Abstract

Background: Central nervous system (CNS) sparganosis is an exceptionally rare parasitic infection caused by the larvae of Spirometra species. Its migratory nature and nonspecific clinical presentation often lead to misdiagnosis, posing significant diagnostic and therapeutic challenges. While CNS involvement typically affects either the brain or spinal cord, disseminated cases involving both regions are exceedingly rare.

Case Description: We report the case of a 34-year-old woman who initially presented with progressive low back pain and paraparesis. She was diagnosed with spinal sparganosis following surgical resection and histopathological confirmation. Despite an uneventful postoperative recovery, she developed progressive headaches 3 years later. Magnetic resonance imaging revealed intracranial lesions, and subsequent surgery confirmed sparganosis in the cisterna magna. One year after brain surgery and ventriculoperitoneal shunt placement, the patient experienced progressive headaches accompanied by confusion. Under the initial misdiagnosis of brain abscess, she was inadvertently treated with intravenous metronidazole for 2 months, resulting in symptomatic improvement. However, a review of imaging demonstrated extensive CNS involvement, including the supratentorial, infratentorial, and upper cervical regions. In addition, there was clear evidence of parasite migration through the cribriform plate into the frontal lobe, highlighting the disseminated and migratory nature of CNS sparganosis.

Conclusion: This case highlights the diagnostic complexity and disseminated nature of CNS sparganosis, underscoring the importance of early surgical intervention and histopathological confirmation. The unexpected clinical response to metronidazole raises the possibility of its adjunctive role in symptom modulation, although its antiparasitic efficacy remains unproven. Given the risk of asymptomatic dissemination and recurrence, long-term follow-up with serial imaging is essential. Clinicians should maintain a high index of suspicion for sparganosis in endemic regions to improve diagnostic accuracy and patient outcomes.

Keywords: Cerebral sparganosis, Disseminated parasitic infection, Metronidazole, Parasite migration, Praziquantel therapy, Spinal sparganosis, Steroid-Induced proliferative sparganosis

INTRODUCTION

Sparganosis is a rare parasitic infection caused by the Plerocercoid larvae of Spirometra species. It is typically acquired through the ingestion of undercooked amphibian or reptile meat, drinking contaminated water, or applying infected raw flesh as a poultice in traditional medicine.[ 13 , 18 ] While the infection most commonly involves subcutaneous tissues, it can also affect the central nervous system (CNS), leading to severe neurological complications.[ 4 ]

Migration is a distinctive feature of sparganosis, and reports have documented cases of the parasite traveling across cerebral structures such as the corpus callosum or even between different regions of the CNS.[ 9 , 12 ] Sparganum larvae exhibit strong tissue invasiveness, leading to inflammation, granuloma formation, and cystic changes within the affected regions.[ 7 ] In addition, the nonspecific radiological findings of CNS sparganosis often mimic neoplasms, tuberculomas, or other infectious lesions, making preoperative diagnosis particularly challenging.[ 5 ]

Although cases of spinal or cerebral sparganosis have been reported individually, literature on patients involving both intracranial and spinal involvement remains scarce.[ 14 ] This report describes a rare case of disseminated and migratory CNS sparganosis, with intracranial and spinal spread confirmed through imaging and histopathological findings. In addition, we review previously reported cases to provide a comprehensive overview of their clinical presentation, diagnostic challenges, and management strategies.

CASE DESCRIPTION

A 34-year-old woman was admitted to our institute with a 10-month history of progressive low back pain radiating to both legs. Two weeks before admission, she developed worsening paresthesia and muscle weakness in her lower extremities. There were no associated bowel or bladder dysfunctions. Notably, she had a history of ingesting undercooked frog meat. Neurological examination revealed paraparesis graded 4/5, normal pinprick sensation, intact proprioception, and hyporeflexia in the lower limbs.

Magnetic resonance imaging (MRI) of the lumbosacral spine revealed multiloculated cystic lesions containing cerebrospinal fluid (CSF)-like content extending from L3 to S1, with peripheral rim enhancement following contrast administration [ Figures 1a - f ]. Based on these findings, spinal cystic schwannoma was initially suspected. The patient underwent a laminectomy from L3 to L5. Intraoperatively, the dura was opened, revealing a thickened arachnoid membrane, diffuse loculated cystic structures, and severe nerve root adhesions. The lesions were nearly completely removed, and lysis of adhesions was performed under nerve root monitoring. Histopathological examination of the surgical specimen from the lumbar region revealed parasitic tissue with three distinct layers: an outer cuticular layer, a middle granular layer, and an inner fibrillary layer [ Figure 1g ]. The most likely diagnosis was sparganosis. The postoperative course was uneventful. One week after surgery, the patient was prescribed a high-dose regimen of praziquantel (75 mg/kg/day) in combination with cimetidine for 7 days. Her motor strength gradually improved, leading to a full recovery. However, she continued to experience intermittent low back and leg pain during follow-up. The pain was attributed to arachnoiditis and was managed with oral corticosteroids, which were gradually tapered over 1 year.

Three years later, she developed progressive headaches over 4 months and returned to our emergency department. Cranial MRI revealed thin-walled cystic lesions at the cisterna magna, right ambient cistern, and anterior to the pons, with mild contrast enhancement and associated obstructive hydrocephalus [ Figures 2 and 3a]. The patient underwent a suboccipital craniectomy with cystic lesion removal from the cisterna magna, followed by occipital external ventricular drainage. Histological examination of the cisterna magna tissue confirmed the presence of parasitic structures, demonstrating the characteristic three-layered composition and calcareous bodies. These findings are consistent with sparganosis. Due to persistent hydrocephalus, a ventriculoperitoneal shunt was placed 2 weeks later. The patient’s headaches resolved, and she remained symptom-free throughout the 1-year follow-up period.

One year after brain surgery, the patient developed progressive headaches for 2 weeks, followed by confusion, leading to readmission. MRI of the brain revealed a loculated cystic lesion in the basal right frontal lobe, characterized by hypointensity on T1-weighted and hyperintensity on T2-weighted images, with irregular rim enhancement and associated perilesional white matter edema. Within the cyst, an intermediate T2 component exhibited hyperintensity on trace diffusion-weighted imaging (DWI) and hypointensity on apparent diffusion coefficient mapping, suggesting high-viscosity content. An air-fluid level was present within the lesion, as well as in the bilateral frontal horns and anterior third ventricle. In addition, a focal dural defect was identified at the right cribriform plate, accompanied by a small air bubble and a cystic lesion above the defect [ Figures 3b - e ]. Thick leptomeningeal enhancement with loculated CSF collections was observed around the brainstem, as well as along the anterior aspect of the spinal cord from the C1 to C5 levels [ Figure 3f ].

The provisional diagnosis was a brain abscess with associated diffuse cerebritis. To cover potential pathogens originating from the sinus, intravenous antibiotics, including vancomycin, meropenem, and metronidazole, were administered for 2 months. The patient gradually improved until all symptoms resolved. Follow-up MRI of the brain, performed 2 months after intravenous antibiotic administration, demonstrated a reduction in the size of the right frontal cystic lesion, along with thick leptomeningeal enhancement and loculated CSF collections in the prepontine and left cerebellopontine angle cisterns, with resolution of the previously noted air content. Diffuse thick dural enhancement was observed along the bilateral cerebral convexities, likely indicative of intracranial hypotension secondary to previous shunt placement [ Figures 4a - d ].

Figure 1:

Magnetic resonance imaging (MRI) of the lumbosacral spine. (a) Sagittal T1-weighted, (b) gadolinium-enhanced T1-weighted, (c) T2-weighted, and (d-f) axial gadolinium-enhanced T1-weighted images at the L3, L4, and L5 levels demonstrate clumping, distortion, and enhancement of the cauda equina nerve roots, with multiloculated cerebrospinal fluid-filled lesions. (g) Histological examination of a lumbar surgical specimen, stained with Hematoxylin and Eosin, ×400 magnification, reveals parasitic tissue characterized by three distinct layers: An outer cuticular layer, a middle granular layer, and an inner fibrillary layer.

Upon reevaluation and review of all imaging, the previously observed lesion at the right ethmoid sinus had disappeared [ Figure 3a and b ]. In addition, susceptibility-weighted imaging and T2*-weighted gradient echo images revealed low signal intensity across the corpus callosum extending to the opposite hemisphere, likely representing hemorrhage along the parasite’s migratory tract [ Figures 4e and f ]. Based on these findings, we speculated that sparganosis had migrated from the right ethmoid sinus into the frontal lobe. The patient declined further surgery to remove the remaining sparganosis and remained asymptomatic at the 3-year follow-up.

DISCUSSION

Literature review of sparganosis involving both spinal and intracranial regions

We identified nine cases of CNS sparganosis involving both the spinal cord and brain, including our own [ Table 1 ].[ 1 - 3 , 5 - 7 , 14 , 18 ] The median patient age was 51 years (range: 26–59), with a male predominance (88.9%). Most cases originated from Thailand (4), South Korea (2), China (1), and Myanmar (1), reflecting the disease’s endemic distribution in East and Southeast Asia.

Figure 2:

Magnetic resonance imaging (MRI) of the brain performed 3 years after spinal surgery. (a-c) Axial fluid-attenuated inversion recovery and (d) sagittal gadolinium-enhanced T1-weighted images reveal focal cyst-like extra-axial lesions with cerebrospinal fluid density in the prepontine cistern (arrowheads in b and d) and cisterna magna (arrows in c and d), demonstrating a mild mass effect and faint peripheral enhancement. (e) Histological examination of a surgical specimen from the cisterna magna, stained with Hematoxylin and Eosin, ×400 magnification, shows the characteristic parasite structure with three distinct layers: An outer cuticular layer, a middle granular layer, and an inner fibrillary layer, along with calcareous bodies within the tissue.

Spinal symptoms, particularly progressive low back pain and paraparesis, were common initial presentations, while headache and cranial nerve deficits occurred in patients with brain involvement. Histopathological confirmation was performed in all cases, establishing it as the diagnostic gold standard. In select cases, serologic tests (enzyme-linked immunosorbent assay on serum or CSF) and polymerase chain reaction served as adjunctive tools.

Surgical resection was the mainstay of treatment, especially for symptomatic or migrating lesions. Most patients underwent spinal surgery, with cranial procedures reserved for significant intracranial disease. Antiparasitic medications were occasionally used as adjunctive therapy.

Outcomes were mixed: five patients had good recovery, while four had persistent deficits, often linked to delayed diagnosis or extensive disease. These findings highlight the importance of early recognition and timely intervention to improve prognosis in CNS sparganosis.

Migration route of sparganum between the brain and spinal canal

The migration route of sparganum within the CNS remains poorly understood, particularly in cases involving both the brain and spinal cord. Unlike other neuroparasitic infections, Sparganum demonstrates a uniquely dynamic and unpredictable migratory pattern, complicating diagnosis and management. This prolonged movement often contributes to delayed detection, necessitating long-term radiological follow-up.[ 12 ]

Feng et al.[ 4 ] analyzed 30 patients with cerebral sparganosis and identified four main migration patterns on MRI: interlobar (50%), transmidline (27.3%), transventricular (13.6%), and cerebellum-brainstem (9.1%). Interlobar migration occurred within the same cerebral hemisphere, while transmidline movement crossed central structures such as the corpus callosum or brainstem. Transventricular migration involved spread through the ventricular system, and cerebellum-brainstem migration, though rare, represented a more severe presentation.

In some cases, MRI findings suggest a descending trajectory from the brain to the spinal canal through ventricular or subarachnoid pathways.[ 7 ] However, in other reports with simultaneous intracranial and spinal involvement, the direction of spread remains ambiguous, whether ascending from the spine or descending from the brain.[ 3 , 14 ] The parasite’s ability to invade dura, soft tissue, and even bone further obscures its migration pathway.[ 2 , 5 ]

Figure 3:

(a) Sequential axial fluid-attenuated inversion recovery (FLAIR) image obtained 3 years after spinal surgery shows mixed hypo- and hyperintense content with mucosal thickening (arrowhead) within the opacified right ethmoid sinus, along with cyst-like extra-axial lesions (asterisks) with cerebrospinal fluid (CSF) density in the right ambient cistern. Axial (b) sequential FLAIR, (c) gadoliniumenhanced T1-weighted, (d) diffusion-weighted imaging (DWI), and (e) apparent diffusion coefficient images acquired 1 year after brain surgery and ventriculoperitoneal shunt placement reveal a right loculated cystic lesion with thin peripheral enhancement. The lesion contains hyperintense FLAIR content and shows restricted diffusion. A small air bubble and a cystic lesion are also observed at the right anterior cranial fossa (arrow in b). Notably, the previously seen mixed signal content within the right ethmoid sinus has resolved. (f) Sagittal gadolinium-enhanced T1-weighted image demonstrates diffuse thick leptomeningeal enhancement with loculated CSF collections extending along the spinal canal from the C1 to C5 levels.

Bone involvement in sparganosis is rare but highly invasive, with cases of osteolytic destruction in the lumbar spine, iliac bone, and humerus mimicking tumors. The parasite likely penetrates bone through enzymatic degradation, facilitating deep tissue migration between CNS compartments. Given this potential, sparganosis should be considered in cases of unexplained osteolytic lesions, particularly in endemic regions.[ 10 ]

In our case, the migration route remains uncertain, with disseminated involvement of the supratentorial, infratentorial, upper cervical, and lumbar spinal regions. In addition, newly identified penetration from the right frontal sinus through the cribriform plate into the frontal lobe highlights the parasite’s ability to traverse anatomical barriers, supporting its invasive and disseminative nature.

Steroid induced proliferative sparganosis

Sparganosis is traditionally considered a nonproliferative infection, as Spirometra larvae do not undergo asexual reproduction in human hosts. However, emerging evidence suggests that chronic immunosuppression, particularly from long-term corticosteroid therapy, may promote parasite persistence, migration, or atypical dissemination.[ 2 , 14 , 17 ] This is especially concerning in patients receiving steroids for autoimmune or inflammatory diseases, where reduced immune surveillance may enable larvae to survive and spread within the CNS.

Figure 4:

Magnetic resonance imaging of the brain performed 2 months after intravenous (IV) antibiotic administration. (a-c) Sequential axial gadolinium-enhanced T1-weighted and (d) T2-weighted images demonstrate a reduction in the size of the right frontal cystic lesion, along with thick leptomeningeal enhancement and loculated cerebrospinal fluid collections in the prepontine and left cerebellopontine angle cisterns, with resolution of the previously noted air content. Diffuse thick dural enhancement is observed along the bilateral cerebral convexities, likely indicative of intracranial hypotension. (e) Axial susceptibility-weighted imaging (SWI) and (f) coronal T2*-weighted gradient echo (GRE) images reveal a small linear hemorrhagic lesion (arrows) in the inferior part of the genu of the corpus callosum, appearing as a focal susceptibility signal on SWI and GRE images, likely representing hemorrhage along the parasite’s migratory tract.

Several clinical reports support this association. Noiphithak and Doungprasert[ 14 ] described a 54-year-old Thai man with bullous pemphigoid on chronic high-dose prednisolone who developed disseminated CNS sparganosis involving the spine and eyes. Carlson et al.[ 2 ] similarly reported a 53-year-old man with pemphigus vulgaris on long-term steroids who presented with both spinal and cerebral involvement. In both cases, extensive parasite dissemination was suspected to be facilitated by steroid-induced immunosuppression.

In addition, a veterinary study by Tokiwa et al.[ 17 ] described proliferative sparganosis in a cat treated with corticosteroids for over a year, resulting in uncontrolled larval expansion in subcutaneous and muscle tissue. While Spirometra mansoni is not known for asexual reproduction, this case raised concerns that steroids may contribute to abnormal parasitic proliferation.

The mechanisms underlying steroid-associated progression remain speculative. It is hypothesized that steroid-induced immunosuppression impairs host clearance and may also alter parasite behavior, including enhanced motility or tissue invasiveness. These findings underscore the need for caution when prescribing corticosteroids in individuals with suspected or confirmed sparganosis, with close clinical and imaging surveillance and consideration of alternative anti-inflammatory therapies where appropriate.[ 2 , 14 , 17 ]

Table 1:

Summary of reported cases of sparganosis involving both spinal and intracranial regions.

Management strategies

Sparganosis may present as either a localized lesion or part of a disseminated infection, raising the need to evaluate for possible systemic involvement. Infections affecting the ocular, subcutaneous, or CNS regions may result from a primary infestation or secondary migration from another site. Because the parasite can spread through CSF, tissue planes, and even bone, comprehensive imaging such as whole-brain and spine MRI or a full-body scan may be necessary. This is particularly important in endemic regions, where co-infections or multiple lesions may be overlooked, delaying diagnosis and treatment.[ 8 ]

Management of CNS sparganosis requires a multidisciplinary approach, combining surgical intervention, pharmacological treatment, and supportive care. Surgical resection remains the preferred option when the lesion is symptomatic, localized, and surgically accessible. Complete removal is essential, as residual larval segments may lead to recurrence. However, surgery may not be feasible in patients with multifocal or deep-seated lesions or in those with contraindications to operative procedures.[ 14 ]

In cases where surgery is not possible, pharmacological therapy with high-dose praziquantel has shown variable success. This approach is sometimes combined with corticosteroids to reduce the inflammatory response associated with parasite disintegration. Although praziquantel may not eliminate the parasite, several studies have reported clinical improvement and radiological stabilization with repeated treatment courses.[ 16 ]

Long-term follow-up with serial imaging is critical to monitor treatment response and detect recurrence. Management should be tailored to each patient based on clinical status, lesion location, and response to therapy.[ 12 ]

Pharmacological treatment

The pharmacological management of CNS sparganosis primarily relies on antiparasitic agents, although their efficacy remains inconsistent. Praziquantel is considered the first-line option in inoperable cases, yet Sparganum often demonstrates high tolerance to low concentrations, limiting its effectiveness. Other agents, such as albendazole and mebendazole, have been used with variable success, particularly in nonCNS involvement.[ 13 , 14 ]

Surgical removal remains the preferred treatment, especially for live or localized lesions, as drug therapy alone rarely leads to complete eradication. When pharmacotherapy is used, dosing strategies vary significantly across studies. High-dose praziquantel regimens, such as 75 mg/kg/day for 7 days, are often combined with cimetidine to boost drug levels.[ 2 ] Some reports recommend even higher doses, up to 120–150 mg/kg/day, divided over 2 days for disseminated or refractory cases.[ 13 ] Prolonged courses have also been described; for example, mebendazole at 40 mg/kg/day for 6 months has shown some success in pulmonary sparganosis, although its CNS efficacy is unproven.[ 15 ]

Shorter praziquantel regimens have yielded mixed outcomes, likely due to differences in parasite burden, lesion location, and host response. This variability underscores the need for standardized treatment protocols based on controlled studies. At present, many experts view praziquantel as an adjunct, not a substitute for surgery, particularly in extensive CNS disease.[ 14 ]

In a notable clinical series, Zhang et al.[ 19 ] reported that high-dose praziquantel (75 mg/kg/day in three divided doses for 10 days per course) led to clinical improvement in 80% of patients, with complete resolution in two. The treatment was administered every 3 months, continuing until clinical improvement and radiologic stability were observed. This regimen was well-tolerated and considered a viable alternative when surgery was not an option.

In our case, the patient received intravenous metronidazole for 2 months, initially for a presumed brain abscess. Unexpectedly, this led to symptomatic improvement despite metronidazole not being a recognized treatment for sparganosis. Given its ability to penetrate the blood–brain barrier and modulate neuroinflammation, it may have contributed to reducing perilesional edema and suppressing inflammatory responses, which could explain the stabilization of lesions and the absence of new symptoms.[ 11 , 16 ] Although speculative, this observation raises the possibility of a supportive role for metronidazole in managing disseminated sparganosis, particularly in nonsurgical candidates. Further studies are needed to investigate its potential benefit in this context.

CONCLUSION

CNS sparganosis is a rare parasitic infection characterized by its migratory nature and potential for dissemination within both the brain and spinal cord. Our case highlights the diagnostic challenges associated with this condition, often mimicking other neurological diseases, which can lead to delayed diagnosis and management. A combination of neuroimaging and histopathological confirmation remains essential for accurate diagnosis, while surgical resection remains the cornerstone of treatment, particularly for symptomatic or accessible lesions. Although antiparasitic agents like praziquantel have shown variable efficacy, their role as adjunctive therapy warrants further investigation. Interestingly, the accidental use of metronidazole in our case may have contributed to symptom relief, suggesting a potential, yet unproven, role in modulating disease activity. Given the risk of recurrence and asymptomatic dissemination, long-term follow-up with serial imaging is crucial. This case, along with our literature review, underscores the importance of maintaining a high index of suspicion for sparganosis, especially in endemic regions, to facilitate early diagnosis and improve neurological outcomes.

Ethical approval:

Institutional Review Board approval is not required.

Declaration of patient consent:

Patient’s consent not required as patients identity is not disclosed or compromised.

Financial support and sponsorship:

Nil.

Conflicts of interest:

There are no conflicts of interest.

Use of artificial intelligence (AI)-assisted technology for manuscript preparation:

The authors confirm that there was no use of artificial intelligence (AI)-assisted technology for assisting in the writing or editing of the manuscript and no images were manipulated using AI.

Disclaimer

The views and opinions expressed in this article are those of the authors and do not necessarily reflect the official policy or position of the Journal or its management. The information contained in this article should not be considered to be medical advice; patients should consult their own physicians for advice as to their specific medical needs.

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