The corneal nerve density in the sub-basal plexus decreases with increasing myopia: a pilot study.

PURPOSE: Myopia can cause many changes in the health of the eye. As it becomes more prevalent worldwide, more patients seek correction in the form of glasses, contact lenses and refractive surgery. In this study we explore the impact that high myopia has on central corneal nerve density by comparing sub basal nerve plexus density measured by confocal microscopy in a variety of refractive errors. METHODS: Seventy healthy adult subjects between the ages of 21-50 years participated in this study. The study took place in two phases with no overlapping subjects (n = 30 phase 1 and n = 40 phase 2). In both phases an autorefraction, keratometry reading, corneal thickness measure and confocal corneal scan of the sub basal nerve plexus were performed for both eyes. There were 11 hyperopes (+0.50 to +3.50DS), six emmetropes (-0.25 to +0.50DS), 30 low myopes (-5.50 to -0.50DS), and 23 high myopes (-5.50DS and above). In the second phase of the study additional tests were performed including an axial length, additional corneal scans, and a questionnaire that asked about age of first refractive correction and contact lens wear. Corneal nerves were imaged over the central cornea with a Nidek CS4 confocal microscope (460 × 345 µm field). Nerves were evaluated using the NeuronJ program for density calculation. One eye was selected for inclusion based on image quality and higher refractive error (more myopic or hyperopic). RESULTS: As myopia increased, nerve density decreased (t1  = 3.86, p < 0.001). We also note a decrease in data scatter above -7 D. The relationship between axial length values and nerve density was also significant and the slope was not as robust as refractive error (t1  = 2.4, p < 0.04). As expected there was a significant difference between the four groups in axial length (F3  = 19.9, p < 0.001) and age of first refractive correction of the myopic groups (14.9 vs 11.5 years; t46  = 2.99 p < 0.01). There was no difference in keratometry readings or corneal thickness between the groups (F3  = 0.6, p = 0.66 and F3  = 1.2, p = 0.33 respectively). CONCLUSION: Corneal nerve density in the sub-basal plexus decreased with increasing myopia. This could have implications for corneal surgery and contact lens wear in this patient population.

Spectral Domain OCT Imaging Techniques in Tamoxifen Retinopathy.

PURPOSE: To highlight the use of high-density spectral domain optical coherence tomography (SD-OCT) in the detection of tamoxifen retinopathy. CASE REPORT: An 82-year-old asymptomatic woman with a history of tamoxifen therapy for breast cancer was found to have bilateral refractile retinal deposits on fundus examination. Detection on SD-OCT was compared across imaging techniques. High-density SD-OCT demonstrated hyperreflective deposits in the inner retinal layers of each eye consistent with the diagnosis of tamoxifen retinopathy. CONCLUSIONS: The optimal SD-OCT scan technique depends on the ocular condition being imaged. High-density scan techniques require longer acquisition time but may enhance the detection of focal retinal pathology.

Loss of protein kinase Cgamma in knockout mice and increased retinal sensitivity to hyperbaric oxygen.

OBJECTIVE: To determine if loss of protein kinase Cgamma (PKCgamma) results in increased structural damage to the retina by hyperbaric oxygen (HBO), a treatment used for several ocular disorders. METHODS: Six-week-old mice were exposed in vivo to 100% HBO 3 times a week for 8 weeks. Eyes were dissected, fixed, embedded in Epon, sectioned, stained with toluidine blue O, and examined by light microscopy. RESULTS: The thicknesses of the inner nuclear and ganglion cell layers were increased. Destruction of the outer plexiform layer was observed in the retinas of the PKCgamma-knockout mice relative to control mice. Exposure to HBO caused significant degradation of the retina in knockout mice compared with control mice. Damage to the outer segments of the photoreceptor layer and ganglion cell layer was apparent in central retinas of HBO-treated knockout mice. CONCLUSIONS: Protein kinase Cgamma-knockout mice had increased retinal sensitivity to HBO. Results demonstrate that PKCgamma protects retinas from HBO damage. CLINICAL RELEVANCE: Care should be taken in treating patients with HBO, particularly if they have a genetic disease, such as spinocerebellar ataxia type 14, a condition in which the PKCgamma is mutated and nonfunctional.