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K M Robertson

Publications and source records attributed to K M Robertson.

25 records · Page 2Linked to original sources

Disparity vergence dynamics and fixation disparity.

The initial velocity of the vergence response to step changes in disparity was examined in two subjects as a function of the retinal locus and spatial frequency of fusion stimuli. Vergence velocity decreased for both subjects as retinal eccentricity increased and it was unaffected by spatial frequency. The same subjects had very different amounts of fixation disparity (FD). The flat forced duction FD curve for one subject who had rapid vergence adaptation remained unaffected by these two stimulus variables. In contrast, the steep forced duction FD curve for the other subject became steeper as retinal eccentricity and target coarseness increased. These results suggest that prism adaptation overshadows the effects of disparity vergence dynamics upon FD, but in the absence of adaptation, two dynamic properties of vergence (velocity and decay during occlusion) determine the slope of the peripheral limits of the forced duction FD curves. The results also suggest that the vergence system is more sensitive to small disparities subtended by high than low spatial frequency detail. We recommend that the slope of the extreme limits of the forced duction curve be used clinically to discriminate between normal and abnormal disparity vergence dynamics.

Adaptation, Ocular↗

Combined effects of spatial frequency and retinal eccentricity upon fixation disparity.

The variations in fixation disparity (FD) with spatial frequency and retinal locus of fusion locks were examined in two groups of subjects having either steep or flat forced-duction FD curves. FD for subjects with flat curves was unaffected by either spatial frequency or diameter of fusion locks. FD of observers with steep forced-duction curves increased with both the coarseness and eccentricity of fusion locks. Panum's horizontal fusion range increased markedly with target spatial period but only modestly with retinal eccentricity. These results indicate that factors other than the dimensions of Panum's fusional area (PFA) result in the increase of FD found in some observers with peripheral fusion locks.

Convergence, Ocular↗

Orthophorization after occlusion-induced exotropia.

A 36-year-old male had been constantly wearing a patch to avoid diplopia since an operation on the right parietal area of the brain. Postsurgical visual field evaluation indicated a complete bilateral left hemianopia with macular splitting. The patient had a constant alternating comitant exotropia with no suppression. By terminating the patching, establishing the appropriate fixing eye, and applying relieving prisms, diplopia was removed. Once binocularity was thus established, it was found (over the course of 7 months) that binocular function was possible with diminishing amounts of prism power. During this 7-month period, measurements of the patient's heterophoria, motor fusion, and sensory fusion revealed that he adapted from his occlusion-induced exotropia toward an habitual heterophoria. Such vergence adaptation has been defined as orthophorization. The occurrence of vergence adaptation after sensory fusion indicates that sensory fusion plays an important role in the etiology of prism adaptation.

Adaptation, Physiological↗

Effect of visual training on the vertical vergence amplitude.

Visual training has an effect on the vertical vergence amplitudes. Three mature symptomatic patients exhibited a significant increase in the vertical vergence which compensates for the vertical heterophoria. Subjects with normal binocularity and hence no vertical heterophoria did not exhibit increased vertical vergence amplitudes after training.

Adult↗

Electrophysiological detection of aniseikonia.

Steady-state and transient Visually Evoked Responses (VERs) were used to verify a paradoxical aniseikonic condition in an anisometropic patient. Testing on the Remole multimeridional horopter apparatus indicated that a 2% overall magnification was required for the more hyperopic eye to eliminate ocular image size differences. A special lens correction for the patient's aniseikonia resulted in a very significant improvement in visual comfort and binocular function.

Adult↗

Characterization of the fertility of male aromatase knockout mice.

Previous studies employing the male aromatase knockout (ArKO) mouse have indicated that local expression of estrogens appears to be important for the progression of spermatogenesis. In the absence of estrogen biosynthesis round spermatids are observed to undergo apoptosis and thus fail to differentiate into mature, elongated spermatids. This lesion appears to arise between the ages of 18 weeks and 1 year. To ultimately determine if the disruption to spermatogenesis arises earlier than 18 weeks, we performed an intensive study to examine the fertility of younger male ArKO mice. This involved an analysis of their mating capacity together with an extensive stereological analysis, determination of the in vitro potential of mature sperm, and sexual behavior. ArKO and wild-type (w/t) males at 7 weeks of age were placed with w/t females for 7 weeks. At age 14 weeks, the males were killed and the testes removed. ArKO mice were observed to sire significantly fewer litters than the w/t mice; 5 out of the 10 sired no litters at all. Stereological analysis performed on the removed testes found a significant decrease in round spermatid numbers between w/t and ArKO mice at this age; however, there were no differences in all other germ cells and Sertoli cell numbers. When mature spermatozoa were analyzed, sperm from 15-week-old ArKO mice had a significant reduction in motility. This was further reduced by 1 year of age with a decrease in concentration. A preliminary examination of sexual behavior found that ArKO mice did not attempt to mount the females, in contrast to the w/t mice, which mounted consistently during the time period. In conclusion, we observed that ArKO mice have reduced fertility at age 14 weeks. This may be due in part to a disruption in spermatogenesis because the phenotype does appear to arise earlier than 18 weeks, possibly leading to abnormalities in the mature spermatozoa. Or, in part, this may be attributable to an impairment in the development of copulatory behavior, which is consistent with the available evidence that points to a crucial role for estrogens in the neural development and initiation of male sexual behavior.

Animals↗