296 Optometry, Vol 81, No 6, June 2010

leakage and PED resulting in a local defect in the RPEleading to a serous detachment of the retina. Pigmented ep-ithelial detachments maybe more common in central serouschorioretinopathy than previous believed.Case Summary: A 35-year-old man presented to theSt. Louis VAMC with a history of an acute change in visionduring his tour of combat duty after exposure to improvisedexplosive devices in Iraq in 2007. He reported blunt headtrauma against the steering wheel of a Humvee after expo-sure to a blast that hit behind his vehicle. He denied loss ofconsciousness. He reported a persistent green after-imagein both his eyes much like an after-image after flash pho-tography. Medical history was significant for deep veinthrombosis, leg pain, and depression treated with Couma-din, lotab, and Zoloft. Entering visual acuities were 20/40OD and 20/30 OS. Pupils and color vision were normalwith no color desaturation. Refraction revealed significanthyperopia with a BVA of 20/25 OD and OS. Anterior seg-ment, intraocular pressures and gonioscopy were normal.Dilated retinal examination revealed a 3/4 sized, elevated,lobulated, creamy lesion with pigment clumping juxta fo-veal OU with corresponding metamorphopsia on Amslergrid. OCT revealed classical large bilateral pigmented epi-thelial detachment s juxta foveal and distorting of the fo-veal pit OU. FA confirmed bilateral PED with pooling.Conclusion: A unique and rare case of bilateral PED fromCentral Serous Chorioretinopathy causing acute hyperopiais presented and discussed. In elderly patients the naturalcourse and prognosis of serous pigment epithelial detach-ments has been associated with progressive vision loss, oc-cult choroidal neovascularization, and disciforms scars. Inyoung individuals, PED are unusual and maybe more com-mon in Central Serous Chorioretinopathy than previouslybelieved.

Poster 61

Unusual Bilateral Upgaze Palsy Secondary toHydrocephalus

Steven J. Grondalski, O.D., and Pinky Weiser, O.D., SaintLouis Veteran Affairs Medical Center, St. Louis, Missouri

Background: Vertical gaze palsy is not well characterizedor understood. It is believed to be caused by lesions disrupt-ing corpora quadrigemia including its fibers and nuclei ofthe posterior commissure of the midbrain. Animal studiesshed light regarding vertical gaze palsy, specifically local-izing lesion to the rostral interstitial nucleus of the mediallongitudinal fasciculus and interstitial nucleus of Cajal.Here we present a case of an unusual bilateral upgaze palsysecondary to hydrocephalus.Case Summary: A 54-year-old white man presented to theSt. Louis VA Medical Center Eye clinic for cataract evalu-ation with reduced vision of his left eye. Systemically itwas significant with multiple cerebrovascular accidents,subdural hematoma, cerebral hemorrhage, left frontoparie-tal craniectomy, hydrocephalus, seizure disorder, and apha-sia. Prior ocular history was unable to obtain. Visual

acuities were 20/30 OD and 20/400 OS. Extraocular motil-ity revealed significant grade 41 restricted upgaze, traceabduction and adduction abnormality of both eyes. A smallconstant left exotropia was noted. Slit lamp examination in-dicated trace nucleus sclerotic cataracts in both eyes. Therest of the dilated eye examination was unremarkable.A computed tomography of the brain indicated enlargedleft ventricles consistent with hydrocephalus and explainedbilateral upgaze palsy where pressure of cerebrospinal fluidinduced damage to the corpora quadrigemia.Conclusion: Bilateral upgaze palsy indicates lesions in themidbrain, mostly caused by compressive or ischemicetiology. Optometrists may be the first to diagnose thesepotentially fatal brain conditions.

Poster 62

The Use of Optical Coherence Tomography (OCT) in theDiagnosis and Management of Central SerousChorioretinoapthy

Nirali Patel, O.D., Meghan Cook, O.D., Crystal DeLuca,O.D., and Nancy Shenouda-Awad, O.D., West HavenVAMC, West Haven, Connecticut

Background: Central serous chorioretinopathy (CSCR) is asyndrome characterized by serous detachment of theneurosensory retina in the macular region. It usually affectsmiddle-aged adults with more male predilection. Themost common symptom is unilateral metamorphopsia;however, patients may also be asymptomatic. CSCR isthought to be idiopathic in nature, although it has beenassociated with systemic corticosteroid use as well asother systemic conditions. Clinical diagnosis isconfirmed by ancillary tests such as optical coherence to-mography (OCT) and fluorescein angiography (FA). Thesetests are necessary to help rule out other similarly present-ing pathologies. CSCR typically resolves spontaneouslyover time. Laser photocoagulation and photodynamic ther-apy are reserved for persisting cases past 6 months.Case Report: A 54-year-old white man presented to the op-tometry service at West Haven VAMC for a routine eye ex-amination. He reported no visual/ocular symptoms. Ocularhistory was remarkable for mild macular pigment changesOU. Visual acuities were 20/20 OD, and 20/25 OS reducedfrom prior 20/20. Amsler grid found no metamorphosiaOD, and metamorphopsia just below fixation OS. Slitlamp examination was unremarkable OU. Dilated fundusexamination showed macular retinal pigment epithelium(RPE) mottling with a suspicious hypopigmented mini-mally elevated lesion above the fovea OS. Differential diag-noses were CSCR, choroidal neovascularization, andpolypoidal choroidal vasculopathy. OCT showed macularpigment epithelium detachment (PED) OD with associatedsub-RPE fluid typical of CSCR confirming the diagnosis.The patient was then referred to the retina clinic wherehe had a FA, which found mild fluid leakage at the levelof RPE.

Poster Presentations 297

Conclusion: CSCR is characterized by a fluid detachmentof the macular layers allowing leakage into the subretinaland sub-RPE spaces. Higher levels of cortisol increasethe risk of the development of CSCR. In this case, thesymptoms fit the diagnosis of CSCR but the clinical appear-ance could have mimicked other pathologies. OCT played asignificant role in the confirmation of the initial diagnosisminimizing the need for repeat FAs during the course ofmanagement.

Poster 63

Left Homonymous Hemianopsia Secondary to BrainMetastasis From Non–Small Cell Lung Cancer

Regina L. Portocarrero, O.D., Malcom Randall VAMC,Gainesville, Florida

Background: Non–small cell lung cancer (NSCLC) is byfar the most common type of lung cancer. Metastasis tothe brain may occur and have visual consequences thatcould help make the initial diagnosis of this deadlycondition.Case Summary: A 73-year-old white man presented to ourclinic with complaints of decreased peripheral vision on hisleft side. He noticed the vision loss 3 weeks prior whiledriving after he inadvertently pulled out in front of a policecar. His past medical history was remarkable for hyperten-sion, hyperlipidemia, COPD, tobacco use disorder, andchronic sinusitis with frontal headache. He reported someweight loss over the past few months, and he complainedof poor balance, which he attributed to his poor vision.He had no history of a stroke and did not have any relatedCVA symptoms. His BCVAs were 20/301 OD and 20/251

OS. His pupils and motilities were without defects. On con-frontation visual fields he had a nasal defect OD and a tem-poral defect OS. The anterior segment and posteriorsegment examinations were unremarkable other than forgrade 2 nuclear sclerotic cataracts. The Humphrey visualfield test revealed a left homonymous hemianopsia. The pa-tient was referred to our emergency room for further eval-uation to rule out a stroke or mass. A CT scan wasperformed the same day, which showed a 2.5-cm lesionin the mesial portion of the right occipital lobe with mod-erate peritumoral edema and local mass effect. Recent chestx-ray showed a right upper lobe lung mass, which made thediagnosis of metastatic carcinoma likely. Further MRI ofthe brain with and without contrast was ordered as wellas consults with neurosurgery and neurology. The lung bi-opsy showed a poorly differentiated non–small cell lungcancer consistent with the primary tumor. A PET/CT scandid not reveal any other metastasis. The patient underwentstereotactic radio surgery, but unfortunately died within 3months of the diagnosis. Copies of visual fields andneuro-imaging are included.Conclusion: It is important to recognize the causes of neu-rological field defects and the proper and timely testing andreferral to elucidate the etiology.

Poster 64

Leutic Optic Neuropathy Masquerading as Glaucoma

Krishna Morar, O.D., Rebecca Rojas, O.D., and Brian Hall,O.D., SUNY State College of Optometry, New York, NewYork

Background: Normal-tension glaucoma is a relativelycommon variant of primary open angle glaucoma in whichintraocular pressure (IOP) is not elevated above the normalrange. This represents a demanding clinical picture, as theclinician must determine whether the IOP is indeed withinthe normal range and whether the optic neuropathy is infact glaucomatous in nature. Toxic, compressive, and infec-tious optic neuropathies can all mimic normal-tension glau-coma and should all be excluded, as they may requiretreatment to avoid further morbidity.Case Report: A 67-year-old black woman presented to ourclinic with a history of being followed up with as a glau-coma suspect by other practitioners. The patient reportedno family history of glaucoma and had no visual com-plaints. Initial examination findings included IOP in thelow teens and optic nerves suspicious for glaucomatousdamage. Visual field testing was consistently of poor relia-bility and as such, correlation with stereo photography ofthe optic nerve was questionable, as was the certainty ofprogression. At this point, it was decided to rule out com-pressive and infectious optic neuropathies, as nothing inthe patient’s history suggested a toxic etiology. The pa-tient’s MRI scan showed no evidence of a space-occupyinglesion. Blood work was positive for syphilis, and once ed-ucated regarding this, the patient admitted to prior treat-ment for the disease. The patient was referred to aninfectious disease specialist to evaluate the need for furthersystemic treatment. She is currently not taking medicationand is seen in our clinic every 6 months.Conclusion: This case highlights the necessity of excludingother forms of optic neuropathy in patients suspected ofnormal-tension glaucoma. Demographic information, pa-tient history, and correlation of subjective and objectivefindings should all be considered when determining themanagement course for these challenging patients.

Poster 65

De Morsier’s Syndrome

Dina Iskander, O.D., SUNY State College of Optometry,New York, New York

Background: De Morsier’s syndrome, also known as septo-optic dysplasia, is a rare developmental anomaly of the braincharacterized by optic nerve hypoplasia, absence of the sep-tum pellucidum, and/or agenesis of the corpus callosum. Pitu-itary gland hypoplasia is highly associated with De Morsier’ssyndrome and hence, De Morsier’s is a common etiology ofcongenital growth hormone deficiency. Associated hypopitu-itarism with midline brain abnormalities is the most signifi-cant cause of morbidity in these patients. De Morsier’s is of