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Biomedical subjects

J R Tian

Publications and source records attributed to J R Tian.

12 recordsLinked to original sources
PubMed2001

Dynamic visual acuity during transient and sinusoidal yaw rotation in normal and unilaterally vestibulopathic humans.

The vestibulo-ocular reflex (VOR) stabilizes gaze to permit clear vision during head movements. It has been supposed that VOR function might be inferred from dynamic visual acuity (DVA), the acuity during imposed head motion. We sought to determine effectiveness of DVA for detection and lateralization of unilateral vestibulopathy, using rigorous psychophysical methods. Seventeen normal and 11 unilaterally vestibulopathic subjects underwent measurement of optically best corrected DVA during head motion. A variable size letter "E" 6 m distant was displayed in oblique random orientations to determine binocular DVA by a computer controlled, forced choice method. Three types of whole-body yaw rotation were delivered by a servo-controlled chair synchronized with optotype presentation. Two types of motion were predictable: (1) steady-state 2.0-Hz rotation at 10-130 degrees/s peak velocity with repetitive optotype presentation only during head velocity exceeding 80% of peak; and (2) directionally predictable transients at peak accelerations of 1000, 1600 and 2800 degrees/s2 with optotype presentation for 300 ms. For neither of these predictable motions did DVA in vestibulopathic subjects significantly differ from normal, with suggestions from search coil recordings that this was due to predictive slow and saccadic eye movements. Unilaterally vestibulopathic subjects experienced a significant decrease in DVA from the static condition during ipsilesional rotation for all three peak head accelerations. Only during directionally unpredictable transients with 75 ms or 300 ms optotype presentation was the sensitivity of DVA in unilaterally vestibulopathic subjects significantly abnormal during ipsilesional rotation. The ipsilesional decrease in DVA with head motion was greater for 75 ms than 300 ms optotype presentation. Search coil recordings confirmed hypometric compensatory eye movements during DVA testing with unpredictable, ipsilesional rotation. Receiver-operator characteristic analysis indicated ideal detection and lateralization of unilateral vestibulopathy by DVA tested with a 75-ms optotype exposure for unpredictable transient rotations to a peak acceleration of 2800 degrees/s. DVA can reliably detect unilateral deafferentation only if precautions are taken to prevent compensation by predictive slow eye movements and saccades.

Adaptation, Physiological↗
PubMed2001

Impairments in the initial horizontal vestibulo-ocular reflex of older humans.

To determine age-related changes, the initial horizontal vestibulo-ocular reflex (VOR) of 11 younger normal subjects (aged 20-32 years) was compared with that of 12 older subjects (aged 58-69 years) in response to random transients of whole-body acceleration of 1,000 and 2,800 degrees/s2 delivered around eccentric vertical axes ranging from 10 cm anterior to 20 cm posterior to the eyes. Eye and head positions were sampled at 1,200 Hz using magnetic search coils. Subjects fixed targets 500 cm or 15 cm distant immediately before the unpredictable onset of rotation in darkness. For all testing conditions, younger subjects exhibited compensatory VOR slow phases with early gain (eye velocity/head velocity, interval 35-45 ms from onset of rotation) of 0.90 +/- 0.02 (mean +/- SEM) for the higher head acceleration, and 0.79 +/- 0.02 for the lower acceleration. Older subjects had significantly (P < 0.0001) lower early gain of 0.77 +/- 0.04 for the higher head acceleration and 0.70 +/- 0.02 for the lower acceleration. Late gain (125-135 ms from onset of rotation) was similar for the higher and lower head accelerations in younger subjects. Older subjects had significantly lower late gain at the higher head acceleration, but gain similar to the younger subjects at the lower acceleration. All younger subjects maintained slow-phase VOR eye velocity to values > or = 200 degrees/s throughout the 250-ms rotation, but, after an average of 120 ms rotation (mean eccentricity 13 degrees), 8 older subjects consistently had abrupt declines (ADs) in slow-phase VOR velocity to 0 degree/s or even the anticompensatory direction. These ADs were failures of the VOR slow phase rather than saccades and were more frequent with the near target at the higher acceleration. Slow-phase latencies were 14.4 +/- 0.4 ms and 16.8 +/- 0.4 ms for older subjects at the higher and lower accelerations, significantly longer than comparable latencies of 10.0 +/- 0.5 ms and 12.0 +/- 0.6 ms for younger subjects. Late VOR gain modulation with target distance was significantly attenuated in older subjects only for the higher head acceleration.

Acceleration↗
PubMed2001

Otolith function in cerebellar ataxia due to mutations in the calcium channel gene CACNA1A.

The vestibulo-ocular reflexes stabilize retinal images during head movements. While there is a wealth of information about the interaction between the cerebellum and vestibulo-ocular reflexes mediated by the semicircular canals, little is known about the role of the cerebellum in the generation of the otolith-mediated linear vestibulo-ocular reflex (LVOR). By means of transient linear acceleration of the whole body along the interaural axis, we examined the LVOR in six patients with hereditary cerebellar ataxia due to mutations of the calcium channel gene CACNA1A, five with spinocerebellar ataxia type 6 (SCA6) and one with episodic ataxia type 2 (EA-2). Six age-matched normal subjects served as controls. Using a peak acceleration of 0.5 g in combination with recording by the binocular scleral magnetic search coil method, it was possible to study the latency and sensitivity of the LVOR in the first 150 ms after motion onset. The normal LVOR showed a significant dependence on viewing distance and covaried with vergence angle, and could be enhanced by the presence of a visible target. In contrast, the LVOR of ataxic patients had normal latency but significantly decreased sensitivity that was not enhanced with visible or nearer targets despite normal vergence. Substituting for the normal smooth LVOR slow phase, ataxic patients employed catch-up saccades 150-250 ms after motion onset. These findings suggest a critical role of the cerebellum in the modulation of otolith-ocular signals that is independent of motor vergence.

Adult↗
PubMed2001

New tests of vestibular function.

The vestibulo-ocular reflex (VOR) is the only drive for short-latency eye movements stabilizing the retina during externally imposed, sudden, high-head accelerations. New strategies can exploit this unique VOR feature to study it under conditions relevant to the daily lives of patients, and to exclude the contributions from confounding nonvestibular mechanisms. Testing of the yaw vestibulo-ocular reflex (VOR) during random, whole-body rotational transients at < or = 2800 degrees/s2 delivered about centered and eccentric axes enables measurement of gains and millisecond latencies of the canal and otolith VORs in humans. Repeated measurements in acute unilateral deafferentation show sequential recovery of canal and otolith VORs to contralesional rotation, but severe and permanent deficits to ipsilesional rotation. Patients with bilateral loss of caloric responses show severe bilateral loss of VORs to transient rotation, suggesting that the apparent preservation of their VORs during sinusoidal rotations at moderate frequencies may be due instead to somatosensory inputs. Since visual acuity is degraded by retinal image motion, dynamic visual acuity (DVA) measured during imposed head-on-body or whole-body transient motion can correlate closely with VOR performance only if optotypes are presented during directionally and temporally unpredictable, high-acceleration head motion. Prediction and efference copy are relentlessly employed by vestibulopathic patients to enable good DVA during predictable or low-acceleration head motion. The linear VOR to transient lateral acceleration is strongly dependent upon viewing distance. The latency of this otolith VOR is slightly longer and more variable than the canal VOR. Unlike the canal VOR, the otolith VOR does not develop a strong directional asymmetry in unilateral deafferentation. The otolith VOR is bilaterally attenuated in bilateral vestibulopathy, and loses target distance dependence in cerebellar degeneration.

Adult↗
PubMed2000

Initial vestibulo-ocular reflex during transient angular and linear acceleration in human cerebellar dysfunction.

During transient, high-acceleration rotation, performance of the normal vestibulo-ocular reflex (VOR) depends on viewing distance. With near targets, gain (eye velocity/head velocity) enhancement is manifest almost immediately after ocular rotation begins. Later in the response, VOR gain depends on both head rotation and translation; gain for near targets is decreased for rotation about axes anterior to the otoliths and augmented for rotation about axes posterior to the otoliths. We sought to determine whether subjects with cerebellar dysfunction have impaired modification of the VOR with target distance. Eleven subjects of average age 48 +/- 16 years (mean +/- standard deviation, SD) with cerebellar dysfunction underwent transients of directionally unpredictable whole-body yaw rotation to a peak angular acceleration of 1000 or 2800 degrees/s2 while viewing a target either 15 cm or 500 cm distant. Immediately before onset of head rotation, the lights were extinguished and were relit only after the rotation was completed. The axis of head rotation was varied so that it was located 20 cm behind the eyes, 7 cm behind the eyes (centered between the otoliths), centered between the eyes, or 10 cm anterior to the eyes. Angular eye and head positions were measured with magnetic search coils. The VOR in subjects with cerebellar dysfunction was compared with the response from 12 normal subjects of mean age 25 +/- 4 years. In the period 35-45 ms after onset of 2800 degrees/s2 head rotation, gain was independent of rotational axis. In this period, subjects with cerebellar dysfunction had a mean VOR gain of 0.5 +/- 0.2, significantly lower than the normal range of 1.0 +/- 0.2. During a later period, 125-135 ms after head rotation about an otolith-centered axis, subjects with cerebellar dysfunction had a mean VOR gain of 0.67 +/- 0.46, significantly lower than the value of 1.06 +/- 0.14 in controls. Unlike normal subjects, those with cerebellar dysfunction did not show modification of VOR gain with target distance in the early response and only one subject showed a correct effect of target distance in the later response. The effect of target distance was quantitatively assessed by subtracting gain for a target 500 cm distant from gain for a target 15 cm distant. During the period 35-45 ms after the onset of 2800 degrees/s2 head motion, only two subjects with cerebellar loss demonstrated significant VOR gain enhancement with a near target, and both of these exhibited less than half of the mean enhancement for control subjects. During the later period 125-135 ms after the onset of head rotation, when VOR gain normally depended on both target location and otolith translation, only one subject with cerebellar dysfunction consistently demonstrated gain changes in the normal direction. These findings support a role for the cerebellum in gain modulation of both the canal and otolith VOR in response to changes in distance. The short latency of gain modification suggests that the cerebellum may normally participate in target distance-related modulation of direct VOR pathways in a manner similar to that found in plasticity induced by visual-vestibular mismatch.

Adult↗
PubMed1996

Functionally defined smooth and saccadic eye movement subregions in the frontal eye field of Cebus monkeys.

1. Intracortical microstimulation was used to localize and define the smooth and saccadic eye movement subregions of the frontal eye field (FEF) and the supplementary eye field (SEF) in nine hemispheres of six Cebus apella monkeys and to map the hand/arm areas in the dorsal premotor area and other adjacent areas in five hemispheres of three C. apella monkeys. Monkeys were anesthetized during experiments with Telazol, a dissociative agent that has no significant effect on microstimulation-induced eye movement parameters (current threshold, velocity, and duration). The functional subregions were defined with the use of low threshold current (< or = 50 microA). Electrically elicited eye movements were videotaped and quantified. The two types of eye movements were clearly distinguished by their significantly different duration and velocity (P < 0.0001) and their different responses to long stimulus trains. 2. The saccadic subregion of the FEF in Cebus monkeys is in the same location as in macaque monkeys (Walker's areas 8a and 45). Most of the functional and anatomic characteristics of the saccadic subregion of Cebus are the same as those reported in the saccadic FEF subregion of macaque monkeys. 3. A subregion in which only smooth eye movements were evoked was found in the posterior shoulder of the superior arcuate sulcus near its medial tip. A band of inexcitable cortex separated the SEF and this smooth eye movement subregion of the FEF. This supports the proposal that the smooth eye movement subregion is independent of the SEF but is analogous to the saccadic subregion of the FEF. The existence of two subregions of the FEF was further confirmed by single-unit recording results. It is proposed that the smooth eye movement subregion in Cebus monkeys may be comparable with the one described in macaque monkeys. 4. Both saccadic and smooth eye movements were also reliably evoked in the SEF in each hemisphere studied. This result strongly indicates that the SEF is concerned with not only saccadic eye movements, as previously reported, but also with smooth (pursuit) eye movements.

Animals↗
PubMed1996

Corticocortical input to the smooth and saccadic eye movement subregions of the frontal eye field in Cebus monkeys.

1. The locations and connections of the smooth and saccadic eye movement subregions of the frontal eye field (FEFsem and FEFsac, respectively) were investigated in seven hemispheres of five Cebus monkeys. The supplementary eye field was also mapped in seven hemispheres and the hand/arm regions of the dorsal and ventral premotor areas were localized in five hemispheres. Monkeys were immobilized during experiments with Telazol, a dissociative anesthetic agent that has no significant effect on microstimulation-induced eye movement parameters (threshold, velocity, and duration). The functional subregions were defined with the use of low threshold intracortical microstimulation (current < or = 50 microA). Then different retrogradely transported fluorescent tracers were placed into these functionally defined regions. 2. The FEFsac in Cebus monkey is in the same location as the one in macaque monkeys, which is in Walker's areas 8a and 45. The FEFsem is located in the posterior shoulder of the superior arcuate sulcus near its medial tip and is therefore more accessible for tracer injections than the one in macaque monkeys. This subregion is within cytoarchitectural area 6a beta, which is distinct from the adjacent area 6a alpha (dorsal premotor area). This smooth eye movement subregion may be comparable with the one in macaque monkeys. 3. Cortical connection patterns of the FEFsac and FEFsem are similar and parallel to each other. The predominant neural input to these two subregions originates in other cortical eye fields, including the supplementary eye field, the parietal eye field, the middle superior temporal area, and the principal sulcus region. These cortical eye fields each contain two separate, almost non-overlapping, distributions of labeled neurons that project to the corresponding frontal eye field (FEF) subregions. These results suggest that there may be similar, but relatively independent, parallel corticocortical networks to control pursuit and saccadic eye movements. The weak connections between the middle temporal area (MT) and FEF suggest that the MT may not provide the major source of visuomotion inputs to the FEF, but that it rather plays a role in mediating visual information that is relayed from the striate and extrastriate cortices via MT to the parietal cortex and then to the FEF. In addition to the well-known neural connections between the lateral intraparietal area and the FEF, additional parietal projections have been demonstrated from the dorsomedial visual area area specifically to the FEFsac and from area 7m specifically to the FEFsem.

Animals↗
PubMed1995

Slow and saccadic eye movements evoked by microstimulation in the supplementary eye field of the cebus monkey.

1. Intracortical microstimulation was used to map the supplementary eye field (SEF) in eight hemispheres of five Cebus apella monkeys. Monkeys were immobilized during experiments with Telazol (tiletamine HCl and zolazepam HCl), a dissociative anesthetic agent that was demonstrated to have no significant effect on microstimulation-induced eye movement parameters compared with similar experiments in alert, behaviorally trained monkeys. The functional subregions were defined with the use of low-threshold current (< or = 50 microA). Electrically elicited eye movements were videotaped and quantified. Both slow and saccadic eye movements were reliably evoked at low threshold by microstimulation in each of eight hemispheres studied. The two types of eye movements were clearly distinguished by their significantly different duration and velocity (P < 0.0001) and their different responses to long stimulus trains. The results strongly support the proposal that the SEF produces not only saccadic eye movements as previously reported but also slow (pursuit) eye movements.

Anesthetics↗
PubMed1991

Saccades in Huntington's disease: predictive tracking and interaction between release of fixation and initiation of saccades.

We compared saccadic eye movements in 21 patients with Huntington's disease (HD) and 21 normal subjects. In a predictive tracking task, HD patients were unable to anticipate normally the timing and location of a visual target that alternated its position predictably (+/- 10 degrees, 0.5 Hz; mean latency of +170 msec in HD and -78 msec in normal subjects). HD patients and normal subjects, however, showed comparable decreases in saccade latency (110 msec in HD, 124 msec in normal subjects) when the fixation target was turned off 200 msec before (gap task) versus 200 msec after (overlap task) the appearance of an unexpected peripheral stimulus. Taken together, these findings support the idea that HD patients show greater defects in initiating internally generated than in initiating externally triggered saccades. This dichotomy is likely due to involvement of frontal lobe--basal ganglia structures in HD, with relative sparing of parietal--superior collicular pathways.

Adult↗
PubMed1991

Postural control in Huntington's disease (HD).

We studied postural control, using quantitative moving-platform posturography, in 20 patients with Huntington's Disease (HD) and in 20 age-matched controls. HD patients showed considerably more anterior-posterior sway than normals, even when a correction for chorea was attempted. This increase in sway was especially true when, by eliminating visual and by attenuating proprioceptive cues, patients were forced to rely primarily on vestibular cues for balance. HD patients also showed increased latencies (30-50 ms) but normal amplitude, in response to translational perturbations of the platform. HD patients showed increased amplitude of responses to rotational perturbations of the platform but a normal decrease in response on successive trials. Thus, patients with HD show a consistent pattern of abnormality on posturography suggesting a role for the basal ganglia in a number of aspects of postural control.

Cognition↗