Neurocysticercosis is a common parasitic neurologic disease worldwide, but in some parts of the world, it remains relatively rare, and the presentation is variable depending on the location of cyst. It is caused by the larvae of pork tapeworm (Taenia solium) and acquired from a human carrier through faecal-oral route. Approximately, 10–20% of patients worldwide [1] are present with IVNCC, which has a high mortality rate owing to secondary obstructive hydrocephalus. Viable cysts are freely mobile and may lodge anywhere in the foramina or the aqueduct resulting in mechanical obstruction or as a result of arachnoiditis in chronic cases [2]. The cysts reach the ventricular space through the choroid plexus and are more frequently found in the fourth ventricle, likely due to gravitational forces which favor migration from supratentorial ventricles or may directly enter through the choroid plexus. The size of the cyst and the ventricular foramina could also be one of the factors responsible for frequent involvement of fourth ventricle. The presenting features of hydrocephalus are headache, nausea, vomiting, altered sensorium, and papilledema. Acute hydrocephalus may present as Bruns’ syndrome in which sudden attacks of headache, vertigo and nausea, or vomiting were precipitated by abrupt head movements which was present in our patient [3]. Episodic hydrocephalus in Bruns’ syndrome is due to intermittent obstruction of cerebrospinal fluid flow by ball valve movement of intraventricular cysts. Mechanism of hydrocephalus is either ventricular obstruction or arachnoiditis (either basal or spinal). Bruns’ syndrome has been originally described in fourth ventricular NCC but has also been reported in other lesions like third ventricular lesions [4, 5]. Lu Zhengqi and colleagues described the first case of Bruns’ syndrome secondary to tuberculoma which mimicked neurocysticercosis and the patient improved on treatment. Such cases especially a single cyst as seen in our case pose a diagnostic dilemma for a clinician and if misdiagnosed as tuberculoma can result in unnecessary side effects of antituberculous drugs. Though serological tests are available for diagnosis, they have a poor sensitivity and specificity. So, majority of cases are diagnosed with help of imaging; however, histopathology is the gold standard for diagnosing NCC. These intraventricular cysts are poorly defined on CT Brain and so routine MRI Brain is used for diagnosis. However, routine MRI sometimes may also not be able to delineate the nature of lesion; as result, newer imaging modalities like constructive interference in steady state 3 dimensional (CISS3D) and fast imaging employing steady-state acquisition (FIESTA) sequence promise improved detection of IVNCC in terms of better sensitivity [6]. In addition, previously missed cases have been diagnosed using 3D CISS sequence [7]. These advanced imaging techniques have also been strongly recommended by Infectious Disease Society of America (IDSA) and the American Society of Tropical Medicine and Hygiene (ASTMH) [8]. Many conditions can cause hydrocephalus and thus mimic extra-parenchymal NCC. These include colloid cysts, cerebellar cystic hemangioblastoma, and tuberculomas. Treatment of IVNCC includes managing hydrocephalus and removal of the cyst. Flexible neuroendoscopy has emerged as the surgical approach for extirpation of the cysts, though surgical removal of fourth ventricular cysterci with or without shunt surgery is recommended in cases where endoscopic removal is not possible [8, 9]. Accurate diagnosis is essential in such cases as it can prevent morbidity and mortality due to unnecessary interventions like lumbar puncture, shunt procedures ,or initiation of antitubercular drugs without confirming the final diagnosis.
Thus, to conclude diagnosis of IVNCC can still pose a challenge despite modern neuroimaging methods because of poor specificity of clinical and imaging findings, a histopathological confirmation may be required to rule out a malignant lesion.