Macular infarction may be a consequence of arterial occlusion, or occasionally it may arise as a complication of drug toxicity especially the aminoglycosides. On fundus examination there is a variable extent of foveal opacification along with retinal hemorrhages. HPE has shown lamellar lysosomal inclusion bodies in the retinal pigment epithelium and accumulation of an amorphous PAS-positive material in the subepithelial space. On OCT there is increased macular thickness with hyperreflectivity of the inner retinal layers, corresponding to the area of retinal pallor and edema. Neurosensory retina may be elevated with accumulation of hyperreflective material under the neurosensory retina (Fig. 28.2) (Venkatesh et al. 2005; Witkin et al. 2006). There is loss of normal alternate layers of hyperreflectivity that represent different layers of the retina. During follow-up OCT though a reduction in the macular edema is observed, the ischemic retina may still remain hyperreflective, and the alternate layers of hyperreflectivity that represent different layers of the retina are generally lost.

Optic nerve head drusen (ONHD) are a common, benign, congenital anomaly of the optic nerve, which rarely lead to decreased visual acuity. Clinically, optic nerve head drusen may be visible on the disk surface or buried within the disk. These lesions often obscure the margins of the optic disk. Buried ONHD may simulate optic disk edema (ODE) and lead to diagnostic uncertainty. Various techniques to differentiate these two conditions include fundus examination, optic disk autofluorescence, fluorescein angiography, B-scan ultrasonography, and OCT. In recent years, there have been a number of reports evaluating OCT to distinguish between ODE and ONHD. The OCT appearance of optic disk drusen is characterized by an elevated optic nerve head with a “lumpy-bumpy” internal optic nerve contour and an abrupt tapering of the hyporeflective space located between the sensory retina and the retinal pigment epithelium and choriocapillaris. Retinal nerve fiber layer thickness, especially in the nasal quadrant, has also been shown to be decreased in ONHD when compared with ODE (Davis and Jay 2003; Johnson et al. 2009; Karam and Hedges 2005) (Fig. 28.3).

Intraocular myelination of the retinal nerve fiber has been reported in 0.3–0.6 % of population by ophthalmoscopy and in 1 % by postmortem examination (Duke-Elder 1963). Normally myelination stops at the lamina cribrosa and does not extend intraocularly. Oligodendrocytes, which are responsible for myelination of the central nervous system, are not normally present in the human retina. However, histological sections confirm their presence in some areas of myelinated nerve fibers (Straatsma et al. 1981). The presence of myelinated nerve fiber has been associated with several ocular and systemic disorders. Extensive unilateral myelination of nerve fibers can be associated with anisometropic high myopia and dense amblyopia which is refractory to treatment by occlusion therapy (Ellis et al. 1987; Moradian and Karimi 2009). They may also be associated with occult microvascular abnormalities (Tabassian et al. 1995) and Gorlin syndrome (de Jong et al. 1985). Myelinated nerve fibers do not usually reduce visual acuity. However, it may produce relative scotomas depending upon their location and the number of fibers present. The scotomas are smaller than what the size of the myelinated fiber would suggest. The time domain and SD-OCT features of myelinated nerve fiber have been described by Salvatore et al. (Salvatore et al. 2011). Increased reflectivity and thickness of the retinal nerve fiber layer (RNFL) in the area of the myelinated fibers were reported. Furthermore this characteristic was accompanied by a posterior cone of shadowing. Three-dimensional OCT features of myelinated nerve fiber were described by Saxena and Jain. They observed an abrupt termination of the structures posterior to the hyperreflective RNFL due to the back shadowing produced by the thickened nerve fiber layer. The steeply elevated area of myelinated nerve fiber as observed on 3D-OCT acted as an optical barrier creating an area of non-reflectivity seen amidst the hyperreflective area as seen on the C-scan (Saxena and Jain 2011) (Fig. 28.4).

Solar retinopathy is a retinal damage, particularly the macula that results from exposure to solar radiation. On fundus examination in the initial period, there is a foveolar yellow spot. With the passage of time, this gets replaced by a very small sharply delimited red lesion or by a hypopigmented lesion with irregular margins. Solar burn is the smallest form of a macular hole. Visual acuity is relatively well maintained. Optical coherence tomography (OCT) is the most sensitive diagnostic imaging technique to detect the subtle macular changes in solar retinopathy which might get missed clinically and on fundus fluorescein angiography. It helps delineating the retinal injury site in vivo. Bechmann et al. for the first time described solar retinopathy as a hyperreflective area at the fovea with all retinal layers affected using time domain OCT (Bechmann et al. 2000).Acute changes seen on OCT predominantly include the RPE and outer photoreceptor segments, while chronic changes (more than 1 year from exposure) mainly affect the inner and outer photoreceptor segments. A tiny punched-out disruption of the pigment epithelial layer on OCT is pathognomonic of solar burn. Other OCT changes which have been observed include transient increase in foveal reflectivity and disruption of the inner and outer segments of the photoreceptor layers with or without underlying RPE defects. In many cases the changes are reversible, but solar retinopathy can lead to permanent visual impairment. Worse long-term vision is significantly related to the presence of photoreceptor layer damage on OCT (Chen et al. 2012; Codenotti et al. 2002; Garg et al. 2004; Hossein et al. 2011; Garg et al. 2004; Kaushik et al. 2004) (Fig. 28.5).