Neurocysticercosis : Clinical Picture, Diagnosis, Treatment

Introduction

• Neurocysticercosis is a type of Intracranial space-occupying lesion.
• It is an important cause of intracranial calcification
  • Calcification occurs in the later part of the disease
• Larva growing in the brain is causing vasogenic cerebral edema that can lead to seizures.
• Patients will have seizures.

• These tapeworms develop in the gut of an individual.
• It is found in both non-vegetarians and vegetarians.
• The length is 3 meters.
• Sticky segments are proglottids that attach to the person’s perianal area after he defecates.
• If he doesn't wash his hands afterward, he is at high risk of ingesting these worms, which can result in the development of adult worms in his guts again.
• This worm lives in the small intestine in the upper jejunum.
• In vegetarians → Cabbage/Lettuce in street food → If these leafy vegetables are grown in fecally contaminated soil  → which means the person ingests the eggs
• In non-vegetarians  → who eat semi-cooked pork, the larvae are ingested, and they form into adult tapeworms in the patient's GI tract.
  • These larvae can migrate out → via the bloodstream → reach the muscle area
  • The person will develop lumps/bumps
  • These lumps/bumps are intramuscular and will limit the mobility of the patient.
  • The larva cannot cross the blood-brain barrier. Hence, there will be no neurocysticercosis.
• Poor personal hygiene person having jet black and dirty nails
  • The person usually doesn't wash their hands after defecating 
  • He is more likely to ingest eggs that are under his nails
  • A person who consumes the eggs is the one whose brain will be infected
    • The eggs are coming into the bloodstream
    • Crossing the blood-brain barrier
    • Hatch into the larva
    • Develop into larva and scolex
    • In later stages, when immunity will kill the worms – intracranial calcifications can be seen.
• Cysticercosis cellulosae involves brain parenchyma, and it contributes to cerebral edema and cerebritis – seizure episodes.
• Racemose - worms are inside the ventricular and can hinder the ventricular system, hence raising the ICP and hydrocephalus in the patients.

Clinical Picture of a Seizure in Neurocysticercosis

• Recurrent episodes
• Jacksonian spread, which has involuntarily spread from the distal part to the proximal part

On Physical examination:

• GCS = 15/15
• Cranial Nerves examination was normal
• DTR was normal
• Fundus Examination: Papilledema ±
• Lumps and bumps all over the body
• There is a possibility of focal neurological deficit (weakness)
• The last step after examinations is to Admit the patient and perform their workup.

Work Up

• To rule out the evidence of neurocysticercosis, LP was performed, and the CSF sample was obtained.
• CSF immunoblot, not CSF ELIZA, for NCC antigen
• Imaging = Gadolinium-enhanced MRI

• Starry sky appearance.
• There will be black spots: hypointense lesion.
• Inside this black spot is a white spot known as scolex.
• As the lesion progresses, a greyish area is seen around. Evidence of cerebral edema is seen.

• Immunity kills the worm, and it becomes disintegrated.
• Patients become symptomatic.
• If you evaluate the patient after 6 months, the black spot will have become white-calcified, killing the whole worm.

Also Read: Acute Kidney Injury (AKI) in Adults

Linking Microbial Aspects with Radiology

• Black spots are the vesicular stage of development of worm
• The subsequent stage would be called Colloidal vesicular
  • Cerebral edema is developed
• When the grey area progresses, and cerebral edema increases it is termed as a granular nodular format.
• The white spot Calcification is termed in nodular calcified format.
  • The patient will become symptomatic at colloidal vesicular and granular nodular stages.
  • The patient might deteriorate or worsen.

Absolute Criteria for NCC 

• There should be a histopathological demonstration of the parasite: brain parenchyma or CSF.
• Fundus examination shows Subretinal cysticercosis 
• Neuroimaging is done using  gadolinium enhanced MRI.
  • It will show Scolex/ evidence of vasogenic cerebral edema.

X-ray of Bilateral Lower Extremities

• Evaluate the lumps and bumps.
• Lesions were diffusely present, the larva was dead and calcified.
• This is known as Rice Grain Calcification.

Differential Diagnosis between Cysticercus Granuloma and Tuberculoma

Treatment

1. Load the patient with steroid - IV Dexamethasone
   1. To reduce hypersensitivity.
   2. To reduce cerebral edema component (Vasogenic cerebral edema).
   3. After 48 hours, when cerebral edema subsides, start with albendazole.
   4. Steroids for a few days to 8 weeks.
2. Albendazole: not concurrently but sequentially
   1. Duration - 8 days
3. Focal seizures: Carbamazepine/ lamotrigine/ oxcarbazepine
   1. AED: asymptomatic for 2 years, then gradual withdrawal 
   2. Never stop antiepileptic drugs immediately
4. Raise ICP: Ventriculoperitoneal shunting
   1. Give Dexamethasone
   2. Suppress cerebral edema
   3. Start albendazole 

It is a simple yet complex disease, as the patient is usually misdiagnosed. The only way to control it is to make a timely diagnosis and complete the proper treatment for Neurocysticercosis. This topic is very important for the NEET PG/ FMGE examination, and at least one sure-shot question can be expected from it. 

To get a better understanding of the topic, it is advised that you watch the “intracranial space-occupying lesion” video from the medicine section which is taught by Dr. Deepak Marwah.

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