PubMed · 7239821
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M A Lemp. 1981. Precorneal fluid and blinking.. https://pubmed.ncbi.nlm.nih.gov/7239821/
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After prolonged fixation, a stationary object placed in the peripheral visual field fades and disappears from our visual awareness, especially at low luminance contrast (the Troxler effect). Here, we report that similar fading can be triggered by visual transients, such as additional visual stimuli flashed near the object, apparent motion, or a brief removal of the object itself (blinking). The fading occurs even without prolonged adaptation and is time-locked to the presentation of the visual transients. Experiments show that the effect of a flashed object decreased monotonically as a function of the distance from the target object. Consistent with this result, when apparent motion, consisting of a sequence of flashes was presented between stationary disks, these target disks perceptually disappeared as if erased by the moving object. Blinking the target disk, instead of flashing an additional visual object, turned out to be sufficient to induce the fading. The effect of blinking peaked around a blink duration of 80 msec. Our findings reveal a unique mechanism that controls the visibility of visual objects in a spatially selective and time-locked manner in response to transient visual inputs. Possible mechanisms underlying this phenomenon will be discussed.
BACKGROUND: Classical conditioning provides a means of addressing mechanisms of learning and can therefore help understand the pathophysiology of memory alteration in schizophrenia. METHODS: Single cue delay and trace eyeblink conditioning were used in patients with schizophrenia and matched normal control subjects to explore, respectively, cerebellar and hippocampal integrity during learning. We measured percent of conditioned (CRs) and unconditioned responses (URs), their amplitude, and onset and peak latencies. We also accounted for spontaneous blink rates and stimulus-induced responses before learning. RESULTS: During delay conditioning, patients showed CRs with longer onset and peak latencies and improved efficiency compared to normal volunteers without there being differences between patients and normal control subjects in the percentage of CRs. During trace conditioning, neither group showed an increase in CRs as a function of conditioned stimulus-unconditioned stimulus pairings, in part because the level of spontaneous blink rates exceeded the level of CRs; however, patients with schizophrenia showed increased responding 150-400 msec after the conditioned stimulus and in the last 100-150 msec before the unconditioned stimulus, whereas normal control subjects showed only the latter type of responses. The former type of response was more frequent in patients with schizophrenia even before either trace or delay conditioning. CONCLUSIONS: These results suggest integrity of cerebellar mechanisms underlying conditioning, although the altered timing of CRs in patients may indicate differences in the modulation of such responses. Both the greater CR onset latency during delay and the presence of early nonadaptive responses during trace are compatible with the pattern of responding seen in animals with hippocampal damage.
It is common in pediatric ophthalmology to see children with eye disorders that have gone undetected for years. Many conditions can progress slowly, are not painful, or are unilateral so as not to be bothersome to the child or noticeable to the parent or physician. Pediatricians often ask what they could have done to confirm the presence of the condition and whether the child should have been referred for specialty examination. The guidelines set forth in this article should clarify for the pediatrician which children warrant referral to the ophthalmologist.