History
Neurocysticercosis (NC) is frequently asymptomatic. Cysticercosis of other tissues is almost always asymptomatic.
Clinical manifestations of NC are variable and dependent on the number and location of cysts as well as the host-immune response to the parasite.
The most frequent clinical manifestations are the following:
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Seizures
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Intracranial hypertension
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Focal neurological deficits
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Mental changes
A myriad of syndromes have been described, including brainstem dysfunction, cerebellar ataxia, sensory deficits, involuntary movements, stroke, dementia, and hydrocephalus.
A survey carried out in Mexico on 205 patients with NC (114 adults and 92 children younger than age 15 y) who were diagnosed by means of neuroimaging reported that seizures were more frequent in children (80% vs 56%), while headache was more frequent in the adults (27% vs 15%). [5]
Ten percent of patients present with ventricular cysts, with seizures, or with meningeal inflammation.
Symptoms include nausea, vomiting, headache, ataxia, and confusion.
Most of these clinical manifestations develop over a period of a few days, weeks, or months, with periods of remission and relapse, probably due to different evolutionary stages of the parasite.
Physical
No pathognomonic physical findings unmistakably identify a patient with NC. Virtually any neurological sign or symptom can occur, depending on the CNS location of the parasite.
Patients with cysts in the basal cisterns can present with meningeal signs, hydrocephalus, vasculitis, and stroke.
Cysticercal encephalitis with multiple parenchymal cysts (ie, associated inflammatory response, diffuse cerebral edema) is a rare presentation often seen in young girls. These patients are at a risk of developing severe neurological sequelae.
In patients with seizures, SECTL or hyperintense lesions on MRI are a common finding. The lesion is usually small, about 5-10 mm, well defined, annular or nodular, contrast enhancing, cortical or subcortical, and generally associated with perilesional edema and minimal mass effect, but without midline shift (see the image below). These patients, mainly children and young adults, have some benign and transitory clinical manifestations, predominantly partial or partial secondary generalized seizures, and occasionally Todd paresis or focal neurological deficits.
Causes
Risk factors associated with the disease include the following:
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Immigration from areas of endemic disease
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Family history of parasitic infestation
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Household visitors from an endemic area
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History of travel to an endemic area
Other diagnostic considerations include the following:
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Focal signs may occur abruptly in patients who develop a cerebral infarction as a complication of subarachnoid NC.
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Some manifestations of spinal NC are nonspecific, and the differential diagnosis with other diseases of the spinal cord is difficult on clinical grounds.
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Arachnoiditis is characterized by root pain and weakness of subacute onset. Cysts in the spinal cord parenchyma usually occur with motor and sensory deficits that vary according to the level of the lesion.
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Diffuse muscle involvement may result in a pseudohypertrophic myopathy. Patients have diffuse swelling of the muscles mimicking hypertrophy, myalgia, and muscle weakness.
Complications
Complications of neurocysticercosis (NC) include the following:
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intracranial herniation
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stroke
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status epilepticus
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hydrocephalus
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Neuroimaging in neurocysticercosis. CT scans showing different phases of neurocysticercosis. Top left: CT scan showing many calcifications and active cysts with scolices in both hemispheres. Top right: T1-weighted MRI showing 2 active cysts with the scolex in their interior (vesicular phase). Bottom left: Postcontrast CT scan showing a ring-enhancing cyst (colloidal phase) on left. Bottom right: Proton density-weighted MRI showing a thick capsule with adjacent scolex and perilesional edema (colloidal phase).
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Neuroimaging in neurocysticercosis. Natural history of neurocysticercosis. Top left: This CT scan shows a large occipital active cyst (vesicle phase), many calcifications, and small cortical cysts. Top right: After 18 months, the occipital cyst has been replaced by a calcification and the remaining cysts have disappeared. Bottom left: A single parietal nodular-enhancing lesion (transitional, nodular-granular phase) is shown. Bottom right: Six months later, the lesion has disappeared.
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Neuroimaging in neurocysticercosis. Noncontrast and contrast-enhanced CT scan of neurocysticercosis. Left: Normal noncontrast CT scan. Right: After administration of the contrast medium, the CT scan of the same patient shows a single parietal nodular-enhancing lesion (transitional, nodular phase).
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Neuroimaging in neurocysticercosis. Cysticercotic encephalitis. Left: Contrast-enhanced CT scan showing multiple, small, nodular, and annular areas of abnormal enhancement in brain parenchyma. Right: Gadolinium-enhanced T1-weighted MRI showing hyperintense lesions.
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Neuroimaging in neurocysticercosis. Cysticercus cellulosae in neurocysticercosis.
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Treatment of Neurocysticercosis
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Neuroimaging in neurocysticercosis. Cysticercus cellulosae showing the invaginated scolex in neurocysticercosis.
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Neuroimaging in neurocysticercosis. Subcortical parenchymatous cysticercosis
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Neuroimaging in neurocysticercosis. Inflammatory reaction in parenchymatous cysticercosis.
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Neuroimaging in neurocysticercosis. Antiepileptic treatment for patients with first seizure due to neurocysticercosis.
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Neuroimaging in neurocysticercosis. Probability of seizure recurrence (Kaplan-Meier curve) after a first seizure in patients with NC as function of cysticidal treatment.