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Biomedical subjects

T C Hain

Publications and source records attributed to T C Hain.

54 records · Page 3Linked to original sources

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↗

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↗

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↗

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↗

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↗

Blink-induced saccadic oscillations.

A patient with a neurodegenerative disease had abnormal saccades only when he blinked. These saccades were hypermetric and were followed immediately, without any intersaccadic interval, by a large, oppositely directed saccade (dynamic overshoot). To explain these findings, we hypothesize that a blink-related neural signal can modulate the activity of pause cells that normally inhibit saccadic burst neurons during fixation. In pathological circumstances, abnormal function of pause cells could lead to large-amplitude saccadic oscillations. In normal subjects, blinks could induce short bursts of low-amplitude flutter.

Adult↗

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↗

Motion of the eye immediately after a saccade.

Dynamic overshoot is a small saccade that follows a main saccade, in the opposite direction, with no delay. To re-examine prior reports of dynamic overshoot, the properties of dynamic over-shoot were studied in six normal subjects. The post-saccadic drift of eye movements was studied as well. Horizontal eye movements were recorded with the magnetic-field/search-coil method. System noise level was 0.05 deg. Dynamic overshoot occurred with a frequency of about 13% and was more frequent for saccades 10 deg or less. Its mean size was 0.15 deg and its peak velocity showed it to be saccadic in nature. Binocular recordings for three subjects showed that when dynamic overshoot occurred it was almost always in the abducting eye which also had the least post-saccadic drift. The abducting eye seldom had dynamic overshoot and consistently had a more pronounced post-saccadic drift, almost always in the onward direction. We suggest that, at the end of a saccade, the eye normally is brought to rest by a braking pulse and dynamic overshoot occurs when the braking pulse is accidentally too large. It would appear to serve no useful purpose. Why dynamic overshoot is monocular and coincides with the eye having less post-saccadic drift is unclear.

Biomechanical Phenomena↗

A model of the nystagmus induced by off vertical axis rotation.

A three-dimensional model is proposed that accounts for a number of phenomena attributed to the otoliths. It is constructed by extending and modifying a model of vestibular velocity storage. It is proposed that the otolith information about the orientation of the head to gravity changes the time constant of vestibular responses by modulating the gain of the velocity storage feedback loop. It is further proposed that the otolith signals, such as those that generate L-nystagmus (linear acceleration induced nystagmus), are partially coupled to the vestibular system via the velocity storage integrator. The combination of these two hypotheses suggests that a vestibular neural mechanism exists that performs correlation in the mathematical sense which is multiplication followed by integration. The multiplication is performed by the otolith modulation of the velocity storage feedback loop gain and the integration is performed by the velocity storage mechanism itself. Correlation allows calculation of the degree to which two signals are related and in this context provides a simple method of determining head angular velocity from the components of linear acceleration induced by off-vertical axis rotation. Correlation accounts for the otolith supplementation of the VOR and the sustained nystagmus generated by off-vertical axis rotation. The model also predicts the cross-coupling of horizontal and vertical optokinetic after nystagmus that occurs in head-lateral positions and the reported effects of tilt on vestibular responses.

Animals↗

Alexander's law: its behavior and origin in the human vestibulo-ocular reflex.

Alexander's law refers to the phenomenon in which the spontaneous nystagmus of a patient with a vestibular lesion is more intense when the patient looks in the quick-phase than in the slow-phase direction. Alexander's law was investigated in normal subjects as well as patients with vestibular lesions. During sinusoidal rotations of normal subjects, there was no trace of this phenomenon when subjects looked 25 degrees left and right in the dark. The phenomenon of Alexander's law is therefore created centrally and is not due to any mechanical properties of the orbit. During rotation at constant velocity in the dark, normal subjects did weakly demonstrate Alexander's law because of a mild gaze-evoked nystagmus present in normal subjects in the dark. Gaze-evoked nystagmus from a cerebellar lesion involved a pronounced demonstration of Alexander's law during rotatory nystagmus. In patients with a vestibular lesion and a mild spontaneous nystagmus in the dark that obeyed Alexander's law, the nystagmus reversed upon far gaze in the slow-phase direction. We propose that in patients with a vestibular lesion, the phenomenon of Alexander's law is created by the sum of vestibular nystagmus and an abnormally large gaze-evoked nystagmus that is consequent to the vestibular lesion. This conclusion has a number of neurological implications concerning the ways in which the nervous system attempts to compensate for vestibular lesions.

Adult↗

Head-shaking nystagmus in patients with unilateral peripheral vestibular lesions.

In certain patients with peripheral or central vestibular lesions, a transient nystagmus appears after shaking the head rapidly for 10 to 20 cycles. We recorded such a "head-shaking nystagmus" using the scleral eye coil in six subjects with unilateral peripheral vestibular lesions. Horizontal head shaking elicited horizontal nystagmus with slow phases that were initially directed toward the side of the lesion and upward. All subjects showed a prolonged, lower-amplitude reversal phase after the initial response following horizontal head shaking. The main features of these results can be explained by an analytic model that incorporates a central velocity-storage mechanism that perseverates vestibular inputs, Ewald's second law, and adaptation of primary vestibular afferent activity.

Adaptation, Physiological↗

Limits of normal for pressure sensitivity in the fistula test.

In patients with perilymphatic fistula (PLF), nystagmus may sometimes be elicited by application of pressure to the external ear canal. The extent to which the normal population also exhibits such 'pressure sensitivity' is presently unknown. Our goal was to determine the limits of normal pressure sensitivity and to quantify the performance of the fistula test. Our subjects consisted of 13 normal controls and 7 patients with a history of pressure sensitivity who later underwent exploratory tympanotomy. We measured nystagmus prior to and following pressurization of the external ear canal. Pressure was applied manually over 60 s with a pneumatic otoscope bulb. In normal subjects, change in nystagmus between prepressure and postpressure tests ranged from -1.3 to 0.9%s. In patients, change in nystagmus greater than the 95th percentile limits of normal was not a reliable indication of PLF.

Acoustic Impedance Tests↗

Tilt suppression of vestibulo-ocular reflex in patients with cerebellar lesions.

The effect of tilt on the time constant of post-rotatory nystagmus was determined in a group of normal subjects and patients with cerebellar lesions. The normal subjects showed a vestibular response that decayed with a time constant of 19.6 s when upright and 7.2 s after tilt prone. Patients with midline cerebellar lesions near the uvula and nodulus had time constants that were normal in the upright position but were unaffected by head tilt. Patients with cerebellar lesions due to the Arnold-Chiari malformation showed behavior that was intermediate between that of normal subjects and the patients with midline lesions. These results provide evidence that in humans, the midline cerebellum regulates a neural network in the brainstem that perseverates peripheral vestibular input.

Adolescent↗

Head-shaking nystagmus: associations with canal paresis and hearing loss.

In 108 patients referred for caloric testing, head-shaking nystagmus (HSN) was noted in 37 electronystagmography (ENG) recordings. A canal paresis was found in 31 patients and a sensorineural or mixed hearing loss in one or both ears was found in 45 patients. Both HSN and canal paresis were insensitive predictors of either hearing loss or of each other. HSN was less sensitive as well as less specific than canal paresis for hearing loss. These data suggest that HSN is not as powerful a test as canal paresis in detecting lesions of the 8th nerve.

Adult↗

[Neck vibration: usefulness in neurotology].

INTRODUCTION: Recently, mechanical vibration on the neck has begun to be used to improve diagnostic sensitivity in patients who have vestibular disorders. METHOD: We review results of studies of this stimulus in normal subjects and patients with vestibular lesions: the ocular responses, changes in the subjective straight ahead, and postural changes generated by the neck vibration. CONCLUSION: Although the underlying mechanism for the responses to neck vibration remains uncertain, it is an excellent addition to the neurotologic exam since it allows us demonstrate vestibular deficit with greater sensitivity than other maneuvers. As vibration is easy to apply it can be useful for screening in patients who complain of dizziness.

Eye Movements↗

[The pharmacology of vestibular disorders].

INTRODUCTION: In recent years, significant advances have been made in the physiology and the pharmacology of vestibular disorders. It is now possible to elaborate an approximation of the mechanisms of action of the drugs used in the symptomatic treatment of vertigo. DEVELOPMENT: These drugs usually have a number of different pharmacological actions and overlapping effects. They can modify the intensity of the symptoms (e.g. vestibular suppressants) or prevent recurrences (e.g. calcium blockers in the case of vestibular migraine). Most of the drugs used for the acute treatment of vertigo can have a negative effect on the central compensation mechanisms. Vestibular rehabilitation exercises and certain drugs can speed up compensation. Choice of medication and the method of administration depend on the severity of the clinical symptoms, the pattern of temporal evolution, the underlying vestibular disease, the associated clinical conditions and the profile of the collateral effects of the drugs utilised. CONCLUSIONS: Vestibular suppressants and antiemetic drugs are still the basis of the acute treatment of vertigo.

Antiemetics↗