Parenchymal Neurocysticercosis as One of the Most Neglected Tropical Diseases: A Case Report

• A report of parenchymal neurocysticercosis with atypical phenomenon, such as focal neurological deficit due to space occupying lesions.
• Neurocysticercosis is one of the most neglected tropical diseases that caused by infection of Taenia solium via fecal-oral route.

Based on clinical symptoms of seizures and CT scan results of the brain parenchyma, the patient was diagnosed had parenchymal neurocysticercosis with symptomatic epilepsy. The patient was given albendazole, phenytoin, pantoprazole, dexamethasone, and folic acid for 1 month. After treatment, the patient's condition improved, MRI results showed no abnormality, and the symptoms of seizures were no longer present.

Neurocysticercosis is classified into two types based on the parasite's location: parenchymal (in the brain and medulla tissues) and extraparenchymal (primarily in the intraventricular and subarachnoid spaces, in between the leptomeninges, arachnoids, and pia mater, where cerebrospinal fluid circulates). The clinical, therapeutic, and prognostic consequences of neurocysticercosis in the parenchymal and extraparenchymal types are completely different.[10], [11] We discovered a parenchymal neurocysticercosis in this patient.

There are four stages of parenchymal neurocysticercosis, and the neuroimaging results varies depending on the stage. In the vesicular stage, the cyst measures 4-5 mm, is filled with clear fluid, has a thin, semi-transparent wall, an eccentric opaque scolex, and usually does not display symptoms. The cyst begins to deteriorate in the colloid stage, causing an inflammatory reaction that culminates in the replacement of clear cyst fluid with gelatinous material due to hyaline degeneration in the larvae. In the granular nodular stage, the cyst wall is replaced by lymphoid nodules and necrosis with the scolex transforming into mineralized granules, edema decreases, and ring enhancement persists in CT scan. In the nodular calcification stage, CT scan reveals granular tissue that has converted into calcified nodules without contrast enhancement.[12] In this case, CT scan showed an oval lesion with heterogeneous density in the right centrum semiovale with minimal perifocal edema and ring contrast enhancement indicating the patient was in the granular nodular stage of parenchymal neurocysticercosis.

Clinical signs of neurocysticercosis range from asymptomatic to severe critical symptoms that are related with larval size, quantity, stage, location, and host immune reaction.[13] In this case, the cyst is located in the white matter (in the right centrum semiovale), that generates adult-onset epilepsy.[6] Headache, which is the second most frequent symptom after epilepsy and focal neurological deficit (unilateral hemiparesis), which is a rare symptom of neurocysticercosis (only 5-15% of cases) are also experienced by this patient.[13]

Seizures are the major or perhaps the sole symptom of parenchymal neurocysticercosis, occurring in 80% of symptomatic patients.[14] Neurocysticercosis is the predominant cause of acquired epilepsy in the majority of the developing world, and it has been regarded as on of the primary disease causing the excess percentage of epilepsy recorded from these areas.[15] According to research, all stages of parenchymal neurocysticercosis are connected with reactive seizure via different mechanisms. At the vesicular stage (viable cysts), it develops as a result of inflammation or compressive effects on the brain parenchyma. Reactive seizure may develop in the colloidal and granular stages as a result of the inflammatory process associated with the host immune system's attack on the parasites. However, at the nodular calcified stage, gliosis occurs around deceased parasites, and late exposure of remaining antigenic material to the brain parenchyma may result in a persistent epileptogenic lesion.[16] Recurrent inflammatory episodes and consequent reactive seizure activity may culminate in persistent local or distant epileptogenic lesions, resulting in acquired epilepsy.[17]

Parenchymal neurocysticercosis is associated with the focal neurological deficit such as pure motor hemiparesis (PMH).[18] PMH can be caused by lacunar infarction or space occupying lesions.[19] In regard to our case, unilateral hemiparesis that occur in this patient was not caused by lacunar infarction based on neuroimaging results. A CT scan of the brain revealed no indication of recent infarction or bleeding. An oval lesion in right centrum semiovale with minimal perifocal edema were the results in CT scan of brain. As this is not owing to a lacunar infarction, the hemiparesis in our case is most likely attributable to the compressive impact of oval lesion with minimal perifocal edema on the right centrum semiovale.

Most focal neurological deficit cases caused by space occupying lesion are irreversible.[20] However, after dexamethasone, phenytoin, and albendazole treatment, the patient’s clinical manifestations  in this case improved significantly during hospital stay. The symptoms of recurrent seizures and focal neurological deficit were gone after one month of medication, and the cyst was no longer visible on MRI findings.

Dexamethasone which is a steroid is used to control local inflammatory effects (cerebral edema) and minimize the worsening of neurological symptoms due to parasite death.[21] Antihelmentic drugs that usually used for neurocysticercosis are praziquantel and albendazole. However, in our case, we used albendazole since it is more effective than praziquantel in eliminating cysts and causing overall clinical improvement, and it also has good pharmacological interactions with dexamethasone. Dexamethasone increases plasma level of albendazole by decreasing the clearance of albendazole sulfoxide, the active metabolite of albendazole.[22] Antiepileptic drugs are frequently utilized since seizures are the most prevalent manifestation of neurocysticercosis. Phenytoin and carbamazepine are the first line therapy for control secondary seizures due to neurocysticercosis.[23]

Conclusion

Neurocysticercosis is one of the most neglected tropical diseases. It caused by infection of Taenia solium via fecal-oral route. In our case, the patient experienced neurocysticercosis through eating undercooked pork that contain Taenia solium eggs. Neurocysticercosis is classified into two types based on the parasite's location, such as parenchymal and extraparenchymal with different clinical manifestation, therapeutic, and prognosis. We report a parenchymal neurocysticercosis with atypical phenomenon, such as focal neurological deficit (unilateral hemiparesis). Although in general focal neurological deficits due to space occupying lesions are irreversible, in this case we report a neurocysticercosis patient with improvement in symptoms and neuroimaging results. This offers up new paths for research into the causes of focal neurological deficit other than infarction and hemorrhage.

Acknowledgement

We would like to thank you to the RSU Premagana for allowing us to submit this case as our experience there.

Author contribution: We declare that all listed authors have made substantial contributions to all of the following three parts of the manuscript:

- Research design, or acquisition, analysis or interpretation of data;

- drafting the paper or revising it critically;

- approving the submitted version.

We also declare that no-one who qualifies for authorship has been excluded from the list of authors.

Funding:None.

Conflict of interest:None.

Ethical considerations: This case report is based solely on anonymized laboratory data without involving direct patient interaction or intervention. No identifiable patient information is included, ensuring compliance with ethical guidelines and does not require formal ethical clearance as it involves retrospective data analysis.