- •PROGRESS IN BRAIN RESEARCH
- •List of Contributors
- •Preface
- •Epidemiology of primary glaucoma: prevalence, incidence, and blinding effects
- •Introduction
- •Prevalence of glaucoma
- •PAC suspect
- •PACG
- •Incidence of glaucoma
- •Blinding effects of glaucoma
- •Abbreviations
- •Acknowledgment
- •References
- •Predictive models to estimate the risk of glaucoma development and progression
- •Risk assessment in ocular hypertension and glaucoma
- •Risk factors for glaucoma development
- •Intraocular pressure
- •Corneal thickness
- •Cup/disc ratio and pattern standard deviation
- •The need for predictive models
- •Predictive models for glaucoma development
- •Predictive models for glaucoma progression
- •Limitations of predictive models
- •References
- •Intraocular pressure and central corneal thickness
- •Main text
- •References
- •Angle-closure: risk factors, diagnosis and treatment
- •Introduction
- •Mechanism
- •Other causes of angle closure
- •Risk factors
- •Age and gender
- •Ethnicity
- •Ocular biometry
- •Genetics
- •Diagnosis
- •Acute primary angle closure
- •Angle assessment in angle closure
- •Gonioscopy technique
- •Ultrasound biomicroscopy (UBM)
- •Scanning peripheral anterior chamber depth analyzer (SPAC)
- •Management
- •Acute primary angle closure
- •Medical therapy
- •Argon laser peripheral iridoplasty (ALPI)
- •Laser peripheral iridotomy (PI)
- •Lens extraction
- •Monitoring for subsequent IOP rise in eyes with APAC
- •Fellow eye of APAC
- •Chronic primary angle-closure glaucoma (CACG)
- •Laser peripheral iridotomy
- •Laser iridoplasty
- •Medical therapy
- •Trabeculectomy
- •Lens extraction
- •Combined lens extraction and trabeculectomy surgery
- •Goniosynechialysis
- •Summary
- •List of abbreviations
- •References
- •Early diagnosis in glaucoma
- •Introduction
- •History and examination
- •Quantitative tests and the diagnostic process
- •Pretest probability
- •Test validity
- •Diagnostic test performance
- •Posttest probability
- •Combing test results
- •Selective tests of visual function
- •Early glaucoma diagnosis from quantitative test results
- •Progression to make a diagnosis
- •Conclusions
- •Abbreviations
- •References
- •Monitoring glaucoma progression
- •Introduction
- •Monitoring structural damage progression
- •Monitoring functional damage progression
- •Abbreviations
- •References
- •Standard automated perimetry and algorithms for monitoring glaucoma progression
- •Standard automated perimetry
- •Global indices
- •HFA: MD, SF, PSD, CPSD
- •Octopus indices: MD, SF, CLV
- •OCTOPUS seven-in-one report (Fig. 2)
- •SAP VF assessment: full-threshold strategy
- •SAP VF defects assessment: OHTS criteria
- •SAP VF defects assessment: AGIS criteria
- •SAP VF defects assessment: CIGTS
- •Fastpac
- •Swedish interactive threshold algorithm
- •SAP VF assessment: the glaucoma staging system
- •SAP: interocular asymmetries in OHTS
- •SAP, VF progression
- •SAP: the relationship to other functional and structural diagnostic tests in glaucoma
- •SAP, FDP-Matrix
- •SAP, SWAP, HPRP, FDT
- •SAP: the relationship between function and structure
- •SAP, confocal scanning laser ophthalmoscopy, SLP-VCC
- •SAP, optical coherence tomography
- •SAP and functional magnetic resonance imaging
- •References
- •Introduction
- •Retinal ganglion cells: anatomy and function
- •Is glaucoma damage selective for any subgroup of RGCs?
- •Segregation
- •Isolation
- •FDT: rationale and perimetric techniques
- •SWAP: rationale and perimetric techniques
- •FDT: clinical data
- •SWAP: clinical data
- •Clinical data comparing FDT and SWAP
- •Conclusions
- •References
- •Scanning laser polarimetry and confocal scanning laser ophthalmoscopy: technical notes on their use in glaucoma
- •The GDx scanning laser polarimeter
- •Serial analysis
- •Limits
- •The Heidelberg retinal tomograph
- •Limits
- •Conclusions
- •References
- •The role of OCT in glaucoma management
- •Introduction
- •How OCT works
- •How OCT is performed
- •Evaluation of RNFL thickness
- •Evaluation of optic disc
- •OCT in glaucoma management
- •New perspective
- •Abbreviations
- •References
- •Introduction
- •Technology
- •Visual stimulation
- •Reproducibility and habituation of RFonh
- •Retinal neural activity as assessed from the electroretinogram (ERG)
- •The Parvo (P)- and Magno (M)-cellular pathways
- •Physiology
- •Magnitude and time course of RFonh in humans
- •Varying the parameters of the stimulus on RFonh
- •Luminance versus chromatic modulation
- •Frequency
- •Effect of pattern stimulation
- •Neurovascular coupling in humans
- •Clinical application
- •RFonh in OHT and glaucoma patients
- •Discussion
- •FLDF and neurovascular coupling in humans
- •Comments on clinical application of FLDF in glaucoma
- •Conclusions and futures directions
- •Acknowledgements
- •References
- •Advances in neuroimaging of the visual pathways and their use in glaucoma
- •Introduction
- •Conventional MR imaging and the visual pathways
- •Diffusion MR imaging
- •Functional MR imaging
- •Proton MR spectroscopy
- •References
- •Primary open angle glaucoma: an overview on medical therapy
- •Introduction
- •When to treat
- •Whom to treat
- •Genetics
- •Race
- •Ocular and systemic abnormalities
- •Tonometry and pachymetry
- •How to treat
- •Beta-blockers
- •Prostaglandins
- •Alpha-agonists
- •Carbonic anhydrase inhibitors (CAIs)
- •Myotics
- •Fixed combinations
- •References
- •The treatment of normal-tension glaucoma
- •Introduction
- •Epidemiology
- •Clinical features
- •Optic disk
- •Central corneal thickness
- •Disease course
- •Risk factors
- •Intraocular pressure
- •Local vascular factors
- •Immune mechanisms
- •Differential diagnosis
- •Diagnostic evaluation
- •Therapy
- •IOP reduction
- •Systemic medications
- •Neuroprotection
- •Noncompliance
- •Genetics of NTG
- •Abbreviations
- •References
- •The management of exfoliative glaucoma
- •Introduction
- •Epidemiology
- •Ocular and systemic associations
- •Ocular associations
- •Systemic associations
- •Pathogenesis of exfoliation syndrome
- •Mechanisms of glaucoma development
- •Management
- •Medical therapy
- •Laser surgery
- •Operative surgery
- •Future treatment of exfoliation syndrome and exfoliative glaucoma
- •Treatment directed at exfoliation material
- •References
- •Laser therapies for glaucoma: new frontiers
- •Background
- •Laser iridotomy
- •Indications
- •Contraindications
- •Patient preparation
- •Technique
- •Nd:YAG laser iridectomy
- •Argon laser iridectomy
- •Complications
- •LASER trabeculoplasty
- •Treatment technique
- •Mechanism of action
- •Indications for treatment
- •Contraindications to treatment
- •Patient preparation and postoperative follow-up
- •Complications of the treatment
- •Selective laser trabeculoplasty
- •Results
- •LASER iridoplasty
- •Indications
- •Contraindications
- •Treatment technique
- •Complications
- •LASER cyclophotocoagulation
- •Introduction
- •Indications and contraindications
- •Patient preparation
- •Transpupillary cyclophotocoagulation
- •Endoscopic cyclophotocoagulation
- •Transscleral cyclophotocoagulation
- •Transscleral noncontact cyclophotocoagulation
- •Transscleral contact cyclophotocoagulation
- •Complications
- •Excimer laser trabeculotomy
- •References
- •Modulation of wound healing during and after glaucoma surgery
- •The process of wound healing
- •Using surgical and anatomical principles to modify therapy
- •Growth factors
- •Cellular proliferation and vascularization
- •Cell motility, matrix contraction and synthesis
- •Drug delivery
- •Future directions: total scarring control and tissue regeneration
- •Acknowledgments
- •References
- •Surgical alternative to trabeculectomy
- •Introduction
- •Deep sclerectomy
- •Viscocanalostomy
- •Conclusions
- •References
- •Modern aqueous shunt implantation: future challenges
- •Background
- •Current shunts and factors affecting their function
- •Shunt-related factors
- •Surface area
- •Plate material
- •Valved versus non-valved
- •Commercially available devices
- •Comparative studies
- •Patient and ocular factors
- •Severity of glaucoma damage
- •Tolerance of topical ocular hypotensive medications
- •Aqueous hyposecretion
- •Previous ocular surgery
- •Scleral thinning
- •Patient cooperation for and tolerance of potential slit-lamp interventions
- •Future challenges
- •Predictability
- •Cataract formation
- •The long-term effect on the cornea
- •References
- •Model systems for experimental studies: retinal ganglion cells in culture
- •Mixed RGCs in culture
- •Retinal explants
- •Glial cultures
- •RGC-5 cells
- •Differentiation of RGC-5 cells
- •RGC-5 cell neurites
- •Advantages and disadvantages of culture models
- •References
- •Rat models for glaucoma research
- •Rat models for glaucoma research
- •Use of animal models for POAG
- •Suitability of the rat for models of optic nerve damage in POAG
- •Methods for measuring IOP in rats
- •General considerations for measuring IOP in rats
- •Assessing optic nerve and retina damage
- •Experimental methods of producing elevated IOP
- •Laser treatment of limbal tissues
- •Episcleral vein cautery
- •Conclusions
- •Abbreviations
- •Acknowledgements
- •References
- •Mouse genetic models: an ideal system for understanding glaucomatous neurodegeneration and neuroprotection
- •Introduction
- •The mouse as a model system
- •Mice are suitable models for studying IOP elevation in glaucoma
- •Tools for glaucoma research
- •Accurate IOP measurements are fundamental to the study of glaucoma
- •The future of IOP assessment
- •Assessment of RGC function
- •Mouse models of glaucoma
- •Primary open-angle glaucoma
- •MYOC
- •OPTN
- •Strategies for developing new models of POAG
- •Developmental glaucoma
- •Pigmentary glaucoma
- •Experimentally induced models of glaucoma
- •Mouse models to characterize processes involved in glaucomatous neurodegeneration
- •Similar patterns of glaucomatous damage occur in humans and mice
- •The lamina cribrosa is an important site of early glaucomatous damage
- •An insult occurs to the axons of RGCs within the lamina in glaucoma
- •What is the nature of the insult at the lamina?
- •Other changes occur in the retina in glaucoma
- •PERG and complement
- •Using mouse models to develop neuroprotective strategies
- •Somal protection
- •Axonal protection
- •Erythropoietin administration
- •Radiation-based treatment
- •References
- •Clinical trials in neuroprotection
- •Introduction
- •Methods of clinical studies
- •Issues in the design and conduct of clinical trials
- •Clinical trials of neuroprotection
- •Clinical trials of neuroprotection in ophthalmology
- •Endpoints
- •Neuroprotection and glaucoma
- •Conclusions
- •Abbreviations
- •References
- •Pathogenesis of ganglion ‘‘cell death’’ in glaucoma and neuroprotection: focus on ganglion cell axonal mitochondria
- •Introduction
- •Retinal ganglion cells and mitochondria
- •Possible causes for ganglion cell death in glaucoma
- •Mitochondrial functions and apoptosis
- •Mitochondrial function enhancement and the attenuation of ganglion cell death
- •Creatine
- •Nicotinamide
- •Epigallocatechin gallate
- •Conclusion
- •References
- •Astrocytes in glaucomatous optic neuropathy
- •Introduction
- •Quiescent astrocytes
- •Reactive astrocytes in glaucoma
- •Signal transduction in glaucomatous astrocytes
- •Protein tyrosine kinases (PTKs)
- •Serine/threonine protein mitogen-activated kinases (MAPKs)
- •G protein-coupled receptors
- •Ras superfamily of small G proteins
- •Astrocyte migration in the glaucomatous optic nerve head
- •Cell adhesion of ONH astrocytes
- •Connective tissue changes in the glaucomatous optic nerve head
- •Extracellular matrix synthesis by ONH astrocytes
- •Extracellular matrix degradation by reactive astrocytes
- •Oxidative stress in ONH astrocytes
- •Conclusions
- •Acknowledgments
- •References
- •Glaucoma as a neuropathy amenable to neuroprotection and immune manipulation
- •Glaucoma as a neurodegenerative disease
- •Oxidative stress and free radicals
- •Excessive glutamate, increased calcium levels, and excitotoxicity
- •Deprivation of neurotrophins and growth factors
- •Abnormal accumulation of proteins
- •Pharmacological neuroprotection for glaucoma
- •Protection of the retinal ganglion cells involves the immune system
- •Searching for an antigen for potential glaucoma therapy
- •Concluding remarks
- •References
- •Oxidative stress and glaucoma: injury in the anterior segment of the eye
- •Introduction
- •Oxidative stress
- •Trabecular meshwork
- •IOP increase and free radicals
- •Glaucomatous cascade
- •Nitric oxide and endothelins
- •Extracellular matrix
- •Metalloproteinases
- •Other factors of interest
- •Therapeutic and preventive substances of interest in glaucoma
- •Ginkgo biloba extract
- •Green tea
- •Ginseng
- •Memantine and its derivates
- •Conclusions
- •Abbreviations
- •References
- •Conclusions on neuroprotective treatment targets in glaucoma
- •Acknowledgments
- •References
- •Involvement of the Bcl2 gene family in the signaling and control of retinal ganglion cell death
- •Introduction
- •Intrinsic apoptosis vs. extrinsic apoptosis
- •The Bcl2 family of proteins
- •The requirement of BAX for RGC soma death
- •BH3-only proteins and the early signaling of ganglion cell apoptosis
- •Conclusion
- •Abbreviations
- •Acknowledgments
- •References
- •Assessment of neuroprotection in the retina with DARC
- •Introduction
- •DARC
- •Introducing the DARC technique
- •Annexin 5-labeled apoptosis and ophthalmoloscopy
- •Detection of RGC apoptosis in glaucoma-related animal models with DARC
- •Assessment of glutamate modulation with DARC
- •Glutamate at synaptic endings
- •Glutamate excitotoxicity in glaucoma
- •Assessment of coenzyme Q10 in glaucoma-related models with DARC
- •Summary
- •Abbreviations
- •Acknowledgment
- •References
- •Potential roles of (endo)cannabinoids in the treatment of glaucoma: from intraocular pressure control to neuroprotection
- •Introduction
- •The endocannabinoid system in the eye
- •The IOP-lowering effects of endocannabinoids
- •Endocannabinoids and neuroprotection
- •Conclusions
- •References
- •Glaucoma of the brain: a disease model for the study of transsynaptic neural degeneration
- •Retinal ganglion cells, retino-geniculate neurons
- •Lateral geniculate nucleus
- •Mechanisms of RGC injury in glaucoma
- •Transsynaptic degeneration of the lateral geniculate nucleus in glaucoma
- •Neural degeneration in magno-, parvo-, and koniocellular LGN layers
- •Visual cortex in glaucoma
- •Neuropathology of glaucoma in the visual pathways in the human brain
- •Mechanisms of glaucoma damage in the central visual pathways
- •Implications of central visual system injury in glaucoma
- •Conclusion
- •Acknowledgments
- •References
- •Clinical relevance of optic neuropathy
- •Is there a remodeling of retinal circuitry?
- •Behavioral consequences of glaucoma
- •Glaucoma as a neurodegenerative disease versus neuroplasticity and adaptive changes
- •Future directions
- •Acknowledgment
- •References
- •Targeting excitotoxic/free radical signaling pathways for therapeutic intervention in glaucoma
- •Introduction
- •Channel properties of NMDA receptors correlated with excitotoxicity
- •Downstream signaling cascades after overactivation of NMDA receptors
- •Relevance of excitotoxicity to glaucoma
- •Therapeutic approaches to prevent RGC death by targeting the pathways involved in NMDA excitotoxicity
- •Drugs targeting NMDA receptors
- •Kinetics of NMDA receptor antagonists
- •Memantine
- •NitroMemantines
- •Drugs targeting downstream signaling molecules in NMDA-induced cell death pathways
- •p38 MAPK inhibitors
- •Averting caspase-mediated neurodegeneration
- •Abbreviations
- •Acknowledgments
- •References
- •Stem cells for neuroprotection in glaucoma
- •Introduction
- •Glaucoma as a model of neurodegenerative disease
- •Why use stem cells for neuroprotective therapy?
- •Stem cell sources
- •Neuroprotection by transplanted stem cells
- •Endogenous stem cells
- •Key challenges
- •Conclusion
- •Abbreviations
- •Acknowledgments
- •References
- •The relationship between neurotrophic factors and CaMKII in the death and survival of retinal ganglion cells
- •Introduction
- •Glaucoma and the RGCs
- •Are other retinal cells affected in glaucoma?
- •Retinal ischemia related glaucoma
- •Excitotoxicity and the retina
- •Signal transduction
- •NMDA receptor antagonists and CaMKII
- •Caspase-3 activation in NMDA-induced retinal cell death and its inhibition by m-AIP
- •BDNF and neuroprotection of RGCs
- •Summary and conclusions
- •Abbreviations
- •Acknowledgments
- •References
- •Evidence of the neuroprotective role of citicoline in glaucoma patients
- •Introduction
- •Patients: selection and recruitment criteria
- •Pharmacological treatment protocol
- •Methodology of visual function evaluation: electrophysiological examinations
- •PERG recordings
- •VEP recordings
- •Statistic evaluation of electrophysiological results
- •Electrophysiological (PERG and VEP) responses in OAG patients after the second period of evaluation
- •Effects of citicoline on retinal function in glaucoma patients: neurophysiological implications
- •Effects of citicoline on neural conduction along the visual pathways in glaucoma patients: neurophysiological implications
- •Possibility of neuroprotective role of citicoline in glaucoma patients
- •Conclusive remarks
- •Abbreviations
- •References
- •Neuroprotection: VEGF, IL-6, and clusterin: the dark side of the moon
- •Neuroprotection: VEGF-A, a shared growth factor
- •VEGF-A isoforms
- •VEGF-A receptors
- •Angiogenesis, mitogenesis, and endothelial survival
- •Neurotrophic and neuroprotective effect
- •Intravitreal VEGF inhibition therapy and neuroretina toxicity
- •Neuroprotection: clusterin, a multifunctional protein
- •Clusterin/ApoJ: a debated physiological role
- •Clusterin and diseases
- •Clusterin and the nervous system
- •Neuroprotection: IL-6, VEGF, clusterin, and glaucoma
- •Rational basis for the development of coenzyme Q10 as a neurotherapeutic agent for retinal protection
- •Introduction
- •Ischemia model
- •Neuroprotective effect of Coenzyme Q10 against cell loss yielded by transient ischemia in the RGC layer
- •Retinal ischemia and glutamate
- •Coenzyme Q10 minimizes glutamate increase induced by ischemia/reperfusion
- •Summary
- •Acknowledgment
- •References
- •17beta-Estradiol prevents retinal ganglion cell loss induced by acute rise of intraocular pressure in rat
- •Methods
- •Morphometric analysis
- •Microdialysis
- •Drug application
- •Statistical analysis
- •Results
- •17beta-Estradiol pretreatment minimizes RGC loss
- •Discussion
- •Acknowledgment
Diagnosis
Acute primary angle closure
The diagnosis of APAC is mainly clinical. There is a sudden, usually symptomatic rise in IOP. This is usually unilateral, but bilateral simultaneous attacks can occur. Patients complain of periocular or ocular pain, headache, nausea, and/or vomiting. The patients also complain of blurring of vision with haloes. Slit lamp examination will reveal conjunctival injection, corneal epithelial edema with a mid dilated sluggish/nonreacting pupil. The IOP is likely to be greater than 30 mmHg. The anterior chamber will be shallow and gonioscopy will show occludable or occluded drainage angles in both eyes. In some instances, if there is a severe anterior chamber reaction, with hypopyon, the IOP maybe normal or low due to ciliary body shutdown. It is important that these episodes of APAC are not misdiagnosed as uveitis. Also, certain types of open angle glaucoma can be
Table 3. Gonioscopy grading systems
35
associated with an acute rise in IOP with ocular pain, conjunctival injection, and corneal edema. These include phacolytic glaucoma, Posner– Schlossman syndrome, pseudoexfoliative glaucoma, and neovascular glaucoma.
Angle assessment in angle closure
In angle closure, the drainage angle is occludable and there are features indicating that trabecular obstruction has occurred like PAS. The gold standard technique to diagnose angle closure is gonioscopy. There are three widely used grading systems. The Scheie scheme is based on the angle structures seen during gonioscopy (Scheie, 1957). The Shaffer system requires the assessment of the angular distance between the iris and cornea (Becker and Shaffer, 1965). The Spaeth scheme allows for more detailed recording of the angle characteristics (geometric angle, iris profile, true and apparent level of insertion) (Spaeth, 1971). Table 3 gives a summary of the grading systems (Scheie,
|
0 |
I |
II |
III |
IV |
|
|
|
|
|
|
|
|
Shaffer |
Closed |
101 |
201 |
|
301 |
401 |
Modified |
Schwalbe’s line not |
Schwalbe’s line |
Anterior trabecular |
Scleral spur is visible |
Ciliary band is visible |
|
Shaffer |
visible |
visible |
meshwork is visible |
|
|
|
Scheie |
Ciliary band is |
Last roll of iris |
Nothing posterior to |
Posterior portion of |
No structures posterior |
|
|
visible |
obscures ciliary |
the trabecular |
trabecular meshwork |
to Schwalbe’s line visible |
|
|
|
body |
meshwork is visible |
is hidden |
|
|
|
|
|
|
|
|
|
Spaeth system |
|
|
|
|
|
|
|
|
|
|
|
|
|
(1) Iris insertion |
|
Anterior to Schwalbe’s line |
|
|
|
|
|
|
Behind Schwalbe’s line |
|
|
|
|
|
|
Centred at scleral spur |
|
|
|
|
|
|
Deep to scleral spur |
|
|
|
|
|
|
Extremely deep/on ciliary band |
|
|
||
(2) Angle width |
|
Slit |
|
|
|
|
|
|
101 |
|
|
|
|
|
|
201 |
|
|
|
|
|
|
301 |
|
|
|
|
|
|
401 |
|
|
|
|
(3) Peripheral iris configuration |
Queerly concave |
|
|
|
|
|
|
|
Regular |
|
|
|
|
|
|
Steep |
|
|
|
|
(4) Trabecular meshwork pigment |
0 (none) to 4 (maximal) |
|
|
|
|
|
|
|
|
|
|
|
|
36
1957; Becker and Shaffer, 1965; Spaeth, 1971; South East Asia Glaucoma Interest Group, 2008). The Goldmann lens gives a stable, clear view of the important landmarks but indentation of appositionally closed angles using this lens has not been validated, and is difficult as the curvature of the lens is more than the corneal curvature. Therefore, the use of a four-mirror, like the Zeiss four-mirror is necessary. This lens has the same radius of curvature as the cornea so the patient’s own tear film functions as a coupling agent. The Goldmann-type lenses require an optical coupling agent.
Gonioscopy technique
Gonioscopy should be carried out in a darkened room. The patient should have adequate topical anasthesia and should be looking in the primary position. The slit lamp beam should be 1 mm high and narrow. The light must be kept away from the pupil, at the lowest illumination that will allow angle visualization. The lens can be moved minimally along the cornea to see over the convexity of the iris, however, care must be taken not to apply pressure and cause indentation. Using high magnification, the termination of the corneal wedge (which marks the anterior edge of the trabecular meshwork) can be identified. Additionally, it is important to locate the scleral spur as the trabecular meshwork is directly anterior to this structure. Assessment of whether the iris is in contact with the trabecular meshwork is done. If it is not, the angle between the trabecular meshwork and adjacent peripheral iris is estimated and the level of the most anterior point of contact between the iris and angle structures is described. This is carried out for all four quadrants, then dynamic gonioscopy can be carried out.
If Goldmann-style lenses are being used, the patient should be instructed to look toward the mirror, the examiner should then press on the rim of the lens overlying the mirror, so as to indent the central cornea. The accuracy of indentation using this method has not been validated. The ideal technique involves using another goniolens with a diameter smaller than the corneal diameter, e.g. a four-mirror Zeiss lens. Pressure should be applied over the cornea, so as to displace aqueous from the centre of the anterior chamber into the periphery,
pushing the iris posteriorly, falsely opening the drainage angle. This allows one to assess whether the iridotrabecular contact is appositional or synechial (i.e. permanent). The extent of the synechial closure should be assessed. Once it is determined that the angle is indeed occludable, the slit beam height and illumination and room lights should be turned up ideally prior to indentation gonioscopy to look for PAS. Any pseudo-PAS would open up with bright light besides the pressure applied on the cornea. Iris processes should not be confused with PAS. Iris processes are uveal extensions from the iris on to the trabecular meshwork and occur in normal angles. Figure 1 shows the normal angle anatomy.
Ultrasound biomicroscopy (UBM)
UBM gives good qualitative information about the drainage angle including visualization of the ciliary body. However, highly reproducible quantitative information is dependent on examiner technique and experience. UBM is usually performed with the patient in the supine position. A suitably sized eye cup (around 20 mm) is inserted between the eyelids and the coupling medium (e.g. methylcellulose and/or normal saline) is inserted into it. The probe is then inserted into the medium and real time images are displayed on a video monitor. These can be stored and/or printed out for analysis. It should be noted that room illumination and accommodation must be kept constant. Also the configuration of the anterior segment and the proportions of the structures seen depends on the plane of the section and any degree of tilt in the scanning probe (Liebmann, 2006). Figure 2 shows an UBM scan of narrow angles.
Kumar et al. (2008) have used the UBM to define plateau iris. The features of UBM are defined in each quadrant, and include the presence of an anteriorly directed ciliary body, an absent ciliary sulcus, a steep iris root from its point of insertion followed by a downward angulation from the corneoscleral wall, presence of a central flat iris plane, and irido-angle contact. At least two quadrants have to fulfill the above criteria for plateau iris to be defined (Kumar et al., 2008). Figure 3 shows the features.
37
Fig. 1. Gonioscopic view of normal angle anatomy, showing iris (I), ciliary body band (CBB), scleral spur (SS), posterior trabecular meshwork (PTM), anterior trabecular meshwork (ATM), and Schwalbe’s line (SL). Iris processes can also be clearly seen (IP). (Courtesy of Lisandro Sakata, MD, PhD, University of Alabama, Birmingham, USA.) (See Color Plate 4.1 in color plate section.)
Fig. 2. The figure shows an ultrasound biomicroscopy scan of a closed angle; there is iridocorneal touch, obstructing the trabecular meshwork.
Anterior segment optical coherence tomography |
angle and anterior chamber using infrared light |
(AS-OCT) |
(Baskaran, 2006). Unlike the UBM it cannot image |
|
the ciliary body. The image capture scan takes a few |
The AS-OCT is a noncontact instrument that |
seconds and is akin to taking a photograph. The |
rapidly obtains high-resolution images of the |
device allows qualitative and quantitative angle |
38
Fig. 3. The figure shows an ultrasound biomicroscopy image of a quadrant showing plateau iris after laser peripheral iridotomy. Features shown: (A) irido-angle touch, (B) anteriorly rotated ciliary process, (C) absent ciliary sulcus, and (D) iris angulation. (Courtsey of Rajesh Kumar, MS, Singapore National Eye Centre, Singapore.)
imaging, which is objective and reproducible. Research comparing UBM, AS-OCT, and gonioscopy shows the AS-OCT is good at identifying narrow angles; however, the device does identify more subjects as having closed angles than gonioscopy (Radhakrishnan et al., 2005, 2007). Figure 4 shows an AS-OCT scan of an eye with narrow angles.
Scanning peripheral anterior chamber depth analyzer (SPAC)
The SPAC does not image the angle per se but takes rapid slit images of the central and peripheral anterior chamber using an optical method and creates an iris anterior surface contour using these measurements. This is then graded and compared to the normative database and the resultant grade gives a risk assessment for the patient (Kashiwagi et al., 2004). The SPAC correlates well with the modified van Herick system in grading peripheral ACD. However, it overestimates the proportion of
narrow angles relative to gonioscopy and the modified van Herick grading system (Baskaran et al., 2007).
Visual-field loss
It has been observed that the pattern of visual-field loss in PACG is different from that of POAG. Gazzard et al. showed that subjects with POAG had greater superior hemifield loss than in the inferior hemifield. This difference between the two hemifields was less pronounced in the PACG patients. However, the PACG group exhibited more severe visual-field loss compared to the POAG group. The authors postulated that POAG is thought to be due to a combination of pressure dependent and independent mechanisms whereas PACG is predominantly pressure related. This may be why there is less of a difference between the two hemifields in PACG patients. The reason for the more severe field loss is less clear and maybe due to the tendency of PACG patients to present later (Gazzard et al., 2002).
