A 33-year-old Indian male was hospitalised for a 3-day history of headache and left lower limb weakness in December 2014. He had experienced no fever or seizures. He had visited New Delhi, India, the year before. Physical examination revealed the patient to be fully conscious with left lower limb monoparesis. There was no sensory deficit. Computed tomography (CT) revealed a superior parietal intra-axial lesion with a calcified focus (Fig 1a). Magnetic resonance imaging (MRI) delineated a 2 x 1.5 x 1.5 cm circumscribed hypointense cystic lesion with a contrast-enhancing wall and an eccentric intracystic signal with perilesional oedema (Figs 1b to 1d). Differential diagnoses included neurocysticercosis, brain abscess, brain metastasis, and malignant glioma. Craniotomy for excision was performed in view of the possibility of malignancy and the surgically accessible superficial location of the lesion. Intra-operatively, a firm capsular mass containing thick opaque material was seen (Fig 2a). Histology revealed a cysticercus within a fibrous capsule, compatible with the diagnosis of neurocysticercosis (Figs 2b and 2c). A 2-week course of oral albendazole was commenced and the patient was discharged with full recovery.

Neurocysticercosis is the most common parasitic infection of the central nervous system (CNS) caused by the larval form of Taenia solium. The peak age of incidence is between 25 and 35 years1 and the condition is endemic to the Indian subcontinent, coastal North Africa, sub-Saharan Africa, Latin America, and China. The main mode of transmission is by faecal-oral ingestion of tapeworm embryos.1 2 Consumption of contaminated poorly cooked pork is a less-frequent alternative source of infection since pigs are intermediate hosts.2 3 Within 72 hours of ingestion, larvae known as oncospheres are released and pass through the intestinal wall into the circulation, subsequently depositing in the CNS, retina, and skeletal muscle as cysticerci.1 2 The parasite can remain viable in the brain for several years after which it undergoes calcific degeneration.3 In endemic areas, the most common presentation is epilepsy, responsible for 30% of cases.1 Focal neurological deficits may occur including cranial nerve palsy due to basal meningitis. Obstructive hydrocephalus develops when lesions occupy the fourth ventricle.1 2

Characteristic radiological features include dystrophic calcification on CT imaging, cyst wall contrast enhancement on T1-weighted MRI and identification of the pathognomonic scolex, an eccentric focus of enhancement representing the tapeworm’s head, best delineated with fluid-attenuated inversion recovery sequences (hole-with-dot sign).3 4 Brain abscess or metastases are important differential diagnoses as they are also similarly located at the grey-white matter junction of the middle cerebral artery distribution, associated with disproportionately significant perilesional cerebral oedema and classically exhibit heterogeneous contrast enhancement. Malignant glioma was less likely in our patient since they are morphologically more infiltrative, and the present lesion was well-circumscribed. For this patient, the major distinguishing feature that supported a diagnosis of neurocysticercosis was the presence of dystrophic calcification on CT and, in retrospect, the presence of a scolex on MRI. Absolute criteria for a definitive diagnosis are either histological parasitic proof, imaging demonstration of a scolex, or subretinal parasites on fundoscopy (Table5). Serological enzyme-linked immunoelectrotransfer blot detection of anti-cysticercus antibodies or cerebrospinal fluid enzyme-linked immunosorbent assays are adjunctive investigations.1 6 Management of active neurocysticercosis includes antiepileptic drug administration, anti-inflammatory glucocorticoid therapy, and definitive antiparasitic therapy with albendazole (15 mg/kg per day) or praziquantel (50 mg/kg per day) for 2 to 4 weeks.1 Surgical excision is reserved for cysts that cause mass effect, hydrocephalus, or if the diagnosis is unclear.2

In an era of increasing migration and international travel, patients from developing countries who present with seizures, raised intracranial pressure symptoms, or focal neurological deficit should be suspected of having neurocysticercosis when characteristic imaging findings are identified. In probable cases, a trial of antiparasitic therapy is recommended with serial scans arranged to monitor treatment response.

1. Garcia HH, Nash TE, Del Brutto OH. Clinical symptoms, diagnosis, and treatment of neurocysticercosis. Lancet Neurol 2014;13:1202-15. Crossref

2. Zymberg ST. Neurocysticercosis. World Neurosurg 2013;79(2 Suppl):S24.e5-8.

3. Dhesi B, Karia SJ, Adab N, Nair S. Imaging in neurocysticercosis. Pract Neurol 2015;15:135-7. Crossref

4. Lerner A, Shiroishi MS, Zee CS, Law M, Go JL. Imaging of neurocysticercosis. Neuroimaging Clin N Am 2012;22:659-76. Crossref

5. Del Brutto OH, Rajshekhar V, White AC Jr, et al. Proposed diagnostic criteria for neurocysticercosis. Neurology 2001;57:177-83. Crossref

6. Gekeler F, Eichenlaub S, Mendoza EG, Sotelo J, Hoelscher M, Löscher T. Sensitivity and specificity of ELISA and immunoblot for diagnosing neurocysticercosis. Eur J Clin Microbiol Infect Dis 2002;21:227-9. Crossref