Effect of age on adult stereoacuity as measured by different types of stereotest.

AIM: To examine how stereoacuity changes with age as measured by a variety of stereotests. METHODS: Stereoacuity has been measured in 60 normal subjects aged 17-83 years by a single observer using TNO, Titmus, Frisby near, and Frisby-Davis distance stereotests. Motor fusion was measured at (1/3) metre and 6 metres. RESULTS: Overall stereoacuity measured by all tests showed a mild decline with age (p<0.001 for all tests; Spearman rank correlation). A marked reduction to screening or absent levels of stereoacuity was seen in five subjects aged over 55, but only with the TNO stereotest. All these subjects were able to achieve a stereoacuity of 200 seconds of arc or better with the Titmus test and 340 seconds of arc or better using the Frisby near stereotest. There was a small decline with age in the base out motor fusion range measured at 6 metres (p<0.05; Spearman rank correlation). No subject described difficulty in judging distances for everyday tasks. CONCLUSIONS: Although subjects showed some decline in stereoacuity with age by all tests, the large drop in stereoacuity seen in some older subjects using the TNO test was probably due to difficulty overcoming the dissociative effect of the test rather than a true reduction in cortical disparity detection. Results of random dot stereotests should be interpreted with caution in older patients, particularly with respect to their ability to perform everyday visual tasks.

Delayed visual evoked potentials in adults after monocular visual deprivation by a dense cataract.

PURPOSE: To study the effect of monocular visual deprivation caused by dense unilateral cataracts in adults. METHODS: Visual evoked potentials have been recorded in 11 patients after removal of a dense unilateral cataract acquired in adulthood. These were compared with those from 8 control patients after removal of a mild lens opacity. RESULTS: Visual evoked potentials recorded on the first day after removal of a longstanding, dense, unilateral cataract showed a marked delay to stimulation of the operated eye compared to the unoperated eye. No delay was found in the operated or unoperated eye of control patients. Delays in the visual evoked potential returned to normal within approximately 3 months after surgery, with the exception of the two patients with the most longstanding cataracts in whom the delays persisted much longer. CONCLUSIONS: The adult central visual system is sensitive to visual deprivation caused by a longstanding, dense, unilateral cataract. The changes found may be important in understanding the causes of intractable diplopia, which sometimes occurs after the removal of such cataracts.

Reduced binocular beat visual evoked responses and stereoacuity in patients with Duane syndrome.

PURPOSE: To study the effects that the abnormal eye movements of patients with Duane retraction syndrome have on the development of binocular function. METHODS: Pattern reversal visual evoked responses (VEPs) to 15-minutes-of-arc and 60-minutes-of-arc checks and binocular beat VEPs to diffuse sinusoidally modulated 18- and 20-Hz stimuli were recorded in 10 patients with Duane retraction syndrome who maintain binocular function by using an abnormal head posture. Visual acuity, stereoacuity, and eye movements were measured. The results have been compared to those from 10 normal subjects. RESULTS: The patients with Duane retraction syndrome had reduced stereoacuity compared to the normal control group (TNO mean, 82.5 seconds of arc compared to 37.5 seconds of arc; Titmus mean, 143 seconds of arc compared to 44 seconds of arc). The binocular beat VEPs showed a significantly reduced difference beat response at 2 Hz in the patients with Duane syndrome compared to normal subjects (mean signal-to-noise ratio 2.40 +/- 1.05 compared to 4.30 +/- 2.66; t = 2.21, df = 18, P < 0.05). Binocular enhancement of the P100 pattern reversal amplitude to 15-minute checks was increased in these patients, because of a reduction of the monocular P100 amplitudes compared to the normal group. CONCLUSIONS: Patients with Duane syndrome who maintain binocular function using an abnormal head posture have reduced stereoacuity and show electrophysiological evidence of reduced cortical binocular interaction.

Increased binocular enhancement of contrast sensitivity and reduced stereoacuity in Duane syndrome.

PURPOSE: To compare the binocular enhancement of contrast sensitivity and stereoacuity in patients with Duane syndrome and normal subjects. METHODS: Monocular and binocular contrast sensitivity functions were determined using a two-alternative, forced-choice method in 14 patients with Duane syndrome and 14 normal subjects. Monocular and binocular log minimum angle of resolution (logMAR) acuities were measured, and stereoacuity was determined using the Titmus and TNO stereotests. RESULTS: In the patients with Duane syndrome, the binocular enhancement of contrast sensitivity was increased across all spatial frequencies, although stereoacuity was reduced compared to that of the normal subjects. The increased enhancement was caused by a reduction in monocular contrast sensitivity rather than an increase in binocular contrast sensitivity. The patients with Duane syndrome also showed a generalized reduction of contrast sensitivity at high spatial frequencies. CONCLUSIONS: It is suggested that the combination of reduced stereoacuity and increased binocular enhancement of contrast sensitivity seen in Duane syndrome can be explained by a partial loss of binocular cortical cells, caused by intermittent misalignment of the eyes during early visual development.

Selective degeneration of interneurons in the motor cortex of infant monkeys following controlled hypoxia: a possible cause of epilepsy.

Infant monkeys have been subjected to hypoxia with an arterial pO2 of 20-22 Torr for 30 min. Following perfusion 1-2 weeks later electron microscopy of the motor cortex shows a selective degeneration of axon terminals making symmetrical synapses and which probably arise from inhibitory GABAergic interneurons. It is suggested that this may be related to the development of epilepsy following hypoxia.

Initial hypertrophy of cells in undeprived laminae of the lateral geniculate nucleus of the monkey following early monocular visual deprivation.

Comparisons of mean cell area in the lateral geniculate nucleus between normal and monocularly deprived Rhesus monkeys show that closure started in the first few days of life produces an initial hypertrophy of up to 25% affecting undeprived parvocellular cells. Hypertrophy is maximal at 4 weeks. Following this there is later shrinkage affecting both deprived and undeprived parvocellular cells so that ultimately undeprived parvocellular cells are about 10% smaller and deprived parvocellular cells about 35% smaller than corresponding cells in normal animals.

Effects of enucleation at different ages on the sizes of neurons in the lateral geniculate nucleus of infant and adult monkeys.

Cell areas have been measured in the lateral geniculate nucleus following enucleation in 7 infant and 3 adult monkeys. Deafferented cells showed rapid transneuronal degeneration. Following enucleation at birth non-deafferented parvocellular LGN cells underwent hypertrophy which was followed by a delayed return to normal size. Enucleation at 7 months of age caused marked shrinkage of non-deafferented parvocellular cells. These changes in the non-deafferented cells are similar to those following monocular lid closure at the same ages. Sizes of non-deafferented cells were unchanged following enucleation of adult monkeys.

Changes in the size of cells in the monocular segment of the primate lateral geniculate nucleus during normal development and following visual deprivation.

Cell areas have been measured in the monocular segment of the lateral geniculate nucleus in a series of 18 normal rhesus monkeys and in 27 following monocular or binocular lid closure or monocular enucleation. Cells in the parvocellular monocular segment shrank by 16% during the later period of normal development, between about 3 and 18 months of age, in contrasts to cells in the binocular segment which did not. Monocular closure at birth caused hypertrophy of cells in the undeprived monocular segment whereas long-term closure started later caused shrinkage of both deprived and undeprived parvocellular cells additional to that occurring during normal development. In both these instances cells in the monocular segment related to the undeprived eye are undergoing changes indicating some form of binocular interactions even in the monocular segment, but these interactions are considerably weaker than in the binocular part of the nucleus. Enucleation caused marked transneuronal degeneration of cells in the contralateral monocular segment of both infant and adult monkeys.

Experiments to study recovery of lateral geniculate nucleus cell size following monocular lid closure and reverse suture in infant monkeys.

Following monocular eyelid closure at birth in macaque monkeys, reverse suture at 3 weeks of age cancels the difference in size between deprived and undeprived parvocellular lateral geniculate nucleus (LGN) cells by causing hypertrophy of the initially deprived cells. This means that two weeks after reversal cells in both initially deprived and initially undeprived parvocellular laminae are approximately 15% larger than normal. However, long term survival shows that there is a second phase of change during which all parvocellular cells shrink, but particularly the initially undeprived cells which become considerably smaller than the initially deprived cells. Reopening the secondarily closed eye after a short period of reversal resulted in normal cell sizes in one animal, but two animals developed marked squints and had very small parvocellular cells in all laminae, and one animal developed bilateral amblyopia. Simply reopening the eye of two animals after two months of late closure started at 7 months of age reversed the shrinkage of all parvocellular cells which is caused by late closure.

A comparison of cell size changes in central and pericentral representations within the primate lateral geniculate nucleus following early monocular deprivation.

Mean cell areas have been measured in the most posterior part of the lateral geniculate nucleus containing the representation of central retina in 8 normal monkeys (Macaca mulatta) and in 5 monkeys following monocular closure from birth. Comparisons with cell size changes at a more anterior level, where pericentral retina is represented, show that size changes of parvocellular cells at the posterior level are significantly less, being only between half and two-thirds of those more anteriorly. The undeprived cells undergo less initial hypertrophy than cells at a more anterior level and subsequently the deprived cells show less shrinkage. There is no comparable difference for magnocellular cells.

Simultaneous hypertrophy of cells related to each eye in the lateral geniculate nucleus of the infant monkey following short-term reverse suture.

Three infant monkeys were monocularly deprived from birth and reverse sutured at 3 weeks of age for a further period of 1, 2 or 5 weeks before perfusion. Cell areas were measured in the lateral geniculate nuclei and compared to those in normal monkeys and in monkeys following monocular closure. One week after reverse suture, cells in the initially deprived parvocellular laminae were 17% larger than normal and those in the initially undeprived laminae were 28% larger than normal. The initially undeprived parvocellular cells then shrank back to 14% larger than normal at 2 and 5 weeks while the initially deprived cells also remained hypertrophied. Following reverse suture at 3 weeks of age cells in parvocellular LGN laminae related to both eyes are simultaneously hypertrophied until at least 8 weeks of age and the LGN is therefore markedly abnormal even though the size difference between initially deprived and undeprived cells has been cancelled.

Cell sizes in the lateral geniculate nucleus of normal infant and adult rhesus monkeys.

Measurements of mean cell area have been made in the lateral geniculate nuclei of 16 normal rhesus monkeys as a control for changes following visual deprivation. There is little variability between animals and no significant growth between 8 days of age and adulthood in the parvocellular laminae. The magnocellular laminae show more variability and some continuing growth after 8 days of age.

Shrinkage of cells in undeprived laminae of the monkey lateral geniculate nucleus following late closure of one eye.

Comparisons of mean cell area in the lateral geniculate nucleus between normal and monocularly deprived rhesus monkeys show that late closure at between 3 months and a year of age produces up to 25% shrinkage of cells in the undeprived parvocellular laminae and up to 30% shrinkage in the deprived parvocellular laminae.

Sizes of neurons in the primate lateral geniculate nucleus during normal development.

Measurements of cell area have been made in the lateral geniculate nuclei (LGNs) of 18 normal rhesus monkeys aged from 8 days to fully adult. There is much less variability between individual animals than had been thought from measurements of undeprived cells in experimental animals following visual deprivation. It is therefore possible to make reliable comparisons of cell size between different animals. There is no change in size of cells in the parvocellular laminae between 8 days of age and adulthood, although cells in the magnocellular laminae grow a little. In the primate, unlike the cat, the period of maximum sensitivity to visual deprivation does not correspond to a period of rapid cell growth in the LGN.

Effects of monocular closure at different ages on deprived and undeprived cells in the primate lateral geniculate nucleus.

This study has examined the effects of monocular visual deprivation on cells in the lateral geniculate nucleus of the primate by comparing the sizes of cells in deprived and undeprived LGN laminae of experimental rhesus monkeys with those of cells in the corresponding laminae of normal animals. A number of conclusions may be drawn from this comparison: monocular visual deprivation has major effects on cells in the undeprived LGN laminae and these vary with age at closure; the initial effect of monocular closure from birth is to cause marked hypertrophy of undeprived parvocellular cells with little shrinkage of the deprived parvocellular cells, whereas late monocular closure (after 2 months of age) causes marked shrinkage of both undeprived and deprived parvocellular cells; following monocular closure at birth, the LGN abnormality continues to evolve until at least 3 months of age, with a marked parallel shrinkage affecting both deprived and undeprived parvocellular cells. The initial hypertrophy of the undeprived cells is reversed and the deprived cells become smaller than normal; cells in the monkey LGN are sensitive to visual deprivation until about 1 year of age, much later than previously thought. Visual experience, however, modifies this sensitivity so that the effects of monocular visual deprivation are both qualitatively and quantitatively different at different ages; there are important differences between the susceptibility of cells in the magnocellular and parvocellular laminae to visual deprivation; and actual shrinkage of cells to markedly below normal size occurs and the smaller size is not simply failure of growth.

Effect of reopening an eye after a period of monocular deprivation on sizes of neurons in the primate lateral geniculate nucleus.

Following monocular closure shortly after birth the deprived eye of 4 rhesus monkeys was reopened at different times. Following long-term recovery, cells in the undeprived laminae of the lateral geniculate nucleus of these animals were of normal size and those in the deprived laminae were markedly shrunken. Comparisons with animals monocularly deprived for similar periods indicate, however, that in 3 of these animals the undeprived parvocellular cells would have been markedly hypertrophied at the time of reopening the deprived eye, and in two of the animals, little shrinkage of the deprived parvocellular cells would have occurred by this time. Both undeprived and deprived parvocellular cells have therefore undergone marked shrinkage after the deprived eye had been reopened. The parallel shrinkage of deprived and undeprived parvocellular cells which occurs following closure at birth thus appears to be a consequence of the initial abnormalities produced by monocular closure rather than a direct result of the continuing lack of visual input to one eye.

The clinical features of albinism and their correlation with visual evoked potentials.

AIM: To investigate the relation between the clinical and electrophysiological abnormalities of patients undergoing visual evoked potential investigation for albinism. METHODS: 40 subjects with a probable or possible clinical diagnosis of albinism underwent pattern appearance and/or flash visual evoked potential (VEP) examination. The VEP findings are correlated with the clinical features of albinism determined by clinical examination and orthoptic assessment. RESULTS: The majority of patients with clinical evidence of albinism showed a contralateral predominance in the VEPs. There was close correlation between the clinical signs of albinism and the degree of contralateral VEP predominance. This manifested as an interhemispheric latency asymmetry to monocular pattern appearance stimulation but amplitude asymmetry to flash stimulation. The strongest correlation for pattern appearance interhemispheric latency difference was with foveal hypoplasia (rho = 0.58; p = 0.0003) followed by nystagmus (rho = 0.48; p = 0.0027) and iris transillumination (rho = 0.33; p = 0.039). The VEP abnormalities were of greater magnitude in those patients with most features of albinism. Several patients with apparently mild disorders of ocular pigmentation had small but significantly abnormal VEP latency asymmetries. CONCLUSION: There is a strong association between the magnitude of the interhemispheric latency asymmetry of the pattern appearance VEP, and of amplitude asymmetry of the flash VEP, with the clinical signs of albinism. The data are consistent with a spectrum of abnormalities in albinism involving both clinical expression and electrophysiological misrouting, which is wider than previously recognised.

A prospective study of the effect of a unilateral macular hole on sensory and motor binocular function and recovery following successful surgery.

AIMS: To examine the effect of a unilateral full thickness macular hole on sensory and motor binocular function and to study recovery after successful surgical closure. METHODS: Twenty eight consecutive patients undergoing surgery for a unilateral macular hole underwent orthoptic examination, including measurements of Titmus and TNO stereoacuity and motor fusion range before surgery. Twenty three patients had successful anatomical closure. Fifteen of these patients, who had both improved acuity in the operated eye following surgery and were available for further testing, underwent repeat orthoptic assessment 2-7 months after surgery. RESULTS: In all patients stereoacuity was reduced before surgery, but few patients were subjectively aware of a deficit of depth perception affecting their everyday life. In those patients with improved Snellen acuity after surgery, stereoacuity measured by the Titmus stereotest also improved significantly, but not that measured by the TNO test. Two patients were aware of a subjective improvement in depth perception. Motor fusion was markedly reduced compared to normal before surgery, with only limited recovery after surgery. CONCLUSION: A unilateral macular hole notably reduced both stereoacuity and motor fusion. Successful closure improved the deficit in stereoacuity associated with the hole when measured by a stereotest using contoured stimuli. The majority of patients were not subjectively aware of the deficit in stereoacuity or its improvement following surgery.

Anomalies of binocular function in patients with longstanding asymmetric keratoconus.

AIMS: To study binocular function in patients with longstanding asymmetric keratoconus. METHODS: In 20 adult patients with longstanding asymmetric keratoconus managed with a scleral contact lens a full clinical and orthoptic assessment was performed with and without the scleral contact lens in the poorer eye. RESULTS: All 20 patients had a corrected acuity of at least 6/9 in their better eye. With the scleral lens in situ the acuity of the poorer eye ranged from 6/6 to 6/60 and without the lens from 6/18 to hand movements. Patients were aged from 18 to 68 years and had worn a scleral contact lens for between 3 and 106 months. Without the contact lens in their poorer eye all patients had a small exotropia and all showed suppression, with the exception of one patient who had a right hypertropia with diplopia. With the scleral lens in situ 12 patients had an exophoria or esophoria, six a microexotropia, and two a manifest exotropia with suppression. CONCLUSIONS: Binocular function breaks down in some adult patients with longstanding asymmetric keratoconus. This is probably caused by longstanding unilateral visual deprivation. There are similarities to the breakdown of binocular function seen in some patients with a longstanding dense unilateral adult onset cataract who can develop intractable diplopia following cataract surgery.

Intensive occlusion therapy for amblyopia.

AIM: To study the effects of supervised inpatient occlusion treatment for amblyopia in children who had failed to respond to outpatient treatment. METHODS: A retrospective study of 39 children admitted to a paediatric ophthalmic ward for 5 days of supervised intensive occlusion therapy having previously failed to respond to outpatient occlusion. Visual acuity of amblyopic and fellow eyes was recorded at each clinic visit before admission, daily during admission, and at each outpatient visit after discharge. RESULTS: There was no significant overall improvement in visual acuity during a mean of 9 months of attempted outpatient occlusion before admission. During the 5 days of admission 26 children (67%) gained at least one line of acuity in their amblyopic eye and five (13%) gained three or more lines (mean gain 1.03 Snellen lines). The acuities of both the amblyopic and fellow eyes subsequently improved with continuing part time patching as an outpatient, including in nine of the children who did not respond during admission. At the last recorded visit, at a median time of 14 months after discharge, 13 (33%) of the patients had an acuity of at least 6/12 in their amblyopic eye. CONCLUSIONS: The acuity of amblyopic eyes did not improve without effective treatment. Subsequent supervised inpatient occlusion therapy was effective in the majority of the children.