Cases reported "Pupil Disorders"

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1/4. Absent relative afferent pupillary defect in an asymptomatic case of lateral chiasmal syndrome from cerebral aneurysm.

    INTRODUCTION: This report documents a case of an asymptomatic 34-year-old female who had right eye subtle temporal optic nerve pallor with absent clinically detectable relative afferent pupillary defect. CASE REPORT: This presentation was secondary to a fusiform paraclinoid aneurysm resulting in lateral chiasmal syndrome. visual fields demonstrated a nasal depression OD. neuroimaging studies revealed the presence of a fusiform paraclinoid aneurysm compressing the right optic nerve and optic chiasm. The lesion was treated surgically without additional visual loss nor systemic and neurological complications. CONCLUSIONS: A clinically detectable relative afferent pupillary defect may be absent in unilateral optic nerve pallor and/or visual field loss and does not preclude the need to attempt to identify an underlying etiology. Neuroradiological examination of orbital and cranial structures is an imperative protocol in the appropriate management of this potential life- and vision-threatening condition.
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2/4. Clinical features associated with lesions other than pituitary adenoma in patients with an optic chiasmal syndrome.

    PURPOSE: Pituitary adenomas are the most common cause of an optic chiasmal syndrome, and treatment of these lesions is considerably different from the treatment of most of the other lesions in this region. Although the diagnosis of a pituitary adenoma is usually inferred from the results of neuroimaging, lesions other than pituitary adenomas can have an appearance that suggests an adenoma. The objective of our study was to determine whether there are clinical findings that suggest a lesion producing a chiasmal syndrome is something other than a pituitary adenoma. DESIGN: Retrospective, case-controlled, analysis of medical record data. methods: The records of the Neuro-ophthalmology Unit of the Wilmer eye Institute were searched for patients with a chiasmal syndrome who had been evaluated before treatment and for whom pathologic or laboratory confirmation of the etiology was available. Presenting clinical features of these patients were recorded, and analyses with both a single variable and multiple variables were performed to determine whether there were any features that could identify with a high degree of probability the etiology of the lesion producing the syndrome. RESULTS: The search revealed 149 patients who met the inclusion criteria, including 90 patients with pituitary adenomas and 59 patients with other lesions. Variables that were highly suggestive of an etiology other than pituitary adenoma included symptomatic visual loss, younger age, unilateral optic disk pallor, a relative afferent pupillary defect, and an absolute or a complete visual field defect or one was greater inferiorly than superiorly. CONCLUSION: Although no single clinical feature can be used to determine the specific nature of a lesion that produces an optic chiasmal syndrome, certain features are highly suggestive of an etiology other than pituitary adenoma. When these features are present, the likelihood that a suprasellar lesion is a pituitary adenoma is much lower, regardless of the appearance on neuroimaging.
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3/4. Hypovolemic ischemic optic neuropathy.

    BACKGROUND: Ischemic optic neuropathy refers to an acute event of ischemia, or decreased blood flow, to the optic nerve resulting in varying degrees of vision loss and visual field defects. Typically this disease affects the elderly population who experience systemic diseases that compromise the blood flow efficiency of the optic nerve head (e.g., giant-cell arteritis, hypertension, diabetes, etc.). However, cases of blood loss to the optic nerve, secondary to traumatic injuries or surgeries, have also been shown to result in ischemic optic neuropathy, regardless of age. It seems that in these cases, the resulting anemia and hypotension play contributing roles in the development of ischemic optic neuropathy. methods: A 41-year-old black man came to us with optic nerve head pallor O.S., count-fingers vision O.S., positive afferent pupillary defect O.S., and a central scotoma O.S. after being hospitalized and treated for a stab wound to his left neck that severed his left carotid artery at the bifurcation. RESULTS: This patient had been seen in the optometry Clinic two years before the stab-wound incident. At that time, he had 20/20 vision in his left eye and no remarkable neurological deficits. His ocular presentation after the traumatic hypovolemic event was probably a direct result of the hypoperfusion to the left optic nerve head. This patient was diagnosed with a hypovolemic, or blood loss-related, ischemic optic neuropathy (O.S.). CONCLUSIONS: patients who experience large amounts of blood loss due to trauma, surgery, internal bleeding, etc. and report vision loss should be screened for possible optic nerve ischemia. As eye care providers, when we are presented with patients who have optic nerve head atrophy, we should inquire about events that may have precipitated blood loss, potentially triggering ischemic optic neuropathy.
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4/4. Visual field loss following vitreous surgery.

    OBJECTIVE: To assess possible causes of visual field loss following vitreous surgery. DESIGN: charts of 8 patients prospectively identified, who developed visual field loss following vitreous surgery, were reviewed to characterize this newly recognized syndrome and assess possible causes. RESULTS: Two patients had preexisting chronic open-angle glaucoma and 1 had ocular hypertension. Indications for surgery included 4 eyes with macular holes, 1 eye with epiretinal membrane, 2 eyes with rhegmatogenous retinal detachment, and 1 eye with retinal detachment and giant retinal tear. All patients received retrobulbar anesthesia. Seven of 8 patients had fluid/gas exchange with installation of long-acting bubbles. In 1 patient with a macular hole, a small hemorrhage was noted along a vessel coming off the nerve superotemporally while attempting to engage the posterior cortical vitreous intraoperatively. This patient developed an inferior visual field defect. No intraocular pressure (IOP) measurements greater than 26 mm Hg were recorded in any eye perioperatively. Visual field defects included 4 eyes with inferotemporal defects, 2 eyes with inferior altitudinal defects, 1 eye with a cecocentral scotoma, and 1 eye with a superonasal defect. Only 1 patient had worsened visual acuity. A relative afferent pupillary defect was observed in 4 eyes and disc pallor in 5 eyes. CONCLUSIONS: Central or peripheral visual field loss can now be recognized as a possible complication of vitreous surgery. In some cases, a relative afferent pupillary defect and optic disc pallor are present, suggesting that the optic nerve is the site of injury. Possible mechanisms include ischemia due to elevated IOP or fluctuations in IOP, optic nerve damage from retrobulbar injection, direct intraoperative mechanical trauma to the optic nerve, indirect injury from vigorous suction near the optic nerve leading to shearing of peripapillary axons or vessels, or a combination of these. Certain optic nerves may be more susceptible to injury because of preexisting compromise from glaucoma or vascular disease.
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