Volume 18Number 2 Reports 213

do VEPs.1 However, the comparison of VEP andbehavioral data on the same individual in Fig. 2(N. B. at 7 to 8 weeks) indicates quite close agree-ment, as does the comparison of the two 3-week-old infants' VEP with the 1-month groupbehavioral data; VEP and behavioral measures ona single 6-month-old individual'; and the indi-vidual VEP-based CSFs reported by Pirchio et al.6

in comparison with behaviorally determined CSFsat 2 to 3 months.2' ;i Comparison of data betweendifferent experiments must also consider the ef-fects of stimulus variables. In the present study,behavioral data were obtained with a stimulusluminance 0.5 log units higher than that used forthe VEP testing; on those grounds, the VEP re-sults might be relative underestimates of per-formance. Further studies employing VEP andbehavioral measures on the same infants by thesame stimuli would be desirable to confirm therelationship between the two measures.

Insofar as data from the different methods maybe compared, the VEP data from the two 3-week-old infants shown in Fig. 1 and the meanbehavioral data for 5-week-olds show only modestimprovements in acuity and contrast sensitivityover our neonatal VEP data. A larger increase insensitivity is shown behaviorally between 1 and 2months. If these comparisons are valid, they sug-gest that visual maturation may accelerate afterthe first month of life.

In interpreting VEP data, it should be borne inmind that each study uses a particular rate of tem-poral modulation of the stimulus. Little is knownof the temporal properties of the infant visual sys-tem, and it is possible that use of different tem-poral parameters might lead to different estimatesof visual spatial performance.

The acuity and sensitivity reported here forneonates may appear extremely poor in compari-son to adult vision. However, they are adequate toprovide useful visual information, especially overthe short distances where most stimuli that aresignificant for the infant appear. For example, anacuity of 0.8 c/deg will preserve the over-all shapeof the mother's face and its principal features atdistances of 50 cm or less.

kinson, Psychological Laboratory, University of Cam-bridge, Downing Street, Cambridge, CB2 3EB, En-gland

Key words: infant vision, contrast sensitivity, acuity, vi-sual evoked potentials

REFERENCES1. Dobson, V., and Teller, D. Y.: Visual acuity in

human infants: a review and comparison of behav-ioral and electrophysiological studies, Vision Res.18:1469, 1978.

2. Atkinson, J., Braddick, O., and Moar, K.: Devel-opment of contrast sensitivity over the first threemonths of life in the human infant, Vision Res.17:1037, 1977.

3. Banks, M. S., and Salapatek, P.: Acuity and contrastsensitivity in 1-, 2-, and 3-month-old human infants,INVEST. OPIITIIALMOL. VISUAL SCI. 17:361, 1978.

4. Marg, E., Freeman, D. N., Peltzman, P. andGoldstein, P. J.: Visual acuity development inhuman infants: evoked potential measurements, IN-VEST. OPIITIIALMOL. 15:150, 1976.

5. Harris, L., Atkinson, J., and Braddick, O.: Visualcontrast sensitivity of a 6 month-old infant measuredby the evoked potential, Nature 264:570, 1976.

6. Pirchio, M., Spinelli, D., Fiorentini, A., and Maf-fei, L.: Infant contrast sensitivity evaluated byevoked potentials. Brain Res. 141:179, 1978.

7. Harter, M. R. Deaton, F. R., and Odom, J. V.:Visual evoked potentials to checkerboard flashes ininfants from six days to six months. In Desmedt, J.,editor: New Developments in Visual Evoked Po-tentials of the Human Brain. Oxford, 1977, OxfordUniversity Press.

8. Regan, D.: Recent advances in electrical recordingfrom the human brain, Nature 253:401, 1975.

9. Campbell, F. W., and MafTei, L.: Electrophysio-logical evidence for the existence of orientation andsize detectors in the human visual system J. Physiol.(Lond.) 207:635, 1970.

10. Gorman, J. J., Cogan, D. G., and Gellis, S. S.: Anapparatus for grading the visual acuity on the basis ofoptokinetic nystagmus, Pediatrics 19:1088, 1957.

11. Dayton, G. D., Jones, M. H., Aiu, P., Rawson, R.A., Steele, B., and Rose, M.: Developmental studyof co-ordinated eye movements in the human infant,Arch. Ophthalmol. 71:865, 1964.

We thank Dr. N. C. R. Roberton for encouragement,advice, and the provision of facilities in CambridgeMaternity Hospital; nursing staff and mothers for theirco-operation; and Dr. F. VV. Campbell for helpful dis-cussion and the generous loan of equipment.

From the Psychological Laboratory, University ofCambridge, Cambridge, England. This work was sup-ported by the Medical Research Council. Submitted forpublication July 24, 1978. Reprints requests: Dr. J. At-

Different rates of functional recovery of eyemovements during orthoptics treatmentin an adult amblyope. KENNETH J. CIUF-

FREDA, ROBERT V. KENYON, AND LAWRENCE

STARK.

Although it is common clinical knowledge that ocu-lomotor control appears to normalize during the course

0146-0404/79/020213+07S00.70/0 © 1979 Assoc. for Res. in Vis. and Ophthal., Inc.

214 ReportsInvest. Ophthalmol. Visual Sri.

February 1979

of successful orthoptics therapy for amblyopia, reportsproviding a quantitative analysis of eye movements dur-ing extended periods of treatment are lacking. We pro-vide for the first time such a report in an adult amblyope.Aspects of eye movement control tluit tended to nor-malize with therapy include drift amplitude and velocity,duration and frequency of steady fixation, and pursuitgain. These results suggest that smooth pursuit controlcan be modified, even in an adult amblyope. Aspects ofeye movement control that remained abnormal through-out therapy, in spite of normalization of visual acuityand centralization of fixation, include increased saccadiclatencies, use of large saccades during small-amplitudepursuit tracking, and static overshooting. These resultssuggest that certain aspects of saccadic and pursuit con-trol could either no longer be modified or would requirelonger periods for this to occur.

Orthoptics is a nonsurgical method of develop-ing comfortable, binocular vision in patients whohave vision anomalies such as amblyopia1 andstrabismus1' 2 which may impede sensory andmotor fusion. It is common clinical knowledge thatoculomotor control appears to normalize duringthe course of successful orthoptics therapy foramblyopia. Although reports are sorely neededwhich provide a quantitative analysis of changes invarious aspects of oculomotor control obtained byobjective eye movement recording performedconcurrent with treatment,1':! they are not evidentin the literature. However, von Noorden andBurian4 provided ac-electro-oculographic record-ings of fixation and saccadic movements in oneyoung amblyope before and after direct occlusiontherapy and found eye movements to be normalonce amblyopia was corrected. However, this in-formation (only a small part of a larger study onfixation in amblyopia) was presented in a non-quantitative manner; furthermore, eye move-ments were not recorded during the course oftreatment. Thus careful quantitative analysis ofthose aspects of oculomotor control that changedduring amblyopia treatment, as well as their rateof change, are unknown. We provide for the firsttime such a report.

In our study, the fixational, saccadic, and pur-suit eye movements of one adult amblyope wererecorded on several occasions over an 8-monthperiod of successful orthoptics treatment foramblyopia.

Methods. A photoelectric method was used torecord horizontal eye position.3 With this method,the amount of infrared light reflected from thehorizontal limbal regions was monitored, and thiswas linear for the range of movements recorded.The bandwidth of the entire recording system was

75 Hz (^3 dB). Resolution was approximately 12min arc. A chinrest and headrest, as well as a bitebar covered with dental impression material, wereused to stabilize the head. Spectacle correctionwas worn throughout test periods.

A PDP8/I minicomputer was used to move asmall spot of light (3.5 to 6.0 min arc) horizontallyon a display monitor placed either 57 or 91 cmaway on the subject's midline. Target luminancewas maintained at least 1 log unit above screenluminance. Fixation was tested by having the sub-ject maintain gaze on (for 15 to 120 sec) the targetwhich was placed either on the midline or 2.5 or5.0 deg to the left or right of the midline. Driftamplitude and velocity during fixation were de-termined at four test sessions; at each session, thesame 15 to 30 sec portion of record was used toobtain all drift measures. Drift amplitude was de-termined in two ways. (1) The maximum peak-to-peak drift amplitude, regardless of time requiredfor completion of the movement, was found, and(2) maximum peak-to-peak drift amplitude duringconsecutive 1 sec fixation intervals was obtainedand averaged. Drift velocity was also determinedin two ways. (1) Maximum drift velocity, regard-less of time required for completion of the move-ment, was obtained, and (2) maximum drift veloc-ity during a 200 msec period for consecutive 1 secintervals was obtained and averaged. Saccadicmovements were tested by having the subjecttrack the spot moving either in random horizontalstep displacements ranging from 0.25 to 8.5 deg inamplitude or in predictable steps having a fre-quency of 0.5 Hz with amplitudes of 0.6, 1.25, 2.5,5.0, or 10.00 deg. Pulse inputs were also used.Pursuit was tested by having the subject follow thetarget moving within a range of constant velocities(0.95 to 6.75 deg/sec) and fixed amplitudes (1, 2,4, or 8 deg) in several possible combinations.Mean smooth-pursuit gain was determined by av-eraging values of smooth-pursuit gain (eye velocitydivided by target velocity) for each individualramp segment of smooth tracking for 5 to 15 cyclesof target motion.

Case history. The patient was an 18-year-oldwhite man who came to our clinic to obtain a re-placement for his spectacles which had been lost 1year earlier. He reported that vision had alwaysbeen poor in the left eye and that due to a birthtrauma, his left eye had been totally occluded dur-ing the first 2 days of life. Refraction was +5.00diopters in the left eye (20/230) and +3.00 diop-ters in the right eye (20/15). Although the initialcover test indicated 3 prism diopters of left eso-

Volume 18Number 2 Reports 215

tropia with 2 prism diopters of left hypertropia,these findings were confounded by unsteady fixa-tion in the amblyopic eye. On later occasions asfixation became steadier, subsequent repeatedcover tests clearly showed the absence of anystrabismus. Initial visuoscopy indicated 10 prismdiopters of temporal and 5 prism diopters of su-perior unsteady eccentric fixation. But again, be-cause of very unsteady fixation and lack of a dis-tinct foveal reflex, this finding was simply an es-timate, although nonfoveal fixation was clearlypresent. Haidinger's brush and afterimage transfertest indicated normal retinal correspondence. Noocular or neurological disease was detected. Thepatient indicated that he would be willing to un-dergo therapy in order to improve vision in hisamblyopic eye.

The initial diagnostic tests and the first phase oforthoptics were conducted prior to the authors'involvement in the case. Orthoptics proceduresincluded occlusion (inverse occlusion during theday and direct occlusion in the evening); placingand maintaining the Haidinger's brush or trans-ferred afterimage on small acuity targets; eye-handcoordination activities such as tracing and trackingobjects; accommodation "jump focus " exercises todevelop facility of accommodation; and at-homeand in-office pleoptics according to Bangerter'smethod. During this 6-month training period, ec-centric fixation decreased to approximately 3 to 5prism diopters temporal, and visual acuity was attimes as high as 20/50. However, neither measurewas stable. The second phase of orthoptics trainingin which new clinicians began their rotation lasted10 months. The authors became involved in eyemovement testing, as well as some phases of clini-cal testing and training, during the last 8 months ofthe second phase. The initial comprehensiveexamination in the second phase showed nochange in refraction and absence of strabismus asjudged by repeated cover tests. Eccentric fixationwas 2 prism diopters temporal as measured byHaidinger's brush, afterimage transfer, and vis-uoscopy. Visual acuity was 20/200. Orthopticstraining procedures similar to those used in thefirst phase were instituted, with the following ad-ditional techniques or modifications introduced atthe indicated improved acuity levels: antisup-pression training (20/90), fusion training (20/70),direct occlusion (20/50), and saccadic and pursuittracking (20/25). A variety of therapeutic measureswere implemented in order to increase the prob-ability of a functional cure. It is difficult to deter-mine whether all procedures were of equal benefit

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Fig. 1. Changes in eccentric fixation, visual reso-lution, and saccadic latency for both eyes duringlast 8 months of orthoptics therapy. Note cen-tralization of fixation and normalization of visualresolution, but maintenance of increased saccadiclatencies in left amblyopic eye. Plotted are mean(and standard deviations for saccadic latency) ofmeasures for each test session.

to the patient, and future clinical research in thisdirection will aid the clinician in optimizing hisamblyopia treatment plan. Stereopsis was lessthan 800 sec arc early in the first phase of training,but it improved to approximately 60 sec arc once20/20 visual acuity was attained. Eye movementswere recorded on six separate occasions duringthis second phase of training. Two months after20/20 acuity was attained, the patient moved toanother state and was therefore not available forfollow-up testing.

ResultsSaccadic eye movements. One of the most con-

sistent findings of our study was the persistence ofincreased saccadic latencies in the amblyopic eye(Fig. 1). As fixation centralized and visual acuitynormalized, saccadic latency remained approxi-mately 100 msec longer for monocular trackingwith the amblyopic eye than for either binoculartracking or monocular tracking with the dominanteye. Saccadic latency did not vary as a function oftarget eccentricity for the relatively small range ofvalues tested. Static overshooting5 (the primarysaccade was larger than required, thus necessitat-ing a secondary corrective saccade occurring ap-

216 ReportsInvest. Ophthahnol, Visual Sci.

February 1979

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Fig. 2. Monocular saccadic tracking amblyopic eye (20/20). Target amplitude and frequency,0.6 deg and 0.5 Hz, respectively. Note frequent large static overshoots, as well as increasedfixation (amplitude) levels following the overshoots. Intersaccadic intervals for overshootsgenerally ranged from 100 to 200 msec. Temporal drift more prominent than nasal drift duringbrief fixation periods. 0Al Eye position amblyopic eye;0T, target position; T, templewardmovements; A', nasalward movements.

proximately 100 to 200 msec later) and glissadicundershooting5 (slow "drifting" eye movementswith return velocities ranging from 2 to 20 deg/secand resulting from pulse-step mismatches in thesaccadic controller signals) were also observed.Large static overshoots (0.8 to 2.4 deg in ampli-tude) were found at times throughout the course oftreatment for both random and predictable steptracking, and this was particularly pronounced fortracking small (0.6 deg), predictable (0.5 Hz) stepdisplacements (Fig. 2). Saccadic gain greater thanunity for small-amplitude step tracking was evi-dent from the large static overshooting. Intersac-cadic intervals for corrective saccades of the over-shoots ranged from 100 to 200 msec and thus didnot exhibit delays. Overshoot amplitude was in-dependent of target amplitude. Also present wereincreased fixation (amplitude) levels following theovershoots. Marked glissadic undershooting wasno longer a frequent finding once 20/20 visualacuity was attained; it occurred approximately30% of the time at 20/110 visual acuity but lessthan 5% of the time at 20/20. Tracking ofrandom-pulse inputs and small-amplitude stepdisplacements was also tested. The amblyopic eyeresponded to pulses as short as 80 msec in dura-tion and, at times, to random step displacementsas small as 0.4 deg in amplitude, at every testsession. The amblyopic eye responded, at times,with multiple saccades to combinations of pulseand step stimuli. After the initial delayed saccade

(~300 msec delay), remaining saccades in such atrain of multiple saccades often had normal initia-tion times (-150 to 200 msec). The normal eyewould also, at times, respond with multiple sac-cades but without the initial delay to combinationsof pulse and step stimuli. This indicates that themotor control aspects of generation and initiationof saccades were not slowed or prolonged; only thesensory processes involved in initiation of the firstsaccade of a train of multiple saccades was pro-longed or delayed consequent to the amblyopicdefect.n~8 Two other aspects of saccadic eyemovements that support normal motor mecha-nisms in this patient were normal saccadic dura-tions for monocular tracking with the amblyopice v e6-s ancj normal saccadic latencies for binoculartracking and monocular tracking with the domi-nant eye.0"8 Saccadic accuracy was normal forbinocular tracking and monocular hacking withthe dominant eye. During binocular tracking,dynamic violations of Herings law, as commonlyfound in normal subjects,9 were found in ouramblyopic patient at each test session.

Fixational eye movements. Fig. 3 shows changesin presence of abnormal drift (number of 1 secintervals in which increased drift was found di-vided by total number of seconds fixation wastested), average maximum drift velocity andamplitude, eccentric fixation, and visual resolutionduring the course of orthoptics treatment. In gen-eral, drift characteristics tended to normalize, and

Volume 18Number 2 Reports 217

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periods of steady fixation became more frequent asvisual acuity and eccentric fixation normalized.The increase in average maximum drift velocity, aswell as its increased variability, at 20/45 acuity isof interest; one might speculate that when certainrelatively fixed patterns of eccentric fixation aredisrupted, control of drift velocity is adversely af-fected until a new region of fixation is established.Not displayed in Fig, 3 are the maximum driftvalues found at each session. Maximum peak-to-peak drift amplitude was 1.7, 3.4, 2.2, and 1.0deg, and maximum drift velocity was 1.5, 3.3, and1.0, and 0.7 deg/sec at visual acuity levels of 20/110, 20/45, 20/20 (first session), and 20/20 (secondsession), respectively. Evident at all test sessionswas the paucity of single, large saccades and sac-cadic intrusions during fixation; an intrusion con-

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Fig. 4. Monocular pursuit with amblyopic eye as afunction of visual acuity level. In each pair of rec-ords, top trace is eye position, and bottom trace isstimulus (1.0 deg amplitude, 3.75 deg/sec veloc-ity, 1.88 Hz). Note persistence of abnormal sac-cadic substitution in spite of acuity improvement;this tracking response was most pronounced at20/45 level. Symbols same as in Fig. 2.

sists of a pair of saccades of approximately equalamplitude but of opposite direction that occur ir-regularly during fixation at a rate of about one persecond with intersaccadic intervals ranging from150 to 500 msec. These intrusions, commonlyfound in strabismic patients,63 result in little net-change in eye position. Rather, as found inamblyopes without strabismus,6 drift was theprominent feature of the records. Drift charac-teristics were similar for all five amplitudes ofhorizontal gaze tested. Binocular fixation andmonocular fixation with the dominant eye were

218 ReportsInvest. Ophthalmol. Visual Sci.

February 1979

within normal limits (<12 min arc drift amplitude,<20 min arc/sec drift velocity).

Pursuit movements. Two pursuit abnormalities,abnormal saccadic substitution and low pursuitgain, were observed during the course of treat-ment. Abnormal saccadic substitution615 duringpursuit of small-amplitude targets (1 and 2 deg)was found at each test session; that is, saccadeshaving amplitudes generally two to five timeslarger than the target amplitude were used totrack the target, rather than smooth movements.Representative examples of abnormal saccadicsubstitution recorded at three acuity levels for thesame small-amplitude stimulus (1 deg, 3.75 deg/sec) are shown in Fig. 4. Large saccades, withlittle evidence of smooth movements, are promi-nent in each trace. Pursuit gain for tracking oftargets having larger amplitudes (4 and 8 deg) wasalso of interest. When visual acuity was 20/110,long duration (up to 1 sec), low gain (0.1 to 0.2range, 0.14 mean value) pursuit, followed by largesaccades correcting for position errors, was ob-served. Low, variable pursuit gain (0.0 to 0.8range, 0.45 mean value) continued at the 20/45acuity level. However, once visual acuity reached20/25, pursuit gain was generally higher and lessvariable (0.5 to 0.8 range, 0.60 mean value). Pur-suit gain for monocular tracking with the dominanteye generally ranged from 0.7 to 0.95, with a meanvalue of 0.85 (within normal limits for our labora-tory). Conjugate movements were always presentduring binocular pursuit tracking.

Discussion. To the best of our knowledge, this isthe first report in the literature providing quanti-tative eye movement analysis in an amblyope dur-ing an extended period of orthoptics treatment.Although only one patient was studied, we believethat our results and their clinical implications areof interest and importance to those involved inclinical, as well as theoretical, aspects of ambly-opia and its treatment.

Several aspects of eye movement control im-proved in the amblyopic eye during treatment:decrease in drift amplitude, decrease in drift ve-locity, increase in frequency and duration ofsteady fixation, and increase in pursuit gain. Thesefindings demonstrate that as amblyopia decreasedand fixation became centralized, certain aspects ofeye movement control (primarily under the pro-vince of the smooth-pursuit system) could be mod-ified by the orthoptics therapy. Furthermore, thefindings suggest that the "critical period" foroculomotor plasticity for these aspects of eyemovement control in our amblyope extended intoadulthood.

However, other aspects of eye movement con-trol in the amblyopic eye remained abnormalthroughout treatment: increased saccadic laten-cies, abnormal saccadic substitution, and staticovershooting. The increase in saccadic latenciessuggests a processing delay over the central retinain the amblyopic eye involving pathways from theamblyopic eye to centers controlling saccadic in-itiation, such as the superior colliculus,8 althoughinvolvement of parietal lobe mechanisms underly-ing directed visual attention remains a distinctpossibility10 Furthermore, the results repre-sented by Fig. 1 suggest that in amblyopia thoseneural channels conveying and/or processing spa-tial resolution information (probably "sustained"channels"), as well as those neural elements re-sponsible for eccentric fixation, can be functionallymodified in the adult amblyope and require a rel-atively short course of therapy for recovery (thevisual acuity recover)' function for our adultamblyope was similar to that measured in a veryyoung amblyope12). This is in contrast to thoseneural channels (probably "transient" channels")involved in saccadic initiation, where recovery inan adult amblyope is either very slow or no longerpossible. This is consistent with a recent finding ofresidual differences in visual-evoked potentialpeak latencies of greater than 5 msec between thetwo eyes of former amblyopic patients now havingequal vision in each eye, thus suggesting that elec-trophysiological changes remain despite a clinicalcure of the amblyopia.i:i The abnormal saccadicsubstitution response found for tracking a smalltarget moving smoothly over the retina suggests adefect in direction sense6'1 (i.e., difficulty in es-timating small angular changes in target location;in this case, overestimation seems to be the rule),and this may be related to the increased saccadicgain and increased fixation (amplitude) levels thatwere prominent during small-amplitude steptracking (Fig. 2).

A possible complicating factor in this case wasthe effect of form deprivation during the first 2days of life. A recent report by Movshon andDursteler1"1 clearly shows significant shifts in ocu-lar dominance, broadening of cortical receptivefield orientation specificity, and reduction in lat-eral geniculate nucleus cell size with only 1 to 2days of unilateral eye closure in kittens during thepeak of the critical period. Although a criticalperiod for man has not yet been firmly estab-lished, the possibility remains that a short periodof form deprivation very early in life could haveadverse effects on the postnatal development ofthe human visual system.15 It is remarkable that

Volume 18Number 2 Reports 219

several aspects of oculomotor control, as well asvisual acuity and fixation, showed such improve-ment in spite of numerous indications of an unfa-vorable prognosis for a functional cure, includinginitiation of therapy in adulthood, presence ofdeep amblyopia with eccentric fixation, minimaluse of spectacles until high school, and possibleeffects of form deprivation.

The fixation and tracking abnormalities re-corded during the course of therapy would bemost difficult to quantitatively assess by standardclinical techniques. Our results suggest that afternormalization of visual acuity and centralization offixation (the hallmarks of cured amblyopia), subtledefects in oculomotor performance may persist,clearly demonstrating that all vision functions inthe amblyopic eye do not improve concurrently.Thus it appears that orthoptics therapy for ambly-opia should perhaps be continued until visualacuity, fixation, and oculomotor control (as well asother vision functions) are normalized and/or re-main stable for a suitable period of time. Objectiverecording and analysis are essential to quantify thedynamic aspects of eye movements in theamblyopic eye and to monitor the return and per-sistence of normal function. Moreover, those par-ticular objectively determined eye movementmeasures that changed and tended to normalizeduring treatment in our patient, if used in con-junction with the subjectively determined visualacuity measures, could provide the clinician afirmer base upon which to decide when the eyehad been satisfactorily treated and therapy couldbe terminated. Perhaps lack of normalization ofthe oculomotor system results in some improvedor "cured" amblyopic patients reverting to theirformer condition after termination of therapy.Thus accurate recordings of eye movement controlbefore, during, and after treatment may be a valu-able tool in assessing the functional cure ofamblyopia.

We thank Drs. Grisham and Poise for their help andsupport.

From the School of Optometry, University of Cali-fornia, Berkeley. This work was supported in part byNIH Training Grant EY00076 (K. J. C. and R. V. K.) andan Auxiliary to the American Optometric Association Re-search Fellowship (K. J. C.). Submitted for publicationJune 12, 1978. Reprint requests: Kenneth J. Ciuffreda,Department of Basic Optometric Sciences, State Collegeof Optometry/SUNY, 100 East 24th St., New York,N. Y. 10010.

Key words: amblyopia, saccades, pursuit, fixation,oculomotor plasticity, orthoptics, vision development,vision deprivation

REFERENCES1. Burian, H. M., and von Noorden, G. K.: Binocular

Vision and Ocular Motility, St. Louis, 1974, TheC. V. Mosby Co., pp. 420-423.

2. Ludlam, W. M.: Orthoptic treatment of strabismus,Am. J. Optom. Arch. Am. Acad. Optom. 3S:369,1961.

3. Simons, K., Moss, A., and Reinecke, R.: Ocularmotility test administration analysis by computer instrabismus and amblyopia evaluation, Comput.Biol. Med. 8:105, 1978.

4. von Noorden, G. K., and Burian, H. M.: Anelectro-oculographic study of the behavior of thefixation in amblyopic eyes in light- and dark-adaptedstate: a preliminary report, Am. J. Ophthalmol.46:68, 1958.

5. Bahill, A. T, Clark, M. R., and Stark, L.: Dynamicovershoot in saccadic eye movements is caused byneurological control signal reversals, Exp. Neurol.48:107, 1975.

6. Ciuffreda, K. J.: Eye movements in amblyopia andstrabismus, Ph.D. dissertation, School of Op-tometry, University of California, Berkeley, 1977.

6a. Ciuffreda, K. J., Kenyon, R. V., and Stark, L.:Saccadic intrusions in strabismus, Arch. Ophthal-mol. (in press).

6b. Ciuffieda, K. J., Kenyon, R. V., and Stark, L.:Abnormal saccadic substitution during small-ampli-tude pursuit tracking in amblyopic eyes, INVEST.OPHTHALMOL. VISUAL SCI. (in press).

7. Ciuffieda, K. J., Kenyon, R. V., and Stark, L.: Pro-cessing delays in amblyopic eyes: evidence fromsaccadic latencies, Am. J. Optom. Physiol. Opt.55:187, 1978.

8. Ciuffieda, K. J., Kenyon, R. V., and Stark, L.: In-creased saccadic latencies in amblyopic eyes, IN-VEST. OPHTHALMOL. VISUAL SCI. 17:697, 1978.

9. Bahill, A. T, Ciuffreda, K. J., Kenyon, R. V., andStark, L.: Dynamic and static violations of Hering'slaw of equal innervation, Am. J. Optom. Physiol.Opt. 53:786, 1976.

10. Mountcastle, V. B.: Brain mechanisms for directedattention. J. R. Soc. Med. 71:14, 1978.

11. Ikeda, H., and Wright, M. J.: Is amblyopia due toinappropriate stimulation of the "sustained path-way during development? Br. J. Ophthalmol.58:165, 1974.

12. Mohindra, I.: Early treatment of anisometropicastigmatism and strabismus, Am. J. Optom. Physiol.Opt. 54:479, 1977.

13. Lawwill, T.: Electrophysiologic aspects of ambly-opia, Trans. Am. Acad. Ophthalmol. Otolaryngol.85:451, 1978.

14. Movshon, J. A. and Diirsteler, M. R.: Effects ofbrief periods of unilateral eye closure on the kitten'svisual system, J. Neurophysiol. 40:1255, 1977.

1.5. Awaya, S., Mikake, Y., Imaizumi, Y., Shiose, Y.,Kanda, T., and Komuro, K.: Amblyopia in man,suggestive of stimulus deprivation amblyopia, Jpn.J. Ophthalmol. 17:69, 1973.