July - August 2009 Lett ers to the Editor 325

Amjad Salman, Pragya Parmar, vary signiÞ cantly. With the increasing use of MRI in all cases Vanila G Coimbatore, Rajmohan Meenakshisunderam, suspected to be a brain syndrome, CVT has been increasing Nelson Jesudasan A Christdas diagnosed. MRI is now the gold standard in the diagnosis of CVT as rightly done in this case. Institute of Ophthalmology, Joseph Eye Hospital, Tiruchirapalli - 620 001, India Visual loss in CVT maybe due to thrombotic ischemia of any structure of the visual pathway or due to pressure on the optic Correspondence to Dr. Salman Amjad, Institute of Ophthalmology, Joseph Eye Hospital, Tiruchirapalli - 620 001, India. nerve due to the transmitt ed raised intracranial pressure (ICP). E-mail: [email protected] All cases of CVT with visual loss require visual Þ eld analysis and measurement of optic nerve sheath diameter using B-scan References ultrasonography (USG). Visual loss in patients with CVT due to transmitt ed raised ICP (indicated by increased optic nerve sheath 1. Gillies MC, Simpson JM, Billson FA, Luo W, Penfold P, Chua W, et al. diameter on USG) not amenable to medical management is an Safety of an intravitreal injection of triamcinolone: Results from a indication for optic nerve sheath decompression (ONSD). ONSD randomized clinical trial. Arch Ophthalmol 2004;122:336-40. as a treatment option for the visual loss in the left eye should have 2. Thompson JT. Cataract formation and other complications of intravitreal triamcinolone acetonide for macular edema. Am J been off ered to the patient in this case, as it has been shown to [4,5] Ophthalmol 2006;141:629-37. be eff ective even in the presence of optic disc pallor. Moreover, 3. Moshfeghi DM, Kaiser PK, Scott IU, Sears JE, Benz M, Sinesterra JP, ONSD is commonly and more easily done by the medial et al. Acute endophthalmitis after intravitreal triamcinolone transconjunctival approach or the lateral orbitotomy approach acetonide injection. Am J Ophthalmol 2003;136:791-6. and not through the orbital roof as mentioned in the report.[1] 4. Degenring RF, Sauder G. Vitreous prolapse and IOL dislocation during intravitreal injection of triamcinilone acetonide. Graefes Suneetha Nithyanandam Arch Clin Exp Ophthalmol 2006;244:1043-4. Department of Ophthalmology, St John’s Medical College Hospital, 5. Chen SD, Chen FK, Patel C. Opaque coating of the intraocular Bangalore, India lens and regression of iris neovascularization following injection of triamcinolone acetonide into the anterior chamber. Clin Exp Correspondence to Dr. Suneetha Nithyanandam, Department of Ophthalmol 2006;34:803-5. Ophthalmology, St John’s Medical College Hospital, Sarjapur Road, Bangalore - 560 034, India. E-mail: [email protected] DOI: 10.4103/0301-4738.53066 References 1. Parija S, Mohapatra MM, Pattnaik BK. Polycythemia vera Polycythemia vera presenting with presenting with bilateral papilledema: A rare case report. Indian J Ophthalmol 2008;56:327-8. bilateral papilledema 2. Ferro JM, Canhao P, Stam J, Bousser MG, Barinagarrementeria F; ISCVT investigators. Prognosis of cerebral vein and dural sinus Dear Editor, thrombosis: Results of the International Study on Cerebral Vein and Dural Sinus Thrombosis (ISCVT) Stroke 2004;35:664-70. I read with interest the brief report by Parija et al.[1] and 3. Biousse V, Ameri A, Bousser MG. Isolated intracranial hypertension appreciate the manner in which the case was diagnosed and as the only sign of cerebral venous thrombosis. Neurology treatment instituted leading to good visual recovery in one eye. 2000;54:2030-6. In this regard, I would like to make the following comments. 4. Lam BL, Schatz NJ, Glaser JS, Bowen BC. Pseudotumour cerebri from cranial venous obstruction. Ophthalmology 1992;99:706-12. The clinical presentation was suggestive of raised 5. Nithyanandam S, Manayath GJ, Batt u RR. Optic nerve sheath intracranial pressure, with the diagnostic workup pointing to decompression for visual loss in intracranial hypertension: Report cerebral venous thrombosis (CVT). CVT is a relatively common from a tertiary care center in South India. Indian J Ophthalmol presentation of polycythemia vera.[2] When we reviewed the 2008;56:115-20. records of 50 CVT patients treated at our hospital over a period DOI: 10.4103/0301-4738.53067 of four years, four cases were secondary to polycythemia vera. Of these four patients three, presented with signs and symptoms similar to the reported patient. In all cases of CVT one should rule out the multiple known causes of CVT Retinitis pigmentosa associated including myeloproliferative disorders like polycythtemia with blepharophimosis, blue dot vera. [2] Hence, the presentation is not as rare as it has been alluded to in the report. cataract and primary inferior oblique This report highlights the diagnosis of an uncommon overaction: A new syndrome complex hematological condition which primarily presented to an or consummate myotonic dystrophy? ophthalmologist. CVT is often under diagnosed even by neurologists. It should be remembered that almost 40% of Dear Editor, CVT patients present with signs and symptoms suggestive of isolated intracranial.[3,4] A thorough diagnostic workup We thank the authors for their equivocations in reply to our including magnetic resonance imaging (MRI) should be done lett er.[1] The reply fails to address the inherent contradictions before labeling a case as idiopathic intracranial hypertension cloaking the report, be it clinical findings, diagnostic (IIH), as the management and outcome of these two conditions oversights or syndromic prophecy, implicitly paraphrasing