Classification and Evaluation of Macular Edema, Glaucoma and Alzheimer’s Disease Using Optical Coherence Tomography

Int. J. of Biomedical Engineering and Technology, Vol. 25, No. 2/3/4, 2018 370-388
Copyright © 2018 Inderscience Enterprises Ltd.
Classification and Evaluation of Macular Edema,
Glaucoma and Alzheimer’s Disease Using Optical
Coherence Tomography
P.S.Jagadeesh Kumar1
, Yang Yung2
,
Mingmin Pan3
, Wenli Hu4
and J.Ruby5
1.2.3.4
Biomedical Engineering Research Centre,
Nanyang Technological University, Singapore.
5
Department of Surgery,
University of Cambridge, United Kingdom.
Abstract:
Optical Coherence Tomography is an imaging test to quantify retinal thickness
and other features related with retinopathy. The benefit of optical coherence
tomography is its quantifiable valuation, rather than the qualitative estimation
realized with angiography and bio-microscopy. The role of optical coherence
tomography in classification and evaluation of macular edema, glaucoma and
alzhemeir’s disease will afford proper eye treatment supervision. Recognizing
and categorizing the structural variations in retina employing optical coherence
tomography may permit more effective supervision of patients. This manuscript
aims at a rigid and accurate classification of retinal disorders that would
intensify the leeway to optimize the cause, to relate and to critic the results of
various therapeutic tactics for different diseases.
Keywords:
Optical Coherence Tomography; Alzheimer’s Disease; Glaucoma; Macular
Edema; Retinal Disorder Classification
Reference to this paper should be made as follows: P.S.Jagadeesh Kumar,
Yang Yung, Mingmin Pan, Wenli Hu, and J.Ruby. (2018) ‘Classification and
Evaluation of Macular Edema, Glaucoma and Alzheimer’s Disease Using
Optical Coherence Tomography’, Int. J. of Biomedical Engineering and
Technology, Vol. 25, No. 2/3/4, 2018, pp.370-388.
Biographical notes: P.S.Jagadeesh Kumar is currently working as Professor in
the School of Computer Science and Engineering at BMERC (Biomedical
Engineering Research Centre), Nanyang Technological University, Singapore.
He received his BE in EEE from the University of Madras in 1999. He obtained
his MBA in HR from the University of Strathclyde, Glasgow, and the UK in
2002. He obtained his ME in 2004 with specialisation in CSE from the
Annamalai University, Chidambaram, India. He achieved his MS in Computer
Engineering from the New Jersey Institute of Technology, Newark, and the
USA in 2006 and his Doctorate from the University of Cambridge, the United
Kingdom in 2013.

PSJ Kumar et al. IJBET, Vol. 25, No. 2/3/4, 2018, pp.370-388
Yang Yung is currently working as a Professor and Research Chair in
Biomedical Engineering Research Centre (BMERC), Nanyang Technological
University, Singapore. He has 20 plus years of experience in research and
development. He completed his Bachelor’s degree in Biomedical Engineering
from the University of Malaya, Malaysia in 1989. He obtained his Master’s in
Biomedical Engineering from Monash University Australia in 1996. He
attained his first Doctorate from Monash University Malaysia in Biomedical
Engineering in 2006. He received his second Doctorate from the University of
Malaya, Malaysia in Medical Image Processing in 2011.
Mingmin Pan is currently working as Associate Professor in Biomedical
Engineering Research Centre (BMERC), Nanyang Technological University,
Singapore. She received her Bachelor’s degree in Biomedical Engineering from
the University of Malaya, Malaysia in 2003. She obtained her Master’s in
Biomedical Engineering from University of Malaya, Malaysia in 2007. In
2015, she achieved her Doctorate from University of Malaya, Malaysia in
Biomedical Engineering.
Wenli Hu is Professor in Biomedical Engineering Research Centre, Nanyang
Technological University, Singapore. He has 15 plus years of experience in
academics and research. He received his doctoral degree from Beijing
University, China in 2012. He is associated with Nanyang Technological
University since 2012 in different cadre. He has published more than 100
publications in reputed journals and conferences. His foremost research interest
includes Biomedical Engineering, Neuroscience and Ophthalmology.
J.Ruby is working as a Medical Professional in the Department of Surgery at
the University of Cambridge, United Kingdom. She completed her post-
graduation in Medical-Surgical and Health Care from the University of
Cambridge, United Kingdom. She completed her undergraduate in Nursing
Education and Health Sciences from the University of Oxford, UK.
1 Introduction
Optical Coherence Tomography (OCT) has been technologically advanced for non-
invasive cross-sectional imaging in biological organizations. OCT imposts low-coherence
interferometry to generate a 2D image of ophthalmic sprinkling from interior tissue
microstructures in a means that is identical to ultrasonic pulse-echo imaging. OCT has
longitudinal and cross latitudinal tenacities of a few micrometers and can distinguish
reproduced signals as trivial as 10(-10) of the occurrence in ocular supremacy (Trichonas
G, Kaiser PK, 2014). It is an imaging technique like ultrasound, but as an alternative in
consuming the change in the flight times of audio waves, it customs light to attain
micrometer axial resolution. OCT is castoff in numerous biomedical applications, with
retinal imaging, exist the utmost fruitful and the powerful force behindhand in its
advance. The axial tenacity of OCT in retinal tissue is around 1-15 µm, which is 10 to
100 times improved than ultrasound or Magnetic Resonance Imaging (MRI). However,
comparatively novel to ophthalmology, a viable OCT scheme has already transformed the
arena, swiftly fetching a crucial device in the analysis and treatment of human retinal

Classification and Evaluation of Macular Edema, Glaucoma and Alzheimer’s
Disease Using Optical Coherence Tomography
disease. The field of OCT has grown up intensely subsequent to its invention in the initial
1990s (Dong ZM et al., 2016). The evolution of OCT in the earlier 25 years has been
tremendously effective; technically, medically, and prudently. Numerous features have
facilitated to initiate this accomplishment, preliminary with the clinical necessity for
novel lucrative, high-resolution, triflingly hostile imaging purposes for several medical
examination and treatment. Nevertheless, similarly significant to this achievement has
been the international bionetwork comprising of the tangled part of researchers, wangles,
clinicians, professional societies, government funding and agencies, monitoring bodies,
impresarios, project financiers, and minor, major commercial entities within the
biomedical optics engineering, in addition to other industries (P Sathyan et al., 2012).
There are numerous traditions to distinguish and measure OCT's influence. In the
antiquity of ophthalmology, limited imaging machineries have been espoused more
rapidly than OCT, and OCT is a vital study and clinical instrument in cardiology and
dermatology. Optical Coherence Tomography is castoff primarily to portray structural
physiognomies. But this multipurpose imaging method is also able to deliver practical
imaging of live, integral tissue, and in topical years, investigators have progressively
hunted leeway to understand this latent. These scopes increase OCT's significance for
clinical work by affording wealthier data about such subtleties as blood flow, collagen
and oxygenation (Dharwadkar S, Nayak BK, 2017).
Optical Coherence Tomography/Scanning Laser Ophthalmoscopy (OCT/SLO) represents
possibly the most significant medically authorised advance in investigative expertise that
the eye care communal has realised in relative period. The capacity to perceive, identify,
stage and regulate the degree of progression of retinal diseases with a firmness that slants
is much healthier than magnetic resonance imaging. In the previous years, OCT/SLO has
combined an enormous and rising admiration in eye care and correctly so. There is no
essential groundwork of the retinal being imaged and very minute is requisite on the
patient’s side (Maalej et al., 2012). The capability to better distinguish and classify
macular edema, along with the aptitude to examine detailed layers of the retina, has
demonstrated to be exceedingly advantageous in the attention of retinal patients.
Furthermore, OCT/SLO arrived on the eye care division at an appropriate time, as life
expectancy of retinal patients’ eye at which macular, neuro-degenerative and optic nerve
complications are more everyday. OCT/SLO is glowing on its means to develop the
standard of attention for retinal diseases like glaucoma. As an alternative, visible
structural injury heralds measurable functional damage most of the time. One cause for
this may be the occurrence of intersection in visual receptor fields (Coppola G, Di Renzo
A, Ziccardi L G, et al., 2015). Another cause may be that the seamless visual field study
fairly doesn’t appear to have been happened. OCT/SLO has now recognised to be
tremendously appreciated at defining the incidence and degree of structural evolution in
Alzheimer’s disease (P.S.Jagadeesh Kumar, J.Ruby, J.Lepika, J.Nedumaan, J.Tisa, 2015).
OCT/SLO is very much appreciated but there are two effects it just doesn’t concoct: think
and diagnose. Additionally, it doesn’t straightaway measure the retinal tissues of the eye.
It as an alternative measures the changes in the light reflectivity of the tissues. The
several tissues and their layers in the eye reflect light at several planes, so they display as
discrete entities on an OCT (Igor Bussel, Gadi Wollstein et al., 2013). Nevertheless, these
diverse levels of reflectivity do permit the device to section the different layers of the
tissue being imaged. OCT/SLO proficiency has really stretched the advantage of

enumerating disease progressions down to few microns. It has augmented the
contemplate in detecting numerous retinal diseases. It perhaps grows more everyday as
many clinicians practise it and advances remain to be made to its existing farfetched
functionalities. Furthermore, growths in the technology permits to custom OCT/SLO in
place of hostile analytical tests, such as fluorescein angiography for retinal and optic
nerve studies (Berisha et al., 2007). Nevertheless, OCT/SLO technology, as erudite as
may be, will at no time produce the similar qualitative data as observed directly at the
tissues of the human eye (Kromer et al., 2014). Afterward, OCT/SLO technology is an
exceptional method to accomplish impartial quantitative information in the occurrence of
retinal diseases such as glaucoma, alzheimer’s disease, and macular edema.
2 Retina and Macular Edema
Macular edema is the paradigm of liquid in the macula, an expanse in the intermediate of
the retina. The retina is the delicate tissue at the posterior of the eye and the macula is the
portion of the retina accountable for persuasive, straight-ahead vision as shown in Fig. 1.
Fluid accumulation sources the macula to swell and congeal, which misrepresents vision.
Macular edema happens when there is irregular outflow and accretion of fluid in the
macula from injured blood vessels in the adjacent retina. A communal source of macular
edema is diabetic retinopathy, a disease that can occur to patients with diabetes
(Trichonas G, Kaiser PK, 2014). Macular edema can also arise after eye surgery, in
connotation with age-related macular degeneration, or provocative ailments that distress
the eye. Any disorder that injures blood vessels in the retina can lead to macular edema.
The principal sign of macular edema is shadowy or crimped vision or together in the
center of the field of vision. Colors might also seem carried away or washed-out.
Furthermost, patients with macular edema will have indications that vary from somewhat
fuzzy vision to obvious vision damage. If only one eye is inflated, the vision may be
blurred till the disorder is matured. Macular edema denotes to an atypical swelling of
fluid in the coatings of the macula. Analogous to a globule of water on the computer
screen, the enflamed retina garbles images; causing it harder to see undoubtedly. The
more prevalent, denser, and unadorned the swelling develops, the more probable one will
realise visual symptoms of fuzziness, falsification, and troubled reading. If not treated
properly, chronic macular edema can cause unalterable harm of the macula and perpetual
vision loss. Macular edema is classically originated by augmented seepage from
incapacitated retinal blood vessels or development of irregular blood vessels in the retina.
The maximum operational treatment stratagems for macular edema report the
fundamental sources such as diabetes in addition to a superfluous of fluid dripping from
irregular blood vessels in and around the macula. Eye drops and surgical procedure can
be dynamic in various retinal diseases, but the backbone of the deed is intravitreal
injections (Maalej et al., 2012).

Fig. 1. Structure of the Eye.
(a) Cystoid macular edema
Cystoid macular edema (CME) includes fluid gathering in the external plexiform coating
inferior to anomalous perifoveal retinal capillary absorbency. It is a trouble-free disorder
which distresses the central retina or macula. When this disorder exists, multiple cyst-like
(cystoid) extents of fluid seems in the macula and reasons for retinal swelling or edema.
The indications include hazy or diminished central vision. Nevertheless, the exact reason
of CME is unknown; it may convoy a diversity of disorders such as retinal vein
occlusion, uveitis, or diabetes (Y M Helmy, H R Atta Allah, 2013). It most frequently
befalls after cataract surgical treatment. About 1-5% of those who have cataract
abstractions will involve diminished vision due to CME, typically within a month after
surgery. If the complaint seems in one eye, there is an augmented jeopardy that it will
also distress the second eye. Providentially, though, most patients recuperate their vision
with proper eye care and therapy.
(b) Diabetic macular edema
Diabetic macular edema (DME) is instigated by an exertion of diabetes called diabetic
retinopathy. Diabetic retinopathy is the most communal diabetic eye disorder and the
foremost reason of permanent loss of vision. Diabetic retinopathy generally affects both
eyes. Diabetic retinopathy is produced by continuing injury to the trivial blood vessels of
the retina (Virgili G, Menchini F et al., 2009). The seepage of fluid into the retina may
cause swelling of the adjacent tissue, together with the macula. DME is the utmost reason
of vision loss in patient with diabetic retinopathy. Deprived blood sugar regulation and
further medical circumstances, such as high blood pressure, upsurge the danger of
blindness for patient with DME. DME can transpire at any phase of diabetic retinopathy,
though it is more prospective to arise later as the disease advances.

3 Retina and Glaucoma
Glaucoma is a syndrome which anguishes the optic nerve and can source sightlessness.
The optic nerve is the nerve that diffuses optical signals from eye to the brain, permitting
vision. In premature stage, glaucoma can generally be cured. Nevertheless, it habitually
has no indications; regular eye inspections are the criterion. Glaucoma typically instigates
when pressure upsurges in the aqueous humor fluid of the ciliary epithelium. This fluid
cleanses the interior of the eye, disparate to the tears, which cleanse the exterior of the
eye (Dong ZM et al., 2016). When the intraocular pressure increases it can harm the
cranial nerve II. The eye continuously secretes aqueous humor fluid. If the usual removal
of liquid from the eye, through trabecular meshwork, develops block, large fluid
accumulates in the eye producing a surge in pressure. There exist two foremost types of
glaucoma namely open angle glaucoma and closed angle glaucoma. Glaucoma is
certainly about the difficulties which transpire due to increased Intraocular Pressure
(IOP). The regular IOP in a usual population is 15-17 mmHg. In a regular population,
pressure equals to 20 mmHg may be inside typical range. A pressure of 21mmHg is
uncertain and perhaps irregular (Dharwadkar S, Nayak BK, 2017). However, not all
people with higher pressure mature glaucoma. It's probable for new-borns and progenies
to develop glaucoma. It may be existing from natal or advanced in the initial few years.
The optic nerve harm may be overcome by removing blocks or by a fundamental
remedial therapy.
(a) Open angle glaucoma
Open angle is the angle where the iris connects the cornea as extensive and exposed as
illustrated in Fig. 2. Open angle glaucoma is similarly termed as primary or chronic
glaucoma. This is the utmost form of glaucoma. It arises deliberately in aged patients.
The drainage extent of the retina develops congestion and the pressure upsurges. This
ground for slow loss of outlying vision. Frequently, the vision damage is not perceived
till it is much matured (Igor Bussel, Gadi Wollstein et al., 2013). Open angle glaucoma,
the greatest general kind of glaucoma, instigating for not less than 50% of all glaucoma
causing:
 Sluggish blockage of the drainage ducts, ensuing augmented eye pressure.
 Gradual progression and is a permanent disorder.
 Warning sign and mutilation that are not observed.
Open angle glaucoma sources no hurt and do not perceive a variation of vision in the
beginning since the initial loss of sight is of lateral or outlying, and the visual acuity is
sustained till later in the disorder. Through the period a patient is conscious of vision loss,
the disorder is relatively matured. Deprived of appropriate diagnoses, glaucoma can
cause impaired vision (P Sathyan et al., 2012). The righteous inform is that with
consistent eye tests, premature discovery, and medication can prevent vision loss. Since
open angle glaucoma has very limited threatening indications before mutilation ensues, it
is sizable to have consistent eye check-ups. If glaucoma is noticed through an eye test, a
pre-emptive action to help guard the sight is arranged. Certain patients with glaucoma
suffer low vision. Low vision causes difficulties undertaking every day, monotonous
things though if wearing lenses or glasses. Glaucoma comprises loss of contrast
sensitivity; the capacity to perceive shades of the identical colour, glitches with glower,
light sensitivity, and moderated visual acuity; the capability to realize tiny facts.

Fig. 2. Open angle glaucoma.
(b) Closed angle glaucoma
Closed angle glaucoma is a disorder in which the pressure within the eye develops too
high. This category of glaucoma is much infrequent than open angle glaucoma. It often
emanates immensely when the drainage zone in the eye abruptly turns into totally
blocked. The pressure in the eye increases rapidly. A distorted vision and rainbow
coronae around illuminations as well as agony, soreness of the eye may be observed. If
not preserved immediately, it can reason sightlessness (Dong ZM et al., 2016). In closed
angle glaucoma, pressure increases quickly since the liquid is not streaming as it must.
Liquid is formed in the back cavity of the eye, late the iris. This fluid usually streams
over the pupil into the anterior cavity of the eyeball. The liquid then moves over a
sequence of canals called the trabecular meshwork and then hooked on to the sclera, the
white potion in the eye. In closed angle glaucoma, since the trabecular meshwork is
congested or injured, the liquid cannot move easily over the drainage alleyway, or is
totally gridlocked. This liquid stoppage upsurges pressure within the eye. Closed angle
glaucoma is not as much of frequent. If left without treatment, glaucoma might spring
injury to the optic nerve and eventually loss of sight. Angle-closure glaucoma is also
termed as closed-angle glaucoma, which happens when the iris swells onward to thin or
condense the drainage slant between the cornea and the iris (P.S.Jagadeesh Kumar,
J.Ruby, J.Lepika, J.Tisa, J.Nedumaan, 2017). Therefore, liquid cannot flow over the eye
and pressure surges. Certain patients have slim drainage slants, pushing them at high
danger of angle closure glaucoma. Angle closure glaucoma may transpire unexpectedly
identified as acute angle closure glaucoma or may transpire gradually acknowledged as
chronic angle closure glaucoma.
4 Retina and Alzheimer’s Disease
Alzheimer’s disease (AD) is a hybrid disease and has several perceptive types. These are
typically split into remembrance, linguistic, decision-making, consecration, and optical
disorders. The abnormalities of AD in which optical indications are protuberant due to
the confined parieto-occipital fissure are usually specified to as optical variant Alzheimer
(Elena Salobrar-Garcia et al., 2015). The connection amid eye and brain proposes that it

is practical to semblance for ocular pointers of neuro-degenerative syndrome and esteem
the eye as a leeway of the Central Nervous System (CNS). Vision grumbles are usual
detections in AD patient and these might have a considerable influence on sovereignty
and eminence of these patients. The general form of vision warning sign is weakening of
longitudinal contrast sensitivity, gesture discernment, shade perspicacity and loss of
sight, which in the former, were ascribed to abrasions distressing the principal visual
cortex and other explicit parts of the brain. Neuroimaging practices are crucial in the
analysis of AD and OTC has developed the furthermost recycled instrument for cerebral
imaging in AD patients, delivering comprehensive evidence about brain (Kromer et al.,
2014). Though revisions have not yet finally clarified the structural and functional
vicissitudes that happen in brains of AD patients, roughly clinical and histologic revisions
propose that the similar neurodegenerative procedure that befalls in the brain, may also
distress the retina, subsequently the later epitomises an outlying portion of CNS. Retinal
obsessive vicissitudes such as loss of Retinal Ganglion Cell (RGC) and their attributes
were established. Consequently, conferring to numerous clinical and histologic revisions
there is substantial indication of frontal optical pathway damage in AD patients, with
principal engrossment of RGC and their tissues (P.S.Jagadeesh Kumar, J.Ruby, 2018).
With the discovery of OCT, in the previous twofold decades, it technologically advanced
to deliver an unswerving clinical quantifiable valuation of retina. Numerous previous
revisions have appraised the Retinal Nerve Fibre Layer (RNFL) thickness restrained by
OCT and all evidences were intelligent to validate that maximum of RNFL constraints
were condensed in patients with AD (Coppola G, Di Renzo A, Ziccardi L G, et al., 2015).
The decrease of RNFL width was suggestively larger than that detected in the age-related
patients and thus cannot be completely recognised to aging. In harmony with these
revisions, the decrease of RFNL thickness happened in respective four retinal quadrants,
recommend that retinal axonal loss in AD patients appears to be the consequence of a
long-winded disintegration procedure of RGCs. World-wide diminution of RNFL typical
width dimensions in AD patients was recognised by numerous self-governing groups. All
suggestions detected a considerable lessening of RNFL thickness in every quadrant, with
preponderance in the larger and smaller quadrants. Assorted groups exposed the retinal
axonal loss with RNFL decreasing in AD patients, though various marketablely obtained
OCT strategies were employed. The advance of the SD-OCT suggests a speedy imaging
procedure that has publicized latent in refining the empathetic of neuro-degenerative
diseases. Apart from smearing this method in the analysis of retinal disorders, it may also
advance the empathy of its role in retinal connexion of neurodegenerative disease
evolution (Berisha et al., 2007). Instantaneously, the usage of SD-OCT methods may be
possibly advantageous in measuring neuronal loss in AD, permitting evaluation of
disease development even in preclinical phases, in addition to appraising treatment in
medical tribunals.
In embryological advance, eyes and brain have an analogous derivation. The eyes are
shaped from the frontal neural conduit, an extent that later stretches its growth to the
brain. Ocular expansion happens over description of the eye arena post neural initiation.
This procedure involves precise transcript features that are also well-maintained in brain
expansion (P.S.Jagadeesh Kumar, J.Ruby, J.Lepika, J.Nedumaan, J.Tisa, 2014). One such
subject, a main controller genetic factors of the growth of the eye field, oculorhombin,
theatres a vivacious role in neural development. When articulated ectopically,
oculorhombin can persuade ocular development in other fragments of the body.

Consequently, owing to its close connotation with the brain, it is not startling that neuro-
degeneration produced by syndromes such as Alzheimer’s disease outspreads into the eye
(Lim JKH, Li Q-X et al., 2016). Therefore, this affords a prospect to custom a triflingly
hostile method to scrutinize the compulsive structures in the brain – over the translucent
standard of the eye as shown in Fig. 3.
Fig. 3. Retina is a true window to the heart and the brain.
5 OCT and Retinal Disease Classification
Reduction in visual acuity in place with diabetic retinopathy most typically happens from
diabetic macular edema. Conventional procedures of assessing DME encompass ancillary
funduscopy, biomicroscopy, angiography and streo-photography. Yet, given the relative
dearth of facility of these approaches to perceive and to enumerate DME, substitute
impartial approaches have been functional. The outline of OCT consents an unbiased
assessment of DME with efficiency in both qualitative and quantifiable portrayal of this
pathology. That is because it developed a typical instrument in the administration of
DME patients (Virgili G, Menchini F et al., 2009). Further 15 years subsequent to Early
Treatment Diabetic Retinopathy Study (ETDRS), OCT significantly improved the
capability to perceive macular clotting and has fetched new perceptions on the
morphology of DME and on the occurrence of vitreo-retinal crossing point irregularities.
With the accurate and valuable data given by OCT, DME can better identified, classified
and trailed.
Glaucoma is a liberal optic neuropathy ensuing distinctive impairment to the optic nerve
and blemishes in the visual arena. Since it can prime to permanent blindness, judicious
recognition of glaucoma is dangerous. Hitherto, examination is regularly indeterminate.
Premature vicissitudes are suitable to be intangible, and physical and practical stains
normally do not give the impression concurrently. Neural mutilation frequently reveals
beforehand statistically substantial visual field deviations, so the capability to steadily
perceive it is vital (Gracitelli et al., 2015). Usually quoted physiognomies of
glaucomatous neuropathy embrace an upsurge in the cup-to-disc ratio, achieving of the
neuro-retinal circumference, nerve fiber coating blemishes, vessel variations inside the

optic nerve cranium, and disc depletion. There is habitually momentous alteration in
arbitrating the optic nerve, even amid skilled clinicians (P.S.Jagadeesh Kumar et al.,
2018). A nerve with a bulky cup might be typical, though one with a trivial cup might be
glaucomatous. Numerous circumstances counting high bigotry, slanted discs, and optic
depths of despair also disturb the optic nerve, creating it further problematic to recognize
glaucomatous optic neuropathy in their occurrence. OCT has been fundamental in clinical
valuation of the optic disc and for tightfitting profounder edifices that cannot be
evaluated in the clinical checkup, like the lamina cribrosa. Topical suggestion provisions
the concept that preliminary glaucomatous injury happens at the lamina. Premature
vicissitudes display later distortion and congealing of laminar muscle, which profounder
OCT imaging can nowadays distinguish. If these vicissitudes can be recognized early in
the disorder, dealing invasions can be complete to envision ailment evolution.
Alzheimer’s disease is controlled by liberal perceptive damage, such as remembrance
shortfall, failure in erudition and supervisory maneuver, and visual irregularities. The
Retinal Nerve Fiber Layer (RNFL) width capacities were abbreviated in all quadrants,
signifying that a prolix axonal deterioration arises in AD patients (P.S.Jagadeesh Kumar,
J.Ruby, J.Lepika, J.Tisa, J.Nedumaan, 2014). It is strengthened by the macular width
decrease, particularly by the damage of internal retinal coatings, which reproduces a
privileged retinal Ganglion cell layer (GCL) loss in AD patients. Hence, OCT constraints
can be recycled to discriminate AD patients from typical aging. Both RNFL and macular
width capacities attained by OCT can be hand-me-down to perceive premature neuronal
forfeiture as established in Mild Cognitive Impairment (MCI) patients, signifying that
OCT might be a capable analytical device in AD diseases (Cunha et al., 2016). OCT is
beneficial in detecting the acclimating patients from cognitive impairment to AD.
Furthermore, neuronal damage appears to associate well with cerebral weakening in AD,
particularly for macular constraints. This specifies the capable part of OCT in the medical
assessment of AD patients. Consequently, OCT is a non-invasive trial, which supposed to
assist as an indicator in AD patients that might be regularly castoff to estimate and survey
the patients, permitting a further inclusive method in sorting disorders.
6 Quantitative Assessment
Nearly 3000 eyes of patients including men, women and children of different age groups
with different retinal disorders were inspected and diagnosed with OCT. In prospective
Trial-I, OCT scans were performed for 900 eyes of 500 Macular Edema patients using
OCT/SLO (Optical Coherence Tomography/Scanning Laser Ophthalmoscopy). The
Spectral OCT/SLO could produce a 3D retinal width plot reserved in a sequence within 5
seconds. This differs with the Stratus OCT, which produces its 3D retinal width plot from
spatial scans (Y M Helmy, H R Atta Allah, 2013). Inimitable to the Spectral OCT/SLO is
its aptitude to do practical examine of the retina. Similarly, since additional scans are
recycled to produce this plot, the width analyses over respective pixel of the retinal plot
can be established. Visual field testing over a minor, further meticulous extent of the
retina is named as microperimetry, which trials the capacity of the patient to distinguish
illuminations of fluctuating concentrations. Consequences are plotted over the SLO
fundus image, and might also be shrouded upon a retinal width plot. In this fashion, the

connection among retinal purpose and width at detailed areas in the retina can be
evaluated as shown in Fig. 4.
In prospective Trial-II, OCT scans were performed for 900 eyes of 500 Glaucoma
patients using OCT/SLO. RNFL thickness examination is significant in evaluating the
impairment from premature glaucoma, as the RNFL has been revealed to develop diluent
earlier to other vicissitudes from glaucoma become obvious (Gracitelli et al., 2015). The
OCT/SLO can generate a topographic plot of the optic nerve extent as publicized in Fig.
5 in the similar method that it is engendered in the macular edema, by means of
longitudinal scans over a 5mm area. With the help of this information, evidence about the
RNFL width can be mined as shown in Fig. 6, moreover as a width plot or as a dimension
of the RNFL width laterally through a static diameter about the optic nerve. Since the 3.4
mm ring is mined from a width plot, the ring may be enthused to inspect dissimilar
extents about the optic nerve deprived of having to scan the patient several times.
Fig. 4. Spectral OCT/SLO based DME patient examining.

Fig. 5. OCT/SLO generates an RNFL thickness of a glaucoma patient.
Fig. 6. Based on data produced from Fig. 5, RNFL width laterally 3.4mm ring.
In prospective Trial-III, OCT scans were performed for 900 eyes of 500 Alzheimer’s
disease patients using OCT/SLO. Spectral OCT/SLO imaging permits to attain imageries
with noticeably healthier obstinacy of the abnormalities of AD in which optic warning
sign are prominent owed to the limited pathology of the retina (Cunha et al., 2016). This
swiftness, firmness in imaging lessens crusade artifacts, and consents numerous disparate
imaging stratagems to be achieved rapidly and with superior precision. Fig. 7 validates
that the GCL+ and GCL++ width is expressively inferior in eyes of Alzheimer’s disease
patients. The RNFL width dimensions in AD eyes were inferior to regular eyes, which
did not influence statistical implication.

Fig. 7. AD testing to map the parieto-occipital region superseding OCT/SLO.
The outcomes establish that interior retinal coats defacement replicate the neuronal
disintegration of the retina in AD, chiefly disturbing the macular expanse. This method
may be auspicious in AD assessment, expressly since the Retinal Ganglion Cell (RGC)
weakening shares correspondences with neuronal forfeiture in the brains of AD patients.
The reduction of complete macular width is probably correlated to the favored connection
of the RGC layer.
In prospective Trial-IV, OCT scans were performed for 300 eyes of 250 general retinal
disorders patients using OCT/SLO. Imaging over a section of the retina with the
OCT/SLO engenders an image of such firmness that the dissimilar coverings of the retina
are visibly understood as revealed in Fig. 8. Due to this, delicate pathologies are
envisaged earlier, and this might lead to premature finding and imposition of retinal
diseases. In OCT/SLO, the cystic vicissitudes are distinct, suggesting that the cystic are
composed of quite a lot of minor cysts. The epiretinal sheath is understood too evidently
outspreading from one culmination of the scan to the other culmination. Supplementary
data is attained with vitreous fragments realized as white spots in the vitreous along with
a posterior vitreous detachment (PVD) as publicized in Fig. 9.

Fig. 8. OCT/SLO longitudinal scan clearly showing the different retinal layers.
Fig. 9. OCT/SLO showing PVD.
Fig. 10. OCT and Percentage of Occurrence (Macular Edema)

7 Results and Interpretation
A complete investigation into the role of Optical Coherence Tomography in classifying
and evaluating retinal disorders in providing proper eye treatment guidance were carried
out. The results of the investigation were shown in Table I and Table II.
In trail-I, 900 eyes of 500 patients exaggerated by macular edema were investigated. The
results show that out of 900 patients, 368 patients were affected by Cystoid Macular
Edema (CME), which donates to about 41% of the overall patients including 15% of men
and 26% of women and children. Diabetic Macular Edema (DME) were classified into
Focal Macular Thickening (FMT), Diffuse Macular Edema (DiME), Tractional Macular
Edema (TME), Serous Retinal Detachments (SRD). The investigation reveals that out of
900 patients, 167 were affected by FMT, which contributes to 19% of the overall patients
including 8% of men and 11% of women and children, 227 were pretentious by DiME,
which contributes to 25% of the overall patients including 15% of men and 10% of
women and children, 38 were pretentious by TME, which contributes to 4% of the overall
patients including 2% of men and 2% of women and children, 89 were pretentious by
SRD, which contributes to 10% of the overall patients including 6% of men and 4% of
women and children. The symptoms and causes for distinct types of macular edema
including their suggested therapy were also evaluated and tabulated. The percentage
occurrence of macular edema analysed through OCT is shown in Fig. 10.
Fig. 11. OCT and Percentage of Occurrence (Glaucoma)
In trail-II, 900 eyes of 500 patients exaggerated by glaucoma were examined. Glaucoma
was classified into Primary Open Angle Glaucoma (POAG), Acute Primary Angle
Closure (APAC), Secondary Angle Closure Glaucoma (SACG), and Developmental
Glaucoma (DG). The investigation reveals that out of 900 patients, 449 were affected by
POAG, which contributes to 50% of the overall patients including 21% of men and 29%
of women and children, 198 were pretentious by APAC, which contributes to 22% of the
overall patients including 10% of men and 12% of women and children, 149 were
pretentious by SACG, which contributes to 17% of the overall patients including 9% of

men and 8% of women and children, 90 were pretentious by DG, which contributes to
10% of the overall patients including 6% of men and 4% of women and children. The
symptoms and causes for distinct types of glaucoma including their suggested therapy
were also evaluated and tabulated. The percentage occurrence of glaucoma analysed
through OCT is shown in Fig. 11.
In trail-III, 900 eyes of 500 patients exaggerated by Alzheimer’s Disease (AD) were
examined. AD was classified into Type 1, Type 2, Type 3 and Type 4. Type 1 includes
Narrowing of the Venous Blood Column Diameter, Reduced Venous Blood Flow Rate;
Type 2 includes Thinning of the RNFL, Visual Field Loss, Retinal Ganglion Cell Loss;
Type 3 includes Diabetes, Age-Related Optic Nerve Degeneration; Type 3 includes Leber
Congenital Amaurosis, Abnormalities in Contrast Sensitivity.
Fig. 12. OCT and Percentage of Occurrence (Alzheimer’s Disease)
The investigation reveals that out of 900 patients, 334 were affected by Type 1, which
contributes to 38% of the overall patients including 20% of men and 18% of women and
children, 234 were pretentious by Type 2, which contributes to 26% of the overall
patients including 12% of men and 14% of women and children, 183 were pretentious by
Type 3, which contributes to 20% of the overall patients including 12% of men and 8%
of women and children, 118 were pretentious by Type 4, which contributes to 14% of the
overall patients including 8% of men and 6% of women and children. The symptoms and
causes for distinct types of Alzheimer’s Disease including their suggested therapy were
also evaluated and tabulated. The percentage occurrence of Alzheimer’s Disease analysed
through OCT is shown in Fig. 12.
In trail-IV, 300 eyes of 250 patients inflated by other retinal disorders were examined.
The investigation reveals that out of 300 patients, 23 were affected by Central Serous
Retinopathy, 36 were affected by Retinoblastoma, 46 were affected by Endophthalmitis,
36 were affected by Retinal Hemorrhage, 28 were affected by Solar Retinopathy, 19 were
affected by Posterior Vitreous Detachment, 104 were affected by Cataract i.e. 35% of the
overall patients were affected by cataract. To summarize, the results are evident that the
major cause for retinal disorders are Macular Edema, Glaucoma, Alzheimer’s Disease
and Cataract; in specific, Cystoid Macular Edema, Diffuse Macular Edema, Primary
Open Angle Glaucoma, Cataract, Alzheimer’s Disease Type 1 and Type 2 contribute
profoundly as evaluated through OCT.

8 Conclusion
The capability to perceive and measure structural damage is crucial for appropriate
analysis and supervision of retinal disorders. Valuation of retinal damage with OCT/SLO
has been demonstrated valuable for detecting and assessing the disease at various levels
of severity, as well as for enumerating distinct therapeutics in macular edema, glaucoma,
Alzheimer’s disease and other distrusts. Moreover, structural assessment from OCT/SLO
combined with functional classification and appraisal is helpful in providing apposite eye
care supervision. The outcomes show a firm and precise classification of retinal disorders
to organize the cause and various therapeutics for diverse diseases assessed by Optical
Coherence Tomography (OCT). OCT suggests a substantial benefit in ophthalmology
revisions consenting the learning of further retinal constraints such as Retinal Ganglion
Cells (RGCs), which might be added subtle than existing constraints used in retinal
disease revisions. Spectral OCT has revealed capable outcomes grounded on Retinal
Nerve Fibre Layer (RNFL) and Ganglion Cell-Inner Plexiform Layer (GC-IPL) revisions,
recognizing the incidence of RGC and optic nerve impairment in retinal disorders.
Currently, SD-OCT expertise is been employed in reviews of Central Nervous System
(CNS) and neuro-degenerative syndromes. Additionally, SD-OCT empowers stronger
recognition and segregation of retinal coatings with the better-quality scan resolution.
Existing revisions of OCT imaging mostly had trivial sample sizes and remained cross-
sectional in strategy, but longitudinal revisions are crucial to evaluate the analytical and
prognostic rate of retinal vicissitudes. In future, longitudinal revisions following the
vicissitudes in retinal constraints over time can be reinforced, permitting the prophetic
capability of retinal variations in assessing the progression of disease.
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TABLE I. CLASSIFICATION AND EVALUATION OF RETINAL DISORDERS USING
OPTICAL COHERENCE TOMOGRAPHY
Trail
Type of
Retinal
Disorder
No. of Eyes
Examined
Sub-Type
Classification/ No. of
Eyes Affected
Symptoms & Causes Suggested Therapy
Trail-I
Macular
Edema
900
Cystoid
Macular
Edema
Eyes with Cysts (368)
Macular thickening,
Retinal swelling,
Retinal inflammation,
Blurred central vision,
Retinal vein occlusion,
Uveitis, Diabetes,
Cataract surgery,
Vitreous gel
Eye drops, Tablets,
Corticosteroids,
Vascular Endothelial Growth
Factor (VEGF),
Acetazolamide (Diamox),
Laser Surgery,
Vitrectomy Surgery
Diabetic
Macular
Edema
Focal Macular
Thickening (167)
Diffuse Macular
Edema (227)
Tractional Macular
Edema (38)
Serous Retinal
Detachments (89)
Others (11)
Age-related macular
degeneration,
Hypertensive retinopathy,
Pars planitis, Choroiditis,
Iridocyclitis,
Diabetic retinopathy,
Irvine–Gass syndrome,
Birdshot retinopathy,
Retinitis pigmentosa
Eye drops, Tablets,
Laser photocoagulation,
Anti-VEGF therapy,
Corticosteroids, mTOR,
Tyrosine kinase,
Protein kinase C,
Nicotinic acetylcholine
receptor, ICAM-1, MMPs,
Renin-angiotensin system,
Ras/Raf/Mek/Erk
Trail-II Glaucoma 900
Chronic
Glaucoma
Primary Open Angle
Glaucoma (449)
Intraocular Pressure
(IOP),
High Degree of Short
Sight (Myopia),
Diabetes,
Ethnicity, Red Eye,
Family History
Eye drops, Tablets,
Visual field test,
Automated Perimetry,
Frequency Doubling
Perimetry,
Electroretinography,
Latanoprost, Brimonidine
Acute
Glaucoma
Acute Primary Angle
Closure (198)
Drastic Rise in Eye
Pressure, High Degree of
Long Sight,
Ethnicity, Family
History,
Halos around Light
Sources, Red Eye, Very
Painful, Cloudy Vision,
Sickness
Eye drops, Tablets,
Laser or Surgical Procedure,
Intravenous Injection,
Laser Trabeculoplasty,
Trabeculectomy,
Peripheral Iridoplasty,
Laser iridotomy
Secondary
Glaucoma
Secondary Angle
Closure Glaucoma
(149)
Pressure in the Eye is
Constantly Higher,
Damaged Trabecular
Meshwork, Eye Ache
with Cloudy Vision,
Milky or Hazy Like
Looking Through Smoke
Eye drops, Tablets,
Diamox, Laser Iridotomy,
Surgical Iridectomy,
Trabeculectomy,
Peripheral Iridoplasty,
Electroretinography
Congenital
Glaucoma
Developmental
Glaucoma (90)
Others (14)
Primary Congenital
Glaucoma in Babies and
Childrens, Axenfeld’s or
Reiger’s Anomaly,
Peter’s Anomaly,
Aniridia,
Sturge Weber Syndrome,
Port Wine Stain,
Arthritis,
Large Eyes, Cloudy Eyes,
Sensitivity to Light,
Watering Eyes,
Poor Vision and Jerky
Eyes (Nystagmus)
Eye drops, Tablets,
Examination under
Antiesthetic (EUA),
Trabeculotomy,
Laser Iridotomy,
Drainage Tubes,
Trabeculectomy,
Needling,
Diode Laser,
Eye Patching,
Surgery Goniotomy

Trail-III
Alzheimer’s
Disease
900
Alzheimer’
Disease
Type 1* (344)
Type 2* (234)
Type 3* (183)
Type 4* (118)
Others (21)
Narrowing of the Venous
Blood Column Diameter,
Reduced Venous Blood
Flow Rate, Thinning of
the RNFL, Diabetes,
Abnormalities in Contrast
Sensitivity,
Retinal Ganglion Cell
Loss, Age-Related Optic
Nerve Degeneration,
Visual Field Loss, Leber
Congenital Amaurosis
Eye drops, Tablets,
Optogenetic, Gene Therapy,
Embryonic Stem Cell
Therapy, Photodynamic
Therapy, Diamox, Laser
Iridotomy, Eye Patching,
Surgery Goniotomy,
Surgical Iridectomy,
Trabeculectomy
Trail-IV
Other
Retinal
Disorders
300 General
Central Serous
Retinopathy (23)
Retinoblastoma (36)
Endophthalmitis (46)
Retinal
Hemorrhage (36)
Solar Retinopathy (28)
Posterior Vitreous
Detachment (19)
Cataract (104)
Unidentified (8)
Sudden Vision Loss,
Loss of Peripheral
Vision,
Light Flashes,
Color Perception
Changes,
Floaters, Eye Pain,
Redness,
Night Blindness,
Vision Loss in Vision
Field,
Trouble Adjusting to
Light Changes,
Photophobia,
Double Vision
Eye Drops, Tablets,
Injection, Glass, Lens,
Scatter Laser
Photocoagulation,
Cryopexy,
Pneumatic Retinopexy,
Scleral Buckling,
Vitrectomy,
Retinal Prosthesis
*Type 1: Narrowing of the Venous Blood Column Diameter, Reduced Venous Blood Flow Rate (250+94=344)
*Type 2: Thinning of the RNFL, Visual Field Loss, Retinal Ganglion Cell Loss (106+72+56=234)
*Type 3: Diabetes, Age-Related Optic Nerve Degeneration (46+137=183)
*Type 4: Abnormalities in Contrast Sensitivity, Leber Congenital Amaurosis (95+23=118)
TABLE II. PERCENTAGE ESTIMATION OF RETINAL DISORDERS USING
OPTICAL COHERENCE TOMOGRAPHY
Type of
Retinal
Disorder
Classification
Evaluation
No. of
Eyes
Examined
No. of
Eyes
Affected
Percentage of Occurrence
(Rounded)
Men
Women &
Children
Overall
Macular
Edema
Cystoid Macular Edema 900 368 15 26 41
Focal Macular Thickening 900 167 8 11 19
Diffuse Macular Edema 900 227 15 10 25
Tractional Macular Edema 900 38 2 2 4
Serous Retinal Detachments 900 89 6 4 10
Glaucoma
Primary Open Angle Glaucoma 900 449 21 29 50
Acute Primary Angle Closure 900 198 10 12 22
Secondary Angle Closure Glaucoma 900 149 9 8 17
Developmental Glaucoma 900 90 6 4 10
Alzheimer’s
Disease
Type 1* 900 250 20 18 38
Type 2* 900 94 12 14 26
Type 3* 900 106 12 8 20
Type 4* 900 95 8 6 14
*Type 1: Narrowing of the Venous Blood Column Diameter, Reduced Venous Blood Flow Rate (28+10=38%)
*Type 2: Thinning of the RNFL, Visual Field Loss, Retinal Ganglion Cell Loss (12+8+6=26%)
*Type 3: Diabetes, Age-Related Optic Nerve Degeneration (5+15=20%)
*Type 4: Abnormalities in Contrast Sensitivity, Leber Congenital Amaurosis (11+3=14%)

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