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Ocular Cysticercosis Clinical Presentation

  • Author: Smita Menon-Mehta, MBBS, DO, FRCS(Glasg); Chief Editor: Hampton Roy, Sr, MD  more...
Updated: Nov 30, 2015


See Physical.



Ocular cysticercosis may affect almost all eye tissues. The vitreous cavity, subretinal space, and subconjunctival space are common sites, while involvement of other regions (eg, extraocular muscles, optic nerve) is relatively less common.[8]

While either eye may be affected, bilateral involvement is rare.[10] Multiple cysts may develop in the same eye.[11]

Ocular manifestations may be devastating as the cysticercus enlarges. The cysticercus may lead to blindness in 3-5 years.[12] Decreased vision, pain, and recurrent redness of the involved eye are common symptoms of intraocular cysticercosis.

Clinically, the cyst appears as a well-defined translucent mass with a dense white spot (scolex) at one region. When alive, the cyst appears motile due to larval invagination or evagination. This motility is absent if the larvae are dead. A live cyst can induce intraocular inflammation because of its motility. Cyst death causes the release of toxic products, which induce a severe inflammatory reaction. The cyst becomes less translucent with a surrounding inflammatory membrane.

The cyst usually presents in the subretinal space or vitreous cavity, where it can be observed ophthalmoscopically. The site of entry into the eye is most probably the choroidal vasculature, from which the cyst migrates into the subretinal space, bores a hole in the retina, and enters the vitreous cavity. This passage incites inflammation, leaving behind a chorioretinal scar.[13] Other sites of entry include the ciliary and retinal blood vessels. Within the vitreous cavity, the cyst may be free-floating[14, 15] and may produce vitritis.

Apart from uveitis,[16] cysticercosis may also lead to retinal hemorrhages, proliferative vitreoretinopathy, retinal detachment, disc edema, cyclitic membrane formation, and phthisis. In individuals with intense inflammation in which the cyst cannot be clinically visualized, imaging modalities help in making the diagnosis.

Cysticerci may develop in the anterior chamber. In these instances, they may produce iridocyclitis and secondary glaucoma.[17] The cyst may be freely mobile or may be attached by inflammatory membranes to surrounding structures, such as the cornea, lens capsule, or iris.[18] The cyst may enter the anterior chamber either from the posterior ciliary arteries or from the angle. Intraocular inflammation may also cause cataract formation[19] and iris atrophy.

Subconjunctival cysticercosis usually presents as a painful, yellowish, nodular subconjunctival mass with surrounding conjunctival congestion. Spontaneous extrusion of an anterior subconjunctival cyst has been reported.[20, 21] Subconjunctival cysticercosis may even present as an eyelid nodule.

Acquired strabismus, diplopia, recurrent redness, and painful proptosis are some of the clinical signs in patients with orbital cysticercosis. One or more extraocular muscles may be simultaneously involved, although a propensity for involvement of the superior muscle complex and the lateral rectus muscles has been reported.[22, 23] Depending on the muscle involved, clinical findings of Duane retraction syndrome or Brown syndrome may be observed. Blepharoptosis may occur due to the presence of the cyst in the superior muscle complex. An intraorbital cyst may cause decreased vision due to external compression of the eyeball.[24]

Optic nerve compression by the cyst may cause decreased vision and disc edema. Optic nerve cysticercosis produces similar symptoms.[23] Lacrimal canalicular obstruction due to adnexal cysticercus has also been reported.[25]



Factors facilitating the spread of T solium infection include inadequate sanitation, breeding pigs in unsanitary conditions, and eating uncooked pork.

Risk factors include a family history of parasitic infestation, history of travel to an endemic area, or household visitors from an endemic area.

Contributor Information and Disclosures

Smita Menon-Mehta, MBBS, DO, FRCS(Glasg) Consulting Staff, Department of Ophthalmology, Bahrain Specialist Hospital

Smita Menon-Mehta, MBBS, DO, FRCS(Glasg) is a member of the following medical societies: All India Ophthalmological Society

Disclosure: Nothing to disclose.

Specialty Editor Board

Simon K Law, MD, PharmD Clinical Professor of Health Sciences, Department of Ophthalmology, Jules Stein Eye Institute, University of California, Los Angeles, David Geffen School of Medicine

Simon K Law, MD, PharmD is a member of the following medical societies: American Academy of Ophthalmology, Association for Research in Vision and Ophthalmology, American Glaucoma Society

Disclosure: Nothing to disclose.

Chief Editor

Hampton Roy, Sr, MD Associate Clinical Professor, Department of Ophthalmology, University of Arkansas for Medical Sciences

Hampton Roy, Sr, MD is a member of the following medical societies: American Academy of Ophthalmology, American College of Surgeons, Pan-American Association of Ophthalmology

Disclosure: Nothing to disclose.

Additional Contributors

Richard W Allinson, MD Associate Professor, Department of Ophthalmology, Texas A&M University Health Science Center; Senior Staff Ophthalmologist, Scott and White Clinic

Richard W Allinson, MD is a member of the following medical societies: American Academy of Ophthalmology, American Medical Association, Texas Medical Association

Disclosure: Nothing to disclose.

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CT scanning of the orbit demonstrating cysticercus within the medial rectus muscle observed as a hypodense area with a central hyperdensity suggestive of the scolex.
B-scan ocular ultrasonography demonstrating cysticercus within an extraocular muscle observed as a well-defined cystic mass with a central hyperechoic area.
MRI of the orbit demonstrating deep orbital cysticercus within superior muscle complex observed as a hypointense area with central hyperintensity compressing the optic nerve posteriorly.
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