- •Preface
- •Contents
- •Contributors
- •1: Living with Diabetic Retinopathy: The Patient’s View
- •My Patient Experience
- •Others’ Experiences
- •Photos of the Meaning of Diabetes
- •References
- •2: Diabetic Retinopathy Screening: Progress or Lack of Progress
- •Definitions of Screening for Diabetic Retinopathy
- •Studies Reporting the Prevalence of Diabetic Retinopathy
- •Reports on Blindness and Visual Impairment
- •Is There Evidence That Treatment for Sight-Threatening Diabetic Retinopathy Is Effective and Agreed Universally?
- •The Evidence That Diabetic Retinopathy Can Be Prevented or the Rate of Deterioration Reduced by Improved Control of Blood Glucose, Blood Pressure and Lipid Levels, and by Giving Up Smoking
- •The Evidence that Laser Treatment Is Effective
- •The Evidence That Vitrectomy for More Advanced Disease Is Effective
- •Progress of Lack of Progress in Screening for Diabetic Retinopathy in Different Parts of the World
- •References
- •3: Functional/Neural Mapping Discoveries in the Diabetic Retina: Advancing Clinical Care with the Multifocal ERG
- •Introduction
- •The Diabetes Epidemic
- •Current Treatment Focus
- •Vasculopathy and Neuropathy of the Retina
- •The Early Efforts
- •Some Breakthroughs
- •Predictive Models of Visible Retinopathy Onset at Specific Locations
- •How Is the mfERG Measured and What is it Measuring?
- •Where Are These Neural Signals Generated in the Retina?
- •Some Key Results
- •Adolescents and Adult Diabetes
- •Type 1 vs. Type 2: Differences in Retinal Function
- •References
- •4: Corneal Diabetic Neuropathy
- •Introduction
- •Corneal Confocal Microscopy
- •Corneal Nerves and Diabetes
- •Conclusion
- •References
- •5: Clinical Phenotypes of Diabetic Retinopathy
- •Natural History
- •MA Formation and Disappearance Rates
- •Alteration of the Blood–Retinal Barrier
- •Retinal Capillary Closure
- •Multimodal Macula Mapping
- •Clinical Retinopathy Phenotypes
- •Relevance for Clinical Trial Design
- •Relevance for Clinical Management
- •Targeted Treatments
- •References
- •6: Visual Psychophysics in Diabetic Retinopathy
- •Introduction
- •Visual Acuity
- •Color Vision
- •Contrast Sensitivity
- •Macular Recovery Function (Nyctometry)
- •Perimetry
- •Microperimetry (Fundus-Related Perimetry)
- •Conclusion
- •References
- •7: Mechanisms of Blood–Retinal Barrier Breakdown in Diabetic Retinopathy
- •The Protective Barriers of the Retina
- •The Inner and the Outer BRB
- •Inflammation and BRB Permeability
- •Leukocyte Mediators of Vascular Leakage
- •Other Mediators of Leukocyte Recruitment in DR
- •Structural Compromise of the BRB
- •Vascular Endothelial Growth Factor
- •Anti-VEGF Properties of Natriuretic Peptides
- •Proposed Model of BRB Breakdown in DR
- •Key Role of AZ in VEGF-Induced Leakage
- •Azurocidin Inhibition Prevents Diabetic Retinal Vascular Leakage
- •References
- •8: Molecular Regulation of Endothelial Cell Tight Junctions and the Blood-Retinal Barrier
- •The Blood-Retinal Barrier
- •The Retinal Vascular Barrier
- •The Junctional Complex
- •ZO Proteins
- •Claudins
- •Junctional Adhesion Molecules
- •Occludin and Tricellulin
- •Vascular Permeability in Diabetic Retinopathy
- •VEGF-Induced Regulation of Endothelial Permeability
- •Occludin Phosphorylation and Permeability
- •Protein Kinase C in Regulation of Barrier Properties
- •Conclusions
- •References
- •9: Capillary Degeneration in Diabetic Retinopathy
- •Vascular Nonperfusion in Diabetes: Mechanisms
- •Molecular Causes of Capillary Degeneration
- •Unexplained Aspects of Diabetes-Induced Degeneration of Retinal Capillaries
- •What Is the Relation Between the Retinal Vasculature and Neuronal Retina Structure and Function in Diabetes?
- •Conclusion
- •References
- •10: Proteases in Diabetic Retinopathy
- •Proteases in Retinal Vasculature
- •Extracellular Proteases
- •Urokinase Plasminogen Activator System (uPA/uPAR System)
- •Matrix Metalloproteinases
- •Endogenous Inhibitors of Proteases
- •Tissue Inhibitors of Metalloproteinases (TIMPs)
- •Plasminogen Activator Inhibitors (PAI)
- •Proteases in Retinal Neovascularization
- •Tissue Inhibitor of Matrix Metalloproteinases in Retinal Neovascularization
- •Inhibition of Retinal Angiogenesis by MMP Inhibitors
- •Inhibition of Retinal Angiogenesis by Inhibitors of the uPA/uPAR System
- •Proteases in Diabetic Macular Edema
- •Conclusion
- •References
- •11: Proteomics in the Vitreous of Diabetic Retinopathy Patients
- •Introduction
- •Vitreous Anatomy
- •A Candidate Approach
- •Proteomic Approaches
- •Vitreous Acquisition
- •Sample Pre-Fractionation
- •Mass Spectrometry
- •Spectral Analysis
- •Data Analysis
- •The Vitreous Proteome
- •2-DE-Based Proteomics
- •1-DE-Based Proteomics
- •Summary and Conclusions
- •References
- •12: Neurodegeneration in Diabetic Retinopathy
- •Introduction
- •Histological Evidence
- •Early Pathology Studies
- •Histological Evidence of Apoptosis
- •Gross Morphological Changes in the Retina
- •Reductions in Numbers of Surviving Amacrine Cells
- •Retinal Ganglion Cell Loss
- •Abnormalities in Ganglion Cell Morphology
- •Centrifugal Axon Abnormalities
- •Nerve Fiber Layer Thickness
- •Biochemical Evidence of Neurodegeneration and Cell Death
- •Functional Evidence of Neurodegenerative Changes
- •Electrophysiological Evidence for Neurodegeneration
- •Optic Nerve Retrograde Transport
- •Other Changes in Visual Function
- •Summary and Conclusions
- •References
- •13: Glucose-Induced Cellular Signaling in Diabetic Retinopathy
- •Introduction
- •Cellular Targets in DR
- •Endothelial Cell (EC) Dysfunction
- •Endothelial-Pericyte Interactions
- •Endothelial-Matrix Interactions
- •Signaling Mechanisms in DR
- •Altered Vasoactive Factors
- •Alteration of Metabolic Pathways
- •Polyol Pathway
- •Hexosamine Pathway
- •Protein Kinase C Pathway
- •Activation of Other Protein Kinases
- •Mitogen-Activated Protein Kinase (MAPK)
- •Increased Oxidative Stress
- •Protein Glycation
- •Aberrant Expression of Growth Factors
- •Transcription Factors
- •Transcription Regulators
- •Concluding Remarks
- •References
- •Introduction
- •The Growth-Hormone/Insulin-Like Growth Factor Pathway in Proliferative Retinopathies
- •Proliferative Diabetic Retinopathy (PDR)
- •Retinopathy of Prematurity (ROP)
- •Animal Models of Proliferative Retinopathies
- •IGFBP-3 as a Regulator of the Growth-Hormone/ Insulin-Like Growth Factor Pathway
- •Conclusion
- •References
- •15: Neurotrophic Factors in Diabetic Retinopathy
- •Diabetic Retinopathy
- •Neurotrophic Factors
- •Neurotrophins and Others
- •Nerve Growth Factor
- •Glial-Cell-Derived Neurotrophic Factor
- •Ciliary Neurotrophic Factor
- •Anti-angiogenic Neurotrophic Factors
- •Pigment-Epithelium-Derived Factor
- •SERPINA3K
- •Brain-Derived Neurotrophic Factor
- •Fibroblast Growth Factors
- •Insulin and Insulin-Like Growth Factor 1
- •Erythropoietin
- •Vascular Endothelial Growth Factor
- •Neurotrophic Factors and the Future of DR Research
- •References
- •16: The Role of CTGF in Diabetic Retinopathy
- •Introduction
- •ECM Remodeling and Wound Healing Mechanisms in Diabetic Retinopathy
- •ECM Remodeling in PCDR
- •Wound Healing Mechanisms in PDR
- •CTGF Structure and Function
- •CTGF in the Eye
- •CTGF in Ocular Fibrosis
- •CTGF in Ocular Angiogenesis
- •CTGF in Diabetic Retinopathy
- •CTGF in BL Thickening in PCDR
- •AGEs and CTGF in BL Thickening in PCDR
- •Role of VEGF in BL Thickening
- •BL Thickening in Diabetic CTGF-Knockout Mice
- •CTGF in PDR
- •Role of CTGF and VEGF in the “Angiofibrotic Switch” in PDR
- •Conclusions
- •References
- •17: Ranibizumab and Other VEGF Antagonists for Diabetic Macular Edema
- •Introduction
- •Pathogenesis of DME and Current Standard of Care
- •Ranibizumab for DME
- •Pegaptanib for DME
- •Bevacizumab for DME
- •VEGF Trap-Eye for DME
- •Other Considerations in the Management of DME
- •Combination Treatment for DME
- •DME and Quality of Life
- •Conclusions
- •References
- •18: Neurodegeneration, Neuropeptides, and Diabetic Retinopathy
- •Introduction
- •Neuropeptides Involved in the Pathogenesis of DR
- •Glutamate
- •Angiotensin II
- •Pigment Epithelial-Derived Factor
- •Somatostatin
- •Erythropoietin
- •Docosahexaenoic Acid and Neuroprotectin D1
- •Brain-Derived Neurotrophic Factor
- •Glial Cell Line-Derived Neurotrophic Factor
- •Ciliary Neurotrophic Factor
- •Adrenomedullin
- •Concluding Remarks and Therapeutic Implications
- •References
- •19: Glial Cell–Derived Cytokines and Vascular Integrity in Diabetic Retinopathy
- •Introduction
- •The BRB Functional Unit Composed of Glial and Endothelial Cells
- •Tight Junctions Between Endothelial Cells Are Substantial Barrier of the BRB
- •Major Cytokines Derived from Glial Cells Affecting Tight Junctions of the BRB
- •VEGF
- •GDNF
- •APKAP12
- •A Possible Treatment of the Retinopathy with Retinoic Acid Analogues
- •Conclusion
- •References
- •20: Impact of Islet Cell Transplantation on Diabetic Retinopathy in Type 1 Diabetes
- •Introduction
- •What Are the Benefits and Risks of Reducing Blood Glucose?
- •On Average, 3 Years Was Required to Demonstrate the Beneficial Effect of Intensive Treatment
- •The Earlier in the Course of Diabetes That Intensive Therapy Is Initiated, Even Before the Onset of Retinopathy, the Greater the Long-Term Benefits
- •Risk Reduction in the Primary Prevention Cohort
- •Risk Reduction in the Secondary Prevention Cohort
- •There Was No Glycemic Threshold Regarding Progression of Retinopathy
- •Diabetic Ketoacidosis (DKA)
- •Efforts to Normalize Blood Glucose Are Associated with Weight Gain in People with Type 1 Diabetes
- •Connecting Peptide (C-Peptide) Responders Have Less Risk of Progression of Retinopathy
- •Effects of Improved Control on Retinopathy Were Sustained in the Long-Term
- •Quality of Life Measure
- •“Metabolic Memory”: A Phenomenon Producing a Long-Term Beneficial Influence of Early Metabolic Control on Clinical Outcomes
- •Need for a More Physiologic Glycemic Control Regimen
- •Effect of Intensive Insulin Therapy on Hypoglycemia Counterregulation
- •b Cell Function
- •Whole Pancreas Transplantation
- •Effect of SPK Transplantation on Diabetic Retinopathy
- •Islet Cell Transplantation
- •Adverse Effects of Chronic Immunosuppression
- •Effect of Islet Cell Transplantation on Retinopathy
- •References
- •Index
Visual Psychophysics in Diabetic Retinopathy |
77 |
was no difference in CS function between diabetics without retinopathy and controls, whereas Ghafour et al. [71], using the same test, found that diabetics without retinopathy were abnormal at 3.2 and 6.3 c/deg. Using the Vision Contrast Test System in patients with little or no retinopathy, Trick et al. [69] found reduced mean CS at each spatial frequencies when compared to controls; however, a post hoc analysis yielded no statistical difference between the groups. Sokol et al. studied separately insulinand non-insulin- dependent diabetes mellitus (IDDM and NIDDM) patients and found that patients with IDDM and no DR had normal CS function, whereas patients with NIDDM, normal VA, and no DR had abnormal CS at high spatial frequencies. If background retinopathy was present, abnormal CS at all spatial frequencies was found [73]. Della Sala et al. [72], using the Cambridge low-contrast sensitivity charts, showed abnormal CS in 9 of 22 patients without diabetic retinopathy and in only 6 of 20 patients with background retinopathy (Table 2). Therefore, the contrast sensitivity losses in IDDM and NIDDM patients may not be similar, and further studies are needed to substantiate this hypothesis. Contrast sensitivity testing, as color vision testing, shows significant changes in diabetics and there is some correlation with glycemic control, although prospective studies are required to assess this relationship over a longer time period. Although both tests show similar patterns in diabetics, direct comparisons of the two tests seem to indicate the CS function test as more sensitive and specific.
MACULAR RECOVERY FUNCTION (NYCTOMETRY)
Macular recovery function (nyctometry) is a dynamic measure of the initial 2-min course of macular recovery function following preadaptation to a strong uniform illumination of a large area of the retina. It is a standardized technique, which lasts only 6.5 min. It quantifies not only the dark adaptation of the cone system but also the macular sensitivity to glare [79]. Gliem and Schulze reported a progressive reduction in macular recovery related to deterioration of DR [80]. Midena et al. [79] showed, in a well-defined series of patients, that reduced nyctometry is directly and strongly related to the progression of retinal (functional and anatomical) derangement due to diabetes mellitus. Different authors suggested, but never definitively proved, that nyctometry can be used to predict the progression of background DR to proliferative DR. They suggested the use of nyctometry as a screening method in selecting patients at high risk for proliferative DR [81–83]. Verrotti et al. [84] found altered nyctometry in microalbuminuric diabetic children vs. normoalbuminuric and normal controls. Reported values were independent of both the level and the fluctuations of glycemia. However, Lauritzen et al. [85] found improved performance of nyctometry in the first year in patients on a intensive insulin regimen. In two separate studies, Andersen et al. [86] and Frost-Larsen et al. [87] found significant improvement in macular recovery function in newly diagnosed juvenile diabetics after a 10-day period of superregulation in the biostator. This indicates that in metabolic dysregulation, the results of nyctometry are reversible to a certain extent provided the reduced values of nyctometry are mainly due to functional changes in the retina [83].
In CSME, 1 week after macular laser photocoagulation, nyctometry was shown to decrease significantly, followed by slow improvement toward the initial value [76].
Table 2. Studies which have investigated contrast sensitivity in patients with diabetic retinopathy
Principal |
|
|
|
|
|
|
investigator/ |
Types |
|
Age in years: |
|
|
|
year of publication |
of study |
Sample size |
mean/range |
DR status and VA |
Nature of stimulus |
Conclusions |
|
|
|
|
|
|
|
Ghafour et al. [71] |
Case-control Cases-93 |
Cases-47 (27–70) |
42-No DR |
Arden grating test |
Diabetic pts without DR |
|
|
|
Controls-80 |
Controls-46 (24–68) |
22-Background DR |
|
have increased thresh- |
|
|
|
|
29-PDR |
|
olds at the higher spatial |
|
|
|
|
VA: 6/5 to 6/36 |
|
frequencies. Significative |
|
|
|
|
|
|
difference CS threshold |
|
|
|
|
|
|
found between each |
|
|
|
|
|
|
group (controls-no |
|
|
|
|
|
|
DR-background-PDR) |
Hyvärinen et al. |
Case-control Cases-19 |
Cases-32 (19–59) |
5-Micro±hemorrhages |
Sinusoidal grating |
CS seems to correlate better |
|
[3] |
|
Controls-from |
|
but normal vision |
(cathode-ray- |
with DR status then with |
|
|
Virsu et al. |
|
(20/20) |
display) |
VA. Diabetic pts without |
|
|
[127] |
|
5-bDR |
|
DR has no significant |
|
|
|
|
6-PDR |
|
reduction of CS in com- |
|
|
|
|
3-PDR + central cataract |
|
parison to normal sub- |
|
|
|
|
|
|
jects. In the third group |
|
|
|
|
|
|
(cataract) CS was better |
|
|
|
|
|
|
than expected |
Regan and Neiman |
Case-control Cases-15 |
Cases-49 (24–75) |
6-VA ³6/7.5 or better |
Regan chart |
Diabetic pts had significa- |
|
[128] |
|
Controls-40 |
|
9-VA <6/7.5 |
|
tive CS loss |
Sokol et al. [73] |
Case-control Cases-64 |
– |
31-IDDM and no DR; |
Sinusoidal grating |
Pts with NIDDM, normal |
|
|
|
Controls-117 |
|
VA: 20/25 or better |
(microproces- |
VA and no DR had |
|
|
|
|
33-NIDDM and no |
sor-controlled |
abnormal CS at high |
|
|
|
|
(n = 16) or back- |
video system) |
spatial frequencies. Pts |
|
|
|
|
ground (n = 17) DR; |
|
with NIDDM and bDR |
|
|
|
|
VA: 20/30 or better |
|
had abnormal CS at all |
|
|
|
|
|
|
spatial frequencies. Pts |
|
|
|
|
|
|
with IDDM and no DR |
|
|
|
|
|
|
had normal CS |
Della Sala et al. |
Case-control |
Cases-42 |
Cases-12–75 |
22-No DR |
Cambridge |
Diabetic pts showed |
[72] |
|
Controls-84 |
Controls-14–68 |
19-bDR |
low-contrast |
decreased CS |
|
|
|
|
1-PDR |
sensitivity |
|
|
|
|
|
VA: 1.0 or better |
charts |
|
Trick et al. [69] |
Case-control |
Cases-57 |
No DR-36.9 ± 11.1 |
37-No DR |
Vistech VCTS |
All diabetic pts showed |
|
|
Controls-35 |
bDR-37.9 ± 8.6 |
20-bDR |
6500 distance |
decreased CS, par- |
|
|
|
Controls-33.3 ± 9.3 |
18-NIDDM |
chart |
ticularly with mid-spatial |
|
|
|
|
39-IDDM |
|
frequency gratings. |
|
|
|
|
VA: 20/30 or better |
|
No difference between |
|
|
|
|
|
|
IDDM and NIDDM pts |
Khosla et al. [129] |
Case-control |
Cases-38 eyes |
No DR-50.0 ± 11.8 |
22 (eyes)-No DR |
Cambridge low- |
Significant decreased CS in |
|
|
(22 pts) |
bDR-47.1 ± 10.3 |
16-bDR |
contrast sensi- |
the retinopathy group. |
|
|
Controls-20 |
Controls-47.2 ± 13.5 |
VA: 6/6 |
tivity charts |
No significant difference |
|
|
eyes (10 |
|
|
|
in CS between non retin- |
|
|
pts) |
|
|
|
opathy group and normal |
|
|
|
|
|
|
subjects |
Midena et al. [76] |
Prospective |
30 Diabetic |
55 (40–70) |
Minimalto mild-bDR |
Arden grating test |
CS improved after photo- |
|
non com- |
pts |
|
CSME |
|
coagulation, with a sig- |
|
parative |
|
|
VA: 1.0 |
|
nificant difference after |
|
study |
|
|
|
|
3 months, but did not |
|
|
|
|
|
|
reach normal values |
Bangstad et al. |
Case-control |
Cases-30 pts |
Micro-albuminuria |
Micro-albuminuria |
Vistech VCTS |
Micro-albuminuric pts |
[130] |
|
with micro- |
group: 19 (14–29) |
group: |
6500 distance |
showed worse CS at |
|
|
albuminuria |
Normo-albuminuria |
12 pts-No DR |
chart |
middle and high spatial |
|
|
Controls-27 |
group: 19 (14–24) |
18 pts-bDR |
|
frequencies, but signifi- |
|
|
pts with |
|
Normo-albuminuria |
|
cantly only for 18 cpd |
|
|
normo- |
|
group: |
|
|
|
|
albuminuria |
|
12 pts-no DR |
|
|
|
|
|
|
15 pts-bDR |
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
(continued) |
Table 2. (continued)
Principal |
|
|
|
|
|
|
investigator/ |
Types |
|
Age in years: |
|
|
|
year of publication |
of study |
Sample size |
mean/range |
DR status and VA |
Nature of stimulus |
Conclusions |
|
|
|
|
|
|
|
Arend et al. [75] |
Case-control |
Cases-20 pts |
Cases-42 ± 12 |
6-No DR |
CSV-1000 (Vector |
Diabetic pts had signifi- |
|
|
Controls- |
|
8-Only microaneurisms |
vision; Dayton, |
cantly lower CS at 6 and |
|
|
Normal |
|
4-Mild retinopathy |
OH) |
12 c/deg than control |
|
|
subjects |
|
1-Severe retinopathy |
|
subjects. Foveal avascu- |
|
|
from data- |
|
1-PDR |
|
lar zone and perifoveal |
|
|
base (arch |
|
VA: 20/25 or better |
|
intercapillary area cor- |
|
|
ophth |
|
|
|
related significantly with |
|
|
75;610) |
|
|
|
CS at 12 cpd |
De Marco [131] |
Case-control Cases-66 |
Cases: |
No DR |
Conel CST auto- |
No difference was found |
|
|
|
IDDM |
30–10 ± 1.22 years |
VA: 1.0 or better |
matic (Roma, |
between diabetic aretino- |
|
|
Controls-66 |
36–16.07 ± 2.3 |
|
ITA) (sinusoi- |
patic pts and controls. |
|
|
|
years |
|
dal gratings) |
CS was not correlated |
|
|
|
Controls: |
|
|
with sexual maturity or |
|
|
|
30–9.93 ± 2.02 |
|
|
duration of diabetes |
|
|
|
years |
|
|
|
|
|
|
36–17 ± 3.16 years |
|
|
|
Verrotti et al. |
Case-control |
Cases-40 + 20 |
Cases-16.9 ± 4.9 |
20-No DR |
CSV-1000 (Vector |
Diabetic pts showed a sig- |
[132] |
|
Controls-20 |
Controls-16.9 ± 4.6 |
30-bDR |
vision; Dayton, |
nificative decrease of |
|
|
|
|
10-Preproliferative/PDR |
OH) |
CS at 12 and 18 c/deg; |
|
|
|
|
|
|
preproliferative and PDR |
|
|
|
|
|
|
pts had decreased CS at |
|
|
|
|
|
|
all frequencies, and sig- |
|
|
|
|
|
|
nificative lower than CS |
|
|
|
|
|
|
of aretinopathic pts |
Mackie et al. [133] |
Case-control |
Cases-90 |
Cases: |
VA: 0.3 or better |
Pelli–Robson |
There was a progressive |
|
|
|
Controls-50 |
Young pts- |
|
chart |
reduction of CS thresh- |
|
|
|
|
33.2 ± 7.9 |
|
|
old through the five |
|
|
|
|
Older pts- |
|
|
groups of diabetic pts (no |
|
|
|
|
65.5 ± 8.2 |
|
|
DR, bDR, PPR, treated |
|
|
|
|
Controls: |
|
|
retinopathy, treated mac- |
|
|
|
|
Young pts- |
|
|
ulopathy), significative |
|
|
|
|
30.8 ± 7.9 |
|
|
between groups in which |
|
|
|
|
Older pts- |
|
|
there was a difference |
|
|
|
|
66.6 ± 10.1 |
|
|
of at least two adjacent |
|
|
|
|
|
|
|
degrees of retinopathy. |
|
|
|
|
|
|
|
No significative differ- |
|
|
|
|
|
|
|
ence was found between |
|
|
|
|
|
|
|
controls and aretino- |
|
|
|
|
|
|
|
pathic pts |
|
Lövestam-Adrian |
Case control |
Cases-20 |
Cases-32 (15–27) |
Cases-Treated PDR or |
Precision Vision |
Pts treated with panretinal |
|
et al. [134] |
|
Controls-19 |
Controls-30 (20–42) |
severe NPDR; VA: |
chart (Preisler |
photocoagulation had |
|
|
|
|
|
0.9 (0.4–1.0) |
instrument AB, |
significative higher |
|
|
|
|
|
Controls-No DR or non |
Illinois, USA) |
contrast threshold than |
|
|
|
|
|
treated mild bDR; |
|
untreated diabetic pts |
|
|
|
|
|
VA: 1.0 (0.5–1.0) |
|
|
|
Talwar et al. [77] |
Prospective |
14 Eyes with |
47–60 years |
CSME |
Cambridge low- |
The CS improved signifi- |
|
|
noncom- |
untreated |
|
VA: 0.49 (1.0–0.1) |
contrast sensi- |
cantly after photocoagu- |
|
|
parative |
CSME |
|
|
tivity charts |
lation treatment |
|
|
study |
|
|
|
|
|
|
Stavrou et al. |
Case-control |
Cases-20 pts |
Cases-62.67 ± 11.21 |
12-No/minimum DR |
Pelli–Robson |
CS was lower in diabetic |
|
[135] |
|
Controls- |
Controls-67.36 ± 7.35 |
4-Mild DR |
chart |
pts than CS of controls, |
|
|
|
24 pts |
|
4-Moderate/severe DR |
|
but significative differ- |
|
|
|
|
|
VA: 6/9.5 or better |
|
ence was observed only |
|
|
|
|
|
8 Pts had macular |
|
between no/minimum |
|
|
|
|
|
edema |
|
DR group and controls. |
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
(continued) |
|
Table 2. (continued)
Principal |
|
|
|
|
|
|
investigator/ |
Types |
|
Age in years: |
|
|
|
year of publication |
of study |
Sample size |
mean/range |
DR status and VA |
Nature of stimulus |
Conclusions |
|
|
|
|
|
|
|
|
|
|
|
|
|
Presence/absence of |
|
|
|
|
|
|
macular edema was |
|
|
|
|
|
|
correlated to decreased |
|
|
|
|
|
|
CS, but there was no |
|
|
|
|
|
|
significative difference |
|
|
|
|
|
|
between the two groups |
Farahvash et al. |
Prospective |
17 Diabetic |
– |
26 Eyes-diffuse macu- |
Metrovision with |
CS had a significative |
[78] |
noncom- |
pts (34 |
|
lar edema |
a high resolu- |
improved after photoco- |
|
parative |
eyes) |
|
8 Eyes-focal macular |
tion cathodic |
agulation treatment only |
|
study |
|
|
edema |
ray tube stimu- |
in the frequency of 6.4 |
|
|
|
|
VA pre-treatment: 0.21 |
lator |
cpd |
|
|
|
|
VA post-treatment: 0.24 |
|
|
|
|
|
|
|
|
|
Pts patients; VA visual acuity; CS contrast sensitivity; DR diabetic retinopathy; bDR background diabetic retinopathy; PDR proliferative diabetic retinopathy; CSME clinically significant diabetic macular edema; IDDM insulin-dependent diabetes mellitus; NIDDM non insulin-dependent diabetes mellitus; cpd cycles per degree
