Press Archive
- Charles Francis: Weakening eye surgery laws places WV patients in jeopardy
- Mark D. Mayle, MD - 2022 Secretariat Award Recipients
- Dr. Larry Schwab recognized with 2020 International Blindness Prevention Award
- Wow Moment with Joseph A. LoCasio | Bio-Tissue | #WowWednesdays
- WVU Today | Moore, Oppe named recipients of Heebink award for Distinguished Service
- Cornea Transplant Restores Young Boy’s Sight After Fishing Accident
- Keep your eyes healthy and safe in the workplace
- Glaucoma Awareness Month
- Ophthalmologists Say 90 Percent of Work-Related Eye Injuries Can be Avoided by Wearing Eye Protection
- Five Tips to Avoid Toy-Related Eye Injuries
- Details
In their editorial, Brodsky and Jung1 describe neurophysiologic mechanisms for the development of intermittent exotropia. They state that “prolonged patching causes it (exotropia) to become manifest.”1
- Details
A choroidal macrovessel appears on fundus photography (Canon CR-2) as an abnormally dilated, tortuous vessel (Fig 1A) that can be misdiagnosed as a parasitic track-like lesion. Evaluation using enhanced depth imaging-optical coherence tomography (OCT) (Spectralis OCT; Heidelberg Engineering, Heidelberg, Germany) reveals prominent hyporeflective vasculature occupying the entire thickness of the choroid (Fig 1B, asterisk), with tent-like elevations of the retinal pigment epithelium and indentation of the photoreceptors (Fig 1B, arrowhead).
- Details
We thank Dr Lempert for his interest in our editorial. Although orbital anatomic derangements can cause exotropia in patients with craniosynostosis or hypertelorism, the natural history of intermittent exotropia is that it generally becomes more severe during the first few years of life (as the orbits become more parallel). This is the opposite of what would occur if the lateral orientation of the neonatal orbits engendered this exodeviation. Dr Lempert's proposed mechanism would, therefore, require some anatomic evidence that the age-related degree of orbital divergence is greater in children with intermittent exotropia.
- Details
We thank Barboni et al for their interest in our recent article describing the optic nerve and retinal morphology using high-resolution optical coherence tomography (OCT) in optic nerve hypoplasia (ONH).1 They highlight that in mitochondrial neuropathies such as dominant optic atrophy (DOA) and Leber's hereditary optic neuropathy (LHON) optic disks can also be small.2,3 We agree that the pathophysiology is poorly understood in ONH and that the importance of OPA1 in embryologic development may warrant a search of common pathophysiologic mechanisms.
- Details
We agree very much with Spaide et al1 that a great advantage of optical coherence tomography (OCT) angiography is its 3-dimensional (3D) nature, and that color coding for the depth of vessels is a natural way to represent this 3D information. However, we think it is disingenuous for Dr Spaide to imply that he was the first to adapt this approach from CT and MR literature and apply it to OCT angiography. He wrote:Instead of imaging the average or densest voxel, volume rendering uses all the voxel values to make an image that retains the sense of depth and is less prone to image artifact.
- Details
We read with great interest the article by Pilat et al,1 in which they described high-resolution imaging of the optic nerve and retina in optic nerve hypoplasia (ONH). They concluded that patients with ONH had significantly smaller optic nerve head parameters, such as disc diameter and cup diameter, and significantly thinner macular layers, including retinal nerve fiber layer (RNFL), ganglion cell layer, inner plexiform layer, and outer nuclear layer, as measured by optical coherence tomography.