INCIDENCE OF COLOUR BLINDNESS AMONG UNIVERSITY STUDENTS IN PORT HARCOURT.

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INCIDENCE OF COLOUR BLINDNESS AMONG UNIVERSITY STUDENTS IN PORT HARCOURT.

TABLE OF CONTENT

Declaration

Dedication

Acknowledgement

Abstract

List of tables and figures

Chapter one: Introduction and literature review

Chapter two: materials and methods

Chapter three: Results and data analysis

Chapter four: Discussion and conclusion

References.

ABSTRACT

Colour blindness testing was done using the Ishihara test chert (1980 Edition) is 1,000 randomly selected male and female University student in Port Harcourt, River state Nigeria.

7.5% of the total number of subjects were found to be colour-blind out of which 6.6% were males and 0.9% females. The differences in percentages between both 0.01 and 0.05 sig. levels. Socio-economic class variation was also found to be significantly statically. These results obtained agreed with the results of most investigations. However no relationship was observed between ages, weight height, defects with the incidence of colour blindness.

From the comparison, one could state that between male and female university students I Port Harcourt, there exists a significant difference in their incidence for colour blindness while there is an insignificant differences along different ages weights, heights distributions but socio-economic class is significant factor is determining colour blindness.

From the comparism, one could state that between male and female university students in differences in their incidence of colour blindness while there is an insignificant difference among different ages weights, heights distributions but socio-economic class is a significant factor is determining colour blindness.

CHAPTER ONE

INTRODUCTION

Colour blindness can be simply defined as the inability to distinguish one or more of the three colours red, green and blue. The ability to see colours exists in only a few vertelerntes including among others man and the other privates, fish, amphibians, sone reptiles and same birds, and in bees and butterflies.

In the retina- the light sensitive layer of tissue that lines the back and sides of the eyeball, there are in human beings three types of cones, the visual cells that function in the perception of colour. One type absorbs high best in wavelengths of blue – violet and another in the wavelength of green. The third type is most sensitive to wavelength of yellow but is also sensitive to red. Colour blind persons may be blind to one, two or all of the colours red, green and blue. (Blindness to red is called protanopia; to green denternopia and to blue tritanopia). Red blind persons are ordinarily able to distinguish between red and green white blue-blind persons cannot distinguish between blue and yellow, Green – blind persons are unable to see the green port of the spectrum.

The Nomenclature of the varieties of colour blindness has become somewhat complicated and therefore something must be said about the theories of colour visions. Unfortunately more of the theories is yet completely established, but as a working hypothesis trichromatic holds the field, though recent work seems to show that at least six receptor work may be operative in the retina. The trichromatic theory was enunciated by Yong in 1807 and later elaborated by Helhotz 91911). In essence, it postulates a subdivision of the ritual receptors into three types, those sensitive to red, green and blue respectively, and that only colour could be matched by a contented of various amounts of these primary colours. The young – Helmotz theory has been explained and more details have been worked out. It now is generally accepted as the mechanism of colour vision.

The photo chemicals in the cones have almost the same chemical composition as that of the rhodopsin in the rods the only difference being that the protein portions, the opsins called photopsins in the cones are different from the scotopsin in the rods. The retinal portions are exactly the same as in the cones as in the rods. The colour-sensitive pigments of the cones, therefore, are combinations of retinal and photosins. Three different types of photopsins. Three different cones, thus making these cones selectively sensitive to the different colours of blue, green and red. These chemicals are called respectively blue sensitive pigment, green-sensitive pigment and red-sensitive pigment. In the three types of cones show peak absorbance’s at might wavelength respectively, of 445, 535, and 570 millimicines.

Normal colour vision is currently accounted by same from or trichromatic opponent modle. Trichromacy has its origin at the receptor level wherein there is found three different foveal photo pigments whose spectra have wavelengths (x) maximum in three different spectral regions viz. long, medium and short wave cones. It has been presumed that the same three photo pigments exist in each persons categorized as having normal trichromacy, that is to say that there are presumptively only three types of cene pigments. Evidence from fundal reflectomety has confirmed this view.

In the case of the basic mechanism involved in defective colour visions, red-green dichronacy (protanopia and deuteranpia) has been accounted for by two alternative hypothesis: (1) a reduction form of normal trichromacy; and (2) a fusion of two of the three fundamental processes. Within the frame work of the reduction hypothesis, were account for red-green dichromacy as follows: protanopes lack the normal long wave sensitive cene photo pigments (Chlorolabe) but have normal long and short wave sensitive cene photo pigments however the fusion hypotheses provides an alternative explanation of dichromatic vision. Here it is postulated that all three cene types are present but the signals are processed by fewer than three channels. The results from most studies employing selective chromatic adaptation and fundal reflectometry support the reduction or loss mechanism for explaining dichromatic colour vision. Our understanding of anomalous trichromacy is less clear and not explained by a reduction mechanism but rather same form of an alteration hypothesis.

The interpretation of colour is mostly done by the central nervous system. As been shown that an range monochromatic high with a wavelength of 580 mill microns stipulates the red cenes to a stimulus value of approximately 99(99 percent of the peak stimulation the green cenes to a stimulus values of approximately 42 and the blue cenes not at all. Thus, the ratios of stipulation of the three different types of cenes in this instance are 99:42:0. The nervous system interprets this set of ratios as the sensation of orange. On the other hand, a monochromatic blue high with a wavelength of 450 millions stipulates the red cenes to a stimulus value of 0, the green cenes to a value of 0. And the blue cenes to a value of 97. This set of ratios 0;0:97 – is interpreted by the nervous system as blue. Aetiology of colour Blindness, colour blindness may be congenital or acquired.

The congenital from resembles haemophilia in its inheritance and is transmitted through the female, who is usually unaffected. Its transmitted in the sex chromosomes (xy in the male and xx in the female) the defect descends through the x chromosome, the gene being dominant in the male and recessive in the fame. It is not an uncommon condition among males, as unselected proportion of which contains at least 4 percent of crudely defective persons. (dichromate’s) and an additional 6 percent of less obviously affected persons (anomalous trichromatic). In females 0.4 percent only of dichromate are found.

Acquired colour blindness, may arise from various diseases of the eye and central nervous system. It often affect only port of the visual field, and is usually associated with depreciation of visual acuity. A common example is afforded by tobacco blindness in which over an area including the fixation and blind sport, there is inability to discriminate between red and green and visual acuity may be as low as 6% 36. Tabetic optic atrophy, exposure to glove (snow blindness) and sensible discoloration of the lens may all give rise to perversions of colour sense known as achromatopsia. Classification of colour Blindness.

Colour vision abnormalities can be classified into several distinct categories according to type and degree of the deficiency. No categorical classification system appears to be entirely satisfactory; some colour refectories will be found to exhibit characteristics that place them simultaneously in more than one category. Nevertheless, most genetic evidence points to the existence of several strickly different abnormalities and most psychophysical measurements also have revealed clustering of results into classifiably different groups. However the simplest classification would seem to be into two main groups, anomalies and blindness with regard to one or all of the three primary colours.

Discrimination of colours
Trichromats: These are those who can perceives all three primaries, the conditions encountered are (a) abnormal perception of red, called protanomally causing weakness in discrimination of red and green; (b) abnormal perception of green called deuteranomaly, in which case again there is weakness in discrimination of red and green; and (c) abnormal perception of blue, called tritanomally, in which there is weakness in discriminating yellow and blue.
Dichromats: Those who are blind to one of the three primary colours, the conditions met with are (a) red blindness called protenopia, in which red and green cannot be distinguished though blue and yellow can; (b) green blindness called deuteranopia in which red and green can be distinguished but not blue from yellow. (iii) monochromats: here there is inability to distinguish any colours as such and the world therefore appears like a photograph though a somewhat blurred one, because the condition is usually associated with nystagmus, bad control vision and phtophobia.
Matching of colours

Another way of classifying the colour blindness is to realize that anyone with normal colour vision, that is a trichromat can match any colour by a mixture of spectral red, green and blue in suitable proportions. Dichromats, can however, produce what is to then a match with a mixture of only two colours, whereas a monochromat will use only one colour which by variation of its intensity, can be made to match only part of the spectrum. Anomalous trichromats, although requiring three colours to produce a match of some given, colour require proportions different from those needed by the normal person, incidence and Heredity of colour Defects.

Among uncivilized races, colour blindness is common and even in civilized communities it is by no means rare, occurring among Europeans in 4% of males and 0.4% of females (Bateson 1913; Vogt 1922) or 8% of males and 0.4% of females (Waaler, 1927; planta, 1928). By far the most usual form met with is dichromatism and of the various types of this condition, denteranopia and protanopia are the more common. Tritanopia on the other hand is very rare. Most cases are pathological and are associated with depression in the function of the rods; it may also be simulated in cases of Jaundice and sclerosis of the liver owing to absorption of high by the yellow pigment total colour blindness is also rare. In the whole of the literature only some 130 cases are known. The condition was noted by Turberville (1984) and the recorded cases have been collected and cannotated by Grunert (1903), Nettle shipo 1909 (84 cases) and Bell 1926 (119 cases); subsequently some 12 additional cases have appeared (Fry, 1930; chance, 1931). Unilateral cases of uncomplicated colour blindness are extremely rare. Holgren (1880) reported 2 protanopes, Hayes (1911) a unilateral protanomalons case, and Reichert (1915) and Urines (1918) deuteranomalons cases. There are three cases or record of individuals with one eye normal (Beckes, 1879; Piper, 1905).

Colour blindness has a very strong hereditary character and a large number of extensive and very complete genealogies are now on record. Generally dichromatism in all its forms is transmitted as a male sex-linked character, recessive in the female due to a gene in the x-chromosons. Normal heterozygous mothers transmite to half their off spring (sons), houszygous mothers to all their sons and half their daughters will be transmitters. Mated to a hetetrozygous woman, a colour blind man will have 50% colour blind daughters and 50% normal but transmitting daughters while 50% of the sons will carry the defect. The defect is evident in a woman, therefore if her mother is a carrier and her father is defective or if both parents are defective. Most of these combinations have been observed in porotanopes and deuteranopes in families in which intermarriages have taken place (Bowditch, 1922; colour blindness is encountered in a pedigree (Waaler, 1927), but when intermarriage has occurred, protanopia is dominant to deuteranopia (Vogt, 1922).

Very rarely however colour blindness acts as a dominant instead of a recessive in which case there is a matriheal descent as a female sex linked character. Thus in the Belgian family described by counter (1839) descent was directly from mother to daughter for 5 generations in the few mother to daughter for 5 generation in the few cases of tritanopia (Yellowhue blinness) which have been followed a recessive – sex linked has been evident (Engelking, 1926; Hartung, 1926). Total colour blindness on the other hand is clearly a recessive character. Since 1880 sene 60 families have been traced in 14 of which consanguinity among the ancestors occurred. Baetger (1929) recorded briefly a pedigree where a sex called inherence seemed to be present and Halberitance was complicated by macular degeneration.

Colour blindness is sex – linked and results from absence of appropriate colour genes in the X – chromosomes. This lack of colour genes is a recessive trait, therefore, colour blindness will not appear as long as another x chromosome carries the genes necessary for development of the respective colour – receptive genes. Because the male human being has only one x chromosome, all three colour genes must be present in this single chromosome if he is not to be colour blind. In approximately one of every fifty times, the x-chromosome lacks the red gene; in approximately one of every sixteen, it lacks the green gene and rarely it lacks the blue gene, thus means that 2 person of all men are red colour blind (Protanopes) and 6 percent are green colour blind deuteranopes, making a total of approximately 8 percent who are red green colour blind. Because a female has two X-chromosomes, red-green colour blindness is a rare abnormality in the females.

Colour vision may become defective as a result of lesion of the macules, optic nerve or visual cortex or because of charges in the optical media for example cataracts. An acquired colour vision defect differs from a congenital one that is often asymmetrical in the two eyes, it may affect blue – yellow as well as red-green vision, it is associated with other defects of visual function, it is more variable and it causes the patient to see the colours of objects differently and therefore to name them incorrectly.

Although some forms of ocular pathology can result in disturbances of colour vision, as can assume charges associated with aging, nearly all colour deficiency of significant degree is hereditary, congenital and permanent. The commonest forms of defective colour vision, the red-green deficiencies are sex-linked, simple recessive hereditary traits. A colour defective male always inherits his deficiency from his mother, who usually has normal colour vision and is therefore a carrier of the defect. She may have received her colour deficiency gene from either her father but only if he were colour defective), or form her mother (who could have been a carrier herself or rarely who was colour defective).

Blue – yellow deficiencies, much rarer that the red-green defects have not been studied in sufficient numbers to establish firstly the mode of inheritance. Wright’s data on tritanopia based on a study of 17 subjects and correspondence with perhaps a dozen other probable tritanopes, indicate that this condition is not sex-linked but is instead on auto soma recessive trait (Wright, 1952; Kalmus 1965).

Typical total colour blindness –achromasy or shed as an autosomal recessive trait (Kalmus, 1965).

` Recent comprehensive studies of acquires colour the deficiency (Francois and verriegt, 1961; coz, 1960, 1961) have provided good understanding of the basis and significance of non-congenital impairments of colour vision. These studies confirm the conclusions reached by kollner (1912) now sometimes referred to as koller’s law:

Lessons of outer retinal layers affect blue-yellow vision, and lessions of inner layers and the optic nerve impair red-green vision. (b) pathological conditions in which blue yellow colour bision defects might be anticipated include (1) Galaucoma (2) Retrival detachment (3) Pigmentary degeneration (5) Myopic ritual degeneration (6) chorioretinitis (7) Retrial vascular occasion (8) Diabetiv retinopathy (9) Hypertensive retropathy (10) papilledema (11) Methyl alcohol poisoning. (c) pathological conditions in which impaired red-green colour vision would be anticipated include (1) lesions of optic nerve and optic pathways (2) tobacco or toxic amblyopia (3) Retrobulbar neuritis (4) Leber’s optic atrophy (5) comprehensive lesions of the optic tract. However, some exceptions to the kollners law have been noted (a) some optic atrophies are accompanied by blue – yellow defects in which cases the observed optic atrophy is probably secondary to atrophy or lesions of deper retinal structures (b) Red – green colour defects are sometimes found in cases of macular degeneration in which case the primary damage may lie superficially in the ganglian cell layer and the visible negative change that suggest deep damage may be secondary and lesson. (c) In juvenile macular degeneration, there is sometimes a deficiency, sometimes a red-green deficiency, occasionally total colour blindness, and sometimes no disturbances of colour vision.
Note also that since red-green deficiency are so common, superimposition of a blue – yellow defect resulting from a deep lesion may result in total colour blindness or more commonly in colour amblyopia. This is a generalized loss of sensitivity to all colours.
Aging could also lead to acquired colour blindness. The ocular media become progressively yellower with age. This may impair blue – yellow discrimination to the expert that vision may appear to be tritanomalous. Errors by elderly observers on color vision tests from tritan defects should be interpreted with caution. Efforts should be made to establish whether such blue – yellow deficiency was present at an earlier age.

TEST FRO COLOUR BLINDNESS

The purposes of colour vision testing as with most optometric procedures will vary according to the needs of the patient. His age, vocational plans and requirements interests, previous difficulties and other pertinent factors should be considered in selecting and administering the most appropriate tests to obtain the deserted information. A great many instruments, tests and materials are readily available for the investigation of colour perception but there is little value in subjecting patients to an exhaustive battery of tests unless there is need for detailed information that cannot be obtained more simply. On the other hand, care should be exercised to assure that sufficient information is obtained to anticipate future questions and needs and that the information is both valid and reliable.

Tests for colour-blindness date back to the time of seebeck (1837), who investigated colour defectives by making them arrange some 300 different coloured pieces of paper, glass and wool. The question, however received little attention until winson, the professor of Technology at Edinburgh, become impressed by the fact that disasters at sea and or the railroad might be attributable to this cause; he published an important book (1855) describing tests on the same principle as that of seebeck, with the result that the great northern railway company imposed colour tests upon the men seeking employment as engine drivers. A railway accident at Laggerlunda induced Holugreen (1877) to devise his wool test for the railway employees of sweden and his researches were responsible for the classical work of Jeffreies, of Bostan (1879) in the united states. Thereafter, tests for colour blindness rapidly become obligatory in the transport service of most civilized countries. Notwithstanding the importance and urgency of the problem, it has not been satisfactorily concluded. Simple and adequate has yet been devised and tests and regulations remain in the unsatisfactory state of varying from company to company and from country to country.

It will be observed that most of the tests are of considerable standing, for although the literature of the subject is large, much of the more recent writing is unfortunately, polemic rather than constructive in nature and the more receipt test which have been devised diverge in unessential deals rather than in basic principles from the classical ones. The test are broadly classified into:

Spectrum tests.
Matching tests
Pseudo – Isochromatic diagrams
Lantern tests
Quantitative tests
Miscellaneous tests

SPECTRUM TESTS

To enable a complete analysis of the colour perception of any individual to be made, the only scientific method for testing colour vision is by spectroscopic investigations; and the expert of the investigations which may be undertaken to determine the link of spectral, the degree of line sensitivity, the position and extent of neural banks, the discrimination of confusion colours and so on, Is limited only by the availability of time and the availability of time and the complexity of the necessary apparatus. Among the more simple tests which are usually employed is to which a portion of one spectrum and ask the tests to match this line in a second spectrum. For this purpose Helmholetz’s (1966) spectrum colour mixing apparatus may be employed or an apparatus based on the principle of Abneys (1906). Edridge-green (1909-20) uses a single spectrum and ask the tests to mark off the monochromatic banks and to describe what he sees as the spectrum is moved along. There spectroscopic tests are of considerable intricacy and for the practice of routine examination may have been suggested.

MATCHING TESTS.

A number of tests have been suggested or introduced which depends on the subjects ability to match various colours in which are deliberately added ‘’confusion colours’’, the identification and matching of which present considerable difficulty to the colour – blind. Among the best of these is the original Holmgreens ‘’wool test’’ (1877) in which skeins of Berlin wools are supplied and the test is required to pick out from the wools those which resemble selected skeins in colour.

PSEUDOISOCHROMATIC OR POLYCHROMATIC PLATES

This is a modification of the earlier tests and possesses considerable advantages. Colour defectives confuse certain colours and colour shades with one another and on a background composed of coloured spots, numerical or letters are marked out in similar spots of the confusion colours. The test can be made extremely varied and be so composed that various types of colour blindness can be detected by the failure of the tests to pick out the pattern or by his appreciation of a pattern different from that seen by a normal. All pseudo so chromatic plates are made up of coloured dots arranged so those of generally similar colours form a figure (a letter, numerical, a geometrical shape or simply a winding path) among a background of dots of another colour. If the difference between the figure colour and the background colour is sufficiently great of an observer, he readily reads the figure. If the colour differences is slight, he can distinguish the figure only with difficulty and hesitation or not at all. Usually several different shades or highnesses of each colour are used in both the figures and the background so as to prevent recognition of the figure or the basis of a lightness difference among, and thus to require that a true or saturation difference to the basis for identification of the figure. The cleverest of plate design are those in which there are two figures, often overlapping, only one of which can be read by a normal observer, while a colour defective can read only the other, another useful design is a diagnostic plate that displays two figures, both of which can be read by a normal observer while one type of colour defective sees only of the figures, and another type sees only the other figure.

The first satisfactory series of plates was produced by stilling (1883), which was modified and improved by Hertel (1926) and other have been devised by Grossman (188), Nagel (1906), Oguchi (1914) Edridge – green (1920), Ishihara (1921) and schaaff (1927). Of these, Ishihara is the most useful.

ISHIHAR’S PLATES.

The Ishihara test for colour-blindness has become almost a world-wide standard. First published in 1917, the test has been revised many times in subsequent editions in which new plates have been added, certain old plates eliminated and others improved. Thus both the number of plates and their quality are variable among the various editions.

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