Neurocysticercosis Clinical Presentation

  • Author: Mohammed J Zafar, MD, FAAN; Chief Editor: Karen L Roos, MD   more...
 
Updated: Jun 7, 2011
 

History

Neurocysticercosis is a pleomorphic disease, although it sometimes produces no clinical manifestation. This pleomorphism is due to variations in the locations of the lesions, the number of parasites, and the host's immune response.[7]

Many patients are asymptomatic; others report vague symptoms such as headache or dizziness. The onset of symptoms is usually subacute to chronic, with the exception of seizures, which present in an acute fashion. Possible symptomatic presentations are briefly reviewed below.

Epilepsy

Epilepsy is the most common presentation (70%) of neurocysticercosis and is also a complication of the disease.[6] Neurocysticercosis is the leading cause of adult-onset epilepsy and is probably one of the most frequent causes of childhood epilepsy in the world.

Seizures secondary to neurocysticercosis may be generalized or partial. Simple and complex partial seizures may be associated with the presence of a single lesion. Generalized seizures are usually tonic-clonic; this is thought to be related to the presence of multiple lesions. However, irritation of focal cortical tissue by one of the lesions most probably leads to focal onset with secondary generalization. Myoclonic seizures also have been described.

Go to First Adult Seizure for complete information on this topic.

Headache

Headaches may be associated with intracranial hypertension and are indicative of hydrocephalus; they may also result from meningitis. Chronic headaches may be associated with nausea and vomiting (simulating migraines).

Intracranial hypertension

Most often, intracranial hypertension is due to obstruction of cerebrospinal fluid (CSF) circulation caused by basal or ventricular cysticercosis. It may also result from large cysts displacing midline structures, granular ependymitis, arachnoiditis, or the so-called cysticercotic encephalitis caused by the inflammatory response to a massive infestation of cerebral parenchyma with cysticerci. Affected patients may have seizures and deterioration of their mental status, mainly due to the host's inflammatory reaction as an exaggerated response to the massive infestation.

Diplopia may also result from intracranial hypertension or arachnoiditis producing entrapment or compression of cranial nerves III, IV, or VI.

Strokes

Ischemic cerebrovascular complications of neurocysticercosis include lacunar infarcts[8] and large cerebral infarcts due to occlusion or vascular damage. Hemorrhage can also occur and has been reported as a result of rupture of mycotic aneurysms of the basilar artery. Strokes may be responsible for paresis or plegias, involuntary movements, gait disturbances, or paresthesias.[9]

Neuropsychiatric disturbances

Neuropsychiatric dysfunction can range from poor performance on neuropsychologic tests to severe dementia. These symptoms appear to be related more to the presence of intracranial hypertension than to the number or location of parasites in the brain.

Hydrocephalus

Ten to thirty percent of patients with neurocysticercosis develop communicating 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. Noncommunicating hydrocephalus may be a consequence of intraventricular cysts.

Presentations of other forms of neurocysticercosis

Patients with intrasellar neurocysticercosis present with ophthalmologic and endocrinologic manifestations mimicking those of pituitary tumors.

Spinal neurocysticercosis is rare and may be either intramedullary or extramedullary. The extramedullary form is the most frequent and is responsible of symptoms of spinal dysfunction such as radicular pain, weakness, and paresthesias. Intramedullary presentation may cause paraparesis, sensory deficits with a level, and sphincter disturbances.

Ocular cysticercosis occurs most commonly in the subretinal space. Patients may present with decreased visual acuity, visual field defects, or monocular blindness.

Systemic cysticercosis is most common in the Asian continent. The parasites may be located in the subcutaneous tissue or muscle. Peripheral nerve involvement as well as involvement of the liver or spleen have been reported.

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Physical Examination

Twenty percent or less of infected patients with neurocysticercosis have abnormal neurologic findings. Physical findings depend on where the cyst is located in the nervous system and include the following:

  • Cognitive decline
  • Dysarthria
  • Extraocular movement palsy or paresis
  • Hemiparesis or hemiplegia, which may be related to stroke, or Todd paralysis
  • Hemisensory loss
  • Movement disorders
  • Hyper/hyporeflexia
  • Gait disturbances
  • Meningeal signs
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Contributor Information and Disclosures
Author

Mohammed J Zafar, MD, FAAN  Associate Clinical Professor of Medicine, Kalamazoo Center for Medical Studies, Michigan State University College of Human Medicine; Neurologist, Clinical Neurophysiologist and Neuroimager, Kalamazoo Nerve Center, PLLC

Mohammed J Zafar, MD, FAAN is a member of the following medical societies: American Academy of Neurology, American Association of Neuromuscular and Electrodiagnostic Medicine, American Society of Neuroimaging, Michigan State Medical Society, and Movement Disorders Society

Disclosure: Nothing to disclose.

Specialty Editor Board

Amy A Pruitt, MD  Associate Professor of Neurology, University of Pennsylvania School of Medicine; Attending Neurologist, Hospital of the University of Pennsylvania

Amy A Pruitt, MD is a member of the following medical societies: American Academy of Neurology

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Florian P Thomas, MD, MA, PhD, Drmed  Director, Spinal Cord Injury Unit, St Louis Veterans Affairs Medical Center; Director, National MS Society Multiple Sclerosis Center; Director, Neuropathy Association Center of Excellence, Professor, Department of Neurology and Psychiatry, Associate Professor, Institute for Molecular Virology, and Department of Molecular Microbiology and Immunology, St Louis University School of Medicine

Florian P Thomas, MD, MA, PhD, Drmed is a member of the following medical societies: American Academy of Neurology, American Neurological Association, American Paraplegia Society, Consortium of Multiple Sclerosis Centers, and National Multiple Sclerosis Society

Disclosure: Nothing to disclose.

Chief Editor

Karen L Roos, MD  John and Nancy Nelson Professor of Neurology, Professor of Neurological Surgery, Department of Neurology, Indiana University School of Medicine

Karen L Roos, MD is a member of the following medical societies: American Academy of Neurology and American Neurological Association

Disclosure: Nothing to disclose.

References
  1. Gubbay AD, Brophy BP, Henley S, Sage M. Neurocysticercosis. J Clin Neurosci. Apr 1998;5(2):203-7. [Medline].

  2. Sinha S, Sharma BS. Neurocysticercosis: a review of current status and management. J Clin Neurosci. Jul 2009;16(7):867-76. [Medline].

  3. Del Brutto OH, Garcia E, Talamas O, Sotelo J. Sex-related severity of inflammation in parenchymal brain cysticercosis. Arch Intern Med. Mar 1988;148(3):544-6. [Medline].

  4. Gaffo AL, Guillen-Pinto D, Campos-Olazabal P, Burneo JG. [Cysticercosis as the main cause of partial seizures in children in Peru]. Rev Neurol. Nov 16-30 2004;39(10):924-6. [Medline].

  5. Bickerstaff ER, Cloake PC, Hughes B, Smith WT. The racemose form of cerebral cysticercosis. Brain. Mar 1952;75(1):1-18. [Medline].

  6. Del Brutto OH, Santibanez R, Noboa CA, Aguirre R, Diaz E, Alarcon TA. Epilepsy due to neurocysticercosis: analysis of 203 patients. Neurology. Feb 1992;42(2):389-92. [Medline].

  7. Chaoshuang L, Zhixin Z, Xiaohong W, Zhanlian H, Zhiliang G. Clinical analysis of 52 cases of neurocysticercosis. Trop Doct. Jul 2008;38(3):192-4. [Medline].

  8. Barinagarrementeria F, Del Brutto OH. Lacunar syndrome due to neurocysticercosis. Arch Neurol. Apr 1989;46(4):415-7. [Medline].

  9. Barinagarrementeria F, Cantu C. Neurocysticercosis as a cause of stroke. Stroke. Aug 1992;23(8):1180-1. [Medline].

  10. Tian XJ, Li JY, Huang Y, Xue YP. Preliminary analysis of cerebrospinal fluid proteome in patients with neurocysticercosis. Chin Med J (Engl). May 5 2009;122(9):1003-8. [Medline].

  11. Garcia HH, Martinez SM, eds. Taenia solium Taeniasis/Cysticercosis. 2nd ed. Lima, Peru: Editorial Universo; 1999.

  12. Odermatt P, Preux PM, Druet-Cabanac M. Treatment of neurocysticercosis: a randomised controlled trial. J Neurol Neurosurg Psychiatry. Sep 2008;79(9):978. [Medline].

  13. Garg RK. Treatment of neurocysticercosis: is it beneficial?. Expert Rev Anti Infect Ther. Aug 2008;6(4):435-40. [Medline].

  14. Garcia HH, Pretell EJ, Gilman RH, Martinez SM, Moulton LH, Del Brutto OH, et al. A trial of antiparasitic treatment to reduce the rate of seizures due to cerebral cysticercosis. N Engl J Med. Jan 15 2004;350(3):249-58. [Medline].

  15. White AC Jr. New developments in the management of neurocysticercosis. J Infect Dis. May 1 2009;199(9):1261-2. [Medline].

  16. Rangel-Castilla L, Serpa JA, Gopinath SP, Graviss EA, Diaz-Marchan P, White AC Jr. Contemporary neurosurgical approaches to neurocysticercosis. Am J Trop Med Hyg. Mar 2009;80(3):373-8. [Medline].

  17. White AC Jr, Weller PF. Cestodes. In: Kasper DL, Braunwald E, Hauser S, et al, eds. Harrison's Principles of Internal Medicine. 16th ed. New York, NY: McGraw-Hill; 2004:Chapter 204.

  18. Garg RK. Medical management of neurocysticercosis. Neurol India. Dec 2001;49(4):329-37. [Medline].

  19. Sotelo J, Escobedo F, Penagos P. Albendazole vs praziquantel for therapy for neurocysticercosis. A controlled trial. Arch Neurol. May 1988;45(5):532-4. [Medline].

  20. Proano JV, Madrazo I, Avelar F, Lopez-Felix B, Diaz G, Grijalva I. Medical treatment for neurocysticercosis characterized by giant subarachnoid cysts. N Engl J Med. Sep 20 2001;345(12):879-85. [Medline].

  21. Bittencourt PR, Gracia CM, Martins R, Fernandes AG, Diekmann HW, Jung W. Phenytoin and carbamazepine decreased oral bioavailability of praziquantel. Neurology. Mar 1992;42(3 Pt 1):492-6. [Medline].

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Massive nonencephalitic neurocysticercosis. Photo courtesy of Cysticercosis Working Group in Peru.
Computed tomographic (CT) scan of the brain in a patient who presented with an episode of generalized tonic-clonic seizure. Note the calcified lesion in the left parieto-occipital region. Subsequent evaluation confirmed the diagnosis of neurocysticercosis.
T2-weighted magnetic resonance image (MRI) of the brain showing the presence of increased signal as a result of edema in the right frontal region; subsequent studies found a cysticercus in that location.
Magnetic resonance image (MRI) of the brain in a patient who presented with an episode of generalized tonic-clonic seizure. Note the cyst in the left parieto-occipital region with perilesional edema.
 
 
 
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