- •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
a very high spatial discrimination, whereas peripheral vision is much less defined. In order to preserve the foveal highly detailed vision, inter receptors connections are absent; this means that receptive fields have no overlapping. On the other hand, in the peripheral retina there is a high interconnection among receptors, intraretinal cells, and ganglion cells, leading to a partial overlapping of the contiguous receptive fields.
The concept of overlapping receptive fields is also known as redundancy. Due to redundancy, a single stimulus may simultaneously stimulate two or more RGCs; in the case of retinal damage, this guarantees a higher probability of the stimulus to be transmitted to the brain. As a consequence, the higher the redundancy, the more minor the probability of detection of early damages of the RGCs. It has been demonstrated that, apart from the foveal area, P-pathway is endowed with high redundancy (Johnson, 1994). On the other hand, it is likely that the receptive fields of a sparse subset of RGCs (such as M- and K-cells) have a lower overlap, though low redundancy has until now been demonstrated only for M-cells (Haymes et al., 2005).
FDT: rationale and perimetric techniques
FDT is based on a phenomenon described about 40 years ago by Kelly, who observed that when an achromatic sinusoidal grating of low spatial frequency undergoes counterphase flickering at a hightemporal frequency, the apparent spatial frequency of the grating appears to be doubled (Kelly, 1966). He reported that this ‘‘frequency-doubling’’ phenomenon occurred for sinusoidal gratings having a spatial frequency less than approximately 3 cyc/degree undergoing a counterphase flickering at a temporal frequency greater than 7 Hz.
The FDT stimulus predominantly stimulates the M-cell pathway, which is primarily involved in motion and flicker detection and represents about 10% of all RGCs. Some believe that the frequency-doubling illusion in humans is mediated by the subgroup of My cells (Maddess and Henry, 1992). However, the existence of M-cells that exhibit nonlinear response properties, My cells, is not universally agreed. White et al. (2002) reported
105
that there is no evidence of a separate nonlinear M-cell class in the primate visual system. They suggested that a cortical loss of temporal phase discrimination is the principal cause of the illusion and proposed that the mechanisms underlying the illusion resemble those underlying the detection of full-field flicker, which appears to be accomplished through the M-cell pathway. Thus, FDT (and particularly Matrix FDT) is most likely a probe of contrast sensitivity: it does not depend on whether the stimulus is perceived as doubled but simply measures detection thresholds of the M-cell pathway.
FDT perimeter (Welch Allyn, Skaneateles Falls, NY; and Humphrey Instruments, San Leandro, CA) uses a vertical sine wave grating of low spatial frequency (0.25–0.50 cyc/degree) that undergoes counterphase flickering at a high-temporal frequency (12–25 Hz). The contrast of the stimulus is modified in each location to calculate threshold sensitivity.
FDT comprises firstand second-generation tests. The major difference between the two groups is the number of tested locations, the dimension, and the characteristics of the stimuli (Table 2); Fig. 1 shows the FDT tests most commonly used in glaucoma practice.
In the first-generation FDT, two programs are available: C-20 and N-30. C-20 consists of a grid of 16 square locations of 10 10 degrees each, projecting on the central 20 degrees of the retina, and a foveal circular grid location of 5 degrees. The N-30 program also tests two additional locations between 20 and 30 degrees of the nasal retina immediately above and below the horizontal line, for a total of 19 locations.
Two strategies are available: screening (suprathreshold) and full-threshold. Both can be performed using the C-20 or the N-30 programs. The average test duration is about 1–1.5 min for the screening test and 4–5 min for the full-threshold mode, and it is directly related to the presence of visual field defects. The greater the visual field loss, the longer the test duration.
The screening strategy compares the point-to- point results with an age-corrected normative database and assigns one of the following values: within normal limits (PX1%), mild relative loss
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Table 2. Features of the programs of the first-generation FDT (above) and the novel programs of Matrix FDT (bottom)
Program |
C-20 screening |
C-20 threshold |
N-30 threshold |
N-30 screening |
|
|
|
|
|
Spatial frequency (cyc/degree) |
0.25 |
0.25 |
0.25 |
0.25 |
Temporal frequency (Hz) |
25 |
25 |
25 |
25 |
Stimulus size |
101a |
101a |
101a |
101a |
Tested area |
201 |
201 |
201 (301 nasally) |
201 (301 nasally) |
Number of tested locations |
17 |
17 |
19 |
19 |
Test time (in normal subjects) |
45 s |
4 min |
5 min |
90 s |
|
|
|
|
|
Program |
24-2 threshold |
30-2 threshold |
10-2 threshold |
Macula screening |
|
|
|
|
|
Spatial frequency (cyc/degree) |
0.5 |
0.5 |
0.5 |
0.5 |
Temporal frequency (Hz) |
18 |
18 |
12 |
12 |
Stimulus size |
51 |
51 |
21 |
21 |
Tested area |
241 (301 nasally) |
301 |
101 |
51 |
Number of tested locations |
55 |
69 |
44 |
16 |
Test time (in normal subjects) |
5 min |
6 min |
4 min |
90 s |
|
|
|
|
|
aThe size of the foveal stimulus is 51.
(Po1%), moderate relative loss (Po0.5%), and severe loss (point not seen; failure to respond to maximum contrast level). In the full-threshold strategy, point-to-point threshold is calculated using a Method of Binary Search (MOBS) procedure (Tyrell and Owens, 1998) that is a different threshold approach compared to the staircase procedure used in Humphrey-SAP. Then the threshold values are compared to the normative database; each location is deemed as normal (PW5%) or abnormal at different levels of probability (Po5%, o2%, o1%, o0.5%) in two maps: total deviation map and pattern deviation map. Point-to-point results are depicted on a colored scale corresponding to the different probability levels.
Reliability indices (fixation errors, false-positive and false-negative) are provided in both strategies. Similarly to the SAP programs with short duration and absence of short-term fluctuation (such as SITA-standard and SITA-FAST), full-threshold FDT also gives two global indices: mean defect (MD) and pattern standard deviation (PSD).
The FDT database contains data from more than 700 eyes of 450 normal subjects with ages ranging from 18 to 85. As it has been shown that FDT sensitivity is lower for the second tested eye versus the first (probably due to cortical
adaptation to the FDT stimulus), the machine automatically adjusts the values of the second eye.
The first FDT version has few manufacturing limitations: a system to monitor fixation throughout testing is unavailable (the operator cannot check whether the patient is fixating properly or pause the test to adjust patient alignment during the examination); in order to examine the two nasal points in the N-30 strategy, the fixation target is moved temporally, which may be confusing or cause improper fixation in some patients. FDT includes a small printer which can provide a brief printout; an external computer using specific software, Windows ViewFinder, is needed to obtain more detailed printouts and store data.
The second-generation FDT perimeters include a new program called Matrix which is very similar to the previous version except for the use of a smaller size of the stimulus (5 degrees for the 24-2 and the 30-2 programs and 2 degrees for the 10-2 program), a higher number of tested points, a more efficient method to calculate threshold, and a slightly longer duration (about 6 min). The programs of this FDT version are closer and more comparable to the same programs of SAP; other advantages are the presence of a video eye monitor to check patient alignment and cooperation during the test, a bigger screen to examine the nasal
107
Fig. 1. Printouts of a C-20 screening test (a), an N-30 full-threshold test (b), and a 24-2 Matrix FDT (c).
108
Fig. 1. (Continued).
targets within the central 301 without a moving fixation target, the possibility to store data on the machine, and an enhanced software for result interpretation. Matrix FDT interpretation is based on a database of 270 subjects with age ranging from 18 to 85.
SWAP: rationale and perimetric techniques
The evidence of a deficiency in color vision, particularly in the blue–yellow axis, has been
clearly demonstrated in patients affected by glaucoma more than 25 years ago (Drance et al., 1981). Information on the blue–yellow axis is projected to LGN by koniocells, which are a small subgroup of RGCs endowed with little redundancy, a fact which is supposed to allow early glaucoma detection.
The commercially available SWAP version is a modification of the SAP test obtained by Humphrey Field Analyzer (Humphrey-Zeiss, Dublin, CA) using a V stimulus (1.8 degree) of blue light at 440 nm projected to a background illuminated
109
Fig. 2. Printout of a full-threshold SWAP.
with yellow light (570–590 nm) at a luminance of 200 cd/m2. The test can be performed over both the 30 and 24 central degrees of the retina; respectively, 76 and 54 locations are tested.
As evident in Fig. 2, SWAP tests are performed and analyzed similarly to SAP: reliability parameters (false-positive, false-negative, and fixation loss) and perimetric indices (MD; PSD; short fluctuation, SF; corrected PSD, CPSD) are calculated, gaze tracking is available and test duration is recorded; the point-to-point sensitivity is reported in decibel and greytone maps (the latter
of which should be ignored; it is usually misleading because it is calibrated on SAP sensitivities, which are higher than SWAP). Point-to-point sensitivities are matched to those of normal subjects of the same age in order to identify diffuse (total deviation map) and localized (pattern deviation map) defects. A glaucoma hemifield test (GHT) is finally performed by comparison of symmetric areas of the superior and inferior hemifields.
The full-threshold strategy is the most commonly used but it has a long duration (up to 20 min per eye) and, as a consequence, a high
