Richard A. Harrad

Interocular suppression in the primary visual cortex: a possible neural basis of binocular rivalry

In an attempt to demonstrate a physiological basis for the alternating suppression of perception when the two eyes view very different contours (binocular rivalry), we studied the responses of neurons in the lateral geniculate nucleus (LGN) and area 17 of cats for drifting gratings of different orientation, spatial frequency and contrast in the two eyes. Almost half of the LGN neurons studied exhibited modest inhibitory interocular interaction, but independent of interocular differences in orientation. Monocularly driven units in layer 4 of area 17 behaved similarly. However, for the majority of binocular cortical cells, the response to a grating of optimal orientation in one eye was suppressed by a grating of very different orientation shown to the other eye, over a wide range of spatial frequency and independent of relative spatial phase. This interocular suppression exhibits a remarkable non-linearity: a grating of non-preferred orientation in one eye causes significant interocular suppression only if the neuron is already responding to an appropriate stimulus in the other eye [Sengpiel and Blakemore (1994) Nature, 368, 847-850]. We propose that the switches in perceptual dominance during binocular rivalry depend on interocular interactions at the level of binocular neurons of the primary visual cortex, which might involve intracortical inhibition between adjacent ocular dominance columns. The spontaneous alternations in perceptual suppression that occur during prolonged viewing of rivalrous patterns remain to be explained, although significant variation in the strength of neuronal suppression in such conditions was occasionally seen.

Binocular rivalry disrupts stereopsis.

Does the shift from binocular rivalry to fusion or stereopsis take time? We measured stereoacuity after rivalry suppression of one half-image of a stereoacuity line target. After the observer signalled that the single stereo half-image had been suppressed, the other half-image was presented for a variable duration. Stereoacuity thresholds were elevated for 150–200 ms. A control experiment demonstrated that the threshold elevation was due to rivalry suppression per se, rather than masking effects associated with the rivalry-inducing target. Monocular Vernier thresholds, measured as the smallest identifiable abrupt shift in the upper line of an aligned Vernier target that had previously been suppressed by rivalry, were elevated for a much longer duration. This result shows that an appropriately matched stereo pair can break rivalry suppression more easily than can monocular changes in position. With the aid of a similar paradigm, we also measured the duration needed to detect a disparate feature in a random-dot stereogram after rivalry suppression of one half-image of the stereogram. Observers could correctly identify the location of the disparate feature (upper or lower visual field) when the other half-image was presented for a duration ranging from 150–650 ms. In the absence of the matching half-image, the first half-image was suppressed by the rival target for a far longer duration (a few seconds). These findings show that although stereopsis and fusion terminate rivalry, both are initially disrupted for a few hundred milliseconds by rivalry suppression.

Fusional suppression in normal and stereoanomalous observers

Observers with normal stereopsis suppress some of the monocular information contained in each stereo half-image, a phenomenon we call fusional suppression. We measured vernier acuity for an ordinary vertical vernier test target, presented to one eye, that was paired stereoscopically with a vernier target with a large fixed offset, presented to the other eye. The size of the fixed offset, and hence, the disparity of the upper target line, was varied parametrically. Vernier thresholds for the test target rose as a function of disparity, reaching a maximum at 20 min of disparity and then decreasing gradually as the disparity exceeded the limits of foveal fusion (40-60 min arc). In the two normal observers, fusional suppression was symmetrical; neither eye had good access to monocular information. In the stereoanomalous observers, fusional suppression was not symmetrical. When they viewed the vernier test target with the stronger of their two eyes, their vernier thresholds were barely affected by the stereo half-image in the other eye, and so were better than those of the normal observers measured in the same condition. When the stereoanomalous observers viewed the test target with their weaker eye, their fusional suppression was similar in range and magnitude to the suppression found in normal observers. Amblyopic suppression in mild amblyopes may be a residual effect of normal fusional suppression, operating to suppress monocular signals in the weaker eye, without conferring the benefits of normal stereopsis and fusion.

Duration of conjunctival redness following adult strabismus surgery

PURPOSE To determine the duration of postoperative conjunctival injection following strabismus surgery and to assess how this is affected by previous extraocular muscle surgery. This would improve preoperative counseling of strabismus patients. METHODS Subjective evaluation of conjunctival redness based on patient questionnaire response. RESULTS Fifty-three patients returned completed questionnaires. A total of 93 muscles were operated on. Of these, 46 had not undergone previous operations; 47 had. Previously unoperated eyes remained red for a median duration of 9.5 weeks; reoperated eyes remained red for a median of 11 weeks. Of the 93 muscles, 50 were sutured with adjustable sutures. These remained red for a median duration of 11 weeks. Muscles tied with nonadjustable sutures remained red for a median of 10 weeks. CONCLUSIONS In both previously unoperated and reoperated eyes, conjunctival redness resolved in approximately 10 weeks; adjustable sutures did not alter the duration of redness significantly.

Disparity tuning of binocular facilitation and suppression after normal versus abnormal visual development.

PURPOSE To study the pattern of facilitatory and suppressive binocular interactions in stereodeficient patients with strabismus and in healthy controls. METHODS Visual evoked potentials were recorded in response to a Vernier onset/offset pattern presented to one eye, either monocularly or paired dichoptically with a straight vertical square-wave grating, which, when fused with the target in the other eye, gave rise to a percept of a series of bands appearing in depth from an otherwise uniform plane or with a grating that contained offsets that produced a standing disparity and the appearance of a constantly segmented image, portions of which moved in depth. RESULTS Participants with normal stereopsis showed facilitative and suppressive binocular interactions that depended on which dichoptic target was presented. Patients with longstanding, constant strabismus lacked normal facilitative binocular interactions. The response to a normally facilitative stimulus was reduced below the monocular level when it was presented to the dominant eye of patients without anisometropia, consistent with classical strabismic suppression of the nondominant eye. The dominant eye of strabismic patients without anisometropia retained suppressive input from crossed but not uncrossed disparity stimuli presented to the nondominant eye. CONCLUSIONS Abnormal disparity processing can be detected with the dichoptic VEP method we describe. Our results suggest that suppression in stereoblind, nonamblyopic observers is determined by a binocular mechanism responsive to disparity. In some cases, the sign of the disparity is important, and this suggests a mechanism that can explain diplopia in patients made exotropic after surgery for esotropia.

Why can't my child see 3D television?

A child encountering difficulty in watching three-dimensional (3D) stereoscopic displays could have an underlying ocular disorder. It is therefore valuable to understand the differential diagnoses and so conduct an appropriate clinical assessment to address concerns about poor 3D vision.