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Imaging in neurocysticercosis Balraj Dhesi,1 Sumit J Karia,1 Naghme Adab,2 Sujit Nair1

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Department of Clinical Radiology, University Hospitals Coventry and Warwickshire NHS Trust, Coventry, UK 2 Department of Neurology, University Hospitals Coventry and Warwickshire NHS Trust, Coventry, UK Correspondence to Dr B Dhesi, Department of Clinical Radiology, University Hospitals Coventry and Warwickshire NHS Trust, Coventry CV2 2DX, UK; [email protected] Accepted 27 October 2014

To cite: Dhesi B, Karia SJ, Adab N, et al. Pract Neurol Published Online First: [ please include Day Month Year] doi:10.1136/practneurol2014-000972

ABSTRACT Neurocysticercosis is a parasitic neurological infection caused by the ingestion of larvae from the adult tapeworm Taenia solium. We describe a man who presented with generalised tonicclonic seizures. He had been previously diagnosed with epilepsy in Malawi, where he had emigrated from 2 years before this episode. An MRI was performed to further investigate the cause of his seizures, as no previous imaging had been performed. His initial MRI showed multiple characteristic cystic lesions in keeping with neurocysticercosis.

Neurocysticercosis is acquired through faecal–oral contamination from a human carrier of the tapeworm, as opposed to taeniasis which is contracted via the ingestion of infected pork. It should be considered as a disease mostly transmitted from person to person contrary to

popular belief of being acquired through infected pigs. With increasing migration and world travel, clinicians should suspect neurocysticercosis in patients with seizures, headache and focal neurological deficits who have spent time in developing countries. The characteristic imaging findings should be recognised and can help to determine the stage of disease. A young man presented with generalised tonic-clonic seizures. He had been previously diagnosed with epilepsy in Malawi; he had emigrated to the UK 2 years before this episode. An MRI scan of brain (not previously performed) showed multiple characteristic cystic lesions, in keeping with neurocysticercosis. Neurocysticercosis is a parasitic neurological infection caused by the ingestion of larvae from the adult tapeworm

Figure 1 MRI scan of brain (axial T2 weighted image) showing lesions in two different stages of the disease. First, simple fluid is seen inside a cyst, as would be seen in the vesicular stage (black arrow). This patient also has mixed type lesions in the granular nodular stage. This is shown by high signal fluid with low signal seen within it. The low signal is thought to be from a mineralised scolex (white arrow).6

Dhesi B, et al. Pract Neurol 2014;0:1–4. doi:10.1136/practneurol-2014-000972

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Figure 2 MRI scan of brain (axial T1 weighted, pregadolinium and postgadolinium contrast images) showing enhancement of the cyst capsule in the colloidal vesicular phase.

Taenia solium. It is endemic in developing countries, but due to immigration and travel, it is more commonly being seen in the developed world.1 Taenia solium has a complex life cycle involving two hosts: humans and pigs. Humans can acquire two forms of infection, depending on the stage of the life cycle at which the parasite is ingested. ▸ Taeniasis: This form of infection is acquired through ingesting undercooked pork infected with parasitic cysts. The scolex ( parasitic head), once ingested, attaches to the small bowel mucosa and gives rise to multiple segments ( proglottids) to produce a tapeworm.2 This is known as taeniasis. Eventually, the proglottids, which contain parasitic eggs, shed from the worm and are excreted in faeces. Pigs then acquire the parasite by ingesting feed that is contaminated with infected human

faeces. These ingested larvae are then absorbed via the intestinal tract and spread and form cysts in the pig’s muscle, thus completing the cycle. ▸ Cysticercosis: This form of infection is acquired in the same way that pigs acquire the infection, through faecal–oral contamination of larvae from a human carrier of the tapeworm. The larvae, once ingested, lose their capsules after being exposed to gastric acid, producing larval cysts called oncospheres. These are absorbed via the gastrointestinal tract where they migrate, commonly to the brain, eyes and muscle, where they form cysts.3

Neurocysticercosis is a term used when the central nervous system is affected by cysticercosis. When it involves the brain parenchyma, the disease can be classified into four discrete disease stages: vesicular,

Figure 3 MRI scan of brain (coronal FLAIR (left) and T2-weighted (right) images) showing oedema secondary to a right-sided occipital lesion in the colloidal vesicular phase. FLAIR, fluid-attenuated sequence.

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Dhesi B, et al. Pract Neurol 2014;0:1–4. doi:10.1136/practneurol-2014-000972

NEUROIMAGING similar to cerebrospinal fluid on CT and all MR sequences. (figure 1).4 2. As the cyst breaks down, fluid from the cyst becomes proteinaceous and leaks into the surrounding tissue, causing a strong immune response: the colloidal vesicular stage. On MRI, these lesions show a thick, wellenhancing capsule following contrast with surrounding oedema (figures 2 and 3); on CT scanning they appear as hyperdense cysts.5 3. The cyst then further degenerates and oedema decreases in the granular nodular stage. MRI shows the transformation of these cysts into either nodular or mixed types. Nodular lesions have surrounding high signal on MRI, with a central nodule that has the same intensity as white matter. Mixed type lesions are high signal, with central hypointensity due to a mineralised scolex inside the cyst (figure 1). On CT this gives the ‘bull’s eye sign’ (figure 4).6 4. Finally, the cyst becomes calcified to form a granuloma in the nodular calcified stage.7 CT shows calcified lesions in the brain parenchyma (figure 4). On MRI, these are micronodular lesions that are isointense on T1-weighted images and low signal on T2-weighted images (figure 5).5 Figure 4 CT scan of head (axial unenhanced) showing lesions in two different stages of the disease. The ‘bull’s eye sign’ (white arrow) is seen in the granular nodular stage. Calcified lesions (black arrow) are seen in the nodular calcified stage.

colloidal vesicular, granular nodular and nodular calcified. 1. In the first vesicular stage, the parasite cyst membrane is intact with little or no host response. In this phase, there is simple fluid within a cyst. The fluid has characteristics

Common presenting symptoms of neurocysticercosis include seizures, headache and focal neurological deficits. It is the most common cause of acquired epilepsy in the world. Hydrocephalus, intracranial hypertension and dementia are common sequelae.8 The treatment of neurocysticercosis should be individualised depending on the presentation, stage of cyst degeneration and inflammation. Albendazole and praziquantel are commonly used anthelminthics that are particularly effective against reducing the number of parenchymal cysts and reducing long-term seizure frequency.9 Sometimes symptoms worsen after 48 hours of treatment due to cyst degeneration and oedema, for which high-dose corticosteroids are recommended. Antiepileptics are the mainstay of seizure control in neurocysticercosis.10 Surgical intervention is indicated for complicated disease, including shunt insertion and cyst removal using neuroendoscopy.11 Contributors BD and SJK reviewed literature, collated images and were involved in drafting the manuscript. NA was involved in the care of the patient and reviewed the manuscript. SN analysed the images and reviewed the manuscript. Competing interests None. Provenance and peer review Not commissioned; externally peer reviewed. Reviewed by Hadi Manji, London, UK.

REFERENCES

Figure 5 MRI scan of brain (axial T2 weighted image) showing low signal calcified micronodules in the nodular calcified stage. Dhesi B, et al. Pract Neurol 2014;0:1–4. doi:10.1136/practneurol-2014-000972

1 Sotelo J, Del Brutto OH. Review of neurocysticercosis. Neurosurg Focus 2002;12:e1. 2 García HH, Gonzalez AE, Evans CA, et al.; Cysticercosis Working Group in Peru. Taenia solium cysticercosis. Lancet 2003;362:547–56. 3 Garcia HH, Gonzalez AE, Tsang VCW, et al. Neurocysticercosis: some of the essentials. Pract Neurol 2006;6:288–97. 4 Lerner A, Shiroishi MS, Zee CS, et al. Imaging of neurocysticercosis. Neuroimaging Clin N Am 2012;22:659–76.

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NEUROIMAGING 5 Dumas JL, Visy JM, Belin C, et al. Parenchymal neurocysticercosis: follow-up and staging by MRI. Neuroradiology 1997;39:12–18. 6 Kramer LD, Locke GE, Byrd SE, et al. Cerebral cysticercosis: documentation of natural history with CT. Radiology 1989;171:459–62. 7 Giorgio CM, Medina MT, Durón R, et al. Neurocysticercosis. Epilepsy Curr 2004;4:107–11. 8 Nash TE, Garcia HH. Diagnosis and treatment of neurocysticercosis. Nat Rev Neurol 2011;7:584–94.

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9 Baird RA, Wiebe S, Zunt JR, et al. Evidence-based guideline: treatment of parenchymal neurocysticercosis: report of the Guideline Development Subcommittee of the American Academy of Neurology. Neurology 2013;80:1424–9. 10 García HH, Evans CA, Nash TE, et al. Current consensus guidelines for treatment of neurocysticercosis. Clin Microbiol Rev 2002;15:747–56. 11 Rajshekhar V. Surgical management of neurocysticercosis. Int J Surg 2010;8:100–4.

Dhesi B, et al. Pract Neurol 2014;0:1–4. doi:10.1136/practneurol-2014-000972

Imaging in neurocysticercosis.

Neurocysticercosis is a parasitic neurological infection caused by the ingestion of larvae from the adult tapeworm Taenia solium. We describe a man wh...
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