Frontolobular Cystic Mass and Hydrocephalus in Woman With Headache and Lethargy


A previously healthy 35-year-old woman was admitted to a New York City hospital after presenting to the emergency department (ED) with a 10- to 14-day history of generalized weakness, progressive frontal headache, and lethargy. She immigrated to Brooklyn, New York, from urban Haiti 9 years previously and had not returned to Haiti since. She denied any recent travel elsewhere and had no pets. An HIV antibody test, performed 4 months before ED presentation, was negative.

Figure 1. This CT scan ofthe brain without contrastshows a large cysticmass with multipleseptations in the rightfrontal lobe with associatedmidline shift andhydrocephalus.

Figure 2. This T1-weightedMRI scan with contrastof the brain showsthe mass extending intothe right frontal horn ofthe lateral ventricle andhigh signal in the subarachnoidspace.

A previously healthy 35-year-old woman was admitted to a New York City hospital after presenting to the emergency department (ED) with a 10- to 14-day history of generalized weakness, progressive frontal headache, and lethargy. She immigrated to Brooklyn, New York, from urban Haiti 9 years previously and had not returned to Haiti since. She denied any recent travel elsewhere and had no pets. An HIV antibody test, performed 4 months before ED presentation, was negative.

On admission, the patient's vital signs were normal. Although lethargic, she opened her eyes to and followed voice commands. Lung, heart, and abdominal examination findings were unremarkable. The patient's gait was normal and coordination was intact, as was her cranial nerve function, sensory function, and motor function in the upper and lower extremities.

The white blood cell count was 8100/µL, with 36% neutrophils and 53% lymphocytes. The C-reactive protein level was 0.6 mg/L. Erythrocyte sedimentation rate was 27 mm/h.

CT scan of the head without contrast performed in the ED revealed a large intra-axial right cystic mass with multiple septations (63 2 45 mm) in the right frontal lobe with associated midline shift and hydrocephalus (Figure 1).

An MRI scan taken on the second hospital day showed the mass extending into the right frontal horn of the lateral ventricle and high signal in the subarachnoid space consistent with meningitis (Figure 2). Treatment with phenytoin and dexamethasone was started.

The following day, the patient became more lethargic and a dilated right pupil was observed. No other focal neurological deficits were noted. She underwent craniotomy and emergent decompression.

The mass lesion from the frontal lobe was evacuated intact and was described as a cluster of clear gelatinous fluid-filled cysts with thin translucent walls.

DIAGNOSIS: Neurocysticercosis
Microscopic evaluation showed the anatomy of the cyst wall to be consistent with cysticercosis. Histological characteristics include microvilli, thin tegument, tegument nuclei, and loose connective tissue (Figure 3); however, no hooklets or scolices were visible.

Figure 3. The anatomy of the cyst wall is shown here: microvilli (A),thin tegument (B), tegument nuclei (C), and loose connective tissue(D) (hematoxylin and eosin stain, ×20).

Neurocysticercosis is caused by the consumption of food contaminated with the feces of a carrier of the tapeworm Taenia solium. The stool contains eggs of the tapeworm. When ingested and exposed to gastric acid in the human stomach, the eggs lose their protective capsule and become larval cysts, or cysticerci, that migrate through the vascular system and settle in the brain, muscle, eyes, and elsewhere. When in the brain, cysticerci can be viable for years with little indication that a parasitic infection is present.

In the developing world, neurocysticercosis is the most common cause of acquired epilepsy.1 In Mexico and Peru, for example, 12% of the persons in neurology units, including 30% to 50% of patients with seizure disorders who are seen in neurology units, have neurocysticercosis.2-6

In the United States, neurocysticercosis is increasingly reported, probably because of the rising number of immigrants infected with T solium. In New Mexico and Los Angeles, 6% and 10%, respectively, of persons who underwent brain imaging in EDs because of seizures had neurocysticercosis.2,7

Most patients with cysticercosis are asymptomatic. However, the most frequently reported symptoms are abdominal pain and distention, diarrhea, and nausea. Persons with neurocysticercosis can present with seizures, focal deficits, stroke, or encephalitis.2


  • Serology mostly has a screening or confirmatory role and should be used in conjunction with neuroimaging.
  • Enzyme-linked immunosorbent assay for T solium has cross-reactivity with Hymenolepis nana and Echi- nococcus granulosus. Even so, it is more useful when applied to samples of cerebrospinal fluid (CSF) than of serum.
  • Enzyme-linked immunoblot assay for serum has better sensitivity (98%) and specificity (100%) for detecting T solium infection. Its sensitivity in patients with only 1 degenerating cysticercus or calcified lesion decreases to 70%.2 The disadvantages of enzyme-linked immunoblot assay are lower sensitivity when using CSF samples and persistent positive results long after the death of the parasite.
  • CT is better than MRI at detecting small areas of calcification in the brain. MRI, however, is more sensitive in detecting perilesional edema and lesions in the posterior fossa, ventricles, eyes, and spinal cord; in evaluating degenerative changes in the parasite; and in visualizing scoleces.


  • Treatment of neurocysticercosis depends on the number and location of the lesions as well as the viability of the parasites.8
  • The currently accepted antiparasitic regimens are 8 days of albendazole or 15 days of praziquantel, both with simultaneous administration of corticosteroids and antiepileptic medication.8
  • Corticosteroids should be used to decrease brain edema and the inflammatory response caused by death of the parasite.8
  • Surgical therapy for neurocysticercosis is indicated for ventricular, ophthalmic, or spinal cysticercosis; a ventricular shunt should be placed for hydrocephalus or life-threatening intracranial hypertension not responsive to medical therapy.8,9
  • A giant subarachnoid cyst (greater than 50 mm in diameter) can cause life-threatening intracranial hypertension with compression and displacement of adjacent brain structures.9,10 In such cases, surgery is the treatment of choice, especially if corticosteroid therapy has failed. Medical treatment alone, however, can effectively manage giant subarachnoid cysts.

Vascular complications of neurocysticercosis are common but frequently unrecognized; most are in the form of an endarteritis involving the small vessels, but large-vessel infarcts have been documented. A high frequency of subarachnoid cysts neighboring the ischemic area also has been reported.11-13

After surgery, the patient experienced impairments in balance, gait, and cognition, and within a few days post-surgery, she experienced visual hallucinations. An MRI scan of the brain showed interval ischemic infarct of the right occipital lobe (Figure 4) although MR angiography of the brain did not show vascular lesions. An ophthalmological examination did not reveal intraocular cysts.

Figure 4. An interval ischemicinfarct of the rightoccipital lobe is shownon this axial flair MRIscan.

Serum and CSF were collected 7 days after admission. Immunoblot assays of serum for detection of cysticercosis and hydatid cyst were negative. However, immunoblot assay of CSF was positive for cysticercosis.

Three weeks after admission, an 8-day course of albendazole (400 mg bid) was started. The patient continued to receive phenytoin and dexamethasone throughout the course of albendazole therapy, which was completed without any serious adverse effects, such as mental status changes or seizures. The patient's level of functioning was continuously assessed throughout her hospitalization by physical and occupational therapy. Follow-up assessment at the time of discharge revealed significant improvement in gait, balance, and cognition. She had no focal neurological deficit when she was discharged.

Whether this case of neurocysticercosis was autochthonous could not be determined. The patient's family dynamics did not allow for the routine testing of other household members for cysticercosis; other recent contacts, if any, from areas where cysticercosis is endemic were not made known. Nevertheless, this case illustrates that neurocysticercosis should be considered in the differential diagnosis of any intracranial mass in persons from areas in which the parasitic infection is endemic.


REFERENCES1. Garcia HH, Pretell EJ, Gilman RH, et al. A trial of antiparasitic treatment to reduce the rate of seizures due to cerebral cysticercosis. N Engl J Med. 2004; 350:249-258.
2. Garcia HH, Gonzalez AE, Evans CA, et al. Taenia solium cysticercosis. Lancet. 2003;362:547-556.
3. Garcia HH, Martinez M, Gilman R, et al. Diagnosis of cysticercosis in endemic regions. The Cysticercosis Working Group in Peru. Lancet. 1991;338: 549-551.
4. Flisser A. Neurocysticercosis in Mexico. Parasitol Today. 1988;4:131-137.
5. Garcia HH, Gilman R, Martinez M, et al. Cysticercosis as a major cause of epilepsy in Peru. The Cysticercosis Working Group in Peru (CWG). Lancet. 1993;341:197-200.
6. Medina MT, Rosas E, Rubio-Donnadieu F, Sotelo J. Neurocysticercosis as the main cause of late-onset epilepsy in Mexico. Arch Intern Med. 1990;150:325-327.
7. Ong S, Talan DA, Moran GJ, et al. Neurocysticercosis in radiographically imaged seizure patients in US emergency departments. Emerg Infect Dis. 2002;8:608-613.
8. Garcia HH, Evans CA, Nash TE, et al. Current consensus guidelines for treatment of neurocysticercosis. Clin Microbiol Rev. 2002;14:747-756.
9. Proano JV, Madrazo I, Avelar F, et al. Medical treatment for neurocysticercosis characterized by giant subarachnoid cysts. N Engl J Med. 2001;345:879-885.
10. Berman JD, Beaver PC, Cheever AW, Quindlen EA. Cysticercus of 60-millimiter volume in human brain. Am J Trop Med Hyg. 1981;30:616-619.
11. Rocha MS, Brucki SM, Ferraz AC, Piccolo AC. Cerebrovascular disease and neurocysticercosis [in Portuguese]. Arq Neuropsiquiatr. 2001;59:778-783.
12. Jha S, Kumar V. Neurocysticercosis presenting as stroke. Neurol India. 2000;48:391-394.
13. Cantu C, Barinagarrementeria F. Cerebrovascular complications of neurocysticercosis. Clinical and neuroimaging spectrum. Arch Neurol. 1996;53: 233-239.

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