- •Pearls of Glaucoma Management
- •Optic Nerve: The Glaucomatous Optic Nerve
- •1.1 Why is the Optic Nerve Important in the Diagnosis and Management of Glaucoma?
- •1.1.1 The Optic Nerve Head (ONH) is the Principal Site of Glaucomatous Damage to the Visual System
- •1.1.3 The Clinical Appearance and Behavior of the ONH Holds Clues as to the Etiology of a Given Optic Neuropathy
- •Summary for the Clinician
- •References
- •Optic Nerve: Clinical Examination
- •Summary for the Clinician
- •2.2 How Does One Establish the Borders of the Nerve and Follow the Neuroretinal Rim Contour?
- •Summary for the Clinician
- •Summary for the Clinician
- •Summary for the Clinician
- •Summary for the Clinician
- •2.6 How Quickly Can I Expect Optic Nerve Change to Occur?
- •Summary for the Clinician
- •2.7 If I See a Disc Hemorrhage on Healthy Appearing Neuroretinal Rim, How Soon Can I Expect to See a Change in the Rim?
- •Summary for the Clinician
- •References
- •Optic Nerve: Heidelberg Retinal Tomography
- •3.1 What Indices Should I Use to Help Me Interpret the Heidelberg Retinal Tomograph (HRT) Printout?
- •Summary for the Clinician
- •3.2 How Big a Change is Meaningful in the Numbers on an HRT Printout?
- •Summary for the Clinician
- •3.3.1 Trend Analysis
- •Summary for the Clinician
- •Summary for the Clinician
- •References
- •Optic Nerve: Scanning Laser Polarimetry
- •4.1 What is the Physical Principle Behind Scanning Laser Polarimetry (SLP)?
- •4.1.1 How has Scanning Laser Polarimetry Evolved?
- •4.1.2 What is GDxVCC (Variable Corneal Compensation)?
- •4.1.3 What is GDxECC (Enhanced Corneal Compensation)?
- •Summary for the Clinician
- •4.2 How is Image Quality and Artifact Assessed on the GDxVCC Printout?
- •Summary for the Clinician
- •Summary for the Clinician
- •4.4.1 Detection of Progression with SLP
- •Summary for the Clinician
- •References
- •Optic Nerve: Optical Coherence Tomography
- •Summary for the Clinician
- •5.2 What Indices Should I Use to Help Me Interpret the “RNFL Thickness Average Analysis Report” Printout?
- •Summary for the Clinician
- •Summary for the Clinician
- •5.4 Can I Use OCT Clinically to Diagnose Glaucoma? How Certain Can I Be that the Diagnosis is Real?
- •Summary for the Clinician
- •Summary for the Clinician
- •References
- •Optic Nerve: Comparison of Technologies
- •6.1 Why Image the Optic Nerve?
- •6.1.3 Scanning Laser Polarimetry (SLP)
- •Summary for the clinician
- •Summary for the Clinician
- •6.3 Is One Imaging Technique Easier to Use and Interpret than Another?
- •Summary for the Clinician
- •Summary for the Clinician
- •References
- •7.1 Should Peripapillary Atrophy (PPA) Concern Me? Should it Be Followed for Enlargement?
- •Summary for the Clinician
- •7.2 In Examining Tilted Optic Discs, How Do I Distinguish Tilt vs. Glaucoma?
- •7.2.1 What are the Characteristics of a Tilted Disc?
- •7.2.5 What Management Strategy Can I Use in Equivocal Cases of Tilt vs. Glaucoma?
- •Summary for Clinicians
- •7.3 With Optic Nerve Head Drusen (OND), How Do I Tell If Visual Field Changes are due to Drusen vs. Glaucoma?
- •7.3.1 Description of Drusen
- •7.3.2 What are the Characteristics of Field Defects in OND?
- •7.3.3 Are There Other Signs that Can Help Me Distinguish Between OND and Glaucoma?
- •7.3.4 Can Imaging Help Me to Distinguish Between OND and Glaucoma?
- •7.3.5 What Management Strategy Can I Use in Equivocal Cases of OND vs. Glaucoma?
- •Summary for the Clinician
- •7.4.1 What is the Significance of Disc Cupping?
- •7.4.3 What is the Significance of Optic Disc Pallor?
- •Summary for the Clinician
- •References
- •8.1 Why is Intraocular Pressure Important in Diagnosing and Treating Glaucoma?
- •8.1.3 Non-IOP Factors May also Be Involved in the Pathogenesis of Glaucoma
- •8.1.4 The Decision to Initiate Treatment by Lowering IOP
- •Summary for the Clinician
- •References
- •IOP: Instruments to Measure IOP
- •9.2.1 Maklakov Tonometer
- •9.2.2 Shiøtz Tonometry
- •9.2.3 Goldmann Tonometry
- •9.2.4 McKay-Marg and Tonopen
- •9.2.5 Air-Puff Tonometry
- •9.2.6 Dynamic Contour Tonometry
- •9.2.7 Trans-Palpebral Tonometers
- •Summary for the Clinician
- •Summary for the Clinician
- •Summary for the Clinician
- •9.5 In Cases of Prosthetic Corneas How Can I Measure the IOP?
- •Summary for the Clinician
- •Summary for the Clinician
- •References
- •IOP: Central Corneal Thickness
- •10.1.1 Goldmann Tonometry
- •10.1.2 The Influence of CCT on Tonometry
- •Summary for the Clinician
- •10.2.1 CCT in Different Populations
- •10.2.2 CCT Over Time
- •Summary for the Clinician
- •10.3 Does CCT Predict Glaucoma?
- •10.3.1 Clinical Trials
- •10.3.2 CCT in Established Glaucoma
- •10.3.3 CCT as a Biological Risk Factor
- •Summary for the Clinician
- •10.4.1 Should IOP Be “Adjusted” for CCT?
- •10.4.4 Should I Measure CCT in All Patients?
- •Summary for the Clinician
- •References
- •IOP: Corneal Hysteresis
- •11.1 What is Corneal Hysteresis and How Does it Influence IOP Measurement?
- •Summary for the Clinician
- •Summary for the Clinician
- •11.3 What Is the Relationship Between CCT, IOP, and Corneal Hysteresis?
- •Summary for the Clinician
- •11.4 Should I Invest in Newer Devices to Measure IOP that Claim Less Influence of CCT?
- •Summary for the Clinician
- •References
- •IOP: Target Pressures
- •Summary for the Clinician
- •12.2 If I Decide to Set a Target IOP, How Should I Set it – Do I Use a Percent Reduction or Aim Toward an Absolute Number?
- •Summary for the Clinician
- •Summary for the Clinician
- •Summary for the Clinician
- •References
- •IOP: Fluctuation
- •13.1 Why is IOP Fluctuation a Topic of Interest?
- •Summary for the Clinician
- •Summary for the Clinician
- •Summary for the Clinician
- •Summary for the Clinician
- •13.5 What is the Significance of Measures of Long-Term IOP Fluctuation?
- •Summary for the Clinician
- •13.6 What is the Impact of Medication on Short-Term and Long-Term IOP Fluctuation?
- •Summary for the Clinician
- •13.7 What is the Impact of Surgery on Short-Term and Long-Term IOP Fluctuation?
- •Summary for the Clinician
- •Summary for the Clinician
- •References
- •Gonioscopy: Why Do Indentation?
- •14.1 Which Patients Should have Gonioscopy?
- •Summary for the Clinician
- •14.2 Of What Use is the Van Herick Angle Examination?
- •Summary for the Clinician
- •14.3 What Lens Should be Used for Gonioscopy?
- •Summary for the Clinician
- •Summary for the Clinician
- •14.5 What Should I Look for in the Angle?
- •Summary for the Clinician
- •14.7 How Narrow is too Narrow? What are the Indications for Laser Iridotomy in a Patient with No Symptoms of Angle-closure?
- •Summary for the Clinician
- •14.8 What Should I Know about Plateau Iris?
- •Summary for the Clinician
- •Summary for the Clinician
- •Summary for the Clinician
- •References
- •Visual Fields: Visual Field Test Strategies
- •15.1.1 Automated vs. Manual
- •Summary for the Clinician
- •Summary for the Clinician
- •15.3 Is There a Visual Field Program of Choice at This Point in Time?
- •Summary for the Clinician
- •Summary for the Clinician
- •15.5 What Program is Best for Use in a General Clinic to Screen for Glaucoma?
- •Summary for the Clinician
- •15.6 How Can I Convert from One Visual Field Strategy to Another to Help Me Interpret and Compare Tests?
- •Summary for the Clinician
- •15.7 What Can be Done to Obtain Visual Field Information in a Patient who Consistently Tests Unreliably?
- •Summary for the Clinician
- •References
- •Visual Fields: Fluctuation and Progression
- •16.1 How Do I Distinguish Between Fluctuation and True Progressive Change on Visual Field Printouts?
- •Summary for the Clinician
- •Summary for the Clinician
- •Summary for the Clinician
- •16.4 What Automated Progression Analysis Software Is Available to Help with Visual Field Interpretation?
- •Summary for the Clinician
- •References
- •Visual Fields: Field Interpretation
- •17.1 How Is Information on a Single Field Printout of the Humphrey Visual Field Analyzer Interpreted?
- •17.1.1 Part 1 of the Visual Field Printout
- •17.1.2 Part 2 of the Visual Field Printout
- •17.1.3 Part 3 of the Visual Field Printout
- •17.1.4 Part 4 of the Visual Field Printout
- •Summary for the Clinician
- •17.2 How Is the Information on the Glaucoma Progression Analysis Printout Interpreted?
- •17.2.1 Part 1 of the GPA Printout
- •17.2.2 Part 2 of the GPA Printout
- •17.2.3 Part 3 of the GPA Printout
- •Summary for the Clinician
- •17.3.2 Automatic Reliance on the Statistical Analysis
- •17.3.3 Visual Field Artifacts
- •Summary for the Clinician
- •References
- •Other Tests in Glaucoma: Genetic Testing
- •18.1.1 Anterior Segment Dysgenesis
- •18.1.3 Congenital Glaucoma
- •18.1.4 Low-Tension Glaucoma
- •18.1.6 Pseudoexfoliation Glaucoma
- •Summary for the Clinician
- •18.2 Are Genetic Tests for Glaucoma of Practical Use in a Clinical Setting Today, or Are They More of Theoretical Use?
- •18.2.1 Anterior Segment Dysgenesis
- •18.2.3 Congenital Glaucoma
- •18.2.4 Low-Tension Glaucoma
- •Summary for the Clinician
- •18.3 How Do I Collect Samples and Where Do I Send Them for Analysis?
- •Summary for the Clinician
- •18.4.1 Genetic Counseling
- •18.4.3 Juvenile-Open Angle Glaucoma
- •18.4.4 Congenital Glaucoma
- •18.4.5 Low-Tension Glaucoma
- •Summary for the Clinician
- •References
- •Summary for the Clinician
- •19.2 Is Abnormal Ocular Blood Flow Causal in Glaucoma and Glaucoma Progression, and Does It Correlate with Disease Severity?
- •Summary for the Clinician
- •19.3.1.2 Patients with Vasospasm
- •19.3.1.3 Patients with Nocturnal Blood Pressure Dips
- •19.3.1.4 Diabetes
- •19.3.2 Patients Who Progress despite Reaching Target IOP or with Fluctuating IOP and Pulse Pressure
- •19.3.3 NTG Patients with Migraine and or Disc Hemorrhages
- •Summary for the Clinician
- •19.4 What are the Most Common Techniques to Measure Optic Nerve Blood Flow and what are Their Limitations?
- •19.4.1 Color Doppler Imaging (CDI)
- •19.4.4 Angiography
- •Summary for the Clinician
- •References
- •20.1 What Evidence Is There that Vascular Alterations Play a Role in Open-Angle Glaucoma (OAG)?
- •Summary for the Clinician
- •Summary for the Clinician
- •20.3.1 Color Doppler Imaging (CDI)
- •20.3.4 Laser Doppler Flowmetry (LDF)
- •20.3.5 Retinal Vessel Analyzer (RVA)
- •Summary for the Clinician
- •20.4.1 Color Doppler Imaging
- •20.4.2 Heidelberg Retinal Flowmeter
- •20.4.4 Laser Doppler Flowmetry
- •20.4.5 Retinal Vessel Analyzer
- •Summary for the Clinician
- •20.5.1 Color Doppler Imaging
- •20.5.2 Heidelberg Retinal Flowmeter
- •20.5.3 Canon Laser Blood Flowmetry
- •20.5.4 Laser Doppler Flowmetry
- •20.5.5 Retinal Vessel Analyzer
- •Summary for the Clinician:
- •20.6 How Can the Data from Ocular Hemodynamic Studies Be Used in Clinical Practice?
- •Summary for the Clinician
- •References
- •21.1.1 The Visual Evoked Potential (VEP)
- •Summary for the Clinician
- •Summary for the Clinician
- •21.3 Is the mfVEP a Useful Test in Glaucoma?
- •21.3.1 The mfVEP Is Not Ready for Routine Screening of Glaucoma Patients
- •21.3.2 The mfVEP Can Provide Clinically Useful Information
- •21.3.2.2 Unreliable Visual Fields
- •21.3.2.3 Inconsistent Visual Fields
- •21.3.2.3 Visual Fields that Need Confirmation
- •Summary for the Clinician
- •References
- •Risk Factors
- •Summary for the Clinician
- •22.2 What are the Main Risk Factors for Primary Open-Angle Glaucoma?
- •22.2.2 Demographic Factors
- •22.2.4 Central Corneal Thickness
- •22.2.5 Systemic Factors
- •Summary for the Clinician
- •Summary for the Clinician
- •References
- •Risk Factors: The Risk Calculator
- •23.1 Is a Risk Calculator Useful?
- •Summary for the Clinician
- •23.2 How Should I Use a Risk Calculator?
- •Summary for the Clinician
- •23.3 Can I Screen for Glaucoma with a Risk Calculator?
- •Summary for the Clinician
- •23.4 What Does It Mean to Me and My Patient If the Risk Score Is High?
- •Summary for the Clinician
- •References
- •24.1 Should Beta Blockers Still Be Used as a First-Line Agent?
- •24.1.1 What is the Topical Beta Blocker Mechanism of Action?
- •24.1.2 What Magnitude of IOP Decrease Is Seen with Beta Blockers?
- •24.1.3 How Should Beta Blockers Be Initiated?
- •24.1.4 What Are the Differences Between Individual Beta Blockers?
- •Summary for the Clinician
- •Summary for the Clinician
- •Summary for the Clinician
- •24.4 Should Miotics Still Be Used?
- •Summary for the Clinician
- •References
- •Summary for the Clinician
- •25.2 What Medications Are Safe to Use in a Nursing Mother?
- •Summary for the Clinician
- •References
- •Summary for the Clinician
- •26.2 How Should Oral CAIs Be Dosed?
- •Summary for the Clinician
- •Summary for the Clinician
- •26.4 Can CAIs Be Used in Pregnant Women or Pediatric Patients?
- •Summary for the Clinician
- •26.5 Can CAIs Be Used in Patients with Sickle Cell Anemia?
- •Summary for the Clinician
- •Summary for the Clinician
- •Summary for the Clinician
- •References
- •Medical Treatment: Osmotic Agents
- •27.1 When Using Hyperosmotics Agents, What Is a Typical Dose for Acutely Elevated Intraocular Pressure (IOP)?
- •Summary for the Clinician
- •Summary for the Clinician
- •27.3 Should Hyperosmotic Agents Be Used to Lower IOP Prior to Surgery?
- •Summary for the Clinician
- •References
- •Medical Treatment: Neuroprotection
- •28.1 What Exactly Is Neuroprotection?
- •Summary for the Clinician
- •Summary for the Clinician
- •28.3.1 Memantine
- •28.3.2 Brimonidine
- •28.3.3 Betaxolol
- •28.3.4 Calcium Channel Blockers
- •23.3.5 Other Possible Treatments
- •Summary for the Clinician
- •Summary for the Clinician
- •References
- •29.2 What Is the Natural History of Treated and Untreated Glaucoma?
- •29.2.1 Olmsted County, MN
- •29.2.2 St. Lucia Study
- •Summary for the Clinician
- •Summary for the Clinician
- •References
- •30.1.1 What Is Adherence?
- •30.1.2 What Is Persistence?
- •Summary for the Clinician
- •30.2 How Can One Help Patients to Be More Compliant with Treatment?
- •Summary for the Clinician
- •Summary for the Clinician
- •References
- •Summary for the Clinician
- •31.2.1 Exercise
- •31.2.2 Smoking
- •31.2.3 Alcohol Consumption
- •31.2.4 Diet
- •Summary for the Clinician
- •31.3.1 Marijuana Use
- •31.3.2 Gingko Biloba
- •31.3.3 Bilberry
- •31.3.4 Acupunture
- •Summary for the Clinician
- •References
- •32.1.2 Does Trabeculoplasty benefit Compliance?
- •32.1.3 How well does Trabeculoplasty control the Diurnal IOP curve?
- •32.1.4 What are the Side Effects/Risks of Trabeculoplasty?
- •32.1.5 What are the Economic Issues Involved with Trabeculoplasty?
- •Summary for the Clinician
- •32.2.1 What is the Efficacy of ALT Versus SLT?
- •32.2.2 What are the Complications of ALT Versus SLT?
- •32.2.3 How does Retreatment compare between ALT and SLT?
- •Summary for the Clinician
- •32.3 When Should SLT or ALT not Be Performed?
- •32.3.1 Types of Glaucoma
- •32.3.2 IOP Reduction
- •32.3.3 Maximal Medical Therapy
- •Summary for the Clinician
- •32.4.1 Argon Laser Trabeculoplasty
- •32.4.2 Selective Laser Trabeculoplasty
- •Summary for the Clinician
- •Summary for the Clinician
- •Summary for the Clinician
- •32.7 What is the Mechanism of Action of ALT and SLT?
- •32.7.1 Mechanical Theory
- •32.7.2 Biologic Theory
- •32.7.3 Repopulation Theory
- •Summary for the Clinician
- •Summary for the Clinician
- •References
- •33.1 When Can or Should Endoscopic Cyclophotocoagulation (ECP) Be Used?
- •Summary for the Clinician
- •33.2 Should ECP Be Used as a Primary Surgery for Glaucoma?
- •Summary for the Clinician
- •33.3 Is Burning the Ciliary Processes a Safe Thing to Do?
- •Summary for the Clinician
- •Summary for the Clinician
- •Summary for the Clinician
- •33.6 What Are Complications that May Be Encountered and How Are They Specifically Managed?
- •Summary for the Clinician
- •Summary for the Clinician
- •33.8 What Is the Long Term Safety Data on this Procedure?
- •Summary for the Clinician
- •References
- •34.1 What is Transscleral Cyclophotocoagulation (TCP)?
- •Summary for the Clinician
- •34.2 When Should I Use TCP? Should it be Used as a Primary Surgery for Glaucoma?
- •Summary for the Clinician
- •34.3 Technically, How is TCP Performed?
- •Summary for the Clinician
- •Summary for the Clinician
- •Summary for the Clinician
- •References
- •Procedural Treatments: Trabeculectomy
- •Summary for the Clinician
- •35.2 Should Antimetabolites be Used in All Cases of Trabeculectomy?
- •35.3 Do You Adjust Antimetabolite Usage and Dose Based on Patient Age or Race?
- •Summary for the Clinician
- •Summary for the Clinician
- •Summary for the Clinician
- •Summary for the Clinician
- •References
- •Summary for the Clinician
- •Summary for the Clinician
- •Summary for the Clinician
- •Summary for the Clinician
- •Summary for the Clinician
- •References
- •Procedural Treatments: Bleb Needling
- •37.1.1 Slit Lamp Bleb Needling
- •37.1.3 Antimetabolite Use with Needling
- •Summary for the Clinician
- •37.2 Is It Ever Too Early or Too Late to Needle a Bleb?
- •Summary for the Clinician
- •Summary for the Clinician
- •Summary for the Clinician
- •37.5 Is It Better to Needle or Reoperate on a Failing Bleb?
- •Summary for the Clinician
- •References
- •38.1 Is One Tube Shunt Design Better than Another at Lowering IOP?
- •Summary for the Clinician
- •Summary for the Clinician
- •Summary for the Clinician
- •Summary for the Clinician
- •Summary for the clinician
- •Summary for the Clinician
- •Summary for the Clinician
- •References
- •39.1.1 Aqueous Shunts for Glaucoma (Supporting Evidence Level I/1c)
- •39.1.2 Cyclodestruction with Diode G-Probe (Supporting Evidence Level III/4)
- •39.1.3 Cyclodestruction with Diode Endocyclophotocoagulation (Supporting Evidence Level I/1c)
- •39.1.8 iScience (Canaloplasty) (Supporting Evidence III/4)
- •Summary for the Clinician
- •References
- •Summary for the Clinician
- •40.2 What Is the Ex-PRESS Mini-Shunt and How Does It Work?
- •Summary for the Clinician
- •Summary for the Clinician
- •Summary for the Clinician
- •Summary for the Clinician
- •40.6 What Complications Are Specific to the Ex-PRESS Shunt Procedure?
- •Summary for the Clinician
- •References
- •41.1.1 When to Add a Trabeculectomy to Cataract Surgery
- •41.1.2 When to Add Phacoemulsification to a Trabeculectomy
- •Summary for the Clinician
- •41.2.1 Glaucoma as the Primary Problem
- •41.2.2 Cataract as the Primary Problem
- •Summary for the Clinician
- •41.3 How Is the Postoperative Course of a Phacotrabeculectomy Different than that After the Individual Surgeries?
- •Summary for the Clinician
- •References
- •42.1 What Is End-Stage Glaucoma?
- •Summary for the Clinician
- •42.2 Should I Operate on a Patient with End-Stage Glaucoma?
- •Summary for the Clinician
- •Summary for the Clinician
- •42.4 How Do Specific Complications of Surgery in End-Stage Glaucoma Lead to Vision Loss?
- •42.4.1 Hypotony Maculopathy
- •42.4.2 Retinal Detachment
- •42.4.3 Endophthalmitis
- •42.4.4 Malignant Glaucoma and others
- •Summary for the Clinician
- •42.5 What Can Be Done to Minimize Potential Vision Loss Due to Surgery in End-Stage Glaucoma?
- •Summary for the Clinician
- •References
- •Summary for the Clinician
- •Summary for the Clinician
- •43.3 What Is the Treatment of Choice in Normal-Tension Glaucoma – Medication, Laser, or Surgery?
- •Summary for the Clinician
- •43.4.1 Risk Factors for Progression in NTG
- •43.4.2 Disc Hemorrhage in NTG
- •Summary for the Clinician
- •References
- •Glaucomas: Pseudoexfoliation Glaucoma
- •44.1 Is There a Gene for Pseudoexfoliation Syndrome?
- •Summary for the Clinician
- •Summary for the Clinician
- •44.3 What Is the Risk of Developing Glaucoma Once PXF Material Is Observed in the Eye?
- •Summary for the Clinician
- •44.4.2 Cataract Extraction Technique
- •Summary for the Clinician
- •References
- •Summary for the Clinician
- •45.2 Is PDG Managed Differently than Primary Open Angle Glaucoma?
- •45.2.1 Medical Treatment
- •45.2.2 Trabeculoplasty
- •45.2.3 Trabeculectomy
- •Summary for the Clinician
- •Summary for the Clinician
- •Summary for the Clinician
- •Summary for the Clinician
- •45.6.1 Medical Therapy
- •45.6.2 Laser and Incisional Surgery
- •Summary for the Clinician
- •Summary for the Clinician
- •References
- •Glaucomas: Sturge Weber Syndrome
- •Summary for the Clinician
- •Summary for the Clinician
- •Summary for the Clinician
- •Summary for the Clinician
- •References
- •Glaucomas: Glaucoma and the Cornea
- •Summary for the Clinician
- •Summary for the Clinician
- •47.3 What Effect Does Laser Glaucoma Surgery Have on the Cornea?
- •Summary for the Clinician
- •Summary for the Clinician
- •Summary for the Clinician
- •References
- •Glaucomas: Uveitic Glaucoma
- •Summary for the Clinician
- •48.2 Is There a Way to Distinguish Between Elevated IOP Due to a Steroid Response vs. Uveitis?
- •Summary for the Clinician
- •48.3 How Do Inflammation and Steroids Cause an Increase in IOP?
- •Summary for the Clinician
- •Summary for the Clinician
- •48.5 Is There a Preferred Surgery for Uveitic Glaucoma (Trabeculectomy vs. Tube vs. Laser)?
- •Summary for the Clinician
- •48.6 Is One Tube Preferred over Another in Uveitic Glaucoma?
- •Summary for the Clinician
- •Summary for the Clinician
- •Summary for the Clinician
- •References
- •Glaucomas: Neovascular Glaucoma
- •49.1.1 IOP Lowering Agents
- •49.1.3 Cycloplegics/Mydriatics
- •Summary for the Clinician
- •Summary for the Clinician
- •Summary for the Clinician
- •Summary for the Clinician
- •References
- •50.1 What Is the Best Way to Measure IOP in the Pediatric Patient?
- •Summary for the Clinician
- •Summary for the Clinician
- •Summary for the Clinician
- •Summary for the Clinician
- •References
- •51.1.1 Which Medications Can Be Used as First Line Agents in Children?
- •Summary for the Clinician
- •Summary for the Clinician
- •References
- •52.1 How Do I Perform Goniosurgery?
- •52.1.2 What Can I Do Technically to Perform a Better Trabeculotomy ?
- •Summary for the Clinician
- •Summary for the Clinician
- •References
- •Summary for the Clinician
- •53.2 Is Trabeculectomy Preferred over Tube Shunt Surgery in Children?
- •Summary for the Clinician
- •Summary for the Clinician
- •53.4 What Factors Help One Decide for or Against One Surgery over the Other?
- •Summary for the Clinician
- •53.5.1 In Trabeculectomy
- •53.5.2 In Tube-Shunts
- •Summary for the Clinician
- •Summary for the Clinician
- •53.7 What Can Be Done Technically to Perform a Better Glaucoma Drainage Device Surgery in Kids?
- •Summary for the Clinician
- •References
- •Angle-Closure Glaucoma: Risk Factors
- •54.1 Who Is at Risk for Acute Angle-Closure?
- •54.1.1 What are the Anatomical Risk Factors?
- •54.1.2 Age, Gender and Ethnicity
- •Summary for the Clinician
- •Summary for the Clinician
- •Summary for the Clinician
- •References
- •Angle-Closure Glaucoma: Iridotomy
- •55.1.1 Settings for Argon LPI
- •55.1.2 Settings for Nd-YAG LPI
- •Summary for the Clinician
- •Summary for the Clinician
- •55.3 If It Is Difficult to Penetrate the Iris, What Adjustments Can Be Made to the Laser Settings?
- •Summary for the Clinician
- •55.4.1 Visual Discomfort
- •55.4.2 Diplopia and/or Glare
- •55.4.3 Hemorrhage
- •55.4.4 Corneal Damage
- •55.4.5 Lens Damage
- •55.4.6 IOP Elevation
- •55.4.7 Progression of PAS Formation
- •55.4.8 Posterior Synechia
- •55.4.9 LPI Closure
- •Summary for the Clinician
- •Summary for the Clinician
- •References
- •Angle-Closure Glaucoma: Imaging
- •Summary for the Clinician
- •56.2.1 Ultrasound Biomicroscopy (UBM)
- •56.2.3 Scheimpflug Photography
- •Summary for the Clinician
- •56.3 When Should UBM and AS-OCT Be Ordered: Is One Device Considered Better than the Other?
- •Summary for the Clinician
- •56.4.1 Qualitative Analysis
- •56.4.2 Quantitative Analysis
- •Summary for the Clinician
- •References
- •Angle-Closure Glaucoma: Medical Therapy
- •57.1.1 Carbonic Anhydrase Inhibitors
- •57.1.2 Beta-Blockers
- •57.1.3 Alpha-Agonists
- •57.1.4 Prostaglandin Analogs
- •57.1.5 Hyperosmotic Agents
- •57.1. 6 Miotics
- •Summary for the Clinician
- •Summary for the Clinician
- •References
- •Summary for the Clinician
- •Summary for the Clinician
- •Summary for the Clinician
- •Summary for the Clinician
- •References
- •Complications: Hypotony
- •59.1 What are the Options in the Treatment of Early Postoperative Hypotony?
- •59.1.1 Compression Sutures
- •59.1.2 Anterior Chamber Reformation
- •59.1.3 Choroidal Drainage
- •59.1.4 Repairing Wound Leaks
- •59.1.5 Resuturing of Trabeculectomy Flap
- •Summary for the Clinician
- •59.2 If There Is Hypotony Maculopathy, What Should Be Done to Manage It?
- •59.2.1 Cataract Surgery and Hypotony
- •Summary for the Clinician
- •59.3 How Can I Manage Late Hypotony Due to a Scleral Melt?
- •Summary for the Clinician
- •Summary for the Clinician
- •References
- •Complications: Bleb Leaks
- •60.1.2 With a Large/Brisk, Early Postoperative Bleb Leak, What Options Are Available to Help It Heal?
- •60.1.3 What Can I Do If the Leak Continues to Persist?
- •Summary for the Clinician
- •60.2.2 Autologous Blood Injection
- •60.2.3 Compression Sutures
- •60.2.4 Laser
- •60.2.5 Surgical Bleb Revision
- •Summary for the Clinician
- •Summary for the Clinician
- •References
- •Complications: Blebitis
- •Summary for the Clinician
- •Summary for the Clinician
- •61.3 How Do I Manage a Patient After the Blebitis Is Resolved?
- •Summary for the Clinician
- •References
- •Subject Index
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[5, 11]. While some of these patients are simply unable to produce reliable fields, others have functional (nonorganic) disorders [5, 11, 12, 25, 26]. In either case, the information from SAP should be discounted.
Occasionally, the SAP visual field is inconsistent with disc abnormalities because nonglaucomatous damage may be contributing to the field loss. In some of these cases, the latency of the mfVEP can signal the presence of another disease process, as mentioned above.
21.3.2.3 Visual Fields that Need Confirmation
The mfVEP can prove useful in confirming a questionable visual field defect prior to initiation or advancement of therapy.
Summary for the Clinician
››The mfVEP can detect glaucomatous damage before it is detected with standard automated perimetry (SAP). For other patients, SAP is more sensitive.
››The mfVEP is not a substitute for SAP.
››Patients in whom diagnosis by SAP and disc examinations is uncertain, a mfVEP test may be beneficial.
››When SAP field defects are questionable or absent, but present on SWAP or FDT, the mfVEP can provide confirmatory evidence. If there are defects in the same area, it suggests the presence of glaucomatous damage and the need for treatment.
››The mfVEP is helpful in patients with unreliable SAP fields or whose fields are inconsistent with disc appearance.
››Moderately prolonged latencies of mfVEP responses can signal the presence of retinal disease, while markedly prolonged latencies or increases in latency are associated with compressive tumors and multiple sclerosis.
››Because of the difficulties involved in recording and analyzing mfVEPs, we recommend that the test be performed in centers with the necessary equipment, expertise, and experience.
References
1. Hood DC (2003) Objective measurement of visual function in glaucoma. Cur Opin Ophthalmol 14:78–82.
2. Holder GE, Brigell MG, Hawlina M, et al.; International Society for Clinical Electrophysiology of Vision (2007) ISCEV standard for clinical pattern electroretinography – 2007 update. Doc Ophthalmol 114:111–6.
3. Brigell MG (2001) The visual evoked potential. In: Fishman, GA, Birch DG, Holder GE, Brigell MG (eds.) Electrophysiologic Testing in Disorders of the Retina, Optic Nerve, and Visual Pathway, 2nd edition (Ophthalmology Monographs) . San Francisco: The Foundation of the American Academy of Ophthalmology, pp. 237–78.
4. Baseler HA, Sutter EE, Klein SA, Carney T (1994) The topography of visual evoked response properties across the visual field. Electroencephalogr Clin Neurophysiol 90:65–81.
5. Hood DC, Greenstein VC (2003) The multifocal VEP and ganglion cell damage: applications and limitations for the study of glaucoma. Prog Retin Eye Res 22:201–51.
6. Hood DC, Zhang X, Greenstein VC, et al. (2000) An intero cular comparison of the multifocal VEP: a possible technique for detecting local damage to the optic nerve. Invest Ophtha lmol Vis Sci 41:1580–7.
7. Goldberg I, Graham SL, Klistorner AI (2002) Multifocal objective perimetry in the detection of glaucomatous field loss. Am J Ophthalmol 133:29–39.
8. Graham SL, Klistorner AI, Grigg JR, Billson FA (2000) Objective VEP perimetry in glaucoma: asymmetry analysis to identify early deficits. J Glaucoma 9:10–9.
9. Graham SL, Klistorner AI, Goldberg I (2005) Clinical application of objective perimetry using multifocal visual evoked potentials in glaucoma practice. Arch Ophthalmol 123:729–39.
10.Fortune B, Hood DC (2003) Conventional pattern-reversal VEPs are not equivalent to summed multifocal VEPs. Invest Ophthalmol Vis Sci 44:1364–7.
11.Hood DC (2004) Electrophysiologic imaging of retinal and optic nerve damage: the multifocal technique. Ophthalmol Clin North Am 17:69–88.
12.Hood D, Odel JG, Winn BJ (2003) The multifocal visual evoked potential (VEP): applications and limitations in neuro-ophthalmology. J Neuro Ophthalmol 23:279–89.
13.Klistorner A, Graham SL (2000) Objective perimetry in glaucoma. Ophthalmol 107:2283–99.
14.Seiple W, Holopigian K, Clemens C, et al. (2005) The multifocal visual evoked potential: an objective measure of visual field? Vision Res 45:1155–63.
15.Grippo TM, Hood DC, Kanadani FN, et al. (2006) A comparison between multifocal and conventional VEP latency changes secondary to glaucomatous damage. Invest Ophthalmol Vis Sci 47:5331–6.
16.Hood DC, Chen, JY, Yang EB, et al. (2006) The role of the multifocal visual evoked potential (mfVEP) latency in understanding optic nerve and retinal diseases. Trans Am Ophthalmol Soc 104:71–7.
17.Klistorner A, Graham SL, Martins A, et al. (2007) Multifocal blue-on-yellow visual evoked potentials in early glaucoma. Ophthalmology 114:1613–21.
18.Rodarte C, Hood DC, Yang EB, et al. (2006) The effects of glaucoma on the latency of the multifocal visual evoked potential. Br J Ophthalmol 90:1132–6.
21 Other Tests in Glaucoma: Multifocal Visual Evoked Potential |
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19.Hood DC, Odel JG, Zhang X (2000) Tracking the recovery of local optic nerve function after optic neuritis: a multifocal VEP study. Invest Ophthalmol Vis Sci 41:4032–8.
20.Semela L, Yang EB, Hedges TR, et al. (2007) Multifocal visual evoked potential in unilateral compressive optic neuropathy. Br J Ophthalmol 91:445–8.
21.Chen JY, Hood DC, Odel JG, Behrens MM (2006) The effects of retinal abnormalities on the multifocal visual evoked potential. Invest Ophthalmol Vis Sci 47:4378–85.
22.Fortune B, Demirel S, Zhang X, et al. (2007) Comparing multifocal VEP and standard automated perimetry in high-risk ocular hypertension and early glaucoma. Invest Ophthalmol Vis Sci 48:1173–80.
23.Thienprasiddhi P, Greenstein VC, Chu DH, et al. (2006) Detecting early functional damage in glaucoma suspect and ocular hypertensive patients with the multifocal VEP technique. J Glaucoma 15:321–7.
24.Hood DC, Thienprasiddhi P, Greenstein VC, et al. (2004) Detecting early to mild glaucomatous damage; a comparison of the multifocal VEP and automated perimetry. Invest Ophthalmol Vis Sci 45:492–8.
25.Massicotte EC, Semela L, Hedges TR (2005) Multifocal visual evoked potential in nonorganic visual field loss. Arch Ophthalmol 123:364–7.
26.Miele DL, Odel JG, Behrens, et al. (2000) Functional bitemporal quadrantopia and the multifocal visual evoked potential. J Neuro Ophthal 20:159–62.
27.Klistorner AI, Graham SL, Grigg JR, Billson FA (1998) Multifocal topographic visual evoked potential: improving objective detection of local visual field defects. Invest Ophthalmol Vis Sci 39:937–50.