DOS_Apr_2008

Compressive Optic Neuropathy Neuro-ophthalmology

Shailesh G.M. MD, DNB, MNAMS, Jatin Ashar MBBS, Rohit Saxena MD, Vimla Menon MS

Optic neuropathy that is caused by compression of the optic Management of compressive optic neuropathy is difficult. Many of
nerve anywhere along its course constitutes the compressive the conditions causing the compression are resistant to current
optic neuropathy. treatment. Even well-performed surgery can worsen vision.

Compressive optic neuropathies include compressive optic History
neuropathies with optic disc swelling (anterior compressive optic
neuropathies) and compressive optic neuropathies without optic Visual complaints may be somewhat vague and nonspecific. The
disc swelling (retrobulbar compressive optic neuropathies). chronicity of the lesion may be indeterminate since patients may
incidentally discover their visual loss when one eye becomes blind.
The various causes of compressive optic neuropathy include lesions Rarely patients with compressive optic neuropathy will have sudden
within the orbit, within the optic canal and rarely intracranially visual loss (eg, pituitary apoplexy, bleeding optic nerve glioma).
compress the optic nerve resulting in optic disc swelling. These
lesions could be tumors, infections, inflammations, and even • Patients with compressive optic neuropathy typically present
adnexal structures that have become enlarged by the diseases.1 with slowly progressive visual loss.

Mechanical compression of the optic nerve causes axonal death or • Compressive optic neuropathy may be found during routine
demyelination without permanent axonal injury. Tumors cause eye examination or refraction.
mechanical pressure and disrupt local perfusion causing ischemia,
which plays major role in the pathogenesis of compressive • It may be discovered following cataract surgery when the
neuropathies. Unlike other cranial nerves, optic nerve axons do not expected improvement in visual acuity does not occur.
regenerate after a lethal injury. However, successful reversal of
optic nerve or optic chiasmal compression can result in significant • Observant patients may complain of ipsilateral
improvement in visual field defects, presumably from recovery of dyschromatopsia (objects seem less bright and colors are
demyelinated and partially injured axons. Prompt diagnosis is subdued in the affected eye compared with the normal eye).
therefore important, as early intervention may offer the best chance
for visual recovery.2

Relevant anatomy

The optic nerve extends from the back of the eye, traverses through
the orbit and optic canal to the optic chiasm. The intraocular optic
nerve is about 1 mm in length, the intraorbital segment 25 mm, the
intracanalicular segment about 9 mm, and the intracranial
component is about 16 mm long (Figure 1). The optic nerve is most
vulnerable to compression where it is adjacent to or surrounded by
bone and is relatively immobile.

Clinical features

The hallmarks of compressive optic neuropathy are:

• Slowly progressive visual loss

• Relative afferent pupillary defect

• Typically a central scotoma.

However, the diagnosis of compressive optic neuropathy is often
delayed because patients may not note early symptoms, or the
visual loss is misinterpreted as optic neuritis.

Compressive optic neuropathy should be considered in the Figure 1: Anatomy of optic nerve
differential diagnosis of all corticosteroid responsive optic
neuropathies. A workup of incidentally discovered optic atrophy
should be completed to exclude a compressive lesion.

Dr. Rajendra Prasad Centre for Ophthalmic Sciences,
All India Institute of Medical Sciences, New Delhi-110029

www.dosonline.org 61

Pathophysiology Compressive lesions causing axial proptosis may result in a
hyperopic shift. Brightness perception usually is reduced in the
Mechanical compression of the nerve affected eye color vision often is reduced in the affected eye.

↓ Desaturation of hue - When a bright color, especially red, is viewed
by each eye separately, the patient usually will describe the color to
Stagnation of flow within the individual neurons, in be less vivid or washed-out in the affected eye.
Both the slow and fast phases of axoplasmic transport
Pupils - Examination of the pupils usually will reveal an ipsilateral
↓ relative afferent pupillary defect (Marcus-Gunn pupil).

Swelling of the axons Proptosis- It is best noted by viewing the globes from above the
patient’s forehead. Formal measurement of the position of the
↓ anterior surface of the cornea in relation to the lateral wall of the
orbit can be recorded with a Hertel exophthalmometer. This is a
Leakage of intracellular “soup” (water, protein, etc.) useful test in all cases of suspected optic nerve dysfunction. If more
into the extracellular space of the prelaminar optic disc than 2 millimeters of proptosis exists, a space-occupying lesion of
the orbit may be suspected, and especially in the setting of decreased
↓ orbital retropulsion. Mild proptosis often is not noticed by patients
and their physicians.
Secondary vascular changes as venous drainage via the central
Retinal vein is impeded Extraocular motility- The movement of the eye often is not affected
by conditions causing compression of the optic nerve. Disturbance
↓ of ocular motility or ptosis along with other signs of compressive
optic neuropathy may suggest an infiltrative process, inflammatory
Hypoxia and disorganization of the normal neural matrix condition, or that the location of the lesion is at the apex of the
orbit.
↓
Visual field examination- Because of the arrangement of nerve
Optic atrophy fibers as they course through the optic nerves and the chiasma, the
site of compression produces specific visual field abnormalities.
• Patients sometimes present with complaints of visual field loss. The most common defects found with compression of the optic
nerve anterior to the chiasma include enlarged blind spot, relative
• It is not uncommon in cases of compressive optic neuropathy central scotoma, and constriction. When compression of the optic
for a friend or relative to note the appearance of proptosis. chiasma occurs, a bitemporal hemianopia usually is found, although
unilateral field loss or homonymous hemianopia may occur if the
Examination lesion is prefixed or postfixed. Nearly all types of visual field
abnormalities have been reported with compression of the optic
Compressive optic neuropathy may affect visual acuity, visual fields, nerve.
pupils, brightness perception, color vision, resistance to retropulsion
of the globe, extraocular motility, and the fundus (Table 1). Dilated fundus examination- A careful examination of the optic
disc is important. Often the optic disc may appear normal or pale.
Visual acuity - Visual acuity usually is reduced in the affected eye Some degree of disc edema is typical, signs of which include
and refraction or at least pinhole acuity should be performed. hyperemia of the neural retinal rim, blurring of the disc margins,
peripapillary retinal edema, circumpapillary retinal folds (“Paton’s
Table 1: Clinical Features lines”), distention and tortuosity of the retinal vasculature, and
occasionally hemorrhages on or adjacent to the disc (“splinter
Visual acuity Reduced in the affected eye hemorrhages”). With chronic compression of the optic nerve, optic
Hyperopia atrophy results. The triad of optic disc swelling followed by optic
Decreased brightness perception atrophy, optociliary shunt veins (optochoroidal collaterals), and
Colour vision decreased progressive visual loss commonly is reported in compressive lesions
Desaturation of hue of the orbital and intracanalicular optic nerve. Optociliary collateral
vessels are noted at the disc margin. There will frequently be
Pupils RAPD (Relative Afferent increased progressive cupping of the optic nerve head similar to
Pupillary Defect) that seen in glaucoma. The main differentiating factor from
glaucomatous optic atrophy is the pallor of the remaining
Proptosis neuroretinal rim in compressive neuropathy. Optochoroidal
collaterals are not pathognomonic of optic nerve sheath
Extraocular motility Disturbance of motility meningioma and can be seen with central retinal vein occlusion,
chronic papilledema, and a variety of compressive optic nerve
Visual field Central scotoma, centrocecal lesions. A finding of unilateral optic disc swelling may be the first
scotoma sign of compressive optic neuropathy. Even in the absence of visual

Fundus examination Disc normal or pallor present
Disc swelling
Panton’s lines
Optociliary shunts
Choroidal folds

62 DOS Times - Vol. 13, No.10, April 2008

and neurologic symptoms and an otherwise unremarkable Although optic neuritis is much more common than compressive
complete ophthalmic examination, unilateral optic disc swelling optic neuropathy, both these conditions should be differentiated:
should be investigated promptly with a CT scan or MRI. If no
intracranial explanation is found, careful evaluation should be made Optic neuritis usually presents with acute or subacute visual loss in
to rule out an intraorbital or intracanalicular mass. The presence of a patient younger than 50 years and frequently is associated with
a swollen optic disc should raise the index of suspicion for a primary pain on eye movement. The vision usually improves substantially
nerve sheath meningioma. However, a great variety of tumors have in optic neuritis with or without steroid treatment.
been reported with this finding. Similarly, swollen discs have been
reported more commonly in the presence of tumors within the Compressive optic neuropathy presents as gradually progressive
orbit. Less frequently there have been reports of disc swelling with visual loss, which may not be painful. Vision may improve with
intracanalicular and intracranial tumors compressing the optic steroid treatment only to deteriorate again when steroids are
nerve. Tumors causing proptosis may result in choroidal folds. withdrawn. Compressive optic neuropathy should be considered
in the following situations:
Associated clinical signs are specific to the root cause of the disease.
For example, restriction of ocular motility is often seen in Graves’ • A patient who is suspected of having acute optic neuritis
disease, orbital cellulitis and orbital pseudotumor, but almost never continues to lose vision after 2 weeks.
encountered in neoplasms such as gliomas or meningiomas.
Carotid-cavernous fistulas result in a corkscrew-like arterialization • Disc swelling increases or optic atrophy is not seen within 6-10
of conjunctival veins, while Graves’ disease may show only modest weeks in a patient who is suspected of having anterior ischemic
conjunctival hyperemia, and orbital cellulitis presents with lids that optic neuropathy.
are literally swollen shut.
• A diagnosis of posterior ischemic optic neuropathy is being
Aetiology: Causes of compressive optic neuropathy are listed in considered in a patient.
(Table 2).
• An MRI of the optic nerves should be obtained promptly in
the situations described above. Patients with incidentally

Table 2: Causes of compressive optic neuropathy

Common causes Other causes to be considered

Primary malignancies or metastases Schwannoma

Optic nerve tumors - Optic nerve gliomas, Optic nerve Pituitary adenoma
meningiomas

Thyroid ophthalmopathy Craniopharyngioma

Cavernous hemangiomas Leukemia

Sarcoidosis Lymphoma

Trauma Aneurysms

Solid orbital tumors –Meningiomas, Hemangiomas, Schwannoma Fibrous dysplasia

Cystic tumors- Dermoid cysts, Cholesterol granuloma, Orbital hemorrhage
Mucoceles, Conjunctival orbital cysts

Inflammatory and infiltrative processes Mucocele, Orbital pseudotumor

Metastatic carcinoma, Carcinomas extending from sinuses

Apical cavernous hemangiomas and meningiomas
enlarging during pregnancy

Following use of intracranial oxidized cellulose hemostat

Fungal hypertrophic cranial pachymeningitis7

Orbital amyloidosis8, Renal osteodystrophy9

Dolichoectatic internal carotid artery, basilar artery,
sclerotic internal carotid artery

Nasal neurofibroma10

www.dosonline.org 63

discovered optic atrophy require neuroimaging to exclude a • A favorable response to treatment with corticosteroids should
possible compressive lesion. not be considered as confirmation of a diagnosis until good
quality MRI and CT scans are obtained.
Management
• A practical approach for those cases in which the MRI and/or
Investigations -Blood tests sometimes are helpful in the diagnosis CT imaging studies strongly indicate a meningioma (both
of compressive optic neuropathy. intraorbital and intracanalicular) is to follow the patient with
serial visual acuity measurements and field testing. If visual
• If thyroid ophthalmopathy is suspected, thyroid-stimulating loss progresses, consider treatment with radiation and if growth
hormone (TSH) may be helpful. continues then also consider surgery.

• An elevated angiotensin-converting enzyme may be seen in • Rapamycin, a fibroblast and T cell inhibitor has been tried in a
sarcoidosis. patient with dysthyroid optic neuropathy refractory to steroids
and orbital decompression. Further investigation of rapamycin
• An elevated prostate specific antigen (PSA) may be helpful in for treatment of dysthyroid orbitopathy is warranted.6
male patients with suspected bony orbital metastases and optic
nerve compression. Many cases of compressive optic neuropathy (eg, thyroid
ophthalmopathy, orbital pseudotumor, lymphoma & sarcoid)
Imaging Studies: Plain x-ray studies play little role in the evaluation will improve at least transiently with steroid treatment. Intravenous
of suspected optic nerve compression. Findings such as asymmetric steroids may hasten visual recovery. It may be difficult to
enlargement of the optic foramen or hyperostosis of the optic nerve withdraw steroid treatment from such patients without
canal require further workup with CT and MRI. deterioration of vision.

• CT and MRI imaging studies are the foundation for determining Surgical- Consider surgical excision or decompression as a
the cause of optic nerve compression. CT better illustrates treatment option when orbital tumors compress the optic nerve.
bony detail, and MRI better delineates soft tissue lesions. The Well circumscribed apical optic nerve tumors (eg, cavernous
two studies often offer complementary information. hemangioma) may require an orbitocranial approach.
Interpretation of both the axial and coronal views, and
occasionally sagittal projections is required. MRI of the orbit • The definitive procedure for optic neuropathy of Graves’s
should be ordered with gadolinium and fat suppression. disease is orbital decompression. Although advocates of
steroids and radiation exist, decompression is the best and
• MRI and CT scans are essential in evaluating cases of most assured way of reversing the compression aspect of this
compressive optic neuropathy. In addition to revealing the disorder.
extent and location of the lesion, the imaging characteristics of
the lesion will probably permit an experienced neuroradiologist • Optic canal decompression for tumors in the intracanalicular
to differentiate between optic nerve sheath meningiomas and area is extremely risky, and not uncommonly results in the loss
optic nerve gliomas. Optic nerve sheath meningiomas will show of any remaining vision, unless the tumor has a large exophytic
“tram tracking” on axial views and a “target sign” on coronal component.
views. Optic nerve glioma may show kinking, especially on
sagittal views. On axial views, fusiform enlargement of the • If the tumor is intimately involved with the optic nerve, as
nerve is present. On coronal views, gliomas may show diffuse often is the case with nerve sheath meningiomas, surgical
enhancement. A characteristic pattern of enlargement of the removal often results is further loss of vision. This is thought
extraocular muscles is found in thyroid ophthalmopathy. to be due to a compromise of the shared blood supply.

• Orbital ultrasound may be useful in lesions affecting the portion Complications
of the optic nerve near the globe, but such cases also should
undergo either MRI or CT scan. • Surgery to remove orbital tumors compressing the optic nerve
frequently is associated with injury to the third, fourth, and/or
Visual-evoked potential in unilateral compressive optic neuropathy: sixth cranial nerves, which may result in paralytic strabismus
Compressive optic neuropathy decreases the amplitude and and ptosis.
increases the latency of the mfVEP. The changes in latency were
similar to those seen in optic neuritis but larger than those in • Surgery to remove lesions that are intimately involved with
ischaemic optic neuropathy and glaucoma. the nerve sheath (eg, meningiomas, schwannomas) often
results in further loss of vision or blindness.
Treatment

Medical- Corticosteroids are useful in compressive optic Prognosis: Prognosis depends on the type of lesion causing
neuropathy caused by inflammation and thyroid ophthalmopathy. compression of the optic nerve, some tumors are relatively easy to
excise, while others are likely to result in loss of vision.
• Symptoms from other causes of compressive optic neuropathy
also may improve with use of corticosteroids. Patients with compressive optic neuropathy should be managed in
consultation with a neuro-ophthalmologist or orbital surgeon
• Radiation therapy often is appropriate for malignant lesions whenever possible.
and may benefit intracanalicular and possibly intraorbital
meningiomas. Prophylaxis for other eye: Prescribe polycarbonate safety glasses to

64 DOS Times - Vol. 13, No.10, April 2008

patients with compressive optic neuropathy to protect the vision in 6. Chang S, Perry JD, Kosmorsky GS, Braun WE .Rapamycin for
the remaining eye. Treatment of Refractory Dysthyroid Compressive Optic Neuropathy.
Ophthal Plast Reconstr Surg. 2007 May/June;23(3):225-226.
References
7. Ismail AR, Clifford L, Meacock WR. Compressive optic neuropathy
1. Miller NR, Newman NJ, editors. Walsh and Hoyt’s clinical neuro- in fungal hypertrophic cranial pachymeningitis. Eye. 2007
ophthalmology, 5th edition; Williams & Wilkins. Pages 247-271. Apr;21(4):568-9.

2. Martin TJ, Corbett JJ, editors. Neuro-ophthalmology in 8. Oishi A, Miyamoto K, Yoshimura N. Orbital amyloidosis-induced
ophthalmology; mosby. Pages 78-80. compressive optic neuropathy accompanied by characteristic eyelid
pigmentation.Ophthal Plast Reconstr Surg. 2006 Nov-Dec;22(6):485-
3. Kline LB, Bajandas FJ: Neuro-Ophthalmology Review Manual. 2003. 7.

4. Shields AJ, Shields CL, Scartozzi R: Survey of 1264 patients with 9. Schmidt RH, Rietz LA, Patel BC, Osborne AG, Pratt D, Digre KB.
orbital tumors and simulating lesions: the 2002 Montgomery Lecture, Compressive optic neuropathy caused by renal osteodystrophy. Case
Part 1. Ophthalmology 2004; 111(5): 997-1008. report. J Neurosurg. 2001 Oct;95(4):704-9.

5. Walsh TJ, ed: Neuro-Ophthalmology: Clinical Signs and Symptoms. 10. Chua CN, Alhady M, Ngo CT, Swethadri GK, Singh A, Tan S.Solitary
Lippincott, Williams & Wilkins; 1997. nasal neurofibroma presenting as compressive optic neuropathy.Eye.
2006 Dec;20(12):1406-8.

First Author
Shailesh G.M. MD, DNB, MNAMS

Answer Quiz No. 10

3. WAVEFRONT 2. ASPHERIC 1. FRESNEL
6. INTERFEROMETRY 5. REFRACTION 4. ABBERATION

Extra Word: OPTICS

www.dosonline.org 65

Ocular Surface Squamous Neoplasia (OSSN) Cornea

Amar Agarwal MS, FRCS, FRCOphth, Soosan Jacob MS, FRCS, DIP NB, Athiya Agarwal MD, DO

Ocular surface squamous neoplasia or OSSN includes Staining with fluorescein sodium or Rose Bengal helps in the
precancerous and cancerous epithelial lesions of the diagnosis by showing up the papillary or granular nature of the
conjunctiva and cornea, that is, dysplasia, carcinoma in situ and lesion and by delineating its extent. Anterior segment OCT may be
squamous cell carcinoma. It can consist of dysplasia, carcinoma in done to find out the extent of deep involvement as well as intra-
situ and squamous cell carcinoma. They generally occur in the ocular and angle invasion. Anterior segment OCT may be done to
interpalpebral fissure, usually at the limbus, although they may be find out the deep extent as well as intra-ocular and angle invasion.
found elsewhere. The limbal transition zone theory of OSSN
proposed by Lee and Hirst is based on the long-living and high Treatment
proliferation rate of the limbal stem cells. Any alteration here may
lead to abnormal epithelial maturation which may result in OSSN (Figure 1) without intra-ocular or orbital invasion requires a
metaplasia. Chronic exposure keratopathy secondary to long non-touch specialized technique of excision to prevent recurrence.
standing facial nerve palsy may be associated with OSSN. OSSN Prior to surgery, the limits of the lesion should be determined and
may also be associated with exposure to sunlight, fair skin, pale iris, any additional foci should be carefully looked for. En toto surgical
HPV, HIV etc. It is more aggressive and occurs at a younger age in excision for OSSN is planned.
patients with HIV.
Absolute alcohol soaked on an applicator is gently applied to the
Clincial Diagnosis entire corneal component. This causes epithelial cellular
devitalization and allows easier release of the tumor cells from
The diagnosis of OSSN is mainly clinical. It may be difficult to Bowman’s layer. 2mm outside the corneal component, a blunt blade
distinguish between intraepithelial and invasive squamous neoplasia. is used to microscopically outline the malignancy within the corneal
Patients may present with a growth, redness and irritation. Visual epithelium. The blade is then used to sweep the affected corneal
acuity is decreased once the visual axis is affected. OSSN may grow epithelium gently towards the limbus, into a scroll that rests at the
within weeks to years; in most cases, the history is of several months. limbus. (Figure 2) A pentagonal or circular conjunctival incision
based at the limbus is then made 4–6 mm outside the
OSSN lesions may be gelatinous with superficial vessels; papilliform tumor margins. The incision is carried through the underlying
with a papillary appearance; or leukoplakic with a white keratin Tenon’s fascia until the sclera is exposed so that full thickness
plaque covering the lesion. It may also be nodular in case of invasive conjuctiva and Tenon’s fascia is incorporated into the excisional
squamous cell carcinoma, or may present as a diffuse lesion biopsy. Cautery is applied to control bleeding. A superficial scleral
mimicking a chronic conjunctivitis. The lesion is usually non- incision approximately 0.2 mm in depth and 2.0 mm outside the
pigmented though pigmented OSSN may also occur. OSSN may base of the overlying adherent conjunctival mass is made and
sometimes mimic a pterygium or a pinguecula. It has also been continued anteriorly to the limbus. Lamellar dissection of this entire
known to occur in a pre-existing pinguecula or pterygium. extent of sclera is done with a crescent knife. During the
entire surgery, a dry field without BSS irrigation is maintained to
prevent tumor cell seeding. The lamellar sclera is dissected in an
attempt to remove en toto a superficial lamella of sclera, overlying
Tenon’s fascia and conjunctiva with tumor, and the scrolled corneal

Figure 1: Ocular surface squamous Figure 2: A blunt blade is used to
Neoplasia. Note the lesion on the limbus. microscopically outline the malignancy

Also see the smaller satellite lesion within the corneal epithelium

Dr. Agarwal’s Group of Eye Hospitals 69
19 Cathedral Road, Chennai

www.dosonline.org

Figure 3: Cryotherapy after tumor resection Figure 4: Amniotic membrane graft being fixed

epithelium. The entire surgery should be done without touching OSSN may spread circumferentially around the limbus in which
the tumor itself, ie., with a no touch technique. The removed case extensive surgical excision of the growth may be required. For
specimen is placed flatly on a paper, labeled according to topography lesions more than 4 clock hours in extent, an incisional biopsy may
and submitted for histopathologic studies. This prevents the be done prior to surgery to confirm the diagnosis. No-touch, alcohol
specimen from folding and allows identification of margins assisted epitheliectomy, conjunctivo-tenonectomy and superficial
histopathologically. All used instruments are then replaced with lamellar sclerectomy is done. The same procedure as described
fresh instruments for subsequent steps, to avoid contamination of earlier is done. If the deep cornea is involved, deep lamellar
healthy tissue with possible tumor cells. Cryotherapy is applied to keratectomy is also done. Double freeze thaw cryotherapy to
the margins of the remaining bulbar conjunctiva by freezing the conjunctival edges is then applied followed by an amniotic
surrounding bulbar conjunctiva as it is lifted away from the sclera membrane graft. Reconstruction may also be done using a
using the cryoprobe.(Figure 3). When the ice ball reaches a size of conjunctival limbal autograft.
4–5 mm, it is allowed to thaw and the cycle repeated once more.
The entire conjunctival margins are treated by this double freeze Chemotherapy in the form of topical mitomicin, 5-FU or interferon
thaw technique. It is not necessary to treat the corneal margins with alpha 2-b has also been used for OSSN either post-surgery or as
cryoapplication. The tumor bed is treated with absolute alchohol primary treatment. Corneal or scleral melt may develop if these
wash on cotton tip applicator and bipolar cautery, avoiding are used prior to conjunctival healing or if used excessively.
cryotherapy directly to the sclera. Using clean instruments, the
conjunctiva is undermined and either directly closed or closed with Eyes with intra-ocular invasion often require a modified enucleation
an amniotic membrane graft (Figure 4). If histopathology shows and those with orbital invasion may require exenteration. Distant
positive margins anywhere, further tissue is resected until margins metastases are rare and may involve lymph nodes, lungs or bones
are reported as negative. In case of positive corneal epithelial and may contribute to the mortality.
margins, alcohol impregnated sponge is applied and an
epitheliectomy is done in an attempt to remove the entire area of Summary
metaplasia. The tissue is sent as two separate specimens. If the
intermediate epithelium is found to be free of involvement, the Ocular surface squamous neoplasias are a surgical challenge
patient can be put on follow-up with or without topical mitomicin- requiring specialized no-touch techniques of surgery. OSSN is
C. Brachytherapy and external beam radiotherapy have also been difficult to handle, both in the physical sense and the metaphorical
used for OSSN sense and it is important that the surgeon use a minimal
manipulation technique for tumor resection to avoid transfer and
implantation of tumor cells into previously uninvolved areas.

First Author
Amar Agarwal MS, FRCS, FRCOphth

70 DOS Times - Vol. 13, No.10, April 2008

Evaluation of Intrastromal Effects of central corneal Abstracts

Injection of Voriconazole as a thickness on the efficacy of topical

Therapeutic Adjunctive for the ocular hypotensive medications

Management of Deep Recalcitrant Johnson TV, Toris CB, Fan S, Camras CB
Fungal Keratitis. Department of Ophthalmology, University of Nebraska Medical

Prakash G, Sharma N, Goel M, Titiyal JS, Vajpayee RB. Center, Omaha, Nebraska.
J Glaucoma. 2008 Mar;17(2):89-99.
Cornea and Refractive Surgery Services, Rajendra Prasad Center for
Ophthalmic Sciences, All India Institute of Medical Sciences, New PURPOSE
Delhi, India.

Am J Ophthalmol. 2008 Apr 23 [Epub ahead of print] To determine the effect of central corneal thickness (CCT) on the
efficacy of intraocular pressure (IOP)-reducing drugs in patients
PURPOSE with ocular hypertension (OHT).
To evaluate the role of intrastromal injection of voriconazole in the
management of deep recalcitrant fungal keratitis. DESIGN: METHODS
Interventional case series.
METHODS This retrospective study analyzed research records of 115 OHT
Setting patients and 97 ocular normotensive (ONT) volunteers. CCT was
Cornea services at a tertiary care teaching hospital. measured by slit-lamp pachymetry and IOP by pneumatonometry.
Patients The OHT patients were divided into Thick (>540 mum, n=52) and
Three eyes of three patients with deep stromal recalcitrant fungal Thin (</=540 mum, n=63) Cornea groups. Measurements in the
keratitis not responding to topical antifungal medications. OHT group were made after washout of all IOP-lowering drugs
Intervention Procedure and at 1 week of treatment with latanoprost 0.005%, dorzolamide
2%, brimonidine 0.2%, apraclonidine 0.5%, pilocarpine 2%, or
unoprostone 0.15% to 1 eye and vehicle contralaterally. ONT
volunteers also were divided into Thick (n=34) and Thin (n=63)
Cornea groups. Results were compared between groups using
unpaired t tests or nonparametric Wilcoxon tests and within groups
using linear regression analyses.

Voriconazole 50 micrograms/0.1 ml was injected circumferentially RESULTS
around the fungal abscess in the corneal stroma as an adjunctive to
the topical antifungal therapy. Baseline IOPs were not different between CCT groups of OHT
patients or of ONT volunteers. After 1 week of drug treatment,
Main Outcome Measure IOP was significantly (P=0.02) lower in the OHT Thin Cornea group
(16.0+/-3.0 mm Hg, mean+/-SD) than the OHT Thick Cornea group
Main outcome measure was a reduction in size of the abscess and (17.4+/-2.8 mm Hg). There was a positive correlation between IOP
resolution of the infection. and CCT (R=0.06, P=0.007) in OHT drug-treated eyes, but not
OHT vehicle-treated or ONT untreated eyes. The final IOP was
RESULTS significantly lower in the Thin than the Thick Cornea group treated
with brimonidine (P=0.02) but not with latanoprost (P=0.91).
Before the intracorneal injection, all three eyes had gradually
worsening lesions on topical medications. After the intervention, a CONCLUSIONS
faster reduction in the size of corneal infiltration was documented
and a complete resolution of the ulcers was seen within three weeks When dosed with IOP lowering drugs, eyes with thinner corneas
in all cases. had lower IOPs than eyes with thicker corneas. This suggests a
reduced efficacy of some glaucoma medications in ocular
CONCLUSION hypertensive patients with thick corneas.

Targeted delivery of voriconazole by intracorneal injection may be
a safe and effective way to treat cases of deep-seated recalcitrant
fungal keratitis responding poorly to conventional treatment
modalities.

www.dosonline.org 73

Changes in corneal endothelial Effect of diode laser

cell density and morphology after cyclophotocoagulation on

Ahmed glaucoma valve the anterior segment:

implantation during the first year an Orbscan Study

of follow-up Arikan G, Yaman A, Ozbek Z, Saatci AO, Durak I.

Kim CS, Yim JH, Lee EK, Lee NH Department of Ophthalmology, Dokuz Eylul University, Izmir,
Department of Ophthalmology, Chungnam National University Turkey.

College of Medicine, Deajeon, Korea. Cornea. 2008 Feb;27(2):152-5.

Clin Experiment Ophthalmol. 2008 Mar;36(2):142-7.
PURPOSE

PURPOSE To evaluate the effect of transscleral contact diode laser
cyclophotocoagulation (TCDLC) on corneal topography, central
To determine the effect of Ahmed glaucoma valve (AGV) corneal thickness (CCT), and anterior-chamber depth (ACD).
implantation on corneal endothelial cells.
METHODS
METHODS
The Orbscan II system was used to determine the changes in corneal
Ahmed glaucoma valves were implanted in 30 eyes of 30 patients topography, CCT, and ACD before and after TCDLC in 25 eyes of
with refractory glaucoma. Corneal endothelial cell density and shape 24 patients. RESULTS: Mean prelaser astigmatism was 4.51 +/-
was prospectively evaluated in both the subject and fellow eyes of 1.81, 4.64 +/- 3.47, and 5.40 +/- 3.04 D at central and 3- and 5-mm
each patient. Corneal specular microscopy was performed on the zones, respectively. Mean postlaser astigmatism was 4.54 +/- 2.59,
superior, superotemporal, superonasal and central corneal areas 4.75 +/- 3.33, and 5.57 +/- 3.12 D at central and 3- and 5-mm zones
before and at 1, 6 and 12 months after surgery. at 10 days and 3.99 +/- 2.01, 4.05 +/- 2.20, 5.52 +/- 4.60 D at 1 month,
respectively, showing no statistically significant difference. Prelaser
RESULTS CCT was 540.72 +/- 103.48 microm. Postlaser CCT was 617.08 +/-
86.35 microm at 10 days and 569.88 +/- 70.36 microm at 1 month.
A statistically significant decrease in average corneal endothelial CCT was significantly thicker at 10 days compared with prelaser
cell density was observed 12 months postoperatively in the subject CCT, whereas CCT at 1 month was not statistically different. ACD
eyes compared with the baseline value (P = 0.001). No such changes showed a nonsignificant decrease after TCDLC from 3.77 +/- 0.81
were observed in the fellow eyes during follow-up period. The to 3.38 +/- 0.85 mm at 10 days and 3.58 +/- 0.78 mm at 1 month.
mean percentage decrease in corneal endothelial cell density in
subject eyes was 3.5% at 1 month, 7.6% at 6 months and 10.5% at 12 CONCLUSIONS
months after surgery. The superotemporal area, which was closest
to the tube, showed the greatest decrease in endothelial cell density TCDLC does not alter corneal topography or ACD significantly.
at 1 year after surgery, while the central cornea showed the least However, CCT increases during the 10 days after TCDLC and
decrease. In terms of endothelial cell morphology, polymegathism returns to normal at 1 month, which might be related to the
and pleomorphism increased in the early postoperative periods, inflammation induced by cyclophotocoagulation. Increased CCT
and then gradually approached the preoperative status by 6 months may lead to artificially high intraocular pressure measurements
after surgery. within the first 4 weeks after surgery.

CONCLUSION

Corneal endothelial cell density progressively decreased after AGV
implantation. These findings indicate that particular care should be
taken during intraoperative and postoperative management of AGV
implantation patients in order to minimize damage to the
endothelium.

Contributed by
Shailesh G.M. MD, DNB, MNAMS

74 DOS Times - Vol. 13, No.10, April 2008

Forthcoming Events : National

July 2008 October 2008
12-13 CHENNAI 2th NEW DELHI

Indian Intraocular Implant & Refractive 13th Dr. R.K. Seth Memorial Symposium on Glaucoma
Surgery Convention Contact Person & Address
Contact Person & Address: Dr. Abhishek B. Dagar
Prof. Amar Agarwal Venu Eye Institute & Research Centre, 1/31, Sheikh Sarai
Dr. Agarwal’s Eye Hospital Institutional Area, Phase II, New Delhi-110017
19, Catheral Road, Chennai-600086 Tel.:- 011-29251155/56, 29250757, Fax - 01129252370
Tel.: 91-44-28112811,Fax: 91-44-28115871 Email : [email protected]
Email: [email protected], Website: www.iirsi2008.com [email protected]

August 2008 3-4 NEW DELHI
21-24 MUMBAI National Workshop on Strabismus
Contact Person & Address
Eye Advance 2008 Prof. Pradeep Sharma
Contact Person & Address: Dr. Rohit Saxena, Assistant Professor
Dr. Kaiki R. Mehta Room No. 485, Dr. Rajendra Prasad Centre for
World Trade Centre, Mumbai Ophthalmic Sciences, All India Institute of
The Mehta International Eye Institute Medical Sciences, Ansari Nagar, New Delhi - 110 029
Sea Side, 147, Shahid Bhagat Singh Road, Mumbai - 5 Tel.: 011-26593185, Fax: 011-26588919,
Tel.: 91- 22-22151303, Fax: 91-22-22150433 Email: [email protected]
Email: [email protected]
Website: eyeadvance.com 31st Oct. CHANDIGARH (U.T.)
2nd Nov.
October 2008
2-5 CHENNAI 18th Annual Conference of the Glaucoma
Society of India
A National Board Post Graduate Program Contact Person & Address
Contact Person & Address Dr. S.S. Pandav
Prof. Amar Agarwal Advanced Eye Centre,
Dr. Agarwal’s Eye Hospital Postgraduate Institute of Medical Education & Research,
19, Catheral Road, Chennai-600086 Chandigarh (U.T.)
Tel.: 91-44-28112811, Fax: 91-44-28115871 Telefax: 0172-2747837, Email: [email protected]
Email: [email protected]
Website: www.kalpavriksha.dragarwal.com

Forthcoming Events : International

June, 2008 July, 2008
20-22 SEOUL, KOREA 7-11 MONTREAL, CANADA

Asia Pacific Society of Ophthalmic Plastic 9th International Conference on Low Vision
and Reconstructive Surgery Annual Meeting Rehabilitation - Vision 2008
Samsung Medical Center, Seoul. Korea Montreal, Province: QC (Canada)
Contact Person: Kyung In Woo, MD Contact: Beatrice Laham
E-mail: [email protected] Phone: 514-906-1979, Fax: 514-395-1801
E-Mail: [email protected]
28th June HONG KONG
2nd July September, 2008
5-7 NEW DELHI, INDIA
XXXI International Congress of Ophthamology
Department of Ophthalmology & Visual Sciences Biennial Meeting SAARC Academy
The Chinese University of Hong Kong of Ophthalmology
Contact: India Habitat Centre, New Delhi
Ms. Angela Cho Contact: Dr. Namrata Sharma
3/F, Hong Kong Eye Hospital, 147K Argyle Street, Phone: 011-26589810,
Kowloon, Hong Kong E-Mail: [email protected]
Tel: (852) 2762-3128, Fax: (852) 2194-0695
Email: [email protected]

www.dosonline.org 77

Delhi Ophthalmological Society

(LIFE MEMBERSHIP FORM)

Name (In Block Letters) __________________________________________________________________________
S/D/W/o _____________________________________________________________ Date of Birth _____________
Qualifications _________________________________________________________ Registration No. __________
Sub Speciality (if any) ___________________________________________________________________________
ADDRESS

Clinic/Hospital/Practice ______________________________________________________________________
_______________________________________________________________ Phone __________________
Residence ________________________________________________________________________________
_______________________________________________________________ Phone __________________
Correspondence ___________________________________________________________________________
_______________________________________________________________ Phone __________________
Email ___________________________________________________________ Fax No. ________________
Proposed by
Dr. ____________________________________ Membership No. _________ Signature __________________
Seconded by
Dr. ____________________________________ Membership No. _________ Signature __________________
[Must submit a photocopy of the MBBS/MD/DO & State Medical Council / MCI Certificate for our records.]

I agree to become a life member of the Delhi Ophthalmological Society and shall abide by the Rules and
Regulations of the Society.
(Please Note : Life membership fee Rs. 3100/- payable by DD for outstation members. Local Cheques acceptable, payable
to Delhi Ophthalmological Society)
Please find enclosed Rs.___________in words ____________________________________________________ by Cash
Cheque/DD No.____________________ Dated_____________ Drawn on______________________________________

Three specimen signatures for I.D. Card. Signature of Applicant
with Date

FOR OFFICIAL USE ONLY

Dr._______________________________________________________________has been admitted as Life Member of

the Delhi Ophthalmological Society by the General Body in their meeting held on________________________________

His/her membership No. is _______________. Fee received by Cash/Cheque/DD No._______________ dated_________

drawn on __________________________________________________________________.

(Secretary DOS)

www.dosonline.org 83

INSTRUCTIONS

1. The Society reserve all rights to accepts or reject the application.

2. No reasons shall be given for any application rejected by the Society.

3. No application for membership will be accepted unless it is complete in all respects and accompanied by a Demand Draft of Rs.
3100/- in favour of “Delhi Ophthalmological Society” payable at New Delhi.

4. Every new member is entitled to received Society’s Bulletin (DOS Times) and Annual proceedings of the Society free.

5. Every new member will initially be admitted provisionally and shall be deemed to have become a full member only after formal
ratification by the General Body and issue of Ratification order by the Society. Only then he or she will be eligible to vote, or apply
for any Fellowship/Award, propose or contest for any election of the Society.

6. Application for the membership along with the Bank Draft for the membership fee should be addressed to Dr. Namrata Sharma,
Secretary, Delhi Ophthalmological Society, R.No. 474, 4th Floor, Dr. R.P. Centre for Ophthalmic Sciences, AIIMS, Ansari Nagar,
New Delhi - 110 029.

7. Licence Size Coloured Photograph is to be pasted on the form in the space provided and two Stamp/ Licence Size Coloured
photographs are required to be sent along with this form for issue of Laminated Photo Identity Card (to be issued only after the
Membership ratification).

NATIONAL SOCIETY FOR THE PREVENTION OF BLINDNESS – INDIA
Requires for its unit at

Ginni Modi Community Ophthalmomic Research Centre,
Modi Nagar (U.P.)

1. Ophthalmic Surgeon

(MS/MD/DNB (Ophth.)

With minimum 3 to 5 years experience Trained & Experienced in:

‰ Phaco Surgery ‰ Post-Segment-Medical/Surgical Retina

2. Resident Eye Surgeon

Post Graduate in Ophthalmology

3. Optometrist

B.Sc. (Ophthalmic Technique) / Diploma optometry
(with minimum 2 to 3 years experience)
Salary and compensation will be commensurate within the prevailing
standards and will not issue for deserving candidates.

Apply with full biodata to:
Secretary General,
NSPB- India, Dr. R.P. Centre, AIIMS, Ansari Nagar, New Delhi – 110 029
Or E-mail the same to [email protected]

84 DOS Times - Vol. 13, No.10, April 2008

DOS Quiz Columns

Anagram Time

Each of the following words is a jumbled ophthalmic or related term. There is, however, an extra letter in every set of letters. These
extra letters will also form a six letter ophthalmic word when unjumbled.

So get cracking.

1. LENSFIRE ___ ___ ___ ___ ___ ___ ___ ____

2. RECAPHIST ___ ___ ___ ___ ___ ___ ___ ___ ____

3. NAVWEFROST ___ ___ ___ ___ ___ ___ ___ ___ ___ ____

4. BEARBATPONI ___ ___ ___ ___ ___ ___ ___ ___ ___ ___ ____

5. CARTOONFIRE ___ ___ ___ ___ ___ ___ ___ ___ ___ ___ ____

6. CRYROMETENTFIRE ___ ___ ___ ___ ___ ___ ___ ___ ___ ___ ___ ___ ___ ___ ____

Answers on page number 65 Saurabh Sawhney DO, DNB Ashima Aggarwal MS, DNB
Insight Eye Clinic, New Delhi

www.dosonline.org 87

List of New Members

A-3046 Dr. Namrata Agarwal C-3013 Dr. Amit Chhabra JD-1361 Dr. Rachna Jain
A-3069 Dr. Smita Agarwal C-3143 Dr. Suresh Chhabra J-3205 Dr. Mitesh T. Jain
A-3129 Dr. Saurabh Agarwal CD-1391 Dr. Ameera D. Chimulkar J-3196 Dr. Ravish Jain
A-3074 Dr. Nandita Agarwal C-3256 Dr. Samiksha Choudhary JD-1381 Dr. Abhishek Jain
A-3154 Dr. Swati Agarwal C-2986 Dr. Parijat Choudhuri J-3228 Dr. Bahubali Jain
A-3160 Dr. Prateek Agarwal C-3010 Dr. Babita Chourasia A-3024 Dr. Shashi Jain Nee Agarwal
A-3222 Dr. Aman Agarwal D-2982 Dr. Shrikant Dalwadi J-3124 Dr. N.S. Jangpangi
A-3279 Dr. Bhartendu Agarwal D-3034 Dr. Sumita S. Das J-3169 Dr. Sandeep Kumar Jha
A-3128 Dr. Pallavi Agrawal D-3183 Dr. Matuli Das J-3229 Dr Amit Kumar Jha
A-3099 Dr. Kanhaiya Lal Agrawal D-3027 Dr. Nilutparna Deori J-3059 Dr. Manish Joshi
A-3158 Dr. Rashmi Agrawal D-3094 Dr. Sejal Bhavesh Desai J-3147 Dr. Rajesh Subhash Joshi
A-3185 Dr. Abhinav Agrawal D-3264 Dr. Roopalee Dhaval Desai J-3244 Dr. Manasi Jayant Joshi
A-3268 Dr. Nisha Ahuja D-3120 Dr. Pooja Deshmukh K-3089 Dr. Devayat V. Kachot
A-3000 Dr. Khilat Alvi D-3045 Dr. Chongtham Sarda Devi K-3212 Dr. Amarjeet S. Kadam
A-3056 Dr. Ahirrao Jayshree Amarraj DD-1379 Dr. Jaideep Dhama K-3213 Dr. Subhash P. Kadam
A-3017 Dr. Anuj K. Amin D-3239 Dr. Rahul Ramesh Dubewar K-3036 Dr. Sukhjiwan Kakkar
AD-1375 Dr. Anupam D-3018 Dr. Harish Dulani K-3246 Dr. Abha Vivek Kanade
AD-1356 Dr. Pratibha Arora D-3161 Dr. Jayanta Dutta K-3248 Dr. Ajay Kumar Kapoor
A-3093 Dr. Jatin N. Ashar F-3127 Dr. Mahavir Singh Faujdar V-3012 Dr. V. Anitha Karthikeyan
A-2983 Dr. Parekh Hemil Ashokkumar F-3066 Dr. Bhavesh Amrutlal Furia KD-1380 Dr. Amit Kathakual
A-3157 Dr. Ashutosh G-3005 Dr. Rahul G. K-2988 Dr. Geetwinder Kaur
A-3257 Dr. MeenakshiAtoot M-3236 Dr. Mahesh G.K. K-3118 Dr. Amanpreet Kaur
B-3220 Dr. Sandeep Bachu G-3080 Dr. (Maj.) Abha Gahlot K-3149 Dr. Mandeep Kaur
B-3021 Dr. Memuna Bahadur G-3058 Dr. Rajesh Garg K-3072 Dr. Md. Amjad Khan
B-3042 Dr. Ujwala Hansraj Baheti G-3190 Dr. Deepak Garg K-3068 Dr. Khalid Khan
BD-1359 Dr. Vishwa Jyoti Bahl G-3176 Dr. Amit Garg K-3178 Dr. Perwez Khan
BD-1387 Dr. Sudha Bajaj G-3218 Dr. Gunjan Garg K-3092 Dr. Parul Khanna
B-3047 Dr. Harshal Chunilal Baldha G-3049 Dr. Urmimala Ghatak K-3171 Dr. Manoj Khatri
B-3106 Dr. Yuvika Bansal G-3214 Dr. Pradip Kumar Ghosh K-3254 Dr. Mukesh Kumar Khatri
B-3141 Dr. Nitesh Bansal GD-1383 Dr. Uttama Ghosh k-3234 Dr. Rohini Khurana
B-3217 Dr. Pardeep Bansal GD-1352 Dr. Shilpa Goel K-3023 Dr. Sonia S. Kothari
B-3095 Dr. Ravi Daulat Barbhaya G-3261 Dr. Sheetal Goel K-3009 Dr. Saumil K. Kothari
B-3115 Dr. Manabjyoti Barman G-3273 Dr. Queen Gogoi K-2981 Dr. Swapnil Kothari
BD-1377 Dr. Rituraj Baruah G-2980 Dr. Deepika Goyal K-3122 Dr. Regu Krishnan
B-3172 Dr. Rajani Battu G-3258 Dr. Megha Goyal K-3065 Dr. Vinod Kumar
B-3016 Dr. Ranjit Singh Beniwal P-3103 Dr. S. Guha Priya K-3040 Dr. Nitish Kumar
M-3249 Dr. Mukesh Bhargava GD-1353 Dr. Kishan Kumar Gupta K-3019 Dr. Abhishek Kumar
BD-1392 Dr. Shibal Bhartiya G-3077 Dr. Madhuri S. Gupta K-2999 Dr. Sanjay Kumar
B-2985 Dr. Aditi Bhattacharyya (Bhaoyal) G-3123 Dr. Vivek Gupta K-3132 Dr. Harish Kumar
B-3133 Dr. Ashish Kumar Bichpuria GD-1370 Dr. Shalini Gupta KD-1368 Dr. Bhupal Chandra Kumar
B-3083 Dr. Anand Kumar Birjashanker GD-1372 Dr. Anushree Gupta K-3150 Dr. Ashish Kumar
B-3035 Dr. Rajendra K. Bisen G-3187 Dr. Amit Kumar Gupta K-3168 Dr. Sunil Kumar
BD-1357 Dr. Jammie B. Blah G-3194 Dr. Saroj Gupta KD-1369 Dr. Ajay Kumar
B-3137 Dr. Vinay Kumar Bohra GD-1384 Dr. Snajay Kumar Gupta K-3177 Dr. Alok Kumar
B-3015 Dr. S.S. Bundela G-3226 Dr. Prashant Gupta K-3216 Dr. Dinesh Kumar
C-3153 Dr. Anuradha Chandra G-3251 Dr. Lalit Gupta K-3204 Dr. Satish Kumar
C-3202 Dr. Navin Chandra G-3267 Dr. Rajiv Kumar Gupta K-3227 Dr. Arvind Kumar
C-3270 Dr. Dolly H. Chandra GD-1386 Dr. Shweta Gupta D-3230 Dr. (Maj.) Sanjay Kumar
CD-1358 Dr. Mayee Rishikesh Charudatta HD-1378 Dr. Madhuri Hans K-3282 Dr. Sudhir Kumar
C-2993 Dr. Sameer Vishnath Chaudhari H-3096 Dr. Galib Hasan K-3271 Dr. Rajesh Kumar
C-3043 Dr. Nilesh Sudhir Chaudhari H-3240 Dr. K. Hemalatha K-3262 Dr. Sandesh Kumar
C-3173 Dr. Ram Krishan Chaudhary H-3008 Dr. Solanki R. Hetalben KD-1390 Dr. Vasu Kumar
C-3247 Dr. Bhupendra Nath Chaudhary H-3086 Dr. Subhankar Home KD-1362 Dr. Shalini Kumari
C-2989 Dr. Rajendra Mahendra Chaudhry I-3210 Dr. (Md) Shabbirul Islam K-3281 Dr. Archana Kumari
CD-1364 Dr. Prashant Chaudhry V-2984 Dr. Jyoti V. Jadhav K-3126 Dr. Lakshmi Kuniyal
C-3100 Dr. Parul Chawla J-3125 Dr. Divya Jain LD-1382 Dr. Garima Lakhotia

www.dosonline.org 89

L-3232 Dr. K.K. Lal R-3003 Dr. Priya Dua Rajvanshi S-3192 Dr. Shilpi Singh
J-3090 Dr. Lalitha K.J. K-3272 Dr. R. Ramakrishnan S-3207 Dr. Rajinder Singh
M-3031 Dr. Kukadia Gautamkumar R-3119 Dr. Soni Shruti Ramesh S-3209 Dr. Inder Preet Singh
Maganlal P-3200 Dr. Pendukar Swati Ramesh S-3241 Dr. Preetam Singh
D-3237 Dr. Desai Beena Mahadev R-3057 Dr. Akshatha Ranganath S-3283 Dr. Sunil Kumar Singh
M-2987 Dr. Rajeev K. Mahajan R-3064 Dr. Rajiv Ranjan S-3280 Dr. Abhay Singh
MD-1371 Dr. Deepankur Mahajan R-3189 Dr. Kesharaju Anand Rao N-3277 Dr. Navpreet Singh
M-3188 Dr. Bairy Venkata Mallikarjun R-3050 Dr. R.D. Ravindran S-3276 Dr. Digvijay Singh
M-3022 Dr. Arundhati Malviya R-3193 Dr. Arindam Ray S-2992 Dr. Niha Singhal
V-3121 Dr. Manoj V. R-2979 Dr. J. Sreenivasulu Reddy S-3159 Dr. Anjini Singhal
M-3136 Dr. Kenshuk Marwah R-3275 Dr. Beeram Pradeep Kumar Reddy S-3101 Dr. Trupti Mahesh Solu
M-3020 Dr. Roopashri Matada R-3098 Dr. Nidhi Relhan S-3145 Dr. R. Srikanth
M-3151 Dr. Thomas Mathew R-3026 Dr. Parveen Kumar Rewri S-3062 Dr. T. Srinivas
M-3163 Dr. Deepti Mathur R-3114 Dr. Karandeep Rishi S-3242 Dr. Shashi Kant Srivastava
M-3225 Dr. Madhu Mathur R-3087 Dr. Sutapa Roy S-3075 Dr. V. Subashini
M-3250 Dr. Vaishali Mathur S-3224 Dr. Lakshminarayanan S. S-3112 Dr. Brahadeesh Subramanian
MD-1366 Dr. Pooja Mehta S-3260 Dr. Debarati Saha S-3253 Dr. Praveen Subudhi
M-3073 Dr. Lakshmi Nisha Menon S-2996 Dr. Sahana G.V. S-3221 Dr. Unaiza Sultana
M-3146 Dr. Peeyush Mishra S-3156 Dr. Mihir Kumar Sahoo T-3181 Dr. Priya Taank
M-3029 Dr. Rajesh Kumar Misra S-3252 Dr. Nikhileshwar Dayal Sahu T-3238 Dr. Ashok Talati
M-2994 Dr. Vaibhev Mittal S-3167 Dr. Jimit Narendrabhai Sanghavi T-3162 Dr. Hemant Kumar Taneja
M-3091 Dr. Sajit Kumar Moitra S-3170 Dr. Preeti Sankaran T-3060 Dr. Chaiti Tarafdar
M-3208 Dr. Sandeep V. Mondkar S-3082 Dr. Hemant Sankpal T-3180 Dr. Tarsem Lal Thapar
M-3243 Dr. Ifat Mujtaba S-3002 Dr. Asima Sarkar T-3006 Dr. Indra Narain Tiwari
N-3054 Dr. Anjali Nagar S-3152 Dr. Kumar Saurabh T-3174 Dr. Anil Kumar Tiwari
N-3233 Dr. D. Nalini S-3265 Dr. Parijat Saurabh T-3195 Dr. Sukhdeo Prasad Tiwari
N-3231 Dr. Madhivanan Natarajan S-3088 Dr. Swapnesh Deepak Sawant T-3097 Dr. Ajay Singh Tomar
N-3076 Dr. Atul Nath S-3070 Dr. Ram Bihari Saxena T-3165 Dr. Celine Sosan Topno
N-3131 Dr. Tirupati Nath S-3117 Dr. Priyata Seth T-3061 Dr. Svetlana Toshniwal
ND-1373 Dr. Pinky Mahanta Nath SD-1374 Dr. Racheline M.M. Shadap T-3278 Dr. Manish Baban Totey
O-3215 Dr. Dinesh Kumar Omre S-3033 Dr. Dishant Chandrakant Shah T-3048 Dr. Shubhi Tripathi
P-2990 Dr. Shivani Pahuja S-3116 Dr. Sagar Shah T-3165 Dr. Mona Tuli
PD-1355 Dr. Monika Pahwa S-3111 Dr. Aloka Shah U-3081 Dr. Syed Umair
P-3107 Dr. Sahil Pahwa S-3184 Dr. Riddhi Shah U-3055 Dr. Sanjay M. Upadhyaya
P-2991 Dr. Swati Pandey S-3219 Dr. Rushabh Aniket Shah V-3144 Dr. Patcha Usha
PD-1388 Dr. Mukti Pandey S-3197 Dr. Rupal Twinklekumar Shah P-3030 Dr. Geetha V.K.P.
P-3245 Dr. Suresh Chandra Pant S-3063 Dr. Seemarani Sharma V-3110 Dr. Raksha J. Vaishnav
P-3206 Dr. Avinash Singh Parihar S-2997 Dr. Kanika Sharma V-3138 Dr.AsifAmin Vakil
P-3175 Dr. Hardik P. Parikh S-2978 Dr. Mayank Sharma V-3007 Dr. Shobh Nath Verma
P-3004 Dr. Navin Tulsidas Patel S-3113 Dr. Neelam Sharma VD-1367 Dr. Neha Verma
P-3001 Dr. Chandradatt Patel S-3164 Dr. Surabh Sharma V-3155 Dr. D.K. Verma
P-3182 Dr. Darshana Thakorbhai Patel S-3255 Dr. Preeti Sharma VD-1376 Dr. Shiv Prakash Verma
P-3259 Dr.Amit Patel SD-1389 Dr. Madhu Bakshi Sharma V-3179 Dr. Anand Verma
P-2998 Dr. Kavita Patil S-3140 Dr. Aniket Narendra Shastri V-3235 Dr. Nidhi Verma
P-3211 Dr. Kishor Bhagwat Patil SD-1354 Dr. Prashant Shukla V-3266 Dr. Rakesh Kumar Verma
P-3201 Dr. Pratibha Bapusaheb Patil S-3186 Dr. Tapan Nikhil Shukla V-3108 Dr. Jisha Vimoj
P-3071 Dr. Sourabh Dileep Patwardhan S-3037 Dr. Atika Javed Siddiqui V-3028 Dr. Yogendra Vinayak
P-3102 Dr. Ritu Pingolia S-3053 Dr. Rinki Singh V-3011 Dr. H.S. Vishwanath
P-3148 Dr. Bhavesh R. Pokar S-3052 Dr. Awadhesh Singh V-3135 Dr. Ravi Vohra
P-3078 Dr. R. Surya Prakash S-3041 Dr. Rajbir Singh W-3223 Dr.Amit Wasil
P-3139 Dr. V. Jaya Prakash S-3025 Dr. Dilpreet Singh R-3269 Dr. Rajashekar Y.L.
P-3067 Dr.Amit Prasad S-3079 Dr. Paramjit Singh Y-2995 Dr. Pankaj Yadav
PD-1385 Dr. Anil Prasad S-3084 Dr. Pravin Kumar Singh YD-1365 Dr. Shilpa Yadav
P-3198 Dr. Eram Praveen S-3134 Dr. Parminder Singh Y-3032 Dr. Hetalkumar R. Yagnik
P-3199 Dr. S. Ranjini Priya S-3130 Dr. Reetesh Kumar Singh Y-3274 Dr. Bhamare Ganesh Yuvraj
R-3263 Dr. Raghunandan S-3104 Dr. Desh Raj Singh Z-3085 Dr. Renny Zachariah
R-3109 Dr. Lubna Amin Tamkin Rahman S-3142 Dr. Archana Singh Z-3203 Dr. Imrana Zameer
RD-1360 Dr. A.R. Rajalakshmi S-3166 Dr. Shabnam Singh Z-3039 Dr. Swati Zargar
RD-1363 Dr. Pallavee Rajbongshi S-3191 Dr. Dilip Singh

90 DOS Times - Vol. 13, No.10, April 2008

Delhi Ophthalmological Society Fellowship for Partial
Financial Assistance to Attend Conferences

Applications are invited for DOS Fellowship for partial financial assistance to attend conference(s).

Conferences Points Awarded

International: Two fellowships per year (two fellowships can be 1) Age of the Applicant Points
awarded at a time if committee feels that papers are very good)
a) < 35 years 10
• Maximum of Rs. 25,000/- per fellowship will be sanctioned
b) 36 to 45 years 07
National: Three fellowships per year (only for AIOS)
c) 45 years plus 05
• Maximum of Rs. 5,000/- per fellowship will be sanctioned 2) Type of Presentation
Eligibility
a) Instructor/ Co-instructor of Course 12
• DOS Life Members (Delhi Members only)
b) Free Paper (Oral) / Video 07
• 75 or More DCRS Points 05
c) Poster
• Accepted paper for oral presentation, poster, video or instruction 3) InstitutionalAffiliation
course.
a) Academic Institution 15
Time since last DOS Fellowship
b) Private Practitioner 20
Preference will be given to member who has not attended conference in 4) DCRS Rating in the immediate previous year
last three years. However if no applicant is found suitable the fellowship
money will be passed on to next year. Members who has availed DOS a) 75-150 05
fellowship once will not be eligible for next fellowship for a minimum
period of three years. b) > 150 08
Authorship
c) < 75 not eligible for fellowship
The fellowship will be given only to presenting author. Presenting author Documents
has to obtain certificate from all other co-authors that they are not attending
the said conference or not applying for grant for the same conference. • Proof for age. Date of Birth Certificate
(Preference will be given to author where other authors are not attending
the same conference). If there is repeatability of same author group in that • Original / attested copy of letter of acceptance of paper for oral presen-
case preference will be given to new author or new group of authors. tation / video / poster or instruction course.
Preference will also be given to presenter who is attending the conference
for the first time. • Details of announcement of the conference
Quality of Paper
• Details of both International & National Conferences attended in
The applicant has to submit abstract along with full text to the DOS previous three years.
Fellowship Committee. The committee will review the paper for its scientific
and academic standard. The paper should be certified by the head of the • Copy of letter from other national or international agency / agencies
department / institution, that the work has been carried out in the committing to bear partial cost of conference if any.
institution. In case of individual practitioner he or she should mention the
place of study and give undertaking that work is genuine. The fellowship • At least one original document should be provided, that is ticket,
committee while scrutinizing the paper may seek further clarification boarding pass or registration certificate along with attendance certifi-
from the applicant before satisfying itself about the quality and authenticity cate of the conference.
of the paper. Only Single best paper has to be submitted by the applicant
for review (6 copies). Quality of the paper will carry 50% weightage while • Fellowship Money will be reimbursed only after submission of all the
deciding the final points. required documents and verified by the committee.
Poster and Video
• Undertaking from the applicant stating that above given information’s
The applicant will need to submit poster and video for review. are true.
Credit to DOS
• If found guilty the candidate is liable to be barred for future fellow-
The presenter will acknowledge DOS partial financial assistance in ships.
the abstract book / proceedings.
The author will present his or her paper in the immediate next DOS Application should reach Secretary’s office and should be addressed to
conference and it will be published in DJO/DOS Times. President, DOS before 31st July and 31st January for International
Conference and before 30th September for National Conference. The
committee will meet thrice in a year in the month of August, October and
February with in 2 weeks of last date of receipt of applications. The
committee will reply within four week of last date of submission in yes/no
to the applicant. No fellowship will be given retrospectively, that means
prior sanction of executive will be necessary.

Dr. Namrata Sharma
Room No. 474, 4th Floor,
Dr. Rajendra Prasad Centre for Ophthalmic Sciences
All India Institute of Medical Sciences,
Ansari Nagar, New Delhi – 110029
Ph.: 91-11-65705229, Fax: 91-11-26588919
E-mail: [email protected], Website: www.dosonline.org

94 DOS Times - Vol. 13, No.10, April 2008

Outline Characteristics of Corneal Dystrophies Tearsheet

NAME OTHER LAYER OTHER HEREDITY AGE AT PROGRESSION LATERALITY
NAME
LAYERS ONSET

INVOLVED

Epith Map dot epith. None AD Any, Self limiting B/L
basement fingerprint, usually
membrane Cogan after 30 yr
dystrophy

Juvenile epith Meesman epith. None AD <1 yr Progressive to B/L
dystrophy 12q13/ middle age
17q12
KRT3/
KRT12

Ring shaped Reis Bucklers Bowman Epith., AD childhood Progressive to
ant. stroma 5q31 early middle age B/L
dystrophy layer TGFβ1

Granular Groenouw I Stroma Bowman AD <10yr Slowly B/L
dystrophy (pan) layer 5q31 progressive
TGFβ1

Lattice none Stroma Epith., AD <20 yr Slowly B/L
dystrophy (esp. ant.) Bowman 5q31 progressive sometimes
layer TGFβ1 U/L

Macular Groenouw II Stroma Epith., AR <10yr Progressive B/L
dystrophy (pan) Bowman 16q21 <1 yr B/L
layer, DM CHST6 Slowly
Central Schnyder Stroma endo. progressive
crystalline Fuchs’ (ant.) AD
dystrophy Schlicting endo Bowman
layer
Late endo.
hereditary DM, AD Middle age Progressive B/L
endo. endo. stroma, F:M=4:1 Asymmetrical
dystrophy bowman (Early onset
layer, epith COL8A2)
Posterior
polymorph DM, AD Congenital Nonprogressive B/L
dystrophy Stroma, Chr 20 or slowly Asymmetrical
Bowman progressive
layer epith

Congen. none DM, AD <2 yr Slowly B/L
hereditary Stroma, (20p11.2- congenital progressive
endo. Bowman q11.2)
dystrophy layer, epith. AR nonprogressive
(20p13)
SLC4A11

www.dosonline.org 101

POSITION EFFECT OTHER HISTOPATHOLOGY HISTO.STAIN MANAGEMENT RECUR-
IN CORNEA ON RENCE
SYMPTOMS IN GRAFT
VISION No

Usually Transient Pain of RE Maps intraepith BM; __ MRE, PTK, LK if Yes
central Dots intraepith cysts severe
F’prints intraepith BM Yes
& fibrillary material
Yes
General Transient Often nil Intracytoplasmic __ Usually nil
Sometimes vacuoles containing Yes
pain of RE fibrillary material

Central Slight at Pain of RE Subepithelial MRE , PTK, LK
first, to early microcysts
increasing middle age

Central Slight at Pain or RE Rods & filaments of Masson SK, PTK, LK, PK
first, uncommon ‘hyaline’ trichrome red in early middle
moderate age
after early
middle age

Central Slight to Pain of RE Aligned fibrils Congo red (red MRE ;PK in
of amyloid & green middle age, LK
moderate at dichroism),
birefringent
first, severe

in middle age

General Moderate to None Excess GAG Alcian blue PK in early Yes
Central severe
Cholesterol crystals Colloidal iron middle age, LK

Slight None Endo atrophic Schultz Screen for Yes
Abnormal collagen (cholesterol metabolism
post to DM blue green) abnormality, PTK

Central later None at Pain of BK Collagen layer None at first, later No
general first, in later PAS +ve manage BK, finally
Progressive stages PK
later

General None None Endothelium epitheloid; Collagen layer None No
Abnormal collagen PAS+ve Yes

post to DM

General Severe __ Endo atrophic __ Early PK
Nystagmus Abnormal collagen
post to DM

BK bullous keratopathy; B/L bilateral; DM descemets membrane; GAG glycosaminoglycan; LK lamellar keratoplasty; MRE managementof
recurrent erosion; PK penetrating keratoplasty; PTK phototherapeutic keratectomy; RE recurrent erosion; SK superficial keratectomy

Jaya Gupta DNB, Preeti Paliwal PhD, Radhika Tandon MD

Dr. Rajendra Prasad Centre for Ophthalmic Sciences, All India Institute of Medical Sciences, New Delhi-110029

102 DOS Times - Vol. 13, No.10, April 2008

Advertisement Tariff : DOS Times

Display One Issue Advertisement One Issue Advertisement
Advertisements Copies 4,500 Copies 8,500

• Full Page B&W Rs. 8,800 Rs. 11,550
• Half page B&W Rs. 5,500 Rs. 6,050
• Quarter page B&W Rs. 3,300 Rs. 4,400
• 1/8 page B&W Rs. 2,200 Rs. 3,300
• Back Inside Cover Colour Rs. 22,000 Rs. 27,500
• Full Page Colour Rs. 16,500 Rs. 19,800
• 2 Page Centre Spread B&W Rs. 22,000 Rs. 27,500
• 2 Page Centre Spread Colour Rs. 44,000 Rs. 55,000

• Discount on Long Term Booking

¾ Three issues 5 % discount

¾ Five issues 10 % discount

¾ Ten issues 20 % discount

o Two Pages ten issue additional 10% discount
o Three pages ten issues additional 15% discount
o Four pages B&W for ten issues additional 20% discount
o Four pages color ten issues Flat 50% discount

Service Tax will be charged extra @ 12.36%.

Please send your bookings at the earliest accompanied by Demand Draft in the name of
“Delhi Ophthalmological Society” payable at Delhi to Dr. Namrata Sharma, Secretary, DOS.

SPECIFICATION : : 7.5" x 10.25"
Size of Advertisement page
Frequency : Monthly (10 Issues in a year)
Model of Printing
Advertisement Material : Offset

For Color : For Black & White: Positive films
Mailing and Contact (With proper density dots)

Email : Positive films with proofs

: Dr. Namrata Sharma, Secretary, DOS
Room No. 474, 4th Floor,
Dr. R.P. Centre for Ophthalmic Sciences,
AIIMS, Ansari Nagar, New Delhi - 110029.
Ph. 011-65705229, Fax : 011-26588919

: [email protected]

www.dosonline.org 103