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Prognosis and Treatment of Visual Field Defects Aniruddha Agarwal, MD1
Sachin Kedar, MD1,2
1 Department of Ophthalmology and Visual Sciences, Stanley M.
Truhlsen Eye Institute, Omaha, Nebraska 2 Department of Neurological Sciences, University of Nebraska Medical Center, Omaha, Nebraska
Address for correspondence Sachin Kedar, MD, Department of Neurological Sciences, 985540 Nebraska Medical Center, Omaha, NE 68154 (e-mail: [email protected]).
Abstract
Keywords
► ► ► ► ► ►
visual field defect hemianopia driving rehabilitation quality of life reading
Visual field deficits are common in neurologic disease conditions such as cerebrovascular disease, traumatic brain injury, and brain tumors. Loss of visual fields may lead to impairment of reading skills (hemianopic dyslexia) and limitations of daily activities such as driving, which can have a significant impact on an individual’s socioeconomic status and quality of life. Moreover, patients with motor deficits from neurologic diseases have a 20% decreased likelihood of achieving independence in ambulation and self-care activities with coexisting hemianopia. Studies on the natural history of homonymous hemianopia have shown that spontaneous improvement of visual fields may occur in less than 40% of individuals early in the disease process. Improvement is usually incomplete, which implies that a significant number of individuals will be left with a disabling visual deficit. Although several methods of rehabilitation (optical, compensatory, and restitution therapy) are used in practice, none, unfortunately, have shown consistent and significant benefits. In this review, the authors focus on the natural history, impact, prognosis, and treatment modalities for neurologic field defects.
Visual field (VF) deficits result from diseases involving visual pathways. They can adversely affect activities of daily living, as well as leisure and social activities, and thus compromise quality of life and socioeconomic status. Visual field deficits account for a significant proportion of legal blindness among individuals with neuro-ophthalmic diseases.1 Increasing severity of VF loss is associated with higher odds of disability, and reduced vision-related function and physical activity. In a large, population-based National Health and Nutrition Examination (NHANES) Survey, activities relying on peripheral vision such as driving were found to be most compromised in individuals with VF loss.2 Patients with compromised vision have a higher prevalence of mental health disorders, and as many as 13.5% individuals above 75 years of age may suffer from depression secondary to poor vision.3 Visual field loss leads to increased fear of falling,4 poor socioeconomic performance,5 reduced higher cognitive functions such as visuospatial imaging capability,6 and increased psychosocial comorbidities.7
Issue Theme Neuro-Ophthalmology; Guest Editor: Beau B. Bruce, MD, PhD
In this review, we will evaluate the natural history, real-life impact, and treatment (rehabilitation) options for VF deficits resulting from neurologic conditions.
Ophthalmologic Diseases Associated with Visual Field Defects Although detailed description of ophthalmologic diseases is beyond the scope of this article, two common ophthalmic diseases that frequently coexist in patients with neurologic diseases and produce significant VF deficits are briefly summarized.
Age-Related Macular Degeneration Age-related macular degeneration (AMD) is the leading cause of central visual loss and legal blindness in patients over the age of 65 years.8,9 Complications such as choroidal neovascularization and pigment epithelial detachments account for 90% cases with severe visual loss.10 Patients with choroidal neovascularization are at risk for retinal thickening,
Copyright © 2015 by Thieme Medical Publishers, Inc., 333 Seventh Avenue, New York, NY 10001, USA. Tel: +1(212) 584-4662.
DOI http://dx.doi.org/ 10.1055/s-0035-1563573. ISSN 0271-8235.
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hemorrhage, and scarring from the new choroidal vessels, which is also called wet age-related macular degeneration. Patients with AMD have decreased mobility, spend less time in moderate-to-robust physical activity, and are less likely to spend time out of home.11 Depression and mood disorders are a significant problem in elderly patients affected by AMD.12 Recent advances in management, such as anti-VEGF agents, have improved the outlook for patients with wet AMD.
Optic Neuritis In the Optic Neuritis Treatment Trial (ONTT), VF defects were seen in 100% of affected eyes and 69% of fellow eyes at baseline. Common VF defects included diffuse visual field loss (48%), altitudinal defects (15%), central or cecocentral scotoma (8.3%), and arcuate defects (5%).21 At 1-year followup, VFs were normal in 56% of affected eyes and 69% of fellow eyes.22 Although visual field deficits are common, they are not commonly used to guide treatment of demyelinating optic neuritis.
Glaucoma Glaucomatous VF defects tend to respect the horizontal meridian13 and include a wide variety of defects, such as arcuate, nasal step, and sectoral field loss.14,15 Loss of the superior hemifield in patients with glaucoma has been shown to affect near activity, whereas inferior VF loss impacts general and peripheral vision.16 Higher grades of VF loss in patients with glaucoma are associated with lower scores on quality-of -life indices.17 Visual field assessment is the most important indicator for disease progression and treatment of this condition.
Neurologic Diseases Associated with Visual Field Defects Visual field deficits in neurologic diseases can occur either in isolation or in combination with other neurologic deficits.18 Although the patterns of VF defects aid in lesion localization, they are not pathognomonic for specific disease entities.19,20
Optic Nerve Disorders Optic neuropathy can present with myriad VF defects, summarized in ►Table 1. Although these are not pathognomonic for any particular disease condition, they occur as a result of the retinotopic arrangement of the retinal ganglion cells and nerve fibers. Below we discuss some of the common conditions seen in practice.
Papilledema Papilledema from raised intracranial pressure leads to blind spot enlargement in the early stages. Untreated papilledema can result in progressive VF loss, which includes nasal step defect, arcuate field defect, and constriction and generalized depression of the field. In patients with idiopathic intracranial hypertension, more than 90% of patients will demonstrate VF defects, whereas 5 to 10% of untreated cases result in blindness.23 Visual field monitoring is important in deciding the urgency of treatment of papilledema.
Anterior Ischemic Optic Neuropathy Visual field defects in nonarteritic ischemic optic neuropathy (NAION) include altitudinal, arcuate, and central defects. In a large cohort study of the natural history of visual outcomes in patients with NAION, visual field improvement at 6-month follow-up was noted in 24% (40/168) and worsening in 13% (16/168) of NAION patients with moderate to severe visual field loss at presentation. Most of the visual field fluctuation (improvement or deterioration) occurred from disease onset to the resolution of optic disc edema. Very little change in visual field defect was noted after 6-month follow-up.24 Rehabilitation of VF defects is currently the only option to improve quality of life in patients with ischemic optic neuropathy.
Table 1 Anatomical basis for patterns of visual field loss in optic nerve diseases25 Pattern of field loss
Characteristics
Anatomical basis of field loss
Enlargement of blind spot
Decreased visual function extending beyond the margins of physiologic blind spot
Edema of optic nerve head resulting in displacement of retinal nerve fibers
Central/cecocentral scotoma
Visual loss involving fixation and extending to the blind spot
Involvement of the papillomacular bundle
Arcuate defect
Visual loss occurring along an arc in the superior or inferior quadrants
Pathology affecting arcuate retinal nerve fibers
Altitudinal defect
Much more extensive arcuate visual loss involving 2 quadrants superiorly or inferiorly
Broader pathology affecting arcuate retinal nerve fibers
Wedge defects (temporal)
Field loss with a broader periphery narrowing toward the blind spot
Pathologic involvement of the nasal arcuate bundle
Nasal step
Scotoma within the nasal visual field with reduced sensitivity on one side of the horizontal raphe and normal sensitivity on the other
Inferior arcuate fibers (more commonly) may be affected more than the superior arcuate fibers
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Visual field defects in disorders of the chiasm respect the vertical meridian and include bitemporal scotoma, quadrantanopia, hemianopia, and junctional scotoma, depending on the position of the lesion with respect to the chiasm.25,26 Common pathologies of the optic chiasm include compression from a pituitary adenoma, parasellar meningioma, or craniopharyngioma.27 Visual field improvement occurs in three stages following surgical resection of pituitary tumors: early fast phase (few days to a week), phase of slow recovery (few weeks to months), and late phase (few months to years).28 Reduced retinal nerve fiber layer thickness and ganglion cell area measurements as well as decreased ganglion cell function (PhNR/b-wave amplitude ratio on the electroretinogram) are indicators for poor postoperative VF recovery in patients with compression of the chiasm from a pituitary adenoma.29
Retrochiasmal Disorders Stroke and traumatic brain injury are the commonest causes of homonymous hemianopia in adults, whereas traumatic brain injury and tumors are more common in children.30 Homonymous hemianopia can be seen in approximately 20% of patients with stroke, which makes it an important neurologic deficit in this group of patients.31
Natural History of Retrochiasmal Visual Field Defects Spontaneous recovery of VFs may be seen in patients with neurologic diseases within the first few months of disease occurrence. The extent of recovery is variable and depends on the magnitude of initial damage, nature of the underlying disease, and topographic location of the lesion. In a retrospective study of the natural history of homonymous hemianopia, spontaneous recovery was noted in 38%, with most of the improvement (60%) being seen in the first month of the neurologic insult.18 Recovery is frequently incomplete and limited to the VF periphery.32 Recovery also seems to be dependent on the site of the lesion, with better chances of recovery in patients with lesions outside the occipital lobe.33 Besides reversibility of the underlying disease process, there is indirect evidence to show that neuroplasticity may play a role in VF improvement. Activation of ipsilateral and contralateral cortical and subcortical visual areas are seen on functional neuroimaging of patients with VF recovery.34 Experience-dependent modifications of the neuronal circuitries implying neuroplasticity were demonstrated in the mammalian and rodent visual systems. Proposed mechanisms include epigenetic alteration of chromatin structure, leading to modification of synaptic connectivity and neural circuitry in the mammalian striate cortex35,36 and remodeling of neuronal pathways.36,37
Impact of Visual Field Defects Quality of Life Depending on the neurologic and ophthalmic disease process, VF loss varies greatly in extent, severity, and potential for
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reversibility, and thus impacts activities of daily living and socioeconomic well-being. Several large population-based studies have demonstrated greater loss of functional ability and increased psychological stress with more severe VF defects.2,38,39 Lower scores on the National Eye Institute Visual Functioning Questionnaire (NEI-VFQ) were noted in patients with VF defects compared with healthy subjects.40,41 Visual difficulties in these patients are frequently compounded by additional deficits, such as impaired light sensitivity, color vision anomalies, and decreased depth perception, which significantly affects mobility in complex environments.42 Subjects may have to depend on gaze adaptation to perform activities of daily living such as shopping in supermarkets.43
Impact on Reading Patients with homonymous VF defects experience varying degrees of difficulty in reading despite normal language function. This acquired reading disorder is called hemianopic dyslexia, which results from an inability to plan and guide reading eye movements.44 Certain VF characteristics are associated with worse reading outcomes, including parafoveal and /or foveal field involvement, bilateral VF defects, right-sided unilateral homonymous field defects, complete hemianopia, and central scotoma. Reading difficulty in leftsided VF defects are secondary to impaired eye movements to the beginning of the next line, whereas right-sided VF defects cause abnormalities of fixation, regressive saccades, and reduced saccades into the blind field.45
Impact on Motor Rehabilitation Visual field defects adversely impact the recovery of patients with additional neurologic deficits such as motor and/or sensory deficits.46 Using life table analyses in patients with motor deficits from hemispheric stroke, the likelihood of achieving independence in ambulation and self-care activities (Barthel index 60) was shown to decrease by more than 20% in the presence of a homonymous hemianopia.47
Impact on Driving Patients with VF defects may experience difficulty in driving and increased risk of traffic accidents compared with normal individuals due to decreased perception of visual stimuli.48 Visual field defects also affect steering stability and risks of collision.49 Visual field defects may thus restrict the outdoor activities of patients, making them homebound, which has a significant economic impact due to inability to work and increased caregiver costs.50 Patients may have to depend on others for activities such as doctors’ visits and grocery shopping. Driver licensing authorities have set basic minimum requirements for issuance and maintenance of driving privileges to ensure safety and minimize risks. Unfortunately, there is no uniformity of these criteria or protocols for standardized VF testing during the application for a driver’s license at local, state, national, or international levels. The international requirements of VF for driving are listed in ►Table 2.50,51 Seminars in Neurology
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Table 2 Visual field requirements for driver’s licensing (except USA) Country
Visual Field Criteria
Australia
Horizontal: 120 degrees by confrontation method
European Union
At least 120 degrees, without diplopia
Japan
150-degree field of view
South Africa
Normal field of vision
United Kingdom
At least 120 degrees without loss of central 20-degree field
United States
Varies by state
Source: Based on the survey conducted by the International Council of Ophthalmology (ICO) in December 2005.51
The driving license requirements within the United States vary from one state to another. Certain states such as California have no restrictions on driver’s licenses based on VF criteria, while others have strict monocular and/or binocular field criteria (see ►Table 3). A detailed discussion about the specific rules and regulations pertaining to the testing methods, outcomes, and reporting requirements is beyond the scope of this text. Readers are encouraged to review the specific testing and reporting rules for their states.
Rehabilitation of Patients with Visual Field Defects Rehabilitation is the cornerstone of management in patients with irreversible VF defects from neurologic diseases. Reha-
bilitation strategies are aimed at providing patients with tools to achieve functional independence. The three broad strategies for treatment and rehabilitation are summarized in ►Table 4 and described in the following sections.
Optical Therapies Optical therapies aim to shift the incident rays of light to noninvolved areas of the VF. The most commonly used device is the prism, which may be fitted over one or both eyes.65,66 Prisms work by changing the path of light from blind areas of the VF toward seeing areas by placing the base of prism toward the hemianopic field. To preserve central vision, the prism is usually displaced 1 to 2 mm away from the pupillary center. Sectoral and peripheral monocular prisms and obliquely oriented prisms (angled at 30 degrees) appear
Table 3 Visual field requirements for driver’s licensing within USA52 State
Visual field criteria
Alabama
110-degree field of view
Alaska
There is no visual field requirement for licensing.
Arizona
70-degree field of view and 35-degree nasal field
Arkansas
Both eyes 105 degrees
California
There is no visual field requirement for licensing.
Colorado
Unspecified (minimum horizontal fields)
Connecticut
100-degree monocular and 140-degree binocular
Delaware
There is no visual field requirement for licensing.
District of Columbia
130 degrees both eyes (may be approved by Director at 110 degrees)
Florida
130-degree horizontal field of view
Georgia
140 degrees each eye and 140 degrees both eyes
Hawaii
70-degree field of vision
Idaho
There is no visual field requirement for licensing.
Illinois
105 degrees for one eye and 140 degrees for both eyes
Indiana
70 degrees for one eye and 120 degrees for both eyes
Iowa
140 degrees for both eyes (with outside mirrors: 70 degrees temporal and 45 degrees nasal for one eye; 115 degrees for both eyes. If less than 95 degrees both eyes and 60 degrees temporal and 35 degrees nasal for one eye, the patient needs recommendation.)
Kansas
55 degrees monocular and 110 degrees binocular
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Table 3 (Continued) State
Visual field criteria
Kentucky
Binocular horizontal field of 35 degrees and binocular vertical field of 25 degrees from fixation
Louisiana
There is no minimum visual field requirement.
Maine
110 degrees for both eyes
Maryland
140 degrees for unrestricted license and 110 degrees for restricted license
Massachusetts
120-degree field of view 110-degree to 140-degree field 105-degree field of view
Mississippi
140-degree field of view; one eye 70 degrees temporal; 35 degrees nasal with 2 outside mirrors
Missouri
Binocular field: minimum 55 degrees; monocular: 85 degrees for restricted license
Montana
There is no requirement for private car drivers.
Nebraska
140 degrees for both eyes; denied at less than 100 degrees
Nevada
Unrestricted: binocular 140 degrees; restricted: 110–140 degrees
New Hampshire
There is no visual field requirement for licensing.
New Jersey
There is no visual field requirement for licensing.
New Mexico
120 degrees; 30 degrees in nasal field of one eye
New York
Minimum 140-degree field of view
North Carolina
60 degrees in one eye (30 degrees on each side)
North Dakota
Both eyes 105 degrees
Ohio
Each eye 70-degree temporal field
Oklahoma
Both eyes 70-degree horizontal field
Oregon
110 degrees in horizontal field (one or both eyes)
Pennsylvania
120 degrees both eyes
Rhode Island
115 degrees in horizontal meridian and 40 degrees for one eye nasally
South Carolina
There is no visual field requirement for licensing.
South Dakota
There is no visual field requirement for licensing.
Tennessee
Only professional drivers require field testing.
Texas
There is no visual field requirement for licensing.
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Michigan Minnesota
Utah
120-degree horizontal field; 20-degree vertical and 90 degrees with restrictions
Vermont
Both eyes should be a minimum of 60 degrees.
Virginia
100-degree monocular and binocular; 70-degree monocular and binocular (daytime only); 40 degrees or better temporal and 30 degrees or better nasal in one eye only
Washington
110 degrees in horizontal meridian (monocular and binocular)
West Virginia
There is no visual field requirement.
Wisconsin
70-degree field of vision
Wyoming
Minimum 120-degree field of view
Note: The table is meant for educational purposes only and should not be construed to represent the legal requirements for the jurisdictions represented. For individual state rules and regulations pertaining to the testing methods, outcomes, and reporting requirements, the readers are encouraged to visit the website for the department of motor vehicles (DMV) for their states.
more beneficial, as they can contribute to expansion of the VF (up to 20 degrees) and allow patients to drive legally in certain states.67,68 Although compliance rates with prisms is approximately 47%,66,67 efficacy of this technique has not been studied in controlled trials. In a recent comparative study, peripheral prism glasses demonstrated higher efficacy
in obstacle avoidance and improvement in mobility compared with sham glasses.69
Restorative Therapies Restorative therapies attempt to restore visual function in the area of VF defects. These strategies employ stimuli in the Seminars in Neurology
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Table 4 Rehabilitative approaches for patients with visual field defects53,54 Optical therapy Prisms
Restorative therapy
55,56
Visual search training
Customized devices
55
Compensatory therapy 54,57
Saccadic eye movement training58
59–61
Ocular movement training62,63
Visual field restitution
Adapted glasses54
Optokinetic therapy63
Eye patches53
Use of visual cues64
Contrast sensitivity training59
Environmental modification
53
Fusional training54
Table 5 Rehabilitative treatments for visual field defects based on the pattern of visual loss Pattern of field defect
Treatment strategies
Blind spot enlargement
Considered ubiquitous in papilledema7; treatment not necessary unless encroaching upon fixation77,78
Central/ring scotoma
Optical assistance with magnification or size scaling79,80 Microperimetry-assisted identification of preferential retinal locus81–83 Biofeedback and training84
Cecocentral scotoma
Eccentric viewing training85 Visual restitution therapy60 Functional training86
Hemianopia
Optical modalities such as monocular or binocular prisms55,66,67 Saccadic compensation training87 Restorative training71
damaged field of vision usually at the borders of field defect or deep into the blind field70 using specifically designed computer-based software. One such example is the visual restitution therapy (VRT) by NovaVision AG (Magdeburg, Germany).71 The hypothesis supporting the therapy is that repeated stimuli above threshold intensity can reactivate neurons, restoring visual function, even with 10 to 15% surviving neurons.1 However, this modality is not universally accepted, largely because of significant discordance between subjective response and results of standard perimetry.1,72 Visual restitution therapy is also an expensive option for the patient, with an estimated cost of $6,000 for 6 months of therapy.73
Compensatory Therapies Compensatory therapies utilize strategies based on oculomotor mechanisms to improve visual function in the affected area. For example, saccadic training involves increasing amplitude and frequency of saccades to increase the chance of visual stimuli falling within the noninvolved half of the VF. In a randomized trial in patients with hemianopia, explorative saccade training for 6 weeks improved search behavior and scene exploration on the blind side as compared with flickerstimulation training.74 Audiovisual training may induce a more organized pattern of explorative behavior.75 Other training techniques include systematic scanning with increased head movements to avoid obstacles.76 Compensatory therapies have been proposed as the preferred approach to rehabilitate hemianopic dyslexics. Interested readers are
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directed to a more detailed review of the various treatment options in patients with hemianopic dyslexia.44 Treatment strategies can be varied based on the etiology, pattern and severity of VF loss (►Table 5). However, evidence to support beneficial effects from any of these techniques in patients with hemianopia is insufficient and prevents generalizability of treatment recommendations at present.54
Conclusions Neurologic VF defects adversely affect socioeconomic status, mental well-being, and quality of life through impairment of reading, navigation, and driving. Coexistence of hemianopia decreases the chance of independent ambulation in patients with motor deficits. Current methods to rehabilitate homonymous hemianopia using optical, compensatory, and restorative strategies have met with limited success. The socioeconomic burden and poor quality of life in this group of patients makes the need for development of newer techniques based on an understanding of neuroplasticity in the visual system urgent.
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impairments and functional outcomes poststroke. Arch Phys Med Rehabil 2000;81(10):1357–1363 Reding MJ, Potes E. Rehabilitation outcome following initial unilateral hemispheric stroke. Life table analysis approach. Stroke 1988;19(11):1354–1358 Lövsund P, Hedin A, Törnros J. Effects on driving performance of visual field defects: a driving simulator study. Accid Anal Prev 1991;23(4):331–342 Coeckelbergh TR, Brouwer WH, Cornelissen FW, Van Wolffelaar P, Kooijman AC. The effect of visual field defects on driving performance: a driving simulator study. Arch Ophthalmol 2002;120(11): 1509–1516 Bron AM, Viswanathan AC, Thelen U, et al. International vision requirements for driver licensing and disability pensions: using a milestone approach in characterization of progressive eye disease. Clin Ophthalmol 2010;4:1361–1369 Visual standards vision requirements for driving safety with emphasis on individual assessment. Report prepared for the International Council of Ophthalmology. 2005. Available at: http://www.icoph.org/dynamic/attachments/resources/visionfordriving.pdf. Accessed March 31, 2015 Physician’s Guide to Assessing and Counseling Older Drivers 2010. Available at: www.nhtsa.gov/staticfiles/nti/older_drivers/pdf/ 811298.pdf. Accessed March 31, 2015 Kerkhoff G. Restorative and compensatory therapy approaches in cerebral blindness - a review. Restor Neurol Neurosci 1999;15(23):255–271 Pollock A, Hazelton C, Henderson CA, et al. Interventions for visual field defects in patients with stroke. Cochrane Database Syst Rev 2011;(10):CD008388 Rowe FJ, Wright D, Brand D, et al. A prospective profile of visual field loss following stroke: prevalence, type, rehabilitation, and outcome. Biomed Res Int 2013;2013:719096 Rossi PW, Kheyfets S, Reding MJ. Fresnel prisms improve visual perception in stroke patients with homonymous hemianopia or unilateral visual neglect. Neurology 1990;40(10): 1597–1599 Nelles G, Pscherer A, de Greiff A, et al. Eye-movement traininginduced plasticity in patients with post-stroke hemianopia. J Neurol 2009;256(5):726–733 Gold DR, Grover LL. Treatment of homonymous visual field defects. Curr Treat Options Neurol 2012;14(1):73–83 Schreiber A, Vonthein R, Reinhard J, Trauzettel-Klosinski S, Connert C, Schiefer U. Effect of visual restitution training on absolute homonymous scotomas. Neurology 2006;67(1):143–145 McFadzean RM. NovaVision: vision restoration therapy. Curr Opin Ophthalmol 2006;17(6):498–503 Mueller I, Mast H, Sabel BA. Recovery of visual field defects: a large clinical observational study using vision restoration therapy. Restor Neurol Neurosci 2007;25(5-6):563–572 Trauzettel-Klosinski S. [Visual rehabilitation training for homonymous field defects]. Ophthalmologe 2012;109(5):496–500 Spitzyna GA, Wise RJ, McDonald SA, et al. Optokinetic therapy improves text reading in patients with hemianopic alexia: a controlled trial. Neurology 2007;68(22):1922–1930 Das A, Tadin D, Huxlin KR. Beyond blindsight: properties of visual relearning in cortically blind fields. J Neurosci 2014;34(35): 11652–11664 Peli E. Field expansion for homonymous hemianopia by optically induced peripheral exotropia. Optom Vis Sci 2000;77(9):453–464 Bowers AR, Keeney K, Peli E. Community-based trial of a peripheral prism visual field expansion device for hemianopia. Arch Ophthalmol 2008;126(5):657–664
peripheral prism glasses for hemianopia. Optom Vis Sci 2009; 86(5):492–502 Goodwin D. Homonymous hemianopia: challenges and solutions. Clin Ophthalmol 2014;8:1919–1927 Bowers AR, Keeney K, Peli E. Randomized crossover clinical trial of real and sham peripheral prism glasses for hemianopia. JAMA Ophthalmol 2014;132(2):214–222 Schofield TM, Leff AP. Rehabilitation of hemianopia. Curr Opin Neurol 2009;22(1):36–40 Kasten E, Wüst S, Behrens-Baumann W, Sabel BA. Computer-based training for the treatment of partial blindness. Nat Med 1998;4(9): 1083–1087 Watanabe K, Shinoda K, Kimura I, Mashima Y, Oguchi Y, Ohde H. Discordance between subjective perimetric visual fields and objective multifocal visual evoked potential-determined visual fields in patients with hemianopsia. Am J Ophthalmol 2007;143(2):295–304 Pelak VS, Dubin M, Whitney E. Homonymous hemianopia: a critical analysis of optical devices, compensatory training, and NovaVision. Curr Treat Options Neurol 2007;9(1):41–47 Roth T, Sokolov AN, Messias A, Roth P, Weller M, TrauzettelKlosinski S. Comparing explorative saccade and flicker training in hemianopia: a randomized controlled study. Neurology 2009; 72(4):324–331 Passamonti C, Bertini C, Làdavas E. Audio-visual stimulation improves oculomotor patterns in patients with hemianopia. Neuropsychologia 2009;47(2):546–555 Wood JM, McGwin G Jr, Elgin J, et al. Hemianopic and quadrantanopic field loss, eye and head movements, and driving. Invest Ophthalmol Vis Sci 2011;52(3):1220–1225 Corbett JJ, Jacobson DM, Mauer RC, Thompson HS. Enlargement of the blind spot caused by papilledema. Am J Ophthalmol 1988; 105(3):261–265 Wall M. Idiopathic intracranial hypertension. Neurol Clin 2010; 28(3):593–617 Amore FM, Silvestri V, Turco S, De Rossi F, Cruciani F. Rehabilitative approach in patients with ring scotoma. Can J Ophthalmol 2013; 48(5):420–426 Johnson A, Gurnsey R. Size scaling compensates for sensitivity loss produced by a simulated central scotoma in a shape-from-texture task. J Vis 2010;10(12):18 Altpeter EK, Blanke BR, Leo-Kottler B, Nguyen XN, TrauzettelKlosinski S. Evaluation of fixation pattern and reading ability in patients with Leber hereditary optic neuropathy. J Neuroophthalmol 2013;33(4):344–348 Pacella E, Pacella F, Mazzeo F, et al. Effectiveness of vision rehabilitation treatment through MP-1 microperimeter in patients with visual loss due to macular disease. Clin Ter 2012;163(6):e423–e428 Verboschi F, Domanico D, Nebbioso M, Corradetti G, Zaccaria Scalinci S, Vingolo EM. New trends in visual rehabilitation with MP-1 microperimeter biofeedback: optic neural dysfunction. Funct Neurol 2013;28(4):285–291 Verdina T, Giacomelli G, Sodi A, et al. Biofeedback rehabilitation of eccentric fixation in patients with Stargardt disease. Eur J Ophthalmol 2013;23(5):723–731 Gaffney AJ, Margrain TH, Bunce CV, Binns AM. How effective is eccentric viewing training? A systematic literature review. Ophthalmic Physiol Opt 2014;34(4):427–437 Sabel BA, Kasten E. Restoration of vision by training of residual functions. Curr Opin Ophthalmol 2000;11(6):430–436 Kerkhoff G, Münßinger U, Haaf E, Eberle-Strauss G, Stögerer E. Rehabilitation of homonymous scotomata in patients with postgeniculate damage of the visual system: saccadic compensation training. Restor Neurol Neurosci 1992;4(4):245–254
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Prognosis and Treatment of Visual Field Defects Aniruddha Agarwal, MD1
Sachin Kedar, MD1,2
1 Department of Ophthalmology and Visual Sciences, Stanley M.
Truhlsen Eye Institute, Omaha, Nebraska 2 Department of Neurological Sciences, University of Nebraska Medical Center, Omaha, Nebraska
Address for correspondence Sachin Kedar, MD, Department of Neurological Sciences, 985540 Nebraska Medical Center, Omaha, NE 68154 (e-mail: [email protected]).
Abstract
Keywords
► ► ► ► ► ►
visual field defect hemianopia driving rehabilitation quality of life reading
Visual field deficits are common in neurologic disease conditions such as cerebrovascular disease, traumatic brain injury, and brain tumors. Loss of visual fields may lead to impairment of reading skills (hemianopic dyslexia) and limitations of daily activities such as driving, which can have a significant impact on an individual’s socioeconomic status and quality of life. Moreover, patients with motor deficits from neurologic diseases have a 20% decreased likelihood of achieving independence in ambulation and self-care activities with coexisting hemianopia. Studies on the natural history of homonymous hemianopia have shown that spontaneous improvement of visual fields may occur in less than 40% of individuals early in the disease process. Improvement is usually incomplete, which implies that a significant number of individuals will be left with a disabling visual deficit. Although several methods of rehabilitation (optical, compensatory, and restitution therapy) are used in practice, none, unfortunately, have shown consistent and significant benefits. In this review, the authors focus on the natural history, impact, prognosis, and treatment modalities for neurologic field defects.
Visual field (VF) deficits result from diseases involving visual pathways. They can adversely affect activities of daily living, as well as leisure and social activities, and thus compromise quality of life and socioeconomic status. Visual field deficits account for a significant proportion of legal blindness among individuals with neuro-ophthalmic diseases.1 Increasing severity of VF loss is associated with higher odds of disability, and reduced vision-related function and physical activity. In a large, population-based National Health and Nutrition Examination (NHANES) Survey, activities relying on peripheral vision such as driving were found to be most compromised in individuals with VF loss.2 Patients with compromised vision have a higher prevalence of mental health disorders, and as many as 13.5% individuals above 75 years of age may suffer from depression secondary to poor vision.3 Visual field loss leads to increased fear of falling,4 poor socioeconomic performance,5 reduced higher cognitive functions such as visuospatial imaging capability,6 and increased psychosocial comorbidities.7
Issue Theme Neuro-Ophthalmology; Guest Editor: Beau B. Bruce, MD, PhD
In this review, we will evaluate the natural history, real-life impact, and treatment (rehabilitation) options for VF deficits resulting from neurologic conditions.
Ophthalmologic Diseases Associated with Visual Field Defects Although detailed description of ophthalmologic diseases is beyond the scope of this article, two common ophthalmic diseases that frequently coexist in patients with neurologic diseases and produce significant VF deficits are briefly summarized.
Age-Related Macular Degeneration Age-related macular degeneration (AMD) is the leading cause of central visual loss and legal blindness in patients over the age of 65 years.8,9 Complications such as choroidal neovascularization and pigment epithelial detachments account for 90% cases with severe visual loss.10 Patients with choroidal neovascularization are at risk for retinal thickening,
Copyright © 2015 by Thieme Medical Publishers, Inc., 333 Seventh Avenue, New York, NY 10001, USA. Tel: +1(212) 584-4662.
DOI http://dx.doi.org/ 10.1055/s-0035-1563573. ISSN 0271-8235.
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hemorrhage, and scarring from the new choroidal vessels, which is also called wet age-related macular degeneration. Patients with AMD have decreased mobility, spend less time in moderate-to-robust physical activity, and are less likely to spend time out of home.11 Depression and mood disorders are a significant problem in elderly patients affected by AMD.12 Recent advances in management, such as anti-VEGF agents, have improved the outlook for patients with wet AMD.
Optic Neuritis In the Optic Neuritis Treatment Trial (ONTT), VF defects were seen in 100% of affected eyes and 69% of fellow eyes at baseline. Common VF defects included diffuse visual field loss (48%), altitudinal defects (15%), central or cecocentral scotoma (8.3%), and arcuate defects (5%).21 At 1-year followup, VFs were normal in 56% of affected eyes and 69% of fellow eyes.22 Although visual field deficits are common, they are not commonly used to guide treatment of demyelinating optic neuritis.
Glaucoma Glaucomatous VF defects tend to respect the horizontal meridian13 and include a wide variety of defects, such as arcuate, nasal step, and sectoral field loss.14,15 Loss of the superior hemifield in patients with glaucoma has been shown to affect near activity, whereas inferior VF loss impacts general and peripheral vision.16 Higher grades of VF loss in patients with glaucoma are associated with lower scores on quality-of -life indices.17 Visual field assessment is the most important indicator for disease progression and treatment of this condition.
Neurologic Diseases Associated with Visual Field Defects Visual field deficits in neurologic diseases can occur either in isolation or in combination with other neurologic deficits.18 Although the patterns of VF defects aid in lesion localization, they are not pathognomonic for specific disease entities.19,20
Optic Nerve Disorders Optic neuropathy can present with myriad VF defects, summarized in ►Table 1. Although these are not pathognomonic for any particular disease condition, they occur as a result of the retinotopic arrangement of the retinal ganglion cells and nerve fibers. Below we discuss some of the common conditions seen in practice.
Papilledema Papilledema from raised intracranial pressure leads to blind spot enlargement in the early stages. Untreated papilledema can result in progressive VF loss, which includes nasal step defect, arcuate field defect, and constriction and generalized depression of the field. In patients with idiopathic intracranial hypertension, more than 90% of patients will demonstrate VF defects, whereas 5 to 10% of untreated cases result in blindness.23 Visual field monitoring is important in deciding the urgency of treatment of papilledema.
Anterior Ischemic Optic Neuropathy Visual field defects in nonarteritic ischemic optic neuropathy (NAION) include altitudinal, arcuate, and central defects. In a large cohort study of the natural history of visual outcomes in patients with NAION, visual field improvement at 6-month follow-up was noted in 24% (40/168) and worsening in 13% (16/168) of NAION patients with moderate to severe visual field loss at presentation. Most of the visual field fluctuation (improvement or deterioration) occurred from disease onset to the resolution of optic disc edema. Very little change in visual field defect was noted after 6-month follow-up.24 Rehabilitation of VF defects is currently the only option to improve quality of life in patients with ischemic optic neuropathy.
Table 1 Anatomical basis for patterns of visual field loss in optic nerve diseases25 Pattern of field loss
Characteristics
Anatomical basis of field loss
Enlargement of blind spot
Decreased visual function extending beyond the margins of physiologic blind spot
Edema of optic nerve head resulting in displacement of retinal nerve fibers
Central/cecocentral scotoma
Visual loss involving fixation and extending to the blind spot
Involvement of the papillomacular bundle
Arcuate defect
Visual loss occurring along an arc in the superior or inferior quadrants
Pathology affecting arcuate retinal nerve fibers
Altitudinal defect
Much more extensive arcuate visual loss involving 2 quadrants superiorly or inferiorly
Broader pathology affecting arcuate retinal nerve fibers
Wedge defects (temporal)
Field loss with a broader periphery narrowing toward the blind spot
Pathologic involvement of the nasal arcuate bundle
Nasal step
Scotoma within the nasal visual field with reduced sensitivity on one side of the horizontal raphe and normal sensitivity on the other
Inferior arcuate fibers (more commonly) may be affected more than the superior arcuate fibers
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Visual field defects in disorders of the chiasm respect the vertical meridian and include bitemporal scotoma, quadrantanopia, hemianopia, and junctional scotoma, depending on the position of the lesion with respect to the chiasm.25,26 Common pathologies of the optic chiasm include compression from a pituitary adenoma, parasellar meningioma, or craniopharyngioma.27 Visual field improvement occurs in three stages following surgical resection of pituitary tumors: early fast phase (few days to a week), phase of slow recovery (few weeks to months), and late phase (few months to years).28 Reduced retinal nerve fiber layer thickness and ganglion cell area measurements as well as decreased ganglion cell function (PhNR/b-wave amplitude ratio on the electroretinogram) are indicators for poor postoperative VF recovery in patients with compression of the chiasm from a pituitary adenoma.29
Retrochiasmal Disorders Stroke and traumatic brain injury are the commonest causes of homonymous hemianopia in adults, whereas traumatic brain injury and tumors are more common in children.30 Homonymous hemianopia can be seen in approximately 20% of patients with stroke, which makes it an important neurologic deficit in this group of patients.31
Natural History of Retrochiasmal Visual Field Defects Spontaneous recovery of VFs may be seen in patients with neurologic diseases within the first few months of disease occurrence. The extent of recovery is variable and depends on the magnitude of initial damage, nature of the underlying disease, and topographic location of the lesion. In a retrospective study of the natural history of homonymous hemianopia, spontaneous recovery was noted in 38%, with most of the improvement (60%) being seen in the first month of the neurologic insult.18 Recovery is frequently incomplete and limited to the VF periphery.32 Recovery also seems to be dependent on the site of the lesion, with better chances of recovery in patients with lesions outside the occipital lobe.33 Besides reversibility of the underlying disease process, there is indirect evidence to show that neuroplasticity may play a role in VF improvement. Activation of ipsilateral and contralateral cortical and subcortical visual areas are seen on functional neuroimaging of patients with VF recovery.34 Experience-dependent modifications of the neuronal circuitries implying neuroplasticity were demonstrated in the mammalian and rodent visual systems. Proposed mechanisms include epigenetic alteration of chromatin structure, leading to modification of synaptic connectivity and neural circuitry in the mammalian striate cortex35,36 and remodeling of neuronal pathways.36,37
Impact of Visual Field Defects Quality of Life Depending on the neurologic and ophthalmic disease process, VF loss varies greatly in extent, severity, and potential for
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reversibility, and thus impacts activities of daily living and socioeconomic well-being. Several large population-based studies have demonstrated greater loss of functional ability and increased psychological stress with more severe VF defects.2,38,39 Lower scores on the National Eye Institute Visual Functioning Questionnaire (NEI-VFQ) were noted in patients with VF defects compared with healthy subjects.40,41 Visual difficulties in these patients are frequently compounded by additional deficits, such as impaired light sensitivity, color vision anomalies, and decreased depth perception, which significantly affects mobility in complex environments.42 Subjects may have to depend on gaze adaptation to perform activities of daily living such as shopping in supermarkets.43
Impact on Reading Patients with homonymous VF defects experience varying degrees of difficulty in reading despite normal language function. This acquired reading disorder is called hemianopic dyslexia, which results from an inability to plan and guide reading eye movements.44 Certain VF characteristics are associated with worse reading outcomes, including parafoveal and /or foveal field involvement, bilateral VF defects, right-sided unilateral homonymous field defects, complete hemianopia, and central scotoma. Reading difficulty in leftsided VF defects are secondary to impaired eye movements to the beginning of the next line, whereas right-sided VF defects cause abnormalities of fixation, regressive saccades, and reduced saccades into the blind field.45
Impact on Motor Rehabilitation Visual field defects adversely impact the recovery of patients with additional neurologic deficits such as motor and/or sensory deficits.46 Using life table analyses in patients with motor deficits from hemispheric stroke, the likelihood of achieving independence in ambulation and self-care activities (Barthel index 60) was shown to decrease by more than 20% in the presence of a homonymous hemianopia.47
Impact on Driving Patients with VF defects may experience difficulty in driving and increased risk of traffic accidents compared with normal individuals due to decreased perception of visual stimuli.48 Visual field defects also affect steering stability and risks of collision.49 Visual field defects may thus restrict the outdoor activities of patients, making them homebound, which has a significant economic impact due to inability to work and increased caregiver costs.50 Patients may have to depend on others for activities such as doctors’ visits and grocery shopping. Driver licensing authorities have set basic minimum requirements for issuance and maintenance of driving privileges to ensure safety and minimize risks. Unfortunately, there is no uniformity of these criteria or protocols for standardized VF testing during the application for a driver’s license at local, state, national, or international levels. The international requirements of VF for driving are listed in ►Table 2.50,51 Seminars in Neurology
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Table 2 Visual field requirements for driver’s licensing (except USA) Country
Visual Field Criteria
Australia
Horizontal: 120 degrees by confrontation method
European Union
At least 120 degrees, without diplopia
Japan
150-degree field of view
South Africa
Normal field of vision
United Kingdom
At least 120 degrees without loss of central 20-degree field
United States
Varies by state
Source: Based on the survey conducted by the International Council of Ophthalmology (ICO) in December 2005.51
The driving license requirements within the United States vary from one state to another. Certain states such as California have no restrictions on driver’s licenses based on VF criteria, while others have strict monocular and/or binocular field criteria (see ►Table 3). A detailed discussion about the specific rules and regulations pertaining to the testing methods, outcomes, and reporting requirements is beyond the scope of this text. Readers are encouraged to review the specific testing and reporting rules for their states.
Rehabilitation of Patients with Visual Field Defects Rehabilitation is the cornerstone of management in patients with irreversible VF defects from neurologic diseases. Reha-
bilitation strategies are aimed at providing patients with tools to achieve functional independence. The three broad strategies for treatment and rehabilitation are summarized in ►Table 4 and described in the following sections.
Optical Therapies Optical therapies aim to shift the incident rays of light to noninvolved areas of the VF. The most commonly used device is the prism, which may be fitted over one or both eyes.65,66 Prisms work by changing the path of light from blind areas of the VF toward seeing areas by placing the base of prism toward the hemianopic field. To preserve central vision, the prism is usually displaced 1 to 2 mm away from the pupillary center. Sectoral and peripheral monocular prisms and obliquely oriented prisms (angled at 30 degrees) appear
Table 3 Visual field requirements for driver’s licensing within USA52 State
Visual field criteria
Alabama
110-degree field of view
Alaska
There is no visual field requirement for licensing.
Arizona
70-degree field of view and 35-degree nasal field
Arkansas
Both eyes 105 degrees
California
There is no visual field requirement for licensing.
Colorado
Unspecified (minimum horizontal fields)
Connecticut
100-degree monocular and 140-degree binocular
Delaware
There is no visual field requirement for licensing.
District of Columbia
130 degrees both eyes (may be approved by Director at 110 degrees)
Florida
130-degree horizontal field of view
Georgia
140 degrees each eye and 140 degrees both eyes
Hawaii
70-degree field of vision
Idaho
There is no visual field requirement for licensing.
Illinois
105 degrees for one eye and 140 degrees for both eyes
Indiana
70 degrees for one eye and 120 degrees for both eyes
Iowa
140 degrees for both eyes (with outside mirrors: 70 degrees temporal and 45 degrees nasal for one eye; 115 degrees for both eyes. If less than 95 degrees both eyes and 60 degrees temporal and 35 degrees nasal for one eye, the patient needs recommendation.)
Kansas
55 degrees monocular and 110 degrees binocular
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Table 3 (Continued) State
Visual field criteria
Kentucky
Binocular horizontal field of 35 degrees and binocular vertical field of 25 degrees from fixation
Louisiana
There is no minimum visual field requirement.
Maine
110 degrees for both eyes
Maryland
140 degrees for unrestricted license and 110 degrees for restricted license
Massachusetts
120-degree field of view 110-degree to 140-degree field 105-degree field of view
Mississippi
140-degree field of view; one eye 70 degrees temporal; 35 degrees nasal with 2 outside mirrors
Missouri
Binocular field: minimum 55 degrees; monocular: 85 degrees for restricted license
Montana
There is no requirement for private car drivers.
Nebraska
140 degrees for both eyes; denied at less than 100 degrees
Nevada
Unrestricted: binocular 140 degrees; restricted: 110–140 degrees
New Hampshire
There is no visual field requirement for licensing.
New Jersey
There is no visual field requirement for licensing.
New Mexico
120 degrees; 30 degrees in nasal field of one eye
New York
Minimum 140-degree field of view
North Carolina
60 degrees in one eye (30 degrees on each side)
North Dakota
Both eyes 105 degrees
Ohio
Each eye 70-degree temporal field
Oklahoma
Both eyes 70-degree horizontal field
Oregon
110 degrees in horizontal field (one or both eyes)
Pennsylvania
120 degrees both eyes
Rhode Island
115 degrees in horizontal meridian and 40 degrees for one eye nasally
South Carolina
There is no visual field requirement for licensing.
South Dakota
There is no visual field requirement for licensing.
Tennessee
Only professional drivers require field testing.
Texas
There is no visual field requirement for licensing.
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Michigan Minnesota
Utah
120-degree horizontal field; 20-degree vertical and 90 degrees with restrictions
Vermont
Both eyes should be a minimum of 60 degrees.
Virginia
100-degree monocular and binocular; 70-degree monocular and binocular (daytime only); 40 degrees or better temporal and 30 degrees or better nasal in one eye only
Washington
110 degrees in horizontal meridian (monocular and binocular)
West Virginia
There is no visual field requirement.
Wisconsin
70-degree field of vision
Wyoming
Minimum 120-degree field of view
Note: The table is meant for educational purposes only and should not be construed to represent the legal requirements for the jurisdictions represented. For individual state rules and regulations pertaining to the testing methods, outcomes, and reporting requirements, the readers are encouraged to visit the website for the department of motor vehicles (DMV) for their states.
more beneficial, as they can contribute to expansion of the VF (up to 20 degrees) and allow patients to drive legally in certain states.67,68 Although compliance rates with prisms is approximately 47%,66,67 efficacy of this technique has not been studied in controlled trials. In a recent comparative study, peripheral prism glasses demonstrated higher efficacy
in obstacle avoidance and improvement in mobility compared with sham glasses.69
Restorative Therapies Restorative therapies attempt to restore visual function in the area of VF defects. These strategies employ stimuli in the Seminars in Neurology
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Table 4 Rehabilitative approaches for patients with visual field defects53,54 Optical therapy Prisms
Restorative therapy
55,56
Visual search training
Customized devices
55
Compensatory therapy 54,57
Saccadic eye movement training58
59–61
Ocular movement training62,63
Visual field restitution
Adapted glasses54
Optokinetic therapy63
Eye patches53
Use of visual cues64
Contrast sensitivity training59
Environmental modification
53
Fusional training54
Table 5 Rehabilitative treatments for visual field defects based on the pattern of visual loss Pattern of field defect
Treatment strategies
Blind spot enlargement
Considered ubiquitous in papilledema7; treatment not necessary unless encroaching upon fixation77,78
Central/ring scotoma
Optical assistance with magnification or size scaling79,80 Microperimetry-assisted identification of preferential retinal locus81–83 Biofeedback and training84
Cecocentral scotoma
Eccentric viewing training85 Visual restitution therapy60 Functional training86
Hemianopia
Optical modalities such as monocular or binocular prisms55,66,67 Saccadic compensation training87 Restorative training71
damaged field of vision usually at the borders of field defect or deep into the blind field70 using specifically designed computer-based software. One such example is the visual restitution therapy (VRT) by NovaVision AG (Magdeburg, Germany).71 The hypothesis supporting the therapy is that repeated stimuli above threshold intensity can reactivate neurons, restoring visual function, even with 10 to 15% surviving neurons.1 However, this modality is not universally accepted, largely because of significant discordance between subjective response and results of standard perimetry.1,72 Visual restitution therapy is also an expensive option for the patient, with an estimated cost of $6,000 for 6 months of therapy.73
Compensatory Therapies Compensatory therapies utilize strategies based on oculomotor mechanisms to improve visual function in the affected area. For example, saccadic training involves increasing amplitude and frequency of saccades to increase the chance of visual stimuli falling within the noninvolved half of the VF. In a randomized trial in patients with hemianopia, explorative saccade training for 6 weeks improved search behavior and scene exploration on the blind side as compared with flickerstimulation training.74 Audiovisual training may induce a more organized pattern of explorative behavior.75 Other training techniques include systematic scanning with increased head movements to avoid obstacles.76 Compensatory therapies have been proposed as the preferred approach to rehabilitate hemianopic dyslexics. Interested readers are
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directed to a more detailed review of the various treatment options in patients with hemianopic dyslexia.44 Treatment strategies can be varied based on the etiology, pattern and severity of VF loss (►Table 5). However, evidence to support beneficial effects from any of these techniques in patients with hemianopia is insufficient and prevents generalizability of treatment recommendations at present.54
Conclusions Neurologic VF defects adversely affect socioeconomic status, mental well-being, and quality of life through impairment of reading, navigation, and driving. Coexistence of hemianopia decreases the chance of independent ambulation in patients with motor deficits. Current methods to rehabilitate homonymous hemianopia using optical, compensatory, and restorative strategies have met with limited success. The socioeconomic burden and poor quality of life in this group of patients makes the need for development of newer techniques based on an understanding of neuroplasticity in the visual system urgent.
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