{'fraction_non_alphanumeric': 0.026990913949759488, 'fraction_numerical': 0.012203812577944059, 'mean_word_length': 4.823132780082988, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Intravitreal cysticercosis presenting as neovascular glaucoma

We report two cases of intraocular cysticercosis which showed a peculiar presentation of neovascular glaucoma which is hitherto unreported. Two young adults presented with symptoms of raised intraocular pressure due to neovascular glaucoma. On dilated fundus examination both were found to have dead intravitreal cysticercosis. The cysts were removed by a three-port vitrectomy and intracameral injection of bevacizumab was given to help in the regression of rubeosis. Trabeculectomy had to be combined in one case. The intraocular pressure returned to normal. No recurrence of rubeosis was seen even after one year.


Discussion
Faulty development of lens zonules during embryogenesis is believed to be the cause of microspherophakia which can cause pupillary block glaucoma. Miotics aggravate the condition by increasing the pupillary block and allowing further forward displacement of the crystalline lens. Cycloplegics are the treatment of choice. However, laser-iridotomy, trabeculectomy, [6] were found useful in relieving angle closure glaucoma in such patients. Management of associated high myopia is always a challenge. Clear lens extraction through anterior route, pars plana lensectomy with or without IOL implantation are the treatment options for myopia and glaucoma in microspherophakia. [7][8][9] Indications for lens extraction in such cases are cataract, corneolenticular touch, high myopia, intermitt ent pupillary block and secondary glaucoma. Literature search revealed only few case reports, where clear lens phacoemulsifi cation was done with appropriate IOL implantation, with excellent postoperative visual recovery. [10,11] In the present case, pupillary block glaucoma was successfully treated with Nd:YAG-Laser PI followed by refractive error correction through clear lens extraction with IOL implantation. During the surgery, the capsulorrhexis needed an innovation in the form of using with an iris hook [ Fig. 5] to stabilize the lens. The option of stabilizing the capsular bag with capsular tension ring (CTR) could not be explored by us, because of nonavailability of such a small CTR [7] and also with apprehension that it will further reduce the capsular bag volume. The acrylic foldable lens was well accommodated in the small capsular bag with the unfolded haptics being in touch with the edge of the optics. The IOL was well centered in spite of zonular instability, but clinically phacodonesis persisted in the postoperative period, without compromising the vision. A similar procedure has been described by Khokhar et al. [10] but in their case there was residual myopia and underestimated visual potential acuitymetry result.
In the present case there was no residual myopia, suggesting that the IOL power calculation by the optical biometer using SRK-II formula as appropriate.

Introduction
Ocular cysticercosis aff ects various tissues of the eye such as the extraocular muscles, subretinal space and the vitreous. The intraocular location of the cyst causes retinal detachment, macular scarring, [1,2] retinal vasculitis and vitritis. [3] Only one case report describes cysticercosis resulting in glaucoma due to pupillary block. [4] We report here two cases of intraocular cysticercosis, which presented with neovascular glaucoma (NVG). To the best of our knowledge this is the fi rst report of NVG due to intraocular cysticercosis.

Case 1
A 26-year-old male, vegetarian by diet, presented with a history of painful decrease in vision of the right eye since 15 days. He had undergone scleral buckling fi ve years ago and was maintaining stable vision. The left eye had no light perception following long standing total retinal detachment. His best-corrected visual acuity in the right eye was 20/200. Slit-lamp biomicroscopy revealed 360-degree fl orid rubeosis, 1+ aqueous cells and fl are. Intraocular pressure (IOP) was 42 mm Hg. Gonioscopy showed open angle and 360 degrees neovascularization. Fundus examination revealed att ached retina with peripheral buckle eff ect. The inferior retina showed pigmentary changes comitant with spontaneous reatt achment. There was no evidence of any vascular occlusion. In addition an elongated cyst was seen projecting into the vitreous cavity adherent to the retina in the inferonasal quadrant of the fundus [ Fig. 1]. Mild optic disc hyperemia was noted. There was no movement of the cyst on examination and no scolex was seen even on ultrasound examination. Based on the above fi ndings a clinical diagnosis of a dead ocular cysticercus cyst with infl ammatory response and secondary     NVG was made. Immediate medical treatment was started with tab acetazolamide 250 mg four times daily, topical timolol maleate twice daily and topical brimonidine thrice daily to control the IOP. With the treatment the IOP reduced to 20 mm Hg. The patient then underwent a three-port pars plana vitrectomy. Retinal att achments of the cyst were cut. The cyst was lift ed into the vitreous cavity with a backfl ush needle and removed intact through sclerotomy. Mild scatt er laser was applied to the site of att achment. Bevacizumab (Avastin) 0.05 ml (1.25 mg) was injected intracamerally with a 30-G needle. Degenerated cysticercus was confi rmed on histopathologic evaluation. Aft er a week, there was complete regression of rubeosis with quiet anterior chamber. The IOP was controlled with topical dorzolamide and brimonidine drops. Fundus examination showed att ached retina and normal optic disc [ Fig. 2]. Gonioscopy done two weeks later revealed complete regression of the angle neovascularization. Aft er one year, the patient is maintaining 20/160 vision in the right eye with IOP of 18 mm Hg (on two medications) and no recurrence of iris or angle neovascularization.

Case 2
An 18-year-old student, non-vegetarian by diet, presented to us with complaints of episodes of decreased vision, redness and haloes in the left eye, since two months. On examination his best-corrected visual acuity was 20/40 in the left eye. Slit-lamp biomicroscopy showed ciliary congestion, corneal edema, aqueous fl are and 360 degree rubeosis iridis [ Fig. 3]. IOP was 44 mm Hg. Angle was closed for 270 degrees due to neovascularization. Fundus examination showed a white opaque cyst in the anterior vitreous cavity [ Fig. 4]. No scolex or movements of the cyst were noted. The optic nerve head showed 0.9 cupping. The retina was att ached throughout with normal vessels and macula. Ultrasound B-scan confi rmed absence of scolex. Humphrey visual fi eld test (24-2) revealed advanced fi eld loss. The right eye was normal.
The patient was started on oral acetazolamide 250mg four times daily, topical timolol maleate twice daily along with topical brimonidine thrice daily. He underwent a three-port pars plana vitrectomy. The cyst was freed from the surrounding vitreous and was removed intact using mild aspiration from the vitreous cutt er. The vitrectomy was completed in usual fashion. A trabeculectomy with Mitomicin C was then performed and intracameral injection of 1.25 mg of bevacizumab (Avastin) was given. One week postoperatively the IOP was well controlled (13 mm Hg) with complete regression of the rubeosis. Two weeks postoperatively a localized retinal detachment was noted inferiorly with a horseshoe tear. The patient was immediately operated with fl uid gas exchange with C3F8 gas and buckling of the break. The IOP remained controlled without any medications, no rubeosis was seen and retina was att ached till the last visit at six months follow-up [ Fig. 5].

Discussion
Cysticercosis is a parasitic infection caused by Cysticercus cellulosae, the larval form of cestode, Taenia Solium. [1] Ocular or adnexal involvement occurs in 13-46% of patients. [3] Reportedly 35% of the cysts are in the subretinal space, 22% in the vitreous, 22% in the subconjunctival space, 5% in the anterior segment and 1% in the orbit. [3] Among the intraocular cysts, 60% are found intravitreally and 40% are subretinal. [1] In our case the cyst was lodged over the retina in Case 1, presumably having broken through the retina at that site. In Case 2 it was seen in the anterior vitreous cavity with no retinal scar. It is postulated that such a cyst could have entered the eye through the vessels of the ciliary body. [1] The cysts did not show any movement. The central scolex was neither visible clinically, nor on ultrasound B-scan or on histopathology in both the patients. The above features and the presence of infl ammation suggest a dead and degenerating cyst. There are reports of dead and degenerating cysticerci causing severe infl ammatory reaction and ultimately loss of the eye. [5,6] The cysts are known to release toxic products that cause severe infl ammation mimicking endophthalmitis [3] and even intraocular tumor. [7] Chronic ocular infl ammation is a known etiological factor for development of rubeosis iridis and NVG. [8] Our patients may have been harboring the dead cysticercus cyst for a prolonged period causing a low-grade infl ammation which eventually led to rubeosis and NVG. No visual symptoms from the cyst were noted presumably due to the location of the cyst. In Case 1 it was in the area of retina showing spontaneous reatt achment and pigmentary changes. In Case 2 it was located quite anteriorly and peripherally and hence would not have caused any symptoms in a normal-sized pupil. As a result the patients presented with the symptoms of raised IOP due to NVG.
Removal of the cyst is mandatory to remove the source of the toxins causing infl ammation and early removal has been advocated by many authors. [1,5] However, both the cases also had NVG, which is known to be refractory to treatment. We are unaware of any previous reports of similar nature involving NVG due to intravitreal cysticercosis and could fi nd no reference to it in PUBMED search. However, recently, there have been many case reports stating the effi cacy of intracameral or intravitreal bevacizumab (Avastin, Genentech, Inc, San Francisco, CA) a recombinant, humanized anti-vascular endothelial growth factor (VEGF) antibody in the treatment of NVG due to other vascular disorders. It has been reported to cause rapid regression of rubeosis with a single application. [9][10][11] It has also been reported to improve success rate by maintaining well-functioning bleb resulting in bett er stabilization of IOP. [12,13] Bevacizumab is now being looked at as a promising adjunct for the treatment of NVG.
In our patients, removal of the causative agent viz. cysticercus would have resulted in the reversal of rubeosis, however, oft en such reversal aft er control of infl ammation is temporary and recurrence is common. [8] Also, in advanced stage such as in Case 2 where already 270 degrees of the angle was closed causing rapid, advanced fi eld loss it was essential to ensure good surgical success with long-term IOP control. Case 1 was one-eyed with the only seeing eye aff ected in this manner. This prompted us to use adjunctive bevacizumab in these two cases, to improve the immediate postoperative results. Good response was seen with no recurrence even aft er one year.