Myopia

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Here is a comprehensive overview of myopia drawn from multiple medical textbooks.

Myopia (Nearsightedness)

Definition & Optics

Myopia is a refractive error in which parallel light rays from distant objects converge to a focal point in front of the retina (rather than on it), resulting in blurred distance vision with relatively preserved near vision. It most commonly results from an excessively long axial length of the eyeball, but can also be caused by excessive refractive power in the lens system.

Parallel light rays focus on the retina in emmetropia, behind the retina in hyperopia, and in front of the retina in myopia

Fig. 50.12 — Guyton & Hall Textbook of Medical Physiology

Classification

Type	Definition
Low myopia	< −3 D
Moderate myopia	−3 D to −6 D
High myopia	> −6 D (axial length usually > 26 mm)
Pathologic/Degenerative myopia	Progressive axial elongation with secondary ocular structural changes

High myopia (WHO defines it as > −5.00 D) affects >2% of Western/American adults and up to 10% of East Asians. Global prevalence is expected to reach 5 billion by 2050, with 1 billion having high myopia.

Aetiology & Risk Factors

Myopia arises from complex hereditary and environmental factors:

Strong association with prolonged near visual work (reading, screen use)
Reduced outdoor time — sunlight exposure appears protective
Genetics — multiple loci identified; family history is a major risk factor

Systemic associations of high myopia (Table 14.4, Kanski's):

Down syndrome
Stickler syndrome
Marfan syndrome
Prematurity
Noonan syndrome
Ehlers–Danlos syndrome
Pierre–Robin syndrome

Pathology of Degenerative (Pathologic) Myopia

Pathologic myopia involves progressive weakening and elongation of the posterior sclera, mechanically stretching all posterior ocular tissues. Key fundus findings include:

Finding	Description
Tessellated (tigroid) fundus	Diffuse RPE attenuation → large choroidal vessels visible
Focal chorioretinal atrophy	Patchy RPE and choroidal loss
Tilted optic disc	Anomalous optic nerve head appearance
Peripapillary atrophy	Temporal crescent of thinned/absent RPE
Lacquer cracks	Ruptures in RPE–Bruch membrane complex (~5% of highly myopic eyes); fine yellow irregular lines at posterior pole
Subretinal "coin" haemorrhage	From lacquer cracks without MNV
Fuchs spot	Raised pigmented macular lesion after subretinal haemorrhage absorbs
Posterior staphyloma	Focal peripapillary or macular scleral ectasia (~1/3 of pathologic myopia eyes)
Lattice degeneration	Peripheral retinal thinning
Macular neovascularization (MNV)	~10% of highly myopic eyes; treated with anti-VEGF
Rhegmatogenous retinal detachment	Increased risk due to PVD, lattice degeneration, atrophic holes
Macular retinoschisis / foveoschisis	From vitreous traction in high myopia with staphyloma

Maculopathy is the most common cause of visual loss in pathological myopia and a significant cause of legal blindness.

Correction of Myopia

Optical

Spectacles with concave (diverging) lenses — diverge rays before they enter the eye, shifting the focal point posteriorly onto the retina
Contact lenses — same optical principle

Surgical (from Kanski's Clinical Ophthalmology)

Procedure	Notes
Surface ablation (PRK/LASEK)	Low–moderate myopia
LASIK	Moderate–high myopia; limited by initial corneal thickness
SMILE (refractive lenticule extraction)	Small-incision technique for myopia and myopic astigmatism
Iris clip implant ("lobster claw")**	Anterior chamber phakic IOL; complications include subluxation, endothelial cell loss, cataract, pupillary-block glaucoma, retinal detachment
Phakic posterior chamber implant (ICL)	Implanted behind iris, in front of lens; power −3 D to −20.5 D; material = Collamer (collagen-derived)
Clear lens exchange	Good visual results; risk of RD (higher in high myopia)
Radial keratotomy	Now predominantly historical

Myopia Control (Slowing Progression in Children)

Intervention	Evidence
Low-dose atropine 0.01% (bedtime)	Significantly slows myopia progression; reasonable to offer ages 5–15 if progressing > 1 D/year; mechanism unclear; side effects dose-dependent (mydriasis, loss of accommodation)
High-add (+2.50 D) multifocal contact lenses	For ages 7–11 with < 5 D myopia; BLINK trial shows dose-dependent slowing of progression
Increased outdoor time in sunshine	Protective; encouraged alongside pharmacological treatment

High Myopia Complication: MNV Treatment

Anti-VEGF therapy is the treatment of choice for myopia-related MNV. Injection frequency is generally less than that needed for AMD, but retinal detachment risk is higher. Prognosis is better in younger patients compared to AMD-related MNV.

High Myopia & Lens Changes

High myopia can cause:

Posterior subcapsular lens opacity
Early-onset nuclear sclerosis — paradoxically may increase the myopic refractive error

Sources:

Kanski's Clinical Ophthalmology: A Systematic Approach, 10th ed., pp. 299, 631–632
Guyton & Hall Textbook of Medical Physiology, p. 625
Goodman & Gilman's The Pharmacological Basis of Therapeutics
Goldman-Cecil Medicine

Fundus picture

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Here are the fundus photographs of high/pathologic myopia from Kanski's Clinical Ophthalmology (10th ed.):

A — Tessellated (Tigroid) Fundus

Diffuse attenuation of the RPE reveals the underlying large choroidal vessels, giving a "tiled" appearance. The optic disc appears pale with surrounding peripapillary atrophy.

B — Focal Chorioretinal Atrophy & Tilted Disc

Focal chorioretinal atrophy and tilted disc

Large confluent white patches of chorioretinal atrophy — both RPE and choroid are lost, exposing bare white sclera. The disc has a tilted configuration with a large temporal crescent.

C — Tilted Disc with Peripapillary Atrophy

The optic nerve head appears tilted and enlarged, surrounded by a wide zone of peripapillary chorioretinal atrophy (white/pale halo). Vessels emerge at an oblique angle.

D — Lacquer Cracks (arrow)

Fine, irregular yellow-white criss-crossing lines at the posterior pole (arrow) representing ruptures in the RPE–Bruch membrane–choriocapillaris complex. Present in ~5% of highly myopic eyes and can be complicated by macular neovascularization (MNV).

E — Subretinal "Coin" Haemorrhage

Subretinal coin haemorrhage in high myopia

A well-circumscribed, dark red-black subretinal haemorrhage near the disc/macula. Arises from lacquer cracks in the absence of MNV. The fovea (small grey spot centrally) is spared here.

F — Fuchs Spot

A raised, circular, pigmented lesion at the macula (right side of image) with surrounding chorioretinal atrophy. This develops after a subretinal haemorrhage absorbs and represents the end-stage of MNV activity.

Source: Kanski's Clinical Ophthalmology: A Systematic Approach, 10th ed., Fig. 14.52

Diabetic retinopathy with fundus picture

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