SAGE Open Medical Case Reports
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SAGE Open Medical Case Reports
Volume 10: 1 –9
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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
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.
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
Sheikh Shoib, Jawahar Lal Nehru Memorial Hospital, Srinagar, Jammu &
1100396SCO0010.1177/2050313X221100396SAGE Open Medical Case ReportsAhmed et al.
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.
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
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
You drive me crazy: a case
report of acute psychosis
First admission to hospital:
Low dose of haloperidol with close supervision,
subsequently increased to 15 mg daily and then
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
Second time psychosis:
No resolution of psychosis and
delusions due to non-compliance.
Bills and Symon,
presentations in a patient:
First presentation with psychosis:
Antibiotics and steroids (presuming it was
Ventriculoperitoneal shunt installed to treat
Revision of ventriculoperitoneal shunt after
Praziquantel (50 mg/kg/day) for 2 weeks.
Resolution of her nausea, vomiting
and headaches. Her gait also
improved considerably, allowing her
to ambulate independently again, and
her incontinence decreased.
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
Psychosis improved within 2 weeks
along with improvement of MMSE
scores after 2 months. Able to
do perform independently after
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
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.
An unusual cause of
Albendazole (15 mg/kg).
28 days. Improved and regained pre-morbid
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.
4 SAGE Open Medical Case Reports
Author Case report Psychosis treatment Treatment duration Outcome
disorder: a case report
Albendazole (15 mg/kg/day) for 7 days.
Prednisolone (2 mg/kg/day) for 7 days.
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
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
presented with acute
psychosis: a case report
Antipsychotics and sedatives to control symptoms.
Albendazole 400 mg twice daily for 4 weeks.
Sodium valproate (was started due to onset of
4 weeks. One episode of GTCS during
treatment for which valproate was
initiated. Symptoms improved and the
patient recovered completely after a
association with cognitive
and aberrant behavioral
symptoms: a case report
Medications records not available. Unknown Treatment did not help in patient
improvement, and only led to
Second treatment (after 12 weeks):
Haloperidol, Carbamazepine, Diazepam,
First treatment duration:
Second treatment duration:
schizophrenia: a case
Haloperidol 20 mg/dL. Phenytoin 300 mg/day in
Albendazole 15 mg/kg/day in divided doses.
Haloperidol 30 mg/day.
First treatment duration:
Second treatment duration:
4 weeks—haloperidol was
tapered and completely
stopped after 3 months.
No improvement in behavior with
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.
presenting with psychosis
Anthelmintic, antipsychotic and steroids. Unknown. Symptoms improved.
psychiatric symptoms: a
Albendazole. 28 days. Complete resolution of psychiatric
symptoms, regression of lesions on
CT scan at day 23.
Table 1. (Continued)
Ahmed et al. 5
Author Case report Psychosis treatment Treatment duration Outcome
Mood and psychotic
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
No delusions nor hallucinations. Her
MMSE score improved from 26 to 30.
A case of
manifestations, course and
Initially treated with haloperidol 2 mg TID and
valproic acid 600 mg TID.
Haloperidol was stopped and olanzapine 5 mg/OD
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
Acute psychosis: an
Albendazole 400 mg BID.
Prednisone 60 mg OD.
Haloperidol 5 mg IM.
7 days. Patient improved and medications
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.
presenting with psychiatric
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. Symptoms resolved; prescribed
hydroxyzine 10 mg BID for 4 weeks
(to treat fear and anxiety).
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
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
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
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
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
Meningitis, intracranial hypertension, cognitive dysfunction
(attention deficit, aging, status and sense of control, delirium)
Verma and Kumar, 201330
Parenchymal lesions (cysts and
Neuropsychiatric manifestations of epilepsy, intracranial
hypertension and space-occupying lesions
Mahajan etal., 20046
Disseminated parenchymal lesion Dementia Mahajan etal., 20046
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
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
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
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-
The authors would like to thank Drs. Rizwan Ahmed and Zeenat
Habibullah for their assistance with the literature search and manu-
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.
Our institution does not require ethical approval for reporting indi-
vidual cases or case series.
The author(s) received no financial support for the research, author-
ship and/or publication of this article.
Written informed consent was obtained from the patient(s) for their
anonymized information to be published.
Sadia Usmani https://orcid.org/0000-0002-0577-8562
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