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Congress: ECR25
Poster Number: C-10358
Type: Poster: EPOS Radiologist (educational)
Authorblock: S. Z. Rahman, B. Rao; New Haven, CT/US
Disclosures:
Saumik Zuhayr Rahman: Nothing to disclose
Balaji Rao: Nothing to disclose
Keywords: CNS, Neuroradiology brain, CT, MR, Diagnostic procedure, Haemorrhage, Infection, Parasites
Findings and procedure details

Taenia solium is a common infectious agent within humans across the world. This infection is spread to humans via the consumption of T. solium eggs via fecal-oral transmission. Once ingested, the eggs hatch within the human intestinal tract and invade the host. The larval parasite most commonly infects the brain, muscles, eyes, and skin of the host. When the brain is involved, the condition is known as neurocysticercosis. NCC is widely prevalent in the developing world, with prevalence quoted between 3-20% of the population [1-3]. NCC is the leading cause of epilepsy worldwide [1,2]. Within the brain, the larvae develop as cysticerci. The parasite lifespan is divided into 4 distinct imaging stages: vesicular, colloidal vesicular, granular nodular, and calcified nodular [2-4].

In the vesicular phase, the larvae can be found within cysts within the central nervous system. These cysts are surrounded with a glycoprotein rich wall which works to avoid detection by the host immune system. The cysts contain a small mural nodule known as the scolex, which represents the larval head. The parasite may survive in the vesicular phase for many years [2-4]. On CT, the vesicular phase is identified as a well circumscribed 1-2 cm hypodense lesion with a peripherally based nodule representing the scolex within the cyst.

Fig 1: Sagittal (A), axial (B), and coronal (C) CT images of the head without IV contrast demonstrate an intraparenchymal cystic lesion (arrows) with central nodular hyperdensity, corresponding to the parasitic scolex.
The cyst appears fluid density and exerts local mass effect. No surrounding parenchymal oedema is seen in the vesicular phase. On MRI, this phase is characterised by a T2 hyperintense cyst with an internal mural scolex; cyst contents suppress on fluid attenuated inversion recovery (FLAIR) images. On post-contrast sequences, there may be minimal smooth thin enhancement of the cyst wall and scolex itself. No parenchymal oedema will be seen on the T2 or FLAIR sequences.
Fig 2: Coronal (A) and axial (B) FLAIR MRI sequence demonstrating a cystic lesion in the right parietal lobe without perilesional parenchymal oedema (arrows). Internal scolex is noted. The cyst contents suppress on FLAIR. Coronal (C) and axial (D) contrast enhanced MRI sequence demonstrates think mild peripheral enhancement along the superior cyst (arrow) . In the vesicular phase, thin enhancement of the cysticerci and scolex may be noted.

Over time, the cysticerci will begin to degrade and leak antigens into the surrounding tissues, causing local inflammation. During this colloidal vesicular phase, there is breakdown of the surrounding blood brain barrier, leading to increased contrast enhancement of the cysticerci with surrounding parenchymal vasogenic oedema. The inflammatory cells invade the walls of the cysticerci, modulating the protein contents of the fluid and changing signal characteristics on MRI [2-4]. On CT, the colloidal vesicular cyst will demonstrate surrounding parenchymal hypodensity, corresponding to vasogenic oedema.

Fig 3: Axial (A) and coronal (B) CT images of the head without intravenous contrast demonstrate a large region of geographic intraparenchymal hypodensity (circled), which correlates to vasogenic oedema in the colloidal vesicular stage of neurocysticercosis. The cysticerci are not well visualised in this case on CT.
On MRI, the vasogenic oedema is appreciable as parenchymal hyperintensity surrounds the cyst on T2 and FLAIR sequences. On post-contrast sequences, the walls of the cyst will thicken and demonstrate ring enhancement.
Fig 4: Axial (A) and coronal (B) FLAIR MRI sequence demonstrating parenchymal hyperintensity (circled) representing vasogenic parenchymal oedema in response to antigen leak from the cysticerci. Axial (C) and coronal (D) contrast enhanced MRI sequence demonstrates ring enhancing cysticerci (arrows) within the region of perilesional oedema.
The increased internal protein contents will lead to increased internal signal on T1 weighted and FLAIR sequences. The scolex may demonstrate diffusion restriction on diffusion weighted imaging.
Fig 5: Axial diffusion weighted sequence (A) and corresponding apparent diffusion coefficient map (B) demonstrates a punctate focus of diffusion restriction (arrows) corresponding to the scolex within the cysticerci. Surrounding T2 shine-through is noted on the apparent diffusion coefficient map, corresponding to parenchymal oedema.

The colloidal cyst will eventually involute, entering the granular nodular stage. On CT, the surrounding parenchymal hypodensity will decrease, representing improvement in oedema. This will correspond to resolving signal abnormalities on the T2/FLAIR sequences on MRI. On post-contrast sequences, the cyst will become small with a small amount of residual wall enhancement.

Fig 6: Image A: Axial contrast enhanced MRI sequence demonstrates persistent thick rim enhancement (arrow) with decreasing size in comparison to the colloidal vesicular stage, consistent with ongoing involution of the parasite. Image B: Coronal FLAIR MRI sequence demonstrates resolving perilesional oedema with a small amount of residual adjacent FLAIR hyperintensity noted (arrow). Image C: Axial susceptibility weight image demonstrates signal loss in the region of the parasite, indicating mineralisation (arrow).
Finally, in the calcified nodular stage, the parasite has died. On CT this will be characterised by focal calcification. On MRI, calcifications will correspond to areas of signal loss on susceptibility weighted imaging, along with resolution of previously seen oedema and enhancement [2-4].
Fig 7: Axial maximum intensity projection non-contrast CT of the head (A) demonstrates multiple scattered intraparenchymal calcifications. On axial susceptibility weighted MRI (B), these represent areas of signal loss, indicating mineralisation. These findings represent the dead larvae of neurocysticercosis. Axial FLAIR MRI sequence (C) and postcontrast axial contrast enhanced MRI (D) demonstrate no associated perilesional oedema or enhancement in the areas of susceptibility artifact during the nodular calcified stage of neurocysticercosis.

The cysticerci may be found in multiple locations throughout the neuraxis. In order of descending frequency, this includes the subarachnoid/cisternal spaces, intraparenchymal location, intraventricular location, and spinal subarachnoid spaces. Within the parenchyma, the cysticerci are most often found peripherally at the grey-white matter junction. Within the ventricles, the lesions are most often located at the fourth ventricle (50% of cases), followed by the lateral ventricles (35% of cases), and the remainder located within the third ventricle and cerebral aqueduct [2]. Perilesional inflammatory changes are the primary pathophysiologic mechanism within the human host. The most common manifestation of this disease is seizure disorder, which may present in patients at any stage of the parasite life cycle [1].

With subarachnoid/cisternal NCC, the inflammation may cause reactive vasculitis [2]. In this exhibit we present a case of vertebral artery aneurysm formation secondary to a case of subarachnoid/cisternal NCC involving the posterior fossa. In this case a 30 year old male patient with known subarachnoid and cisternal vesicular stage NCC  presented with seizure-like activity and poor neurologic examination secondary to an acute subarachnoid haemorrhage.

Fig 8: Axial CT of the head without IV contrast (A) demonstrates a vesicular stage cysticercus in the right subarachnoid space (arrow). Axial thin-slice T2 weighted sequence through the posterior fossa (B) and axial T2 weighted sequence of the brain (C) demonstrate multiple scattered cysticerci in the premedullary and pontocerebellar cisterns as well as within the retrocerebellar subarachnoid space (arrows).
CT angiography demonstrated a right vertebral artery aneurysm, most likely related to multiple adjacent cysticerci in the posterior fossa as demonstrated on prior pre-haemorrhagic MRI and CT images found in Figure 8.
Fig 9: Axial CT of the head without IV contrast (A) shows subarachnoid haemorrhage collecting in the posterior fossa, surrounding the brainstem and filling the cisternal spaces. Sagittal CT of the head without IV contrast (B) demonstrates multiple hypodensities within the cisterns, surrounded by blood products, representing cysticerci (arrows). CT angiography of the head (C) reveals the source of haemorrhage: a saccular aneurysm arising from the right vertebral artery (arrow).
The patient underwent catheter angiography of the aneurysm with coil embolisation.
Fig 10: Catheter angiogram of the right vertebral artery (A) demonstrates a saccular aneurysm arising from the V4 segment (arrow). The aneurysm underwent endovascular coiling (B). Angiography via the right vertebral artery demonstrates no residual filling of the aneurysm following coil placement (C).
Unfortunately in this case, the patient died shortly after intervention secondary to worsening cerebral oedema and worsening neurologic status. The etiology of this aneurysm is most likely attributable to a reactive vasculitis secondary to the adjacent cysticerci given the location of aneurysm formation and young age of the patient without additional risk factors. Cases of both aneurysmal and non-aneurysmal subarachnoid haemorrhage attributable to NCC have been described in the literature as sparse case reports of a rare complication of this parasitic infection [5]. The vasculitis caused by NCC has also been described in the literature to cause ischaemic complications, most commonly lacunar infarcts [2]. These infarcts may be indistinguishable from other etiologies of infarction on imaging examinations.

The arachnoiditis/meningitis of NCC within the subarachnoid and cisternal CSF containing spaces may be a focal reaction to the cysticerci themselves or present as a more diffuse process as well on imaging examinations [2-4]. Here, we present a case of a 37 year old male with chronic history of headaches found to have a communicating hydrocephalus with MRI findings of meningitis.

Fig 11: Figure A: T1-weighted sagittal MRI of the brain demonstrates hydrocephalus involving the lateral ventricles, third ventricle, and fourth ventricle. Figures B & C: Sagittal and axial contrast enhanced MRI of the brain demonstrates leptomeningeal enhancement along the anterior surface of the pons (arrows), concerning for meningitis. Figure D: Axial contrast enhanced MRI of the upper cervical spinal cord demonstrates additional areas of meningeal thickening and enhancement (arrow).
Imaging of the lumbar spine demonstrated multiple circumferentially enhancing cysts along the cauda equina, correlating to the clinical diagnosis of NCC in this patient, along with findings of arachnoiditis.
Fig 12: Screen Left: Sagittal short tau inversion recovery (left) and contrast enhanced fat suppressed MRI sequences demonstrate multiple peripherally enhancing cystic structures along the spinal canal involving the cauda equina (arrows). Screen Right: Axial T2 weighted MRI of the lumbar spine shows clumping of the cauda equina nerve roots is noted, consistent with arachnoiditis.
The patient’s hydrocephalus was felt to be secondary to a chronic impairment of CSF resorption and related increased intracranial pressure. The patient’s symptoms improved following a course of steroids and anthelmintic treatment.

Intraventricular NCC may lead to obstructive hydrocephalus, which may be fatal in certain cases [2-4]. When small, the cysts may be difficult to detect on CT imaging given the isoattenuation to adjacent cerebrospinal fluid (CSF). On MRI, these may be isointense to CSF on T1 and T2 weighted sequences with some cysts showing slight FLAIR hyperintensity compared to CSF. A patient presented to our centre with headaches and cervical spine tenderness. CT demonstrated a large septated cystic mass expanding the fourth ventricle. On MRI, a multiseptated cystic structure is seen within the fourth ventricle, with a calcified mural nodule, most consistent with intraventricular NCC. Supratentorial hydrocephalus with transependymal flow of CSF was noted on MRI and ultimately the patient underwent ventriculostomy catheter placement for decompression.

Fig 13: Top Row: Axial CT of the head (left), axial thin slice T2 weighted MRI sequence of the brain (centre), and axial susceptibility weighted MRI sequence (right) demonstrates expansile cysticerci within the fourth ventricle. A scolex is noted within one of the cysticercus (arrows) with associated susceptibility, indicating mineralisation. Bottom Row: Sagittal contrast enhanced MRI sequence (left) and axial FLAIR MRI sequence (right) demonstrates supratentorial hydrocephalus secondary to expansile obstructive cysticerci in the fourth ventricle. FLAIR image demonstrates transependymal flow of CSF.

Reactivation of the calcified nodular previously quiescent NCC has also been described in the literature in a handful of isolated case reports [6-8].The term reactivation may serve as a misnomer; unlike tuberculosis, NCC is not typically thought to reactivate - the parasite dies within the central nervous system leading to its calcification on imaging. A patient with known nodular calcified NCC of the left frontal lobe presented with new generalised seizures, with imaging features concerning for reactivation.

Fig 14: Screen Left: Axial CT of the head (left) and axial T2 weighted MRI sequence (right) demonstrate parenchymal calcifications with associated susceptibility artifact in the left frontal lobe, consistent with nodular calcified neurocysticercosis (arrows). Screen Right: Axial CT of the head (A), axial T2 weighted MRI sequence (B), axial susceptibility weighted MRI sequence (C), and axial contrast enhanced MRI sequence (D), demonstrated perilesional vasogenic oedema surrounding the region of known nodular calcified neurocysticercosis. There is enhancement associated in the region of the calcifications (arrow).
This complication is characterised with worsening oedema and enhancement surrounding the calcified remnant of the dead larval parasite. It is currently unclear what the pathologic mechanism is behind this “reactivation”. Current theories describe possible antigen leak from the dead larva as a possible explanation for this pathophysiology and imaging findings. Although more research into this clinical entity is required, radiologists should be aware of the pertinent imaging findings which may explain new neurological symptoms in a patient with known calcified nodular NCC.
GALLERY