....... MYOPIA
± Short
sightedness
± term
myopia was derived by Galen (131-201 AO) from the words myein ("to
close") and ops ("eye").
± Parallel
rays of light coming from infinity are focused in front of the retina with
minimal accommodation.
Ø Mechanism
of production of ametropia
± Ametropia,
or the absence of emmetropia, may be produced by variations in :
- The
relative location of the optical elements of the eye with respect to the
retina.
- The
relative refractive power of the optical elements with respect to the
location of the retina.
Ø Optics
of myopia
± Far
point is finite (In front of the eye)
± Emmetropic eye it is at infinity
± Higher
the myopia the shorter the distance
± Far point is 1mt from the eye ,there is 1D of
myopia
± Nodal
point is further away from retina
± CLASSIFICATION
The proposed classifications may be grouped under the
following broad headings:
± Rate
of myopic progression
± Anatomical
features of myopia
± Degree
of myopia
± Physiological
and pathological myopia
± Hereditary
and environmentally induced myopia
± Theory
of myopic development
± Age
of myopia onset
± Rate
of myopic progression
Donders" classified myopia on the basis of its rate of
progression, describing three categories of myopia:
± Stationary
(low degree: -1.50 to -2.00 D) and arises "in the years of
development.“ The degree of myopia remains stationary during adulthood and may
occasionally diminish with the approach of old age. However, Donders
incorrectly suggested that the apparent reduction in myopia with increasing age
was probably due to age-related pupillary miosis with an associated increase in
the depth of focus of the eye.)
± temporarily
progressive (Temporarily progressive myopia generally arises in the early
teens and progresses until the late 20s. After this age, the rate of myopia
progression approaches zero. Interestingly, Donders reported that it was rare
for myopia to develop after 15 years of age in previously normal eyes and,
falsely, that it never developed after the 20th year of life )
± permanently
progressive.(Permanently progressive myopia ascends rapidly until around
25 to 35 years of age, and thereafter advances more slowly. Subsequent
increases in myopia are said to occur in jumps, rather than in a smooth
progression. Donders observed that because of pathological conditions such as
retinal detachment and macular degeneration, in these cases it was rare at 60
years of age "to find a tolerably useful eye
± Classification
by anatomical features of myopia
Berish" stated that myopia could be:
Axial, whereby the eye is too long for its refractive
power.•
Refractive, whereby the refractive system is too
powerful for the axial length of the eye. An increase in axial length may occur
in the anterior or posterior portions of the globe individually, or may occur
throughout the eye. The site of elongation may have implications for
determining the etiology. For example, it has been suggested that expansion of
the posterior portion of the globe may be related to the actions of the
superior and inferior oblique muscles during vergence. 12
Berish" further divided refractive myopia into:
• Index myopia, in which one or more of the
refractive indices of the media are anomalous.
• Curvature myopia, in which the reduced radius of
curvature of one or more refractive surfaces produces increased dioptric power.
• Anterior chamber myopia, in which a decrease in
anterior chamber depth increases the refractive power of the eye.
± Classification
by Degree of myopia
± Hirsch
divided the population into three groups on the basis of the degree of myopia,
which he designated the alpha, beta, and gamma groups,
respectively.
± Alpha
group followed a normal distribution curve, with a theoretically assumed peak
of +0.50 D.
± The
beta group was represented by a second normal distribution curve, with its peak
around -4 D. Hirsch suggested that the myopia in this group may be hereditary
in origin.
± The
gamma group ranged from -9 to -15 D, and this degree was described by Hirsch as
malignant, pathological, degenerative, or congenital.
± Classification
by Physiological and pathological myopia
± Physiological
myopia was defined by Curtin as myopia in which each component of
refraction lies within the normal distribution for that population. Thus, the
myopia arises from a failure of correlation between the refractive components.
However, physiological myopia may be defined as normal as opposed to pathologic
myopia Therefore, physiological myopia might simply and more accurately be
defined as nonpathological myopia.
± Pathological
refractive errors ( by Duke-Elder and Abrams) as "those refractive
anomalies determined by the presence in the optical system of the eye of an
element which lies outside the limits of the normal biological
variations." Pathological myopia may also be described as malignant
or degenerative myopia. These authors adopted the term degenerative myopia to
describe myopia that is accompanied by degenerative changes, particularly in
the posterior segment of the globe. This is most frequently found in high
(>6 D) degrees of myopia, but Duke-Elder and Abrams suggested that a
classification merely by degree of ametropia is inappropriate because
degenerative changes may also occur in cases of low myopia. Moreover, in 1913
Harman" described a case of more than 17 D of myopia without any
pathological changes.
± Classification
into Hereditary and
Environmentally Induced Myopia
± The
debate of hereditary versus environmental influences on the development of
myopia has persisted for more than 400 years and is still unresolved."
Kepler, writing in 1604, was the first to have suggested an association between
the development of myopia and the performance of sustained near-vision tasks.'
However, Rosenfield' noted that the case for such an association remains
unproven. It is frequently impossible to distinguish between environmental and
hereditary influences, and hence other means of classification have been
adopted (e.g., age of onset or degree of myopia) in an attempt to provide
additional information regarding the etiology of refractive error development.
± Classification
According to Theory of
Myopic Development
± In
a review of the etiology of refractive error, Mc-Brien and Barnes"
described three major theories of myopic development:
• The
biological-statistical theory
• The use-abuse
theory
• The theory of
emmetropization
± The
biological-statistical theory
± The
biological-statistical theory" considered variations in refractive error
as forming a biological continuum ranging from high myopia to high hyperopia.
Thus, ametropia simply represented the normal biological variation of a
physiological component. However, data by both Stenstrom" and Sorsby et
al. clearly demonstrated that the distribution of refractive error was not
normal.
± The
use-abuse theory
± The
so-called use-abuse theory proposed by Cohrr“ suggested that myopia onset was
an adaptation to use or abuse of the eyes during sustained near vision. Cohn
examined the prevalence of myopia in more than 10,000 German schoolchildren. He
observed that in the youngest children there was little myopia, but the
prevalence increased with age. Cohn concluded that because the increased
prevalence of myopia occurred during the educational process, a substantial
portion of which entailed reading and other close work, the onset of myopia was
related to increased near-vision activities.
± Numerous
investigators have reported a higher prevalence of myopia among people whose
occupations involve substantial amounts of close work, In addition, Young"
demonstrated that when adolescent monkeys are restricted to a near-vision
environment they exhibit significant increases in myopia. Other studies
indicated an increased prevalence of myopia in an Eskimo population after the
introduction of formal education, with its increased near-vision requirement.
However, other factors, such as intelligence and changes toward a Western diet,
may also have been at least partly responsible for the change in refractive
error distribution in this population.
± The
theory of emmetropization
± In
view of the higher prevalence of emmetropia than might be predicted on purely
statistical grounds, it would appear that the components of the eye do not grow
independently, but rather undergo a process of coordinated growth. This
proposed correlated growth of the ocular biometric components has been referred
to as emmetiopizauon. Van Alpherr“ suggested that emmetropization was
achieved by a negative- feedback, self-focusing control system. Variations in
ciliary muscle tone could produce changes in refractive error by interfering
with this self-focusing mechanism.
± Classification
Based on Age of Onset
Grosvenor" classified myopia into the following
categories:
• Congenital
myopia-Myopia is present at birth and persists through infancy.
• Youth-onset
myopia-The onset of myopia occurs between 6 years of age and the early
teens.
• Early
adult-onset myopia-The onset of myopia occurs between 20 and 40 years of
age.
• Late
adult-onset myopia-Myopia onset occurs after 40 years of age.
± Late-Onset
Myopia
Late onset Myopia can be categorized the change in myopia
during adulthood (i.e., beyond 18 years of age) into the following three
groups:
± Adult
stabilization-Rapid increases in myopia during early adolescence were followed
by stabilization during early adulthood. Minor adjustment of the refractive
error sometimes occurred after stabilization, but this change was generally
small, on the order of ±0.25 D. Sixty-eight percent of male subjects and 87% of
female subjects fell into this category.
± Adult
continuation-The rapid myopic progression seen during adolescence continued
through adulthood. This pattern represented 25% of male subjects and 13% of
female subjects.
± Adult
acceleration-Myopic progression increased after adolescence. This was the
least common pattern, representing 6.3% of male subjects and no female
subjects.
± Other
Myopias
Night myopia
± The
phenomenon of increased myopia under low luminance conditions was first
reported in 1789 by the Reverend Nevil Maskelyne, the Astronomer Royal. He
found that his astronomical observations at night were facilitated by the use
of concave spectacle lenses.
± More
recent evidence has demonstrated that night myopia is produced by an increased
accommodative response (typically on the order of 0.50 to 1.00 D) under
degraded stimulus conditions. However, there is also some suggestion that
changes in chromatic aberration may also be involved in this myopic shift. The
chromatic aberration of the eye results in blue light being refracted more than
red light.“Furthermore, as the eye transfers from photopic to scotopic
luminance
levels, its peak sensitivity shifts from approximately 55 nm
to around 510 nm. This change in sensitivity is termed the Purkinje shift.78
Thus, at extremely low luminance levels, the eye becomes most sensitive to
those wavelengths undergoing a greater degree of refraction, and therefore
appears to be more myopic than it is under photopic viewing conditions. To
determine the extent to which chromatic aberration could account for the myopic
shift under reduced illumination, Wald and Criffin" used a spectral
stigmatoscope to measure the refractive state of the eye under monochromatic
light. They assessed axial chromatic aberration by measuring the eye's
refractive state under nine narrow monochromatic conditions over a range of 365
to 750 nm. They concluded that the Purkinje shift in spectral sensitivity would
produce a myopic shift in refractive power of approximately 0.35 to 0.40 D.
However, the mean magnitude of the refractive error shift observed under
reduced illumination in their study was -0.59 D (range =-1.40 to +3.40 D).
Thus, chromatic aberration may account for a significant proportion of the
increased myopia observed under degraded stimulus conditions. Direct evidence
that night myopia is primarily produced by ocular accommodation comes from
researchers who examined variations in the form of the third Purkinje image
(reflected from the anterior surface of the crystalline lens) to assess the
accommodative response under very low illumination levels.8 ! - 84 These
investigators all reported mean changes in accommodation of approximately 0.75
D.
This confirmed that the change in the dioptric power of the
eye resulted directly from a shift in accommodation, that is, a change in the
refractive power of the crystalline lens. Indirect evidence that changes in
accommodation must be the primary source comes from the observation of
equivalent levels of tonic accommodation under a number of widely varying test
conditions. For example, in the measurement of tonic accommodation, the
accommodative loop may be opened by having the subject view a Ganzfeld field, a
low spatial frequency difference of Gaussian (DOG) grating, a distant target
through a 0.5 mm pinhole, or by placing the subject in total darkness.“’:”
Clearly, the magnitude of spherical and/or chromatic aberration will exhibit
wide variations under these different conditions, and yet equivalent values of
tonic accommodation have been recorded." Therefore, both chromatic
aberration and tonic accommodation appear to be the main determinants of the
relative myopic shift observed under degraded stimulus conditions.'
± Pseudomyopia
Pseudomyopia has been defined as a reversible form of
myopia that results from a spasm of the ciliary muscle? It is apparent that
this does not meet the standard definition of a refractive error, that is, one
that occurs under conditions of minimal accommodation. The excessive
accommodative response produces an apparent myopic shift that will disappear
when a cycloplegic agent is administered to produce relaxation of accommodation.
These patients are frequently detected by the presence of a significantly
greater (more than 1 D) amount of relative plus power (i.e., more hyperopia or
less myopia) on retinoscopy compared with the subjective refractive findings,
or by the observation of either an eso shift in oculomotor balance or a
reduction in distance visual acuity, particularly toward the end of a working
day.
Clinical
Classification
± Congenital
Myopia
± Simple
Myopia
± Degenerative
Myopia
± Nocturnal
Myopia
± Pseudo
Myopia
± Induced
Myopia
Degree of Myopia
± Low
Myopia(<3D)
± Medium
Myopia(3-6D)
± High
Myopia(>6D)
AGE OF ONSET
± Congenital
Myopia
± Youth-Onset
Myopia(<20 yrs of age)
± Early
Adult-Onset Myopia(20-40 yrs of age)
± Late
Adult-Onset Myopia(>40 yrs of age)
Congenital myopia
ü Frequently
seen in
ü Premature
babies
ü Marfan’s
syndrome
ü Homocystinuria
ü Increase
in axial length
ü Increase
inOverall globe size
ü Since
birth, diagnosed at age 2-3 years
ü If
unilateral, as anisometropia, may develop amblyopia, strabismus
ü Usually
8-10 D, remain constant
ü Bilateral-
difficulty in distant vision, hold things very close
Ø Associated
conditions
ü Convergent
squint
ü Cataract
ü Microphthalmos
ü Aniridia
ü Megalocornea
ü Congenital
Separation of retina
Management
Ø Early Correction is desirable
Ø Retinoscopy under full cycloplegia
Ø Early full correction desirable
Ø Poor prognosis
± Simple
/ developmental myopia
ü Physiological
error not associated with any disease of the eye
Ø Etiology
:
ü Normal
biological variation in development of eye
ü Inheritence
Ø Associated
factors
ü Role
of diet
ü Theory
of excessive near work
Ø Clinical
picture
ü Rarely
present at birth
ü Rather
born hypermetropic, become myopic
ü Begins
at 7-10 years, stabilizing around mid teens
ü Usually
around 5D, never exceeds 8D
Ø Symptoms
ü Poor
vision for distance
ü Asthenopic
symptoms develop due to dissociation between accommodation and convergence
q Convergence
weakness, exophoria, suppression
q Excessive
accommodation inducing ciliary spasm and artificially increasing the amount of
myopia
ü Psychological
outlook
Ø Signs
ü Large
and prominent
ü Deep
AC
ü Large,
sluggishly reacting pupils
ü Normal
fundus, rarely crescent
ü Usually
doesn't exceed 6-8D
± Retinoscopy
under full cycloplegia
± Pathological
/ degenerative / progressive myopia
ü Rapidly
progressive associated with degenerative changes in the eye
Ø Etiology
ü Rapid
axial growth of the eyeball outside the normal biological variations of
development
ü Role
of heredity
ü Role
of general growth process
Genetic factors General growth process
More
growth of retina
Stretching of sclera
Increased axial length
Degeneration of choroid
Degeneration of retina
Degeneration of vitreous
Symptoms
ü Defective
vision
ü Muscae
volitantes / floating black opacities
Signs
- EYE
Large, prominent eyes simulating exophthalmos
- CORNEA
large
- ANTERIOR
CHAMBER deep
- LENS
show opacities at the posterior pole due to aberration of lenticular
metabolism and due to overstretching anterior dislocation may also occur
- VITEROUS
degeneration,viterous liquefication,vitreous detachment present as WEISS
REFLEX
- SCLERA
thinning resulting in formation of STAPHYLOMA
- VISUAL
FIELD DEFECTS show Contraction and in some ring scotomas present
- DISC
ü Large in size
ü Myopic
Crescent on the temporal side of the disc
ü Choroidal
Crescent
ü Supertraction
of the retina
ü Inverse
myopia Myopic crescent situated nasally and supertraction of the retina
temporally
ü called
as INVERSE CRESCENT
ü Peripapillary
Atrophy
- MACULA
Foster-Fuchs fleck
Ø RETINAL
DETACHMENT
Ø POSTERIOR STAPHYLOMA
Ø RETINAL
HOLES
Ø TESSELATED
FUNDUS
Treatment
Optical treatment
ü Appropriate
concave lenses
ü Minimum
acceptance providing maximum vision
± Guidelines
LOW DEGREES OF MYOPIA (Up to -6D)
Ø IN YOUNG SUBJECTS
Defect should
never be overcorrected and advised for constant use to avoid squinting and
develop a normal ACCOMMODATION-CONVERGENCE reflex
Ø IN
ADULTS
Receiving
spectacle for the first time,have the ciliary muscle that are unaccostomed to
accommodate efficiently so that lens of slightly lower power(1 or 2 D) may be
prescribed for reading,especially if engaged in to any greater extent.Above the
age of 40 years,when accommodation fails physiologically, a weaker glass for
near work is essential
ADVANTAGES
OF SPECTACLES
Ø Economical
Ø Allow
incorporation of prism, bifocals, pal which can be used for the management of
esophoria or any accommodative disorders accompanying myopia
Ø Spectacles
require less accommodation than contact lens for myopia that likelihood of
accommodative asthenopia or near point blur in patients approaching presbyopia
may be less
DISPENSING SPECTACLES IN HIGH MYOPIA
± High-index
lens materials
± Lighter
lens materials
± Reduced
eye size of selected frames
± Minus
lenticular lens designs
ADVANTAGES OF
CONTACT LENS
± Contact
lens provides cosmesis
± Large
retinal image size and slightly better visual acuity in severe myopia
SURGICAL TREATMENT
ü Epikeratophakia
ü RK
ü PRK
ü ISCR
ü Phakic IOL’S
ü LASIK
Photorefractive Keratectomy- (PRK)
± Involves
direct laser ablation of corneal stroma after removal of corneal epithelium
mechanically or using a laser beam.
± Done
using Excimer laser
± MUNNERLYN
EQN: depth of ablation (micrometer)=[diameter of optical zone(mm)]² ×
1/3power(Diopter)
± For
myopic a large amount of ablation is done in central cornea than in the
periphery.
± Give
good results for -2D to -6D of myopia
LASIK- Laser Assisted
In situ Keratomileusis
± Method:Anterior
flap of cornea is lifted with a keratome and excimer laser is used to sculpt
the stromal bed to change the refractive error of eye
± Corrects
0.5 to 12D of myopia and upto 8D of astigmatism
± Guidelines:Age
more than 18yrs
BCVA better than 6/12
Stable refraction for last 1yr
Absence of corneal disease & ectasia
± Note:
± (1)
In no case the residual bed thickness after the ablation should measure
250microns so as to avoid central corneal ectasia
± (2)
Ideally the ablation should be done within 30sec of the preparation of flap
LASEK- Laser
subepithelial Keratomileusis
± Indications:
± Low
myopia
± Irregular
astigmatism
± LASIK
complications in contralateral eye
± Thin
corneal pachymetry
± Predisposition
to trauma
± Glaucoma
suspect
± Method:
± Simple
inexpensive procedure that involves creation of epithelial flap after exposure
to 18% alcohol for 25sec & subsequent replacement of flap after laser
ablation
RK- Radial Keratotomy
± It
refers to making deep corneal incisions(initially 16,now down to 4) in the
peripheral part of cornea leaving about 4mm central optical zone
± The
incisions are made almost down to the level of Descemet’s Membrane
± These
incisions on healing flatten the central cornea thereby reducing its refractive
power
± For
low to moderate degree of myopia(-1.5 to
-6D of myopia)
Epikeratophakia
± For
high degree of myopia (upto 20D)
± Method:
± The
epithelium is removed & then a pocket is fashioned under the edge of the
remaining epithelium & into this is inserted the cryolathed donor homograft
± Preserved
material can also be used
NON CORNEAL
INTERVENTIONS
± (A)
REMOVAL OF CLEAR LENS
± We
know that an aphakic eye is strongly hypermetropic
± If
an eye with an axial myopia of -24D is deprived of its lens it will become
emmetropic without any correcting lens
± Note:
± Whenever
surgery on clear lens is contemplated the eye is examined thoroughly for
abnormalties like Raised IOP,Vitreous & retinal degeneration etc
± (b)Phakic
intraocular lenses
± An
IOL of appropriate power is implanted inside the eye without touching normal
crystalline lens thus without disturbing accomodation
± Method
can be used to correct both myopia & hypermetropia
Phakic IOL types:
± PC
IOL
± Angle
supported IOL
± Iris
claw lens
INTRA CORNEAL
RING(ICR) IMPLANTATION
± ICR
implantation into the peripheral cornea approx.upto 2/3rd of stromal
depth can also be considered for correction of myopia
± It
results in a vaulting effect that flattens the central cornea decreasing the
myopia
± The
procedure has the advantage of being reversible
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