Write a short note on neurocysticercosis.

Definition and Aetiology

Neurocysticercosis (NCC) is infection of the central nervous system by the larval stage (cysticercus) of the pork tapeworm *Taenia solium*. It is the commonest parasitic disease of the CNS worldwide and, critically for Indian practice, the leading cause of acquired epilepsy in India and other endemic regions.

The life cycle explains everything about the disease:

• Definitive host — humans, who harbour the adult tapeworm in the intestine after eating undercooked pork containing cysticerci, causing taeniasis (usually asymptomatic) and passing eggs in faeces.
• Intermediate host — pigs, which ingest eggs and develop cysticerci in muscle.
• Humans become accidental intermediate hosts by ingesting EGGS — through faeco-oral transmission from a tapeworm carrier, contaminated food or water, or autoinfection. The embryos penetrate the intestinal wall and disseminate haematogenously to brain, muscle, eye and subcutaneous tissue.

The crucial public health point: cysticercosis is acquired from human faeces containing eggs, NOT from eating pork. Eating undercooked pork gives you the tapeworm; eating food contaminated by a tapeworm carrier's faeces gives you cysticercosis. Vegetarians can therefore develop neurocysticercosis — a fact frequently misunderstood and often examined.

Pathogenesis and Stages

Symptoms arise mainly from the host inflammatory response to degenerating cysts, not from viable cysts, which are often silent. Four stages are recognised on imaging:

1. Vesicular — viable cyst with a clear fluid-filled vesicle and an eccentric scolex; little surrounding inflammation

2. Colloidal vesicular — the cyst begins to degenerate; surrounding oedema and ring enhancement appear — this is the symptomatic stage

3. Granular nodular — retracting, thickened cyst wall with reducing oedema

4. Calcified nodular — the end stage: a small calcified nodule, which may still cause seizures

Clinical Features

Determined by the number, size, location and stage of the cysts and by the intensity of the inflammatory response.

• Seizures — the commonest presentation (70–90%), usually focal with or without secondary generalisation. A young adult in India presenting with a first seizure and a solitary ring-enhancing lesion has neurocysticercosis until proved otherwise.
• Headache and features of raised intracranial pressure — vomiting, papilloedema; particularly with intraventricular cysts causing obstructive hydrocephalus.
• Focal neurological deficits — depending on location.
• Cognitive decline and psychiatric symptoms.
• Racemose neurocysticercosis — grape-like clusters of cysts in the basal cisterns and ventricles, causing arachnoiditis, communicating hydrocephalus, cranial nerve palsies and stroke from vasculitis; carries a much worse prognosis and needs prolonged treatment.
• Cysticercotic encephalitis — a heavy infection with massive inflammatory response and cerebral oedema, mostly in children and young women; anthelmintics are contraindicated in this situation as they worsen the inflammation.
• Extraneural: subcutaneous nodules, muscle involvement (with the "millet-seed" calcifications on plain X-ray of the thigh), and ocular cysticercosis — which may cause visual loss.

Investigations

• Neuroimaging is the mainstay:
• CT is better for calcified lesions, which are often the only finding in chronic disease.
• MRI is superior for cysts in the posterior fossa, brainstem, ventricles and subarachnoid space, and for visualising the scolex, which is the most specific radiological sign.
• A cystic lesion with an eccentric scolex ("hole-with-dot" sign) is essentially diagnostic.
• Serology — EITB (enzyme-linked immunoelectrotransfer blot) is the most specific; ELISA is less reliable. Serology is often negative in solitary lesions and positive in past exposure, so it supports but does not establish the diagnosis.
• Fundoscopy before starting anthelmintic therapy — mandatory, to exclude ocular cysticercosis, because treatment can cause blinding inflammation within the eye.
• Stool examination for *Taenia* eggs or proglottids, and screening of household contacts for tapeworm carriage — a step routinely omitted but essential to prevent reinfection.
• Supporting: CBC (eosinophilia is often absent), and CSF examination in suspected subarachnoid disease (lymphocytic pleocytosis, raised protein, low glucose — mimicking tuberculous meningitis).

Differential diagnosis of a ring-enhancing lesion in India: tuberculoma (the principal alternative — usually larger, irregular, more oedema, often with basal meningeal enhancement), pyogenic abscess, toxoplasmosis (in HIV), primary or metastatic tumour, and fungal granuloma.

Management

1. Symptomatic treatment first — and often it is all that is needed

• Antiepileptic drugs for seizure control — the priority. Most patients with a solitary lesion do well, and drugs can often be withdrawn after the lesion resolves and the patient is seizure-free.
• Corticosteroids to control perilesional oedema and inflammation.
• Management of raised intracranial pressure and hydrocephalus — including ventriculoperitoneal shunting or endoscopic removal of intraventricular cysts.

2. Antiparasitic (cysticidal) therapy — used selectively

• Albendazole (preferred, better CNS penetration) or praziquantel, or both in combination for heavy infection.
• ALWAYS give corticosteroids before and during cysticidal therapy — killing the cysts provokes an intense inflammatory reaction that can cause seizures, cerebral oedema and clinical deterioration.
• Indications: multiple viable (vesicular or colloidal) cysts. Not indicated for calcified-only disease (the parasite is already dead), and contraindicated in cysticercotic encephalitis and untreated ocular cysticercosis.
• For solitary lesions — a common presentation in India — most resolve with antiepileptics and steroids alone, and the benefit of cysticidal therapy is modest, chiefly hastening radiological resolution.

3. Follow-up — repeat imaging at intervals to document resolution, guiding the duration of antiepileptic therapy.

Prevention

Sanitation and safe disposal of human faeces (the key measure — it breaks the cycle at its source), hand washing, washing of vegetables and salads with safe water, thorough cooking of pork, meat inspection, treatment of human tapeworm carriers (mass or targeted), improved pig husbandry preventing access to human faeces, and health education. WHO classifies *T. solium* as a potentially eradicable parasite because the cycle depends entirely on human faecal contamination.