Pediatric Neurocysticercosis Clinical Presentation

  • Author: Vinod K Dhawan, MD, FACP, FRCP(C); Chief Editor: Russell W Steele, MD   more...
 
Updated: Jul 22, 2011
 

History

Several recent publications have reviewed the clinical features of neurocysticercosis.[12, 13, 14, 15, 16] The most characteristic feature in children is the acute onset of focal seizures.

Approximately 65-80% of children diagnosed with neurocysticercosis present with seizures, most often focal in nature. Often, these children are brought to medical attention within 2 days of their initial seizure. In many countries where T solium is endemic, cysticercosis is the major cause of epilepsy.

Increased intracranial pressure (due to hydrocephalus, which can occur in 15-25% of cases) causes other common clinical symptoms, including headache, nausea, and vomiting.

Less common presentations include hemiparesis, visual changes, progressive obtundation, sciatica (from cauda equina involvement), and sensory disturbances.

In a 1996 study by Rosenfeld et al of 753 children in Chicago, none presented with fever.[17]

Risk factors include the following:

  • Children who present with neurocysticercosis frequently have emigrated from an endemic area or are children of emigrants from such an area. In the past, many children were exposed to infection through Hispanic food handlers, but this occurrence is less common now.
  • Neurocysticercosis is endemic in certain communities because of poor sanitation, use of sewage for fertilizer, and lack of controlled pens for pigs.
  • If neurocysticercosis is a possible diagnosis in a child without such risk factors, question the family as to household contacts who have traveled to an endemic area. Remember that infection can precede symptoms by as much as 5 years.
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Physical

  • Most children with neurocysticercosis have normal findings on physical and neurologic examinations.
  • Some patients may present with hemiparesis due to either a cyst or Todd paralysis after a focal seizure.
  • Rarely, children may present with papilledema, hemiparesis, sensory disturbances, or palpable subdermal cysts.
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Causes

  • Larvae (cysticercus) of the tapeworm T solium cause neurocysticercosis. Larvae are acquired by ingestion of T solium ova, found in the feces of humans infected with the pork tapeworm.
  • The disease is most common in the developing world, especially in environments where sanitation is poor. Such environments exist in rural areas of Latin America, Asia, Africa, Spain, and Eastern Europe.
  • Since the 1980s, this disease has been recognized more commonly in the United States, frequently in the states of California and Texas and in the city of Chicago, where Hispanics make up a large proportion of the community. The emergence of CT scanning and MRI studies as diagnostic tools also probably accounts for the increased detection since the 1980s.
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Contributor Information and Disclosures
Author

Vinod K Dhawan, MD, FACP, FRCP(C)  Professor, Department of Clinical Medicine, University of California, Los Angeles, David Geffen School of Medicine; Chief, Division of Infectious Diseases, Rancho Los Amigos National Rehabilitation Center, Downey, California.

Vinod K Dhawan, MD, FACP, FRCP(C) is a member of the following medical societies: American College of Physicians, American Society for Microbiology, American Society of Tropical Medicine and Hygiene, Infectious Diseases Society of America, and Royal College of Physicians and Surgeons of Canada

Disclosure: Pfizer Inc Honoraria Speaking and teaching

Coauthor(s)

Eric HW Kossoff, MD  Assistant Professor, Departments of Pediatrics and Neurology, Associate Director of Pediatric Neurology Residency Program, Johns Hopkins School of Medicine

Eric HW Kossoff, MD is a member of the following medical societies: American Academy of Neurology, American Academy of Pediatrics, American Epilepsy Society, and Child Neurology Society

Disclosure: Nothing to disclose.

Specialty Editor Board

Ashir Kumar, MD, MBBS, FAAP  Professor Emeritus, Department of Pediatrics and Human Development, Michigan State University College of Human Medicine

Ashir Kumar, MD, MBBS, FAAP is a member of the following medical societies: American Association of Physicians of Indian Origin and Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Mary L Windle, PharmD  Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Leslie L Barton, MD  Professor Emerita of Pediatrics, University of Arizona College of Medicine

Leslie L Barton, MD is a member of the following medical societies: American Academy of Pediatrics, Association of Pediatric Program Directors, Infectious Diseases Society of America, and Pediatric Infectious Diseases Society

Disclosure: Nothing to disclose.

Robert W Tolan Jr, MD  Chief, Division of Allergy, Immunology and Infectious Diseases, The Children's Hospital at Saint Peter's University Hospital; Clinical Associate Professor of Pediatrics, Drexel University College of Medicine

Robert W Tolan Jr, MD is a member of the following medical societies: American Academy of Pediatrics, American Medical Association, American Society for Microbiology, American Society of Tropical Medicine and Hygiene, Infectious Diseases Society of America, Pediatric Infectious Diseases Society, Phi Beta Kappa, and Physicians for Social Responsibility

Disclosure: GlaxoSmithKline Honoraria Speaking and teaching; MedImmune Honoraria Speaking and teaching; Merck Honoraria Speaking and teaching; Sanofi Pasteur Honoraria Speaking and teaching; Baxter Healthcare Honoraria Speaking and teaching; Novartis Honoraria Speaking and teaching

Chief Editor

Russell W Steele, MD  Head, Division of Pediatric Infectious Diseases, Ochsner Children's Health Center; Clinical Professor, Department of Pediatrics, Tulane University School of Medicine

Russell W Steele, MD is a member of the following medical societies: American Academy of Pediatrics, American Association of Immunologists, American Pediatric Society, American Society for Microbiology, Infectious Diseases Society of America, Louisiana State Medical Society, Pediatric Infectious Diseases Society, Society for Pediatric Research, and Southern Medical Association

Disclosure: Nothing to disclose.

References

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Case 1: Coronal image MRI of a 6-year-old boy from Peru with single right frontal cyst.
Case 1: Axial image MRI of a 6-year-old boy from Peru with single right frontal cyst.
Case 2: MRI of a 40-year-old patient with a single parietal calcified cyst.
Case 2: CT scan of a 40-year-old patient with a single parietal calcified cyst.
Case 3: MRI of a 47-year-old man with 2 right parietal cysts, one with edema.
Case 3: MRI of a 47-year-old man with 2 right parietal cysts, one with edema, after the larger cyst had involuted.
Case 4: CT scan of 28-year-old woman with occipital headaches and diplopia; imaging reveals a superior cerebellar cyst, mild ventricular dilatation, and old calcifications in the right insular region. Image courtesy of Gholam Motamedi, MD.
Case 4: MRI of 28-year-old woman with occipital headaches and diplopia; MRI discerns prepontine and suprasellar lesions, as well as the superior cerebellar cyst. Image courtesy of Gholam Motamedi, MD.
MRI of multiple cysts. Image courtesy of the Centers for Disease Control and Prevention.
MRI of an 87-year-old patient from Europe with bitemporal lesions found incidentally. Image courtesy of Jon Poling, MD.
Two parietal lesions observed on autopsy specimen.
MRI of a 40-year-old woman with severe epilepsy and a left temporal single cyst.
MRI of a 21-year-old woman with left temporal lobe epilepsy and a single cyst.
 
 
 
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