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Revalence and causes of low vision in children and adolescents in owerri municipal council of imo state, nigeria




The purpose of this study is to determine the prevalence and causes of low vision in adolescents and children in Owerri Municipal council of Imo State. The samples were randomly selected and was analyses using cross sectional study design. Of the 400 low vision case files reviewed at Federal Medical Center Owerri’s eye clinic from 2017 to 2021, 50 patients were below 20years of age, the acceptable age bracket to be classified as children or adolescents. This shows a prevalence of 12.5% (12.5/100 or 125/1000). This is high compared to the prevalence in developing countries. The study further revealed that cataract contributed the highest prevalence of low vision (24%) followed by myopia (16%) and optic atrophy(16%), aphakia/ dislocated lens(12%), retinitis pibmentosa(12%), macular degeneration (4%), nystagmus (4%) and glaucoma (4%) respectively, idiopathic causes (8%). This study also revealed that the percentage of cataract among males was 33.33% while females is 10%, myopia is 13.33% among males and 20% in females, optic atrophy was 20% in males but 10% in females, macular degeneration was 0 in males but 10% in females, nystagmus was 6.67% in males and 0 in females, glaucoma was 0 in males and 10% in females, aphakia/ dislocated lens was 6.67% in males and 20% in females, retinitis pigmentosa was 13.33% in males and 20% in females while idiopathic was 6.67% in males but 10% in females. The high Prevalence rate of adolescents and children who visited the Federal Medical Center, Owerri could be attributed to alot of factors which includes ignorance or lack of education of parents. Reports show that a lot of uneducated mothers, and even the educated ones, take drugs they are not supposed to take during pregnancy, such as steroids which have been proven to cause congenital cataract in the unborn. Most pregnant women do not know what to eat during pregnancy or cannot afford good diet. In conclusion, the causes of low vision in children and adolescents are largely preventable as the leading cause, Cataract and other pathological causes as well as refractive errors can be treated.



1.1.0 Background to the Study

According to the 10th revised International Classification of Diseases and Health-related Problems, a person has low vision when his or her best-corrected visual acuity is between 6/18 and 3/60 (visual impairment grade categories 1 and 2), and the person is considered blind when this value falls below 3/60 (categories 3, 4, and 5 ).The World Health Organization (WHO) estimates that, worldwide, 140 million people have low vision and 45 million are blind. Visual impairment in childhood is underestimated, and its prevalence is only partially known, ranging from 0.3 to 1.5/1,000, depending on the regional socioeconomic development (between 80 and 100 blind children per 1 million in industrialized countries and 400 blind children per 1 million in the poorest areas of the world). There are an estimated 1.5 million blind children in the world, with three fourths of this total living in the poorest areas of Asia and Africa, of these, 40% of the cases could be avoided, either by prevention or treatment. The worldwide incidence of blindness in childhood is 500,000 new cases each year, of which 60% to 80% of the children will die before the end of the second year of life from problems related to the causes of blindness or as a consequence of it. Prevention of blindness in childhood has been set as a priority by the WHO because of the reduced life expectancy of the child with visual impairment and the social, economic, and emotional repercussions.

Low vision or partial sight is a sub-specialty in Optometry. It is a bilateral visual impairment that has significance on the impairment of the functioning of the patient, and cannot be adequately corrected with surgical, medical, therapy, or  best optical correction provided by lenses. Visual field loss or central acuity loss is often observed, also loss of contrast, light sensitivity and distorted visions are observed. Generally, it is agreed that vision is low when acuity is  6/18 or poorer for the better eye with the best corrective lenses. Also a patient with a visual acuity of 6/6 may be termed low vision patient if the visual field is less than 30 degrees.

The control of blindness and low vision in children was one of the main priorities of the World Health Organization’s VISION 2020 (The Right to Sight). There are several reasons for this, first, the causes of low vision in children are very different from the causes in adults, and the strategies to combat low vision in adults will not result in the control of low vision in children and adolescents. Secondly, unlike in adults, a delay in treatment can lead to amblyopia. There is therefore a level of urgency about managing eye diseases in children. Thirdly, children’s eyes are not like small adult eyes, they respond differently to treatment, and specific expertise, equipment and training is required.

1.1.1 Prevalence of low vision

The prevalence of low vision issues has been difficult to tackle due to to mainly inadequate difference between low vision patients and the legally blind. Inadequate statistics are with respect to the group that has low vision but not legally blind group, Accurate figures are nearly completely lacking. Only educated guess can be made based on the inadequate statistics available. There is useful residual vision as reported by the U.S.A department of health education and welfare among 60% of the legally blind children (20/200VA or less or visual field of 20degree or less). The prevalence of low vision starts from 0-5 years of age and increases steadily with increasing age. Between 70% and 78% of those classified as legally blind should be treated as low vision patients. Genesky( 1984) estimated the numbers of USA partially sighted as slightly over 1.6million. Fonder (1991) has an estimate of low vision population to be 2.5million people. Legge(1991) estimated about 2million Americans with low vision. Goldfish and Marx(1976) estimated the US low vision patients to be 6million including 1.3million functioning as legally blind. Here in Nigeria, the work to estimate accurately the number of low vision patients is still ongoing. This is not easy in Nigeria because most children with low vision are classified as legally blind and most parents don’t allow their children with low vision to come out. These children have never had any adequate examination on low vision. Most of the children belongs to the lower class, and since their is little or no facility to assist them, they are cast aside. parents of the children most times cannot afford to send them to school for low vision and the blind. Hence with this, it is not easy to get a near accurate estimate of the prevalence of low vision in children here in Nigeria.

1.1.2 Causes of low vision in children

There is variation in the causes of low vision in children. It could be due to trauma, illness, pathology or congenital defects that disrupts the normal functioning of the eyes. The most common causes of low vision in children are the following

  1. Glaucoma

Glaucoma is a group of eye diseases which result in damage to the optic nerve and cause vision loss. The most common type is open-angle (wide angle, chronic simple) glaucoma, in which the drainage angle for fluid within the eye remains open, with less common types including closed-angle (narrow angle, acute congestive) glaucoma and normal-tension glaucoma. Open-angle glaucoma develops slowly over time and there is no pain.  Peripheral vision may begin to decrease, followed by central vision, resulting in blindness if not treated. Closed-angle glaucoma can present gradually or suddenly. The sudden presentation may involve severe eye pain, blurred vision, mid-dilated pupil , redness of the eye, and nausea. Vision loss from glaucoma, once it has occurred, is permanent. Eyes affected by glaucoma are referred to as being glaucomatous .

Signs and Symptoms

Open-angle glaucoma is usually painless with no symptoms early in the disease process, thus screening via regular eye check-ups is important. The only signs are gradually progressive visual field loss , and optic nerve changes (increased cup-to-disc ratio on fundoscopic examination ). About 10% of people with closed angles present with acute angle closure characterized by sudden ocular pain, seeing halos around lights, red eye, very high intraocular pressure (>30 mmHg (4.0 kPa)), nausea and vomiting, suddenly decreased vision, and a fixed, mid-dilated pupil. It is also associated with an oval pupil in some cases. Acute angle closure is an emergency. Opaque specks may occur in the lens in glaucoma, known as glaukomflecken.

Risk factors

Risk factors for glaucoma include increasing age, high pressure in the eye , a family history of glaucoma, and use of steroid medication. For eye pressures, a value of greater than 21 mmHg or 2.8 kPa is often used, with higher pressures leading to a greater risk.However, some may have high eye pressure for years and never develop damage.  Conversely, optic nerve damage may occur with normal pressure, known as normal-tension glaucoma. The mechanism of open-angle glaucoma is believed to be slow exit of aqueous humor through the trabecular meshwork, while in closed-angle glaucoma thebiris blocks the trabecular meshwork.

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Screening for glaucoma is usually performed as part of a standard eye examination performed by optometrists and ophthalmologists. Testing for glaucoma should include measurements of the intraocular pressure via tonometry, anterior chamber angle examination or gonioscopy, and examination of the optic nerve to look for any visible damage to it, or change in the cup-to-disc ratio and also rim appearance and vascular change. A formal visual field test should be performed. The retinal nerve fiber layer can be assessed with imaging techniques such as optical coherence tomography, scanning laser polarimetry, and/or scanning laser ophthalmoscopy (Heidelberg retinal tomogram).


The modern goals of glaucoma management are to avoid glaucomatous damage and nerve damage, and preserve visual field and total quality of life for patients, with minimal side-effects. This requires appropriate diagnostic techniques and follow-up examinations, and judicious selection of treatments for the individual patient. Although intraocular pressure (IOP) is only one of the major risk factors for glaucoma, lowering it via various pharmaceuticals and/or surgical techniques is currently the mainstay of glaucoma treatment. A review of people with primary open-angle glaucoma and ocular hypertension concluded that medical IOP-lowering treatment slowed down the progression of visual field loss. Vascular flow and neurodegenerative theories of glaucomatous optic neuropathy have prompted studies on various neuroprotective therapeutic strategies, including nutritional compounds, some of which may be regarded by clinicians as safe for use now, while others are on trial.

  1. Retinitis pigmentosa

Retinitis pigmentosa ( RP) is a genetic disorder of the eyes that causes loss of vision .Symptoms include trouble seeing at night and decreased peripheral vision (side vision).  As peripheral vision worsens, people may experience ” tunnel vision “.  Complete blindness is uncommon. Onset of symptoms is generally gradual and often in childhood. Retinitis pigmentosa ( RP) is a genetic disorder of the eyes that causes loss of vision  often in childhood. Retinitis pigmentosa is generally inherited from a person’s parents .  Mutations in one of more than 50 genes are involved. The underlying mechanism involves the progressive loss of rod photoreceptor cells in the back of the eye . This is generally followed by loss of cone photoreceptor cells . Diagnosis is by an examination of the retina finding dark pigment deposits. Other supportive testing may include an electroretinogram , visual field testing , or genetic testing . There is currently no cure for retinitis pigmentosa.  Efforts to manage the problem may include the use of low vision aids, portable lighting, or orientation and mobility training. Vitamin A palmitate supplements may be useful to slow worsening.  A visual prosthesis may be an option in certain people with severe disease. It is estimated to affect 1 in 4,000 people.

Signs and Symptoms

The initial retinal degenerative symptoms of retinitis pigmentosa are characterized by decreased night vision ( nyctalopia ) and the loss of the mid-peripheral visual field. The rod photoreceptor cells, which are responsible for low-light vision and are orientated in the retinal peripherpy, are the retinal processes affected first during non-syndromic forms of this disease. Visual decline progresses relatively quickly to the far peripheral field, eventually extending into the central visual field as tunnel vision increases. Visual acuity and color vision can become compromised due to accompanying abnormalities in the cone photoreceptor cells, which are responsible for color vision, visual acuity, and sight in the central visual field. The progression of disease symptoms occurs in a symmetrical manner, with both the left and right eyes experiencing symptoms at a similar rate.  A variety of indirect symptoms characterize retinitis pigmentosa along with the direct effects of the initial rod photoreceptor degeneration and later cone photoreceptor decline. Phenomena such as photophobia, which describes the event in which light is perceived as an intense glare, and photopsia, the presence of blinking, swirling or shimmering lights within the visual field, often manifest during the later stages of RP. Findings related to RP have often been characterized in the fundus of the eye as the “ophthalamic triad”. This includes the development of  a mottled appearance of the retinal pigment epithelium (RPE) caused by bony spicule formation, a waxy appearance of the optic nerve, and the attenuation of blood vessels in the retina. Non-syndromic RP usually presents a variety of the following symptoms:

Night blindness

A.Tunnel vision (due to loss of peripheral vision)

B.Latticework vision (due to loss of peripheral vision)

C.loss of depth perception

D.Photopsia (blinking/swirling/shimmering lights)

E.Photophobia (aversion to bright lights)

F.Development of bone spicules in the fundus

G.Slow adjustment from dark to light environments and vice versa

H.Blurring of vision

I.Poor color separation

J.Loss of central vision

K.Eventual blindness.


An accurate diagnosis of retinitis pigmentosa relies on the documentation of the progressive loss photoreceptor cell function, confirmed by a combination of visual field and visual acuity tests, fundus and optical coherence imagery, and electroretinography (ERG)


There is currently no cure for retinitis pigmentosa, but the efficacy and safety of various prospective treatments are currently being evaluated. The efficiency of various supplements, such as vitamin A, DHA , and lutein, in delaying disease progression remains an unresolved, yet prospective treatment option.

  1. Corneal problems

Many corneal problems such as keratitis, corneal apathies, corneal abrasions, corneal ulcers, corneal opacities, keratoconus and corneal injuries can lead to low vision.

  1. Ectopia lentis

Ectopia lentis is a displacement or malposition of the eye ‘s crystalline lens from its normal location. A partial dislocation of a lens is termed lens subluxation or subluxated lens ; a complete dislocation of a lens is termed lens luxation or luxated lens. In ectopia lentis, the lens may be partially or totally displaced from it’s pupillary space. There is tremulous movement of the lens. Patients reports photophobia upon dilation. Ectopia lentis may be herodofamiliar(autosomal recessive or autosomal dominants) or acquired due to trauma or a very large eye, myopia or bulphthalmos. The major complications are optical distortion produced by lenticular myopic astigmatism or lens edge effects, glaucoma due to pupil block or dislocation into the anterior chamber and rarely lens induced uveitis. Aphakia surgery or correction usually improves visual acuity.

5.Illness( Measles)

Measles is a systemic illness due to viral infection. The virus invades an organ and produces characteristic lessons on them. The virus replicate in the the mouth and upper respiratory tract and spreads via the blood to other tissues. When the symptoms appear 9-11 days after infection, virus replicate takes place in cells in many organs including the conjunctiva, respiratory, alimentary, central nervous system etc. The complications includes blindness due to lessons of the conjunctiva, deafness and encephalitis etc.

  1. Retinopathy of prematurity

Retinopathy of prematurity ( ROP ), also called retrolental fibroplasia (RLF) and Terry syndrome , is a disease of the eye affecting prematurely born babies generally having received neonatal intensive care , in which oxygen therapy is used due to the premature development of their lungs. It is thought to be caused by disorganized growth of retinal blood vessels which may result in scarring and retinal detachment. ROP can be mild and may resolve spontaneously, but it may lead to blindness in serious cases. Thus, all preterm babies are at risk for ROP, and very low birth-weight is an additional risk factor. Both oxygen toxicity and relative hypoxia can contribute to the development of ROP.


By the fourth month of pregnancy, the fetal retina has begun to develop vascularization. Such formation of blood vessels appears to be very sensitive to the amount of oxygen supplied, either naturally or artificially. In rare cases ROP has been found in some patients with a mutation in the NDP gene which is normally associated with the more formidable Norrie disease.

Risk factors

Various risk factors contribute to the development of ROP. They are:


  1. High exposure to oxygen
  2. Low birth weight
  3. Various types of infections

E.Cardiac defects


Treatment of retinopathy of prematurity involves the following procedures

A.Peripheral retinal ablation which is the mainstay of ROP treatment

B.Scleral buckling and/or vitrectomy surgery may be considered for severe ROP (stages 4 and 5) for eyes that progress to retinal detachment.

C.Intravitreal injection of bevacizumab ( Avastin) has been reported as a supportive measure in aggressive posterior retinopathy of prematurity.

D.Oral propranolol is being evaluated for counteracting the progression of ROP, but safety is a concern.

  1. Macular Degeneration

Macular degeneration, also known as age-related macular degeneration ( AMD or ARMD ), is a medical condition which may result in blurred or no vision in the center of the visual field. Early on there are often no symptoms. Over time, however, some people experience a gradual worsening of vision that may affect one or both eyes.] While it does not result in complete blindness , loss of central vision can make it hard to recognize faces, drive, read, or perform other activities of daily life. Visual hallucinations may also occur but these do not represent a mental illness .Macular degeneration typically occurs in older people. Genetic factors and smoking also play a role. It is due to damage to the macula of the retina. Diagnosis is by a complete eye exam . The severity is divided into early, intermediate, and late types.  The late type is additionally divided into “dry” and “wet” forms with the dry form making up 90% of cases.  Preventive efforts include exercising, eating well, and not smoking. There is no cure or treatment that returns vision already lost.  In the wet form, anti-VEGF medication injected into the eye or less commonly laser coagulation or photodynamic therapy may slow worsening. Antioxidant vitamins and minerals do not appear to be useful for prevention. However, dietary supplements may slow the progression in those who already have the disease. In 2015 it affected 6.2 million people globally. In 2013 it was the fourth most common cause of blindness after cataracts, preterm birth , and glaucoma . It most commonly occurs in people over the age of fifty and in the United States is the most common cause of vision loss in this age group. About 0.4% of people between 50 and 60 have the disease, while it occurs in 0.7% of people 60 to 70, 2.3% of those 70 to 80, and nearly 12% of people over 80 years old.

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Signs and Symptoms

A.Distorted vision in the form of metamorphopsia , in which a grid of straight lines appears wavy and parts of the grid may appear blank: Patients often first notice this when looking at things like miniblinds in their home or telephone poles while driving. There may also be central scotomas , shadows or missing areas of vision

B.Slow recovery of visual function after exposure to bright light ( photostress test)

C.Visual acuity drastically decreasing (two levels or more), e.g.: 20/20 to 20/80

D.Blurred vision: Those with nonexudative macular degeneration may be asymptomatic or notice a gradual loss of central vision, whereas those with exudative macular degeneration often notice a rapid onset of vision loss (often caused by leakage and bleeding of abnormal blood vessels).

E.Trouble discerning colors, specifically dark ones from dark ones and light ones from light ones

F.A loss in contrast sensitivity

G.Formed visual hallucinations and flashing lights have also been associated with severe visual loss secondary to wet AMD

Risk factors

Key risk factors are age, smoking, and family history .  Advanced age is the strongest predictor of AMD, particularly over 50.


Treatment of AMD varies depending on the category of the disease at the time of diagnosis. In general, treatment is aimed at slowing down the progression of AMD. As of 2018, there are no treatments to reverse the effects of AMD.  Early-stage and intermediate-stage AMD is managed by modifying known risk factors such as smoking and atherosclerosis and making dietary modifications. For intermediate-stage AMD, management also includes antioxidant and mineral supplementation. Advanced-stage AMD is managed based on the presence of choroidal neovascularization (CNV): dry AMD (no CNV present) or wet AMD (CNV present). No effective treatments exist for dry AMD. The CNV present in wet AMD is managed with vascular endothelial growth factor ( VEGF ) inhibitors.

8.High Myopia

High myopia is a condition classified by a very high level of nearsightedness. Since myopia is the medical name for nearsightedness, “high myopia” is another way of saying “severe nearsightedness.”If left untreated, high myopia can exponentially increase your risk of developing sight-threatening eye disease later in life. People who go on to develop high myopia become nearsighted during early childhood. Their nearsightedness then progresses and worsens over time, roughly between grade-school age and young adulthood (ages 18-20). In some cases, nearsightedness will continue to progress past age 20.After myopia has completely progressed, it will stabilize.High myopia is a growing concern around the world. In 2015, the World Health Organization estimated that 2.8% of the global population had high myopia. They believe that number will nearly quadruple over the next few decades, rising to 10% of the world’s population by 2050.Refractive errors like nearsightedness and farsightedness are measured in units called diopters. The term “high myopia” is generally used to describe a refractive measurement of -6.00 diopters or higher. For reference, mild nearsightedness usually falls between -0.25 and -3.00 diopters.

9.Congenital Cataract

Congenital cataracts refers to a lens opacity which is present at birth . Congenital cataracts cover a broad spectrum of severity: whereas some lens opacities do not progress and are visually insignificant, others can produce profound visual impairment. Congenital cataracts may be unilateral or bilateral. They can be classified by morphology, presumed or defined genetic cause, presence of specific metabolic disorders, or associated ocular anomalies or systemic findings. [1]

Signs and symptoms

Congenital cataract in an adult

Congenital cataracts occur in a variety of morphologic configurations, including lamellar, polar, sutural, coronary, cerulean, nuclear, capsular, complete, membranous.


In general, approximately one-third of congenital cataracts are a component of a more extensive syndrome or disease (e.g., cataract resulting from congenital rubella syndrome), one-third occur as an isolated inherited trait, and one-third result from undetermined causes. Metabolic diseases tend to be more commonly associated with bilateral cataracts.

A.Genetic & Metabolic Infections Anomali

B.Down syndrome

C.Hallermann-Streiff syndrome

D.Lowe syndrome


F.Varicella-Zoster ,

G.HIV , and Parvo B19)

  1. Rubella


J.Herpes Simplex ( HSV-1 , HSV-2 ) Aniridia

J.Anterior segment dysgenes

L.Persisten fetal vasculatu (PFV)

N.Posterior lenticonu


All newborns should have screening eye examinations, including an evaluation of the red reflexes.

Red reflex test is best performed in a darkened room and involves shining a bright direct ophthalmoscope into both eyes simultaneously from a distance of 1– 2 ft. This test can be used for routine ocular screening by nurses, pediatricians, family practitioners, and optometrists.

Retinoscopy through the child’s undilated pupil is helpful for assessing the potential visual significance of an axial lens opacity in a pre-verbal child. Any central opacity or surrounding cortical distortion greater than 3 mm can be assumed to be visually significant.

Laboratory Tests : In contrast to unilateral cataracts, bilateral congenital cataracts may be associated with many systemic and metabolic diseases. A basic laboratory evaluation for bilateral cataracts of unknown cause in apparently healthy children includes:

– Urine test for reducing substance, galactose 1-phosphate uridyltransferase, galactokinase, amino acids

– Infectious diseases: TORCH and varicella titers, VDRL zzz

– Serum calcium, phosphorus, glucose and ferritin


Surgeryngenital cataract should be detected and removed before age 6 weeks, and visually significant bilateral congenital cataracts should be removed before age 10 weeks.

Some congenital cataracts are too small to affect vision, therefore no surgery or treatment will be done. If they are superficial and small, an ophthalmologist will continue to monitor them throughout a patient’s life. Commonly, a patient with small congenital cataracts that do not affect vision will eventually be affected later in life; generally this will take decades to occur.


Albinism is a congenital disorder characterized in humans by the complete or partial absence of pigment in the skin, hair and eyes. Albinism is associated with a number of vision defects, such as photophobia, nystagmus , and amblyopia . Lack of skin pigmentation makes for more susceptibility to sunburn and skin cancers. In rare cases such as Chédiak–Higashi syndrome , albinism may be associated with deficiencies in the transportation of melanin granules. This also affects essential granules present in immune cells leading to increased susceptibility to infection.

Albinism results from inheritance of recessive gene alleles and is known to affect allvertebrates , including humans . It is due to absence or defect of tyrosinase , a copper-containing enzyme involved in the production of melanin. It is the opposite of melanism . Unlike humans, other animals have multiple pigments and for these, albinism is considered to be a hereditary condition characterised by the absence of melanin in particular, in the eyes, skin, hair, scales, feathers or cuticle. While an organism with complete absence of melanin is called an albino, an organism with only a diminished amount of melanin is described asleucistic or albinoid.The term is from the Latin albus, “white.

Signs and Symptoms

There are two principal types of albinism, oculocutaneous affecting the eyes, skin and hair, and ocular affecting the eyes only. There are different types of oculocutaneous albinism depending on which gene has undergone mutation. With some there is no pigment at all. The other end of the spectrum of albinism is “a form of albinism called rufous oculocutaneous albinism, which usually affects dark-skinned people”. According to the National Organization for Albinism and Hypopigmentation , “With ocular albinism, the color of the iris of the eye may vary from blue to green or even brown, and sometimes darkens with age. However, when an optometrist or optometrist examines the eye by shining a light from the side of the eye, the light shines back through the iris since very little pigment is present.” Because individuals with albinism have skin that entirely lacks the dark pigment melanin, which helps protect the skin from the sun’s ultraviolet radiation , their skin can burn more easily from overexposure.


Genetic testing can confirm albinism and what variety it is, but offers no medical benefits, except in the case of non-OCA disorders. Such disorders cause other medical problems in conjunction with albinism, and may be treatable. Genetic tests are currently available for parents who want to find out if they are carriers of ty-neg albinism. Diagnosis of albinism involves carefully examining a person’s eyes, skin and hairs. Genealogical analysis can also help.

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Since there is no cure for albinism, it is managed through lifestyle adjustments. People with albinism need to take care not to get sunburnt and should have regular healthy skin checks by a dermatologist. For the most part, treatment of the eye conditions consists of visual rehabilitation. Surgery is possible on the extra-ocular muscles to decrease strabismus. Nystagmus -damping surgery can also be performed, to reduce the “shaking” of the eyes back and forth.  The effectiveness of all these procedures varies greatly and depends on individual circumstances.

Glasses, low vision aids, large-print materials, and bright angled reading lights can help individuals with albinism. Some people with albinism do well using bifocals (with a strong reading lens), prescription reading glasses, hand-held devices such as magnifiers or monoculars or wearable devices like eSight and Brainport.

  1. Nystagmus

Nystagmus is a condition of involuntary (or voluntary, in some cases) eye movement, acquired in infancy or later in life, that may result in reduced or limited vision . Due to the involuntary movement of the eye, it has been called “dancing eyes”.In normal eyesight, while the head rotates about an axis, distant visual images are sustained by rotating eyes in the opposite direction of the respective axis.  The semicircular canals in the vestibule of the ear sense angular acceleration, and send signals to the nuclei for eye movement in the brain. From here, a signal is relayed to the extraocular muscles to allow one’s gaze to fix on an object as the head moves. Nystagmus occurs when the semicircular canals are stimulated (e.g., by means of the caloric test, or by disease) while the head is stationary. The direction of ocular movement is related to the semicircular canal that is being stimulated. There are two key forms of nystagmus: pathological and physiological , with variations within each type. Nystagmus may be caused by congenital disorder or sleep deprivation , acquired or central nervous system disorders, toxicity , pharmaceutical drugs, alcohol , or rotational movement. Previously considered untreatable, in recent years several drugs have been identified for treatment of nystagmus. Nystagmus is also occasionally associated with vertigo .


The cause of pathological nystagmus may be

congenital , idiopathic, or secondary to a pre-existing neurological disorder . It also may be induced temporarily by disorientation (such as on roller coaster rides) or by some drugs ( alcohol , lidocaine , and other central nervous system depressants, inhalant drugs, stimulants , psychedelics , and dissociative drugs).


  1. Congenital nystagmus has long been viewed as untreatable, but medications have been discovered in recent years that show promise in some patients. In 1980, researchers discovered that a drug called baclofen could stop periodic alternating nystagmus. Subsequently, gabapentin, an anticonvulsant, was led to improvement in about half the patients who took it. Other drugs found to be effective against nystagmus in some patients include memantine, levetiracetam , 3,4-diaminopyridine (available in the US to eligible patients with downbeat nystagmus at no cost under an expanded access program , 4-aminopyridine, and acetazolamide . Several therapeutic approaches, such as contact lenses , drugs, surgery , and low vision rehabilitation have also been proposed. For example, it has been proposed that mini-telescopic eyeglasses suppress nystagmus. Surgical treatment of congenital nystagmus is aimed at improving head posture, simulating artificial divergence, or weakening the horizontal recti muscles. Clinical trials of a surgery to treat nystagmus (known as tenotomy ) concluded in 2001. Tenotomy is now being performed regularly at numerous centres around the world. The surgery aims to reduce the eye oscillations, which in turn tends to improve visual acuity.

B.Acupuncture tests have produced conflicting evidence on its beneficial effects on the symptoms of nystagmus. Benefits have been seen in treatments in which acupuncture points of the neck were used, specifically points on the

c.sternocleidomastoid muscle.Benefits of acupuncture for treatment of nystagmus include a reduction in frequency and decreased slow phase velocities, which led to an increase in foveation duration periods both during and after treatment. By the standards of evidence-based medicine, the quality of these studies is poor (for example, Ishikawa’s study had sample size of six subjects, was unblinded, and lacked proper controls), and given high quality studies showing that acupuncture has no effect beyond placebo, [ citation needed] the results of these studies have to be considered clinically irrelevant until higher quality studies are performed.

Physical or occupational therapy is also used to treat nystagmus. Treatment consists of learning strategies to compensate for the impaired system.

  1. Trauma( injury)

Trauma or injury can lead to many complications. It’s effect on the eyes cannot be over emphasized. If any of the structures is affected, it can lead to cataract, uveitis, glaucoma, dislocation etc. If the retina is affected, it can result to retinal detachment, retinopathies and even blindness. If the vitreous is affected, it can lead to vitreous harmorrhages etc.

1.2 Statement of problem

Low vision  in childhood has implications in all aspects of the child’s development. It poses educational, occupational and social challenges, with affected children being at risk of behavioral, psychological and emotional difficulties, impaired self-esteem and poor social integration. Moreover, visual problems are an important contribution to poor school performance (MOPHS and MOE, 2009). There is an estimated 1.5 million children living with low vision and blindness worldwide. Among the blind and visually impaired children, 90% live in the developing countries such as Nigeria(Clare, 2001). Here in Nigeria, there are limited studies suggesting the Prevalence and cause of low vision in children and adolescents. Therefore there is need to investigate the prevalence and cause of low vision in children and adolescents in other to bring to the knowledge of the public, parents and caregivers their causes, signs and symptoms, in other to curb their morbidity and burden on children and adolescents.

1.3 Aims and Objectives

1.3.1 Aim

The aim of this study is to determine the prevalence and causes of low vision in children and adolescents in Owerri municipal council of Imo State.

1.3.2 Objective

  1. To determine the gender-specific prevalence of low vision in children and adolescents.
  2. To determine the age-specific prevalence of low vision in children and adolescents.

1.4 Research questions

  1. What is the gender-specific prevalence of low vision in children and adolescents?
  2. What is the age-specific prevalence of low vision in children and adolescents?

1.5 Research Hypothesis

  1. There is no statisically significant association between gender and low vision in children and adolescents.
  2. There is no statistically significant association between age and low vision in children and adolescents.

1.6 Significance of the Study

  1. General public

It holds the significance of adding to the existing body of knowledge on the prevalence and causes of lt holds the significance of adding to the existing body of knowledge on the prevalence and causes of low vision in children and adolescents, shows the trend of ocular morbidity and also help to provide basic data for planning and designing adequate intervention strategies to mitigate the problem.

  1. in children and adolescents, shows the trend of ocular morbidity and also help to provide basic data for planning and designing adequate intervention strategies to mitigate the problem.


This research work will encourage more optometrists to embrace low vision practice with respect to adequate examination, diagnosis and prescription of low vision aids.

  1. Government

This research work will serve as a pointer to enable the government map out health policy measures to improve the visual abilities of the people.

1.7 Scope/ Delimitation of the study

Due to limited time and resources, this study focused only on case files from Federal medical center Owerri, Imo state, thus limiting my findings to an urban setting.

1.8 Justification of Study

Low vision has been recognized in several studies as one major problem affecting children and adolescents. These problems therefore demand special attention and justify inclusion in the VISION 2020 program as most causes are either preventable or treatable. Knowledge  about the prevalence  and causes of low vision is desirable for planning, monitoring and evaluation of eye care service. Although several studies have been carried out among general populations, there is little data on the prevalence and  causes of low visionI and blindness among children and adolescents in Nigeria.This research work holds the significance of adding to the existing body of knowledge on the prevalence and causes of low vision in children and adolescents, shows the trend of ocular morbidity and also help to provide basic data for planning and designing adequate intervention strategies to mitigate the problem.

Pages:  79

Category: Project     

Format:  Word & PDF        

Chapters: 1-5                                 

Material contains Table of Content, Abstract and References.


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