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Ординатура / Офтальмология / Английские материалы / Essentials in Ophthalmology Pediatric Ophthalmology Neuro-Ophthalmology Genetics_Lorenz, Borruat_2008

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XII Contents

8.9Visual Maps of Higher Visual Function: V4  . . . . . . .   126

8.10Visual Maps of Higher Visual Function: V3A, V3B and KO    126

8.11Segmenting Extrastriate Areas and MT+ into

 

Functional Subregions 

. .   127

8.12

Responses to Optic Flow 

.   128

8.13Disparity and Motion-in-

Depth Stimulation  . . . .   129

8.14Interface Between Visual and Oculomotor

Systems  . . . . . . . . .   129

8.15Parietal Lobe Maps

of Visuotopic Space  . . . .  130

8.16Working Memory for Visual Stimuli  . . . . . . . . . .  130

8.17Role of V1 in Visual Consciousness  . . . . . .   132

8.18Summary   . . . . . . . .   132

Chapter 9

Investigating Visual Function with Multifocal Visual Evoked Potentials

Michael B. Hoffmann

9.1Introduction  . . . . . . .   139

9.2Multifocal Principle and Characteristics of Multifocal

VEPs  . . . . . . . . . . .  140

9.2.1Basics – Multifocal Stimulation, First-

and Second-Order Kernels    140

9.2.2Stimulus Display for mfVEP Recordings  . . . . . . . .  143

9.2.3Recording mfVEPs and Practical

Considerations  . . . . . .  143

9.2.4Dependence

of mfVEPs on Visual Cortex

 

Morphology  . . . . . .

.   146

9.3

Assessment of mfVEPs   .

.   148

9.3.1Response Magnitude  . . .   148

9.3.2Response Latency  . . . . .  149

9.4mfVEP Investigations

 

of Diseases  . . . .

. .

.

.  151

9.4.1

mfVEP in Glaucoma 

. .

.

.  152

9.4.2mfVEP in Optic Neuritis  . .   153

9.4.3

mfVEP in Albinism 

. .

.

.   154

9.5

Conclusion  . . .

. . .

.

.  157

Part III  Retinal Disorders

Chapter 10

Autoimmune Retinopathies

Jennifer K. Hall, Nicholas J. Volpe

10.1Autoimmune Disease

Overview  . . . . . . . . . . . . . . . . .  163

10.2Autoimmune Retinopathy Overview  . . . . . . . . . . . . . . . . .  164

10.3Paraneoplastic

Retinopathies  . . . . . .   164

10.3.1Cancer-Associated

Retinopathy   . . . . . . .  164

10.3.1.1

Clinical Presentation 

.

.

.   166

10.3.1.2

Diagnostic Studies 

. .

.

.   166

10.3.1.3Pathophysiology  . . . . .   166

10.3.1.4Treatment  . . . . . . . .   168

10.3.2Melanoma-Associated Retinopathy  . . . . . . .   168

10.3.2.1

Clinical Presentation 

.

.

.   168

10.3.2.2

Diagnostic Studies 

. .

.

.   168

10.3.2.3Pathophysiology  . . . . .   169

10.3.2.4Treatment  . . . . . . . .   169

10.3.3Bilateral Diffuse Uveal Melanocytic Proliferation  .   169

10.3.3.1

Clinical Presentation 

.

.

.   170

10.3.3.2

Diagnostic Studies 

. .

.

.   170

10.3.3.3Pathophysiology  . . . . .   170

10.3.3.4Treatment  . . . . . . . .   171

10.4AutoimmuneRelated Retinopathy

and Optic Neuropathy  . . .  171

10.5Acute Outer Retinopathies with Blind

Spot Enlargement  . . . .   172

10.5.1Acute Idiopathic

Blind Spot Enlargement   . .  173

10.5.1.1

Clinical Presentation 

.

.

.   173

10.5.1.2

Diagnostic Studies 

. .

.

.   173

10.5.1.3Pathophysiology  . . . . .   173

10.5.1.4Treatment  . . . . . . . .   176

10.5.2Multiple Evanescent White

 

Dot Syndrome   . .

.

.

. .  176

10.5.2.1

Clinical Presentation 

.

.

.   176

10.5.2.2

Diagnostic Studies 

. .

.

.   176

10.5.2.3Pathophysiology  . . . . .   177

10.5.2.4Treatment  . . . . . . . .   178

10.5.3Acute Zonal Occult Outer Retinopathy  . . . . . . .   178

Contents XIII

10.5.3.1

Clinical Presentation 

.

.

.   178

10.5.3.2

Diagnostic Studies 

. .

.

.   178

10.5.3.3Pathophysiology  . . . . .   179

10.5.3.4Treatment  . . . . . . . .   179

10.5.3.5AZOOR Complex of Disease    179

10.6Summary  . . . . . . . .   180

Chapter 11

Retinal Research: Application to Clinical Practice

Ludwig Aigner, Claudia Karl

11.1Introduction   . . . . . . .  185

11.1.1Retinitis Pigmentosa   . . .   185

11.1.2Age-Related Macular Degeneration   . . . . . .   186

11.1.3Glaucoma   . . . . . . . .  186

11.2

Cell Death in the Retina  . .  186

11.2.1Major Characteristics

and Pathways of Apoptosis     187

11.2.1.1Caspase-Dependent

Apoptosis  . . . . . . . .   187

11.2.1.2Caspase-Independent Apoptosis  . . . . . . . .   188

11.3Therapeutic Strategies in Degenerative Retinal

Diseases  . . . . . . . . .  189

11.3.1Strategies

for Neuroprotection   . . .   189

11.3.1.1Animal Models in Retinal Degeneration Research  . . . .  189

11.3.1.2Strategies

for Neuroprotection Interfering

with the Induction Phase

of Apoptosis  . . . . . . .   190

11.3.1.3Strategies

for Neuroprotection Interfering with the Early

Phase of Apoptosis  . . . .   191

11.3.1.4Strategies Using Neuroprotective Cytokines that Showed Effects in Other

Tissues  . . . . . . . . . .  191

11.3.2Cell Therapy

for the Diseased Retina   . .  192

11.3.2.1Cell Transplantation

in the Retina   . . . . . . .  193

11.3.2.2Application of Transgenes or Genetically Engineered

Stem and Progenitor Cells     198

11.3.2.3Endogenous Cell

Replacement in the Retina    199

Part IV  Systemic disease

Chapter 12

Chorioretinal Lesions in Infectious

Diseases of Neuroophthalmic Interest

Yan Guex-Crosier

12.1Introduction  . . . . . . .   206

12.2

Ocular Zoonosis  . . . .

.   206

12.2.1

Ocular Toxoplasmosis  . .

.  206

12.2.1.1

Congenital Toxoplasmosis 

.  206

12.2.1.2Reactivation

of Toxoplasmosis

in Immunocompetent

Patients  . . . . . . . . .   207

12.2.1.3Ophthalmic Toxoplasmosis

in AIDS Patients  . . . . . .  209

12.2.1.4Neurologic Manifestation of Toxoplasmosis in AIDS

Patients  . . . . . . . . .   209

12.2.1.5Radiologic Manifestation

of Toxoplasmosis in AIDS  .   209

12.2.2Toxocariasis  . . . . . . .   210 12.2.2.1 Introduction  . . . . . . .   210 12.2.2.2 Ocular Manifestations  . . .  210 12.2.2.3 Neurologic Manifestations    210

12.2.3Diseases Transmitted

by Ticks   . . . . . . . . .   210

12.2.3.1Introduction  . . . . . . .   210

12.2.3.2Tick-Borne Encephalitis  . .   210

12.2.3.3Lyme Disease  . . . . . . .  211

12.2.4

Cat Scratch Disease  . . . .  214

12.2.4.1Introduction  . . . . . . .   214

12.2.4.2Ocular

and Neuroophthalmologic Manifestations  . . . . . .   214

12.2.4.3Neurologic Manifestations    215

12.2.4.4Therapy  . . . . . . . . .   215

12.3Sexually Transmitted

Diseases  . . . . . . . . .  215

12.3.1 Syphilis  . . . . . . . . .   215

12.3.1.1Introduction  . . . . . . .   215

12.3.1.2Ocular

and Neuroophthalmologic

Manifestations  . .

.

.

.

.   215

12.3.1.3 Diagnostic Tests  .

.

.

.

.   216

XIV Contents

12.3.1.4 Therapy  . . . . . . . . .   216

12.3.2Human Immunodeficiency Virus (HIV)

 

and Ocular Infection 

. . .   216

12.3.2.1 Introduction  . .

.

.

. . .   216

12.3.2.2

HIV Retinopathy 

.

.

. . .   217

12.3.2.3

CMV Retinitis  . .

 

.

. . . .  218

12.4Encephalopathies Due to Viral and Non-

Conventional Agents  . . .   220

12.4.1Lymphocytic

Choriomeningitis Virus   . .   220

12.4.2Creutzfeldt–Jakob

Disease  . . . . . . . . .   220

12.4.3JC Virus

and Progressive Multifocal Leukoencephalopathy  . .   221

12.4.4Herpetic Encephalopathy and Acute Retinal Necrosis

Syndrome  . . . . . . . .   222

12.5Conclusion  . . . . . . . .  222

Chapter 13

Giant Cell Arteritis

Aki Kawasaki

13.1Pathophysiology

of Giant Cell Arteritis  . . .   227

13.1.1Epidemiology  . . . . . .   227

13.1.2

Triggering Event  . . . . .   228

13.1.3Tropism to Certain Vascular

Beds  . . . . . . . . . . .  228

13.1.4Macrophage Recruitment

and Vascular Injury  . . . .   229

13.1.5Systemic Inflammation  . .   230

13.2Clinical (Non-Ophthalmic) Manifestations of GCA  . . .  231

13.2.1

Natural History  . . . . . .  231

13.2.2Systemic Signs

and Symptoms  . . . . . .  231

13.2.3Headache

and Craniofacial Pain  . . .   231

13.2.4Auditory Manifestations  . .  232

13.2.5Neurologic Manifestations    232

13.2.6Occult GCA  . . . . . . . .  232

13.3Visual Manifestations

of GCA  . . . . . .

. .

.

.  233

13.3.1 Transient Visual Loss 

.

.

.   233

13.3.2Anterior Ischemic Optic Neuropathy  . . . . . . .   234

13.3.3Other Types

of Ischemic Visual Loss  . .   235

13.3.4Diplopia  . . . . . . . . . . . . . . . . . .  235

13.3.5Orbital Manifestations  . . .  236

13.4

Clinical Subtypes of GCA  .   236

13.4.1Systemic Inflammatory Syndrome  . . . . . . . .   236

13.4.2

Cranial Arteritis  . . .

.

. .  236

13.4.3

Large-Vessel Vasculitis  

.

.   237

13.5Laboratory Investigations

in GCA  . . . . . . . . . .  238

13.5.1Erythrocyte Sedimentation

Rate  . . . . . . . . . . .  238

13.5.2

C-Reactive Protein 

.

.

.

.   239

13.5.3

Thrombocytosis  .

.

.

.

.   239

13.5.4Interleukin-6

and Other Cytokines  . . .   239

13.5.5Anemia  . . . . . . . . .   240

13.5.6Others  . . . . . . . . . .  240

13.6

Diagnosis of GCA  . . . . .  240

13.6.1Temporal Artery Biopsy  . . . .  241

13.6.2American College

of Rheumatology Criteria  .   241

13.6.3

Role of Ultrasound  . . . .   243

13.6.4Other Non-Invasive Imaging

of the Cranial Arteries  . . .  243

13.7Treatment and Prognosis

of GCA  . . . .

.

.

.

.

.

.  244

13.7.1 Corticosteroids 

.

.

.

.

.

.  244

13.7.1.1Starting Dose  . . . . . . .  245

13.7.1.2Maintenance Dose  . . . .   245

13.7.1.3

Tapering Regimen  . .

.

.   245

13.7.1.4

Duration of Treatment  .

.

.  245

13.7.2Visual Outcome

on Corticosteroids  . . . .   245

13.7.3Methotrexate   . . . . . .   246

13.7.4 Other Adjuvant Therapies  .  246

13.7.5Treatment of Large-Vessel Involvement  . . . . . . .   247

Part V  Oculomotility

Chapter 14

Cerebral Control of Eye Movements

Charles Pierrot-Deseilligny

14.1Introduction  . . . . . . .   254

14.2Brainstem  . . . . . . . .   255

Contents XV

14.2.1Horizontal Eye Movements    255

14.2.1.1

Final Common Pathway 

.

.  255

14.2.1.2

Premotor Structures

 

 

 

and Afferent Pathways   .

 

.   257

14.2.2

Vertical Eye Movements 

.

.  259

14.2.2.1

Final Common Pathway 

.

.  259

14.2.2.2

Premotor Structures

 

 

 

and Brainstem Afferents  

 

.   259

14.3

Suprareticular Structures 

 

.   261

14.3.1Cerebellum  . . . . . . . .  261

14.3.2Cerebral Hemispheres  . . .  262

14.4Abnormal Eye Movements    263

14.4.1Nystagmus  . . . . . . . .  263

14.4.2Non-Nystagmic Abnormal

Eye Movements  . . . . . .  264

Chapter 15

Chronic Progressive External

Ophthalmoplegia – A Common

Ocular Manifestation

of Mitochondrial Disorders

Marcus Deschauer, Stephan Zierz

15.1Introduction  . . . . . . .   267

15.2

Clinical Features  . . . . .   268

15.2.1Ophthalmoplegia

and Ptosis  . . . . . . . .   268

15.2.2CPEO Plus: Multisystemic Involvement  . . . . . . .   268

15.2.2.1

Muscle Impairment 

. . .

.  268

15.2.2.2

Visual Impairment 

. . .

.   268

15.2.2.3Specific CPEO Plus

Syndromes  . . . . . . . .  268

15.3Genetics  . . . . . . . . .  270

15.3.1General Mitochondrial

Genetics  . . . . . . . . .  270

15.3.2Single Deletions of mtDNA    270

15.3.3Defects of Intergenomic Communication with Multiple Deletions

of mtDNA  . . . . . . . .   271

15.3.4Point Mutations

of mtDNA  . . . . . .

.

.   272

15.3.5 Coenzyme Q Deficiency 

.

.  273

15.3.6Genotype–Phenotype Correlation  . . . . . . . .  273

15.4Diagnostics  . . . . . . . .  274

15.4.1Myohistological

Investigations  . . . . . .   275

15.4.2Biochemical Investigations    275

15.4.3Molecular Genetic Investigations  . . . . . .   275

15.5Treatment  . . . . . . . .   276

15.5.1Pharmacological Therapy  .   276

15.5.2 Symptomatic Treatment   .   277

15.5.3Gene Therapy   . . . . . .   277

15.6

Differential Diagnosis   . . .  278

15.6.1Oculopharygeal Muscular Dystrophy   . . . . . . . .  278

15.6.2 Myasthenic Syndromes   . .  278

15.6.3Congenital Fibrosis

 

of the Extraocular Muscles  

279

15.6.4

Ocular Myositis  . . . . .

.  279

15.6.5

Endocrine

 

 

Ophthalmopathy  . . . .

.  279

15.6.6Myotonic Dystrophy   . . .   279

15.6.7Facioscapulohumeral

Muscular Dystrophy  . . . .  279

15.6.8Congenital Myopathies  . .   279

Chapter 16

Treatment of Specific Types

of Nystagmus

Marianne Dieterich

16.1Introduction  . . . . . . .   284

16.2Peripheral Vestibular

and Ocular Motor Disorders    284

16.2.1Acute Peripheral Vestibulopathy, Vestibular

Neuritis  . . . . . . . . .   284

16.2.1.1Etiology  . . . . . . . . .   286

16.2.1.2Therapeutic

Recommendations  . . . .   287

16.2.2Superior Oblique

Myokymia  . . . . . . . .   288

16.2.2.1Etiology  . . . . . . . . .   288

16.2.2.2Therapeutic

Recommendations  . . . .   288

16.3Supranuclear Ocular Motor Disorders  . . . . . . . . .  289

16.3.1Central Vestibular Disorders    289 16.3.1.1 Vestibular Syndromes

in the Sagittal (Pitch) Plane     289

16.3.2Central Ocular Motor

Disorders  . . . . . . . . .  294

16.3.2.1Acquired Pendular

Nystagmus  . . . . . . . .  294

16.3.2.2Opsoclonus and Ocular

Flutter  . . . . . . . . . .  296

XVI Contents

Part VI  Rehabilitation

Chapter 17

Rehabilitation

in Neuroophthalmology

Susanne Trauzettel-Klosinski

17.1Introduction  . . . . . . .   301

17.2Psychophysics of Normal Reading  . . . . . . . . .   302

17.3Diseases of the Visual Pathways and their

 

Functional Deficits  . . .

 

.   303

17.3.1

Optic Neuropathies  . .

.

.  303

17.3.1.1

Central Scotomas  . . .

.

.  303

17.3.1.2

Arcuate Scotomas: Nerve

 

 

 

Fiber Bundle Defects  . .

 

.   305

17.3.1.3Ring Scotomas  . . . . . . . . . . . .  305

17.3.1.4Constricted Fields  . . . . .  305

17.3.1.5The Impact of Visual Field Defects on Reading

Performance  . . . . . . .  305

17.3.2Optic Chiasmal Syndromes    307

17.3.3Suprachiasmatic Lesions

of the Visual Pathways  . . .  307

17.3.3.1Hemianopic Reading

Disorder  . . . . . . . . .  308

17.3.3.2Hemianopic Orientation Disorder  . . . . . . . . .  310

17.3.4Cortical Visual Impairment    311

17.4Diagnostic Procedures

to Examine Reading Ability    311

17.5Rehabilitation Programs  . .  312

17.5.1Visual Aids in Reading

Disorders  . . . . . . . . .  312

17.5.2Visual and Other Aids in Spatial Orientation

Problems  . . . . . . . . .  313

17.5.3Training  . . . . . . . . .   314

17.5.3.1 Training for Patients with Circumscribed Scotomas in the Central

Field  . . . . . . . . . . .  314

17.5.3.2Training for Patients with Homonymous Field

Defects  . . . . . . . . .   315

17.5.4Counseling Regarding

Public Support  . . . . . . . . . . . .  316

17.6Summary and Conclusions    316

Subject Index  . . . . . . . . .  321

Contributors

Ludwig Aigner, Prof. Dr.

François-Xavier Borruat, MD, PD, MER

Klinik und Poliklinik für Neurologie

Department of Neuro-Ophthalmology

der Universität Regensburg

Hôpital Ophtalmique Jules Gonin

Im Bezirksklinikum

Avenue de France 15

Universitätsstraße 84

CH-1004 Lausanne

93053 Regensburg

Switzerland

Germany

 

 

Marcus Deschauer, Priv.-Doz. Dr.

Anthony C. Arnold, MD, Prof.

Neurologische Klinik

Neuro-Ophthalmology Division

der Universität Halle-Wittenberg

Director, UCLA Optic Neuropathy Center

Ernst-Grube-Straße 40

Jules Stein Eye Institute

06097 Halle/Saale

UCLA Department of Ophthalmology

Germany

100 Stein Plaza

 

Los Angeles, CA 90095-7005

Marianne Dieterich, Prof. Dr.

USA

Neurologische Klinik, Universität Mainz

 

Langenbeckstraße 1

Edward J. Atkins, MD

55101 Mainz

Division of Neurology

Germany

University of Saskatchewan

 

RUH Box 239

Marc Dinkin, MD

103 Hospital Drive

Brigham and Women’s Hospital

Saskatoon, SK, S7N 0W8

75 Francis Street

Canada

Boston, MA 02115

Michelle Banks, MD

USA

 

100 Stein Plaza

Mark W. Greenlee, Prof. Dr.

Los Angeles, California

Institut für Experimentelle Psychologie

USA

Universität Regensburg

 

Universitätsstraße 31

Valérie Biousse, MD, Prof.

93053 Regensburg

Departments of Ophthalmology and Neurology

Germany

Emory University

 

Neuro-ophthalmology Unit

Stephan Grewe, Dr.

Emory Eye Center

Institut für Experimentelle Ophthalmologie

1365-B Clifton Road, NE, Atlanta, Georgia 30322

Klinik und Poliklinik für Augenheilkunde

USA

Domagkstraße 15

 

48149 Münster

 

Germany

XVIII Contributors

Yan Guex-Crosier, MD, PD, MER

Ocular Immunology and Inflammation Unit Jules Gonin Eye Hospital

15 av. de France CH 1004 Lausanne Switzerland

Jennifer K. Hall, MD

Scheie Eye Institute

University of Pennsylvania Department

of Ophthalmology

51 North 39th Street

Philadelphia, Pennsylvania 19104

USA

Michael B. Hoffmann, Dr.

Universitäts-Augenklinik

Visual Processing Laboratory

Leipziger Straße 44

39120 Magdeburg

Germany

Claudia Karl, Dr.

Institut für Neurologie

Universität Regensburg

Germany

Aki Kawasaki, MD, MER

Department of Neuro-ophthalmology Hôpital Ophtalmique Jules Gonin Avenue de France 15

1004 Lausanne Switzerland

Birgit Lorenz, MD, FEBO, Prof.

Klinik und Poliklinik für Augenheilkunde Universitätsklinikum Gießen und Marburg GmbH, Standort Gießen

Friedrichstraße 18 35392 Gießen Germany

Tim D. Matthews, MBBS, FRCS, FRCOphth

Department of Ophthalmology

Selly Oak Hospital

Raddlebarn Rd

Birmingham B29 6 JD

UK

Nancy J. Newman, MD, Prof.

Departments of Ophthalmology Neurology, and Neurological surgery

Emory University, Neuro-ophthalmology Unit Emory Eye Center

1365-B Clifton Road, NE, Atlanta Georgia 30322 USA

Charles Pierrot-Deseilligny, MD, Prof.

Hôpital La Pitié-Salpêtrière 47-83, Boulevard de l'Hôpital 75651 Paris Cedex 13 France

Joseph F. Rizzo III, MD, Prof.

Massachussetts Eye and Ear Infirmary Department of Neuro-Ophthalmology 243 Charles Street, 9th FL

Boston, MA 02114 USA

Tobias Stupp, PD, Dr.

Institut für Experimentelle Ophthalmologie Klinik und Poliklinik für Augenheilkunde Domagkstraße 15

48149 Münster Germany

Solon Thanos, Prof. Dr.

Institut für Experimentelle Ophthalmologie Klinik und Poliklinik für Augenheilkunde Domagkstraße 15

48149 Münster Germany

Susanne Trauzettel-Klosinski, Prof. Dr.

Augenklinik der Universität Tübingen Schleichstraße 12–16

72076 Tübingen Germany

Peter U. Tse. Dr.

Institute für Experimentelle Psychologie der Universität Regensburg

93053 Regensburg Germany

Contributors XIX

Nicholas J. Volpe. MD, Prof.

Stephan Zierz, Prof., Dr.

Scheie Eye Institute

Neurologische Universitätsklinik

University of Pennsylvania Department

Ernst-Grube-Straße 40

of Ophthalmology

06120 Halle (Saale)

51 North 39th Street

Germany

Philadelphia, Pennsylvania 19104

 

USA

 

Marcela Votruba, MA, BM, BCh, FRCOphth, PhD

 

School of Optometry & Vision Science

 

Cardiff University

 

Maindy Road

 

Cathays

 

Cardiff CF24 4LU

 

UK

 

Part  I

Optic Nerve

Chapter 1

 

Optic Neuritis

1

and Multiple Sclerosis

Edward J. Atkins, Valérie Biousse, Nancy J. Newman

Core Messages

Idiopathic optic neuritis, an isolated inflammatory optic neuropathy secondary to demyelination, is the most common cause of optic neuropathy in the young and is often the first sign of multiple sclerosis (MS).

It is now possible to predict the risk of subsequent MS in selected patients with optic neuritis, allowing the anticipatory use of immunomodulatory agents to reduce the risk and severity of MS in those patients.

A number of recent studies have clarified the natural history of optic neuritis, the largest being the Optic Neuritis Treatment Trial (ONTT).

The ONTT confirmed that spontaneous visual recovery begins rapidly (within 3 weeks) in about 80% of patients and continues for up to 1 year; if at least some improvement does not occur within 5 weeks, the diagnosis of idiopathic optic neuritis should be reconsidered.

The initial magnetic resonance imaging (MRI) helps to stratify the risk of MS. In the ONTT, the 10-year risk of MS in patients with at least one MRI T2 lesion was 56%, as compared to 22% in those with a normal baseline MRI. A normal MRI in combination with painless optic neuritis, severe optic nerve head edema, peripapillary hemorrhages, or a macular star defines a very low MS risk subgroup.

In the ONTT, treatment with a lower dose of oral corticosteroids (1 mg/kg per day) was associated with an increased risk of recurrent optic neuritis, with a 41% chance of recurrence at 5 years among patients who received oral prednisone, versus 25% for those who received highdose intravenous methylprednisolone (1000 mg/day) or placebo.

High-dose steroids hasten the rate, but not the final extent, of visual recovery in optic neuritis, and the decision to use this therapy should be individualized.

Interferon beta-1a or beta-1b therapy should be considered in selected highrisk patients.