Biomedical subjects

T C Hain

Publications and source records attributed to T C Hain.

At least 19 recordsLinked to original sources

PubMed1992

Velocity storage in labyrinthine disorders.

We studied 13 patients with unilateral peripheral vestibular lesions following removal of acoustic neurinomas. The time constant of the VOR after surgery was 6.4 +/- 2.6 seconds (normal is 18.5 +/- 7.7 seconds). The time constant of OKAN after surgery was 7.2 +/- 1.8 seconds (normal is 11.3 +/- 3.2 seconds). The mean initial velocity of OKAN after surgery was 9.7 +/- 2.4 deg/second (normal is 11.7 +/- 5.9 deg/second). These data suggest that unilateral peripheral vestibular loss is associated with a complete loss of velocity storage for canal input but only a partial loss of velocity storage for visual input. These results can be accounted for by current mathematical models of the velocity storage mechanism.

Humans↗

PubMed1992

Slow cumulative eye position to quantify optokinetic afternystagmus.

In 30 normal subjects we computed the slow cumulative eye position (SCEP) of optokinetic afternystagmus (OKAN) that followed 60 seconds of full-field optokinetic stimulation at 60 degrees/s. The mean SCEP was 112.8 degrees +/- 65.0 degrees. The lower and upper fifth percentile limits for directional preponderance of the SCEP were -38.8% and 44.3%, respectively. The time constant, which we calculated by dividing the SCEP by the initial velocity, was 12.0 +/- 7.4 seconds. This value is nearly identical to the time constant obtained from semilogarithmic regression of the decay of OKAN slow-phase velocity versus time. We conclude that the SCEP is a good measure of OKAN and that it reflects the substantial amount of variability and directional asymmetry observed in the optokinetic responses of normal subjects.

Algorithms↗

PubMed1992

Clinical implications of otolith-ocular reflexes.

While difficult to test clinically, otolith-induced vestibular responses play an important role in both vestibulo-ocular and vestibulo-spinal reflexes, and are likely a source of symptoms in patients with vestibular disorders. Here we review basic aspects of otolith-induced vestibulo-ocular reflexes and consider some clinical implications of disordered otolith function. Emphasis is placed on ocular responses to translation and to tilt and the influence of gravity on vestibulo-ocular responses induced during head rotation.

Adaptation, Physiological↗

PubMed1991

Microsaccadic flutter.

Microsaccadic flutter is a rare symptomatic saccadic oscillation that has been reported only twice previously. Here we describe 5 patients with this disorder. The oscillation is horizontal, has a frequency of 15-30 Hz, an amplitude of 0.1-0.5 degrees, and cannot be seen with the unaided eye. It is usually not associated with any underlying neurological disorder. We hypothesize that microsaccadic flutter is due to malfunction of the brainstem omnipause neurons.

Abducens Nerve↗

PubMed1991

Abolition of optokinetic afternystagmus by aminoglycoside ototoxicity.

We studied optokinetic afternystagmus in eight subjects with loss of or impairment of vestibular function due to ototoxic antibiotics. We found that the initial amplitude, the time constant, and the slow-phase cumulative eye position of optokinetic afternystagmus were significantly reduced in the patients. Slow-phase cumulative eye position most reliably distinguished our patients' responses from those of a normal group.

Adult↗

PubMed1990

Static roll and the vestibulo-ocular reflex (VOR).

We measured the effect of static lateral tilt (roll) on the gain and time constant of the vestibulo-ocular reflex (VOR) in five normal subjects by recording both the horizontal and vertical components of eye velocity in space for rotation about an earth vertical axis with the head either upright or rolled to either side. The time constant of the VOR in the upright position was 19.6 +/- 3.2s (mean +/- standard deviation). The time constant of the horizontal component with respect to the head decreased to 15.7 +/- 4.0s for 30 degrees roll and to 12.7 +/- 2.7s for 60 degrees roll. The time constant of the vertical component with respect to the head was 11.0 +/- 1.4s for 30 degrees roll and 7.5 +/- 1.6s for 60 degrees roll. The gain of the horizontal VOR with respect to space did not vary significantly with roll angle but a small space-vertical component to the VOR appeared during all rotations when the head was rolled away from upright. This non-compensatory nystagmus built up to a maximum of 2-3 degrees/s at 17.0 +/- 4.7s after the onset of rotation and then decayed. These data suggest that static otolith input modulates the central storage of semicircular canal signals, and that head-horizontal and head-vertical components of the VOR can decay at different rates.

Adult↗

PubMed1990

Optokinetic nystagmus and afternystagmus in human beings: relationship to nonlinear processing of information about retinal slip.

In four normal human subjects we measured eye movements during full-field optokinetic stimulation (10-220 deg/s) and determined the relationship among retinal-slip velocity (drum velocity minus slow-phase eye velocity), the slow-phase velocity of optokinetic nystagmus (OKN) and the initial value of the slow-phase velocity of optokinetic afternystagmus (OKAN) measured in darkness. OKN and OKAN were maximum (63-84 and 11-19 deg/s, respectively) when retinal slip ranged from 30-100 deg/s. For higher values of retinal slip, OKN and OKAN fell (in 3 subjects) or reached a plateau (in the fourth). The amplitude of OKAN in human beings was much less than that reported in monkeys. The shape, however, of the curve relating retinal slip to the amplitude of OKAN was similar to that of monkeys. Furthermore, in both cases the curve resembles that obtained by plotting the results of experimental recordings of neural discharge in the nucleus of the optic tract as a function of retinal slip. These results imply that the processing of visual information for generation of OKAN is similar in monkeys and human beings but that the gain of the system is much less in human beings. We also found that fixation of a small target during optokinetic stimulation nearly completely prevented the development of OKAN while fixation of a small target for short periods after optokinetic stimulation did not alter the pattern of decay of OKAN. Thus, fixation may actively prevent the coupling of visual information into the velocity-storage mechanism.

Adult↗

PubMed1990

Ipsiversive eye deviation and epileptic nystagmus.

We studied an 11-year-old boy with focal seizures in the right temporo-occipital cortex. During the seizure, there was a 1- to 2-second period of ipsiversive (rightward) conjugate eye deviation, followed by 10 to 15 seconds of horizontal jerk nystagmus with slow phases that were directed to the right and appeared linear. The patient was conscious throughout the seizure. These findings fit the description of epileptic nystagmus. We postulate that the eye deviation and slow phases of the nystagmus in this patient were induced by epileptic activation of a cerebral smooth pursuit pathway originating from temporoccipital cortex.

Child↗

PubMed1990

Phoria adaptation in patients with cerebellar dysfunction.

The authors studied phoria adaptation to horizontal base-out prism in 17 patients with well-documented cerebellar lesions. There was no significant difference between mean adaptation measured in the patients and ten normal controls. Individually, normal adaptation was found in 12 patients. Abnormal adaptation was found in five patients, all but one of which had other neurologic lesions. These results suggest that phoria adaptation to base-out prism is not diminished by a cerebellar lesion unless it is accompanied by another nervous system lesion(s).

Adaptation, Ocular↗

PubMed1989

Central adaptation models of the vestibulo-ocular and optokinetic systems.

A theoretical analysis of two models of the vestibulo-ocular and optokinetic systems was performed. Each model contains a filter element in the vestibular periphery to account for peripheral adaptation, and a filter element in the central vestibulo-optokinetic circuit to account for central adaptation. Both models account for 1 adaptation, i.e. a response decay to a constant angular acceleration input, in both peripheral vestibular afferent and vestibulo-ocular reflex (VOR) responses and 2 the reversal phases of optokinetic after-nystagmus (OKAN) and the VOR and 3 oscillatory behavior such as periodic alternating nystagmus. The two models differ regarding the order of their VOR transfer function. Also, they predict different OKAN patterns following a prolonged optokinetic stimulus. These models have behavioral implications and suggest future experiments.

Adaptation, Physiological↗

PubMed1989

Optokinetic afternystagmus in humans: normal values of amplitude, time constant, and asymmetry.

It has been suggested that the appearance of directional asymmetry and/or a reduced time constant of optokinetic afternystagmus (OKAN) might be a clinical index of vestibular imbalance. However, we do not know the limits for OKAN parameters in normal humans. Accordingly, we studied OKAN in 30 normal subjects using a "sampling" method, in which a number of values of OKAN are obtained by turning out the lights periodically during optokinetic stimulation. We found that the initial velocity of OKAN has a large intrasubject variability. Accordingly, if precision is desired so as to obtain 95% confidence that the measured mean of the initial velocity of OKAN is within 25% of the true mean in an individual subject, at least eight measurements of the initial OKAN velocity must be taken. When 12 measurements are made, all subjects had a minimum value of 5 degrees/s initial OKAN, and there was little directional asymmetry (mean of -0.47 degree/s +/- 3.13 degrees/s). The intrasubject variability of the time constant of OKAN was similar to the variability of initial OKAN velocity. However, because it is not possible to obtain repeated measures of the time constant in a short period of time, the time constant of OKAN is less likely to be useful in clinical testing.

Adult↗

PubMed1989

Vergence.

Explore the source record for details and available documents.

Convergence, Ocular↗

PubMed1988

Smooth pursuit eye movements in schizophrenics: quantitative measurements with the search-coil technique.

Eye movements of five schizophrenic and five normal subjects were measured with the magnetic-field search-coil technique. Subjects followed targets moving smoothly at various speeds, either unpredictably in a step-ramp fashion or predictably in a triangular wave. The tracking stimulus was either a small dot or a large, richly-textured image that occupied a large portion of the visual field. Tracking by schizophrenics was abnormal; it was punctuated by catch-up saccades that corrected for smooth following movements of inadequate velocity. We did not, however, find saccadic intrusions, such as square wave jerks. Under all tracking conditions steady-state gains (eye velocity/target velocity) and, in the case of step-ramps, average acceleration in the first 120 ms were lower in patients than in normal subjects. The differences were most pronounced for tracking of the small target, moving at the highest speed tested (30 degree/s), in the nonpredictable, step-ramp waveform. With this stimulus mean steady-state gain was 0.36 (SD +/- 0.12) for the schizophrenic patients and 0.73 (SD +/- 0.11) for the normal subjects. When the target was changed to the large-field stimulus or moved in a predictable (triangular-wave) fashion, tracking improved in both patients and normal subjects, and even more so when these features were combined.

Adult↗

PubMed1988

Saccades in Huntington's disease: slowing and dysmetria.

Eye movements were recorded from 20 mildly affected patients with Huntington's disease (HD) who were divided into two groups, 10 patients with onset of symptoms before age 30 and 10 with onset of symptoms after age 30. In the younger onset group (HD less than 30), peak saccade velocities were low (less than 255 deg/sec for 20-deg saccades) in six of the 10 patients, whereas none of the 10 patients in the older onset group (HD greater than 30) had peak saccade velocities lower than 300 deg/sec. Latencies for volitional saccades were greater than normal in the HD greater than 30 group, but were normal for the HD less than 30 group. The ability to maintain steady fixation in the face of a distracting visual stimulus was decreased, to the same degree, in both groups of HD patients. In addition, 70% of the HD less than 30 group had an affected father, while 70% of the HD greater than 30 group had an affected mother. These findings suggest that the pathophysiology of the slow saccades, initiation deficit, and excessive distractibility in HD are different.

Adolescent↗

PubMed1987

Abduction nystagmus in internuclear ophthalmoplegia.

We tested the hypothesis that abnormalities of the abducting eye in internuclear ophthalmoplegia reflect an adaptive process that helps overcome the adduction weakness of the opposite eye. This response operates under the constraints of Hering's law of equal innervation: any attempt to increase the innervation to a weak muscle in one eye must be accompanied by a commensurate increase in innervation to the yoke muscle in the other eye. In 4 patients with internuclear ophthalmoplegia, we patched one eye for 1 to 5 days to allow time for the central nervous system to optimize innervation for the habitually viewing eye. We predicted that there would be a conjugate adjustment of innervation that would diminish the abduction overshoot and backward postsaccadic drift made by the habitually viewing eye. This was the case in 3 of our 4 patients. Our findings show that the abduction nystagmus is a manifestation of a normal adaptive response in some patients with INO.

Adaptation, Physiological↗

PubMed1987

Adaptive changes in post-saccadic drift induced by patching one eye.

A prior study showed that after horizontal saccades the abducting eye has little post-saccadic drift (about 0.5 deg/sec) while the abducting eye has considerable onward drift (about 1.7 deg/sec). To investigate this further, five subjects patched one eye for three days. This reduced the drift after adducting saccades in the viewing eye to the level of that after abducting saccades. The changes were a combination of conjugate and disconjugate alterations. Decreases in drift in the viewing eye did not cause increases in drift in the covered eye. These changes appear functional in that retinal image slip is decreased in the viewing eye but why this goal is not attained when both eyes habitually view is not understood. Also, post-saccadic drift could depend on which eye was used to view the target.

Adaptation, Ocular↗

PubMed1987

Saccades in Huntington's disease: initiation defects and distractibility.

We recorded saccadic eye movements in patients mildly affected with Huntington's disease. Most showed an increase in saccade latencies that was greater for saccades made on command than to the sudden appearance of a visual target. All patients showed excessive distractibility during attempted fixation. They had particular difficulty suppressing a saccade to a suddenly appearing visual target when simultaneously trying to initiate a saccade in the opposite direction. Our results are compatible with a posited role of the basal ganglia in both the initiation of volitional saccades and in the maintenance of fixation. Saccade abnormalities--especially distractibility--are sensitive but probably not specific indicators of Huntington's disease.

Adolescent↗

PubMed1986

Influence of eye and head position on the vestibulo-ocular reflex.

For the vestibulo-ocular reflex (VOR) to function properly, namely to ensure a stable retinal image under all circumstances, it should be able to take into account varying eye positions in the orbit and varying orientations of the head with respect to the axis about which it is rotating. We tested this capability by quantifying the gain and the time constant of the horizontal component of the VOR during rotation about an earth vertical axis when the line of sight (optical axis) was moved out of the plane of head rotation--either by rotating the eyes up or down in the orbit or by pitching the head up or down with respect to earth-horizontal. In either case the gain of the horizontal component of the VOR was attenuated precisely by the cosine of the angle made between the optical axis and the plane of head rotation. Furthermore, if the head was pitched up or down but the eye rotated oppositely in the orbit so as to keep the line of sight in the plane of head rotation the gain of the horizontal component of the VOR was the same value as with the head and eyes both straight ahead. In contrast, the time constant of the VOR varied only as a function of the orientation of the head and not as a function of eye position in the orbit. During rotation about an earth vertical axis, the time constant was longest (about 18 s) when the head was pitched forward to place the lateral canals near earth-horizontal and shortest (about 11 s) when the head was pitched backward to place the vertical canals near earth-horizontal.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗