[NEURORETINAL RIM DEFECTS IN RELATIONSHIP TO DISC DAMAGE October 28, 2011 LIKELYHOOD SCALE IN PRIMARY OPEN ANGLE GLAUCOMA]

laucoma is defined as multi factorial optic neuropathy which is a potentially blinding disease which affects 66.8 million people worldwide or Approximately 15% of cases of blindness. The most common type, primary open-angle glaucoma, having a prevalence of 1/200 in the general population over 40 years of age. Glaucoma is the second leading cause of blindness. Risk assessment of the disease goes a long way in diagnosis and management of the disease. Although the raised intra ocular pressure (IOP) is a significant risk factor for developing glaucoma, there is no set threshold for IOP that causes glaucoma. This can result in decreased peripheral vision and eventually leads to blindness. Glaucoma is associated with a diminution of optic nerve fibres leading to a decrease of The most common type of neuroretinal rim area. This rim loss occurs in glaucoma is primary open all sectors of the optic disc with regional angle glaucoma, having a preferences depending on the stage of the prevalence of 1,200 in the disease. In eyes with modest glaucomatous general population over 40 damage, rim loss is found predominantly at years of age. the inferotemporal and superotemporal disc regions. Early glaucomatous damage can be difficult to detect, requiring careful observation of the optic nerve and Retinal Nerve Fiber Layer. The detection of glaucoma through Optical Coherence Tomography (OCT) and Heidelberg Retinal Tomography (HRT) are very expensive compared to digital fundus images. With the help of image processing, the features of the fundus images such as optic disc and cup could be localized to suspect the glaucoma. The detection of OD position and automated feature extraction is a pre-requisite for the computation of some important diagnostic indexes like glaucoma.

BY Akpotowho Godwin Ellis

| NEUROPATHOLOGY OPT 526 LECTURER: DR. P OMOKHUA

[NEURORETINAL RIM DEFECTS IN RELATIONSHIP TO DISC DAMAGE October 28, 2011 LIKELYHOOD SCALE IN PRIMARY OPEN ANGLE GLAUCOMA]

NEURORETINAL RIM It is a term used in describing the area of the optic disc which contains the neural elements and is located between the edge of the disc and the physiological cup. When describing the neuroretinal rim, as is often done in cases of glaucoma, one must include its colour, size, slope and uniformity. Syn. neural rim. Characteristics of the normal ONH The ONH or optic disc is a round/oval plughole, down which more than a million nerve fibres descend through a sieve-like sheet known as the lamina cribrosa. These fibres are then bundled together behind the eye as the optic nerve which continues towards the brain. The retinal nerve fibres are spread unevenly across the surface of the retina in a thin layer which has a feathery appearance, best seen immediately above and below the disc. As the nerve fibres converge on the edge of the disc they pour over the scleral ring (which marks the edge of the disc) and then down its inner surface. This dense packing of nerve fibres just inside the scleral ring is visualised as the neuroretinal rim. The cup is the area central to the neuroretinal rim. The cup edge (where it meets the neuroretinal rim) is best seen by the bend in small and mediumsized blood vessels as they descend into the cup. The neuroretinal rim is usually

broadest in the Inferior disc region, followed by the Superior disc region, the Nasal disc area, and finally the Temporal disc region (ISNT rule).
In normal eyes, the neuroretinal rim is based on the vertically oval shape of the optic disc and the horizontally oval shape of the optic cup.

BY Akpotowho Godwin Ellis

| NEUROPATHOLOGY OPT 526 LECTURER: DR. P OMOKHUA

[NEURORETINAL RIM DEFECTS IN RELATIONSHIP TO DISC DAMAGE October 28, 2011 LIKELYHOOD SCALE IN PRIMARY OPEN ANGLE GLAUCOMA]

The optic nerve head can be classified by using direct and indirect ophthalmoscopy into six categories: 1. Inferior neuro-retinal rim loss: a disc with tissue loss localised to the inferior/infero-temporal pole, including shelving, or generalised loss of the inferior rim, but not focal notching. 2. Superior neuro-retinal rim loss: a disc with tissue loss localised at the superior/supero-temporal pole, including shelving and generalised loss of the rim, but not focal notching. 3. Concentric cupping: a disc with generalised enlargement of the optic cup without a localised defect in the neuro-retinal rim. 4. Age-related atrophic (senile sclerotic): a disc with a saucerized, shallow cup and parapapillary atrophy. 5. Myopic glaucomatous disc: a myopic disc with a temporal crescent and additional evidence of glaucomatous damage. 6. Focal ischaemic: a disc with a focal notch. ABNORMAL NEURORETINAL RIM WITH DISC DAMAGE The characteristic shape of the rim is of utmost importance in the diagnosis of early glaucomatous optic nerve damage. The physiologic shape of the neuroretinal rim is associated with the diameter of the retinal arterioles, which are significantly wider in the inferotemporal arcade than in the superotemporal arcade; the visibility of the retinal nerve fiber bundles that are significantly more often better detectable in the inferotemporal region than in the superotempora neuroretinal rim. Neuroretinal rim area can be measured by configuration to suspect glaucoma. The shape of the neuroretinal rim, the ratio of the inferior to temporal rim width and the ratio of the superior to temporal rim width were calculated. The photographs were evaluated in a masked fashion without knowledge of the clinical diagnosis and the visual field data.

BY Akpotowho Godwin Ellis

| NEUROPATHOLOGY OPT 526 LECTURER: DR. P OMOKHUA

[NEURORETINAL RIM DEFECTS IN RELATIONSHIP TO DISC DAMAGE October 28, 2011 LIKELYHOOD SCALE IN PRIMARY OPEN ANGLE GLAUCOMA]

Fig: Photograph of an abnormally large, otherwise normal optic disc. Optic disc data: area, 5.7 mm 2; neuroretinal rim width (arrows) inferior, 0.57 mm; superior, 0.35 mm; temporal, 0.18 mm; ratio of inferior to temporal rim width, 3.17; ratio of superior to temporal rim width, 1.94 . Note physiological shape of the neuroretinal rim.

Variables that may also be associated with the pattern of glaucomatous, neuroretinal rim loss are: (1) The physiological configuration of the rim being broader at the inferior and superior disc poles than at the nasal and temporal poles. (2) The morphology of the inner surface of the lamina cribrosa with the larger pores and the higher ratio of pore to interpore connective tissue area in the inferior and superior regions compared with the temporal and nasal regions; a high ratio of pore area to total area is considered to predispose to glaucomatous nerve fibre loss; (3) The glaucomatous bowing of the lamina cribrosa to the outside mainly in the inferior and superior disc regions as shown on scanning electron microscope photographs of glaucomatous eyes; and (4) The regional distribution of thin and thick retinal nerve fibres with thin nerve fibres coming from the foveola, passing mainly through the temporal aspect of the optic disc and being less glaucoma susceptible than thick nerve fibres which originate predominantly in the fundus periphery, lead to the inferior, superior, and nasal disc regions and are more glaucoma sensitive than thin retinal ganglion cell axons. The latter parameter may explain why glaucomatous rim loss occurs later in the temporal horizontal disc sector with predominantly thin nerve fibres than in the temporal inferior or temporal superior disc sectors containing thin and thick axons. It is contradictory to the fact that in far advanced 4 BY: Akpotowho Godwin Ellis | NEUROPATHOLOGY OPT 526 LECTURER: DR. P OMOKHUA

[NEURORETINAL RIM DEFECTS IN RELATIONSHIP TO DISC DAMAGE October 28, 2011 LIKELYHOOD SCALE IN PRIMARY OPEN ANGLE GLAUCOMA]

glaucoma rim remnants are usually located in the nasal disc sector. There, preferentially thick retinal ganglion cell axons leave the eye. As an additional parameter for the pattern of glaucomatous rim loss, the distance from the central retinal vessel trunk in the lamina cribrosa may be considered. In both the normal and glaucomatous eyes of the present study, the retinal vessel trunk was slightly decentred into the nasal upper disc quadrant. Similar results have been obtained in a histomorphometric study of the lamina cribrosa surface. In the latter investigation, the exits of the retinal artery and vein were located 0-15 (O.09) mm and 0 07 (0-14) mm, respectively, nasal to the vertical optic disc axis and 0-02 (0-11) mm and 005 (O 09) mm, respectively, superior to the horizontal optic disc axis. Taking into account the vertically oval optic disc shape, one may infer that the distance between the retinal vessels in the lamina cribrosa and the neuroretinal rim may be associated with the pattern of glaucomatous rim loss. The sector distant to the retinal vessel trunk is the temporal inferior disc region followed by the superior temporal and temporal horizontal disc regions. The nasal disc sector is the one closest to the retinal vessels with the nasal upper portion located closer to the retinal vessel trunk than the nasal inferior portion. In the same sequence, the glaucomatous rim loss has been reported to take place: temporal inferior - temporal superior and temporal horizontal - nasal inferior - nasal superior. Correspondingly, glaucomatous neuroretinal rim notches do not occur on an average at the inferior and superior disc poles but at about 13 degrees temporal to the vertical optic disc axis. These locations are more distant to the retinal vessel trunk than the vertical disc poles at the 6 o'clock and 12 o'clock position. For strengthening the hypothesis that the local glaucoma susceptibility is correlated with the distance to the retinal vessel trunk, the following facts can be listed: (1) In glaucomatous eyes with an unusual location of the retinal vessel trunk or an abnormal optic disc shape, the rim had an unusual form. Conversely, in eyes with an unusual glaucomatous rim configuration, the retinal vessel trunk was abnormally positioned (Figs A-C). Also in these glaucomatous eyes, the rim loss was usually most and least marked in that sector with the longest and shortest distance to the central retinal vessel trunk, respectively.

BY Akpotowho Godwin Ellis

| NEUROPATHOLOGY OPT 526 LECTURER: DR. P OMOKHUA

[NEURORETINAL RIM DEFECTS IN RELATIONSHIP TO DISC DAMAGE October 28, 2011 LIKELYHOOD SCALE IN PRIMARY OPEN ANGLE GLAUCOMA]

(2) The location of early glaucomatous visual field defects in the upper nasal or lower nasal field quadrants close to the horizontal line '9-22 indicates a 6

BY Akpotowho Godwin Ellis

| NEUROPATHOLOGY OPT 526 LECTURER: DR. P OMOKHUA

[NEURORETINAL RIM DEFECTS IN RELATIONSHIP TO DISC DAMAGE October 28, 2011 LIKELYHOOD SCALE IN PRIMARY OPEN ANGLE GLAUCOMA]

ganglion cell loss in the region of the temporal fundus raphe. The axons of these ganglion cells lie in the deepest part of the retinal nerve fibre layer. They are closest to the optic disc border. Within the optic disc, they are more distant to the central retinal vessel trunk than ganglion cell axons originating in the vicinity of the optic nerve head. These are located more centrally in the optic nerve head and are lost in a later stage of the disease. Diagnostically, it may indicate that in eyes with an abnormal position of the central retinal vessels or an unusual optic disc form, early glaucomatous rim changes should be looked for not only in the temporal inferior disc sector but also in that disc sector that is most distant to the central retinal vessel trunk. It may explain why eyes with open angle glaucoma and a temporal cilioretinal artery retain longer central visual field than open angle glaucomatous eyes without a temporal cilioretinal artery. Pathogenetically, one may infer that the retinal vessel trunk could act as a stabilising element. It could render more difficult a mechanical distortion and backward bowing of the lamina cribrosa in glaucoma. This hypothesis is supported by photographs of a W-shaped lamina cribrosa in glaucomatous eyes. The lamina cribrosa is more condensed and bowed more to the back in the inferior and superior disc regions than close to the lamina cribrosa centre where the retinal vessels emerge. If the vessel trunk is decentred into the superior half of the optic disc, the inferior disc portion without vessel trunk support is larger than the superior one. Consequently, it can be deformed to a greater extent than the smaller superior disc part. It could explain the greater frequency of neuroretinal rim notches in the inferior temporal disc region compared with the superior temporal area. As a variation to this mechanical theory, one could also speculate that in the close vicinity of the retinal vessel trunk the vascular supply to the adjacent tissue is better than in the periphery. A vitally important participation of branches of the central retinal vessels in the nourishment of the optic nerve fibres in the lamina cribrosa, however, has not yet been demonstrated. As a factor limiting the scope of the present study one can mention that the position of the central retinal vessel trunk was measured in eyes in which the trunk on the lamina cribrosa surface was clearly detectable. This is possible only in discs showing central cupping. Due to the correlation between optic cup and optic disc size it implies that these selected optic discs were on average larger than normal optic nerve heads. In another histomorphometric investigation on the lamina cribrosa surface, however, 7 BY: Akpotowho Godwin Ellis | NEUROPATHOLOGY OPT 526 LECTURER: DR. P OMOKHUA

[NEURORETINAL RIM DEFECTS IN RELATIONSHIP TO DISC DAMAGE October 28, 2011 LIKELYHOOD SCALE IN PRIMARY OPEN ANGLE GLAUCOMA]

the retinal vessel trunk was also located in the upper nasal quadrant.That study consisted of eyes of varying optic size including also small optic discs. Characteristics of a glaucomatous ONH generalised/focal enlargement of the cup disc haemorrhage (within 1 disc diameter of ONH) thinning of neuroretinal rim (usually at superior & inferior poles) asymmetry of cupping between patients eyes loss of nerve fibre layer parapapillary atrophy (more common in glaucomatous eyes). Distinguishing a glaucomatous ONH from a normal ONH Learn the features of a normal and a glaucomatous ONH (above). Strategy: 1 Dilate pupils, if possible and safe to do so. 2 Identify disc edge and cup edge thereby identifying rim. 3 Does the rim thickness obey the ISNT rule? 4 Is there a haemorrhage? 5 Estimate vertical cup/disc ratio. 6 Measure size of ONH. 7 Examine the retinal nerve fibre layer (using green light).* 8 Draw an annotated diagram of the ONH. *may only be possible with slit lamp and posterior pole lens

BY Akpotowho Godwin Ellis

| NEUROPATHOLOGY OPT 526 LECTURER: DR. P OMOKHUA

[NEURORETINAL RIM DEFECTS IN RELATIONSHIP TO DISC DAMAGE October 28, 2011 LIKELYHOOD SCALE IN PRIMARY OPEN ANGLE GLAUCOMA]

Is the glaucomatous optic neuropathy getting worse/ progressing? The appearance of any of the features of a glaucomatous ONH, or the exacerbation of these features compared to a previous record, is indicative of a progression/worsening of the disease. Disc haemorrhages may be present for two weeks to three months and are an important prognostic sign of progression. An accurate record requires careful observation and a detailed drawing, at the very least. Photographic documentation (preferably stereophotography) is highly recommended. Other imaging devices offer progression analyses, but these are not a surrogate for a detailed clinical examination. Progressive worsening of the visual fields should correlate with structural changes at the ONH.

Pitfalls and pearls

BY Akpotowho Godwin Ellis

| NEUROPATHOLOGY OPT 526 LECTURER: DR. P OMOKHUA

[NEURORETINAL RIM DEFECTS IN RELATIONSHIP TO DISC DAMAGE October 28, 2011 LIKELYHOOD SCALE IN PRIMARY OPEN ANGLE GLAUCOMA]

The hallmark of glaucomatous optic neuropathy is excavation of the neuroretinal rim. Advanced glaucomatous ONH can result in a pale optic disc but disc pallor should raise a suspicion of another cause such as optic atrophy. A colour difference should not be used to distinguish the cup edge; change in direction of the blood vessels is a more reliable indicator. The optic disc abnormality should correlate with the visual field defect. Where this is not the case, further investigations (e.g., CT/MRI scan) may be indicated. The size of the cup always appears smaller when viewed monoscopically than in stereo. A measurement of cup/disc ratio (CDR) alone is insufficient and may be misleading as small discs will have smaller cups and hence a smaller CDR.

Using a study carried out by S.Kavitha, S.Karthikeyan, Dr.K.Duraiswamy (Asst. Professor, Nandha Engineering College, Erode, India. K.S.R. College of Engineering, Tiruchengode, India. Dean, K.S.Rangasamy College of Technology, Tiruchengode, India)on Neuroretinal rim Quantification in Fundus Images to Detect Glaucoma, we can also see the relationship between neuroretinal rim damage and its likelihood in causing primary open angle glaucoma.

PRIMARY OPEN-ANGLE GLAUCOMA (POAG) Primary open angle glaucoma (POAG) encompasses a spectrum of disorders, typified by a characteristic optic neuropathy and field loss in eyes with open drainage angles. It is currently a leading cause of blindness worldwide, and in the future stands to become more important, as populations increasingly age throughout the world. Recently, we have witnessed a number of exciting advances in glaucoma. Developments have occurred regarding diagnosis, treatment, genetics and the relationship of intraocular pressure (IOP) to disease progression. 10

BY Akpotowho Godwin Ellis

| NEUROPATHOLOGY OPT 526 LECTURER: DR. P OMOKHUA

[NEURORETINAL RIM DEFECTS IN RELATIONSHIP TO DISC DAMAGE October 28, 2011 LIKELYHOOD SCALE IN PRIMARY OPEN ANGLE GLAUCOMA]

DISEASE DEFINITION Primary open-angle glaucoma is a progressive, chronic optic neuropathy in adults in which intraocular pressure (IOP) and other currently unknown factors contribute to damage and in which, in the absence of other identifiable causes, there is a characteristic acquired atrophy of the optic nerve and loss of retinal ganglion cells and their axons. This condition is associated with an anterior chamber angle that is open by gonioscopic appearance. CLINICAL FINDINGS CHARACTERISTIC OF PRIMARY OPEN-ANGLE GLAUCOMA Primary open-angle glaucoma is a chronic ocular disease process that is progressive, generally bilateral, but often asymmetric. It is associated with the following characteristics. Evidence of optic nerve damage from either, or both, of optic disc or retinal nerve fiber layer structural abnormalities. Diffuse thinning, focal narrowing, or notching of the optic disc rim, especially at the inferior or superior poles. Documented, progressive thinning of the neuroretinal rim with an associated increase in cupping of the optic disc. Diffuse or localized abnormalities of the peripapillary retinal nerve fiber layer, especially at the inferior or superior poles. Disc rim or peripapillary retinal nerve fiber layer haemorrhages. Optic disc neural rim asymmetry of the two eyes consistent with loss of neural tissue. Reliable and reproducible visual field abnormality considered a valid representation of the subjects functional status - Visual field damage consistent with retinal nerve fiber layer damage (e.g., nasal step, arcuate field defect, or paracentral depression in clusters of test sites)

11

BY Akpotowho Godwin Ellis

| NEUROPATHOLOGY OPT 526 LECTURER: DR. P OMOKHUA

[NEURORETINAL RIM DEFECTS IN RELATIONSHIP TO DISC DAMAGE October 28, 2011 LIKELYHOOD SCALE IN PRIMARY OPEN ANGLE GLAUCOMA]

- Visual field loss in one hemifield that is different from the other hemifield, i.e., across the horizontal midline (in early/moderate cases) Pathophysiology: Even today, much remains unknown about this disease. Elevated IOP almost certainly plays a significant role, but the process is poorly understood. According to the mechanical theory of POAG, chronically elevated IOP distorts the lamina cribrosa, crimping the axons of retinal ganglion cells as they pass through the lamina cribrosa and eventually killing the cells. The vascular theory suggests that with elevated IOP, reduced blood flow to the optic nerve starves the cells of oxygen and nutrients.

More recent research suggests another mechanism of ganglion cell death. Some glaucoma patients exhibit elevated levels of the neurotransmitter glutamate within the vitreous. Ganglion cells contain protein receptors that, when activated by glutamate, increase intr acellular calcium to toxic levels, forming destructive free radicals that kill the cells. This Advanced cupping and plays into the apoptotic theory of glaucoma--a nerve fiber layer defect in neurocellular process in which a retinal ganglion primary open angle cell will commit "suicide." Apoptosis is a normal glaucoma. cellular event designed to ensure a healthy neurological system where non-viable cells are removed. Glaucoma is an abnormal expression of this normal process. Excess glutamate accumulation--which may result from ischemia--may trigger apoptosis. Another possible inciting event: the deprivation of vital neurotrophic nutrients for the retinal ganglion cells from the lateral geniculate nucleus. The vital nutrient--brain derived neurotrophic factor 12
BY Akpotowho Godwin Ellis

| NEUROPATHOLOGY OPT 526 LECTURER: DR. P OMOKHUA

[NEURORETINAL RIM DEFECTS IN RELATIONSHIP TO DISC DAMAGE October 28, 2011 LIKELYHOOD SCALE IN PRIMARY OPEN ANGLE GLAUCOMA]

(BDNF)--reaches the retinal ganglion cells from the lateral geniculate nucleus via axoplasmic transport. Elevated IOP and ischemia disrupt axoplasmic transport and deprive the retinal ganglion cells of this vital nutrient. PATIENT POPULATION The patient population consists of adults 18 or older with POAG. ACTIVITY Identification and management of a patient with POAG. PURPOSE To identify and treat POAG and to preserve visual function while minimizing adverse effects of therapy, thereby enhancing the patients health and quality of life. GOALS Document the status of optic nerve structure and function on presentation. Estimate an IOP below which further optic nerve damage is unlikely to occur. Attempt to maintain IOP at or below this target level by initiating appropriate therapeutic intervention(s) Monitor the structure and function of the optic nerve for further damage and adjust the target IOP to a lower level if deterioration occurs. Minimize the side effects of treatment and their impact on the patients vision, general health, and quality of life. Educate and involve the patient and appropriate family members/caregivers in the management of the disease. PATIENT OUTCOME CRITERIA Preservation of visual function Maintenance of quality of life DIAGNOSIS The comprehensive initial glaucoma evaluation (history and physical examination) includes all components of the comprehensive adult medical eye evaluation102 in addition to, and with special attention to, those factors that specifically bear upon the diagnosis, course, and treatment of POAG. The examination may require more than one visit. For instance, an individual might be suspected of having glaucoma on one visit but may return for further evaluation to confirm the diagnosis, including additional IOP 13
BY Akpotowho Godwin Ellis

| NEUROPATHOLOGY OPT 526 LECTURER: DR. P OMOKHUA

[NEURORETINAL RIM DEFECTS IN RELATIONSHIP TO DISC DAMAGE October 28, 2011 LIKELYHOOD SCALE IN PRIMARY OPEN ANGLE GLAUCOMA]

measurements, gonioscopy, CCT determination, visual field assessment, and optic nerve head and retinal nerve fiber layer evaluation and documentation. Evaluation of Visual Function Patients with glaucoma may have sufficient visual field loss to impair night driving, near vision, and outdoor mobility. Ophthalmic Evaluation In completing the elements in the comprehensive adult medical eye evaluation, the ophthalmic evaluation specifically focuses on the following elements: History Visual acuity measurement Pupil examination Anterior segment examination Intraocular pressure measurement Gonioscopy Optic nerve head and retinal nerve fiber layer examination Fundus examination History Ocular, family, and systemic history (e.g., asthma). The severity and outcome of glaucoma in family members, including history of visual loss from glaucoma, should be obtained during initial evaluation. Review of pertinent records, with particular reference to the past IOP levels, status of the optic nerve, and visual field. Current ocular and systemic medications (e.g., corticosteroids) and known local or systemic intolerance to ocular or systemic medications. Ocular surgery: A history of LASIK or photorefractive keratectomy is associated with a falsely low IOP measurement due to thinning of the cornea. Cataract surgery may also lower the IOP compared with the presurgical baseline. A history of prior glaucoma laser or incisional surgical procedures should be elicited. Visual acuity measurement Visual acuity with current correction (the power of the present correction recorded) at distance and, when appropriate, at near should be measured. Refraction may be indicated to obtain the best-corrected visual acuity. 14

BY Akpotowho Godwin Ellis

| NEUROPATHOLOGY OPT 526 LECTURER: DR. P OMOKHUA

[NEURORETINAL RIM DEFECTS IN RELATIONSHIP TO DISC DAMAGE October 28, 2011 LIKELYHOOD SCALE IN PRIMARY OPEN ANGLE GLAUCOMA]

Pupil examination The pupils are examined for reactivity and an afferent pupillary defect. Anterior segment examination A slit-lamp biomicroscopic examination of the anterior segment can provide evidence of physical findings associated with narrow angles, such as shallow peripheral anterior chamber depth and crowded anterior chamber angle anatomy, corneal pathology, or a secondary mechanism for elevated IOP such as pseudoexfoliation (exfoliation syndrome), pigment dispersion with Krukenberg spindle and/or iris transillumination defects, iris and angle neovascularization, or inflammation. Intraocular pressure measurement Intraocular pressure (IOP) remains the single most important risk factor for the development of glaucomatous optic neuropathy, and its measurement is vital in the initial diagnosis and management of the glaucomas. It is also the only major risk factor that can be treated. There has been much recent interest in the ability to monitor continuous, 24 hour IOP, in order to evaluate sleep IOP profiles and potentially to combine such data with measures of diurnal blood pressure. Such technology is not yet available but promises to be a significant advance of great clinical potential. Intraocular pressure is measured in each eye, preferably by Goldmann applanation tonometry, before gonioscopy or dilation of the pupil. Recording time of day of IOP measurements may be helpful to assess diurnal variation. Unrecognized fluctuations in IOP may lead to progression of POAG. Therefore, additional measurements may be indicated, either at different hours of the day on the same day or on different days. Gonioscopy The diagnosis of POAG requires careful evaluation of the anterior chamber angle to exclude angle closure or secondary causes of IOP elevation, such as angle recession, pigment dispersion, peripheral anterior synechiae, angle neovascularization, and inflammatory precipitates. The careful examination of the anterior chamber angle is essential in evaluating glaucoma suspects and diagnosing glaucoma. Gonioscopy enables the visualization of the anterior angle and its assessment permits the exclusion of angle closure, angle recession, plateau iris or secondary angle block as the cause of raised IOP. Gonioscopy is most commonly performed indirectly by using a contact lens with a mirror system that 15 BY: Akpotowho Godwin Ellis | NEUROPATHOLOGY OPT 526 LECTURER: DR. P OMOKHUA

[NEURORETINAL RIM DEFECTS IN RELATIONSHIP TO DISC DAMAGE October 28, 2011 LIKELYHOOD SCALE IN PRIMARY OPEN ANGLE GLAUCOMA]

overcomes the inherent total internal reflection of the angle anatomy. The angle is graded to relate information of its visible anatomical features. Several non-contact OCT devices can be used to evaluate the angle; these include the stand alone Visante (Carl Zeiss Meditec) and Slit Lamp (SL)-OCT (Heidelberg Engineering), and the analysis modules available on some of the new generation spectral domain (SD) OCTs including the RTVue (Optovue Inc.), Cirrus HD-OCT (Carl Zeiss Meditec) and Spectralis (Heidelberg Engineering) 1). Although considerably more expensive than a classic contact goniolens, they have the advantage of being objective and quantitative. In addition, these devices can accurately measure and map corneal thickness. They can also image bleb quality following trabeculectomy and the integrity of peripheral iridotomies. However, due to the nature of OCT its is often not possible to see the complete angle due to the signal being blocked and therefore assumptions need to be made for the positioning of the sclera spur when measuring the angle. Optic nerve head and retinal nerve fiber layer examination Examination of the optic nerve head and retinal nerve fiber layer provides valuable structural information about glaucomatous optic nerve damage. Visible structural alterations of the optic nerve head or retinal nerve fiber layer and development of peripapillary choroidal atrophy frequently occur before visual field defects can be detected. Careful study of the optic disc neural rim for small hemorrhages is important, since these hemorrhages often precede visual field loss and further optic nerve damage in patients with glaucoma. In the Ocular Hypertension Treatment Study, the incidence of POAG in eyes with disc hemorrhage was 13.6% compared with 5.2% in eyes without disc hemorrhage over 8 years.146 In the Early Manifest Glaucoma Trial, 13% of patients had disc hemorrhages at baseline examination, and hemorrhages were associated with progression. The preferred technique for optic nerve head and retinal nerve fiber layer evaluation involves magnified stereoscopic visualization (as with the slitlamp biomicroscope), preferably through a dilated pupil. In some cases, direct ophthalmoscopy complements magnified stereoscopic visualization, providing additional information of optic nerve detail due to the greater magnification of the direct ophthalmoscope. Red-free illumination of the posterior pole by stereo-biomicroscopy with an indirect 16
BY Akpotowho Godwin Ellis

| NEUROPATHOLOGY OPT 526 LECTURER: DR. P OMOKHUA

[NEURORETINAL RIM DEFECTS IN RELATIONSHIP TO DISC DAMAGE October 28, 2011 LIKELYHOOD SCALE IN PRIMARY OPEN ANGLE GLAUCOMA]

lens at the slit lamp, the direct ophthalmoscope, or with digital red-free photography may aid in evaluating the retinal nerve fiber layer. Fundus examination Examination of the fundus, through a dilated pupil whenever feasible, includes a search for other abnormalities that may account for optic nerve changes and/or visual field defects (e.g., optic nerve pallor, disc drusen, optic nerve pits, disc edema from central nervous system disease, macular degeneration, retinovascular occlusion, and other retinal disease). Supplemental Ophthalmic Testing Supplemental ophthalmic testing includes the following components: Central corneal thickness measurement Visual field evaluation. Optic nerve head and retinal nerve fiber layer analysis MEASUREMENT OF VISUAL FUNCTION Visual function is generally evaluated by measuring the visual field via standard automated perimetry. In glaucoma, the central vision is not affected until late in the disease process. Consequently there is little diagnostic value in evaluating only central visual function by way of visual acuity. Clinical evaluation of automated perimetry charts remains a standard for the detection of glaucoma. Typical glaucomatous visual field defects were first described by von Graefe in 1869 and result from apoptotic death of the retinal ganglion cells. The field defects reflect damage to the NFL bundles as they track from the optic nerve, although the primary site of damage is thought to be at the level of the lamina cribrosa within the optic nerve. Classic defects include early isolated paracentral, arcuate, nasal step and occasional temporal wedge defects. It is likely that a generalized defect due to diffuse loss of axons is present in many glaucomatous visual fields, but such defects have limited diagnostic value as they are difficult to distinguish from the effects of media opacity and pupil size. The standard clinical application of static threshold automated perimetry entails the assessment of the central 30 degrees. A variety of threshold estimation algorithms are available, with the faster strategies based on Baysian methodsfor example the SITA strategy found on the Humphrey 17
BY Akpotowho Godwin Ellis

| NEUROPATHOLOGY OPT 526 LECTURER: DR. P OMOKHUA

[NEURORETINAL RIM DEFECTS IN RELATIONSHIP TO DISC DAMAGE October 28, 2011 LIKELYHOOD SCALE IN PRIMARY OPEN ANGLE GLAUCOMA]

Field Analyzer (HFA). It is important to re-test abnormal looking visual fields to ensure repeatability, particularly in the nave patient, as there is a clearly defined learning curve that can mimic early defects. Interpretation can be aided by statistical packages that analyze the data relative to age matched normal values (Total Deviation), and scan for focal defects by removing the influence of diffuse loss (Pattern Deviation). There are also analyses that judge subjects intra-test reliability and the symmetry between the upper and lower field, such as the glaucoma hemifield test. It is essential to establish good quality baseline data for both the early diagnosis and the management of manifest disease. Indeed, recent recommendations have stated the need for six fields in the first two years in order to appropriately manage patients with glaucoma. To successfully identify those patients with a -2dB/year change, leading to profound loss within seven to eight years, it is necessary to have multiple fields to confidently interpret the measurement within the noise. This was inspired by the important findings of studies such as the EMGT, within which a small but significant percentage of patients exhibited dramatic and rapid progression even at the earliest manifestation of their glaucoma. This is also the thinking behind the excellent new Visual Field Index available for interpretation of rate of progression on the Humphrey Field Analyzer (HFA). There are several standard analyses for glaucomatous progression, the most common being the Humphrey Field Analyzers Glaucoma Progression Analysis (GPA). The analysis empirically compares serial fields to results collected in a group of patients with stable glaucoma. The original application used age-matched normal data to perform the analysis (Total Deviation), but the EMGT found results to be more accurate when based on the Pattern Deviation analysis, by reducing the influence of diffuse loss.

Figure: New glaucoma progression analysis printout for the HFA, incorporating the Visual Field Index, which quantifies the rate of progression and illustrates the projected loss. The left printout shows a

18

BY Akpotowho Godwin Ellis

| NEUROPATHOLOGY OPT 526 LECTURER: DR. P OMOKHUA

[NEURORETINAL RIM DEFECTS IN RELATIONSHIP TO DISC DAMAGE October 28, 2011 LIKELYHOOD SCALE IN PRIMARY OPEN ANGLE GLAUCOMA]
relatively stable patient with a slow rate of progression, whereas the right printout shows a rapid rate of progression in a patient who underwent a change in therapy before the rate of progression reduced as seen in the last 6 fields plotted in the VFI.

Central corneal thickness measurement Measurement of CCT aids the interpretation of IOP readings and helps to stratify patient risk for ocular damage. An overestimation of the real IOP may occur in eyes with corneas that are thicker than average, while an underestimation of the real IOP tends to occur in eyes with corneas that are thinner than average. Several studies have sought to quantify the relationship between measured IOP level and CCT, but there is no generally accepted correction formula. There is a controversy over whether CCT represents a risk factor for glaucoma due to its effect on IOP measurement or whether CCT is a risk factor itself, unrelated to IOP. While it is clear that thinner CCT is a risk factor for the development of POAG, studies of progression have had variable findings. Visual field evaluation Automated static threshold perimetry is the preferred technique for evaluating the visual field. The frequency doubling technology (FDT) method with the central 20-degree test program (C-20) and shortwavelength automated perimetry (SWAP) with the central 24-degree test program (24-2) are two of several alternative testing methods to screen for a defect before conducting more definitive threshold testing. Visual field testing based on SWAP and FDT may detect defects or progression of defects earlier than conventional white-on-white perimetry in some patients. Careful manual combined kinetic and static threshold testing (e.g., Goldmann visual fields) is an acceptable alternative when patients cannot perform automated perimetry reliably or if it is not available. Repeat, confirmatory visual field examinations may be required for test results that are unreliable or show a new glaucomatous defect before changing management. It is best to use a consistent examination strategy for visual field testing. MANAGEMENT Goals The goals of managing patients with POAG are to achieve the following: Controlled IOP in the target range Stable optic nerve/retinal nerve fiber layer status 19
BY Akpotowho Godwin Ellis

| NEUROPATHOLOGY OPT 526 LECTURER: DR. P OMOKHUA

[NEURORETINAL RIM DEFECTS IN RELATIONSHIP TO DISC DAMAGE October 28, 2011 LIKELYHOOD SCALE IN PRIMARY OPEN ANGLE GLAUCOMA]

Stable visual fields Because elevated IOP is a treatable cause of POAG damage, one can expect to reduce the risk of disease progression in many patients by lowering the IOP by means of medication, laser therapy, or incisional glaucoma surgery. Management is a challenge for the patient and the doctor, because POAG is a chronic, often asymptomatic, condition that may require frequent use of multiple and expensive medications that may cause side effects or may require laser or incisional surgery. The effects of treatment, the patients quality of life, and the patients life expectancy are important to consider when choosing therapy. The diagnosis, severity of the disease, prognosis and management plan, and likelihood of long-term therapy should be discussed with the patient.Substantial field loss in glaucoma is associated with a decrease in quality of life measures. Therapeutic Choices The IOP can be lowered by medical treatment, laser therapy, or incisional glaucoma surgery (alone or in combination). The choice of initial therapy depends on numerous considerations, and discussion of treatment with the patient should include the relative risks and benefits of the three options. Medical treatment Management: Significant advances have been made in recent years in diagnostic devices for glaucoma. A scanning laser ophthalmoscope (Heidelberg Retinal Tomograph II) can identify abnormalities in optic disc morphology and compare them against a normative database, documenting changes to the optic disc topography over time. A scanning laser polarimeter (GDx Nerve Fiber Analyzer by Laser Diagnostic Technologies) can accurately identify changes in the retinal nerve fiber layer. Here again, a normative database assigns statistical significance and can identify abnormalities in the nerve fibers. Genetic testing (Ocugene) can identify patients with genetic characteristics of glaucoma and possibly predict the course of the disease. Despite advances in diagnostic technology and new research into neuroprotection, the mainstay of glaucoma treatment remains IOP reduction. Beta-blockers are still very popular medications and used in many cases of POAG. Timoptic (timolol maleate, Merck) is the most commonly prescribed beta-blocker, but others are also noteworthy. 20
BY Akpotowho Godwin Ellis

| NEUROPATHOLOGY OPT 526 LECTURER: DR. P OMOKHUA

[NEURORETINAL RIM DEFECTS IN RELATIONSHIP TO DISC DAMAGE October 28, 2011 LIKELYHOOD SCALE IN PRIMARY OPEN ANGLE GLAUCOMA]

Betoptic S (betaxolol 0.25% suspension, Alcon) selectively blocks beta-1 receptors, largely sparing beta-2 receptors in the lungs (making it a safer option for patients with certain pulmonary conditions, though other classes of medication may ultimately be safer for these patients). Other unique beta-blockers include Ocupress (carteolol, Novartis)--which has less propensity than other beta-blockers to elevate total cholesterol levels Endstage primary openand reduce HDL cholesterol levels--and Timoptic- angle glaucoma. XE (timolol maleate, Merck), which allows for once-a-day therapy. Alpha-adrenergic medications advanced with the development of Alphagan (brimonidine 0.2%, Allergan), a selective alpha-2 adrenergic agonist. This medication has an excellent safety profile and IOP-lowering potential similar to beta-blockers. While clinicians have frequently prescribed Alphagan bid, clinical studies show that it should be prescribed tid, especially when used as monotherapy. Otherwise, IOP control could be lost at times throughout the day. The most common adverse effect has been allergic reactions. A new formulation, Alphagan P (brimonidine 0.15% in Purite), has reduced the incidence of local allergic reactions by 41%.1

Topical carbonic anhydrase inhibitors such as Trusopt (dorzolamide, Merck) and Azopt (brinzolamide, Alcon) have been successful in lowering the IOP in many patients. However, few clinicians use these medications as first-line therapy. Cosopt (Merck), which combines timolol 0.5% with dorzolamide, can be effective when a single agent fails to control IOP. IOP control was revolutionized with the development of prostaglandin analogs and prostaglandin-like medications. Xalatan (latanoprost, Pharmacia) has enjoyed considerable success, offering outstanding IOP lowering, long-term control, and minimal local and systemic effects. Rescula (unoprostone, Novartis), actually a docosanoid, has a similar safety profile to Xalatan, though its IOP-lowering is not as great and it requires bid dosing. More recently developed is Lumigan (bimatoprost, Allergan). Like Xalatan, this medication increases uveoscleral outflow of aqueous and has 21
BY Akpotowho Godwin Ellis

| NEUROPATHOLOGY OPT 526 LECTURER: DR. P OMOKHUA

[NEURORETINAL RIM DEFECTS IN RELATIONSHIP TO DISC DAMAGE October 28, 2011 LIKELYHOOD SCALE IN PRIMARY OPEN ANGLE GLAUCOMA]

outstanding IOP-lowering ability. The medication is well tolerated systemically, hyperemia being the main adverse effect. Another new prostaglandin analog, Travatan (travoprost, Alcon) apparently has a greater IOP-lowering potential in patients of African descent. It, too, is well tolerated systemically and ocularly. Travatan has been shown to be more effective than Timoptic in IOP reduction. The ophthalmologist should consider the balance between side effects and effectiveness in choosing a regimen of maximal effectiveness and tolerance to achieve the desired IOP reduction for each patient. Frequent dosing and side effects (such as depression, exercise intolerance, and impotence with topical beta-blockers) may affect adherence to therapy. To determine the effectiveness of topical therapy, it is necessary to distinguish between the therapeutic impact of an agent on IOP and ordinary background fluctuations of IOP. It may be useful to begin by treating only one eye and comparing the relative change of the IOP in the two eyes at follow-up visits. However, because the two eyes of an individual may not respond equally to the same medication, and because of the possibility of asymmetric spontaneous fluctuations and the potential for contralateral effect of monocular topical medications, it is acceptable to compare the effect in one eye relative to multiple baseline measurements. Additional studies are needed to compare directly monocular and binocular drug trials to find out whether a monocular trial is better at determining a nonresponder than a binocular trial. If a drug fails to reduce IOP sufficiently despite good adherence to therapy, it can be replaced with an alternate agent until effective medical treatment is established. If a single medication is effective in lowering IOP but the target pressure is not reached, combination therapy or switching to an alternative therapy may be appropriate. The patient and ophthalmologist together decide on a practical and feasible regimen to follow in terms of dosing, cost, and adherence in the context of the patients age and preferences. The ophthalmologist should assess the patient who is being treated with glaucoma medication for local ocular and systemic side effects; toxicity, including interactions with other medications; and potential life-threatening adverse reactions. To reduce systemic absorption, patients should be educated about eyelid closure or nasolacrimal duct occlusion when applying topical medications. 22
BY Akpotowho Godwin Ellis

| NEUROPATHOLOGY OPT 526 LECTURER: DR. P OMOKHUA

[NEURORETINAL RIM DEFECTS IN RELATIONSHIP TO DISC DAMAGE October 28, 2011 LIKELYHOOD SCALE IN PRIMARY OPEN ANGLE GLAUCOMA]

New Technologies in the Diagnosis and Management of Glaucoma The last decade has seen an explosion of new technologies that have begun to challenge our understanding of the structural and functional relationships 23
BY Akpotowho Godwin Ellis

| NEUROPATHOLOGY OPT 526 LECTURER: DR. P OMOKHUA

[NEURORETINAL RIM DEFECTS IN RELATIONSHIP TO DISC DAMAGE October 28, 2011 LIKELYHOOD SCALE IN PRIMARY OPEN ANGLE GLAUCOMA]

in early glaucoma, while at the same time introducing potentially new standards of care. There are several of the latest technologies and developments. Methods for the non-invasive, objective, quantitative, structural assessment include: Scanning laser tomography. Optical coherence tomography for the optic nerve (ON) and retinal nerve fiber layer (RNFL); and Scanning laser polarimetry for exclusive RNFL analysis. All three technologies are reported to have excellent diagnostic performance in the detection of early glaucoma. These instruments are not meant for stand-alone use but rather support the clinical evaluation of the ON/RNFL. They may provide corroboration of a working diagnosis or require the clinician to re-evaluate his or her assessment of the ON/RNFL. They may also be used to follow for change over time. Surgical for Glaucoma Management Surgical intervention becomes an option in the management of open-angle glaucoma when the intraocular pressure (IOP) cannot be sufficiently reduced with medical or laser therapy to prevent progressive optic nerve damage and/or visual field loss. Surgery should also be considered when medical treatment is unavailable, the patient cannot adhere to the treatment regimen or the cost of medical therapy exceeds their means. Consideration for surgical intervention should include disease severity, advanced optic nerve damage or visual field defects with threat to central vision, and the age and systemic status of the patient. Adequate treatment of glaucoma requires a high level of adherence to therapy. Frequently this is not achieved; studies indicate relatively poor adherence to therapy. Even with instruction, free medication, once-daily administration, use of a dosing aid, and electronic monitoring of adherence, nearly 45% of patients in one study took fewer than 75% of their prescribed doses. Instilling eyedrops correctly is difficult for patients, and their ability to do so may worsen as glaucoma progresses. Repeated instruction and counselling in proper techniques for using medication as well as a clearly written medication regimen and follow-up telephone calls may improve adherence to therapy. At each examination, medication dosage and frequency of use should be recorded.

24

BY Akpotowho Godwin Ellis

| NEUROPATHOLOGY OPT 526 LECTURER: DR. P OMOKHUA

[NEURORETINAL RIM DEFECTS IN RELATIONSHIP TO DISC DAMAGE October 28, 2011 LIKELYHOOD SCALE IN PRIMARY OPEN ANGLE GLAUCOMA]

Reviewing the time medication was taken may be useful. Adherence to the therapeutic regimen and recommendations for therapeutic alternatives or diagnostic procedures should be discussed. Cost may be a factor in adherence, especially when multiple medications are used. Patient education and informed participation in treatment decisions may improve adherence and overall effectiveness of glaucoma management. Laser trabeculoplasty Laser trabeculoplasty can be considered as initial therapy in selected patients or an alternative for patients who cannot or will not use medications reliably due to cost, memory problems, difficulty with instillation, or intolerance to the medication. Laser trabeculoplasty lowers IOP by improving aqueous outflow and can be performed using argon, diode, and frequency-doubled YAG lasers. Argon and diode laser trabeculoplasty Studies using continuous-wave argon laser with a wavelength spectrum that peaks at 488 nm (argon laser trabeculoplasty [ALT]) found that treatment increases aqueous outflow and provides a clinically significant reduction of IOP in more than 75% of initial treatments of previously unoperated eyes. Since these initial studies, more compact solid-state diode lasers have mostly replaced the original argon laser with equal IOP lowering efficacy. Follow-up Evaluation Guidelines for follow-up of patients with POAG are summarized in Table below. These recommendations apply to ongoing glaucoma management and not to visits for other purposes. Follow-up evaluation includes examination as well as optic nerve head and visual field assessment as indicated.

25

BY Akpotowho Godwin Ellis

| NEUROPATHOLOGY OPT 526 LECTURER: DR. P OMOKHUA

[NEURORETINAL RIM DEFECTS IN RELATIONSHIP TO DISC DAMAGE October 28, 2011 LIKELYHOOD SCALE IN PRIMARY OPEN ANGLE GLAUCOMA]

History The following interval history can be elicited at POAG follow-up visits: Interval ocular history Interval systemic medical history Side effects of ocular medications Frequency and time of last IOP-lowering medications and review of use of medications. Ophthalmic examination The following components of the ophthalmic examination should be performed at POAG follow-up visits: Visual acuity measurement Slit-lamp biomicroscopy Intraocular pressure measurement Based on the understanding of the effect of CCT on IOP measurements, measurement of CCT should be repeated after any event (e.g., refractive surgery) that may alter CCT. Gonioscopy Gonioscopy is indicated when there is a suspicion of an angle-closure component, anterior chamber shallowing or anterior chamber angle abnormalities, or if there is an unexplained change in IOP. Gonioscopy may also be performed periodically (e.g., 1 to 5 years).

26

BY Akpotowho Godwin Ellis

| NEUROPATHOLOGY OPT 526 LECTURER: DR. P OMOKHUA

[NEURORETINAL RIM DEFECTS IN RELATIONSHIP TO DISC DAMAGE October 28, 2011 LIKELYHOOD SCALE IN PRIMARY OPEN ANGLE GLAUCOMA]

Optic nerve head and visual field evaluation Optic nerve head evaluation and documentation by imaging, photography, or drawing and visual field evaluation should be performed at the recommended intervals. Within each of the recommended intervals, factors that determine frequency of evaluations include the severity of damage (mild, moderate, severe, with more frequent evaluations for more severe disease), the rate of progression, the extent to which the IOP exceeds the target pressure, and the number and significance of other risk factors for damage to the optic nerve.[A:III] In certain cases, follow-up visual field testing may be required more frequently than the recommended intervals (e.g., a second test to establish a baseline for future comparisons, to clarify a suspicious test result, or to overcome an apparent testing artifact). For example, a patient with glaucomatous damage who has shown long-term stability can be followed every 6 to 12 months, depending on how severe the damage is, while a patient with evidence of glaucomatous progression may receive a change in care plan with more frequent follow-up. Risk Factors for Progression The risk factors for progression in eyes already diagnosed with OAG are related to the level of IOP and factors independent of IOP: Intraocular pressure: Several multicenter randomized clinical trials have investigated the relationship between IOP and risk of glaucomatous progression. Higher baseline IOP, higher mean IOP during follow-up, and higher yearly average IOP were associated with greater progression of glaucoma as measured by visual field or optic nerve changes. Greater IOP fluctuation in some, but not all studies, has also been shown to be related to visual field progression, but this strongly correlated with absolute IOP level and may not be an independent risk factor. Beta-zone peripapillary atrophy: Either the baseline presence or the size of peripapillary atrophy adjacent to the optic nerve (beta zone) has been related to visual field or optic nerve progression in several large prospective and retrospective studies. Disc hemorrhage: Either presence of a disc hemorrhage or percentage of visits with disc hemorrhage have been associated with progression of visual field defect or optic nerve damage. The association has been reported in both normal-tension and in high-pressure glaucoma. Larger cup-to-disc ratio or small optic nerve rim area 27
BY Akpotowho Godwin Ellis

| NEUROPATHOLOGY OPT 526 LECTURER: DR. P OMOKHUA

[NEURORETINAL RIM DEFECTS IN RELATIONSHIP TO DISC DAMAGE October 28, 2011 LIKELYHOOD SCALE IN PRIMARY OPEN ANGLE GLAUCOMA]

Thinner central cornea: Strong evidence exists for thinner central cornea as a risk factor for progression from ocular hypertension to POAG, but evidence is mixed for thinner central cornea as a risk factor for progression in glaucoma. Damage in one eye is associated with an increased risk of future damage in the other eye. A retrospective study in eyes with OAG and severe visual field damage in one eye showed a risk of progression in the other eye (Kaplan Meier estimate of visual field progression = 12.1%). Risk factors for progression were larger initial cup-to-disc ratio and lower calculated ocular perfusion pressure. In a separate retrospective study, progression in visual field damage between eyes showed a significant correlation. In a large retrospective study of eyes with normal-tension glaucoma and unilateral visual field damage, the risk factors for progression in the normal eye were greater visual field damage in the eye with glaucoma and smaller neuroretinal rim area. PROVIDER AND SETTING The performance of certain diagnostic procedures (e.g., tonometry, pachymetry, perimetry, optic disc imaging, and photography) may be delegated to appropriately trained and supervised personnel. However, the interpretation of results and medical and surgical management of the disease require the medical training, clinical judgment, and experience of the ophthalmologist. Most diagnostic and therapeutic procedures can be safely undertaken on an outpatient basis. In some instances, however, hospitalization may be required. This includes, for example, patients who have special medical or social needs. COUNSELING/REFERRAL It is important to educate and engage patients in the management of their condition. Patients should be educated about the disease process, the rationale and goals of intervention, the status of their condition, and the relative benefits and risks of alternative interventions so that they can participate meaningfully in developing an appropriate plan of action. Patients should be encouraged to alert their ophthalmologists to physical or emotional changes that occur when taking glaucoma medications. The diagnosis of glaucoma can itself lead to negative psychological effects and to fear of blindness. 28
BY Akpotowho Godwin Ellis

| NEUROPATHOLOGY OPT 526 LECTURER: DR. P OMOKHUA

[NEURORETINAL RIM DEFECTS IN RELATIONSHIP TO DISC DAMAGE October 28, 2011 LIKELYHOOD SCALE IN PRIMARY OPEN ANGLE GLAUCOMA]

Numerous studies have been performed to characterize the psychological profile of the glaucoma patient, and some have shown the prevalence of anxiety to be higher in this population. It has been much harder to demonstrate a consistent presence of depression in glaucoma patients; numerous studies have been unable to do soand only a minority do. Glaucoma affects the patients visual and health-related quality of life in many ways,this includes employment issues (e.g., fear of loss of job and insurance from diminished ability to read and drive), social issues (e.g., fear of negative impact on relationships and sexuality), and loss of independence and activities that require good visual acuity (e.g., sports and other hobbies). The ophthalmologist should be sensitive to these problems and provide support and encouragement. Some patients may find peer-support groups or counseling helpful. Patients considering keratorefractive surgery should be informed about the possible impact laser vision correction has on reducing contrast sensitivity, altering visual field testing results, and decreasing the accuracy of IOP measurements.During the conduct of LASIK the IOP will briefly increase from the effect of the suction ring to make the eye rigid during creation of the superficial flap. This effect may cause additional damage in patients whose optic nerves already have advanced damage. Therefore, LASIK may be relatively contraindicated in such individuals, but photorefractive keratectomy may be possible. In addition, postoperative fluid may develop in the corneal flap-stromal interface and lead to temporary underestimation of the applanation IOP in patients treated aggressively with topical corticosteroids to resolve interface inflammation, who may actually have an undetected, corticosteroid-induced elevation of IOP. Conversely, corticosteroid-induced IOP elevation may cause interface fluid that mimics interface inflammation and leads to IOP underestimation. Patients with glaucomatous optic neuropathy considering implantation of a multifocal intraocular lens should be informed of the risk of reduced contrast sensitivity. It is important to establish preoperative and baseline documentation of optic nerve head status and visual field to facilitate subsequent glaucoma management. If the diagnosis or management of POAG is in question or if the condition is refractory to treatment, consultation with or referral to an ophthalmologist with special training or experience in managing glaucoma should be considered. Patients with substantial visual impairment or blindness can be 29
BY Akpotowho Godwin Ellis

| NEUROPATHOLOGY OPT 526 LECTURER: DR. P OMOKHUA

[NEURORETINAL RIM DEFECTS IN RELATIONSHIP TO DISC DAMAGE October 28, 2011 LIKELYHOOD SCALE IN PRIMARY OPEN ANGLE GLAUCOMA]

referred for and encouraged to use appropriate vision rehabilitation and social services. Clinical Pearls:

Glaucoma is a long-term disease. Accumulate the necessary information so that you can diagnose with confidence. Do not to rush to a diagnosis. It typically is not necessary to diagnose the disease and start treatment at the patient's initial presentation. A single IOP measurement does not accurately represent the patient's true status, but is merely a snapshot pressure at that moment. Before making a diagnosis or initiating treatment, take repeated IOP measurements at different times on different days so that you have a more accurate picture of the patient's IOP "baseline range." While scanning lasers have not supplanted visual fields in the diagnosis and management of glaucoma, they provide useful information on optic nerve head and nerve fiber layer structure. Prostaglandins and prostaglandin-like medications are not FDAapproved as first-line therapy due to the possibility of inducing ocular inflammation and iris color changes. Yet many clinicians use them as first-line therapy.

CONCLUSION
Early detection of structural damage to the optic nerve head is critical in diagnosis of glaucoma, because such glaucomatous damage precedes clinically identifiable visual loss. Glaucoma is the second leading ocular 30
BY Akpotowho Godwin Ellis

| NEUROPATHOLOGY OPT 526 LECTURER: DR. P OMOKHUA

[NEURORETINAL RIM DEFECTS IN RELATIONSHIP TO DISC DAMAGE October 28, 2011 LIKELYHOOD SCALE IN PRIMARY OPEN ANGLE GLAUCOMA]

disease and early detection of glaucoma can prevent progression of the disease and consequent loss of vision. Segmentation of optic disc cup and neuroretinal rim can provide important parameters for detecting and tracking this disease.

REFERENCES
1. Community Eye Health Journal | Vol 19 No. 59 | SEPTEMBER 2006. 2. Review of optometry supplement, the handbook of glaucoma, Semptember 2009. 31

BY Akpotowho Godwin Ellis

| NEUROPATHOLOGY OPT 526 LECTURER: DR. P OMOKHUA

[NEURORETINAL RIM DEFECTS IN RELATIONSHIP TO DISC DAMAGE October 28, 2011 LIKELYHOOD SCALE IN PRIMARY OPEN ANGLE GLAUCOMA]

3. Kirsch RE, Anderson DR. Clinical recognition of glaucomatous cupping. Am J Ophthalmol. 1973 Mar;75(3):442454. 4. Pederson JE, Anderson DR. The mode of progressive disc cupping in ocular hypertension and glaucoma. Arch Ophthalmol. 1980 Mar;98(3):490495. 5. Tuulonen A, Airaksinen PJ. Initial glaucomatous optic disk and retinal nerve fiber layer abnormalities and their progression. Am J Ophthalmol. 1991 Apr 15;111(4):485490. 6. Jonas JB, Fernndez MC, Strmer J. Pattern of glaucomatous neuroretinal rim loss. Ophthalmology. 1993 Jan;100(1):6368. [PubMed]. 7. Jonas JB, Fernandez MC. Shape of the neuroretinal rim and position of the central retinal vessels in glaucoma. Br J Ophthalmol. 1994;78:99102. 8. Jonas JB, Budde WM, Nemeth J, Grundler AE, Mistlberger A, Hayler JK. Central retinal vessel trunk exit and location of glaucomatous parapapillary atrophy in glaucoma. Ophthalmology. 2001;108: 10591064. 9. Jonas JB, Budde WM, Panda-Jonas S. Ophthalmoscopic evaluation of the optic nerve head. Surv Ophthalmol. 1999;43:293320. 10. Littmann H. Zur Bestimmung der wahren Grosse eines Objektes auf dem Hintergrund des lebenden Auges. Klin Monatsbl Augenheilkd. 1982;180:286289. 11. Jonas JB, Fernandez MC, Naumann GOH. Glaucomatous parapapillary chorioretinal atrophy: occurrence and correlations. Arch Ophthalmol. 1992;110:214222.

32

BY Akpotowho Godwin Ellis

| NEUROPATHOLOGY OPT 526 LECTURER: DR. P OMOKHUA