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Neurocysticercosis

Neurocysticercosis (NCC) is the most common parasitic disease of the nervous system. It is the most common cause for seizures in India. Every day I see 2 to 5 patients with NCC or its complications.

NCC is the result of accidental ingestion of eggs of Taenia solium (ie, pork tapeworm), due to contamination of food with fecal material. The increase in the prevalence of NCC reflects poorly on the public health system of our country. It shows that the sewage disposal is poor and unhygienic food is consumed by people.

Life cycle of T solium - T solium (pork tape worm) resides in the intestine of man and its larval (a developing stage) form (cysticerci) resides in pig. NCC is acquired through consumption of food contaminated with eggs of T solium (tape worm carrier). Eggs of tapeworm are shed in stool and contaminate food through poor hygiene. The common cause for this is improper disposal of human excreta. When eggs are ingested and exposed to gastric acid they convert into oncosphere which cross into blood vessels and migrate to the brain, muscles. Once in the brain the larval cysts (cysticerci) remain there for years as viable cysts (neurocysticercosis).

Symptom
NCC sometimes produces no clinical manifestation. This is due to variations in the locations of the lesions, the number of parasites, and the host's immune response.
- Many patients are asymptomatic
- Some report nonspecific symptoms such as headache or dizziness.
- The onset of symptoms is usually acute, subacute to chronic. Patients may present with the following:
- Epilepsy
  a. Epileptic seizures are the most common presentation
  b. NCC is the leading cause of adult-onset epilepsy and is probably one of the most frequent causes of childhood epilepsy.
  c. Seizures secondary to NCC may be generalized or partial (simple and complex partial seizures) may be associated with the presence of a single lesion. Irritation of focal cortical tissue by one of the lesions most probably leads to focal onset with secondary generalization.
- Headache
  a. Migraine like headache-Chronic headaches with nausea and vomiting
  b. Headaches associated with intracranial hypertension and indicative of hydrocephalus
  c. Headaches due to meningitis
- Intracranial hypertension (increased pressure within the skull)
  a. Most often, intracranial hypertension is due to obstruction of cerebrospinal fluid (CSF) circulation caused by cysticercosis blocking its flow. It may also result from large cysts displacing midline structures, or the so-called cysticercotic encephalitis caused by the inflammatory response to a massive infestation of cerebral parenchyma with cysticerci.
  b. These patients may have seizures and deterioration of their mental status with drowsyness and encephalopathy, mainly due to the host's inflammatory reaction as an exaggerated response to the massive infestation.
  c. Stroke like presentation
    i. Stroke may be responsible for the following signs and symptoms: weakness, involuntary movements, gait disturbances, or paresthesias.
  d. Neuropsychiatric disturbances
    i. Poor performance on neuropsychological tests to severe dementia
    ii. Due to many parasites in the brain.
  e. Double vision: This is a result of intracranial hypertension, brainstem cysticercosis, or arachnoiditis producing entrapment or compression of cranial nerves III, IV, or VI.
  f. Hydrocephalus (Increased water content in the brain)
    i. Ten to thirty percent of patients with NCC develop hydrocephalus due to inflammation and fibrosis of the arachnoid villi or inflammatory reaction to the meninges and subsequent occlusion of the foramina of Luschka and Magendie.
    ii. Noncommunicating hydrocephalus as a consequence of cysts blocking CSF flow.
- Rare presentation of NCC:
  a. Spinal NCC: This is rare. It is responsible of symptoms of spinal dysfunction such as radicular pain, weakness, and paresthesias.
  b. Ocular cysticercosis:. Patients may present with decreased visual acuity, visual field defects, or blindness.
  c. Systemic cysticercosis: The parasites may be located in the subcutaneous tissue or muscle leading to swelling. Peripheral nerve, liver or spleen involvement has been reported.

Diagnosis and workup
CT scan
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CT scan is the preferred imaging study for detection of parenchymal calcifications.
 
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Depending on the stage of evolution of the infestation, the findings are variable.
 
image
CT Scan showing multiple NCC

MRI
- MRI is the imaging modality of choice.MR is also more helpful in evaluation of cystic degeneration and pericystic inflammatory reaction.

MRI, CT findings may sometimes not be conclusive. In such situation the following tests may be done:
- Enzyme-linked immunosorbent assay (ELISA) of CSF
- Enzyme-linked immune-electrotransfer blot assay in serum Stool examination
- Tapeworm carriers may be identified by examining the stool of the patient or relatives of a patient with cysticercosis encephalitis.

Treatment
Treatment of neurocysticercosis depends upon the life stage of the cyst and its complications. Management includes symptomatic treatment as well as treatment directed against the parasite. If the parasite is dead, the treatment is directed primarily against the symptoms (e.g., anticonvulsants for management of seizures). Duration of the treatment remains undefined. Treatment duration is decided on an individual patient basis. Treating patients with viable cysts with a course of anticysticercal drugs in order to achieve better control of seizures is common practice. If the parasite is viable or active and the patient has encephalitis, a course of steroids is recommended before the use of anticysticercal drugs.

Follow up
Careful follow-up is mandatory in cases who have complications related to NCC and in which anticysticercal medications are used.