Cases reported "Scotoma"

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1/111. Compression of the prechiasmatic optic nerve produces a junctional scotoma.

    PURPOSE: To demonstrate the clinical-radiologic correlation between a junctional scotoma and a focal lesion compressing the prechiasmatic segment of the distal optic nerve. methods: Case report involving a man with a pituitary adenoma. Clinical correlation was determined by reviewing visual field evaluations and magnetic resonance images. RESULTS: The tumor compressed the prechiasmatic segment of the distal optic nerve but not the optic chiasm, producing a junctional scotoma documented by Goldmann and automated perimetry. The visual field defect resolved after neurosurgical decompression of the anterior visual pathway. CONCLUSIONS: A junctional scotoma can be caused by focal as well as large and diffuse lesions injuring the anterior visual pathway, specifically at the junction of the optic nerve and chiasm. This finding supports the existence of Wilbrand fibers.
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2/111. Toxic optic neuropathy after concomitant use of melatonin, zoloft, and a high-protein diet.

    melatonin is a neuromodulating hormone found in the pineal gland and retina. It is involved in light-dark circadian rhythms and mediates retinal processes in a manner antagonistic to that of dopamine. Zoloft (sertraline) is an antidepressant drug that blocks the reuptake of serotonin at the neural synapse. serotonin is the natural precursor of melatonin. A 42-year-old woman sought treatment for visual acuity loss, dyschromatopsia, and altered light adaptation. Neuro-ophthalmologic examination was otherwise normal except for evolving bilateral cecocentral scotomas. She had taken Zoloft for 4 years and began a high-protein diet with melatonin supplementation 2 weeks before onset of visual symptoms. visual acuity and color vision improved within 2 months after melatonin and the high-protein diet were discontinued. Combined use of melatonin, Zoloft, and a high-protein diet may have resulted in melatonin/dopamine imbalance in the retina, manifesting as a toxic optic neuropathy. physicians and patients should be alerted to this potential drug interaction.
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3/111. coffee and doughnut maculopathy: a cause of acute central ring scotomas.

    AIMS: To report the clinical features of five patients with non-progressive central ring scotomas of acute onset associated with excellent retained visual acuity. methods: Complete neuro-ophthalmological examinations were performed. visual fields were performed by tangent screen, Goldmann, or Humphrey perimetry. In some cases further testing was carried out including fundus photography, fluorescein angiography, ERG, VEP, and neuroimaging. RESULTS: The patients were three women and two men whose ages ranged from 25 to 57 years. Four patients were heavy caffeine consumers while the fifth patient experienced an episode of hypotension. Vision loss was acute in all cases. The onset of vision loss was bilateral/simultaneous in three cases, bilateral/sequential in one case, and unilateral in one case. All affected eyes retained visual acuities of 20/25 or better. Colour vision was subnormal in three of four cases. Visual field defects were characterised by a central ring scotoma having an outer diameter less than 10 degrees. Fundus examination demonstrated temporal optic nerve pallor in three patients (five of 10 affected eyes) and reddish, petaloid macular lesions in one patient. Good visual acuity was maintained for the duration of follow up in all five patients. CONCLUSION: Central ring scotomas with excellent retained visual acuity may present as an acute, bilateral syndrome in patients who are heavy caffeine consumers. The configuration of visual field loss and its location, combined with the presence of temporal pallor in five eyes, suggest that the defect localises to the inner layers of the macula. While these cases could be considered an expansion of the clinical spectrum of acute macular neuroretinopathy, some may represent a distinct entity.
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4/111. Visual field defect associated with laser in situ keratomileusis.

    PURPOSE: To report a case of visual field defect associated with laser in situ keratomileusis. methods: Case report. A 28-year-old woman with high myopia (-10D) and a family history of normal tension glaucoma underwent bilateral laser in situ keratomileusis keratorefractive surgery. Preoperatively, both eyes had normal intraocular pressure and visual field. RESULTS: At the first postoperative visit 1 day after apparently uncomplicated laser in situ keratomileusis, the patient reported a scotoma in the right eye. At 3-month follow-up, visual fields revealed the patient had developed a near-superior altitudinal visual field defect in the right eye. The defect did not progress over 1 year of follow-up examinations. CONCLUSION: Increased intraocular pressure associated with the microkeratome vacuum ring used during laser in situ keratomileusis may have precipitated optic nerve head ischemia and visual field defect.
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5/111. Scanning laser entoptic perimetry for the screening of macular and peripheral retinal disease.

    OBJECTIVE: To determine the effectiveness of scanning laser entoptic perimetry as a noninvasive platform for screening for retinal damage in visually asymptomatic patients within the central 120 degrees (diameter) of vision. DESIGN: A masked study comparing entoptic perimetry with fundus photographs. SETTING: The Shiley eye Center and the AIDS Ocular research Unit at the University of california, San Diego. patients: Fifty-eight patients recruited during ophthalmologic visits for treatment or follow-up of ocular disease. MEASUREMENTS: For each testing session, we compared the presence of a disturbance in the entoptic stimulus with the presence of retinal disease within the central 120 degrees of vision, centered on the fovea. RESULTS: Scanning laser entoptic perimetry has a sensitivity and specificity of more than 90%, a positive predictive value of 100%, and a negative predictive value of 89% for screening retinal lesions within the central 120 degrees diameter of vision. CONCLUSION: Scanning laser entoptic perimetry may be an effective and inexpensive screening test for diagnosing retinal disease in hospitals and community clinics. Arch Ophthalmol. 2000;118:1205-1210
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6/111. Amsler grid examination and optical coherence tomography of a macular hole caused by accidental Nd:YAG laser injury.

    PURPOSE: To compare a macular hole from accidental Nd:YAG laser injury with idiopathic macular holes. methods: Case report. In a 24-year-old man with accidental Nd:YAG laser injury, right eye, Amsler grid testing and optical coherence tomography were performed. RESULTS: Nd:YAG laser injury was responsible for a macular hole about 700 microm in diameter. The visual acuity was 20/100. Amsler grid testing displayed a central scotoma with no surrounding distortion. Optical coherence tomography showed a defect in all retinal layers at the macula. CONCLUSION: The scotoma caused by Nd:YAG laser injury is not surrounded by distortion; the hole is produced by the defect of all retinal layers. In contrast, idiopathic macular holes generally produce a pincushion pattern on Amsler grid testing and have no tissue loss.
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7/111. Measurement of venous outflow pressure in the central retinal vein to evaluate intraorbital pressure in Graves' ophthalmopathy: a preliminary report.

    PURPOSE. To evaluate the intraorbital pressure in patients with Graves' ophthalmopathy (GO) in relation to the intraocular pressure (IOP) and proptosis and to find out whether optic nerve compression is predictable. methods. The venous outflow pressure (VOP) in the central retinal vein was measured by the perviously described technique of oculodynamometry.1 Since the central retinal vein passes through the orbit, the VOP cannot be lower than the intraorbital pressure if outflow is to be guaranteed. The IOP was measured either in primary position or with slight chin elevation to avoid restriction of the globe. Fifty-seven patients underwent a complete ophthalmologic examination, including VOP measurements, Hertel exophthalmometry and visual fields. RESULTS. The IOP in primary position ranged between 10 and 29 mmHg and in most (n=54) cases the VOP was 0-4 mmHg higher than the IOP. These patients had neither scotomas nor visual deterioration during an observation period of up to 2 years. In those cases (n=3) where the difference between IOP and VOP was 35 mmHg, the patients developed scotomas and visual deterioration and had to be treated (high-dose steroids or orbital decompression). The elevation in VOP did not correlate with the degree of proptosis. In one unilateral case, treatment of high IOP (32 mmHg) with dorzolamide drops led to a decrease in visual acuity of two lines, inferior field depression and relative afferent pupillary defect. The difference between IOP and VOP was 10 mmHg. Stopping treatment normalized visual function, the IOP rose to its original level and the difference between IOP and VOP was 4 mmHg. CONCLUSION. The increased IOP in GO is not caused by primary glaucoma but by elevated intraorbital pressure. The difference between IOP and VOP must be <5 mmHg to guarantee normal perfusion. We interpret these findings to suggest that loss of visual acuity and visual field defects may not only be caused by optic nerve compression at the apex but also by deterioration of optic nerve head perfusion.
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8/111. Axonal loss in a patient with anterior ischemic optic neuropathy as measured with scanning laser polarimetry.

    PURPOSE: To report Nerve Fiber Analyzer (NFA/GDx; Laser Diagnostic Technologies, San Diego, california) measurements in a patient during the early phase of an anterior ischemic optic neuropathy. methods: Case report. A 58-year old man with acute anterior ischemic optic neuropathy had repeated NFA/GDx scans of the nerve fiber layer adjacent to the optic nerve head of the involved eye, as well as repeated HFA 30.2 (Humphrey Field Analyzer; Humphrey Systems, San Leandro, california) visual field examinations. RESULTS: At presentation (day 0), he had a normal superior nerve fiber bundle on the NFA/GDx, with a deep inferior hemifield scotoma. By day 21 and day 36, the superior nerve fiber bundle thinned on the NFA/GDx, whereas the scotoma remained practically unchanged. CONCLUSION: These findings suggest that after the onset of an anterior ischemic optic neuropathy, acute loss of axonal function results in scotoma, presumably from ischemia. This is followed by a gradual disappearance of nerve fiber tissue, as measured with the NFA/GDx, within several weeks.
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9/111. Retinal arteriovenous communication.

    BACKGROUND: Disturbances in development of the embryonic vascular system, though uncommon, may cause formation of retinal arteriovenous communications (RAC). Such anomalies may also involve the intracranial, orbital, and maxillofacial blood vessels. Field loss, neovascular glaucoma, optic atrophy, Parinaud syndrome, hemiparesis, hemiplegia, and proptosis may be associated with RAC. CASE REPORT: A 27-year-old woman was referred for photography of a vascular anomaly in her left eye. I noted a large arteriovenous malformation joining major temporal branches of the left central retinal artery and vein. External and internal examination of both eyes was otherwise unremarkable. Visual-field testing revealed nasal field disturbances for the left eye, but none for the right eye. CT scan showed no obvious intracranial abnormalities. CONCLUSIONS: Visual-field testing may show scotomas associated with retinal arteriovenous communications. It is possible for patients with RAC to have no associated vascular abnormalities elsewhere in the circulation of the head.
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10/111. Location of lesions in multiple evanescent white dot syndrome and the cause of the hypofluorescent spots observed by indocyanine green angiography.

    PURPOSE: To determine the location of the lesions in the retina of a patient with multiple evanescent white dot syndrome (MEWDS) and to resolve the conflict in the cause of the hypofluorescent spots observed in the late phase of indocyanine green angiography (ICGA). CASE REPORT: A 27-year-old woman presented with a unilateral enlarged blind spot and a central scotoma. Fundus examination of the left eye showed many round, indistinctly circumscribed white dots extending from the posterior pole toward the periphery. fluorescein angiography demonstrated hyperfluorescence due to staining at the location of the white dots. Staining was also observed on the venous wall which was consistent with periphlebitis. The location of the scotomas corresponded with the hypofluorescent spots observed around the optic disc and in the macula in the late phase of ICGA. The scotomas disappeared with the resolution of the hypofluorescent spots, and the sites of other hypofluorescent spots were in accord with the sites of periphlebitis. Visual evoked cortical potentials disclosed no laterality, and the critical fusion frequency was reduced but normalized with the disappearance of the scotoma. CONCLUSION: The initial lesions of MEWDS occur in the retinal pigment epithelium and photoreceptor cells, but when MEWDS is complicated by periphlebitis, the inflammatory lesions extend to the inner layers of the retina. The inflammatory changes involve the choroid and all layers of the retina, which then block the weak background fluorescence in the later phase of ICGA and cause the hypofluorescent spots. The visual field defects are probably caused by retinal dysfunction due to the inflammatory changes.
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