Ординатура / Офтальмология / Английские материалы / Age-Related Changes of the Human Eye_Cavallotti, Cerulli_2008

Fig. 20.23 Distal insertion of human extraocular muscles described by Ruskell et al in: Ruskell GL, Haugen IB, Bruenech JR, Van der Werf F (2005) Double insertion of extraocular rectus muscles in man and the pulley theory. Journal of Anatomy 206, 295–306

play a vital role in human eye movement, then these structures must also be taken into consideration when the process of senescence is addressed.

This was done in a recent study where normal functional anatomy of rectus muscles and pulleys in older humans was compared with previously reported findings in younger subjects.69 The results from this study demonstrated significant changes in the functional anatomy of the horizontal rectus muscles with age, suggesting that the pulleys in older people have a different location on the globe than in younger people. The inferior displacement of the pulleys was argued to convert the force of the rectus muscles to depression. These findings could explain the impairment of elevation observed in older people and their predisposition to incomitant oculomotor anomalies. The structural organization of the extraocular connective tissue and its potential role in ocular motility is still a matter of debate and awaits further investigation.70

Restitution of the Oculomotor System

The oculomotor system must be able to execute very fine graded and synchronized contractions to maintain binocularity. Even minute structural changes at any level of this system should, in principal, have large functional implications and disrupt ocular motility. Yet, the vast majority of the population enjoys good binocular vision throughout their old age—seemingly unaffected by the progressively increasing number of age-related changes as described in this chapter. This has led to the contention that cells in the oculomotor system must have regenerative properties that counteract the process of senescence.45

Authorities within the field have recently provided evidence suggesting that extraocular muscles have the unique ability to retain a population of activated satellite cells that provide for continuous myofiber remodeling throughout life.71 The myogenic precursor cells are believed to retain their proliferative properties even in aging muscles, and may be more robust and long-lived than their counterparts in limb muscles. These findings suggest that extraocular muscles have unique abilities to survive aging, injury, functional degeneration and disease. Furthermore, the authors of the same study have raised exciting questions regarding the potential use of this tissue in repair or reconstruction of other tissues, such as nervous tissue and bone.71 This opens new possibilities for treatment of oculomotor anomalies, as well as a broad spectrum of other clinical conditions.

Although embryonic origin and histological composition determine much of the regeneration properties of a given tissue, there are other factors that can influence the speed and extent of cellular repair. Experimental studies in cell cultures, and in vivo, show that activity-dependent production of neurotrophic factors plays a role in promoting neuronal survival and growth.4 This is supported by epidemiological studies that suggest that humans with active minds have a reduced risk of developing neural decline as they age4. The use it or loose it concept has prevailed for a long time, and has formed the basis for many treatment regimes, including the management and treatment of binocular anomalies.

The fact that muscle function can be restored through systematic activation—such as orthoptic exercises or other forms of neuromuscular stimulation—is well-docu- mented. The literature also offers documentation of the reverse effect in cases of neuromuscular inactivity. Vacuolization, loss of tissue substance, and other evidence of atrophy has been found in extraocular muscles obtained from strabismus patients and other conditions associated with reduced muscle tone. However, activated satellite cells have been found in the same type of muscles, suggesting that there is also a regenerative process taking place.72 The speed and extent of this process seem to vary between individuals suffering from the same oculomotor anomalies. The notion that the unique regenerative properties of extraocular muscles can be enhanced through specific activity or treatment regimes cannot be dismissed.

This could account for some of the individual differences in regenerative activity observed in the aged population, and may explain why the chronological age of the patient is not a precise indicator of the process of senescence. Furthermore, it may also explain some of the functional improvements obtained through various unconventional treatment regimes used in clinical practice.

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pressure is the mainstay of management. At present topical acetazolamide and prostaglandin molecules are also commonly used. Surgical treatment is reserved for cases with poor response to topical drugs and progression of disease with elevated intraocular pressure and optic fiber damage. Age-related macular degeneration (AMD) has several forms. Wet AMD is caused by choroidal neovascularization and if unrecognized and untreated can result in rapid deterioration of vision. Initially laser photocoagualtion was the only clinically proven management in neovascular AMD. At present veteporfin therapy with photodynamic treatment is used in patients with predominantly classic subfoveal choroidal neovascularization. Dry AMD is the most common form and tends to progress more slowly compared to the wet form. The most advanced form of AMD, geographic atrophy, also causes central vision loss. Early detection and prompt treatment will help optimize treatment outcome. New forms of treatment of wet AMD like injecting antivascular endothelial growth factor, pegaptanib (Macugen) e Avastatin, have effectively reduced the progression of disease in some randomized trials. Vision loss from diabetic retinopathy can result from several diabetes related retinal changes but early recognition and treatment, including laser therapy, can prevent blindness. The retinopathy depends on the duration of hyperglycemia rather than age. Therefore, prevention emphasizes the need for blood glucose level control to reduce the incidence, progression, and severity of diabetic retinopathy. Degenerative myopia is another cause of visual impairment not only in the elderly but also in the younger population. Total refractive error correction and healthy nutrition are fundamental in reducing the progression of degenerative retinal alterations.

A cataract is a progressive, irreversible opacity of the lens which causes reduction of visual acuity. The lens is a transparent biconvex organ which is situated perpendicular to the optical axis behind the iris and in front of the vitreous body. It can be divided into a central portion, the nucleus; a peripheral portion, the cortical (anterior and posterior); and a capsule.

The principle function of the lens is accomodation; that is, to focus images on the retina similar to a camera. Its peculiar optical structure and transparency characteristics allow the passage of light rays to reach the retina. The lens is the only organ that continues variable development throughout life, changing in thickness, elasticity, and above all transparency.1 Aging and any pathogenetic noxae that alter the biochemical and structural integrity of the lens cause opacities,2 resulting in a significant reduction of visual acuity. This pathology, earlier described by the ancient Greeks, Romans, and Arabs as “a rapid fall of humour from the brain,” is defined as a “cataract,” which means “a falling downwards.” It is the primary cause of blindness. The surgical removal of cataracts is the most frequently performed operation in the medical field.

The following types of cataract can be described.

Senile cataract: This is the most frequent form and is due to aging. A slow but progressivelossoflenstransparencyistypicaloftheelderlypopulation.Epidemiological studies have shown that in western countries cataracts first appear among the population over age 50, and the incidence progressively increases with age. Indeed, about 50 percent of the population over 60 years of age and 100 percent of people over 80 have lens opacities.

Congenital cataract: This form can occur in one or both eyes at birth or appear in the following months. There can be various degrees of opacity, leading to reduced visual acuity and a secondary amblyopia (permanent reduction of vision). Therefore early diagnosis and management are of extreme importance. Congenital opacities may remain stable or worsen over the years. An exception are total cataracts associated with leukokoria (white pupillary reflex) with nistagmus in bilateral forms and strabismus in monolateral cases. Among the causes of congenital cataract are genetic factors, x-rays, the use of medication in pregnancy, and maternal metabolic alterations such as diabetes, hypothyroidism, alimentary defects, or premature birth. However, the most frequent causes are infectious diseases contracted by the mother during pregnancy, such as rubella, systemic herpes infection, toxoplasmosis, etc.

Complicated cataract: This term is used when the cataract follows ocular pathol- ogy—most frequently, anterior and posterior uveitis, acute glaucoma, high myopia, intraocular tumors, and retinal detachment.

Cataract associated with systemic disease: Cataracts arise four times more frequently in patients with diabetes than in the general population. The cataract is similar to the senile form but arises in younger patients with a more rapid evolution. In cases with poor glycemic control it is frequently bilateral.3,4

Cataract associated with drugs: This is the type secondary to long term use of cortisone or topical treatment (drops) used in glaucoma.

Traumatic cataract: This occurs following closed or perforating trauma and is generally monolateral.

The principle symptom of a cataract is a slow and progressive quantitative and qualitative reduction of visual acuity. This can be described as blurred or unfocused vision, alteration of colour perception, difficulty in night vision, vision of coloured rings around artificial and solar light, double vision, etc. In some elderly patients it can be described as a transitory improvement of near vision due to a myopic shift that delays presbyopia. When the opacity is central, visual acuity improves at night when illumination is dim and there is mydriasis. Slit lamp examination of the anterior segment with pharmacological pupillary dilatation allows detailed examination of the lens.

Until the begining of the 1980s topical medication was prescribed to delay the progression of cataract. However, there is no valid pharmacological agent at present. The sole approach to this pathology is the surgical removal of the lens.

The increased frequency of cataract extraction results not only from the aging of the population but also from an improvement of surgical success rates. This in turn results from the improvement of surgical methods, with more sophisticated technology and faster postoperative visual recuperation. Among the surgical methods employed are intracapsular cataract extraction (ICCE), which is rarely used nowadays; extracapsular cataract extraction (ECCE); and the latest and most frequent method, facoemulsification, which consists of the use of ultrasound for cataract fragmentation.

Once the cataract is extracted, an intraocular lens is usually implanted to replace it. At present facoemulsification can be carried out with topical anesthesia with nearly immediate functional recovery.5-8 This does not imply that the surgical process is simple and without risks; it is extremely sophisticated microsurgery which requires much experience and postoperative follow-up. A severe complication can be internal infection of the eye (endophthalmitis) due to pathogenic germs during

or after surgery. Fortunately, this has a very low frequency, only about four of 1000 operations. Another complication can be rupture of the posterior capsule, where the intraocular lens is usually placed. This can cause the slipping of cataract fragments into the vitreous fluid. Minor complaints are redness, tearing, and foreign body sensation, which are resolved with local medical applications such as antibiotics and anti-inflammatory agents.

A frequent secondary event which can occur both in ECCE and in facoemulsification is secondary cataract formation. This consists of opacification of the posterior capsule. The incidence is 10-50 percent in 3.5 years following surgery.9,10 This opacification causes a progressive reduction of visual acuity. The management at present is a NeoDymion YAG-laser capsulotomy.11-13 A small central opening is created in the posterior capsule, allowing a return to the visual acuity values reached after the original surgery.14 Nd-YAG laser capsulotomy is considererd a safe and effective procedure which can, however, present some complications such as ocular hypertension, cystoid macular edema, and retinal detachment.15

Management of Glaucoma

Glaucoma is characterized by damage to the retinal ganglion cells, which is clinically manifested by alterations of the optic disk cup and typical visual field defects. The traditional definition includes high intraocular pressure and damage to the optic nerve shown by defects of the visual field. Glaucoma has a silent progression. The disease progresses and symptoms appear late, when the patient complains of bumping into objects and tripping. This is due to the loss of lateral vision, as central vision is maintained until the terminal stages of the disease. Indeed, visual acuity is good, but the visual field is progressively reduced.16,17 In advanced disease, without adequate treatment, the loss of the visual field becomes so severe as to cause permanent blindness.18,19 Two principle hypotheses for the pathogenesis have been advanced. The first emphasizes the importance of reduced vascular perfusion to the optic nerve and the nerve fibers layer. The second considers mechanical damage to the lamina cribrosa.20-22 At present the physiopathological mechanisms are not completely clear; however in both theories the alterations of the optic nerve seem to be caused by: 1) the intrinsic vulnerability of the optic disk, and 2) the increase of intraocular pressure up to a critical level for the optic disk.

The etiopathogenetic cause is an abnormal deflux of aqueous humor from the anterior chamber, with an increase of intraocular pressure (IOP). This is the most important factor,23,24 and the higher the IOP the higher the risk of developing glaucomatous optical neuropathy.25,26 Visual field studies have shown that the optic nerve head is where the most damage occurs.27,28 Patients with optic nerve damage can be divided into two groups: those with IOP higher than 21 mmHg, and those with IOP below 18 mmHg, glaucoma sine hypertension.29 Axonal flux studies have shown that with high IOP, the nerve fiber and axons are vulnerable during the passage from the optical disk.30 Two hypotheses have been advanced to explain the

damage: 1) indirect ischaemic damage, in whch elevated IOP causes the degeneration of nerve fibers by compromising the microcirculation of the optic disk; and 2) direct mechanical damage, in which high IOP causes direct damage to the retinal nerve fibers. The factors which determine IOP are the amount of aqueous humour production and the resistance of the drainage system. Aqueous humour is secreted from the ciliary processes in the posterior chamber and diffuses through the iris and the pupil to the sclerocorneal trabecular meshwork situated in the angle of the anterior chamber.31,32 About 80 percent of the drainage is through the trabecular meshwork, Schlemm’s canal, and the Fontana spaces to the episcleral vessels; whereas about 20 percent is uveal scleral drainage, where the aqueous humour passes through the ciliary body to the suprachoroidal space and through the venous circulation of the ciliary body, the choroid, and sclera.33 This continuous cycle is programmed to maintain a slight positive pressure in the eye. Alterations of this delicate equilibrium can cause elevated IOP, leading to damage.34-38 The statistical approach indicates 21 mmHg as the value above which glaucoma is suspected.39-41 The diagnosis of disease cannot be made solely on IOP; other factors such as familiarity, myopia, diabetes, race, age, and trauma must be considered.

Primary open angle glaucoma: This is the most frequent type of glaucoma and leads to blindness in 13 percent of cases. It occurs with the same frequency in males and females but more frequently in the elderly, afflicting 2 percent of the population over 70 years of age with initial alterations after 40 years of age. Both eyes are generally involved, with initial manifestations in one eye. Subjective symptoms are absent and early management can only be based on prevention, since visual acuity is perfectly conserved even with visual field alterations. It is universally accepted that the risk of irreversible damage of visual function increases in relationship to the increase in IOP.

Primary angle closure glaucoma: This form is relatively rare, occurring only in about 0.1 percent of subjects above 40 years of age, though four times more frequently in women. It is also called acute glaucoma, as the anterior chamber angle is rapidly blocked, which causes a sudden increase of IOP up to 60 mmHg or more. The main symptom is extremely intense pain (similar to migraine) accompanied by nausea, vomiting, headache, and rapid deterioration of vision.

Secondary glaucoma: Secondary glaucoma follows other ocular diseases such as inflammation, trauma, or drug side effects. This represents 25-30 percent of all glaucomas and can occur in either open or closed angle forms. Secondary glaucoma can also occur in the course of dismetabolic diseases such as diabetes, ocular hypertension, and advanced cataract.42

Congenital glaucoma: Congenital glaucoma is a very rare form that is present from birth due to a congenital malformation of the iridocorneal angle. The increase in intraocular pressure determines the typical aspect of “bufthalmous” by the third year of age; the eyeball is large due to scleral and corneal enlargement, since in children high intraocular pressure causes distortion of the ocular layers. This condition necessitates early surgical management aimed at eliminating the iridocorneal malformation.

Examination ophthalmology: The increase of IOP is not always synonymous with glaucoma. Certainly IOP increases the risk, but the amount of pressure that the