• Clindamycin, clarithromycin,
trimetrexate, piritrexim, and atovaquone are
alternative drugs in patients in whom
skin reactions to sulfadiazine develop
33. Role of surgery: settling DX
A) in patient with a negative toxo titer
b) accessible lesion(s) atypical for toxo (i.e., Non-enhancing, sparing
basal ganglia, periventricular location)
c) in the presence of extraneural infections or malignancies that may
involve the CNS
d) lesion that could be either lymphoma or toxo (e.g. Single lesion
e) in patients who have lesions not inconsistent with toxo but fail to
respond to appropriate anti-toxo medications in the recommended
time
F) the role of biopsy for non-enhancing lesions is less well-defined as
the diagnosis does not influence therapy
G) stereotactic biopsy may be especially well-suited, with up to 96%
efficacy, fairly low morbidity (major risk: significant hemorrhage, ≈ 8%
incidence), and low mortality
35. Spinal vs cerebral schistosomiasis
• Schistosoma mansoni is the primary cause of spinal
cord disease among all species of Schistosoma.
• Acute myelopathy is the most common neurological
complication.
• Schistosoma japonicum appears to cause more clinical
cerebral involvement than S. mansoni.
• Symptomatic acute cerebral schistosomiasis due to S.
japonicum has been recorded in approximately 2—4%
of patients.
• Neurological complications can occur during all
phases of schistosomiasis
36. Pseudotumoral encephalic
schistosomiasis (PES)
• The tumor-like mass can be located in any
region of the brain, but the cerebellum is the
most common site, followed by the occipital
and frontal lobes.
37. DX
• Biopsy of the nervous tissue is the only method that
gives a definite diagnosis of SCS
• However, this procedure should be avoided because of
its risks. The diagnosis of SCS has been established
according to the following criteria:
1. Evidence of lower thoracic or upper lumbar
neurological lesions;
2. Detection of exposure to schistosomiasis through
parasitological or serological techniques; and
3. Exclusion of other causes of myelitis.
38. Treatment
• Schistosomicidal drugs, steroids and surgery
are currently the available treatments for
neuroschistosomiasis.
• Praziquantel is the treatment of choice for all
schistosome species.
39. Indication for Surgery
• VPS for hydrocephalus and intracranial
hypertension in cerebellar schistosomiasis.
• Surgical intervention such as decompressive
laminectomy when acute s. Mansoni myelitis
deteriorates despite clinical treatment.
• Refractory epilepsy
