Acute Cerebral
Paragonimiasis
Presenting as
Hemorrhagic Stroke
in a Child
Zhi Chen, MD, Gang Zhu, MD, PhD,
Jiangkai Lin, MD, PhD,
Nan Wu, MD, and Hua Feng, MD, PhD

A hemorrhagic stroke in children is rarely secondary
to cerebral paragonimiasis. We describe a 9-year-old
boy in whom an intracerebral hemorrhage was the
leading clinical indication of acute cerebral paragonimiasis. He was hospitalized because of a sudden onset
of headache, right hemiparesis, and dysarthria. A
computed tomography scan revealed an intracerebral
hemorrhage in the left parietal lobe. Magnetic resonance angiography did not confirm any vascular abnormalities at the location of the hematoma. Four
weeks later, he presented with right hemiparesis again,
and fever. A diagnosis of cerebral paragonimiasis was
based on repeated magnetic resonance imaging of
the brain and an enzyme-linked immunosorbent
assay for paragonimiasis. The patient gradually recovered with praziquantel treatment. Cerebral paragonimiasis should be considered in the differential
diagnosis of hemorrhagic strokes in children in areas
where paragonimiasis is epidemic. © 2008 by
Elsevier Inc. All rights reserved.

Chen Z, Zhu G, Lin J, Wu N, Feng H. Acute cerebral
paragonimiasis presenting as hemorrhagic stroke in a
child. Pediatr Neurol 2008;39:133-136.

From the Department of Neurosurgery, Southwest Hospital, Third
Military Medical University, Chongqing, China.

© 2008 by Elsevier Inc. All rights reserved.
doi:10.1016/j.pediatrneurol.2008.04.004 ● 0887-8994/08/$—see front matter

Introduction
Paragonimiasis is a parasitic disease caused by the
genus Paragonimus. As a typical foodborne parasitic
zoonosis, this disease is prevalent in Asia, West Africa,
and Latin America [1,2]. In addition, paragonimiasis was
also described among immigrants in the United States
[1,3] and Australia [4]. Human infection is mainly spread
by eating raw or inadequately cooked crabs or crayfish,
which are the second intermediate hosts for the organism
during its transition from cercaria to metacercaria. The
lung is the principal habitat in the human host. The
encysted metacercariae penetrate the gut wall and migrate
to the lung, where they mature into adult worms and
produce eggs. The eggs are discharged from bronchial
secretions, and are coughed up or passed in feces. These
then hatch and pass through a suitable snail host (first
intermediate host) before encysting in the tissues of a
freshwater crustacean (crabs or crayfish) to repeat the life
cycle [1,3,5].
Cerebral paragonimiasis is probably caused by the migration of worms from the lungs through the soft tissues of the
neck to the jugular foramen and to the brain [5]. The reported
frequency of cerebral involvement varies between 0.845% [5,6]. Cerebral paragonimiasis with hemorrhagic
stroke is rarely reported [2,7,8], but its incidence may be
underestimated. We describe an unusual pediatric case
presenting clinically and radiologically with acute intracerebral hemorrhage. He was diagnosed with cerebral paragonimiasis 1 month after onset of the hemorrhage.
Case Report
This 9-year-old, previously healthy boy presented with sudden onset of
headache associated with nausea and vomiting after getting up in the
morning. He soon developed right hemiparesis and dysarthria. He was
sent to a nearby hospital. A computed tomography scan (Fig 1) was
performed the next day, and revealed an acute intracerebral hematoma in
the left parietal lobe. The patient was transferred to our hospital on day
3 of his previous admission. A neurologic examination revealed dysarthria and right hemiparesis (grade II in his upper limb, and grade IV in
his lower limb), with moderate ipsilateral hyperreflexia. No meningeal
signs were found. Chest x-ray films produced normal results. Routine
laboratory findings such as a complete blood count, erythrocyte sedimentation rate, urinalysis, and stool examination produced normal
results, except for low blood sodium (130 mmol/L). Magnetic resonance
findings of the brain were consistent with the computed tomography
scan, and were suggestive of an acute intracerebral hemorrhage. There

Communications should be addressed to:
Dr. Feng; Department of Neurosurgery, Southwest Hospital; Third
Military Medical University; Gaotanyan Street; Shapingba District;
Chongqing 400038, People’s Republic of China.
E-mail: a65427851@cta.cq.cn
Received January 24, 2008; accepted April 7, 2008.

Chen et al: Cerebral Paragonimiasis With Stroke 133

Discussion

Figure 1. Axial computed tomography scan reveals an acute cerebral
hemorrhage in the parietal lobe.

was no other enhancement on the postcontrast magnetic resonance
images (Fig 2), and no obvious vascular abnormity on magnetic resonance angiography. Conventional angiography was suggested, but was
not accepted by his family. The patient was treated without surgery, and
his dysarthria and right hemiparesis improved.
One month later, the patient developed a cough, chill, and fever, as
well as a recurrence of right hemiparesis. A neurologic examination
revealed mild hemiparesis in his right upper limb (grade III). Follow-up
magnetic resonance imaging of the brain revealed multiple newly
developed lesions located medially to the partly absorbed hematoma.
These lesions proved to be hyperintense on a T2-weighted image, with a
slightly hyperintense wall on a T1-weighted image. Postcontrast magnetic resonance images (Fig 3) revealed clustered ring-enhancing lesions
and an enhancement of meninges beside the lesions and the previous
hematoma, resembling the characteristic appearance of cerebral paragonimiasis. His total white blood cell count consisted of 13.5 ⫻ 109 cells/L,
and an absolute count of his eosinophils consisted of 0.5 ⫻ 109 cells/L,
which increased 3 days later to 3 ⫻ 109 cells/L. A computed tomography
scan of the chest revealed patchy opacity in the right lower lung zone,
combined with pleural effusion. His dietary history was retaken, and
it disclosed that he and his classmates had eaten raw crabs that they
had caught in the rural creeks, without adult supervision. Enzymelinked immunosorbent assays for multiple parasites were performed
on his serum, which was positive for P. skrjabini specific immunoglobulin G antibody and negative for others. When the diagnosis of
cerebral paragonimiasis was established, therapy with praziquantel
was initiated. The patient was treated with praziquantel at a dose of 75
mg/kg/day for 3 days, and with another course of praziquantel at the
same dosage 1 week after the first course. His hemiparesis improved
rapidly, without any other signs. His eosinophil count decreased to
1.38 ⫻ 109 cells/L 4 days after treatment, and reached a normal level
2 weeks later. A follow-up computed tomography scan of his chest
indicated that the lesions had mostly diminished. The patient was
discharged and remained neurologically normal during a follow-up
period of 3 months, during which time he refused serial brain
magnetic resonance imaging.

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Among Paragonimus species, Paragonimus westermani,
followed by P. skrjabini complex, are the major pathogens
for human paragonimosis in Asia [1]. Our patient came from
Sichuan Province, where the main identified worms were
P. skrjabini, according to the literature [9,10]. Therefore, we
presumed that his infection was probably attributable to
P. skrjabini, though no definite eggs or adult parasites were
demonstrated.
Cerebral signs rarely occur without evidence of chest
disease. In the majority of cases (70%), pulmonary signs
occur first [11]. Various nonspecific neurologic manifestations may develop in patients with cerebral paragonimiasis, including epilepsy, headache, nausea, vomiting,
hemiplegia, and aphasia [5,11]. The radiologic findings of
cerebral paragonimiasis are variable, depending on the evolutional stage of the cerebral infection. In the acute stage, the
most common and characteristic computed tomography or
magnetic resonance imaging findings are conglomerate, multiple, ring-shaped enhancements with surrounding edema of
variable degree, resembling “grape clusters.” Nonspecific
features of computed tomography and magnetic resonance
imaging include nonenhancing, edema-like lesions, parenchymal hemorrhage, and irregularly enhancing solid lesions [2,11-13]. Pure or massive hemorrhagic lesions are
rarely reported [2,7,11-13]. The enzyme-linked immunosorbent assay has proven to be efficiently sensitive and
specific for detecting pulmonary and extrapulmonary paragonimiasis [3,11].
Cerebral paragonimiasis presenting as an intracranial
hemorrhage is rarely reported, especially without pulmo-

Figure 2. Initial magnetic resonance findings. Postcontrast axial T1weighted image (TR/TE ⫽ 500/7 ms) indicates the acute hematoma,
without other abnormalities.

Figure 3. Follow-up magnetic resonance imaging 1 month later. A
postcontrast coronal and axial T1weighted image (TR/TE ⫽ 500/7 ms)
reveals multiple, coalesced, ring-enhancing lesions with an obvious enhancement of meninges beside the
lesions and the hematoma.

nary signs. In this circumstance, the diagnosis may be
mistaken or delayed. Hara et al. [7] reported on a 38-yearold man with sudden-onset headache and visual disturbance, who was diagnosed with intracerebral hemorrhage
during his first admission. A diagnosis of cerebral paragonimiasis was not considered until 3 months later, when
respiratory signs developed. In the present case, the
intracerebral hemorrhage was also the initial finding. More
unusual, characteristic radiologic findings of coalesced,
ring-enhancing lesions developed near the follow-up magnetic resonance imaging. To the best of our knowledge, a
childhood case of cerebral paragonimiasis with an intracerebral hemorrhage as the initial finding has not been
reported.
In the reported cases of cerebral paragonimiasis
combined with intracranial hemorrhage, the types of
intracranial hemorrhage included intracerebral hemorrhage, subdural hematoma, and subarachnoid hemorrhage [2,7,8,13,14]. Though the hemorrhage in most
reported cases was attributed to cerebral paragonimiasis,
the causality between cerebral paragonimiasis and intracranial hemorrhage should be considered. Choo et al [8]
reported on a 38-year-old man with chronic cerebral
paragonimiasis combined with a diffuse subarachnoid
hemorrhage, whose subarachnoid hemorrhage was thought
to be secondary to a carotid posterior communicatingartery aneurysm. In childhood, an intracerebral hemorrhage is most often the result of an arteriovenous malformation, hematologic abnormality, or brain tumor; among
these causes, arteriovenous malformations account for
nearly 50% of intraparenchymal hemorrhages [15]. Other
etiologies include cavernous hemangioma, vasculopathy,
vasculitis, and rarely, infections and illicit drug use [15].
Our patient had no history of illicit drug use, and no signs
of vascular abnormalities, brain tumor, or hematologic
abnormalities according to repeated magnetic resonance
imaging, magnetic resonance angiography, and laboratory
examinations. Taken together with the lesions of cerebral
paragonimiasis that developed closely around the hema-

toma, we think that the intracerebral hemorrhage was
attributable to paragonimiasis infection. Surgical treatment
is not always necessary for the management of cerebral
paragonimiasis, whereas praziquantel is the drug of choice
for the treatment of paragonimiasis, and is virtually 100%
effective against all species of Paragonimus [3,11]. Therefore, diagnosis at an early stage is regarded as important in
such cases.
In conclusion, our patient serves as a rare pediatric case
of cerebral paragonimiasis presenting clinically and radiologically as an intracerebral hemorrhage, which made the
early diagnosis difficult. Our case suggests that cerebral
paragonimiasis should be considered in the differential
diagnosis of hemorrhagic stroke in children in areas where
paragonimiasis is epidemic.

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