The use of fibrin coagulum fixation in ocular surgery; in intraocular surgery.
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Spontaneous palinopsia (visual perseveration) and bitemporal visual extinction provoked only by ocular fixation developed in a patient with multiple sclerosis who had chronic bilateral retrobulbar optic neuritis. There were no signs of hemispheral compromise. The intermittent visual symptoms seemingly arose from the lesioned optic nerves, but were probably integrated at a cortical level. Palinopsia, classically considered diagnostic of posterior hemispheral cortical lesions, can also occur in patients with peripherally placed lesions of the visual pathways.
We examined ocular fixations during line bisection in five patients with left hemianopia, two patients with right hemianopia, nine patients with left hemi-neglect and nine normal control subjects. Compared with measures in control subjects, the median fixation, and left- and rightmost fixations were shifted contralaterally in patients with hemianopia alone and ipsilaterally in patients with hemi-neglect. The fixation with the longest duration and the bisection point were also shifted contralaterally with hemianopia and ipsilaterally with hemi-neglect. However, the number of fixations and the spatial range spanned by fixations did not differ between the groups, showing that ocular exploration was not truncated in any group. Only some patients showed a previously reported directional search bias. Overall, there was no directional bias in saccadic number or amplitude. The distribution of fixations was most dense at the centre of the line in normal subjects, while hemianopic patients fixated most frequently at the ends of lines in their contralateral (blind) hemispace and at a central locus that was biased slightly contralaterally, as was their bisection judgement. This contralateral bias may reflect either an adaptive contralateral attentional gradient or a non-veridical spatial representation within the remaining normal hemifield. Hemi-neglect patients had a broad distribution of fixation peaks in the ipsilateral hemispace. Of two hemi-neglect patients with many fixations, one clustered fixations at a position right of centre, as if a normal fixation pattern was shifted rightward, while the other had two fixation peaks: one to the far right and the other near the centre of the line, reminiscent of the dual peaks of activity seen in some recent hemi-neglect models. These data reveal a heterogeneity in the routes by which right-biased judgements of spatial centre are reached by hemi-neglect patients.
We studied the strategic (presumably cortical) control of ocular fixation in experiments that measured the fixation offset effect (FOE) while manipulating readiness to make reflexive or voluntary eye movements. The visual grasp reflex, which generates reflexive saccades to peripheral visual signals, reflects an opponent process in the superior colliculus (SC) between fixation cells at the rostral pole, whose activity helps maintain ocular position and increases when a stimulus is present at fixation, and movement cells, which generate saccades and are inhibited by rostral fixation neurons. Voluntary eye movements are controlled by movement and fixation cells in the frontal eye field (FEF). The FOE--a decrease in saccade latency when the fixation stimulus is extinguished--has been shown to reflect activity in the collicular eye movement circuitry and also to have an activity correlate in the FEF. Our manipulation of preparatory set to make reflexive or voluntary eye movements showed that when reflexive saccades were frequent and voluntary saccades were infrequent, the FOE was attenuated only for reflexive saccades. When voluntary saccades were frequent and reflexive saccades were infrequent, the FOE was attenuated only for voluntary saccades. We conclude that cortical processes related to task strategy are able to decrease fixation neuron activity even in the presence of a fixation stimulus, resulting in a smaller FOE. The dissociation in the effects of a fixation stimulus on reflexive and voluntary saccade latencies under the same strategic set suggests that the FOEs for these two types of eye movements may reflect a change in cellular activity in different neural structures, perhaps in the SC for reflexive saccades and in the FEF for voluntary saccades.
Electro-oculographic recordings of horizontal eye movements in two patients with dorso-mesencephalic lesions are analysed. Tracings shows essentially: (A) dysconjugate glissadic dysmetria, with adduction overshoot and abduction undershoot, and (B) instability of ocular fixation. Fixation instability consists of bursts of 2 or 3 bilateral to-and-fro eye movements, of 4 degree or less amplitude. During a burst there is no evident latency between successive ocular movements. Bursts often appear following horizontal refixation saccades, and are then repeated once or twice with regular intervals. In one patient, fixation instability phases are more often elicited by saccades to the right than to the left. The typical occurrence of fixation instability after the fast phase of optokinetic nystagmus is described. The alteration of ocular fixation described in our patients belongs to the general group of "saccadic intrusions" as defined by Daroff et al. (1977). Resemblance with "lightning eye movements" (Atkin and Bender, 1964) and "opposed adducting saccades" in the Sylvian aqueduct syndrome (Ochs et al., 1979) is discussed.
The behavior of 64 normal subjects was studied after they had been submitted to excentric lateral ocular fixation of gaze of more than 40 degrees for periods of one the three minutes. A significant proportion developed vertigo, slow segmental deviations and nystagmus. Nystagmus appearing during gaze fixation (physiological nystagmus of extreme lateral gaze) was distinguished from nystagmus in the opposite direction which appeared after cessation of fixation and was named "post-fixation nystagmus". The possible role of proprioceptive receptors in the extra-ocular muscles is discussed and a hypothesis proposed of an oculo-oculogyric reflex possibly through the vestibular nuclei and influencing the control mechanisms of posture and balance.
Extraretinal and visual afferent sources of ocular fixation instability were investigated in a group of strabismic amblyopes. Extraretinal drift-bias was revealed by fixational eye movements in darkness. The resulting dark drift-bias was highly correlated with an imbalance of the vestibulo-ocular reflex (VOR). No significant difference in dark drift-bias or VOR imbalance was found between normal and amblyopic observers. Visual afferent sources of fixation instability were revealed by after-effects of nasalward and temporalward retinal image motion upon ocular drifts in the dark (motion after nystagmus) (MAN). Nasalward biases of MAN were significantly greater in amblyopic than nonamblyopic subjects. Directional biases of optokinetic nystagmus in amblyopia were accounted for by normal unindirectional extraretinal drift sources and by an abnormal visual afferent nasal drift-bias of the fixating eye coupled with reduced sensitivity for detecting errors of retinal slip.
As prior studies indicated abnormal cerebellar-vestibular-based sensorimotor mechanisms and neurological and ENG diagnostic parameters in anxiety disorders and because ocular fixation and sequential scanning are cerebellar-vestibular-modulated, it appeared reasonable to measure these and related ocular functions in matched samples of anxiety-disordered and control subjects. In this study, the optokinetically-determined fixation, sequential scanning, and perceptual span capacities obtained by means of a newly revised blurring-speed method were significantly lower or impaired in 70 anxiety-disordered patients vs 70 controls. Such data supported further the hypothesis that there may be cerebellar-vestibular predispositions to anxiety disorders and the optokinetically-based tracking method may prove useful in separating a diverse array of CV-determined or related anxiety symptoms from those of other origins. However, independent validation as well as additional studies of anxiety disorders using larger samples vs random or "normal" controls are required before conclusions are justified.
Fourteen patients with a chronic, unilateral lesion restricted to the frontal lobe (twelve involving the frontal eye field (FEF)), nine patients with a chronic, unilateral lesion restricted to posterior association cortex (eight involving the intraparietal sulcus (IPS)), and twelve neurologically normal control subjects were studied in an anti-saccade task. A combination of manipulating cuing and fixation offset enabled us to examine the effects of chronic oculomotor lesions on both saccade preparation and voluntary control over ocular fixation. Patients with lesions of the FEF made more errors (reflexive glances) toward contralesional targets, whereas patients with IPS lesions made fewer errors toward contralesional targets. Patients with IPS lesions had increased latencies to initiate saccades away from contralesional targets. For FEF patients, the presence of a fixation point inhibited the initiation of contralesionally directed saccades less than those directed ipsilesionally. Saccade preparation in response to a cue did not reduce the inhibitory effect of a fixation point on initiating anti-saccades directed either ipsilesionally or contralesionally for either patient group. We conclude that chronic IPS lesions result in a reduced contralesional visual grasp reflex (VGR) and delayed utilization of visual signals in the contralesional field for planning voluntary eye movements. In contrast, patients with chronic FEF lesions are impaired in inhibiting the VGR toward contralesional signals, and manifest an asymmetry in the balance between fixation and saccade activity. Moreover, voluntary control of fixation is compromised after chronic damage to either frontal or parietal oculomotor cortex.
1. The introduction of a period of darkness between the disappearance of an initial fixation target and the appearance of a peripheral saccade target produces a general reduction in saccadic reaction time (SRT)-known as the gap effect- and often very short latency express saccades. To account for these phenomena, premotor processes may be facilitated by release of visual fixation and advanced preparation of saccadic programs. The experiments described in this paper were designed to test the relevance of the ocular fixation disengagement and oculomotor preparation hypotheses by identifying the influence of different factors on SRTs and the occurrence of express saccades in the monkey. 2. The SRTs of two monkeys were measured in two behavioral paradigms. A peripheral saccade target appeared at the time of disappearance of a central fixation target in the no-gap task, whereas a 200-ms period of no stimuli was interposed between the fixation target disappearance and the saccade target appearance in the gap task. The distribution of SRTs in these tasks was generally bimodal; the first and second mode was composed of express and regular saccades, respectively. We measured the mean SRT, mean regular saccade latency, mean express saccade latency, and percentage of express saccades in both tasks. We also estimated the gap effect, i.e., the difference between the SRTs in no-gap trial and the SRTs in gap trials. 3. Once the animals were trained to make saccades to a single target location and produce express saccades, SRTs in both no-gap and gap trials displayed a broad tuning with respect to the spatial location of the trained target when the target location was varied randomly in a block of trials. Express saccades were made only to a restricted region of the visual field surrounding the trained target location. A gap effect was present for nearly all target locations tested, irrespective of express saccade occurrence. Finally, the probability of generating an express saccade at the trained target location decreased with the introduction of uncertainty about target location. 4. The occurrence of express saccades increased with the duration of the visual and nonvisual (gap) fixation that the animal was required to maintain before the onset of a saccade target. The gap duration was effective in reducing the mean SRT for gaps < or = 300 ms, and it was more influential than comparable variation in the visual fixation duration. 5. The occurrence of express saccades made to targets of identical eccentricity increased when the initial eye fixation position was shifted eccentric in a direction opposite to the saccade direction. Concomitantly, mean SRT decreased by approximately 2 ms for each 1-deg change in initial eye fixation position. 6. The occurrence of express saccades depended upon contextual factors, i.e., on both the behavioral task (no-gap or gap) and the latency of the saccade that the monkey executed to the same target in the preceding trial. The highest percentage of express saccades was observed after an express saccade in a no-gap trial, whereas the lowest percentage was obtained after a regular saccade in a gap trial. 7. These findings indicate that training-dependent express saccades are restricted to a specific spatial location dictated by the training target, and their incidence is facilitated by high predictability of target presentation, long-duration foreperiod, absence of visual fixation, eccentric initial eye position opposite to the saccade direction, and express saccade occurrence in the previous trial. The release of fixation afforded by the gap accounts for the general gap effect, but has only a modulatory influence on express saccade generation. We conclude that advanced motor preparation of saccadic programs generally reduces SRT and is primarily responsible for the occurrence of express saccades, which therefore may be caused mainly by neuronal changes restricted to a specific locus-coding for the trained movemen
In this study, the execution of delayed saccades in 15 DSM-III-R-schizophrenic patients and 15 normal subjects was investigated. While looking at a central fixation cross, a peripheral target was randomly presented at 10 degrees eccentricity. Subjects were instructed to saccade to the target when the fixation cross was switched off after 500 ms. Two experiments were conducted: (a) a delayed-saccade task and, (b) a memory-guided saccade task, that is, the peripheral target was switched off together with the fixation cross. In the delayed-saccade task, amplitudes of regular saccades did not differ between schizophrenic patients and normals. In the memory-guided saccade task, schizophrenic subjects showed marked hypometric saccades. Incorrect delayed saccades (while the fixation cross was on) were also hypometric in schizophrenics, but not in normal controls. The final eye position, i.e., the position reached after the execution of correction saccades, however, did not differ between patients and controls. This means that schizophrenics show a deficit in the programming of primary saccades, if the fixation point and the peripheral target are (a) both visually presented or (b) both memorized. The results support the hypothesis that these saccades are the result of an averaging effect between the fixation point and the peripheral target. It is further hypothesized that these deficits might be explained by a lack of prefrontal inhibition of ocular fixation areas.
103 consecutive patients attending the Visby County Hospital due to vertiginous symptoms were included in the present study. All patients underwent conventional audiometric investigation, brainstem audiometry (ABR), electronystagmography including spontaneous, -gaze-, and positional nystagmus in darkness and under fixation, caloric tests with and without ocular fixation, pendular smooth pursuit test and saccade analyses. Optokinetic nystagmus-test and visual evoked potential recording were performed in some of the patients. Half of the patients underwent CT brain-scan. Abnormal otoneurophysiologic findings suggesting a central origin (pons, mesencephalon, cerebellum) was noted in 55% of the cases. CT brainscan displayed acoustic neuromas in three patients and a cerebellar affection in three patients. Otherwise the CT-scan was normal in the examined patients. In the present investigation the most sensitive tests for diagnosing disorders of central origin resulting in vertiginous symptoms were found to be the brainstem audiometry and smooth pursuit testing. In only two patients the results of the otoneurophysiologic examinations was found to be normal despite a convincing history suggesting a central nervous system disorder.
The eyelid of a patient with apparent unilateral blepharoptosis and a preference for fixation with the contralateral eye, was corrected surgically. However, postoperatively when the preferred (unoperated) eye was used for fixation, the ptosis appeared to have been overcorrected. When the non-preferred (operated) eye was forced to take up fixation, the overcorrected lid position resolved, but ptosis of the unoperated eyelid was unmasked. Surgical correction of this previously masked ptosis ultimately produced a satisfactory result. Our experience emphasizes the importance of ocular fixation preference when evaluating patients with blepharoptosis.
The realisation of combined movements of the head and eyes requires the capacity to modulate the vestibulo-ocular reflex (VOR) but the absence of sufficiently rapid visual feed back results in an open loop function. This reflex must be modulated by other mechanisms. Two options are discussed. A modulation of the gain of the reflex loop is not satisfactory for small combined movements of the head and eyes as it would no longer permit the effective compensation for unexpected perturbations of movement of the head. An additive mechanism modifying the VOR through the addition of an other ocular movement is limited by the constrictions of latency, speed and amplitude of such movement. According to experimental conditions, varying complementary effect of the two mechanisms seems to result in maximum efficiency. This paper attempts to include the mechanism of the ocular fixation index (OFI) among the models of study. The OFI applied to a pendular test is, by the nature of its stimulus, more physiologic and more capable of being integrated into existing models. In the usual conditions of the test, the additive model is probably dominant with a preponderant role in the ocular pursuit system. But whatever may be the part of each mechanism, the OFI is not only dependent on the integrity of the floccular inhibition of the VOR but on the numerous cortical and subcortical structures involved in the realisation of voluntary ocular movements. This information should encourage clinicians to investigate the ocular movements of patients presenting vertigo, particularly those with visual instability on head movements.
We investigated the effect of strategic suppression of reflexive eye movements on external control over fixation using a fixation offset paradigm. A visual signal at fixation facilitates the fixation reflex and inhibits eye movements. Certain preparatory states render the fixation reflex less reactive to visual stimulation at fixation, as evidenced by a reduction in the fixation offset effect (FOE). For example, past studies have suggested that the reduced FOE during anti-saccade tasks results from the requirement to inhibit reflexive eye movements. We tested whether suppressing reflexive saccades reduces external control over ocular fixation using a go-nogo saccade paradigm. During each trial, one of two targets appeared in the periphery. Participants were instructed to saccade to one target (go), but when the other target appeared they either had to maintain fixation (nogo) or move their eyes in the direction opposite the target (anti). When nogo trials were admixed with target-directed saccades a large FOE was observed compared to when target-directed saccades occurred alone (experiment 1); however, when anti-saccades were mixed with target-directed saccades, a small FOE was observed for both types of eye movements (experiment 2). We conclude that suppressing reflexive eye movements does not reduce external control over fixation. Further research is necessary to elucidate which other component of preparing to make an anti-saccade diminishes the FOE.
Perception of stability of the visual world and control of ocular fixation and tracking are altered in subjects submitted to high frequency vibration. Studies of the eye movements induced in man by passively rotating the head sinusoidally around a vertical axis show that beyond 8 Hz, the amplitude of the eye movements increases and reaches 2.5 times the amplitude of head movement at 30 hz. The high amplitude eye oscillation may, at least in part, explain the perception of visual world instability and the decrease of visuo-oculomotor system performance in man submitted to high frequency vibration. Two interpretations of this phenomenon have been proposed (9). High amplitude eye movements induced at high frequency may be due to either a non-linearity of the vestibulo-ocular reflex (VOR) or mechanical resonance oscillations of the orbital apparatus. To test these hypotheses, baboons were trained to fixate visual targets. Each animal's head was rigidly attached to a rotating frame through a block of dental cement bolted to the skull. Head rotation was produced by a servo-controlled vibrator. Rotations in the frequency range 1 to 20 Hz were successively applied with the animal in darkness or fixating a stationary target. The results showed that gain curves obtained with baboons are similar to those obtained with man. Paralysis of the muscles of one eye by injection of lidocaine disclosed a behavioral asymmetry of the two eyes at low frequency. The paralysed eye showed no movement below 8 Hz, while the normal eye behaved as in the normal situation. Beyond 8 Hz, the gain of the treated eye increased gradually so that beyond 12 Hz, the two eyes responded.(ABSTRACT TRUNCATED AT 250 WORDS)