Apparent movement and eye movements.
Explore the source record for details and available documents.
SEARCH · Search PubMed
Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Explore the source record for details and available documents.
The hallmark of a supranuclear eye movement disorder is a functional impairment of one or several types of different eye movements while other types of eye movements still work. All eye movement information is conveyed via the nuclei of the eye muscle nerves. However, the information for a specific type of eye movement is generated in prenuclear cortical and subcortical areas which are activated depending on the type of eye movement performed. Knowledge about the anatomy of these areas enables us to make a clinical diagnosis or to localize the pathological process to a specific area in many neurological conditions. Examination of eye movements are thus a valuable clinical tool in many neurological and neuroophthalmological diseases. The first part of this two-part contribution presents the different types of eye movements, the concept of neural integration, and prenuclear structures important for horizontal eye movement as well as the pertinent pathology. The second part will appear in the next issue and deals with the cerebral structures that are relevant for vertical eye movements including their pathology.
To evaluate whether mouthing movement in the human fetus is related to advance in gestational age and whether such movement is concurrent with rapid eye movement or non-rapid eye movement phases, 26 fetuses from 28 to 41 weeks' gestation were observed for 60 continuous minutes with real-time ultrasonography. It was evident that regular mouthing movement every 300 to 600 msec concurred with the non-rapid eye movement period, from 35 weeks' gestation to term. Random mouthing movements that occurred at a wide range of intervals from 300 msec to approximately 525 seconds were observed predominantly during the rapid eye movement period and were unrelated to advance in gestational age. These observations were discussed in relation to biologic implications.
Evidence suggests that IL-1beta is involved in promoting physiological nonrapid eye movement (NREM) sleep. IL-1beta has also been proposed to mediate NREM sleep enhancement induced by bacteria or their components. Mature and biologically active IL-1beta is cleaved from an inactive precursor by a cysteinyl aspartate-specific protease (caspase)-1. This study aimed to test the hypothesis that inhibition in brain of the cleavage of biologically active IL-1beta will reduce in rats both spontaneous NREM sleep and NREM sleep enhancement induced by the peripheral administration of components of the bacterial cell wall. To test this hypothesis, rats were intracerebroventricularly administered the caspase-1 inhibitor Ac-Tyr-Val-Ala-Asp chloromethyl ketone (YVAD; 3, 30, 300, and 1,500 ng) or were pretreated intracerebroventricularly with YVAD (300 ng) and then intraperitoneally injected with the gram-negative bacterial cell wall component LPS (250 microg/kg). Subsequent sleep-wake behavior was determined by standard polygraphic recordings. YVAD administration at the beginning of the light phase of the light-dark cycle significantly reduced time spontaneously spent in NREM sleep during the first 12 postinjection hours. YVAD pretreatment also completely prevented NREM sleep enhancement induced by peripheral LPS administration at the beginning of the dark phase. These results, in agreement with previous evidence, support the involvement of brain IL-1beta in physiological promotion of NREM sleep and in mediating NREM sleep enhancement induced by peripheral immune challenge.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Recent investigation demonstrate that ocular motility in eyes with retinal pathology may show a lower propensity to visit such areas of the retina as compared to non-pathological retinal sites. While current ophthalmic instruments with the ability to image both the retina and visual function test target placement on the retina have provided this observation, the ability to quantify in real time these images as an eye movement measurement is presently lacking and the objective of this paper. A Rodenstock confocal scanning ophthalmoscope (CSLO) was used to image the retina during the performance of a visual fixation task. Direct observation of acuity target placement at the retina under continuous viewing conditions was possible with this apparatus. Target fixation eye movement images of the retina were rapidly digitized from video tape records and registered using a specialized rapid retinal image tracking algorithm. Fixational eye movement pattern densities at the retina were derived from these data. Preliminary data obtained demonstrate the utility of this technique in quantifying fixation eye movement patterns observed in three human patients with vocation-related laser retinal injury. In all patients, areas of severe retinal damage was generally avoided. The density of ocular eye movement tends to reflect regions of retinal normality and avoidance of retinal regions with severe pathology. Variation in eye movement density may exist where pathology is less severe.
Smooth pursuit eye movements are known to be driven by a mixture of visual feedback and predictive strategies. Prediction in pursuit allows humans to track predictable stimuli with minimal phase lag. But in certain disease states and focal neurological lesions, normal phase relationships are lost and humans track with increased phase errors. Using a sinusoidal pursuit paradigm, we sorted patients into those with large phase errors and those without. Then, working on the premise that large phase errors may have resulted from lack of prediction, we compared predictive and non-predictive ocular pursuit in patients with large phase errors, patients with normal phase errors and control subjects. Subjects sat in darkness and pursued an intermittently illuminated target moving with constant velocity to the right or left. When the movements were in alternate directions and predictable, all the groups possessed the ability to preprogramme appropriate anticipatory eye movements before target onset, and to use this for predictive pursuit. The difference between patients with large phase errors and normal subjects was not an absolute lack or possession of predictive ability but a difference in the timing at which a preprogrammed motor behaviour was initiated or terminated. The timing variability was wide and formed a graded continuum, the control subjects initiating anticipatory pursuit earlier, and the patients with large phase errors initiating much later. In a second experiment, subjects pursued a predictable ramp stimulus presented at various fixed frequencies. We found that in patients where anticipatory pursuit seemed abolished at one frequency of target presentation, changing the frequency of presentation elicited an anticipatory response. Patients adjusted their pursuit latencies to match the temporal demands of target presentation. At target frequencies above 0.8 Hz, there was a significant positive correlation between latencies in ramp pursuit and phase lags in sinusoidal pursuit. None of our patients showed complete loss of prediction irrespective of how large the phase errors were. Even when severe time delays in the system made it impossible for a subject to initiate anticipatory pursuit before target onset, prediction could still be demonstrated by the significant velocity and timing advantage the subject had in the pursuit of a predictable target stimulus or by the technique of unexpectedly blanking the target.
The aim of this study was to assess whether age-related changes in thoracic shape modify patterns of thoracoabdominal asynchrony (TAA) or applicability of phase angle analysis during sleep in young children with increased respiratory loads. We assessed TAA during polysomnographic monitoring in 14 young children (mean age 32 months, range 19 to 46; mean weight 12.5 kg, range 9.3 to 17) with severe bronchopulmonary dysplasia (BPD). Of the patients 10 were severely enough affected to require tracheostomy. We measured asynchrony of rib cage (RC) and abdominal (AB) movements at midinspiration and the corresponding phase angle from oscillographic recordings during both non-REM and REM sleep. We measured the amplitude of "paradoxical" displacement of either RC or AB during inspiration and expressed this as a percentage of the total displacement of the compartment. Of 9 children who manifested early inspiratory AB paradox during non-REM sleep, 7 showed a figure eight on the Konno-Mead diagram. The magnitude of abdominal paradox during non-REM sleep was significantly positively correlated with age (n = 14, r = 0.68; p < 0.01). Phase angle was significantly negatively correlated with dynamic lung compliance (n = 14, r = -0.66; p < 0.01). During REM sleep, expiratory abdominal muscle activity was abolished and all patients with abdominal paradox "converted" to an open loop with RC paradox during inspiration. Graphic assessment of the Lissajous figure on the Konno-Mead diagram indicated when midinspiratory phase angle analysis did not reflect the severity of TAA and can be used to infer patterns of respiratory muscle recruitment. We conclude that young children manifest patterns of TAA that differ from the early inspiratory RC paradox commonly observed in infants. Comparison of RC-AB loops between non-REM and REM sleep in the same child can assess increased thoracic inspiratory efforts and expiratory muscle activity as potential mechanisms for abdominal paradox, as distinct from diaphragm ineffectiveness.
Objective: To replicate the left minus right (L-R) hemisphere EEG power shifts coupled to rapid eye movement (REM) and non-rapid eye movement (NREM) sleep observed in 1972 by Goldstein (Physiol Behav (1972) 811), and to characterize the L-R EEG power spectra for total EEG, delta, theta, alpha and beta bands.Background: Ultradian alternating cerebral hemispheric dominance rhythms are observed using EEG during both waking and sleep, and with waking cognition. The question of whether this cerebral rhythm is coupled to the REM-NREM sleep cycle and the basic rest-activity cycle (BRAC) deserves attention.Methods: L-R EEG signals for ten young, normal adult males were converted to powers and the means were normalized, smoothed and subtracted. Sleep hypnograms were compared with L-R EEGs, and spectra were computed for C3, C4 and L-R EEG powers.Results: Significant peaks were found for all C3, C4 and L-R frequency bands at the 280-300, 75-125, 55-70 and 25-50 min bins, with power dominating in the 75-125 min bin. L-R EEG rhythms were observed for all bands. Greater right hemisphere EEG dominance was found during NREM stage 4 sleep, and greater left during REM for total EEG, delta and alpha bands (Chi-squares, P<0.001). Theta was similar, but not significant (P=0.163), and beta was equivocal.Conclusions: Earlier ultradian studies show that lateral EEG and L-R EEG power have a common pacemaker, or a mutually entrained pacemaker with the autonomic, cardiovascular, neuroendocrine and fuel-regulatory hormone systems. These results for L-R EEG coupling to sleep stages and multi-variate relations may present a new perspective for Kleitman's BRAC and for diagnosing variants of pathopsychophysiological states.
We adopted the estimate of the intraclass coefficient of reliability, R, to evaluate the reliability of saccadic eye movements quantitative analysis. At a one-week interval we recorded refixative saccadic eye movements twice from fifteen healthy subjects by means of the binocular electrooculographic technique. R was computed for the constants and the slopes of the amplitude/duration and the amplitude/peak velocity relationships, for the mean precision values and for the mean latency values adjusted for subject's age. Our data demonstrated that the reliability of saccade parameters is fairly good for the amplitude/peak velocity relationship, good for the precision and very good for the amplitude/duration relationship. Finally, we believe that the normal variability values we obtained can be usefully employed in neurophysiological longitudinal studies not only in normal subjects, but also in pathological condition provided the more reliable parameters and the more adequate strategies to compute normal variability values are chosen.
Abnormal eye movements and nystagmus are, when present, useful for diagnosis of localization of the lesion. Observations of mortality and range of eye movements, pursuit and saccadic eye movements, ability of visual fixation, nystagmus and involuntary eye movements as well as head and eye position, palpebral fissures, ptosis, pupils are important for assessment of eye movements. Anatomical pathways important for horizontal eye movements locate in the caudal pons and for vertical eye movements, in the rostral mesencephalon. In those structures two types of saccade related neurons--burst cells and pause cells-are present and generate premotor saccadic commands. The gaze directed nystagmus results from the central vestibular disorder, not from the peripheral labyrinthine lesion. Bruns' nystagmus characterized by low-frequency, large amplitude nystagmus on looking ipsilaterally and high-frequency, small-amplitude nystagmus on looking contralaterally, is seen in the brainstem lesion. Ocular bobbing consists of rapid downward movement of the eyes followed by a slower return to the primary position and is a sign of pontine lesion. Opsoclonus, multidirectional saccadic oscillation with out intersaccadic interval and flatter-like oscillation, purely horizontal saccadic oscillation are seen in patients with cerebellar and brainstem lesions and may be due to dysfunction of pause cells.
Eye movement desensitization is a new and effective procedure for post-traumatic stress disorder that requires explanation. Reverse learning is a model developed in artificial neural networks as a theoretical explanation of rapid-eye-movement sleep. It demonstrates that an overloaded node within a network can be consolidated with a series of non-specific activations. Rapid-eye-movement sleep is suspected to have a memory consolidation function. Ponto-geniculo-occipital spikes, which occur in rapid-eye-movement sleep, are a candidate for such activations in the real brain. In cats, the phasic functions of rapid-eye-movement sleep are driven by ponto-geniculo-occipital spikes, which are non-specific, at highest amplitude in the visual system but present in other parts of the cortex. Such spikes can be evoked by sensory events such as eye movements. There is evidence of similar events in the human brain. Induced eye movements could generate ponto-geniculo-occipital equivalent spikes and eye movement desensitization/reprocessing could be explained as a focused and artificial exploitation of the rapid-eye-movement sleep mechanism. This theory of eye movement desensitization/reprocessing enables some explanation of current results and may be relevant to other problems, such as stereotyped behaviour.
1. Intracortical microstimulation of a portion of the monkey frontal eye field (FEF) lying in the floor and posterior bank of the arcuate sulcus evokes smooth, rather than saccadic eye movements. To further explore this region's involvement in pursuit, we recorded from FEF neurons in the vicinity of sites from which smooth eye movements (SEMs) were elicited electrically and studied their responses during smooth-pursuit and saccadic tasks. In this report, we describe the neurons' responses during visually guided smooth pursuit and compare their locations and response properties with those of elicited SEMs. 2. One hundred and ninety-three neurons, recorded from the FEF region in six hemispheres of three rhesus monkeys, were classified as "pursuit neurons". These neurons responded during smooth-pursuit tracking of moving visual stimuli but had no, or only minimal, responses in conjunction with visually guided saccades. Pursuit neurons were located in a small region of the arcuate fundus and posterior bank that overlapped, and extended slightly beyond, the region from which SEMs were elicited with microstimulation. 3. All pursuit neurons had a preferred pursuit direction, and all directions were represented with no strong bias toward ipsilateral, contralateral, up, or down. The directional tuning of 80 pursuit cells was measured quantitatively by testing pursuit in several directions and fitting the responses to a Gaussian function. Tuning indices (the sigma parameter of the Gaussian fit) varied between 13 degrees and 136 degrees. The median tuning index, 44.5 degrees, corresponds to a full width at half maximum of 105 degrees. The ubiquity of selectivity for pursuit direction and the wide distribution of preferred directions indicates that pursuit direction uses a place-code type of representation in FEF; however, the broad directional tuning of most neurons suggests that pursuit direction is given by a weighted average of optimal directions across the population of pursuit neurons active at any given time. 4. In general, the responses of pursuit neurons increased with pursuit velocity. Of 13 neurons formally tested with 2 s of constant-velocity tracking in their preferred direction across a range of target speeds, pursuit velocity sensitivity ranged from 0.24 to 1.42 spikes.s-1.deg-1.s-1, with an average sensitivity of 0.70. This relationship suggests that pursuit neurons represent pursuit magnitude using a rate code; this parallels our previous observation that at most SEM sites, the velocity and acceleration of the electrically elicited eye movements increased as a function of the stimulation current.(ABSTRACT TRUNCATED AT 400 WORDS)
1.) Eye movements were recorded in four Java monkeys (M. fascicularis) after unilateral microinjections (1 microliter, concentration 1 micrograms/microliter) of the GABA antagonist, bicuculline, and the GABA agonist, muscimol, into oculomotor related regions of the vestibular nuclei. Eye movements were investigated in the dark and light during spontaneous eye movements, vestibular stimulation (sinusoidal: 0.2 Hz, +/- 40 deg/s, and velocity trapezoid: 40 deg/s2 acceleration, 120 deg/s constant velocity), and visual-vestibular conflict stimulation. 2.) Bicuculline and muscimol injections consistently led to specific eye movement changes, which were maximal 5-10 min after bicuculline injection (muscimol 10-30 min), and lasted 90-120 min (muscimol 2-4 h). Control injections with NaCl (0.9%) into the responsive area and with bicuculline 2-3 mm more lateral showed no effect. 3.) Bicuculline induced a spontaneous nystagmus of 40.9 deg/s (average, range 10.5-93 deg/s), beating in 60% of the cases to the contralateral and in 40% to the ipsilateral side. The analysis of the slope of the slow phase gave no evidence for an additional gaze holding deficit. The VOR gain in the dark showed a slight decrease (pre: 0.96; post: 0.86) on average. The time constant of decay for slow phase nystagmus velocity after vestibular ramp stimulation was reduced, reflecting a 'velocity storage' deficit. After bicuculline injections nystagmus suppression in the light and during visual-vestibular conflict stimulation was generally well preserved. 4.) After muscimol injections horizontal gaze holding was severely affected. Each saccade was followed by an exponentially decreasing postsaccadic drift with a time constant as short as 250 ms (average 414 ms). The eyes always drifted towards a null-position, which generally did not coincide with the midposition of the eye. The null-position could move up to 35 deg to the contralateral or ipsilateral side. The highly distorted eye movements after muscimol injections prevented VOR-measurements based on eye velocity. Instead vestibular stimulation led to a shift of the null-position with an amplitude corresponding to a gain (eye position/stimulus position) of 0.17 (average) at 0.2 Hz (+/- 40 deg/s). Vertical eye movements did not show a major gaze holding deficit. 5.) From the experiments it can be concluded that the inhibitory transmitter GABA plays an important role for eye movement generation within the vestibular nuclei. Bicuculline induces mainly a vestibular imbalance with little evidence for a neural integrator deficit. In contrast unilateral muscimol injections lead to a complete, reversible loss of function for the common horizontal neural integrator, which converts eye velocity into eye position signals. The accompanying shift of the null-position reflects an additional vestibular imbalance.
After the discovery of rapid eye movement (REM) sleep in 1953, oneiric activity was long thought to be associated uniquely with REM sleep. Subsequent evaluation of sleep in humans combining neurophysiologic, psychophysiologic, and, more recently, functional neuroimaging investigations, has instead shown that dreaming also occurs during non-REM (NREM) sleep. It has been documented that hallucinatory activity during sleep is a normal phenomenon that is not constant throughout the night but increases toward morning when it tends to become present to the same extent in REM and NREM sleep. The role of sleep mechanisms in the generation of visual hallucinations is well-recognized in narcolepsy in the case of hypnagogic hallucinations, which are thought to derive from a REM-dissociation state in which dream imagery intrudes into wakefulness. Similar mechanisms have been hypothesized to play a role in the physiopathogenesis of visual hallucinations in various neuropsychiatric disorders. Furthermore, a growing body of evidence indicates that not only REM but also NREM processes, such as arousal-related processes, may play a role in the physiopathogenesis of hallucinations in the aforementioned disorders. The role of these processes has been most extensively documented in visual hallucinations occurring in the context of delirium tremens and Parkinson's disease.
Lateral eye movements evoked by linear head motion were evaluated in human subjects by subtracting the eye movement responses to head-centred angular oscillation in the dark, about a vertical axis, from the responses evoked by similar oscillation with the head displaced 30 cm eccentrically from the axis. The centred oscillation gave a purely angular stimulus whereas the eccentric oscillation gave an additional tangential linear acceleration acting laterally to the head. The stimuli used were relatively unpredictable, enveloped sinewaves at 0.02 to 1.2 Hz, 60 degrees/s peak angular velocity, 0.004 to 0.24 g peak tangential acceleration, and subjects were either given no instructions or were told to imagine fixating on targets at 60 cm or 5 m distance. Eye movements of significantly higher velocity were evoked in the eccentric position, particularly at the higher frequencies and when subjects imagined near targets. The increase in velocity of eye movement was attributed to the linear stimulus and probably derives from stimulation of the otolith organs. The frequency response of the gain (degree/s/g) of these movements gave an approximate slope of -1, indicating that the eye velocity bears a constant proportionality to linear head velocity. The findings are in accord with the theoretical prediction that eye movements compensating for linear head motion should only be required for viewing near targets. These otolithic influences on eye movements could either the mediated by a direct "otolith-ocular reflex" which is subservient to viewing conditions, or, alternatively, the otolith signals may modify the activity of other oculomotor mechanisms.