This document describes a case of neurocysticercosis. It begins with an introduction to neurocysticercosis including what causes it, the different types, epidemiology, diagnosis, management, and treatment. It then presents a hypothetical case of a 38-year-old male who experienced a convulsive episode. His past medical history revealed multiple calcifications on a previous brain CT suggestive of cysticercosis. He had traveled to an endemic area two years prior.

1. NEUROCYSTICERCOSIS
CASE PRESENTATION
PRESENTED BY
DIYA WILSON
VTH PHARM.D
15P02362

2. INTRODUCTION [1]
Neurocysticercosis is a neurologic infection caused by the larval
stage of the tapeworm Taenia solium
It is the most common preventable parasitic disease of the central
nervous system and the most common cause of acquired epilepsy
worldwide.
The disease is the result of accidental ingestion of eggs of Taenia
solium (i.e., pork tapeworm), usually due to :
contamination of food by people with Taeniasis.
consuming undercooked pork, or contaminated water.
The parasite can grow in the brain and spinal cord within the
nervous system,
causing severe headache and seizures beside other
pathological manifestations.
2

3. TYPES [1]
The two basic types of neurocysticercosis are:
PARENCHYMAL:
 Associated with headaches, seizures, intellectual impairment, behavioral
changes, and hydrocephalus.
 Impairment of the ability to coordinate voluntary movements (ataxia) and
muscular weakness on one side of the body (hemiparesis) may also occur
with this form of neurocysticercosis.
EXTRAPARENCHYMAL
 Subarachnoid: associated with chronic inflammation of the membranes
covering the brain (meninges).
 Intraventricular: causes obstructive hydrocephalus. A variant of this form of
cysticercosis known as racemose cysticercosis may occur.
• Racemose cysticercosis: characterized by accumulation of cysts at
the base of the brain potentially resulting in mental deterioration,
coma and life-threatening complications.
3

4. EPIDEMIOLOGY [2]
The World Health Organization (WHO) lists neurocysticercosis as a “Neglected
Tropical Disease.”
It estimates that about 50 million people worldwide have neurocysticercosis and
that it causes about 50,000 deaths each year.
It is also responsible for more than 50% of the cases of late-onset epilepsy in
developing countries.
The T. solium taeniasis/cysticercosis complex is endemic in many developing
countries in sub-Saharan Africa, Latin America, and Asia.
Although T. solium had virtually disappeared in developed countries due to
industrialization, improved methods of husbandry, and health checks;
Cysticercosis and neurocysticercosis are diagnosed anew in North America,
Europe and Australia due to increased immigration from endemic areas.
4

5. 5
Although neurocysticercosis appears to affect men and women equally,
there is some evidence to suggest that inflammation around the parasites
may be more severe in women than in men.
In addition, despite the fact that neurocysticercosis appears to be the most
frequent cause of seizures in children and adults (peak incidence, 30-40 y),
the exact incidence in children is not known.

6. A complex idea can be conveyed
with just a single still image,
namely making it possible to
absorb large amounts of data
quickly.
6

7. INCIDENCE IN INDIA [3]
In a community-based survey involving over 50,000 individuals in a district
in Tamil Nadu in southern India,
 NCC was found to be the cause of active epilepsy (at least one seizure in
the five years before the survey) in at least a third of the patients .
Based on the results of this large survey, the prevalence of NCC as a cause of
active epilepsy in India was calculated to be one per 1000 population.
 Thus, at least 1.2 million persons in India are suffering from active epilepsy
due to NCC.
The most common form of the disease in India was the Solitary Cysticercus
Granuloma (SCG) ( first identified in 1989) which was seen in up to 60 per
cent of patients with NCC.
7

8. 8
The disease is prevalent in all states of India,
although the prevalence varies between the states.
The National Institute of Mental Health and
Neuron Sciences (NIMHANS),Bangalore reported a
diagnosis of NCC in 2% of unselected
series of epilepsy patients.
Low proportion of pork eaters amongst Indian
patients is the other unusual feature of the disease
and more than 95% of Indian patients with
NCC are vegetarians.

9. ETIOPATHOGENESIS [4]
 NCC is caused by the dissemination of the larval
form of the pork tapeworm, Taenia solium in
humans which then form cysts in various organs.
 When the eggs of Taenia solium are ingested by
humans, the tapeworm eggs hatch and the
embryos penetrate the intestinal wall and reach
the bloodstream.
 The formation of cysts in different body tissues
leads to the development of symptoms, which will
vary depending on the location and number of
cysts.
9

10. RISK FACTORS FOR ACQUIRING
NEUROCYSTICERCOSIS [4]
 Living in areas where the parasite is endemic (most
commonly in rural developing countries where pigs roam freely
and come into contact with human feces)
 Drinking water or eating food contaminated with
tapeworm eggs
 Living in a household where another family
member has intestinal tapeworm infection
(taeniasis).
 Individuals who have taeniasis and poor hygiene
are also at increased risk of infecting themselves.
10

11. PATHOPHYSIOLOGY [5]
11

12. 12

13. 13
STAGE 1:
1-2 week after the oncospheres lodges in the brain, it expands to form a
edematous lesion.
If the cysts are small in number-does not produce any symptoms
If they are many-increased intracranial pressure
A diagnosis can rarely be made in this case.
During this phase, a protoscolex develops.
Patients remain asymptomatic usually in this phase.
But those with massive infections uncontrolled seizures and progressive
dementia may develop.
STAGE 2:
Approximately 2 months after ova ingestion, the cystecerci cellulosae matures and the
cyst has a protoscolex surrounded by a bladder with clear fluid.
The living cyst produces only a mild inflammatory reaction and this protects the cyst
from the hosts immune system.
The patient remains asymptomatic till the cysts remains viable (around 2-10 years +)
until there are massive in number.
Neuroimaging done during this stage shows that the cysts do not typically grow
beyond their mature size

14. 14
STAGE 3
2-10 years later, the mature cystecercus dies; the clear fluid becomes thicker
and more opaque.
Hyaline degeneration and mineralization begins.
At this time, the C.cellulosae antigens begins to leak eliciting intense
inflammatory response (this immune response is both humoral and cell-
mediated with fibroblasts forming a capsule-like structure around the cysts.)
The cyst degeneration takes around 6-18 months
Usually the oncospheres lodge in the brain parenchyma but in 10-15% of
patients, they lodge in the ventricles or meninges and these do not become
typical cysts.

15. 15
Sometimes, the cysticerci lodges in the subarachnoid space and can expand
up to 5 cms
These giant cysticerci produce focal neurological signs and increased
intracranial pressure.
Chronic inflammation in the subarachnoid space can cause vasculitis of the
traversing arteries, resulting in thrombosis of brain stem & some may develop
focal neurological signs from a stroke due to vasculitis.
The arachoiditis can lead to lead to obstructive CSF pathways and cause
hydrocephalus which leads to patients developing an altered mental status
with dementia, confusion and stupor.
Patients at this stage show signs and symptoms frequently with the
common one being seizures which can be focal or generalized.

16. 16
STAGE 4
At this final stage, the cyst dies spontaneously or from the anthelmentic
treatment.
The wall collapses, and the cyst becomes a granoulous tissue with a thick
collagenous capsule.
As time passes, the granulomas calcify, therefore the CT scans show no
lesions.
As the cyst is already dead, the patient is asymptomatic; but some patients
do develop frequent seizures.

17. 17
SIGNS AND SYMPTOMS [6]

18. COMPLICATIONS [6]
• Headache, dizziness
• Stroke
• Neuropsychiatric
dysfunction
• Cognitive decline
• Dysarthria
• Extra ocular
movement palsy or
paresis
• Hemiparesis or
hemiplegia, which
may be related to
stroke
• Hemisensory loss
• Movement disorders
• Hyper/hyporeflexia
• Gait disturbances
• Death
18

19. DIAGNOSIS [5]
 HISTORY AND PHYSICAL EXAMINATION:
Signs and symptoms caused by NCC are usually not specific.
The most common symptoms are :
seizures
focal findings,
headache
intracranial hypertension.
Focal neurological findings are less common, non-specific and due to a
variety of types of lesions and mechanisms.
 IMAGING: CNS imaging is essential to establish the diagnosis and to
determine the type of disease, emergency measures required, choice of
treatments.
MRI is much superior to CT scanning to visualize brain structures and
anatomy as well as cysts. However CT is superior to detect
calcifications. 19

20.  SEROLOGY:
The best documented and most useful is a serum Western blot employing a
specific fraction of T. solium cysts.
The test is very specific for exposure and/or disease and to confirm the
diagnosis. However, it lacks sensitivity in patients with minimal
disease
Antigen detection tests using monoclonal antibodies (developed against
the closely related T. saginata) in a capture ELISA format have been
developed.
They are specific for current viable infection, The concentration of antigen
is higher in the CSF than the serum. Levels grossly correlate with the
extent of involvement.
 STOOL EXAMINATION :
Taeniasis may be established by detecting T.solium eggs and proglottids in
a patient's stool.
20

21. MANAGEMENT [7]
21
• Albendazole &praziquantel
• To kill the cystic larvae&/or tapeworm
Larvicidal Agents
• Dexamethasone &prednisone
• To decrease or prevent inflammation
Corticosteroids
• Carbamazepine ,phenytoin ,lamotrigine etc.
• To prevent/decrease severity & no. of seizures
Anti -Seizure meds
•To decrease mass effect with/without inflammation
Surgical based therapies
• Symptomatic treatment like analgesics, antibiotics etc.
General supportive measures

22. TREATMENT OF VIABLE
INTRAPARENCHYMAL NCC
 In patients with untreated hydrocephalus or diffuse cerebral edema,
management of elevated intracranial pressure alone is required
 For diffuse cerebral edema treatment should be done using anti-
inflammatory therapy such as corticosteroids and surgical approach is
required for treatment of hydrocephalus
 In the absence of elevated intracranial pressure, we recommend the
use of antiparasitic drugs in all patients with VPN .
 For patients with one to two viable parenchymal cysticerci:
 Albendazole monotherapy :15 mg/kg/day divided into two daily
doses for 10–14 days with food (maximum dose of 1,200 mg/day)
22

23. Between the second and fifth days of antiparasitic therapy, there is usually
an exacerbation of neurological symptoms, attributed to local
inflammation due to the death of the larvae.
For this reason, both albendazole and praziquantel are generally given
simultaneously with steroids in order to control the edema and
intracranial hypertension that may occur as a result of therapy.
 Albendazole (15 mg/kg/day) combined with Praziquantel (50
mg/kg/day) for 10–14 days.
 Retreatment with antiparasitic therapy for parenchymal cystic lesions
persisting for 6 months after the end of the initial course of therapy is
required.
23

24. TREATMENT OF DEGENERATING INTRAPARENCHYMAL
NCC INCLUDING PATIENTS WITH SOLITARY
CYSTICERCUS GRANULOMA (SEL) DUE TO NCC
› Patients with multiple enhancing lesions and seizures be initially
treated with antiepileptic drugs, antiparasitic therapy, and
corticosteroids.
› Albendazole (15 mg/kg/day in twice daily doses up for 1–2 weeks)
with meal
› Patients with SEL treated with antiparasitic drugs should also be
treated with corticosteroids initiated before antiparasitic therapy.
24

25. TREATMENT OF CALCIFIED PARENCHYMAL
NEUROCYSTICERCOSIS (CPN)
 Symptomatic therapy alone is recommended instead of
antiparasitic drugs in patients with calcified parenchymal lesions
 It is suggested that corticosteroids not be routinely used in
patients with isolated CPN and perilesional edema.
 In patients with refractory epilepsy and CPN, evaluation for
surgical removal of seizure foci is recommended
25

26. MANAGEMENT OF OCULAR
CYSTICERCOSIS (OC)
 Intraocular cysticerci should be treated with
surgical removal rather than with antiparasitic
drugs.
26

27. CORTICOSTEROIDS [8]
 Corticosteroids are frequently used to decrease neurological
symptoms due to the death of the parasite and are the primary
management for chronic cysticercosis arachnoiditis (Upto 32 mg of
dexamethasone per day is needed to reduce the brain edema
accompanying this condition.)
 Administration of adjunctive corticosteroid therapy should begin
before antiparasitic drugs .
 The most frequent regimen is dexamethasone at doses of between 4.5
and 12 mg/day.
 Prednisone at 1 mg/kg/day may replace dexamethasone when long-
term steroid therapy is required.
 Mannitol, at doses of 2 g/kg/day, is also used for acute intracranial
hypertension secondary to neurocysticercosis.
27

28. ANTI-SEIZURE MEDICATIONS
 Antiepileptic drugs are recommended in all NCC patients with seizures.
 Seizures secondary to neurocysticercosis usually respond well to first-
line antiepileptic.
Seizures are often well controlled with a single antiepileptic drug
(AED).
 Duration remains undefined and depends neither on the type of seizure
at presentation nor on other risk factors for recurrence, such as age at
onset and number of seizures before diagnosis.
 Recurrence of seizures after AED withdrawal is correlated with the
presence of multiple lesions prior to starting cysticidal therapy, and
persistence or calcification of lesions after therapy.
 In patients with few seizures before antiparasitic therapy, resolution of
the cystic lesion on imaging studies, and no seizures for 24 consecutive
months, tapering off and stopping antiepileptic drugs can be
considered. 28

29. 29

30. SURGERY
 Surgical procedures are key in the treatment of complicated
disease such as
 neuroendoscopy
 open surgery
 shunt placement.
 Neuroendoscopy is useful to remove cysts that are easily
approached and causing symptoms; this may prevent prolonged
use of corticosteroids and anthelminthics.
 A treatment series of 4th ventricular lodged cysts, suggested
medical therapy, sometimes requiring a shunt to control
hydrocephalus, could successfully be employed.
30

31. HYPOTHETICAL CASE [9]
31

32. SUBJECTIVE
 NAME: Mr.X
 AGE : 38 years
 SEX :Male
 CHIEF COMPLAINTS : An episode of convulsion,
presenting without fever or other neurological
symptoms
32

33. PAST MEDICAL HISTORY:
 Six years previously, he had been admitted to the
emergency department after collapsing.
 A cranial computed tomography (CT) scan revealed
multiple punctiform calcifications in both cerebral
hemispheres and in the cerebellum, surrounded by a small
cyst and with an eccentric position, suggestive of parasitic
infestation - cysticercosis.
SOCIAL HISTORY:
 His last trip to Cape Verde had been two years previously.
 He has a history of alcohol and tobacco dependence.
33

34. PAST MEDICATION HISTORY:
 On the infectious diseases ward, treatment began with
Albendazole and Dexamethasone.
 Beyond cysticidal treatment for NCC, Carbamazepine was
started as the diagnosis of secondary epilepsy was
established.
34

35. OBJECTIVE
Physical examination:
› He had undergone a cranial CT scan (Figs. 1 and 2 ,3) that
showed similar findings to those found 6 years earlier.
35

36. 8 days later:
 He presented with sudden onset of left
eyelid edema and left ocular pain that
increased with horizontal eye movements.
 An orbital CT scan revealed thickening and
densification of the left lateral rectus
muscle (fig. 4) with an apparent cystic
lesion with hypodense centre, suggestive of
infiltration by cysticercosis.
36

37. LABORATORY PARAMETERS
37
PARAMETERS PATIENT VALUES REFERENCE
Haemoglobin 136 g/L 138 to 172 g/L
WBC 6.57× 109/L (4.5 to 11.0 × 109/L).
Neutrophils 82% 40% to 60%
Eosinophils 0.3% 1% to 4%
Platelets 228× 109/L 150 to 400 × 109/L
C-Reactive Protein 3 mg/L <3.0 mg/L
Bilirubin 17.1 μmol/L, 1.71 to 20.5 µmol/L
Alkaline Phosphatase 63 IU/L, 20 to 140 IU/L

38. ADDITIONAL DATA
The patient’s carbamazepine levels were measured to
assess his medication adherence
 Carbamazepine level <0.5 mg/L
[Normal therapeutic range: 4-12 mg/L]
38

39. ASSESSMENT
Intra –Ocular cysticercosis & Seizures
related to Neurocysticercosis & Non-
compliance to Carbamazepine.
39

40. PLAN [9]
INITIAL PLAN:
 He was treated with dexamethasone 10 mg 8/8h,
carbamazepine, albendazole and, 4 days later, praziquantel.
8 DAYS LATER: AFTER DIAGNOSIS OF INTRA-OCULAR
CYSTICERCOSIS
 Analgesia was started, and the dexamethasone dose was
increased from 10 mg 8/8h to 10 mg 6/6h, with significant
clinical improvement.
 The patient was discharged and the outcome was favourable.
 At re-evaluation, he continued taking carbamazepine, and
confirmed no recurrence of seizures or ocular symptoms.
40

41. INTERVENTIONS [7,9]
 In the initial treatment plan, it was already understood that the patient
had calcified cysts and was still administered anthelminthic drugs.
According to the 2017 Clinical Practice Guidelines by the Infectious Diseases
Society of America (IDSA) and the American Society of Tropical Medicine
and Hygiene (ASTMH) :
 Anthelminthic treatment is not indicated in calcified NCC because
parasites are non-viable and only consist of calcified encapsulated cyst
remnants along with varying degrees of host inflammatory reaction.
 Also ,Medical treatment has no role in the management of intraocular
cysticerci due to the potential sight-threatening side-effects of toxin
release following the death of the parasite.
 Surgical treatment is the best choice in intraocular cysticercosis,
41

42.  In this patient symptoms started 8 days after beginning treatment.
Symptom exacerbation is common during the first week after
antiparasitic treatment is initiated.
 The use of steroids is important at this point in order to decrease
the effect of the strong inflammatory response, secondary to the
release of toxins following the death of parasite.
 Steroids should have been administered for around 3 days before
the cysticidal drugs are started, then continued for approximately 1
week following the end of the course.
 It is also likely that the dose of steroids was probably not
sufficient.
 The combination of albendazole and praziquantel increases the
parasiticidal effect in patients with multiple brain cysticercosis and
are ineffective against calcified cysts.
 Hence antiparasitic therapy should be discontinued.
42

43. MY PLAN [7,11 13]
 Stop the antiparasitic treatment
 Dexamethasone :10 mg q 6th hourly for a week
 Carbamazepine :200 mg orally twice a day.
Continue for a period of 2 years.
 Surgical removal of calcified cysts and
intraocular cyst
43

44. PATIENT COUNSELING
REGARDING DISEASE [10]
 Neurocysticercosis is a preventable parasitic infection of the
central nervous system and is caused by the pork
tapeworm Taenia solium.
 Humans become infected after consuming undercooked food,
particularly pork, or water contaminated with tapeworm
eggs, or through poor hygiene practices.
44

45. REGARDING DRUGS [11]
▲ Carbamazepine should not be stopped suddenly
▲ Carbamazepine may affect your judgment and slow your reaction
time so be cautious when driving a vehicle or operating machinery.
▲ Do not drink alcohol while you are taking carbamazepine because
this may increase the sedative effect of carbamazepine.
▲ Carbamazepine may cause hyponatremia (low sodium levels)
 Tell your doctor if you experience any symptoms such as a
headache, confusion, new or increased seizure frequency,
weakness
▲ Tell your doctor if your mood becomes depressed, or you start
having thoughts of suicide or self-harm while taking carbamazepine.
45

46. REGARDING LIFE STYLE MODIFICATION [12]
 Wash your hands with soap and warm water after using the toilet,
changing diapers, and before handling food
 Teach children the importance of washing hands to prevent infection
 Wash and peel all raw vegetables and fruits before eating
 Use good food and water safety practices while travelling in endemic
countries such as:
 Drink only bottled or boiled (1 minute) water or carbonated
(bubbly) drinks in cans or bottles
 Filter unsafe water through an “absolute 1 micron or less” filter &
dissolve iodine tablets in the filtered water [“absolute 1 micron”
filters can be found in camping and outdoor supply stores]
46

47. MONITORING PARAMETERS [11,13]
47
DRUG ADR MONITOING
PARAMETERS
BRAND
NAME
Dexamethasone Alteration in
glucose tolerance,
behavioral and
mood changes,
increased appetite,
and weight gain;
Hemoglobin,
blood pressure,
serum potassium,
glucose, bone
mineral density
DECDAN,
DEXONA,
WYMESONE
Carbamazepine Nausea, vomiting,
Leucopenia,
Dizziness,
somnolence
CBC with platelet
count, liver and
renal function
tests, urinalysis,
BUN, serum
sodium
TEGRITAL,
VERSITOL ,
ZEPTOL

48. TAKE AWAY POINTS [10]
 NEUROCYSTICERCOSIS AND TAENIASIS ARE TWO DIFFERENT
DISEASES CAUSED BY THE SAME PARASITE
When the parasite T. solium is transmitted to human beings, it causes an
intestinal infection of the adult tapeworm known as taeniasis.
 Cysticercosis develops when the larvae of T. solium invade body
and develop in the muscles, skin and eyes. If larvae invade the
central nervous system, the infection leads to
Neurocysticercosis.
 T. SOLIUM WAS RECENTLY NAMED THE FOOD-BORNE PARASITE OF
“GREATEST GLOBAL CONCERN”
 WHO together with the Food and Agriculture Organization recently
issued the warning to highlight the importance of cross-sector
collaboration in tackling the spread of the disease.
48

49.  FOOD HANDLERS CAN ALSO TRANSMIT T. SOLIUM
 Neurocysticercosis is not just limited to rural areas or disadvantaged
communities lacking basic sanitation.
 A growing concern is the lack of hygiene practices among food handlers
where the practice of regular hand-washing is important.
 ELIMINATING NEUROCYSTICERCOSIS REQUIRES BREAKING THE LIFE
CYCLE OF T. SOLIUM
 WHO is working with countries to tailor intensified control strategies
for T. solium and improve management of neurocysticercosis patients.
 Fortunately, pigs can now be treated with anti-parasitic medications and
vaccinated against T. solium. This prevents the parasite from being
transmitted to humans.
49

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51