Racemose Neurocysticercosis Complicated by Meningitis and Lacunar Infarcts

A 30-year-old female presented with complaints of intermittent headaches of increasing severity for the past 2 years, with blurring of vision and loss of memory during the same time frame. On neurological examination, there were no focal deficits. Cranial nerve assessment, motor and sensory examinations, cerebellar function tests, and gait evaluation were all within normal limits. Routine blood investigations were unremarkable. Magnetic resonance imaging (MRI) of the brain revealed multiple T2 hyperintense cystic lesions, with few septations within, in the suprasellar region within the subarachnoid space, extending along the bilateral MCA into the Sylvian fissures up to the insular surface [Figure 1]. There was focal mass effect with inferior displacement of the optic chiasma. They showed complete suppression on fluid-attenuated inversion recovery (FLAIR) sequences. Post-gadolinium T1-weighted sequences showed mild peripheral enhancement around the cystic lesions. Diffusion restriction was absent.Figure 1: Coronal and Axial T2 weighted images show multiple hyperintense cystic lesions, with few septations within, in the suprasellar region within the subarachnoid space, extending along the bilateral MCA into the Sylvian fissures up to the insular surface (a and b). They show complete suppression on FLAIR sequences (black arrows) with additional areas of focal hyperintensity in bilateral gangliocapsular regions (white arrows), signifying chronic lacunar infarcts (c). Leptomeningeal enhancement is seen along the higher cerebral sulcal spaces (white dashed arrows) on post-contrast FLAIR (d) suggestive of meningitis. Post-gadolinium T1-weighted sequence (e) show mild peripheral enhancement (black dashed arrows) around the cystic lesions. Axial non-contrast CT (f) shows fluid density within the cystic lesions (asterisk)T2/FLAIR hyperintense areas were also seen in bilateral gangliocapsular regions, suggesting chronic lacunar infarcts. Leptomeningeal enhancement was seen along the sylvian fissures, and higher cerebral sulcal spaces. Cerebrospinal fluid (CSF) analysis revealed eosinophilia, with an eosinophil count of 258 cells/μL. The patient underwent a treatment course with corticosteroids followed by surgical debulking, resulting in symptomatic improvement. Histopathological examination of the resected ‘cyst wall’ confirmed the diagnosis, revealing a convoluted, layered structure with surface foldings and acellular rounded protrusions consistent with the cuticular layer. The underlying layer showed uniform nucleated cell bodies, and the innermost layer contained loosely arranged fibers characteristic of reticular architecture. These findings, along with imaging features and CSF eosinophilia, confirmed racemose neurocysticercosis. Discussion The final diagnosis in this case was racemose neurocysticercosis (NCC). Cysticercosis, caused by the parasitic tapeworm Taenia solium, is a common helminthic infection affecting the central nervous system. Transmission occurs through ingestion of T. solium eggs, which hatch and release oncospheres, which enter the bloodstream and develop into cysticerci in the brain or muscles.[1] NCC is categorized into intraparenchymal and extra-parenchymal forms.[2] The clinical presentation can be varied, with seizures being the most common symptom. Peripheral eosinophilia is a non-specific laboratory finding. Extraparenchymal NCC occurs when cysticerci migrate to the ventricles via the choroid plexus. Racemose NCC is a subtype that develops due to cysts segmentation, which expand into CSF spaces. It lacks typical evolutionary stages, and does not show significant enhancement on imaging. Additionally, calcifications, are not usually seen.[2] Racemose NCC may cause intracranial hypertension, secondary to cerebrospinal fluid (CSF) outflow obstruction or inflammatory arachnoiditis/meningitis. Host inflammatory responses can lead to endarteritis, vasculitis, and nerve entrapment. Rarely, it may provoke Bruns’ syndrome. Spinal cord involvement is rare, accounting for 1-5% of all cases.[3] Symptomatic treatment includes antiepileptics, corticosteroids to reduce inflammation and antihelminthic therapy.[3] CSF diversion procedures may be performed to manage intracranial hypertension. Declaration of patient consent Appropriate patient consent was obtained for using the anonymized DICOM images and clinical history for making this manuscript. Financial support and sponsorship Nil. Conflicts of interest There are no conflicts of interest.