Study of macular thickness in relatiion to axial lengthin myopic eyes

Abstract

The anatomic macula or area centralis is about 5.5-6 mm in diameter, centered on the fovea. The posterior pole is subdivided into four concentric regions; the parafovea, the perifovea, the foveal slope, and the foveola. The foveola is created by peripheral displacement of the inner nuclear and ganglion cells. The density of RPE cells is greater in the fovea and they are most tightly packed. Rods and cones are tightly stacked together into a single pallisading layer of photoreceptors. The displacement of the inner retinal layers away from the foveola leads to an aggregation of bipolar and ganglion cells around the edge of the fovea making this region the thickest part of the fundus. The ganglion cells are responsible for transmitting visual information from the retina to the brain. Ganglionic axons travel towards the optic nerve head within the NFL. The superficial retina in the macular region receives blood from macular branches of the superior and inferior temporal arteries. The central 500 µm of the fovea contains no retinal capillaries and so it is referred to as the FAZ. In the macular region the choriocapillaris is supplied by the short posterior ciliary arteries. Myopia is the state of refraction in which parallel rays of light are brought to focus in front of the retina of a resting eye. Prevalence rates of myopia are higher in whites than in blacks with higher preponderance in females. The prevalence of myopia changes considerably with age; it usually develops between the ages of 6 and 14 years. Traditionally, myopia has been classified as either refractive or axial. Axial myopia is brought about by increased axial length and is classified as either physiological or pathological (degenerative) which is caused by an abnormal progressive lengthening of the eyeball beyond normal limits with a refractive error of at least 6 D and/or axial length greater than 26-27mm and involves the posterior segment more significantly where serious ocular complications develops. Etiology of myopia is diverse and con¬troversial. Different modes of Mendelian inheritance, including autosomal dominant, autosomal recessive, and sex-linked, have been suggested by different authors. Thirteen autosomal loci have been mapped for myopia, but no causative gene has been identified. Progressive axial myopia is interpretted as a precocious growth which has failed to get ar¬rested. Also close up work causes myopia as seen in the higher prevalence of myopia among persons who are more highly educated. It is likely that genetic and environmental factors interact in a complex manner in the development of myopia. Pathological changes in myopia could be classified into biomechanical changes as lacquer cracks and posterior staphyloma, neovascular changes as CNV and Fuchs’ spot or degenerative changes as chorioretinal atrophy and lattice degeneration. The myopia progression makes the sclera thinner. The choroidal changes are essentially at¬rophic in nature. Atrophic changes in the retina progress coin¬cidentally with those in the choroid. The major threat to vision in the myopic eye is retinal detachment. A posterior staphyloma is a backward ectasia of the fundus, the hallmark being tessellation and pallor of the area involved. Posterior staphylomas are often progressive and result in vision loss. Highly myopic patients with posterior staphyloma are predisposed to develop macular pathologies such as myopic foveoschisis. Macular hole develops in eyes with the severer myopia at the younger age. Fuchs' spot is produced by hyperplasia of the RPE over a subretinal membrane. Macular CNV is one of the most vision threatening complications. Lattice degeneration is the most important peripheral retinal degeneration. Lacquer cracks are thought to be healed spontaneous linear ruptures in the RPE-Bruch’s membrane-choriocapillaris complex. Myopic patients had significantly higher rates of larger, tilted, rotated discs, larger disc areas and longer disc-foveola distances. Although these abnormalities may appear innocuous, they are important clinically because they can be difficult to evaluate. PVD develops increasingly with the degree of myopia and with age. Eyes with greater vitreous depths tended to have flatter anterior corneal surfaces and significantly less corneal endothelial density but there was no significant change in the endothelial function. Posterior subcapsular, nuclear and occasionally cortical cataract may be associated with high and low myopia. Eyes with increased axial length appear to have higher cup/disc ratios, increased NFL defects and possibly greater deformability of the lamina cribrosa, leading to higher susceptibility to glaucomatous optic disc changes. OCT is a non-invasive high-resolution imaging modality which employs non-ionizing optical radiation. In time domain OCT, there is a mechanical moving part that performs the A-scan, and the information along the longitudinal direction is accumulated over the course of the longitudinal scan time while in Fourier domain OCT, the information in an entire A-scan is acquired simultaneously. OCT imaging employs software that allows customized cross sectional optical cut sections to suit to a particular subject for the disease under study. OCT is suited for measurement of retinal thickness. Measurement of retinal thickness is dependent on definition of the anterior and posterior retinal surfaces. The macular thickness map scan protocol consisted of six radial lines through a common central axis centered on the fovea at equally spaced angular (30°) orientation. Each of the six linear scans has a length of 6 mm and is composed of 128 transverse A-scans. The macular thickness and volume map is displayed as three concentric circles including a central circle, an inner ring and an outer ring with diameter of 1 mm, 3 mm and 6 mm respectively. The limitation of the Stratus OCT macular thickness map is that it is derived from only six linear scans over a 360° area in the transverse plane. Another limitation relates to the magnification factor in myopic eyes. We designed a casual research study included two hundred eyes of 108 randomly selected Egyptian healthy subjects. We excluded eyes with refractive myopia, posterior segment pathology or with past history of intraocular surgery or trauma. Also patients with concurrent systemic diseases or medications that are expected to affect the macula. Studied eyes were stratified based on refraction and the age of the subject and formed three main refractive groups; emmetropic, moderate myopic and severe myopic groups; each of them is further divided according to age into young and old subdivisions. Full ophthalmic examination was performed including VA, BCVA, automated refraction and keratometry, slit lamp examination, IOP measurement and dilated fundus examination. Axial length was measured by A-scan. OCT was performed with Stratus OCT. Mean axial length was highest in the severe myopic and lowest in the emmetropic control group. The parafoveal, perifoveal and total macular thickness and the macular volume are highest in the emmetropic group in contrast to the foveal thickness being highest in the moderate myopic group and lowest in the emmetropic group. Axial length was not significantly correlated to macular thickness parameters in nearly all groups except in the old moderate myopic group. The presence of significant difference between macular measurements among refractive groups in the absence of regular direct positive or negative correlation between axial length and these measurements suggests a non-linear correlation which is difficult to be standardized. Moreover, pathological changes of macular thinning in myopic eyes may be genetically determined rather than simply related to the degree of axial elongation and mechanical stretching. Change of macular thickness with age differs according to refraction. There was no difference between young and old in emmetropic or severe myopic groups, conversely, there is thinning of peripheral rather than central macular measurements in eyes with moderate myopia with age. There is no constant precise value for foveal thickness. The cause for this discrepancy may be related to the ethnicity of the study group, the OCT model, type of scan and analysis protocol. There was increased foveal thickness with axial length which may be related to the retinomotor movements of the photoreceptors or an early sign of vitreoretinal traction in highly myopic eyes. There was no change of foveal thickness with age.