pharmacotherapy

1. PHARMACOTHERAPY OF
NEUROCYSTICERCOSIS
Dr. Prerna Singh
Junior Resident (3rd year)
Department of
Pharmacology
JNMC, AMU

2. INTRODUCTION
Most common parasitic disease of the CNS worldwide
Most common cause of acquired epileptic seizure In developing
countries
Causative agent: larval stage T. solium/pork tapeworm
Ingestion of food contaminated with the eggs of the parasite T.
solium

3. INTRODUCTION
Cysticerci: most commonly detected in the brain, CSF, skeletal muscle,
subcutaneous tissue, or eye.
Clinical presentation:
 Depends on the number and location of cysticerci
 Extent of associated inflammatory responses or scarring

4. LIFE CYCLE
Human: definitive
host
Pigs: intermediate
host

5. CLINICAL FEATURES
Neurologic manifestations are the most common
Seizures: generalized/focal
Hydrocephalus may result from CSF flow obstruction by cysticerci
and accompanying inflammation or by CSF outflow obstruction from
arachnoiditis.

6. CLINICAL FEATURES
Symptoms of increased intracranial pressure
Headache
Nausea
Vomiting
Changes in vision
Dizziness
Ataxia

7. CLINICAL FEATURES
Patients with hydrocephalus may develop papilledema or
display altered mental status.
When cysticerci develop at the base of the brain or in the sub-
arachnoid space, they may cause chronic meningitis or
arachnoiditis, communicating hydrocephalus, haemorrhages, or
strokes

8. DIAGNOSIS
MRI or CT scans - appear as cystic lesions/scolex can often be
visualized
Lesions may appear as contrast- enhancing lesions surrounded
by edema.
Parenchymal brain calcifications are the most common finding
and evidence that the parasite is no longer viable.
CSF- to rule out other causes

9. STAGES
Stage
Vesicular Cyst & scolex
Colloidal Ring enhancement and
edema
Granular Decreased enhancement
and edema
Involution Calcification

10. STAGES

11. MANAGEMENT
Anti epileptic drugs
Anti parasitic drugs
Steroids
Surgery

12. ANTIEPILEPTICS
Initiated when the patient presents with a seizure
Stopped once the follow-up CT scan shows resolution of the
lesion
Long-term antiepileptic therapy is recommended when
seizures occur after resolution of edema and resorption or
calcification of the degenerating cyst.

13. ANTHELMINTIC
Cysticidal drugs accelerate the destruction of the parasites,
resulting in a faster resolution of the infection
For lesions that are in the “granulo-nodular” stage (surrounded
by a contrast-enhancing ring)
Calcified lesions do not need to be treated with anticysticidal
therapy.
Albendazole
Praziquantel

14. ALBENDAZOLE
Mechanism of action: Binds to free β-tubulin in nematodes,
inhibiting the polymerization of tubulin and the microtubule-
dependent uptake of glucose. Irreversible damage occurs in
gastrointestinal (GI) cells of the nematodes, resulting in
starvation, death, and expulsion by the host.
Dose: 15 mg/kg per day in two doses for 8 – 28 days
Maximum 800 mg/day

15. ALBENDAZOLE
Poorly absorbed from the GI tract
Metabolized in the liver
Administration with a high-fat meal (~40 g) increases the
drug’s absorption
Albendazole sulfoxide (metabolite) crosses the blood–brain
barrier

16. ALBENDAZOLE
Prolonged courses- associated with liver function abnormalities
and bone marrow toxicity.
Drug should be administered in treatment cycles of 28 days
interrupted by 14-day intervals off therapy

17. PRAZIQUANTEL
Mechanism of action: increases the permeability of the
membranes of schistosome cells towards calcium ions.
Induces contraction of the parasites muscle, resulting in
paralysis
Dose: 50–100 mg/kg daily in three divided doses for 15–30
days
A combination of albendazole and praziquantel is more
effective in patients with more than two cystic lesions.

18. PRAZIQUANTEL
Rapid absorption orally
Excreted in urine
Side effects: headache, anorexia, drowsiness, allergic reactions

19. STEROIDS
Prednisone- 1-2 mg/kg/day
Dexamethasone – 0.1mg/kg/day IV starting one day before
anthelmintic
To reduce the host inflammatory response to degenerating
parasites
Glucocorticoids induce first-pass metabolism of praziquantel
and may decrease its antiparasitic effect, cimetidine should be
co-administered to inhibit praziquantel metabolism
Serum levels of phenytoin and Carbamazepine may also be
altered

20. FOR HYDROCEPHALUS
In the case of obstructive hydrocephalus, the preferred
approach is removal of the cysticercus via endoscopic surgery.
Alternative approach - diverting procedure-
ventriculoperitoneal shunting
Prolonged courses of antiparasitic drugs
Methotrexate should be used as a steroid-sparing agent in
patients requiring prolonged therapy

21. MULTIPLE LESIONS
Glucocorticoids are the mainstay of therapy
Antiparasitic drugs should be avoided

22. CALCIFIED LESIONS
No anthelmintic needed – cyst dead
Edema around calcification- anti inflammatory

23. PREVENTION
 Good personal hygiene
 Treatment and prevention of human intestinal infections.
 Adequate cooking of pork viscera
 Exposure to temperatures as low as 56°C for 5 min will destroy
cysticerci

24. PREVENTION
 Refrigeration/salting for long periods or freezing at –10°C for 9 days also
kills cysticerci
 Inspection of beef and proper disposal of human feces
 Mass chemotherapy - in efforts at disease eradication
 Vaccines are under development.

25. THANK YOU