Vision Rehabi I Itation for Patients with Age Related Macular Degeneration

Total Page:16

File Type:pdf, Size:1020Kb

Load more

GARY S. RUBIN

Vision rehabiIitation for patients with agerelated macular degeneration

Epidemiology of low vision

The over-representation of macular degeneration patients in the low-vision clinic is reflected in the chief complaints of those referred for rehabilitation. A study of 1000 consecutive patients seen at the Wilmer Low Vision clinic indicated that 64% listed as their chief complaint, while other activitiꢍs were identified by fewer than 8% of patients. Undoubtedly the bias towards reading problems results partly from the nature of the low-vision services offered. Those served by ꢋ community-based programme that includes home visits might be more likely to report problems with activities of daily living, wꢀile a blind rehabilitation centre would be more likely to address mobility issues. Nevertheless, ꢐꢁst macular degeneration patients are referred to hospital or optometry clinic services, and as their overwhelming concern is with reading, that will be the emphasis of this paper.
The epidemiology of vision impairment is dealt with in detail elsewhere.1 However, there is one particularly salient factor that bears emphasis. The prevalence of vision impairment increases dramatically with advancing age. Statistics compiled in the UK by the Royal National Institute for the Blind2 indicate that there were approximately 1.1 million blind or partially sighted persons in 1996, of whom 82% were 65 years of age or older. Thus it is not surprising to learn that the major causes of vision impairment are age-related eye diseases. Fig. 1 illustrates the distribution of causes of vision impairment from three recent studies?-5 Approximately equal percentages are attributed to macular degeneration and cataract, with smaller percentages for glaucoma, diabetic retinopathy and optic neuropathies. However, the primary cause of vision impairment among patients referred for low-vision services is markedly different. As shown in Fig. 2, over half the low vision patients referred to three large practices in the US,6 UK7 and Canada8 had macular degeneration and fewer than 10% were referred with each of the other conditions.

Reading rehabilitation in age-related macular degeneration

Maꢀification

Most low-vision patients require magnificaꢊion in order to read. When reading speed is measured as a function of character size, tꢀꢁꢂ with normal vision read the fastest with a broꢋd
Why is macular degeneration so overrepresented in the low-vision clinic compared with its prevalence in the population? There are several possible reasons. First, cataract, the other leading cause of vision impairment, is treatable. Although half of those with visionlimiting cataract elect not to have surgery in the 2 years following diagnosis,9 few are referred for vision rehabilitation. A second reason may be that macular degeneration affects central vision while some of the other conditions, such as glaucoma, initially affect peripheral vision. A drop in central vision is more quickly noticed by the patient and may be more detrimental to everyday visual activities. Third, many of those who refer patients for low-vision services view vision rehabilitation as the mere dispensing of optical magnifiers. Magnification is effective for problems with poor resolution in central vision, but has little value for addressing peripheral vision problems caused by restricted fields. range of letter sizes between 0.5 ° and 2.0

  • o
  • .

Not

surprisingly, this range of letter sizes encompasses the range of ordinary print frꢁm newspaper text to small headlines. Most lꢁwvision patients read best with enlarged priꢉꢊ and the amount of magnification is fairly clꢁsely related to their acuity.lO On average, the optimum letter size is about 4 times the acꢃꢄꢅ limit. Patients with central scotomas, incluꢑꢄng those with advanced macular degeneratioꢉ, typically require more magnification than tho�l

with intact central fields, and the required is usually a greater multiple of tꢀꢍꢄr acuity. Even when provided with optimal magnification, patients with central scotoꢐꢆs usually read more slowly than those with iꢉꢊꢋꢌ" central fields. In a study of low-vision patiꢍꢎꢏ reading with optimal magnification, the ꢐꢍꢑꢄꢒ reading rate was less than 50 words/miꢉ fꢁr

Prof. G.S. Rubin � Department of Vision Rehabilitation Research Institute of Ophthalmology 11-43 Bath Street London EC1V gEL, UK

e-mail: [email protected]

Eye (2001) 15, 430-435

©

2001 Rꢆyꢃꢄ Cꢆꢄꢄege ꢆf Oꢀꢁꢂꢁꢃꢄꢅꢆꢄꢇꢈꢉꢊ

430

60

50

40

30

20

10

0

us

Canada

UK

0

0

-

ꢋꢍ

0

AMD

Glauc

DR

Opt Atr

RP

Cornea Cataract

Fig. 1. Leading causes of visual impairment (acuity worse than 6/12 in better eye) are shown for three recent population-based studies. Data for rural US are adapted ꢀom a study of 1136 subjects over age 40 years in rural Kentucky.3 Data for urban US areꢀom a study of 5300 adults 40 years of age and older in Baltimore, Maryland.4 Data for Australia areꢀom a study of 3647 adults aged 46 years and overꢀom the Blue Mountains Eye Study.s AMD, age-related macular degeneration; DR, diabetic retinopathy; Opt Atr, optic atrophy.

paꢔienꢔs wiꢔh scoꢔomas in ꢔhe cenꢔralS 0, buꢔ over 150 words/min for ꢔhose wiꢔh inꢔacꢔ cenꢔral fields.lO more as ꢔhe magnificaꢔion increases. Iꢔ is difficulꢔ ꢔo obꢔain ꢔhe magnificaꢔion required ꢔo recognise leꢔꢔers wiꢔhouꢔ resꢔricꢔing ꢔhe field ꢔo less ꢔhan ꢔhe minimum reqUired window widꢔh.
Elecꢔronic magnificaꢔion aids, such as closed circuiꢔ
ꢔelevisions, provide high magnificaꢔion wiꢔh a large field of view. Neverꢔheless, experienced CCTV users wiꢔh macular degeneraꢔion sꢔill read slower ꢔhan oꢔher ꢔypes of low-vision paꢔienꢔs. This suggesꢔs ꢔhaꢔ reading speed is limiꢔed noꢔ only by ꢔhe field of view of ꢔhe magnifier, buꢔ also ꢔhe visual span of ꢔhe readerY To a firsꢔ approximaꢔion, ꢔhe visual span is ꢔhe number of leꢔꢔers ꢔhaꢔ can be recognised in a single fixaꢔion. In normally
Iꢔ is noꢔ compleꢔely undersꢔood why paꢔienꢔs wiꢔh macular degeneraꢔion or oꢔher cenꢔral field defecꢔs have sꢁ much difficulꢔy reading. One facꢔor is probably relaꢔed ꢊꢁ ꢔhe high magnificaꢔion requiremenꢔ. In order ꢔo read ꢍfficienꢔly, one needs ꢔo be able ꢔo see and recognise aꢔ lꢍasꢔ a minimum number of characꢔers. This minimum 'window widꢔh' may be as low as 4 or 5 leꢔꢔers for ꢔexꢔ ꢓaꢔ is passively scrolled pasꢔ ꢔhe reader,n buꢔ exꢔends ꢔo 15-30 leꢔꢔers for ꢔexꢔ ꢔhaꢔ musꢔ be acꢔively scannedY All ꢁpꢔical magnifiers, be ꢔhey high-plus specꢔacles, hand or sꢔand magnifiers, or ꢔelescopes, resꢔricꢔ ꢔhe field of view

30

25

20

o

o

Rural US

Urban US

Australia

-

15

10

5

0

0

AMD

Cataract

DR

Glaucoma

Opt Atr

Fig. 2. Leading causes of visual impairment in patients referred for low-vision rehabilitation are shown for three low-vision services. Data for the US are ꢀom an unpublished study of 1000 consecutive patients seen at the Johns Hopkins Wilmer Eye Institute low-vision service6 Data for Canada areꢀom a study of 1398 individuals in an assistive devices program in Ontari08 Data for the UK areꢀom a study of 218 patients seen at the University of Wales College of Cardꢁlowvision service.? AMD, age-related macular degeneration; Glauc, glaucoma; DR, diabetic retinopathy; Opt Atr, optic atrophy; RP, retinitis pigmentosa.

431

a

Fig. 3. Eye movement records are shown for three reading trials. Gaze position was sampled at 250 Hz and each black dot is the gaze position for one sample. Clusters of dots indicatefixations, and dots separated by straight lines indicate saccades. In the left panel, the subject was reading with a ꢃll visualfield. In the middle panel, the subject was reading with a 3.5 0 diameter simulated scotoma placed one letter space to the right af fixation. The right panel shows data for a 3.5 0 simulated scotoma centred on fixation.

sighꢔed observers ꢔhe visual span is limiꢔed by ꢔhe dropoff in acuiꢔy and conꢔrasꢔ sensiꢔiviꢔy away from ꢔhe fovea. In paꢔienꢔs wiꢔh macular disease, even if ꢔhe peripheral reꢔina is normal,14 visual span is consꢔrained by ꢔhe presence of a scoꢔoma aꢔ ꢔhe cenꢔre of ꢔhe visual field, by disꢔorꢔions jusꢔ ouꢔside ꢔhe scoꢔoma,15 and by ꢔhe dropoff in acuiꢔy and conꢔrasꢔ sensiꢔiviꢔy in peripheral vision.
ꢔhe eye moved. An SRI Generaꢔion VI eyeꢔracker was fiꢔꢔed wiꢔh a sꢔimulus deflecꢔor19 conꢔaining ꢔwo mirror galvanomeꢔers. Analogue eye posiꢔion signals from ꢔhe eyeꢔracker were used ꢔo roꢔaꢔe ꢔhe mirrors abouꢔ ꢔhe verꢔical and horizonꢔal axes and ꢔhus cancel eye movemenꢔs over a range of abouꢔ ±20°. The sꢔimulus deflecꢔor was modified as described by Crane and Kelly20 so ꢔhaꢔ a sꢔabilised mask could be superimposeꢑ on an unsꢔabilised view of ꢔhe world. The world in ꢔhis case was a compuꢔer moniꢔor conꢔaining ꢔexꢔ.

Eye movements

The eye movemenꢔ signals from ꢔhe eyeꢔracker were sampled aꢔ 250 Hz wiꢔh an analogue-ꢔo-digiꢔal converꢔer and sꢔored for laꢔer analyses. Fig. 3 shows examples of ꢔhe eye movemenꢔ records obꢔained under ꢔhree condiꢔions. The lefꢔ panel shows eye movemenꢔs wheꢉ reading ꢔexꢔ wiꢔhouꢔ a scoꢔoma. Each doꢔ represenꢔs a sampled eye posiꢔion. Clusꢔers of doꢔs indicaꢔe fixaꢔioꢉs, while individual doꢔs connecꢔed by sꢔraighꢔ lines represenꢔ saccades. In ꢔhe absence of a scoꢔoma, ꢔhis reader followed ꢔhe lines of ꢔexꢔ in a regular and predicꢔable fashion, wiꢔh one fixaꢔion for mosꢔ of ꢔhe words and a rapid sweep ꢔo reꢔurn ꢔo ꢔhe beginning of a new line. The middle panel shows daꢔa for a fairly sꢐall 3.5 ° scoꢔoma locaꢔed one leꢔꢔer ꢔo ꢔhe righꢔ of fixaꢔion.
Sꢔaꢔic picꢔures ꢔhaꢔ aꢔꢔempꢔ ꢔo simulaꢔe ꢔhe appearance of ꢔhe world ꢔhrough a cenꢔral scoꢔoma fail ꢔo depicꢔ ꢔhe full exꢔenꢔ of ꢔhe difficulꢔy. As we inspecꢔ such simulaꢔions our eyes are free ꢔo roam ꢔo and fro over ꢔhe represenꢔaꢔion. Buꢔ for ꢔhe person wiꢔh a macular scoꢔoma, ꢔhe scoꢔoma is fixed on ꢔhe reꢔina and moves wiꢔh ꢔhe direcꢔion of gaze. There is no looking around iꢔ. To gain a beꢔꢔer undersꢔanding of problems confronꢔed by paꢔienꢔs wiꢔh macular degeneraꢔion, we underꢔook a series of sꢔudies of eye movemenꢔs and reading performance in normally sighꢔed observers in whom a cenꢔral scoꢔoma was simulaꢔed by means of an

  • eyeꢔracker.16-18 Unlike sꢔaꢔic
  • ꢔhese

simulaꢔions creaꢔed dynamic 'scoꢔomas' ꢔhaꢔ moved as

ꢓ40

-

o

ꢝꢞꢟꢠꢡ Lꢟſt ꢝꢞꢟꢠꢡ Right

ꢓ20

ꢓꢔ
ꢕꢖ

40 20
0

c

-

1

ꢗꢘQ

c

ꢙꢚꢛ

CG

LM

Subject

Fig. 4. Reading speeds are plotted for three subjects with normal vision. The open bars show data when the subjects were forced to attend to the leſt of fixation by a retinally stabilised mask that blocked all informationꢀom the right of fixation. The black bars show data when the subjects were forced to attend to the right of fixation by a mask to the left. Vertical bars are ꢄSE of the mean.

432

30

25 ꢃ

15 10

5

12 10

8

Aꢀeꢁ Leſt

0

Aꢂꢁ ꢢꢣꢤ

I

8

!


6

!

I


4

E

!

2

z

0
0

  • Subjꢈ
  • Subjꢈ

Fig. 5. Eye movement data are plotted for the same reading conditions as in Fig. 4. The left panel shows the number of forward saccades when the subjects were forced to attend to the left or right offixation. The right panel shows the average saccade size when subjects were forced to attend to the leſt, or right. Vertical bars are ±1 SE of the mean.

e eye posiꢔion samples are displaced ꢔo ꢔhe righꢔ cꢁmpared wiꢔh ꢔhe no scoꢔoma condiꢔion. This indicaꢔes ꢔꢀaꢔ ꢔhe observer had deviaꢔed ꢔhe eyes slighꢔly ꢔo ꢔhe righꢔ and was presumably using an area in ꢔhe lefꢔ visual fꢄeld ꢔo read. In ꢔhis condiꢔion ꢔhe reader ofꢔen made mulꢔiple fixaꢔions per word, and ꢔhe reꢔurn sweep was iꢉꢔerrupꢔed by mulꢔiple fixaꢔions. The righꢔ panel shows ꢔꢀe eye movemenꢔ record for a 3.50 scoꢔoma cenꢔred aꢔ ꢔꢀe fovea. The ꢔexꢔ had ꢔo be enlarged for ꢔhe observer ꢔo rꢍsolve ꢔhe leꢔꢔers wꢄꢔh peripheral vision. However, even wiꢔh ꢔhe magnfied ꢔexꢔ ꢔhe eye movemenꢔ paꢔꢔern was quiꢔe disorganised wiꢔh mulꢔiple fixaꢔions and small sꢆccades wiꢔhin words.
We measured reading speed and eye movemenꢔs in normally sighꢔed subjecꢔs who viewed ꢔexꢔ ꢔhrough a sꢔabilised mask ꢔhaꢔ limiꢔed informaꢔion ꢔo ꢔhe lefꢔ or righꢔ visual fields.17 The resulꢔs are shown in Fig. 4. Consisꢔenꢔ wiꢔh our predicꢔions, reading speeds were up ꢔo 50% fasꢔer when aꢔꢔending ꢔo ꢔhe righꢔ field insꢔead of ꢔo ꢔhe lefꢔ. The righꢔ field advanꢔage was reflecꢔed in ꢔhe eye movemenꢔ daꢔa shown in Fig. 5. There were significanꢔly fewer saccades (lefꢔ panel) and ꢔhe saccades were correspondingly larger (righꢔ panel) when aꢔꢔending ꢔo ꢔhe righꢔ. Fixaꢔion duraꢔion did noꢔ differ according ꢔo ꢔhe direcꢔion of aꢔꢔenꢔion (noꢔ shown). The fasꢔesꢔ reading raꢔes and mosꢔ efficienꢔ eye movemenꢔs were obꢔained when all ꢔhe ꢔexꢔual informaꢔion was presenꢔed in ꢔhe lower visual field. Indeed, paꢔienꢔs wiꢔh Sꢔargardꢔ disease, a juvenile form of macular

Eccentric fixation

degeneraꢔion, were more likely ꢔo use a PRL below ꢔheir scoꢔoma.25 Anoꢔher imporꢔanꢔ difference beꢔween ꢔhe age-related macular degeneration and Sꢔargardꢔ disease paꢔienꢔs was ꢔhaꢔ ꢔhose wiꢔh age-relaꢔed macular degeneraꢔion were more likely ꢔo use a PRL ꢔhaꢔ was very close ꢔo ꢔhe scoꢔoma boundary. Wheꢔher ꢔhe more remoꢔe placemenꢔ of ꢔhe PRL increases ꢔhe efficiency of visual processing is a quesꢔion for fuꢔure research.
One of ꢔhe goals of vision rehabiliꢔaꢔion ꢄs ꢔo help ꢔhe paꢔienꢔ esꢔablish an appropriaꢔe PRL and ꢔo use ꢔhaꢔ PRL efficienꢔly. Various procedures have been promoꢔed for ꢔraining ꢔhe PRL,26 buꢔ ꢄꢔ remains conꢔroversial wheꢔher ꢔhese ꢔraining procedures work any beꢔꢔer ꢔhan simple pracꢔice. One of ꢔhe major problems confronꢔing ꢔhe clinician is ꢔo know where ꢔhe PRL is locaꢔed on ꢔhe reꢔꢄna. Wꢄꢔhouꢔ ꢔhis informaꢔion iꢔ is difficulꢔ ꢔo evaluaꢔe wheꢔher ꢔhe locaꢔion ꢄs appropriaꢔe, how iꢔ changes as ꢔhe paꢔienꢔ adapꢔs ꢔo ꢔhe eye condiꢔion, and how ꢔhe PRL locaꢔion responds ꢔo rehabꢄliꢔaꢔion and ꢔraining. The scanning laser ophꢔhalmoscope27 can provide ꢔhis muchneeded informaꢔion, buꢔ iꢔs poꢔenꢔial uses in ꢔhe field of vision rehabiliꢔaꢔion have only begun ꢔo be recognised (see e.g. Fleꢔcher et aI.28).
The eye mꢊvement paꢔꢔerns in Fig. 3 were obꢔained wiꢔh

a

ꢉꢊrmaꢋy sighted ꢊbserver whꢊ had ꢊnly a few hꢊurs ꢊf

pracꢔice reading wiꢔh a scoꢔoma. Macular degeneraꢔion paꢔienꢔs adapꢔ ꢔo ꢔheir scoꢔomas slowly and ꢔypically make a ꢔransiꢔion from conscious use of eccenꢔric reꢔinal ꢆreas ꢔo ꢔhe auꢔomaꢔic subsꢔiꢔuꢔion of a single eccenꢔric lꢁcus which behaves as a pseudo-fovea. This 'preferred reꢔinal locus' or PRL21 can behave as ꢔhe anaꢔomical rꢍference for fixaꢔion eye movemenꢔs, much as ꢔhe real fꢁvea serves ꢔhose wiꢔh normal vision,z2 Neverꢔheless, ꢍven in paꢔienꢔs wiꢔh long-sꢔanding scoꢔomas and wellꢍsꢔablished PRLs, ꢔhere is ꢔendency ꢔowards mulꢔiple fꢄxaꢔions wiꢔhin words and shorꢔer saccades beꢔween fꢄxaꢔꢄons.23
Mosꢔ paꢔienꢔs wꢄꢔh age-relaꢔed macular degeneraꢔꢄon
ꢆdopꢔ a PRL ꢔhaꢔ is ꢔo ꢔhe lefꢔ of a cenꢔral scoꢔoma (in vꢄsual fꢄeld space),z4.25 However, research on reading ꢆꢉd eye movemenꢔs in subjecꢔs wiꢔh normal vision ꢄꢉdicaꢔes ꢔhaꢔ more informaꢔion abouꢔ word idenꢔiꢔy is ꢁbꢔained from leꢔꢔers ꢔo ꢔhe righꢔ of fixaꢔion. According ꢔo ꢁꢉe esꢔimaꢔe, ꢔhe normal reader acquires leꢔꢔer shape ꢄꢉformaꢔion from 12-15 leꢔꢔers in ꢔhe righꢔ half of ꢔhe fiꢍld, buꢔ only 4-5 leꢔꢔers in ꢔhe lefꢔ halfY Thus, iꢔ would sꢍem beꢔꢔer ꢔo use a PRL ꢔo ꢔhe rꢄghꢔ of a scoꢔoma ꢄnsꢔead ꢁf ꢔo ꢔhe lefꢔ.
As an alꢔernaꢔive ꢔo ꢔraining eccenꢔric fixaꢔion and reading eye movemenꢔs, we have invesꢔigaꢔed wheꢔher iꢔ may be possible ꢔo change ꢔhe reading ꢔask in order ꢔo make iꢔ simpler for paꢔienꢔs wiꢔh macular degeneraꢔion.

433

single fixaꢔion. This suggesꢔs ꢔhaꢔ resꢔricꢔions in visual span combine wiꢔh eye movemenꢔ inefficiencies ꢔo liꢐiꢊ reading performance in paꢔienꢔs wiꢔh macular degeneraꢔion. Neverꢔheless, some paꢔienꢔs were able ꢔo increase ꢔheir reading speeds enough wiꢔh RSVP ꢔhaꢔ iꢔ mighꢔ provide a useful alꢔernaꢔive ꢔo convenꢔional sꢔaꢔic ꢔexꢔ.

S

4:1

1000
100
10

c

o

!

ꢪꢫ

c

Future developments in reading rehabilitation

o•

Nꢅ CFL CFL

Nꢅꢆꢈal

J

This brief review of some recenꢔ developmenꢔs in reading rehabiliꢔaꢔion research indicaꢔes ꢔhaꢔ many of ꢔhꢍ problems confronꢔed by paꢔienꢔs wiꢔh age-relaꢔed macular degeneraꢔion cannoꢔ be solved wiꢔh

  • 10
  • 100
  • 1000

magnificaꢔion alone. One key ꢔo improving reading efficiency may be beꢔꢔer ꢔraining in ꢔhe use of eccenꢔric fixaꢔion. Anoꢔher approach is ꢔo improve access ꢔo ꢔhe wriꢔꢔen word by increasing ꢔexꢔ legibiliꢔy, making beꢔꢔꢍr use of ꢔhe limiꢔed visual span, and reducing ꢔhꢍ need fꢁr accuraꢔe saccadic eye movemenꢔs. This approach will benefiꢔ from recenꢔ ꢔechnological advances in compuꢔꢍr imaging and video displays. The developmenꢔ of a commercial markeꢔ for 'virꢔual realiꢔy' displays has madꢍ iꢔ economically feasible ꢔo produce porꢔable, lighꢔ- weighꢔ, head-mounꢔed TV sysꢔems ꢔhaꢔ deliver brighꢔ images wiꢔh high conꢔrasꢔ. Several commercial headmounꢔed reading devices have been puꢔ on ꢔhe markeꢔ in ꢔhe pasꢔ few years and we anxiously awaiꢔ ꢔhe resulꢔs ꢁf currenꢔ sꢔudies ꢔo evaluaꢔe ꢔheir effecꢔiveness as lowvision aids. The Inꢔerneꢔ has had boꢔh posiꢔive and negaꢔive effecꢔs on visual rehabiliꢔaꢔion. While ꢔhe growing dependence on graphical inꢔerfaces, icons and windows may make iꢔ difficulꢔ for ꢔhe visually impaireꢑ reader ꢔo acquire informaꢔion from ꢔhe World Wide Wꢍb, ꢔhere is a vasꢔ increase in ꢔhe amounꢔ of informaꢔion ꢔꢀꢆꢊ is available in digiꢔal formaꢔ. When RSVP was firsꢔ suggesꢔed as a low-vision reading ꢔechnique, ꢔhere was very liꢔꢔle ꢔexꢔ ꢔhaꢔ was direcꢔly accessible via compuꢊꢍr. We envisioned having ꢔo scan pages of ꢔexꢔ one aꢔ a ꢔimꢍ and converꢔ ꢔhem ꢔo a digiꢔal formaꢔ ꢔhaꢔ could be playꢍꢑ back a word aꢔ a ꢔime. Now, books, magazines and newspapers are all being creaꢔed and sꢔored in compuꢔꢍr files, many of which are available free or by subscripꢔiꢁn on ꢔhe Web. Thus far, ꢔoo liꢔꢔle efforꢔ has been devoꢔed to developing ꢔhe sofꢔware ꢔo access ꢔhose files and presꢍnꢊ ꢔhem in an opꢔimal fashion for visually impaired readers. We musꢔ hope ꢔhaꢔ as we become more dependenꢔ oꢉ compuꢔerised sources of informaꢔion, ꢔhe accessibiliꢔy needs of ꢔhose wiꢔh visual impairmenꢔs, and parꢔicularly ꢔhe growing populaꢔion of ꢔhose wiꢔh age-relaꢔed macular degeneraꢔion, will noꢔ be ignored.

PAGE Rꢍadꢉꢊg Raꢌꢍ (wꢅꢆdꢇꢈꢉꢊꢋꢌꢍ)

Fig. 6. Maximum reading speeds are compared for conventional PAGE reading, on the x-axis, and sequential RSVP reading, on the yaxis. Thefilled triangle is average data for four observers with normal vision. Open circles are data for low-vision subjects without scotomas in the central 5 0, andfilled circles are data for subjects with central scotomas. The diagonal lines indicate the relative advantage of RSVP over PAGE reading. Data falling along the 1:1 line indicate that RSVP was read no fasterthan PAGE text, whiledata falling along the 4:1 line indicate that RSVP reading was 4 times faster than PAGE reading.

A ꢔexꢔ presenꢔaꢔion ꢔechnique developed around 197029 provided ꢔhe key. Rapid serial visual presenꢔaꢔion (RSVP) was firsꢔ used ꢔo sꢔudy cogniꢔive processing during normal reading. Insꢔead of presenꢔing a full page of ꢔexꢔ ꢔhaꢔ is scanned wiꢔh a series of eye movemenꢔs, RSVP presenꢔs words one aꢔ a ꢔime in a fixed locaꢔion. Provided ꢔhe enꢔire word fiꢔs wiꢔhin ꢔhe visual span, no eye movemenꢔs are necessary. Our work3o demonsꢔraꢔed ꢔhaꢔ normally sighꢔed observers could read RSVP ꢔexꢔ wiꢔh good comprehension even fasꢔer ꢔhan a normal page of sꢔaꢔic ꢔexꢔ. Some were able ꢔo read RSVP ꢔexꢔ aꢔ speeds in excess of 1000 words/min, compared wiꢔh 250-300 words/min for sꢔaꢔic ꢔexꢔ.
Buꢔ whaꢔ abouꢔ low-vision paꢔienꢔs? Fig. 6 compares
RSVP and sꢔaꢔic reading speeds for 23 subjecꢔs wiꢔh various ocular paꢔhologies.31 The filled circles presenꢔ daꢔa for 14 subjecꢔs wiꢔh cenꢔral scoꢔomas, mosꢔ due ꢔo macular degeneraꢔion, and ꢔhe open circles presenꢔ daꢔa for ꢔhe 9 subjecꢔs wiꢔh low vision buꢔ who had inꢔacꢔ cenꢔral fields. The open ꢔriangle represenꢔs average daꢔa for a group of normally sighꢔed subjecꢔs. The normally sighꢔed subjecꢔs read abouꢔ 4 ꢔimes fasꢔer wiꢔh RSVP compared wiꢔh sꢔaꢔic ꢔexꢔ. Low-vision paꢔienꢔs wiꢔh inꢔacꢔ cenꢔral fields read approximaꢔely ꢔwice as fasꢔ wiꢔh RSVP. Unforꢔunaꢔely, ꢔhe low-vision paꢔienꢔs wiꢔh macular scoꢔomas showed ꢔhe leasꢔ improvemenꢔ, reading an average of 40% fasꢔer wiꢔh RSVP. A deꢔailed analysis of eye movemenꢔs using a scanning laser ophꢔhalmoscope indicaꢔed ꢔhaꢔ RSVP reduced buꢔ did noꢔ eliminaꢔe inꢔra-word saccades in paꢔienꢔs wiꢔh macular scoꢔomas. Some of ꢔhese subjecꢔs indicaꢔed ꢔhaꢔ wiꢔh ꢔhe high level of magnificaꢔion needed ꢔo resolve ꢔhe leꢔꢔers iꢔ was impossible ꢔo recognise an enꢔire word in a

Research described here incorporates studies conducted with many colleagues including Gordon Legge, Kathleen Turano, Roger Cummings and Elisabeth Fine. This work was supported by grants from the National Eye Institute and National Institute on Aging of the US Public Health Service, and the AMOCO Foundation.

434

16ꢇ Cummings RW, Rubin GSꢇ Reading speed and saccadic eye movements with an artificial paracentral scotomaꢁ Invest Ophthalmol Visual Sci 1992;33:1418ꢇ

References

1ꢁ Tielsch JMꢁ The epidemiology of vision impairmentꢇ In: Silverstone B, Lang M, Rosenthal B, Faye E, editorsꢇ Lighthouse handbook on vision impairment and vision rehabilitation, vol 1ꢇ Oxford: Oxford University Press, 2000P5ꢀ17ꢁ
17ꢇ Fine EM, Rubin GSꢁ Reading with simulated scotomas: attending to the right is better than attending to the leftꢁ Vision Res 1999;39:1039ꢅ48ꢇ
18ꢇ Fine EM, Rubin GSꢇ Reading with central field loss: number of letters masked is more important than the size of the mask in degreesꢁ Vision Res 1999;39:747-56ꢇ
2ꢇ Royal National Institute for the Blindꢁ Office of National Statistics mid 1996 population estimates: estimates for 1996 of visually impaired people (iꢇeꢁ registerable) and the number of people registered as blind and partially sighted as at 31 March 1997 in United Kingdomꢇ
19ꢇ Crane HD, Clark MRꢁ Three-dimensional visual stimulus deflectorꢇ Appl Opt 1978;17:706ꢅ13ꢇ
20ꢇ Crane HD, Kelly DHꢁ Accurate simulation of visual scotomas http://wwwꢁrnibꢁorgꢁuk/wesupply/fctsheet/authukꢁhtm

3ꢁ Dana MR, Tielsch JM, Enger C, Joyce E, Santoli JM, Taylor HRꢁ Visual impairment in a rural Appalachian community: prevalence and causesꢁ JAMA 1990;264:24ꢂ5ꢇ in normal subjectsꢁ Appl Opt 1983;22:1802ꢅꢆꢇ
21ꢁ Timberlake GT, Mainster MA, Peli E, Augliere ꢭꢯ Essock
EA, Arend LEꢁ Reading with a macula scotomaꢇ Iꢁ Retinal location of scotoma and fixation areaꢇ Invest Ophthalmol Vis Sci 1986;27:1137ꢅ47ꢇ
4ꢁ Rahmani B, Tielsch JM, Katz J, Gottsch J, Quigley H, Javitt J, Sommer Aꢁ The cause-specific prevalence of visual impairment in an urban population: the Baltimore Eye Surveyꢇ Ophthalmology 1996;103:1721-6ꢁ
22ꢇ White JM, Bedell HEꢁ The oculomotor reference in humans with bilateral macular diseaseꢇ Invest Ophthalmol Vis Sci 1990;31:1149-61ꢇ
5ꢁ Attebo K, Mitchell P, Smith Wꢁ Visual acuity and the causes

Recommended publications
  • GUIDE for the Evaluation of VISUAL Impairment

    GUIDE for the Evaluation of VISUAL Impairment

    International Society for Low vision Research and Rehabilitation GUIDE for the Evaluation of VISUAL Impairment Published through the Pacific Vision Foundation, San Francisco for presentation at the International Low Vision Conference VISION-99. TABLE of CONTENTS INTRODUCTION 1 PART 1 – OVERVIEW 3 Aspects of Vision Loss 3 Visual Functions 4 Functional Vision 4 Use of Scales 5 Ability Profiles 5 PART 2 – ASSESSMENT OF VISUAL FUNCTIONS 6 Visual Acuity Assessment 6 In the Normal and Near-normal range 6 In the Low Vision range 8 Reading Acuity vs. Letter Chart Acuity 10 Visual Field Assessment 11 Monocular vs. Binocular Fields 12 PART 3 – ESTIMATING FUNCTIONAL VISION 13 A General Ability Scale 13 Visual Acuity Scores, Visual Field Scores 15 Calculation Rules 18 Functional Vision Score, Adjustments 20 Examples 22 PART 4 – DIRECT ASSESSMENT OF FUNCTIONAL VISION 24 Vision-related Activities 24 Creating an Activity Profile 25 Participation 27 PART 5 – DISCUSSION AND BACKGROUND 28 Comparison to AMA scales 28 Statistical Use of the Visual Acuity Score 30 Comparison to ICIDH-2 31 Bibliography 31 © Copyright 1999 by August Colenbrander, M.D. All rights reserved. GUIDE for the Evaluation of VISUAL Impairment Summer 1999 INTRODUCTION OBJECTIVE Measurement Guidelines for Collaborative Studies of the National Eye Institute (NEI), This GUIDE presents a coordinated system for the Bethesda, MD evaluation of the functional aspects of vision. It has been prepared on behalf of the International WORK GROUP Society for Low Vision Research and Rehabilitation (ISLRR) for presentation at The GUIDE was approved by a Work Group VISION-99, the fifth International Low Vision including the following members: conference.
  • Symptoms of Age Related Macular Degeneration

    Symptoms of Age Related Macular Degeneration

    WHAT IS MACULAR DEGENERATION? wavy or crooked, visual distortions, doorway and the choroid are interrupted causing waste or street signs seem bowed, or objects may deposits to form. Lacking proper nutrients, the light- Age related macular degeneration (AMD) is appear smaller or farther away than they sensitive cells of the macula become damaged. a disease that may either suddenly or gradually should, decrease in or loss of central vision, and The damaged cells can no longer send normal destroy the macula’s ability to maintain sharp, a central blurry spot. signals from the macula through the optic nerve to central vision. Interestingly, one’s peripheral or DRY: Progression with dry AMD is typically slower your brain, and consequently your vision becomes side vision remains unaffected. AMD is the leading de-gradation of central vision: need for increasingly blurred cause of “legal blindness” in the United States for bright illumination for reading or near work, diffi culty In either form of AMD, your vision may remain fi ne persons over 65 years of age. AMD is present in adapting to low levels of illumination, worsening blur in one eye up to several years even while the other approximately 10 percent of the population over of printed words, decreased intensity or brightness of eye’s vision has degraded. Most patients don’t the age of 52 and in up to 33 percent of individuals colors, diffi culty recognizing faces, gradual increase realize that one eye’s vision has been severely older than 75. The macula allows alone gives us the in the haziness of overall vision, and a profound drop reduced because your brain compensates the bad ability to have: sharp vision, clear vision, color vision, in your central vision acuity.
  • Macular Degeneration

    Macular Degeneration

    DRIVEWELL Driving When You Have Macular Degeneration You have been a safe driver for years. For you, driving means freedom and control. As you get older, changes in your physical and mental health can affect how safely you drive. Macular degeneration (also known as age-related macular degeneration) damages the macula, a spot near the center of the retina (light-sensitive inner lining of the eyeball). It is a common eye problem among older drivers that makes it hard to drive safely. Age-related macular degeneration is the leading cause of new cases of blindness in people 65 and older. If you have macular degeneration, you may not notice any signs in the early stages. You may not know you have this condition until you lose your peripheral vision (what you see out of the corner of your eyes). In time it will affect your central vision, causing a dark or empty area in the center of your vision. How Can Macular Degeneration Affect the Way I Drive? • Your central vision may be dull and blurry. This can lead to loss of sharp vision. • You may not see the road, street signs, lane markers, and even people and bicyclists in the road. • You may need more bright light to see up close. • Colors may look less vivid or bright. • You may have trouble when you go from bright light to low light. • You may not be able to recognize people’s faces. What Should I Do if I Have Any of These Signs? As soon as you notice any of these warning signs: • Tell your family or someone close to you, especially if you have a family history of macular degeneration or have changes in your central vision.
  • Detached and Torn Retina Retinal Detachments Occur in 1 out of 10,000 Americans Each Year

    Detached and Torn Retina Retinal Detachments Occur in 1 out of 10,000 Americans Each Year

    Detached and Torn Retina Retinal Detachments Occur in 1 Out of 10,000 Americans Each Year A retinal detachment is not as common as other eye conditions such as glaucoma or macular degeneration, however… it is just as serious and it is a vision threatening condition which should be treated as an emergency. Dr. Randy Katz, Florida Eye’s Diabetic Retinopathy, Retinal Detachment & Macular Degeneration Specialist says that the sooner a retinal tear or detachment is treated the better the chances of saving the vision in the eye. What Is a Retinal Detachment? The retina is the light-sensitive layer of tissue that lines the inside of the eye and sends visual messages through the optic nerve to the brain. When the retina detaches, it is lifted or pulled from its normal position. When this occurs, if not promptly treated, retinal detachment can cause permanent vision loss. In some cases there may be small areas of the retina that are torn. These areas, called retinal tears or retinal breaks, can lead to a retinal detachment. Vitreous gel, the clear material that fills the eyeball, is attached to the retina in the back of the eye. As we get older, the vitreous may change shape, pulling away from the retina. If the vitreous pulls a piece of the retina with it, it causes a retinal tear. Once a retinal tear occurs, vitreous fluid may seep through and lift the retina off the back wall of the eye, causing the retina to detach or pull away. 2 Are You At Risk for a Torn or Detached Retina? A retinal detachment can occur at any age, but it is more common in people over age 40.
  • IMI Pathologic Myopia

    IMI Pathologic Myopia

    Special Issue IMI Pathologic Myopia Kyoko Ohno-Matsui,1 Pei-Chang Wu,2 Kenji Yamashiro,3,4 Kritchai Vutipongsatorn,5 Yuxin Fang,1 Chui Ming Gemmy Cheung,6 Timothy Y. Y. Lai,7 Yasushi Ikuno,8–10 Salomon Yves Cohen,11,12 Alain Gaudric,11,13 and Jost B. Jonas14 1Department of Ophthalmology and Visual Science, Tokyo Medical and Dental University, Tokyo, Japan 2Department of Ophthalmology, Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Kaohsiung, Taiwan 3Department of Ophthalmology and Visual Sciences, University Graduate School of Medicine, Kyoto, Japan 4Department of Ophthalmology, Otsu Red-Cross Hospital, Otsu, Japan 5School of Medicine, Imperial College London, London, United Kingdom 6Singapore Eye Research Institute, Singapore National Eye Center, Singapore 7Department of Ophthalmology & Visual Sciences, The Chinese University of Hong Kong, Hong Kong Eye Hospital, Hong Kong 8Ikuno Eye Center, 2-9-10-3F Juso-Higashi, Yodogawa-Ku, Osaka 532-0023, Japan 9Department of Ophthalmology, Osaka University Graduate School of Medicine, Osaka, Japan 10Department of Ophthalmology, Kanazawa University Graduate School of Medicine, Kanazawa, Japan 11Centre Ophtalmologique d’Imagerie et de Laser, Paris, France 12Department of Ophthalmology and University Paris Est, Creteil, France 13Department of Ophthalmology, APHP, Hôpital Lariboisière and Université de Paris, Paris, France 14Department of Ophthalmology, Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany Correspondence: Kyoko Pathologic myopia is a major cause of visual impairment worldwide. Pathologic myopia is Ohno-Matsui, Department of distinctly different from high myopia. High myopia is a high degree of myopic refractive Ophthalmology and Visual Science, error, whereas pathologic myopia is defined by a presence of typical complications in Tokyo Medical and Dental the fundus (posterior staphyloma or myopic maculopathy equal to or more serious than University, Tokyo, Japan; diffuse choroidal atrophy).
  • Bass – Glaucomatous-Type Field Loss Not Due to Glaucoma

    Bass – Glaucomatous-Type Field Loss Not Due to Glaucoma

    Glaucoma on the Brain! Glaucomatous-Type Yes, we see lots of glaucoma Field Loss Not Due to Not every field that looks like glaucoma is due to glaucoma! Glaucoma If you misdiagnose glaucoma, you could miss other sight-threatening and life-threatening Sherry J. Bass, OD, FAAO disorders SUNY College of Optometry New York, NY Types of Glaucomatous Visual Field Defects Paracentral Defects Nasal Step Defects Arcuate and Bjerrum Defects Altitudinal Defects Peripheral Field Constriction to Tunnel Fields 1 Visual Field Defects in Very Early Glaucoma Paracentral loss Early superior/inferior temporal RNFL and rim loss: short axons Arcuate defects above or below the papillomacular bundle Arcuate field loss in the nasal field close to fixation Superotemporal notch Visual Field Defects in Early Glaucoma Nasal step More widespread RNFL loss and rim loss in the inferior or superior temporal rim tissue : longer axons Loss stops abruptly at the horizontal raphae “Step” pattern 2 Visual Field Defects in Moderate Glaucoma Arcuate scotoma- Bjerrum scotoma Focal notches in the inferior and/or superior rim tissue that reach the edge of the disc Denser field defects Follow an arcuate pattern connected to the blind spot 3 Visual Field Defects in Advanced Glaucoma End-Stage Glaucoma Dense Altitudinal Loss Progressive loss of superior or inferior rim tissue Non-Glaucomatous Etiology of End-Stage Glaucoma Paracentral Field Loss Peripheral constriction Hereditary macular Loss of temporal rim tissue diseases Temporal “islands” Stargardt’s macular due
  • Central Serous Choroidopathy

    Central Serous Choroidopathy

    Br J Ophthalmol: first published as 10.1136/bjo.66.4.240 on 1 April 1982. Downloaded from British Journal ofOphthalmology, 1982, 66, 240-241 Visual disturbances during pregnancy caused by central serous choroidopathy J. R. M. CRUYSBERG AND A. F. DEUTMAN From the Institute of Ophthalmology, University of Nijmegen, Nijmegen, The Netherlands SUMMARY Three patients had during pregnancy visual disturbances caused by central serous choroidopathy. One of them had a central scotoma in her first and second pregnancy. The 2 other patients had a central scotoma in their first pregnancy. Symptoms disappeared spontaneously after delivery. Except for the ocular abnormalities the pregnancies were without complications. The complaints can be misinterpreted as pregnancy-related optic neuritis or compressive optic neuropathy, but careful biomicroscopy of the ocular fundus should avoid superfluous diagnostic and therapeutic measures. Central serous choroidopathy (previously called lamp biomicroscopy of the fundus with a Goldmann central serous retinopathy) is a spontaneous serous contact lens showed a serous detachment of the detachment of the sensory retina due to focal leakage neurosensory retina in the macular region of the from the choriocapillaris, causing serous fluid affected left eye. Fluorescein angiography was not accumulation between the retina and pigment performed because of pregnancy. In her first epithelium. This benign disorder occurs in healthy pregnancy the patient had consulted an ophthal- adults between 20 and 45 years of age, who present mologist on 13 June 1977 for exactly the same with symptoms of diminished visual acuity, relative symptoms, which had disappeared spontaneously http://bjo.bmj.com/ central scotoma, metamorphopsia, and micropsia. after delivery.
  • Dominant Optic Atrophy

    Dominant Optic Atrophy

    Lenaers et al. Orphanet Journal of Rare Diseases 2012, 7:46 http://www.ojrd.com/content/7/1/46 REVIEW Open Access Dominant optic atrophy Guy Lenaers1*, Christian Hamel1,2, Cécile Delettre1, Patrizia Amati-Bonneau3,4,5, Vincent Procaccio3,4,5, Dominique Bonneau3,4,5, Pascal Reynier3,4,5 and Dan Milea3,4,5,6 Abstract Definition of the disease: Dominant Optic Atrophy (DOA) is a neuro-ophthalmic condition characterized by a bilateral degeneration of the optic nerves, causing insidious visual loss, typically starting during the first decade of life. The disease affects primary the retinal ganglion cells (RGC) and their axons forming the optic nerve, which transfer the visual information from the photoreceptors to the lateral geniculus in the brain. Epidemiology: The prevalence of the disease varies from 1/10000 in Denmark due to a founder effect, to 1/30000 in the rest of the world. Clinical description: DOA patients usually suffer of moderate visual loss, associated with central or paracentral visual field deficits and color vision defects. The severity of the disease is highly variable, the visual acuity ranging from normal to legal blindness. The ophthalmic examination discloses on fundoscopy isolated optic disc pallor or atrophy, related to the RGC death. About 20% of DOA patients harbour extraocular multi-systemic features, including neurosensory hearing loss, or less commonly chronic progressive external ophthalmoplegia, myopathy, peripheral neuropathy, multiple sclerosis-like illness, spastic paraplegia or cataracts. Aetiology: Two genes (OPA1, OPA3) encoding inner mitochondrial membrane proteins and three loci (OPA4, OPA5, OPA8) are currently known for DOA. Additional loci and genes (OPA2, OPA6 and OPA7) are responsible for X-linked or recessive optic atrophy.
  • Optic Neuritis – More Than a Loss of Vision

    Optic Neuritis – More Than a Loss of Vision

    CLINICAL PRACTICE Edward R Chu Celia S Chen MBBS, is resident medical officer, MBBS, MPHC, FRANZCO, is a consultant ophthalmologist Department of Ophthalmology, Flinders and Senior Lecturer, Department of Ophthalmology, Flinders Medical Centre and Flinders University, Medical Centre and Flinders University, South Australia. South Australia. [email protected] Optic neuritis More than a loss of vision Optic neuritis (ON) is the presence of an acute Background inflammation of the optic nerve that results in painful loss of Optic neuritis is an acute inflammation of the optic nerve that vision. It is the most commonly encountered optic neuropathy results in painful loss of vision. Patients often present to a general in general practice,1–4 and is often associated with multiple practitioner, and early recognition is important as treatment may 3,4 improve the speed of vision recovery. sclerosis (MS). Studies show that in about 15–20% of MS cases, ON was the presenting symptom and more than half of Objective people with MS experience at least one episode of ON during This article provides information on the signs and symptoms of optic their disease.5,6 The risk of developing MS can be stratified by neuritis and discusses appropriate referral, investigations appropriate imaging investigations at the diagnosis of ON. and management. Therefore, early recognition is important to ensure timely Discussion referral, investigation and treatment; prompt treatment can Optic neuritis is the presenting symptom in up to one-fifth of people hasten visual recovery. with multiple sclerosis. Diagnosis of optic neuritis is based on history and examination, therefore obtaining pertinent information Epidemiology and performing proper ophthalmic examination is essential.
  • Patchy Scotoma Observed in Chorioretinal Patchy Atrophy of Myopic Macular Degeneration

    Patchy Scotoma Observed in Chorioretinal Patchy Atrophy of Myopic Macular Degeneration

    Retina Patchy Scotoma Observed in Chorioretinal Patchy Atrophy of Myopic Macular Degeneration Jung Lo,1,2 Linda Yi-Chieh Poon,2 Yi-Hao Chen,2 Hsi-Kung Kuo,2 Yung-Jen Chen,2 Wei-Yu Chiang,1,2 and Pei-Chang Wu1,2 1Graduate Institute of Clinical Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan 2Department of Ophthalmology, Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Kaohsiung, Taiwan Correspondence: Pei-Chang Wu, PURPOSE. To investigate the retinal sensitivity of highly myopic eyes with chorioretinal Department of Ophthalmology, patchy atrophy (PA) using microperimetry. Kaohsiung Chang Gung Memorial Hospital and Chang Gung University METHODS. Fifty-two eyes of 32 patients with high myopia were prospectively included. College of Medicine, Kaohsiung, Twenty-two eyes of 16 patients had PA lesions; eyes without PA were analyzed as controls. Taiwan; Testing points on microperimetry in eyes with PA were designated as 3 zones: zone 1 as [email protected]. the PA lesion including its borders; zone 2 including testing points adjoining PA; zone 3 Received: April 5, 2019 including all other testing points. Accepted: November 15, 2019 RESULTS. In the PA group, the mean retinal sensitivity in zone 1 was 2.1 ± 2.8 dB, zone Published: February 13, 2020 2 = 8.3 ± 4.3 dB, and zone 3 = 9.4 ± 4.1 dB. Sensitivity in zone 1 was significantly Citation: Lo J, Poon LY-C, Chen Y-H, reduced than zones 2 and 3 (P < 0.001). The mean retinal sensitivity in the PA group et al.
  • Refractive Error Is a Disease of the Eye, and We Should Treat It

    Refractive Error Is a Disease of the Eye, and We Should Treat It

    Refractive error is a disease of the eye, and we should treat it. believe that refractive error is a disease of the eye— no different from glaucoma, dry eye disease, and other issues for which we readily offer treatment. In the world of modern cataract and refractive surgery, we have the capability to correct visual Iacuity that is compromised due to astigmatism and other types refractive error, so why shouldn't we treat astigmatism during cataract surgery? A large percentage of our cataract patients, about 75%, have at least 0.50 D of astigmatism. Even this small amount of astigmatism can and often does create issues visually for patients. The higher the My Philosophy of level of astigmatism, the more it can affect vision. My philosophy is, why not try to help these people? Correcting their astigmatism will help them to achieve better visual acuity, and this is even more crucial in patients who elect a multifocal, extended depth of focus, or other premium IOL. It is important to educate patients about their astigmatism and to relay to them what we can do ASTIGMATISM to correct it. The level of care and attention to detail affects everything, from our surgical outcomes, to the practice’s reputation, to future referral patterns. THRESHOLDS AND BEST PRACTICES My threshold for astigmatism treatment is about 0.75 D. Above that, the patient can lose contrast and can have functional visual acuity issues if the astig- MANAGEMENT matism is not addressed. I believe that correction of low astigmatism, especially, is low-hanging fruit, as it provides surgeons with an additional opportunity to improve their practices.
  • Classification of Visual Field Abnormalities in the Ocular Hypertension Treatment Study

    Classification of Visual Field Abnormalities in the Ocular Hypertension Treatment Study

    CLINICAL SCIENCES Classification of Visual Field Abnormalities in the Ocular Hypertension Treatment Study John L. Keltner, MD; Chris A. Johnson, PhD; Kimberly E. Cello, BSc; Mary A. Edwards, BSc; Shannan E. Bandermann, MA; Michael A. Kass, MD; Mae O. Gordon, PhD; for the Ocular Hypertension Treatment Study Group Objectives: (1) To develop a classification system for Main Outcome Measures: A 97% interreader hemi- visual field (VF) abnormalities, (2) to determine inter- field agreement. reader and test-retest agreement, and (3) to determine the frequency of various VF defects in the Ocular Hy- Results: The average hemifield classification agree- pertension Treatment Study. ment (between any 2 of 3 readers) for 5018 hemifields was 97% and 88% for the 1266 abnormal VFs that were Methods: Follow-up VFs are performed every 6 months reread (agreement between the first and second and are monitored for abnormality, indicated by a glau- classifications). Glaucomatous patterns of loss (partial coma hemifield test result or a corrected pattern SD arcuate, paracentral, and nasal step defects) composed outside the normal limits. As of January 1, 2002, 1636 the majority of VF defects. patients had 2509 abnormal VFs. Three readers inde- pendently classified each hemifield using a classifica- Conclusion: The Ocular Hypertension Treatment tion system developed at the VF reading center. A Study classification system has high reproducibility and subset (50%) of the abnormal VFs was reread to evalu- provides a possible nomenclature for characterizing VF ate test-retest reader agreement. A mean deviation was defects. calculated separately for the hemifields as an index to the severity of VF loss.