Outer retinal structure after closed-globe blunt ocular trauma.

PURPOSE: To evaluate outer retinal structural abnormalities in patients with visual deficits after closed-globe blunt ocular trauma. METHODS: Nine subjects with visual complaints after closed-globe blunt ocular trauma were examined between 1 month after trauma and 6 years after trauma. Spectral domain optical coherence tomography was used to assess the outer retinal architecture, whereas adaptive optics scanning light ophthalmoscopy was used to analyze the photoreceptor mosaic integrity. RESULTS: Visual deficits ranged from central scotomas to decreased visual acuity. Spectral domain optical coherence tomography defects included focal foveal photoreceptor lesions, variable attenuation of the interdigitation zone, and mottling of the outer segment band, with one subject having normal outer retinal structure. Adaptive optics scanning light ophthalmoscopy revealed disruption of the photoreceptor mosaic in all subjects, variably manifesting as foveal focal discontinuities, perifoveal hyporeflective cones, and paracentral regions of selective cone loss. CONCLUSION: We observe persistent outer retinal disruption in subjects with visual complaints after closed-globe blunt ocular trauma, albeit to a variable degree. Adaptive optics scanning light ophthalmoscopy imaging allows the assessment of photoreceptor structure at a level of detail not resolvable using spectral domain optical coherence tomography or other current clinical imaging tools. Multimodal imaging seems to be useful in revealing the cause of visual complaints in patients after closed-globe blunt ocular trauma. Future studies are needed to better understand how photoreceptor structure changes longitudinally in response to various traumas.

Venous sinus pulsatility and the potential role of dural incompetence in idiopathic intracranial hypertension.

BACKGROUND: Idiopathic intracranial hypertension (IIH) remains a poorly understood and therapeutically challenging disease. Enthusiasm has emerged for endovascular therapy with stent reconstruction of dural sinus narrowing; however, a complete understanding of the hydrodynamic dysequilibrium is lacking. OBJECTIVE: To review and characterize catheter manometry findings including pulsatility changes within the venous sinuses in IIH. METHODS: Cases of venous sinus stent implantation for IIH were retrospectively reviewed. RESULTS: Three cases of venous sinus stent implantation for treatment of IIH are reported. All cases demonstrated severe narrowing (>70%) within the transverse sinus and a high pressure gradient across the lesion (>30 mm Hg). Stent implantation resulted in pulsatility attenuation, correction of pressure gradient, and improvement of flow. CONCLUSION: We report the finding of high venous sinus pulsatility attenuation after stent implantation for dural sinus narrowing and propose the hypothesis that this finding is a marker of advanced dural sinus incompetence. This characteristic may be useful in identifying patients who would benefit from endovascular stent remodeling.

Leiomyosarcoma of the uterus with sphenoid bone and orbital metastases.

A 55-year-old woman presented with a 1-week history of vision loss in the right eye associated with proptosis and diplopia. Past medical history was significant for high-grade leiomyosarcoma of the uterus status post total abdominal hysterectomy and bilateral salpingo-oophorectomy and postoperative pelvic radiation 18 months prior to presentation. Staging studies at the time of initial diagnosis of uterine leiomyosarcoma showed no evidence for metastatic disease. At presentation, CT and MRI showed a well-circumscribed 3.0 cm x 3.6 cm x 2.4 cm mass centered in the right greater sphenoid wing, extending into the middle cranial fossa and the superior and lateral orbital wall. Biopsy of the orbital mass revealed a poorly differentiated high-grade leiomyosarcoma, consistent with recurrent metastatic disease from the uterus. The patient subsequently underwent radiation treatment followed by a left orbital exenteration 6 months after the orbital biopsy. A left thoracostomy was performed 8 months after the orbital biopsy for a metastatic nodule in the left lower lobe of the lung. The clinicopathologic findings of this rare metastatic orbital lesion are presented.

The hypoplastic maxillary sinus and the orbital floor.

PURPOSE OF REVIEW: Hypoplastic maxillary sinus is a relatively rare clinical problem that has a variable presentation. The purpose of this article is to review the recent literature with regard to evaluation and treatment. RECENT FINDINGS: Most authors suggest that hypoplastic maxillary sinus results from the development of negative pressure resulting from an obstruction of maxillary sinus ventilation. Patients most frequently present with unilateral enophthalmos but some cases may be identified incidentally on imaging studies. SUMMARY: Hypoplastic maxillary sinus is a rare clinical entity with variable presentation. Evaluation and management are tailored to each individual patient's degree of disease and symptoms.

Orbital inflammation.

Orbital inflammation is a common problem in adults and children, accounting for the majority of all orbital processes. The presentation may be acute, subacute, or insidious. When the onset is acute, the process can be mistaken for orbital cellulitis. In insidious cases, such as the sclerosing subtype of inflammation, the chronic painless course may prompt concerns about a neoplastic infiltration such as lymphoma. Orbital inflammation can be divided into nonspecific, idiopathic, and other specific diagnoses. The differential diagnosis includes allergic, infectious (fungal, mycobacterial, and parasitic), and neoplastic (lymphoma or metastatic) disease. Orbital inflammation impacts neurologists and neuro-ophthalmologists because all of the entities can cause afferent dysfunction (decreased vision, abnormal color perception, afferent pupillary defect, and visual field defect) and dysmotility. The pattern of motility deficit may mimic the more familiar cranial nerve palsies. Advances in the diagnosis and management of nonspecific orbital inflammation and the specific entities that cause orbital inflammation are discussed.