Brain Pathology Case of the Month - January 2004

DIAGNOSIS:   Neurocysticercosis

DISCUSSION: Crush preps for intraoperative consultation of suspected parenchymal brain neoplasms has been recommended. This is to facilitate accurate interpretation of the cellular components of the lesion as well as the underlying tissue architecture (4). Crush preparation has been reported to improve the sensitivity and specificity of diagnosing cystic brain lesions in revealing malignant cells has also been reported (5). The crush smear in this case revealed a prominent inflammatory tissue reaction in the absence of malignant cells. The abundance of foreign body giant cells in conjunction with parasitic tissue elements prompted the search for scolex and hooklets that verified the diagnosis of neurocysticercosis.

The solitary parenchymal lesion seen in this case is one in a spectrum of pathologic features found in neurocysticercosis. Neurocysticercosis rarely causes death. Patients are often asymptomatic (7). However, when this disorder causes neurologic symptoms, the infestation may present as a ring-enhancing lesion or be a cystic lesion on CT and/or MRI imaging. This case has features of both. Such lesions lead to surgical excision for establishing the diagnosis and planning further care.

Neurocysticercosis presenting as a single ring enhancing lesion-prompting surgery for suspected malignancy has been documented (6). In this case a solitary lesion demonstrated both cystic and solid components. The solid component containing the degenerative parasite was likely responsible for symptomatology. The parasite typically dies 2 to 6 years after infection leading to leakage of parasite antigens into surrounding tissue, stimulating a vigorous inflammatory response (8). A viable cysticercus tends to be asymptomatic (2).

Neurocysticercosis is the most common parasitic infection of the central nervous system worldwide (2). This pleomorphic clinical entity is also a leading cause of acquired symptomatic epilepsy in the world (8). The disease is caused by Taenia solium, the pork tapeworm, which is endemic in Mexico, Central ans South America, Eastern Europe, and various parts of Asia (2). An increase in travel and immigration of people from endemic areas has lead to a recent increase in the incidence of the disease in the United States (3).


  1. Carrangelo B., Erra S., Del Basso De Caro ML, Bucciero A, Vizioli L, Panagiotopoulos K, and Cerillo A (2001) Neurocysticercosis Case Report. J Neurosurg Sci 45:43-6.
  2. Davis LE and Kornfeld M (1991) Neurocysticercosis: Neurologic, Pathogenic, Diagnostic, and Therapeutic Aspects. Eur Neurol 31: 229-240.
  3. Garcia HH and Del Brutto OH (2000) Taenia solium cysticercosis. Infectious Disease Clinics of North America 14: 97-117.
  4. Namiki H, Hardman J and Yang E (1997) The Central Nervous System, In: Principles and Practices of Surgical Pathology and Cytopathology, pp 2905-2906, Churchill-Livingstone, Inc., New York.
  5. Mabati A, Kumar PV and Kamkarpour A (2000) Intraoperative Cytodiagnosis of metastatic brain tumors confused clinically with brain abscess. A report of three cases. Acta Cytol 44(3): 437-41.
  6. Michael AS, Levy JM, Paige ML (1990) Cysticercosis mimicking brain Neoplasm: MR and CT appearance. J Comput Assist Tomogr 14(5):708-11.
  7. Pitella JEH (1997) Neurocysticercosis. Brain Pathology 7: 681-693.
  8. Scully RE, Mark EJ, McNeely WF, Ebeling SH, Ellender SM, Peters CC (2000) Case Records of the Massachusetts General Hospital. NEJM 343(6) 420-7.

Contributed by David Wada, Michon Morita, and John M Hardman

International Society of Neuropathology