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Biomedical subjects

T Raphan

Publications and source records attributed to T Raphan.

69 records · Page 4Linked to original sources
PubMed1985

Dynamic modification of the vestibulo-ocular reflex by the nodulus and uvula.

The time constant of the decay of slow-phase eye velocity of postrotatory nystagmus or optokinetic after-nystagmus is reduced during exposure to a stationary visual surround (visual suppression). It is also reduced after tilting the head (tilt suppression). A "dump" mechanism in the vestibulo-ocular reflex has been proposed to rapidly discharge activity from the central vestibular system during both types of suppression. Monkeys lost this mechanism after lesions of the nodulus and uvula. They also lost the ability to habituate the time constant of nystagmus on repeated exposure to optokinetic and vestibular stimuli. Periodic alternating nystagmus, which is believed to represent an instability in the vestibulo-ocular reflex, was observed in two of three monkeys. These data indicate that the nodulus and uvula play an important role in suppressing, habituating, and stabilizing the vestibulo-ocular reflex.

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PubMed1985

Horizontal saccades induced by stimulation of the central mesencephalic reticular formation.

The central mesencephalic reticular formation (cMRF) was electrically stimulated in the alert monkey. Saccadic eye movements were induced to the contralateral side in the horizontal plane at latencies of 18-35 ms. Smooth or slow eye deviations were not produced by cMRF stimulation. If the stimulus was given during slow phases of nystagmus, rapid eye movements were elicited, and the velocity of the slow phases was not affected. The function of cMRF neurons and/or of pathways that lie within it appear primarily related to generation of rapid eye movements in the horizontal plane. The amplitude of induced saccadic eye movements depended solely on the region of cMRF that was activated. When the stimulation frequency was lower, the latency was longer, but the size and characteristics of the induced movement were the same. The product of latency and stimulus frequency was approximately constant, suggesting that saccades had been triggered after a fixed number of pulses had been given. Stimulation of cMRF at frequencies that were too low to elicit rapid eye movements had a tonic effect on saccade generation. When the animal was having optokinetic nystagmus (OKN), stimulation modulated beat frequency according to the direction of the nystagmus: contralateral quick phases were facilitated and ipsilateral quick phases were suppressed. The frequencies of stimulation necessary to suppress ipsilateral quick phases increased as slow phase eye velocity increased. This demonstrates that both cMRF activity and slow phase velocity affect quick phase triggering. When the cMRF on both sides were simultaneously stimulated, the eyes were fixed in place, and no further rapid movements occurred until the stimulus had ended. Thus, activity in pathways and/or cells in cMRF is not only able to trigger saccades, but can also change the excitability of saccade generating mechanisms and promote fixation by suppressing eye movements. Two types of rapid eye movements were elicited from cMRF. From dorsal portions of cMRF saccades were induced whose size was relatively constant and not dependent on the initial position of the eyes in the orbit. The size of saccades increased from small to large as the stimulating electrode was advanced through cMRF from dorsal to ventral. This suggests that the tecto-bulbo-spinal efferents coursing through cMRF and/or cMRF neurons related to this input, are organized in a topographic fashion, with cells and fibers related to eye movements of increasing size being layered one beneath another.(ABSTRACT TRUNCATED AT 400 WORDS)

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PubMed1983

Role of the otolith organs in generation of horizontal nystagmus: effects of selective labyrinthine lesions.

Selective labyrinthine lesions were made to study the origin of excitation in the labyrinth during off-vertical axis rotation. Plugging the semicircular canals abolishes the response to rotation about a vertical axis, but optokinetic after-nystagmus (OKAN) and the sustained horizontal nystagmus induced by off-vertical axis rotation (OVAR) are maintained. After cutting the nerves of the lateral semicircular canals, neither horizontal OKAN nor the continuous horizontal nystagmus associated with off-axis rotation can be induced, although vertical OKN, OKAN and vestibular nystagmus are intact. This supports the theory that labyrinthine activity responsible for the nystagmus induced by OVAR arises in the otolith organs and couples to the oculomotor system through the velocity storage mechanism.

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PubMed1983

Nystagmus generated by sinusoidal pitch while rotating.

Sinusoidal pitch while rotating about a vertical axis in darkness causes continuous horizontal compensatory nystagmus in the monkey which persists for the duration of stimulation. The steady-state velocity sums with post-rotatory nystagmus to reduce or cancel it, suggesting involvement of the velocity storage mechanism. Analysis of the labyrinthine excitation during pitch while rotating suggests that the vertical canals play a predominant role in generating the response. Effects of selective labyrinthine lesions are in agreement with this hypothesis. Plugging the lateral canals, leaving the vertical canals intact, blocked the initial rapid response at the onset of rotation, but did not interrupt the continuous nystagmus induced by pitch while rotating. On the other hand, plugging the vertical canals abolished the response. If the lateral canal nerves were cut so that the velocity storage mechanism was inactivated, the continuous response to pitch while rotating also disappeared. The dominant labyrinth activation responsible for the nystagmus during pitching while rotating appears to arise in the vertical semicircular canals and to couple to the oculomotor system through the velocity storage mechanism.

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PubMed1983

Role of the flocculus and paraflocculus in optokinetic nystagmus and visual-vestibular interactions: effects of lesions.

Optokinetic nystagmus (OKN), optokinetic after-nystagmus (OKAN), vestibular nystagmus and visual-vestibular interactions were studied in monkeys after surgical ablation of the flocculus and paraflocculus. After bilateral flocculectomy the initial rapid rise in slow phase eye velocity of horizontal and vertical OKN was severely attenuated, and maximum velocities fell to the preoperative saturation level of OKAN. There is generally little or no upward OKAN in the normal monkey, and upward OKN was lost after bilateral lesions. Unilateral flocculectomy affected the rapid rise in horizontal velocity to both sides. Consistent with the absence of a rapid response to steps of surround velocity, animals were unable to follow acceleration of the visual field with eye accelerations faster than about 3-5 degrees/s2. The slow rise in OKN slow phase velocity to a steady state level was prolonged after operation. However, rates of rise were approximately equal for the same initial retinal slips before and after operation. The similarity in the time course of OKN when adjusted for initial retinal slip, and in the gain, saturation level and time course of OKAN before and after flocculectomy indicates that the lesions had not significantly altered the coupling of the visual system to the velocity storage integrator or its associated time constant. When animals were rotated in a subject-stationary visual surround after flocculectomy, they could not suppress the initial jump in eye velocity at the onset of the step. Despite this, they could readily suppress the subsequent nystagmus. The time constant of decline in the conflict situations was almost as short as in the normal monkey and was in the range of the peripheral vestibular time constant. This suggests that although the animals were unable to suppress rapid changes in eye velocity due to activation of direct vestibulo-oculomotor pathways, they had retained their ability to discharge activity from the velocity storage mechanism. Consistent with this, animals had no difficulty in suppressing OKAN after flocculectomy. Visual-vestibular interactions utilizing the velocity storage mechanism were normal after flocculectomy, as was nystagmus induced by rotation about a vertical axis or about axes tilted from the vertical. Also unaffected were the discharge of nystagmus caused by tilting the head out of the plane of the response and visual suppression of nystagmus induced by off-vertical axis rotation. The flocculus does not appear to play an important role in mediating these responses. The data before and after flocculectomy were simulated by a model which is homeomorphic to that presented previously.(ABSTRACT TRUNCATED AT 400 WORDS)

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PubMed1979

Velocity storage in the vestibulo-ocular reflex arc (VOR).

Vestibular and optokinetic nystagmus (OKN) of monkeys were induced by platform and visual surround rotation. Vision prolonged per-rotatory nystagmus and cancelled or reduced post-rotatory nystagmus recorded in darkness. Presumably, activity stored during OKN summed with activity arising in the semicircular canals. The limit of summation was about 120 degrees/s, the level of saturation of optokinetic after-nystagmus (OKAN). OKN and vestibular nystagmus, induced in the same or in opposite directions diminished or enhanced post-rotatory nystagmus up to 120 degrees/s. We postulate that a common storage mechanism is used for producing vestibular nystagmus, OKN, and OKAN. Evidence for this is the similar time course of vestibular nystagmus and OKAN and their summation. In addition, stored activity is lost in a similar way by viewing a stationary surround during either OKAN or vestibular nystagmus (fixation suppression). These responses were modelled using direct pathways and a non-ideal integrator coupled to the visual and peripheral vestibular systems. The direct pathways are responsible for rapid changes in eye velocity while the integrator stores activity and mediates slower changes. The integrator stabilizes eye velocity during whole field rotation and extends the time over which the vestibulo-ocular reflex can compensate for head movement.

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PubMed1977

Quantitative analysis of the velocity characteristics of optokinetic nystagmus and optokinetic after-nystagmus.

1. Velocity characteristics of optokinetic nystagmus (OKN) and optokinetic after-nystagmus (OKAN) induced by constant velocity full field rotation were studied in rhesus monkeys. A technique is described for estimating the dominant time constant of slow phase velocity curves and of monotonically changing data. Time constants obtained by this technique were used in formulating a model of the mechanism responsible for producing OKN and OKAN.2. Slow phase velocity of optokinetic nystagmus in response to steps in stimulus velocity was shown to be composed of two components, a rapid rise, followed by a slower rise to a steady-state value. Peak values of OKN slow phase velocity increased linearly with increases in stimulus velocity to 180 degrees /sec. Maximum slow phase eye velocities in the monkey are 2-3 times as great as in humans.3. At the onset of OKAN, slow phase velocity falls by about 10-20%, followed by a slower decline to zero. Peak OKAN slow phase velocities were linearly related to optokinetic stimulus velocities up to 90-120 degrees /sec. Above 120 degrees /sec OKAN slow phase velocity saturated although OKN slow phase velocity continued to increase.4. The charge and discharge characteristics of OKAN were studied. The OKAN mechanism charged in 5-10 sec and discharged over 20-60 sec in darkness. The time constants of decay in OKAN slow phase velocity decreased as stimulus velocities increased. They also decreased on repeated testing. In several monkeys there was a consistent difference in the rate of decay of OKAN slow phase velocity to the right and left.5. Extended visual fixation discharged the activity responsible for producing OKAN. Short fixation times caused only a partial discharge of the OKAN mechanism. Following brief periods of fixation, OKAN resumed but with depressed slow phase velocities.6. A model based on a state realisation of a peak detector was formulated which approximately reproduces the salient characteristics of OKN and OKAN. This model predicts the three dominant characteristics of OKAN: (1) charge over 5-7 sec, (2) slow discharge in darkness, and (3) rapid discharge with visual fixation. With the addition of direct fast forward pathways, it also correctly predicts the rapid and slow rise in OKN. We postulate that OKAN is produced by a central integrator which is also active during OKN. Presumably this integrator acts to maximize velocities during OKN and to smooth and stabilize ocular following during movement of the visual surround.

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