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Neurocysticercosis presenting as psychosis: A case report and a brief literature review

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Neurocysticercosis presenting as psychosis: A case report and a brief literature review

Abstract

Patients with neurocysticercosis, a common infection of the central nervous system caused by Taenia solium, have been reported to develop neuropsychiatric complications. We report a unique case of recurrent psychosis caused by neurocysticercosis in a 37-year-old El Salvador immigrant woman and discuss the underlying pathophysiological mechanisms of the complications. We reviewed published case reports of neurocysticercosis that presented with psychotic features and compared their diagnostic evaluation, the underlying pathophysiology of complications and treatment regimen with our case. This review concludes that neurocysticercosis should be considered in the differential diagnosis of patients presenting with psychosis with a history of residence in an endemic area.
https://doi.org/10.1177/2050313X221100396
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DOI: 10.1177/2050313X221100396
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Introduction
Neurocysticercosis (NCC) is the most severe form of cyst-
icercosis to cause infection of the central nervous system
(CNS) and is the leading cause of acquired epilepsy in
humans globally.1 The total number of individuals suffering
from NCC is about 2.56–8.30 million worldwide, while it is
estimated that the total symptomatic cases in endemic
regions are roughly 400,000.1 NCC is endemic in Latin
America, Asia, Africa and Central Europe, where 30% of all
epilepsy cases are caused by it.2 Recently, it is being diag-
nosed more often in the United States due to increased
migration.3 However, very little attention has been paid to its
surveillance, prevention and treatment.4
NCC is caused by the feco-oral transmission of Taenia
solium eggs. Humans ingest these parasite eggs, and their
embryos invade the mucosa of the small intestine, from
where they enter the circulation and subsequently into the
CNS.5 NCC is classified into six clinical syndromes: asymp-
tomatic, parenchymal, intraventricular, subarachnoid, spinal
and ocular forms.5 Clinical manifestations of NCC depend
on the location of the lesions and the number of cysts;
however, commonly associated neurological symptoms are
chronic headache, increased intracranial hypertension (ICH)
with symptoms of vomiting, nausea, dizziness and changes
in vision and focal neurological deficits.3 NCC may also
cause psychiatric manifestations like depression and psy-
chosis.6 In psychosis, a person loses contact with reality;
symptoms include delusions, hallucinations, bizarre behav-
ior and incoherent speech.7
Psychosis is a rare presenting complaint in NCC. One in
twenty NCC patients present with psychosis, and only 5% of
NCC patients present with psychosis in the emergency
department (ED)6 (2004). NCC remains underdiagnosed in
most patients as it is asymptomatic in approximately 50% of
cases.8 The variability in its clinical presentation and neuro-
pathology makes it challenging to diagnose, highlighting the
importance of thorough history taking, early detection and
Neurocysticercosis presenting as psychosis:
A case report and a brief literature review
Saeed Ahmed1, Sadia Usmani2, Sana Javed3, Aakash Hans4,
Sundas Saboor5, Aunsa Hanif6, Sheikh Mohd Saleem7
and Sheikh Shoib8
Abstract
Patients with neurocysticercosis, a common infection of the central nervous system caused by Taenia solium, have
been reported to develop neuropsychiatric complications. We report a unique case of recurrent psychosis caused by
neurocysticercosis in a 37-year-old El Salvador immigrant woman and discuss the underlying pathophysiological mechanisms
of the complications. We reviewed published case reports of neurocysticercosis that presented with psychotic features and
compared their diagnostic evaluation, the underlying pathophysiology of complications and treatment regimen with our case.
This review concludes that neurocysticercosis should be considered in the differential diagnosis of patients presenting with
psychosis with a history of residence in an endemic area.
Keywords
Neurocysticercosis, psychosis, psychotic manifestations, hallucinations, delusions
Date received: 11 October 2021; accepted: 22 April 2022
1Rutland Regional Medical Center, Rutland, VT, USA
2Psychiatry, Dow University of Health Sciences, Karachi, Pakistan
3Nishtar Medical University, Multan, Pakistan
4Hamdard Institute of Medical Sciences and Research, New Delhi, India
5Khyber Medical College, Peshawar, Pakistan
6Sharif Medical and Dental College, Jati Umrah Lahore, Pakistan
7Independent Public Health Consultant, Jammu & Kashmir, India
8Jawahar Lal Nehru Memorial Hospital, Srinagar, Jammu & Kashmir, India
Corresponding Author:
Sheikh Shoib, Jawahar Lal Nehru Memorial Hospital, Srinagar, Jammu &
Kashmir, India.
Email: sheikhshoib22@gmail.com
1100396SCO0010.1177/2050313X221100396SAGE Open Medical Case ReportsAhmed et al.
case-report2022
Case Report
2 SAGE Open Medical Case Reports
treatment. In this literature review, we present a rare case of
recurrent psychosis, along with a detailed review of previous
case reports of psychotic presentation with NCC, along with
associated features, diagnostic evaluation and treatment
options. This review will help clinicians recognize and treat
NCC presenting with psychotic symptoms.
Case presentation
A 37-year-old female immigrant from El Salvador presented
with a headache, strange behavior, auditory hallucinations
and paranoid delusions to the ED. She admitted to being
depressed, having a decreased appetite, sleep deprivation
and forgetfulness. She was admitted to the medical floor to
rule out delirium, and the consultation–liaison (CL) team
was contacted. When the CL team saw the patient, she was
still paranoid, delusional and experiencing auditory halluci-
nations. A review of systems revealed no evidence of a focal
neurological deficit. The general physical examination
revealed no abnormalities. On mental status examination,
her appearance was unkempt; the behavior was strange with
poor eye contact. She described her mood as “depressed,”
and her affect was constricted. Her thought process was con-
crete with circumstantiality at times; thought content was
positive for paranoid delusions, “her husband making plans
with his girlfriend to murder his wife and daughters.” On
perceptions disturbances, she was positive for auditory hal-
lucinations. She lacked insight/judgment, but her orientation
and memory were intact. The Mini Mental State Examination
(MMSE)9,10 score was 27. The CL team began her on risperi-
done 1 mg two times a day (BID) targeting psychotic symp-
toms. Collateral history revealed that the patient had a
history of generalized tonic–clonic seizures (GTCSs), for
which an antiepileptic medication was started. During the
same period, she was diagnosed with NCC and was pre-
scribed albendazole 400 mg BID for 28 days, but she did not
take the medication due to a lack of insurance. During the
current hospitalization, the medical team obtained a com-
puted tomography (CT) scan and a magnetic resonance
imaging (MRI) of the brain. The CT brain indicated
hypodense regions in the right frontal and parietal lobes, as
well as abnormal and irregular calcifications (Figure 1). The
MRI revealed encephalomalacia in the upper right frontal
and parietal lobes, as well as a rim of adjacent gliosis. On
the following day of her admission, she was cleared by the
medical team and transferred to psychiatry for psychosis.
Risperidone was increased to 6 mg/day in two divided
doses of 3 mg BID due to the patient’s persistent psychotic
symptoms. After her psychosis had resolved, she was dis-
charged with an aftercare follow-up appointment at a nearby
facility.
Discussion
This article aims to highlight the difficulties in diagnosing
and treating NCC in patients with psychosis in the United
States or other NCC-prevalent countries. In addition to the
case, presented here, we conducted a literature review of 21
similar cases (Table 1). Thirteen case reports came from
India, the remaining instances came from Nepal, Brazil,
Haiti, Portugal and Africa. Thirteen were male, and eight
were female. Fifteen cases were between the ages of 21 and
50 years, four were between the ages of 10 and 20 years, and
two were elderly (>51 years). The current case was diag-
nosed with NCC and presented to the ED with psychosis in
2017. However, due to non-compliance, she explained to the
ED again after 3 years with psychosis. This demonstrates a
high probability of recurrence of NCC if the disease is not
treated optimally or if patients do not adhere to their recom-
mended medication. Cases were reported in the literature
where patients were non-compliant and presented with psy-
chosis, most likely due to reinfection.16,28,29 In NCC, psychi-
atric symptoms may be triggered by inflammatory injury to
the brain caused by degenerating cysts and mechanical alter-
ations in cerebrospinal fluid (CSF) pressure.6 The classifica-
tion of psychiatric manifestations is based on the location of
the lesion6 (Table 2). The parietal lobe is involved in many
neuropsychological functions, including its engagement
Figure 1. Computed tomography scan of the brain showing areas of calcified lesions; inactive parenchymal neurocysticercosis.
Ahmed et al. 3
Table 1. Case reports of neurocysticercosis causing psychosis.
Author Case report Psychosis treatment Treatment duration Outcome
Shriqui and
Milette, 199228
You drive me crazy: a case
report of acute psychosis
and neurocysticercosis
First admission to hospital:
Low dose of haloperidol with close supervision,
subsequently increased to 15 mg daily and then
2 mg.
2 weeks trial of praziquantel.
Steroids were administered, tapered off and
discontinued after 1 month.
Second admission to hospital:
Continuation of haloperidol 2 mg.
First time psychosis
symptoms: 6 weeks
treatment.
Second time psychosis:
22 months.
No resolution of psychosis and
delusions due to non-compliance.
Bills and Symon,
199226
Cysticercosis producing
various neurological
presentations in a patient:
case report
First presentation with psychosis:
Antipsychotic medication.
Second presentation:
Antibiotics and steroids (presuming it was
encephalitis).
Third presentation:
No treatment.
Fourth presentation:
Ventriculoperitoneal shunt installed to treat
hydrocephalus.
Revision of ventriculoperitoneal shunt after
2 months.
Praziquantel (50 mg/kg/day) for 2 weeks.
Steroids (dexamethasone).
First presentation:
2 weeks.
Second presentation:
Not mentioned.
Fourth presentation:
2 weeks.
Resolution of her nausea, vomiting
and headaches. Her gait also
improved considerably, allowing her
to ambulate independently again, and
her incontinence decreased.
Verma and
Kumar, 201330
Neurocysticercosis
presenting as acute
psychosis: a rare case
report from rural India
Steroid (prednisolone) 1 mg/kg of body weight.
Acetazolamide 250 mg twice daily.
Antipsychotic drugs olanzapine 20 mg/day and
clonazepam 2 mg/day.
Prednisone for 28 days
and acetazolamide for
2 months.
Psychosis improved within 2 weeks
along with improvement of MMSE
scores after 2 months. Able to
do perform independently after
6 months.
Mahajan etal.,
20046
Neurocysticercosis
presenting with psychosis
Antipsychotic drugs risperidone 4 mg/day and
clonazepam 2 mg/day.
Phenytoin sodium 300 mg once a day.
Mannitol injection with prednisolone 40 mg once
a day.
Olanzapine 10 mg/day with venlafaxine 75 mg/day
(as psychotic symptoms worsened).
10 weeks. Free of seizures and psychiatric
symptoms on follow-up at 8 weeks
and 6 months.
Singh etal.,
200441
An unusual cause of
psychosis (2004)
Albendazole (15 mg/kg).
Prednisolone.
Antihistamine.
28 days. Improved and regained pre-morbid
lucidity.
Anjana etal.,
202023
An unusual presentation
of neurocysticercosis as
psychosis with tics
Risperidone 2 mg (for psychiatric symptoms).
Intravenous mannitol twice daily for 3 days.
Tapered albendazole 400 mg twice daily for 14 days.
Oral antiepileptic drugs.
14 days. Symptoms improved within 1 week of
treatment and MMSE reached 30 at
the end of 14 days.
(Continued)
4 SAGE Open Medical Case Reports
Author Case report Psychosis treatment Treatment duration Outcome
Sarangi etal.,
201320
Neurocysticercosis
masquerading psychotic
disorder: a case report
Albendazole (15 mg/kg/day) for 7 days.
Prednisolone (2 mg/kg/day) for 7 days.
Valproate.
7 days. Discharged on valproate. At 3 months
follow-up, there was a significant
decrease in psychotic symptoms and
resolution of CT scan lesions.
da Silva Miranda
etal., 202029
Neurocysticercosis
presenting as acute
psychosis: an unusual case
Albendazole for 1 month.
Corticosteroid for 1 month.
Aripiprazole (to be continued).
1 month. Improvement after 1 month, but
developed psychotic symptoms after
discontinuation of antipsychotic
therapy with several relapses due to
non-compliance.
Thapa etal.,
201622
Neurocysticercosis
presented with acute
psychosis: a case report
Antipsychotics and sedatives to control symptoms.
Albendazole 400 mg twice daily for 4 weeks.
Steroids.
Sodium valproate (was started due to onset of
GTCS-1 episode).
4 weeks. One episode of GTCS during
treatment for which valproate was
initiated. Symptoms improved and the
patient recovered completely after a
few days.
Verma etal.,
201131
Neurocysticercosis
association with cognitive
and aberrant behavioral
symptoms: a case report
and review
Medications records not available. Unknown Treatment did not help in patient
improvement, and only led to
increased sleep.
Mishra and
Swain, 200440
Psychiatric
morbidity following
neurocysticercosis
First treatment:
Haloperidol PO.
Carbamazepine.
Second treatment (after 12 weeks):
Haloperidol, Carbamazepine, Diazepam,
Praziquantel, Steroid.
First treatment duration:
6 weeks.
Second treatment duration:
Unknown.
Complete recovery.
Bhatia etal.,
199413
Neurocysticercosis
presenting as
schizophrenia: a case
report
Haloperidol 20 mg/dL. Phenytoin 300 mg/day in
divided doses.
Albendazole 15 mg/kg/day in divided doses.
Haloperidol 30 mg/day.
First treatment duration:
3 weeks.
Second treatment duration:
4 weeks—haloperidol was
tapered and completely
stopped after 3 months.
No improvement in behavior with
first treatment.
With the second treatment, CT
scan at 3 months showed a decrease
in number of pinhead lesions, but
persistent calcified lesions. Complete
recovery in 4 months.
ElemamaliI
etal., 201721
Neurocysticercosis
presenting with psychosis
Anthelmintic, antipsychotic and steroids. Unknown. Symptoms improved.
Reis etal.,
201417
Racemose
neurocysticercosis with
psychiatric symptoms: a
case report
Albendazole. 28 days. Complete resolution of psychiatric
symptoms, regression of lesions on
CT scan at day 23.
Table 1. (Continued)
(Continued)
Ahmed et al. 5
Author Case report Psychosis treatment Treatment duration Outcome
Bourgeois etal.,
200224
Mood and psychotic
symptoms with
neurocysticercosis
Drainage of the right temporal lobe cyst and
trapped ventricle was performed.
Rifampin, vancomycin and albendazole prescribed.
Risperidone 0.5 mg BID.
12 days. Feeling less depressed at 12 days
after admission. Neuro-vegetative
symptoms improved.
No delusions nor hallucinations. Her
MMSE score improved from 26 to 30.
Gournellis
etal., 201916
A case of
neurocysticercosis:
neuropsychiatric
manifestations, course and
treatment
Initially treated with haloperidol 2 mg TID and
valproic acid 600 mg TID.
Haloperidol was stopped and olanzapine 5 mg/OD
was started.
Long-acting injectable olanzapine 210 mg twice a
month in monotherapy before discharge.
18 days. Five-year follow-up period, the
patient presented cyclical periods
of manic-like and depressive-like
episodes lasting about 1 month each,
with periods of 1⁄2 to 1 month of
normothymia in-between.
Reyazuddin M
etal., 201418
Acute psychosis: an
unusual presentation
in disseminated
neurocysticercosis
Albendazole 400 mg BID.
Prednisone 60 mg OD.
Antiepileptic medication.
Haloperidol 5 mg IM.
7 days. Patient improved and medications
were discontinued.
Mustafa etal.,
202047
Neuropsychiatric
manifestations of
neurocysticercosis
Albendazole 400 mg BID.
Dexamethasone 2 mg IV TID.
Intubated and shifted to the intensive care unit
(ICU) for mechanical ventilation support.
Unknown. Patient expired.
Garieballa and
Hakam, 200812
Neurocysticercosis
presenting with psychiatric
manifestations
Albendazole 500 mg orally BID for 10 days.
Dexamethasone 2 mg BID for 7 days.
Ranitidine 300 mg OD for 5 days.
Phenytoin 300 mg orally QHS for 7 days.
Lorazepam 2 mg BID for 2 days, then 1 mg BID for
3 days.
3 days. Symptoms resolved; prescribed
hydroxyzine 10 mg BID for 4 weeks
(to treat fear and anxiety).
Bhushan etal.,
202015
Neurocysticercosis
presenting with acute
and transient psychotic
disorder: a case report
Risperidone 2 mg QHS.
Lorazepam 1 mg BID.
Valproate 500 mg BID.
Unknown. Symptoms improved.
OD: once a day; BID: two times a day; TID: three times a day; QID: four times a day; IV: intravenous; IM: intramuscular; MMSE: Mini-Mental State Examination; GTCS: generalized tonic–clonic seizure;
QHS: every night at bedtime; CT: computed tomography.
Table 1. (Continued)
6 SAGE Open Medical Case Reports
with the frontal lobe to store and retrieve verbal information.
Both the parietal and frontal lobes have solid anatomical
connections and are activated simultaneously in performing
cognitive tasks.14 In addition to changes in the cortical areas
responsible for the normal physiological function of hearing
and vision, the limbic system is also involved in developing
psychotic phenomena such as auditory and visual hallucina-
tions. However, limbic structures play a central role in the
psychopathology of psychosis, involving frontal and parietal
structures.26
The case reports support the high frequency of neuro-
psychiatric symptoms in patients with NCC. Ms Ana had
headaches with psychotic symptoms, as recorded in nine
other case reports.6,12,18,23,24,26,30,31 Many intracranial infec-
tions cause headaches.32 Most headaches subside once the
infection is resolved, but chronic post-infectious headaches
can last for months.33 Infectious headaches require antimi-
crobial therapy due to viable microorganisms.33 People with
calcified parenchymal brain cysticercosis are more likely to
suffer from primary headache disorders than head trauma
and cerebrovascular disease.34
The current case suffered from depression, which was
also reported in three other case reports.6,23,26 Depression
generally accounts for 56.2% of NCC cases.35 It has been
associated with various neurobiological mechanisms, such
as changes in neural biology, abnormal neuronal adaptive
capability, decreased neurotransmitter levels and endocrine
variations.36 Neuroinflammation is also thought to cause
depression.37 Although there is no established causal rela-
tionship between neuroinflammation and depression, studies
show that neuroinflammation caused by various diseases
alters an individual’s risk profile for developing depression
either immediately or later in life.38
One study examined the prevalence of depression in
NCC patients.39 The researchers reported depression rates
of 83% in the NCC group with epilepsy, 88% in the NCC
without epilepsy group, 92% in epilepsy without NCC
group and 100% in the epilepsy without headache group.
The study found a link between moderate-intensity depres-
sion and chronic illnesses. Another study that measured the
activity of NCC disease through total protein levels in the
cerebrospinal fluid (CSF-TP) found an inverse relation-
ship between NCC and the presence of depression, with
patients with higher CSF-TP readings having minimal or
no depression.19
Seizures are NCC’s most common neurological manifes-
tation in intraparenchymal, enhancing and discrete lesions.3
Nine cases had GTCSs, one had focal seizures, and one case
report presented with partial seizures.2,3,5,8,15,26,27,29,30,40 Focal
seizures occur when cysticercosis invades the temporal-lim-
bic area of the cerebral cortex, whereas GTCS occurs when
the cerebral cortex develops multiple parenchymal cysts and
calcifications.2,5 GTCS is caused by changes in CSF pressure
and inflammation in the brain’s frontal lobe.29,26,40 Similarly,
genetic predispositions to seizures have been observed in
patients with NCC.21 Matrix metallopeptidase-9 (MPP-9)
is an enzyme involves NCC calcified cysts, triggering
seizures.21 Furthermore, Toll-like receptors (TLRs) are
thought to be responsible for the brain’s immune response to
NCC, resulting in seizures.21
Diagnostic imaging
Imaging modalities like CT (with contrast) and MRI are the
mainstays for the diagnosis of NCC. When imaging was per-
formed to look for anatomical causes, CT imaging revealed
multiple hypodense lesions or cysts with calcifications in
both the right frontal and parietal lobe, consistent with cys-
ticercus cellulose. This was also reported by other case
reports.12,20,24,40 MRI showed blurred cortical margins in
the parietal region. Fourteen case reports showed scattered
lesions all over the cerebrum.6,13,17,18,22,23,26,28–31,41,42 Features
consistent with cysticercus racemosus were reported by only
one case report.42 Imaging techniques like CT and MRI have
considerably improved the accuracy of diagnosing NCC by
providing information about the number and location of
the lesions.43 The appearance of these lesions on imaging
depends on whether the cysticerci are living, degenerating
or dead. Living cysticerci appear as well-marginated cysts
with no surrounding inflammation; degenerating cysticerci
are irregularly shaped with surrounding inflammation while
dead or calcified cysticerci look like hyperdense lesions
but are smaller without any surrounding edema or contrast
enhancement.44 False negatives are commonly seen in CT
and MRI in the remission phase of NCC.45
Antibody testing
Other tests that can be used to diagnose NCC are enzyme-
linked electroimmunotransfer blot (EITB) as mentioned in
Table 2. Psychiatric manifestations based on site of lesion.
Location of lesion in NCC Presentation Reference
Ventricular cysticercosis;
subarachnoid cysticercosis
Meningitis, intracranial hypertension, cognitive dysfunction
(attention deficit, aging, status and sense of control, delirium)
Verma and Kumar, 201330
Parenchymal lesions (cysts and
calcifications)
Neuropsychiatric manifestations of epilepsy, intracranial
hypertension and space-occupying lesions
Mahajan etal., 20046
Disseminated parenchymal lesion Dementia Mahajan etal., 20046
NCC: neurocysticercosis.
Ahmed et al. 7
previous case reports and enzyme-linked immunosorbent
assay (ELISA) test.22,23,29–31 The EITB has a sensitivity
ranging from 90% to 100% and a specificity of 100% in indi-
viduals with multiple cysticerci, while the sensitivity drops
to 65% in patients with a single cyst.25 The ELISA test meas-
ures immunoglobulin G (IgG) antibodies against either the
somatic antigen or the excretory–secretory (ES) antigens.46
The sensitivity of the ELISA test for somatic antigen is 76%
in serum and 75% in CSF samples, while specificity is 97%
in serum and 96% in CSF.46 The sensitivity of the ELISA test
for ES antigen is 88% in serum and 64% in CSF, while speci-
ficity is 96% in serum and 97% in CSF.46
Treatment in case studies
The treatment modalities used to treat NCC psychosis in
our patient were albendazole, an antiparasitic and halop-
eridol, an antipsychotic. Similarly, albendazole was pre-
scribed in 11 out of the other 20 cases.12,13,18,20,22,23,24,29,41,47
Other medications used to treat NCC were dexamethasone
in 11 cases to reduce brain edema caused by perilesional
inflammation.12,18,20,22,23,29,41,47 Praziquantel was used in
three cases.26,28,40 Ventriculoperitoneal shunting was per-
formed to improve symptoms of hydrocephalus in three
cases.24,26,42
Although our patient was discharged with a complete
recovery similar to most other case reports, only one patient
succumbed to his illness in the intensive care unit (ICU) after
1 month of extensive treatment due to profuse cerebral
edema/diffuse global hypoxic ischemia.47 These treatments
mentioned above are effective against NCC. However, con-
tinuation may be difficult if the symptoms do not resolve
sooner or due to side effects associated with antipsychotic
medicines. Non-compliance is an essential factor to consider
for the recurrence of NCC in these patients. Non-compliance
can be attributed to the lower socio-economic status of
some of these patients rendering them incapable of acquir-
ing the recommended treatments. Several cases of NCC
psychosis have shown that long-term therapy, particularly
with antipsychotics (haloperidol, olanzapine, risperidone,
aripiprazole), continued for approximately 6 weeks to
22 months.2,3,22,26,28 When the treatment was interrupted for
any reason, the symptoms of psychosis resurfaced, resulting
in rehospitalizations for those individuals.2,3,22,26,28
Lesion localization and psychosis
Koropouli E et al.48 found a distinct region in the right rostral
tectum, near the lesion, whose activity is inversely connected
to the activity of the left amygdala, whereas the left amyg-
dala is functionally coupled with select areas of the temporal,
parietal and occipital lobes. Psychiatric disorders can occa-
sionally be linked to structural changes in the brain. Corpus
callosum lesions, in particular, appear to have a role in the
change in patients’ behavior. Pavesi G et al.49 described a case
of a rapid psychotic crisis caused by a hemorrhagic cavernous
angioma of the corpus callosum, which was surgically
excised and the symptoms were completely resolved.
Although a developmental abnormality such as agenesis or
lipoma is present in the majority of these instances, a devel-
oping corpus callosum lesion is only rarely the underlying
cause. Clinicians should be aware of this link since it is pos-
sible to cure these people.
Barahona-Corrêa JB et al.50 collected 211 lesional mania
cases among 201 individuals with focal lesions, 60.7% had
lesions affecting just the right hemisphere, while 11.4% had
lesions involving only the left hemisphere. The right-sided
predominance of lesions was confirmed across multiple
brain regions, including the temporal lobe, fusiform gyrus
and thalamus, in additional analyses of 56 eligible lesion
images.
Recommendations
The literature indicates various antiepileptic drug (AED)
treatment durations. Two years of therapy with AED was
found to be similar to 1-year treatment in terms of rate of
seizure recurrence.51 Lesions caused by NCC take a long
time to calcify,52 AEDs are gradually tapered down through
incremental doses and eventually broken.53 Abrupt discon-
tinuation of AEDs is not recommended in patients with
multiple cysts as many would develop calcified lesions,
which increases the risk of repeated episodes of seizures.52
Although steroids have been used as an anti-inflammatory
to combat perilesional edema and inflammation, rebound
edema can commonly occur if steroids are not tapered
appropriately.54 Vesicular cysts are immune-tolerant and do
not degrade on their own with time, and increases the fre-
quency of seizures.55 Therefore, it is recommended to treat
with antiparasitic drugs as evidence suggests better outcomes
when compared to no treatment or placebos.56 The treatment
regimen for NCC is albendazole (15 mg/kg per day for
2 weeks) and praziquantel (50 mg/kg per day for 2 weeks),
which are the two most commonly used antiparasitic drugs,
with the former being more effective than the latter. Since
both these antiparasitic drugs have different mechanisms of
action, combining the two can increase the efficacy of treat-
ment. It has also been observed that treatment with albenda-
zole and praziquantel simultaneously increases the plasma
concentration of albendazole by 50%.56
It is also recommended that antiparasitic treatment is
not needed in patients with calcified lesions and NCC
encephalitis.43 Encephalitis is an inflammatory process, and
beginning antiparasitic treatment can exacerbate the inflam-
mation. Steroids and osmotic diuretics can be used to prevent
ICH.8 A craniotomy can decompress if medical treatment
fails.57
Conclusion
Diagnosis of NCC psychosis can be challenging despite
advances in neuroimaging and immunological diagnostic
8 SAGE Open Medical Case Reports
tests. Clinical manifestations can be non-specific, and neuro-
imaging findings are mostly not pathognomonic. Immune
diagnostic tests lack sensitivity and specificity. A thorough
history and a full workup to rule out any organic cause of
psychosis are vital to prevent the consequences of undiag-
nosed and untreated NCC. Early detection and timely treat-
ment are critical because untreated NCC mortality can reach
up to >50%. NCC must be placed in the top differential
diagnosis in patients in endemic areas with psychiatric symp-
toms and a history of seizures who poorly respond to stand-
ard treatment.
Acknowledgement
The authors would like to thank Drs. Rizwan Ahmed and Zeenat
Habibullah for their assistance with the literature search and manu-
script preparation.
Author contributions
Dr S.A., Dr S.U., Dr S.J., Dr A.H., Dr Su.S., Dr A.H., S.M.S. and
S.S. have been involved in the conception and design of the study,
along with acquisition of data. All authors have participated in the
drafting of the article and revising it critically for important intel-
lectual content. All authors have provided final approval of the ver-
sion to be submitted.
Declaration of conflicting interests
The author(s) declared no potential conflicts of interest with respect
to the research, authorship and/or publication of this article.
Ethical approval
Our institution does not require ethical approval for reporting indi-
vidual cases or case series.
Funding
The author(s) received no financial support for the research, author-
ship and/or publication of this article.
Informed consent
Written informed consent was obtained from the patient(s) for their
anonymized information to be published.
ORCID iD
Sadia Usmani https://orcid.org/0000-0002-0577-8562
References
1. World Health Organization. Taeniasis/cysticercosis, 2021,
https://www.who.int/news-room/fact-sheets/detail/taeniasis-
cysticercosis (accessed 4 March 2022)
2. Srivastava S, Chadda RK, Bala K, et al. A study of neuropsy-
chiatric manifestations in patients of neurocysticercosis.
Indian J Psychiatry 2013; 55(3): 264–267.
3. Coyle CM and Tanowitz HB. Diagnosis and treatment of neu-
rocysticercosis. Interdiscip Perspect Infect Dis 2009; 2009:
180742.
4. CDC-Parasites Features Neurocysticercosis—CME, https://
www.cdc.gov/parasites/features/ncc_cme_feature.html
(accessed 4 March 2022)
5. Nikolić S and Stevanović G. [Neurocysticercosis—pathogen-
esis and clinical aspects]. Srp Arh Celok Lek 2006; 134(5–6):
246–250, http://europepmc.org/abstract/MED/16972416
6. Mahajan SK, Machhan PC, Sood BR, et al. Neurocysticercosis
presenting with psychosis. J Assoc Physicians India 2004; 52:
663–665.
7. NIMH Website. NIMH » What is Psychosis? National
Institute of Mental Health, 2018, https://www.nimh.nih.gov/
health/topics/schizophrenia/raise/what-is-psychosis (accessed
4 March 2022).
8. Fogang YF, Savadogo AA, Camara M, et al. Managing neu-
rocysticercosis: challenges and solutions. Int J Gen Med 2015;
8: 333–344.
9. Mini-Mental State Examination Physiopedia, https://www.
physio-pedia.com/Mini-Mental_State_Examination (accessed
18 April 2022).
10. Mahendran R, Chua J, Feng L, et al. The mini-mental state
examination and other neuropsychological assessment tools
for detecting cognitive decline. In: Martin C and Preedy V
(eds) Diet and Nutrition in Dementia and Cognitive Decline.
New York: Elsevier, 2015, pp. 1159–1174.
11. Oyebode F. The neurology of psychosis. Med Princ Pract
2008; 17(4): 263–269.
12. Garieballa SS and Hakam AM. Neurocysticercosis present-
ing with psychiatric manifestations. Qatar Med J 2008; 17(2):
61–62.
13. Bhatia B, Mishra S and Srivastava AS. Neurocysticercosis
presenting as schizophrenia: a case report. Indian J Psychiatry
1994; 36(4): 187–189.
14. Yildiz M, Borgwardt SJ and Berger GE. Parietal lobes in
schizophrenia: do they matter? Schizophr Res Treatment
2011; 2011: 581686.
15. Bhushan A, Nain V, Singh P, et al. presenting with acute and
transient psychotic disorder : a case report. Int J Curr Res
2020; 12(4): 10913–10914.
16. Gournellis R, Tournikioti K, Papathanasiou MA, et al. A
case of neurocysticercosis: neuropsychiatric manifestations,
course, and treatment. Indian J Psychiatry 2019; 61(5):
537–538.
17. ElemamaliI A, Talyb S and Awad A. Neurocysticercosis
presenting with psychosis. New Horizons Clin Case Reports
2017; 1: 23.
18. Reyazuddin M, Hussain K, Ibrahim A, et al. Acute psychosis:
an unusual presentation in disseminated neurocysticercosis.
Southeast Asian J Case Rep Rev 2014; 3(6): 1191–1196.
19. de Almeida SM and Gurjão SA. Is the presence of depres-
sion independent from signs of disease activity in patients
with neurocysticercosis? J Community Health 2011; 36(5):
693–697.
20. Sarangi R, Sahoo S and Mohapatra S. Neurocysticercosis mas-
querading psychotic disorder: a case report. J Acute Dis 2013;
2(1): 79–81.
21. Gripper LB and Welburn SC. The causal relationship
between neurocysticercosis infection and the development
of epilepsy—a systematic review. Infect Dis Poverty 2017;
6(1): 31.
Ahmed et al. 9
22. Thapa DK, Limbu CP, Gurung A, et al. Neurocysticercosis
presented with acute psychosis: a case report. Nepal J Neurosci
2016; 13(1): 54–56.
23. Anjana KK, Suresh V, Poornima C, et al. An unusual presen-
tation of neurocysticercosis as psychosis with tics. Arch Ment
Heal 2020; 21(1): 55–58.
24. Bourgeois JA, Motosue J and Mehra N. Mood and psychotic
symptoms with neurocysticercosis. Psychosomatics 2002;
43(4): 337–338.
25. Wilson M, Bryan RT, Fried JA, et al. Clinical evaluation of
the cysticercosis enzyme-linked immunoelectrotransfer blot
in patients with neurocysticercosis. J Infect Dis 1991; 164(5):
1007–1009.
26. Bills DC and Symon L. Cysticercosis producing various neu-
rological presentations in a patient: case report. Br J Neurosurg
1992; 6(4): 365–369.
27. Del Brutto OH. Neurocysticercosis. Handb Clin Neurol 2014;
121: 1445–1459.
28. Shriqui CL and Milette PC. You drive me crazy: a case report
of acute psychosis and neurocysticercosis. Can J Psychiatry
1992; 37(2): 121–124.
29. da Silva Miranda CC, Fernandes Dos Santos CFS and
Cordeiro de Medeiros AB. Neurocysticercosis presenting
as acute psychosis: an unusual case. Psychiatr Danub 2020;
32(3–4): 445–446.
30. Verma A and Kumar A. Neurocysticercosis presenting as
acute psychosis: a rare case report from rural India. Asian J
Psychiatr 2013; 6(6): 611–613.
31. Verma R, Anand KS, Chandra M, et al. Neurocysticercosis
association with cognitive and aberrant behavioural symp-
toms: a case report and review. J Behav Brain Sci 2011; 1(4):
229–233.
32. Locker T, Mason S and Rigby A. Headache management--are
we. doing enough? An observational study of patients present-
ing with headache to the emergency department. Emerg Med J
2004; 21(3): 327–332
33. Gotkine M, Kennedy PG and Steiner I. Post infectious CNS
disorders: towards a unified approach. J Neurol 2010; 257(12):
1963–1969.
34. Del Brutto OH and Del Brutto VJ. Calcified neurocysticerco-
sis among patients with primary headache. Cephalalgia 2012;
32(3): 250–254.
35. Forlenza OV, Filho AH, Nobrega JP, et al. Psychiatric mani-
festations of neurocysticercosis: a study of 38 patients from
a neurology clinic in Brazil. J Neurol Neurosurg Psychiatry
1997; 62(6): 612–616.
36. Oglodek E, Szota A, Just M, et al. The role of the neuroendo-
crine and immune systems in the pathogenesis of depression.
Pharmacol Rep 2014; 66(5): 776–781.
37. Bakunina N, Pariante CM and Zunszain PA. Immune mecha-
nisms linked to depression via oxidative stress and neuropro-
gression. Immunology 2015; 144(3): 365–373.
38. Benatti C, Blom JM, Rigillo G, et al. Disease-induced neu-
roinflammation and depression. CNS Neurol Disord Drug
Targets 2016; 15(4): 414–433.
39. Almeida SM and de Gurjão SA. Frequency of depression among
patients with neurocysticercosis TT—Depressão em pacientes
portadores de neurocisticercose. Arq Neuropsiquiatr 2010;
68(1): 76–80, http://www.scielo.br/scielo.php?script=sci_
arttext&pid=S0004-282X2010000100017
40. Mishra BN and Swain SP. Psychiatric morbidity following
neurocysticercosis. Indian J Psychiatry 2004; 46(3): 267–278.
41. Singh S, Dhikav V, Agarwal N, et al. An unusual cause of
psychosis. Lancet 2004; 363: P1522.
42. Fabiano Reis Lisiane Seguti L and de SQ. Racemose neu-
rocysticercosis with psychiatric symptoms: a case report. J
Neuroinfectious Dis 2015; 6(1): 163.
43. Garcia HH, Nash TE and Del Brutto OH. Clinical symptoms,
diagnosis, and treatment of neurocysticercosis. Lancet Neurol
2014; 13(12): 1202–1215.
44. Singh G, Rajshekhar V, Murthy JMK, et al. A diagnostic
and therapeutic scheme for a solitary cysticercus granuloma.
Neurology 2010; 75: 2236–2245.
45. Agapejev. Central nervous system agents in medicinal
chemistry, https://benthamscience.com/journals/central-
nervous-system-agents-in-medicinal-chemistry/ (accessed 4
March 2022)
46. Sahu PS, Parija SC, Narayan SK, et al. Evaluation of an IgG-
ELISA strategy using Taenia solium metacestode somatic and
excretory-secretory antigens for diagnosis of neurocysticerco-
sis revealing biological stage of the larvae. Acta Trop 2009;
110(1): 38–45.
47. Mustafa N, Al Ayyat D, Awad M, et al. Neuropsychiatric
Manifestations of Neurocysticercosis. Dubai Med J 2020; 3(1):
37–40, https://www.karger.com/DOI/10.1159/000506365
48. Koropouli E, Melanitis N, Dimitriou VI, et al. New-onset psy-
chosis associated with a lesion localized in the rostral tectum:
insights into pathway-specific connectivity disrupted in psy-
chosis. Schizophr Bull 2020; 46(5): 1296–1305.
49. Pavesi G, Causin F and Feletti A. Cavernous angioma of
the corpus callosum presenting with acute psychosis. Behav
Neurol 2014; 2014: 243286.
50. Barahona-Corrêa JB, Cotovio G, Costa RM, et al. Right-sided
brain lesions predominate among patients with lesional mania:
evidence from a systematic review and pooled lesion analysis.
Transl Psychiatry 2020; 10(1): 139.
51. Singhi PD, Dinakaran J, Khandelwal N, et al. One vs. two
years of anti-epileptic therapy in children with single small
enhancing CT lesions. J Trop Pediatr 2003; 49(5): 274–278.
52. Del Brutto OH. Prognostic factors for seizure recurrence after
withdrawal of antiepileptic drugs in patients with neurocyst-
icercosis. Neurology 1994; 44(9): 1706–1709.
53. Callaghan N, Garrett A and Goggin T. Withdrawal of anti-
convulsant drugs in patients free of seizures for two years: a
prospective study. N Engl J Med 1988; 318(15): 942–946.
54. Mejia R and Nash TE. Corticosteroid withdrawal precipitates
perilesional edema around calcified Taenia solium cysts. Am J
Trop Med Hyg 2013; 89(5): 919–923.
55. Zee CS, Go JL, Kim PE, et al. Imaging of neurocysticercosis.
Neuroimaging Clin N Am 2000; 10(2): 391–407.
56. Garcia HH and Del Brutto OH; Cysticercosis Working Group
in Peru. Neurocysticercosis: updated concepts about an old
disease. Lancet Neurol 2005; 4(10): 653–661.
57. Del Brutto OH and Sotelo J. Neurocysticercosis: an update.
Rev Infect Dis 1988; 10(6): 1075–1087.
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