The Effect of Hypertension in IOP, Color Vision, Vision, and Visual Field By: Hind Hassan Mohammed Saleh (B.Sc

Home , Intraocular pressure

AL-Neelain University

Graduate Studies Collage

Faculty of Optometry & Visual Sciences

The Effect of Hypertension in IOP, Color Vision, Vision,

and Visual Field

Thesis submitted as a partial fulfillment for requirement of M.Sc. Degree in Optometry and Visual Sciences

By: Hind Hassan Mohammed Saleh B.Sc. in Optometry

Supervisor Dr. Madiha Sid Ahmed PhD in optometry

2016

اآليــــــــــه

بسمميحرلا نمحرلا هللا

) اَل ال َّش ْم ُس يا ْنبا ِغي ال اها أا ْن تُ ْد ِر اك ا ْل اق ام ار او اَل اللَّ ْيل ُ اسابِ ُق النَّ اها ِر ۚ او ُ ل ِي اِ ال ك يا ْسبا ُُو ان ﴿ ٠٤﴾

صدق هللا العظيم

سورة يس

Al-Neelain University Graduate Studies College The Effect of Hypertension in IOP, Color Vision, Vision, and Visual Field By: Hind Hassan Mohammed Saleh (B.Sc. in Optometry) Supervisor: Madiha Sid Ahmed (PhD in Optometry)

Abstract

Aim: To show the effect of hypertension in IOP, color vision, vision, and visual field.

Material and methods: Done at Makkah Eye complex -Alkalakla and El-Neelain University Hospital, in the period from (March to June 2016), A total of 100 subjects; (29) of them have hypertensive their ages ranged from (44-80) years they were free from other systemic or ocular disease, and (25) subjects of (control group) free from ocular and systemic disease. Snellen’s chart was used to assess vision of patients, Goldenman tonometr and Schiotz tonometer to measure intraocular pressure, Ishihara pseudo Isochromatic plates to evaluate color vision, automated perimeter Octopus 9000 to examine visual field.

Results: Sixty four percent of the hypertension subjects had low vision 0.3 (6/18) or worse comparing with case control 78% had vision of 6/18 or better. 19% of the hypertension subjects had IOP >20 mmHg and all subjects of case control were normal; a significant difference in means was founded with control group (P value 0.000). In color vision results 56.9% of the research sample had deutan, 12.1% were totally color blind and 3.4% were with protan while in case control 25% have color vision defect. Furthermore; visual field defect was severe in 24.1% of study subject opposite to case control all subjects were normal.

Conclusion: hypertension patient increased IOP, defect in color vision and visual field.

Keywords: hypertension, intraocular pressure, vision, color vision, visual field.

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جامعة النيمين الدراسات العميا تاثير ضغط الدم عمى ضغط العين وحدة االبصار ورؤية االلوان وميدان النظر اعداد: هند حدن دمحم صالح بكالريوس في عموم البصريات اشراف: د/ مديحة سيد احمد دكتواره في عموم البصريات ممخص الدراسة

الهدف: تهدف الدراسة لطعرفة تاثير ضغط العين عمى مرضى ضغط الدم، وحدة االبصار، رؤية االلهان وميدان الظظر .

المواد والطرق : هذه الد ارسة وصفية مقظعية اجريت في مجطع مكة لظب العيهن بالخرطهم )الكالكمة( وستشفى العيهن الجامعي في الفترة من )مارس الى مايه 2016( من مجطهع مائة مريض )50( مظهم مرضى ضغط الدم وتراوحت اعطارهم ما بين )44-80( عامهلس لديهم اي امراض عضهية او بصرية وخطسهن طبيعيهن، تم استخدام لهحة اسظيمين لقياس حدة االبصار وقهلد مان تهنهميتر وسجهتيذ تهنهميتر لقياس ضغط العين ولهحة ايشارا القياس رؤية االلهان و automated perimeter لقياس ميدان الظظر.

النتائج: سبعهن بالطائة من مرضى ضغط الدم لديهم حدة ابضار ما بين )6/18 – 1/60( وعد االصابع وؤية الضؤ وحركة اليد كانها 4% و 11% و 9% عمى التهالي مقارنة مع االشخاص الظبيعين 78% لديهم حدة ابصار 6/18 وافضل. 31% من مرضى ضغط الدم كان ضغط العين لديهم اكبر من 20 ممم مقارنة مع الظبيعين، جطيعهم كانه في الطدى الظبيعي ووجد ان هظالك فروقات ذات دالالت احصائية بقيطة معظهية )0.000(. رؤية االلهان لدى مرضى ضغط الدم 48% مظهم لديهم ديهتان 31% لديهم عطى الهان و 3% بروتان مقارنة مع االشخاص الظبيعين 25% لديهم مشاكل في رؤية االلهان. اما ميدان الظظر 36% لديهم مشاكل حادة مقارنة مع االشخاص الظبيعين.

الخالصة: مرضى ارتفاع ضغط الدم يعانهن من الرؤية الطتدههرة، وزيادة الضغط داخل الطقمة، خمل في رؤية األلهان، والطجال البصري.

كممات المفتاحية: ارتفاع ضغط الدم، ضغط العين، والرؤية، رؤية األلهان، الطجال البصري.

Dedication

To My

Mother,,

Father,,

Husband,,

Brothers, sisters,,

And Friends,,

Acknowledgement

After thanks Allah,

My full thanks to my supervisor Dr. Madiha Sid Ahmed

All the patients who agreed to participate in this study.

My thanks also to Al-Neelain University Hospital and Makah Eye Complex for permission.

List of contents

Topic Pg. Holly Quran I Abstract English ii Abstract Arabic iii Dedication iv Acknowledgement v List of content vi List of tables ix List of figures x Chapter One Introduction 1.1 Introduction 1 1.2 Statement of problem 1 1.3 Aim of study 2 1.4 Hypotheses 2 1.5 Structure of study 2 Chapter Two Literature Review 2.1 Hypertension 3 2.1.1 The Definition 3 2.1.2 Classification 3 2.1.2.1 Primary hypertension 3 2.1.2.2 Secondary hypertension 4 2.1.3 Symptoms 4 2.1.4 Causes of hypertension 4 2.1.5 Physiological factor affect in hypertension 4 2.1.6 Clinical features of hypertension 5 2.1.7 Risk factor of hypertension 5 2.1.8.2 Sign and Symptom 5 2.1.9 Diagnosis of hypertension 6 2.1.10 Treatment of hypertension 6 2.1.8 Ocular Complication of hypertension 6

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2.1.8.2 Other complications 6 2.2 Intraocular Pressure (IOP) 7 2.2.1 Definition 7 2.2.2 Physiology of intraocular pressure 7 2.2.3 Importance of measuring IOP 7 2.2.4 Factors affect IOP 8 2.2.5 Range of intraocular pressure in population 8 2.2.5.1 Fluctuation 9 2.2.5.2 Ocular hypertension 9 2.2.6 Intraocular pressure assessment 9 2.2.6.1 Tonometry 9 2.3 Color vision 10 2.3.1 Normal color vision 10 2.3.4 Properties of color vision 11 2.3.5 Physiology of color vision 11 2.3.3 Defective color vision 11 2.3.6 Color Blindness 13 2.3.7 Color vision testing 13 2.4 Visual Field 14 2.4.1 The definition 14 2.4.2 Visual Pathways 14 2.4.3 Size and Shape 14 2.4.4 Visual field defects 15 2.4.5 Visual filed test 16 2.5 Previous studies 17 Chapter Three Material and Methods 3.1. Introduction 23 3.2 Study area 23 3.3 Group of the study 23 3.3.1 Hypertensive group 23 3.3.2 Control group 23 3.4 Material 23

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3.5 Clinical procedure 24 3.5.1 Snellen’s chart 24 3.5.2 Goldman Tonometer 24 3.5.2.1 Technique 25 3.5.3 Schiotz tonometer 25 3.5.4 Ishihara Pseudo Isochromatic Plates 26 3.5.4.1 Technique 26 3.5.4.2 Interpretation 27 3.5.5 Automated (computerized) perimeter: (Octopus 9000) 28 Chapter Four Results 4.1 Subjects Demographic Data 29 4.2 Vision 32 4.3 Intraocular pressure IOP 33 4.4 Color Vision 33 4.5 Visual field 34 4.6 CD/ratio 34 Chapter five Discussion 5. Discussion 35 Chapter Six Conclusion and Recommendations 6.1 Conclusion 36 6.2 Recommendations 36 6.3 Suggestion for future study 36 References 37 Appendices 39

List of tables

Tables Pg. Table (4.1) Shows the demographic and statistics of clinical data of the two 30 study groups Table (4.2) Measurement of vision of the two groups 32 Table (4.2) Measurement of IOP of the two groups 33 Table (4.2.1) measurement of IOP in hypertensive according to gender 34 Table (4.3) measurement of color vision in hypertensive according to 34 gender Table (4.4) distribution of visual field result in hypertensive depending on 34 genders 34 Table (4.5) distribution of CD/ratio result in hypertensive and case control

List of figures

Figures Pg. Figure (3.1) Snelen’s vision chart 24 Figure (3.2) Goldman Tonometer 24 Figure (3.3) Schiotztonometer 26 Figure (3.4) Ishihara Pseudo Isochromatic Plates 27 Figure (4.1) the gender of the sample 29 Figure (4.2.1) Mean of vision in hypertension and case control 32 Figure (4.4.1) Types of color vision between hypertension and case control 33 subjects

CHAPTER ONE

INTRODUCTION

1.1 Introduction

Hypertension is another name for high blood pressure. It can lead to severe complications and increases the risk of heart disease, stroke, and death. Blood pressure is the force exerted by the blood against the walls of the blood vessels. The pressure depends on the work being done by the heart and the resistance of the blood vessels. Medical guidelines define hypertension as a blood pressure higher than 130 over 80 millimeters of mercury (mmHg), according to guidelines issued by the American Heart Association (AHA) in November 2017.

Hypertension is classifieds as primary or secondary, 90-95% of cases are primary hypertension which means high blood pressure with no obvious cause (Michele 2012)

Hypertension is a chronic medical condition in which blood pressure in the arteries is evaluated. Blood pressure is summarized by two measurements systolic and diastolic depend on whether heart muscle is contracting or relaxed (Michele 2012).

Clinically available color vision test are used to diagnose and differentiate congenital and acquired color confusions abnormal wave length discrimination experienced by color defectives and are designed to perform different functions (Nicola 2009).

Intraocular pressure (IOP) the fluid pressure inside the eye, tonometry is the method eye care professional used to determine. The measurement of intraocular pressure is an important part of the full eye examination and has important implication in screening for eye disease (Nicola 2009)

Visual field describes the visual function within an area that is defined by the limits of visual space to steadily fixating eye (Timothy J 2013).

1.2 Statement of problem

Hypertension is very common in the developed world depending on the diagnostic criteria; it can affect all organs of the body. In the eye hypertension may cause retinopathy in the retina and other compilations of blood.

1.3 Aim of the study

 To show the effect of hypertension in IOP, color vision, vision, and visual field.

1.4 Hypotheses

 Dose hypertension increase the IOP?  Dose hypertension change the color discrimination?  Dose hypertension affect vision?  Is there specific visual field defect associated with hypertension?

1.6 Structure of study

The study will include the following chapters:

Chapter one: introduction.

Chapter two: literature review.

Chapter three: subjects, materials and methods.

Chapter four: Results.

Chapter five: Discussion

Chapter six: conclusions and recommendations, then followed by references and appendices.

CHAPTER TWO

LITERATURE REVIEW

2.1 Hypertension

2.1.1 The Definition

High blood pressure also is a common medical condition in which the long term force of the blood against artery walls is high or too strong, when blood puches harder against the arteries, blood pressure goes up, that it may eventually cause health problems. (Norman,2006)

Blood pressure (BP) above 140/90 is considered as hypertension, the upper number is systolic pressure is the highest pressure in the arteries when the heart beats and fills the arteries, the lower number is diastolic pressure; is the lowest pressure in the arteries when the heart relaxes between beats (Norman, 2006)

2.1.2 Classification

2.1.2.1 Primary hypertension

Borderline and labile hypertension: About one third of patients found to have an abnormal blood pressure at their first visit to the doctor will have lower blood pressure on subsequent visits. Some individuals appear to have wide swing in blood pressure and have been called labile hypertensive.

Isolated systolic hypertension: Due to arteriosclerotic change in the major vessels of the elderly, the pulse pressure widens with greater rise in systolic compared to diastolic pressure.

Benign or essential hypertension: Hypertension is never essential and rarely benign. This disease is which affect the vast majority of those suffering from high blood pressure, diagnosis depend on an established elevated systemic pressure in the absence of change in the ocular funds. (Sunil and Gergory 2009).

2.1.2.2 Secondary hypertension

The cause of secondary hypertension:

Renal disease the precise cause of high blood pressure in chronic renal failure is not clear there is no justification for surgical removal of kidney in unilateral renal disease, since medical treatment of hypertension is now likely to be more effective; endocrine disease Hypertension, which may be severing, usually accompanies Cushing syndrome.

Drug induced hypertension: some drug of combination of drug may induce hypertension. (Sunil and Gergory 2009)

2.1.3 Symptoms

High blood pressure itself is usually without sign and symptoms (asymptomatic) it can do damage silently. Although few people with early stage high blood pressure may have dull headaches, dizzy, spells, or few more nose bleeds than normal, this signs and symptoms don’t occur until high blood pressure sever. (Nema, 2012)

2.1.4 Causes of hypertension

 Pregnancy  Hormonal problems such as an underactive thyroid ,diabetes, or low blood sugar  Heart failure heart arrhythmias(abnormal heart rhythms)  Liver disease (Melinda, 2012)

2.1.5 Physiological factor affect in hypertension

 Blood volume.  Resistance in circulatory system this resistance of the blood vessels.  Viscosity or thickness of fluid.  Level of different body hormones.  Condition of the kidney (Parveen 2011).

2.1.6 Clinical features of hypertension

 Until complications appear, essential hypertension is condition without symptoms has no associated physical signs save for the elevated blood pressure.  Headaches once widely regarded as indicators of hypertension.  Breathlessness may be present, due to elevated left ventricular.  Once complication of essential hypertension are present they reflected in symptom and physical signs lead to cardiac failure and renal disease. Investigations have two aims:  To determine the effect that elevated blood pressure. they already had on various organ systems.  To identify a cause of hypertension. (Nichi et al 2010)

2.1.7Risk factor of hypertension

Urban black population have a higher incidence of hypertension environmental and genetic factor are likely to be responsible; stroke is most common complication amongst black hypertensive; the opposite is the case for white hypertensive the effectiveness of treatment is similar among black and whites. (Kanski 2007)

2.1.8.2 Sign and Symptom

 Hypertensive retinopathy it is usually discovered during eye exam.

 Headaches.

 Vision problem.

 Narrowing of blood vessels.

 Cotton wool exudates.

 Swelling of the macula.

 Optic nerve bleeding. (Web M D. medical, 2011)

2.1.9 Diagnosis of hypertension

Diagnosis of high blood pressure is made by measuring it over number of clinic visit via the familiar upper arm cuff device.

Other tests also help to identify the causes and determine any complication including urine test, kidney echo cardiography. (Nichi et al 2010)

2.1.10 Treatment of hypertension

 Dietary measure for each kilogram loss of weight blood pressure can be expected to fall by 3- mm hg systolic and `1.5- diastolic.

 Relaxation, teaching patient to relax – using formal programmers.(Nichi et al 2010)

Measured the hypertension

. Blood pressure is measured with an instrument called a sphygmomanometer. (Melinda, 2012)

2.1.8 Ocular Complication of hypertension

2.1.8.1 Hypertensive retinopathy

Can cause damage to the blood vessel in the retina, this eye disease is known hypertensive retinopathy the damage can be serious if hypertension is not treating (Nema, 2010). Hypertension retinopathy has the following grades;-

 Grade (1) visible arteriolar narrowing  Grade (2) obvious arteriolar narrowing with localized irregularities  Grade (3) multiple flame, shape, hemorrhage, exudates.  Grade (4) called malignant hypertension, the presence of papilledema. (Nema, 2010)

2.1.8.2 Other complications

 Strok  Heart disease  Kidney disease

 Metabolic syndrome  Erectile dysfunction

2.2 Intraocular Pressure (IOP)

2.2.1 Definition

The IOP is determined by the balance between the rate of aqueous secretion and aqueous outflow. The latter is in turn related to the resistance encountered in the outflow channels and to the level of episcleral venous pressure. The rate of aqueous outflow is proportional to the difference between the intraocular and episcleral venous pressure.

Tonometry is the method used to determine the eye pressure. Elevated of intraocular pressure is probably the most significant ocular risk factor for glaucomatous optic nerve damage. (Rosenfield M 2009).

2.2.2 Physiology of intraocular pressure

Ocular pressure is related to the secretion and draying of aqueous fluid. The regulation of aqueous production and drange allow control of IOP. The aqueous is secreted from epithelial layer of the process of the ciliary body at a rate of around 5mm per minute. Aqueous pass through the narrow passage between the anterior crystalline lens surface and iris into the anterior chamber, and drange away via one of two route, about 80 -90 per cent of aqueous drains via the trabecular routes.

The fluid passes via the trabicular meshwork into the canal of schlemm passes into the suprachoroidal space from the iris root and anterior ciliray muscle, to drain it into the sclera vascular system (Nema HV, 2012).

2.2.3 Importance of measuring IOP

 It helps to identify individuals at higher risk of developing glaucoma.

 Initial IOP measurements guide subsequent treatment approach and help set the desired pressure for each patient.

 Subsequent I measurements help to decide the need to be more aggressive in treating the individual s glaucoma.

 Treatment efficacy can be monitored by measuring the IOP accurately (Rosenfield M 2009).

2.2.4 Factors affect IOP

 Accommodation.

 Age.

 Gender.

 Blinking.

 Extra ocular muscle action.

 Respiration.

 Ocular pulse.

 Diurnal variation

 Seasonal variation.

 Food and drug.( www.wikipidea.org)

2.2.5 Range of intraocular pressure in population

The normal range of IOP is defined from population surveys, and a cutoff value of 11- 21 mmHg is widely used to differentiate between normal and abnormal IOP. Although there is no absolute pathological point, 21 mmHg is considered the upper limit of normal and levels above this are viewed with suspicion. However, in some patients glaucomatous damage occurs with IOPs less than 21mmHg (normal - tension or normal- pressure glaucoma) whilst others remain unscathed with IOPs up to 30 mmHg (ocular hypertension). Although the actual level of IOP is important in the development of glaucomatous during age, other factors are also significant (Timothy J 2013).

2.2.5.1 Fluctuation

Normal IOP varies with the time of day, heartbeat, blood pressure level and respiration. The diurnal pattern varies, with a tendency to be higher in the morning and lower in the afternoon and evening. Normal eyes manifest a mean diurnal pressure variation of 5mmHg. Ocular hypertensive or glaucomatous eyes, however, exhibit a wider fluctuation (Timothy J 2013).

2.2.5.2 Ocular hypertension

Ocular hypertension as any ocular condition presenting with an IOP >21 mmHg, but with normal appearing optic disc and visual field. Careful evaluation of optic nerve head and visual filed should be performed along with IOP measurement in all patients evaluates for glaucoma.

Investigators have reported an increased central corneal thickness in eyes of patient with ocular hypertension. A strong relationship exists between increase IOP and greater risk of developing glaucomatous neuropathy. (Nema HV 2012).

2.2.6 Intraocular pressure assessment

2.2.6.1 Tonometry

a) Goldman tonometer

The standard device for measuring IOP has been the Goldman applanation tonometer (GAT). This is because it is reasonably priced, fits easily into the slit- lamp examination, provides seemingly accurate IOP measurement and is based on easily understood principles.

b) Schiotz tonometer

Uses the principle of indentation tonometry, in which the extent of corneal indentation by a plunger of known weight is measured; it is now seldom used in clinical practice.

c) Other types of tonometers

 Pneumotonometers.

 Reichert ocular response analyzer.

 Dynamic contour tonometry.

 Perkins applanation tonometer.

 Tono-Pen.

 iCare. (Kanski J 2011)

2.3 Color vision

Color sense is the ability of the eye to discriminate between colors excited by light of different wave lengths. Color vision is a function of cones and thus better appreciated in photo vision (Khurana 2006).

Clinically available color vision tests are used to diagnose and different congenital .and acquired color deficient, they exploit the isochromatic color confusions and abnormal wavelength discriminations experienced by color defectives and are designed to perform different functions. (Rosenfield M 2009)

2.3.1 Normal color vision

In normal healthy human eye there are three different classes of cones photoreceptors, this lead to trichromatic, because a person having normal color vision required three primary color to match any given color stimulus.

All spectral hues can be matched by an additive mixture of three primary colors taken from long wave length (red 558nm) maximum absorption, and medium wave length (green 531nm) maximum absorption and short wave length (blue 419nmm) maximum absorption region of spectrum.

The three types of cone differ in their overall numbers and distribution over retina, blue photo receptors are absent from central fovea.

Normal color vision vary from males and female the light that reaches the photo receptors is composed of mixture of wave length and it is the dominant wave length which determines the color.(Bruce , J, 2007)

2.3.4 Properties of color vision

 Hue, which is closely related to wavelength, and which is used to name a color  Saturation, which describes the intensity of a color  Brightness, which indicates the intensity of light emitted or reflected by the surface. (Bruce J 2007)

2.3.5 Physiology of color vision

The initial processing of color information occurs in the retina.

The m1agnocellular visual pathway can provide luminance information but not color- opponent information.

Retinal ganglion cells and cells in the lateral geniculate nucleus of the brain show chromatic and spatial opponency.

Cerebral achromatopsia suggests that there is a specialized cortical area for the perception of color. (David 2007)

2.3.3 Defective color vision

Inherited color vision defects

The most common form of color deficiency are inherited congenital defects are binocular, symmetrical and do not change with time unless the individual acquires a disease that causes damage to the visual pathway. They arise from alteration in the genes encoding the posing molecules and are characterized by abnormal color matching and color confusions; genes are either lost, rendered non-functional, or altered.

The results of the gene alterations are:

 Monochromatism

Rod monochromatism occur in about 1 in 30000 of the population; such individuals have true a chromatic vision, low visual acuity (0.1-0.3), find high intensity light uncomfortable, display nystagmus, and may have some signs of macular dystrophy.

These patients do have morphologically normal cones in their outer retina but their functional status is unclear. It has been suggested that they have a single type of blue cone.

Cone monocromatism is very rare (1 in 100000). These individuals have normal visual acuity but cannot discriminate colored light of equal luminosity. Apparently cone monochromatis possess all three types of cones, indicating that the defect occurs in cortical processing, probably. (David 2007)

 Dichromatiosm

Dichromatism occurs when the affected individual matches all color with mixtures of two primaries. Therefore, the range of secondary colors is restricted. Protanopes are missing the red wave length, deutranope the green, and tritanopes the blue. Mixing of the two color will produce a sensation of white at certain specificities, which for protanopes is 495 nm, for deutranopes 500 nm, the dichromate cannot distinguish the chart of no spectral hues from spectral hues as the trichromate can, leading to a much narrower range of color detection by the color charts.(David 2007)

 Anomalous Trichromatism

Anomalous trichromats use different proportions of the three primaries to match color. Protans use more red, deutans more green, and tritans more blue. The color anomalous individual differ from the trichromate and the dichromate in that he or she will not accept those matches that the other two agree . This is the common from of ‘color blindness’ occurring in 6% of the male population. (David 2007).

Acquired color deficiency

Acquired color vision deficiencies occur as a secondary feature to pathology and can arise at any time throughout life as a result of general or ocular disease, trauma, and medication, or as a result of exposure to toxic substances. Some changes in color vision occur throughout life even in healthy individuals.

Acquired defects often fluctuate in severity, tend to be monocular and often affect blue perception. Hence, changes in color vision can be used as a useful indicator of potentially more serious damage to the visual system.

The classification of acquired color vision deficiencies is not as straightforward as that for congenital color vision defect can be distinguished:

 Type 1 (red/green):similar to a congenital protan defect.

 Type 2 (red/green):similar to a congenital deutan defect.

 Type 3 (blue): similar to a tritan defect. (Rosenfield M ,2009)

2.3.6 Color Blindness

Some of the defined color defects can be explained in simple terms of loss of one or other specific type of receptor. However, in practice the situation is often more complex involving not the loss of one particular but the production of combination genes as the result, for instance, of aberrant crossing over in meiosis; these proteins that are intermediate in their spectral sensitivities thus reducing the rang of responsiveness of the protein (Timothy J 2013).

2.3.7 Color vision testing

Color vision testing can be extremely valuable in making the correct diagnosis concerning the cause of a patient s decreased vision. In addition, color vision testing can help monitor the progression of a disease

There are two main types of color vision test: a) The color plate Test: Ishihara, pseudoisochromatic, or Dvorine color plates, b) The color arrangement tests: The Farnsworth (D-15) test, Farnsworth- munsell 100 – hue test and the angel anomaloscope (Rosenfield M 2009).

Pseudoisochromatic color plates

The Ishihara and the Hardy-Rittler-Rand color plates offer a fairly rapid assessment of color discrimination, and arc routinely used clinically (unlike the FM-l00). In these tests, numbers, letters, or other characters arc hidden in a matrix of seemingly random dots the shades and colors are chosen such that patients with congenital color deficits

13 are not able to distinguish between pigments, and thus arc unable to identify the hidden character. Color plate tests were originally designed for detecting congenital color deficits, but the total number of plates missed is often helpful to gauge acquired color vision defects. (Timothy J- 2013)

2.4 Visual Field

2.4.1 The definition

The field of vision is that portion of space in which objects are visible at the same moment during steady fixation of gaze in one direction. The monocular visual field consists of central vision, which includes the inner 30 degrees of vision and central fixation, in the peripheral visual field objects must be larger or more intense to be identified.(Timothy J, 2013)

2.4.2 Visual Pathways

The visual pathway comprises of retina, optic nerve, optic chiasma, optic tract, lateral geniculate body, optic radiation and occipital cortex.

•The first visual neuron is formed by rods and cones.

•The second visual neuron is formed by the bipolar cells.

•The third visual neuron is formed by the ganglion cells. The axons from the ganglion cells forms the nerve fiber layer and passes out as optic nerve that crosses at chiasma to emerge as optic tract and ends in the lateral geniculate body.

•The fourth visual neuron emerges from the lateral geniculate body. The axons of fourth visual neuron emerge as optic radiations and ends in the visual cortex in the calcarine area of occipital lope.

•The course of fiber is associated with crossing, shifting, looping and intermingling and final rearrangement in the cortex (Ml Agarwal 2007).

2.4.3 Size and Shape

The visual field represents the extent of the visual world perceived by the eye, and includes an expansive area that stretches from 90˚ temporally to 60˚ nasally, and

14 approximately 70˚ both superiorly and inferiorly, light entering the eye is focused by the cornea and lens to form an inverted image on the retina. Axons that convey information from the retina to the brain from the optic disc as they exit the eye, interrupting the otherwise continuous blanket of retina. The optic disc is approximately 12˚ to 15˚ on the nasal side of the visual axis and contains no photoreceptors. Thus, a blind, oval-shaped spot, measuring approximately 5˚ in width and 7˚ in height, is projected into the temporal visual field of each eye. This physiological blind spot is rarely noticed, even with monocular viewing. (Timothy J 2013)

2.4.4 Visual field defects

It is important to remember that the image is projected on to the retina upside down and inverted. Hence, a lesion of the top right of the retina or in the pathway beyond will cause a defect in the bottom left of the visual field (Timothy J 2013).

Visual field defect - a portion of the visual field is missing. This may be central (eg, an optic disc or nerve problem) or peripheral (along the visual pathways from the optic chiasm back).

Scotoma - this is a type of visual field defect. It is a defect surrounded by normal visual field.

Relative scotoma - an area where objects of low luminance cannot be seen but larger or brighter ones can.

Absolute scotoma - nothing can be seen at all within that area.

Hemianopia - a binocular visual defect in each eye's hemifield.

Bitemporal hemianopia - the two halves lost are on the outside of each eye's peripheral vision, effectively creating a central visual tunnel.

Homonymous hemianopia - the two halves lost are on the corresponding area of the visual field in both eyes, either the leftor the right half of the visual field.

Altitudinal hemianopia - refers to the dividing line between loss and sight being horizontal rather than vertical, with visual loss either above or below the line.

Quadrantanopia - is an incomplete hemianopia referring to a quarter of the schematic 'pie' of visual field loss.

Sectoral defect - is also an incomplete hemianopia.( www.wikipidea.org)

2.4.5 Visual filed test a. Tangent screen test

The simplest form of perimetry uses a white tangent .vision is tested by present different sized pins attached to a black background. This test stimulus (pins) a white or colored. (Timothy J, 2013) b. Goldmann perimeter test

The goldmann perimeter is a hollow white spherical bowl positioned a set distance in front of the patient. The goldmann method is able to test the entire range of peripheral vision, and has been used for years to follow vision changes in glaucoma patients. However, now automated perimetry is more commonly used. ( Elliott D.B,2007) c. Automated Perimetry test

Automated perimeter strategies are mostly static specific preselected threshold points in the visual field are tested. Determination of a threshold is performed by projecting a stimulus light of a given size and intensity for a brief duration, varying the intensity of the stimulus above and below the suspected threshold level to isolate the dimmest stimulus intensity that the patient can detect at a given point. Thus, a given point in the visual field receives many stimuli of varying intensities presented in a way to optimally determine the threshold. The computer tests and retests a number of points in a seemingly random fashion, until thresholds are obtained for all points. (Timothy J, 2013). d. Confrontations test

The confrontation visual field exam is a basic exam performed, and not accurate as some of the other visual field test. However, this test can help the specialist to decide if further visual field testing is needed. (Timothy J, 2013)

16 e. Amsler charts test

The amsler grid,used since 1945,isagrid of horizontal and vertical lines used to monitor a person’s central visual field.The grid was developed marc amsler, a swiss ophthalmologist.

It is a diagnostic tool that aids in the detection of visual disturbance caused by changes in the retina, particularly the macula (e.g. macular degeneration), as well as the optic nerve and the visual pathway to the brain.( Elliott D.B,2007)

2.5 Previous studies

B E K Klein, R Klein, and M D Knudtson, Intraocular pressure and systemic blood pressure: longitudinal perspective: the Beaver Dam Eye Study 2005

Abstract

Aim: To investigate the relation between change in systemic blood pressures and change in intraocular pressure.

Methods: This was a population based study of people 43–86 years old living in Beaver Dam, Wisconsin. Measurements at baseline (1988–90) and 5 year follow up of systemic blood pressures, intraocular pressures, and history of use of blood pressure medications.

Results: Intraocular pressures were significantly correlated with systolic and diastolic blood pressures at both baseline and follow up. There were significant direct correlations between changes in systemic blood pressures and changes in intraocular pressure. There was a 0.21 (95% CI: 0.16 to 0.27) mm Hg increase in IOP for a 10 mm Hg increase in systolic and 0.43 (0.35 to 0.52) mm Hg increase in IOP for a 10 mm Hg increase in diastolic blood pressure. Further adjustment for diabetes and medication use did not alter these associations. Decreased systolic or diastolic blood pressures of more than 10 mm Hg over 5 years were significantly associated with decreased IOP.

Conclusions: Reduced systemic blood pressure is associated with reduced intraocular pressure. This finding should be evaluated in other studies, especially with respect to the possibility of resultant decreased risk of open angle glaucoma.

The Effect of Hypertension on Intraocular Pressure and Apoptosis of Retinal Ganglion Cell Through ET-1 Signaling Pathway Activation in Trabecular Meshwork of Hypertension Rat Model

S. Prayitnaningsih, H. Sujuti, A. Abdullah Hamid, N. Permatasari andM. Aris Widodo,2015.

Purpose: To evaluate the effect of Deoxycorticoacetate (DOCA)-salt Hypertension model on IOP,retinal ganglion cell (RGC) apoptosis, ratio of endothelin (ET-1)/ endothelial Nitric Oxide Synthase (eNOS), ETA and ETB Receptor (ETRA and ETRB), Myosin Light Chain Kinase (MLCK), and Caldesmon (CaD) in endothelial cells of Trabecular Meshwork (TM).

Methods: Experimental study was performed on 20 male Spraque Dawley rats divided into control group(1), hypertension group (2–4): DOCA subcutaneous 10 mg/kg BW twice a week+ NaCl 0.9% daily for 2, 6, and 10 weeks respectively. Blood pressure were measured by BP analyzer with animal tail-cuff method and IOP measured by handheld tonometry before study and before enucleation. ET-1 signaling pathway and RGC apoptosis were evaluated by immunofluorescent staining, then observed by laser scanning confocal microscopy. Data were analyzed by one way Anova.

Results: Peak of IOP elevation occurred on 2 weeks of hypertension (7.78 ± 4.14 mmHg). The average ratio of ET-1/eNOS was highest on 2 weeks (1.31 ± 0.025 au). The ETRA were significantly increased in 2 and 6 weeks (1476.3 ± 20.9 au and 1209.7 ± 6.1 au), while ETRB only in 2 weeks (1160.5 ± 18.2 au).The highest average of MLCK (1916.68 ± 6.41 au), CaD (1676.37 ± 7.72 au), and RGC apoptosis (576.15 ± 33.28 au) were found in 2 weeks hypertension.

Conclusions: Hypertension induced by DOCA-salt stimulated significant activation of ET-1 signaling pathway on TM, elevation of IOP, and RGC apoptosis. The peak of activation was achieved at 2 weeks of hypertension.

Acquired color vision and visual field defects in patients with ocular hypertension and early glaucoma, 2005

Dimitris Papaconstantinou, Ilias Georgalas, George Kalantzis, Efthimios Karmiris, Chrysanthi Koutsandrea, Andreas Diagourtas, Ioannis Ladas, and Gerasimos Georgopoulos

Abstract

Purpose:To study acquired color vision and visual field defects in patients with ocular hypertension (OH) and early glaucoma.

Methods:In a prospective study we evaluated 99 eyes of 56 patients with OH without visual field defects and no hereditary color deficiencies, followed up for 4 to 6 years (mean = 4.7 ± 0.6 years). Color vision defects were studied using a special computer program for Farnsworth–Munsell 100 hue test and visual field tests were performed with Humphrey analyzer using program 30–2. Both tests were repeated every six months.

Results:In fifty-six eyes, glaucomatous defects were observed during the follow-up period. There was a statistically significant difference in total error score (TES) between eyes that eventually developed glaucoma (157.89 ± 31.79) and OH eyes (75.51 ± 31.57) at the first examination (t value 12.816, p < 0.001). At the same time visual field indices were within normal limits in both groups. In the glaucomatous eyes the earliest statistical significant change in TES was identified at the first year of follow-up and was −20.62 ± 2.75 (t value 9.08, p < 0.001) while in H eyes was −2.11 ± 4.36 (t value 1.1, p = 0.276). earson’s coefficient was high in all examinations and showed a direct correlation between TES and mean deviation and corrected pattern standard deviation in both groups.

Conclusion:Quantitative analysis of color vision defects provides the possibility of follow-up and can prove a useful means for detecting early glaucomatous changes in patients with normal visual fields.

Changes of color vision in ocular hypertension. 1995.

Mäntyjärvi M1, Tuppurainen K.

Abstract

Fifty-six ocular hypertension (OHT) patients were examined for 2-3 days in the Eye Clinic of Kuopio University Hospital. No glaucomatous changes were found. Twenty- seven of them were found to have several risk factors for developing glaucoma and medication was started. Twenty-nine of the patients did not show risk factors and had no medication. Color vision was examined with the Farnsworth-Munsell 100 (FM 100) hue test and Besançon anomalometer, later Color Vision Meter 712 at the beginning of the study and 3 years later. None of the 56 patients showed any glaucomatous changes after 3 years of the study. In the treatment group, the FM 100 test showed significantly (paired t-test, p = 0.004) improved error scores after 3 years. In the non-treatment group, 19 patients did not develop risk factors; they had no significant changes in the color vision results. In 10 patients of the non-treatment group, risk factors had developed with elevated intraocular pressure and medication was started for them after 3 years. Their color vision results in the blue anomalous quotient (AQ) of the anomalometer had significantly shifted to the blue part of the equation (paired t-test, p = 0.04). The other color vision results had not changed significantly. The significantly improved FM 100 scores in the treatment group could mean, that the treatment has a beneficial effect for the OHT eyes at risk for developing glaucoma.

Effect of IOP on the visual field in ocular hypertension and glaucoma 1989

Anders Heijl

Abstract

The traditional opinion that increased intraocular pressure is the cause of glaucoma is controversial, probably mainly because of the fact that firm evidence for the value of pressure reduction is largely lacking. The present article reviews results from short term studies of visual fields before and after pressure reduction. It also reviews published and unpublished preliminary results from studies addressing the problem of

20 whether the long term visual field prognosis, in glaucoma and inocular hypertension, is affected by pressure lowering therapy. There is no convincing agreement among results from modern studies using computerized perimeter indicating that acute lowering of the ocular tension results in an improvement of the glaucomatous visual field. Long-term result are equally conflicting, and often negative. We have noted from a preliminary analysis of our own masked, prospective study of patients with ‘high risk’ ocular hypertension, that the same results may be interpreted in quite different ways. The results of available studies certainly indicate that pressure reduction does not automatically lead to clear and positive effects on the visual field. The studies have often been small, however, and have usually not had the power of detecting small effects of treatment. Also, pressure reduction has usually not been dramatic and many treated patients have maintained ‘elevated’ pressure levels. atients with very high pressures have not been included, and the effect of pressure reduction in this situation has therefore not been investigated at all. More controlled, prospective therapeutic studies are necessary and ethical. It seems particularly important to study the long- term effects of non-pharmacologically induced pressure reduction in patients with manifest field loss. It is necessary to make every effort to avoid bias not only in the design of such studies, but also in the interpretation of their results.

Myron Yanoff 2009

in the Baltimore eye study, IOP was 1.5 mmHg higher for patients with a systolic blood pressure over 160mmHg when compared to systolic blood pressures lower than 1 10mmHg.The same study, however, did not find a statistically significant association between hypertension and glaucoma. Likewise, no association was seen between POAG and hypertension in south indiansM or southwest United States Hispanies.

The idea that insufficient perfusion of the optic nerve may contribute to glaucoma led the Baltimore eye study investigators to examine the relationship between POAG and diastolic perfusion pressure (defined as the difference between diastolic blood pressure and intraocular pressure). They found a significant increase in the rates of

POAG for diastolic perfusion pressures under 50, with a greater than sixfold odds of having POAG noted when the diastolic perfusion pressure dipped below 30. More recently, similar findings were also reported for Caribbean and Hispanic populations.

CHAPTER THREE

MATERIAL AND METHOD

3.1. Introduction

This chapter represents the materials, methods, criteria for selecting patient and procedure used in this study.

3.2 Study area

This is a cross sectional study which conducted at Makkah Eye complex -Alkalakla and El-Neelain University Hospital from (March to April 2016)

3.3 Group of the study

The study include two groups with the following criteria

3.3.1 Hypertensive group

. Have no other systemic disease . They were free from ocular disease. . Their age over 35.

3.3.2 Control group

. The same range of age . They were free from ocular and systemic disease

3.4 Material

 Snellen’s chart to assess the vision of patient.  The Goldman Tonometer to measure intraocular pressure.  The Schiotz Tonometer to measured intraocular pressure.  Ishihara pseudo isochromatic plate to assess color vision test.  Automated (computerized) perimeter to assess visual field.

3.5 Clinical procedure

3.5.1 Snellen’s chart

Snellen’s chart was used to measure patient visual acuity, the visual acuity was measured for distance about 6m, set the patient comfortable in examination chair, also in brightly and evenly illumination, then measure the right eyes.

Standard visual acuity first, cover the left eye with occluder, after that ask the patient to read the top line if he/she can’t read then move the chart toward the patient if not read count finger (CF) then hand moved in front of the patient face (HM), and finally put pen light in front the patient eye or around the eye, if he/she can see light (PL) if can’t see ( N L ), repeat this procedure with left eye

Figure (3.1) Snelen’s vision chart

3.5.2 Goldman Tonometer

Goldman tonometer (GAT) was used to measure IOP

Figure (3.2) Goldman Tonometer

3.5.2.1Technique:

a. The patient is positioned at the slit-lamp with the forehead firmly against the headrest.

b. Topical anaesthetic and flurescien are instilled into the conjunctiva sac.

c. With the cobalt blue filter and the brightest beam projected obliquely at the prism, the prism is centered in front of the apex of the cornea.

d. The dial is preset between 1 and 2 (i.e. 10-20mmHg).

e. The prism is advanced until it just touches the apex of the cornea

f. Viewing is switched to the ocular of the slit-lamp.

g. A pattern of two semicircle mires will be seen, one above and one below the horizontal midline, which represent the fluorescein-stained tear film touching the upper and lower outer halves of the prism.

h. The dial on the tonometer is rotated to align the inner margins of the semicircles

i. The reading on the dial, multiplied by 10, gives the IOP.

3.5.3 Schiotz tonometer

The instrument measures the degree of corneal indentation produced by known weight that rest upon the cornea.

Putting the patient up right and open the eye and the anesthesia instelated in eye put schiotz in center of cornea and observed to the indicater when stop take the reading and return to the sheet of schiotz to see equivalent reading to determine the measured of intraocular pressure.

Figure (3.3) Schiotztonometer

3.5.4 Ishihara Pseudo Isochromatic Plates:

. Full version 38 plates was used. . Test conducted in natural daylight or fluorescent light

3.5.4.1 Technique:

The subject was seated comfortably under adequate day light illumination; the various polychromatic plates were presented to the subject, who was asked to identify the patterns.

The plates were held 75cm. from the subject and tilted so that the plane of the paper is right angle to the line of vision.

The subject was asked to read or trace the figure or the line in the first page, which can be recognized by normal or abnormal person, if he read or trace the line, then the second page showed to him, if he passes it, then the pages showed one after one till the end of the test. But if the subject could not read or trace the frest page, he was asked many times to distinguish what was there in the page, if still he was not seeing, that means he did not pass the color vision test.

3.5.4.2 Interpretation:

 The first plate should be seen by all subjects.

 2-9 (screening transforming) one number seen by normal patient and another seen by red-green defeat.

 10-17 (screening vanishing) number seen by normal but not seen by color deficient.

 18-21 (Hidden digits) numbers not detected by normal but color deficient individuals.

 22-25 (classification plates) differentiate between protan and deutan.

 Each plate contain (2) numbers on grey background.

 Reddish-purple invisible to protons.

 Bluish-purple invisible to deutan

 26-38 drawing pathways for children or illiterates.

 Each plate presented for 3 seconds.

Figure (3.4) Ishihara Pseudo Isochromatic Plates

3.5.5Automated (computerized) perimeter: (Octopus 9000) a. The instrument turn on and allow to calibrate. b. The test was explained to the patient. c. The patient correction was entered (if any). d. Correcting lens was placed in lens cell. e. The patient seat at the instrument and the height of the instrument adjusted to ensure patient comfort. . f. Patient age entered. g. The right eye was tested first. h. The response button holed by the patient after placing head and chin in place. i. the patient was confirmed to stare at the green dot in the center of bowel and to press the bottom when seeing the light flash. k. Following completion of the one eye test, slide the patient visor to the other eye position and repeat the test. l. At the end of the test printout paper was taken.

CHAPTER FOUR

RESULTS

4.1 Subjects Demographic Data

A total of (54) subjects (108) eyes included in this the study, (32) males and (22) females; their age mean was 53.5±9.40 ranged between (40-76) years.

70.0% 58.6% 60% 60.0%

50.0% 41.4% 40% 40.0%

30.0%

20.0%

10.0%

0.0% Hypertension group Case control group

Male Female

Figure (4.1) the gender of the sample

The total subjects were two groups; group (1) hypertension subjects contains 29 person; group (2) contains 25 normal subjects as case control.

Table (4.1) Shows the demographic and statistics of clinical data of the two study groups

Data Hypertension Case control N =29 N = 25 Age (years) (mean ± SD) 55.8 ± 10.2 50.8 ± 7.62 Range (40 - 76) years (40 - 68) years

Gender Male 17 (58.6%) Male 15 (60%) Female 12 (41.4%) Female 10 (40%)

Vision (mean ± SD) 0.33±0.26 0.41±0.22 Range (NPL-1) (0.25-1)

IOP (mmHg) (58 eyes) (50 eyes) (mean ± SD) 15.3±4.88 13.9±1.88 Range (10-30) (10-18)

Color vision Normal 16 (27.6%) Normal 41 (82%) (58 eyes) Deutan 33 (56.9%) Deutan 9 (18%) Protan 2 (3.4%) Total color blindness 7 (12.1%)

Visual field Normal 22 (75.9%) Normal (100%) (29 eyes) Mild 3 (10.3%) Moderate 2 (6.9%) Severe 2 (6.9%)

Duration (mean ± SD) 9.75±6.80 Range (1-25) years ------

Fundus CD/ratio (mean ± SD) 0.34±0.09 0.36±0.09 Range (0.3-0.7) (0.3-0.6)

Treatment Use 27 (93.1%) ------Not use 2 (6.9%)

Hypertension Control 12 (41.4%) ------High 17 (58.6%)

Hypertension group

Mean age of this group was 55.8±10.2, 17 male (58.6%) and 12 female (41.4%). Vision mean was 0.33±0.26. IOP mean was 15.3±4.88, color vision showed Normal 16 (27.6%) Deutan 33 (56.9%) Protan 2 (3.4%) Total color blindness 7 (12.1%). Visual field Normal 22 (75.9%) Mild 3 (10.3%) Moderate 2 (6.9%) Severe 2 (6.9%). The duration of hypertension has mean 0.34±0.09, and cup disc ratio defect mean 0.48±0.22. Treatment was used in 27 (93.1%) of patients, hypertension was un- controlled in 12 (41.4%) high 17 (58.6%).

Case control

Mean age of this group was 50.8±7.62, 15 males (60%) and 10 females (40%). Vision mean was 0.41±0.22. IOP mean was 13.9±1.88. Color vision Normal 41 (82%) Deutan 9 (18%), All subjects had normal visual field. Cup disc ratio mean 0.36±0.09.

4.2 Vision

Table 4.2.1 measurement of vision

Hypertension Case control Vision Frequency Percent Freq. Percent 0.00 6 10.3 0 0 0.05 1 1 0 0 0.1 6 10.3 0 0 0.15 1 1.7 0 0 0.16 5 8.6 0 0 0.25 6 10.3 16 32 0.3 13 22.4 14 28 0.5 15 25.9 10 20 0.6 1 1.7 7 14 1 4 6.9 1 2 1.2 0 0 2 4 Total 58 100 50 100

Paired sample t-test showed no significant difference in vision between hypertension and case control P > 0.05

0.5 0.45 0.4 0.35 0.3 0.25 0.2 0.15 0.1 0.05 0 Hypertension group Case control group

Figure 4.2.1 compare between mean of vision

4.3 Intra ocular pressure Table (4.2) Measurement of IOP of the two groups Hypertension (N 58) Case control (N 50) IOP Freq. (%) Freq. (%) <10 0 (0) 0 (0) 10 – 20 47 (81) 50 (100) >20 11 (19) 0 (0) 10 – 20 = Normal range

A paired sample t-test was used to compare IOP between hypertension subjects and case control. The test showed no significant difference between them, df (49) t = 1.5, P value 0.123.

0 Hypertension group Case control group

Figure (4.3) mean of IOP in hypertension and case control

Table (4.2.1) measurement of IOP in hypertensive according to gender Male (34) Female (24) Total IOP Freq. (%) Freq. (%) Freq. (%) < 10 0 (0) 0 (0) 0 (0) 10-20 29 (50) 18 (31) 47 (81) >20 5 (8.6) 6 (10.6) 11 (19)

4.4 Color Vision

90.0% 82% 80.0% 70.0% 60.0% 56.9% 50.0% 40.0% 27.6% 30.0% 18% 20.0% 12.1% 10.0% 3.4% 0.0% Normal Dutan Protan Blindness

Hypertension group Case control group

Figure (4.4.1) Types of color vision between hypertension and case control subjects

Chi squire test was used to compare between hypertension subjects and case control in color vision. The test showed significant differences between them, P value0.000.

Table (4.3) measurement of color vision in hypertensive according to gender Male (34) Female (24) Color vision Freq. % Freq. % Deutan 18 (31) 15 (25.9) Protan 2 (3.4) 0 (0) Total color blindness 5 (8.6) 2 (3.4) Normal 9 (15.5) 7 (12.1)

4.5 Visual field

Table (4.4) distribution of visual field result in hypertensive depending on genders

Male (17) Female (12) VF Freq. % Freq. % Normal 14 (48.3) 8 (27.6) Mild 2 (6.9) 1 (3.4) Moderate 1 (3.4) 1 (3.4) Sever 0 (0) 2 (6.9)

(0-2) Normal, (2-6) Mild, (6-12) Moderate, (>12) Marked for MD

4.6 CD/ratio

Table (4.5) distribution of CD/ratio result in hypertensive and case control

CD/ratio Hypertension (N 58) Case control (N 25) Freq. (%) Freq. (%) 0.3 46 (50) 15 (60) 0.4 6 (10.3) 6 (24) 0.5 2 (3.4) 2 (8) 0.6 2 (3.4) 2 (8) 0.7 2 (3.4) 0 (0)

CHAPTER FIVE

DISCUSSION

This study was aimed to show the effect of hypertension in IOP, color vision, vision, and visual field. (54) Subjects included in the study, (32) males and (22) females; their age mean was 53.5±9.40 ranged between (40-76) years.

People over 40 years, African-Americans, and those with a family history of hypertension or glaucoma are at higher risk of having high IOP. Generally, women are more prone to develop hypertension than men. (Vision Service Plan USA 2016); this agree with our study which showed that the range of age of hypertension subjects was ≥ 38year but disagree with this study in that males were more than females.

Nineteen percent of the subjects had IOP >20 mmHg, comparing with case control subjects no significant difference was present; P value >0.05. A study done by B E K Klein2005; reported that there was a significant direct correlation between changes in systemic blood pressures and changes in intraocular pressure. S. Prayitnaningsih study in 2015; mentioned that hypertension induced by DOCA-salt elevated IOP, Myron Yanoff Zoog also found an association between high systemic blood pressure and increased IOP. Hence all these studies are compatible with ours.

Referring to color vision results of this study agree with (72.4%) hypertension subjects had abnormal color vision, comparing with case control P value was 0.000. and this is agree with study done by Dimitris Papaconstantinou and others 2005.

Eventually; (24.1%) of subject had some types of visual field defect comparing with normal subjects P value 0.000, this is agree with Brangava 2012; who said that hypertension may result in a series of retinal vascular changes. Andres 1989; said that it seems particularly important to study long term effects of non-pharmacologically induced reduction in patients with manifest field loss.

CHAPTER SIX

CONCLUSION & RECOMMENDATIONS

6.1 Conclusion

This study was aimed to find the effect of hypertension in IOP, color vision, vision, and visual field. 100 subjects included in the study, 46% males and 54% females; their age mean was 50.42±10.00 ranged between (38-82) years.

 64.6% of the hypertension subjects had low vision <0.3 (6/18).

 81% had normal IOP 10-20 mmHg.

 72.4% had defect in color vision.

 24.1% had defect in visual field.

 20.5% of the hypertension subject had abnormal C/D ratio.

6.2 Recommendations

 Eye examinations should be undertaking routinely especially for hypertension patient.  Increase the awareness and vigilance compilation of hypertension and the importance of treatment.

6.3 Suggestion for future study

 Increase sample size.  Other test like contrast sensitivity should be used.  Study other ocular compilation of hypertension

REFERENCES

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Appendix (A)

CONSENT FORM FOR A RESEARCH PROJECT

Title of project:

The Effect of hypertension in Vision, IOP, Color Vision, and Visual field

Consent

I have informed about the purpose of this project by researcher. I understand the objectives of all clinical tests that will conducted to me. I retain the absolute right over the examination and my withdraw at any time. I also have the right to know about the research information including the result of the research.

I...... (ID no)......

Agree/Disagree to undergo all the examination needed in this research and allow the records to be kept and used for continuing research in the future.

Signature...... Date......

Appendix (B)

Al-Neelain University

Faculty of Optometry and Visual Sciences

Data form

Name:…………………………………………………No:……………………..

Age:…………………………………… Gender:………………………………..

Vision: RE:………………………………LE:…………………………………...

I : RE:………………………………LE:…………………………………......

Color vision: RE:………………………………LE:……………………………..

Visual field: RE:………………………………LE:………………………………

Duration: …………………………………………………………………………..

Fundus: RE:………………………………LE:…………………………………...

Treatment: use not use

Hypertension: control un control high

Data base (hypertension subjects)

No Gender Age IOP CV VF Treatment Onset Fundus Hypertension RE LE RE LE RE LE 1. F 60 12 10 Deutan Deutan Sever Use 6 0.6 0.6 High 2. F 42 14 10 Normal Normal Normal Use 5 0.3 0.3 Normal 3. M 55 12 10 Normal Deutan Moderate Use 15 0.4 0.4 High 4. M 52 14 10 Deutan Deutan Normal Use 10 0.3 0.3 High 5. F 59 10 10 Deutan Deutan Early Use 14 0.4 0.4 Normal 6. M 50 10 10 Normal Normal Normal Use 25 0.3 0.3 High 7. M 59 14 16 Deutan Deutan Early Use 6 0.3 0.3 High 8. M 40 14 10 Normal Deutan Normal Use 0.3 0.3 High 9. M 72 17 17 Protan Deutan Normal Use 5 0.3 0.3 Normal 10. M 50 22 22 T.C. blindness Deutan Normal Use 8 0.3 0.3 High 11. M 55 16 16 Deutan T.C. blindness Normal Use 25 0.3 0.3 High 12. F 47 14 12 Normal Deutan Normal No use 6 0.3 0.3 High 13. F 76 13 10 Normal Normal Normal Use 2 0.3 0.3 Normal 14. M 71 17 17 Deutan Deutan Normal No use 10 0.3 0.3 Normal 15. F 58 22 23 Deutan T.C. blindness Normal Use 20 0.3 0.3 High 16. M 63 18 18 Protan T.C. blindness Normal Use 15 0.3 0.3 Normal 17. M 55 12 12 Deutan Deutan Normal Use 6 0.3 0.3 High 18. F 69 25 30 Deutan T.C. blindness Sever Use 25 0.3 0.3 High 19. M 55 16 22 Deutan Normal Early Use 1 0.7 0.7 High 20. M 62 23 18 T.C. blindness Deutan Normal Use 5 0.4 0.4 Normal 21. F 40 10 10 Deutan Deutan Moderate Use 8 0.5 0.5 High

22. M 44 11 12 Deutan Deutan Normal Use 7 0.3 0.3 Normal 23. F 40 11 11 Normal Normal Normal Use 5 0.3 0.3 High 24. F 66 12 10 Deutan Deutan Normal Use 10 0.3 0.3 Normal 25. M 67 15 15 Normal Normal Normal Use 7 0.3 0.3 Normal 26. F 49 12 20 Deutan Deutan Normal Use 10 0.3 0.3 High 27. F 44 22 22 Deutan Deutan Normal Use 3 0.3 0.3 Normal 28. M 65 18 18 Normal Normal Normal Use 5 0.3 0.3 Normal 29. M 55 20 22 Deutan T.C. blindness Normal Use 9 0.3 0.3 High

Data base (normal subjects)

No Gender Age IOP CV VF CD/ratio RE LE RE LE F 50 12 12 Normal Normal Normal 0.4 1. M 45 15 14 Normal Normal Normal 0.6 2. F 55 16 15 Normal Normal Normal 0.3 3. M 43 14 14 Normal Normal Normal 0.4 4. M 40 16 15 Deutan Deutan Normal 0.3 5. F 50 14 13 Normal Normal Normal 0.5 6. F 45 15 15 Normal Normal Normal 0.4 7. F 60 15 15 Deutan Deutan Normal 0.3 8. M 58 18 17 Normal Normal Normal 0.3 9. F 44 15 16 Normal Normal Normal 0.3 10. M 68 16 16 Normal Normal Normal 0.3 11. M 50 14 12 Deutan Normal Normal 0.6 12. F 40 14 11 Normal Normal Normal 0.3 13. M 42 14 14 Normal Normal Normal 0.5 14. M 50 10 11 Normal Normal Normal 0.3 15. M 58 15 15 Normal Normal Normal 0.3 16. F 45 11 13 Normal Normal Normal 0.4 17. M 50 11 11 Normal Normal Normal 0.3 18. F 55 14 15 Normal Normal Normal 0.3 19. M 43 16 16 Normal Normal Normal 0.4 20. M 48 15 17 Normal Normal Normal 0.3 21. M 59 11 13 Normal Normal Normal 0.3

22. M 50 14 15 Deutan Deutan Normal 0.4 23. F 59 11 13 Normal Normal Normal 0.3 24. M 63 12 13 Deutan Deutan Normal 0.3

T-Test

Paired Samples Statistics

Mean N Std. Deviation Std. Error Mean VisionH 0.3330 50 .26034 .03682 Pair 1 VisionN 0.4160 50 .22620 .03199

Paired Samples Correlations

N Correlation Sig. Pair 1 VisionH & VisionN 50 -.144- .318

Paired Samples Test

Paired Differences t df Sig. (2- Mean Std. Std. Error 95% Confidence tailed) Deviation Mean Interval of the Difference Lower Upper Pair VisionH - - - .36867 .05214 -.18778- .02178 49 .118 1 VisionN .08300- 1.592-

Chi-Square Test

Test Statistics

CVH CV

Chi-Square 43.920a 83.540b

Df 3 2

Asymp. Sig. .000 .000 a. 0 cells (.0%) have expected frequencies less than 5. The minimum expected cell frequency is 25.0. b. 0 cells (.0%) have expected frequencies less than 5. The minimum expected cell frequency is 33.3.

CVH

Observed N Expected N Residual

Deutaus 48 25.0 23.0

Total color blindness 31 25.0 6.0

Normal 18 25.0 -7.0

Protans 3 25.0 -22.0

Total 100

Observed N Expected N Residual

Deutaus 22 33.3 -11.3

Protans 3 33.3 -30.3

Normal 75 33.3 41.7

Total 100

T-Test

Paired Samples Statistics

Mean N Std. Deviation Std. Error Mean

Pair 1 IOPH 17.2900 100 6.22360 .62236

IOP 13.5500 100 2.17132 .21713

Paired Samples Correlations

N Correlation Sig.

Pair 1 IOPH & IOP 100 -.058 .565

Paired Samples Test

Paired Differences

95% Confidence Interval of the Difference Std. Std. Error Sig. (2- Mean Deviation Mean Lower Upper t df tailed)

Pair IOPH - 3.74000 6.70989 .67099 2.40861 5.07139 5.574 99 .000 1 IOP

T-Test

Paired Samples Statistics

Mean N Std. Deviation Std. Error Mean

Pair 1 VisionH .2418 100 .24083 .02408

Vision .5390 100 .30323 .03032

Paired Samples Correlations

N Correlation Sig.

Pair 1 VisionH & Vision 100 -.044 .667

Paired Samples Test

Paired Differences

95% Confidence Interval of the Difference Std. Std. Error Sig. (2- Mean Deviation Mean Lower Upper t df tailed)

Pair VisionH – -.29724 .39537 .03954 -.37569 -.21879 -7.518 99 .000 1 Vision

Chi-Square Test

Test Statistics

VFH

Chi-Square 49.120a

Df 3

Asymp. Sig. .000 a. 0 cells (.0%) have expected frequencies less than 5. The minimum expected cell frequency is 25.0.

VFH

Observed N Expected N Residual

Normal 48 25.0 23.0

Moderate 8 25.0 -17.0

Sever 36 25.0 11.0

Early 8 25.0 -17.0

Total 100

Observed N Expected N Residual

Normal 100 100.0 .0

Total 100a a. This variable is constant. Chi-Square Test cannot be performed.