Human vertical optokinetic nystagmus and after-response, and their dependence upon head orientation with respect to gravity.

Characteristics of human vertical optokinetic nystagmus (VOKN) and afternystagmus (VOKAN) were examined by electro-oculography in 18 normal human subjects by means of the analysis of slow phase velocity (SPV) and area under the regression curve of the VOKAN decay. Under normal gravity, subjects were tested in upright and left ear down (90 degrees roll) positions, respectively, using a hemisphere onto which stripes were projected at a velocity of 40 degrees/s in left, right, up and down directions. Analysis of the VOKN and VOKAN revealed a significant asymmetry of vertical eye movements in the subjects' sagittal plane, ie, stronger upward SPV than downward in both VOKN and VOKAN decay. This asymmetry became even more prominent when the head was in the 90 degrees roll position. It is postulated that the asymmetry of VOKN and VOKAN in humans, as in animals, is due to the asymmetrical storage capability of the vertical velocity storage mechanism which mainly contributes to upward eye movements. In addition, it is postulated that the vertical storage mechanism is modified by the action of gravity on the otolith organs. However, only two out of our 18 subjects demonstrated cross-coupling, as reported in animals, from the horizontal to the vertical mode of storage when the head was tilted away from the spatial vertical.

Stimulus velocity dependence of human vertical optokinetic nystagmus and afternystagmus.

Stimulus velocity dependence of human VOKN and VOKAN was investigated using 20 degrees, 40 degrees, 60 degrees, and 80 degrees/s optokinetic stimulation. In our experimental conditions, 40 degrees/s was found to be the most appropriate stimulus velocity for inducing reliable VOKN and VOKAN based on the analysis of SPV, gain, and the area under the VOKAN decay curve. There was a clear trend toward up/down asymmetry of VOKN gain, with higher upward OKN SPV than downward at 40 degrees/s. VOKAN with both short and long time constant components was induced in 5 of 11 subjects, but only when the stimulus was upgoing. Stimulation at 20 degrees/s in either direction produced a decay with only a short time constant. VOKN-SPV and the area under VOKAN decay curve at 40 degrees/s showed no significant difference from the corresponding values at 60 degrees/s or 80 degrees/s, indicating that following and the velocity storage mechanism had saturated at 40 degrees/s. However, the gain at 60 degrees/s and 80 degrees/s became low and eye movement regularity was poor. Stimulation at 20 degrees/s may activate mainly the vertical pursuit mechanism, as it did not produce up/down asymmetry. It is proposed that, as in the horizontal case, two kinds of mechanisms are involved in vertical stripe-following eye movements, which represent smooth pursuit and optokinetic systems respectively.

Suppression of optokinetic velocity storage in humans by static tilt in pitch.

The effects of static tilts about the pitch axis on human horizontal optokinetic after-nystagmus OKAN (HOKAN) were examined. Static tilts in pitch produced tilt-dependent HOKAN suppression. The slow decay (indirect pathway) component (coefficient C and long time constant 1/D) of the two-component model for OKAN was significantly reduced, while the short decay (direct pathway) component (coefficient A and short time constant 1/B) remained invariant as angle of tilt was increased. These results provide further evidence that otolith organ activity can couple to horizontal velocity storage in humans, in accordance with models proposed in the literature.

Suppression of optokinetic velocity storage in humans by static tilt in roll.

The effects of static tilts about the roll (anterior-posterior) axis on human horizontal optokinetic afternystagmus (HOKAN) were examined. Static tilts in roll, with subjects lying on their left side, produced significant tilt-dependent HOKAN suppression. Only the slow (indirect pathway) component time constant (1/D) of the double exponential model for human HOKAN decreased with angle of roll tilt. The effect was direction specific in that suppression occurred only following a leftward-going stimulus. These findings provide further support for the postulate that otolith-organ-mediated activity can couple to the horizontal velocity storage mechanism in humans. A slight trend towards a tilt-dependent reduction of coefficient A (initial slow phase velocity of fast component decay) was revealed, suggesting the possibility that otolith-organ-mediated activity could couple to direct (pursuit-mediated?) pathways as well. No horizontal-to-vertical cross-coupling occurred, indicating that this aspect of the 3-dimensional model for velocity storage proposed by Raphan & Cohen (1988) may not completely apply to humans.

The influence of active versus passive head oscillation, and mental set on the human vestibulo-ocular reflex.

We compared passive (manual) whole body, and active head oscillation in normal human subjects attempting mentally to influence the vestibulo-ocular reflex (VOR). Our objective was to establish simple procedural guidelines for vestibular test procedures in clinical settings. Using a head-fixed target, both methods of oscillation yielded virtually zero gain. Using an Earth-fixed target, active oscillation gain was unity, while passive gain was slightly less than 1. Using an imagined Earth-fixed target in the dark, both active and passive gains were reduced considerably, but passive gain was reduced more. Using an imagined head-fixed target in the dark, VOR gain was near zero at low frequencies but increased as frequency increased. Again, passive gain was less than active gain. At frequencies above 1 Hz, VOR gain in all conditions approached a value between 0.7 and 0.9. We conclude that active and manual passive rotation are simple and effective methods to test the VOR, but emphasize that visual and mental influences must be carefully controlled.

Concussion. Acceleration limits causing concussion.

Among the many features common to all species of the animal kingdom is the transient loss of function of the nervous system as the result of a jarring blow, a phenomenon known as concussion. Understanding of concussion has been hampered by the lack of a uniform definition, with many authors including cases with gross, irreversible changes. The phenomenon occurs only with a blow that significantly accelerates and thus is best defined as "a transient disturbance of neuronal function as a result of acceleration." There must be a threshold beneath which no loss of function occurs and a ceiling beyond which changes are not reversible. Experiments with nonanesthetized frogs revealed that at 33 g only the occasional frog would be stunned. From 50 to 230 g, consciousness was always lost but rapidly regained and retained, while beyond, the loss was not always reversible. The time of functional loss was increasingly proportional to acceleration.

Effect of active head movements about the pitch, roll, and yaw axes on human optokinetic afternystagmus.

Effects of active head movements about the pitch, roll, or yaw axes on horizontal optokinetic afternystagmas (OKAN) were examined in 16 subjects to test the hypothesis that otolith organ mediated activity induced by a change in head position can couple to the horizontal velocity storage in humans. Active head movements about the pitch axis, forwards or backwards, produced significant OKAN suppression. Pitch forward head movements exerted the strongest effect. Active head movements about the roll axis towards the right also produced OKAN suppression but only if the tilted position was sustained. No suppression was observed following sustained yaw. However, an unsustained yaw left movement after rightward drum rotation significantly enhanced OKAN. Sustained head movement trials did not significantly alter subsequent control trials. In contrast, unsustained movements about the pitch axis, which involve more complex interactions, exerted long-term effects on subsequent control trials. We conclude that otolith organ mediated activity arising from pitch or roll head movements couples to the horizontal velocity storage in humans, thereby suppressing ongoing OKAN. Activity arising from the horizontal canals during an unsustained yaw movement (observed mainly with yaw left), following drum rotation in a direction contralateral to the movement, may also couple to the velocity storage, resulting in increased activity instead of suppression.

Convergent effects from vestibulospinal tract and primary cutaneous afferent fibers on motoneurons to proximal lower limb flexor and extensor muscles in humans.

In human subjects, the latency and magnitude of cutaneomuscular test reflexes, evoked by stimulation of the sural nerve in the contralateral and ipsilateral quadricep and hamstring muscles, were investigated during static tilts in the pitch axis. The ANOVA demonstrated a highly significant, tilt-dependent modulation of the magnitude of the test reflex for the initial phase of both ipsilateral quadriceps and ipsilateral hamstrings. These results are consistent with results from a similar study on human ankle muscles and provide further evidence that the tilt-dependence of these cutaneomuscular reflexes originates from activity in the otolith receptors.

Human optokinetic afternystagmus. Is the fast component of OKAN decay due to smooth pursuit?

Eye movement after-effects subsequent to pursuit of a single LED target were studied in human subjects to test the hypothesis that constant velocity pursuit activates a velocity storage system in the neuronal pathway. The temporal characteristics of observed after-effects fall within those predicted from the Robinson model of eyeball mechanics, indicating that neuronal integration was not a factor.

Convergent effects from vestibulospinal tract and primary cutaneous afferent fibers on motoneurons to ankle extensor and flexor muscles in humans.

The latency and magnitude of cutaneomuscular reflexes, evoked by stimulation of the sural nerve in the contralateral and ipsilateral tibialis anterior and soleus, were investigated in normal human subjects during static tilts in the pitch axis. For all subjects the test reflex consisted of oscillating sequences of excitation and inhibition, each muscle exhibiting a characteristic pattern defined by its latency and sign of the initial phase. The latency of the various components and the sign of the initial phase did not vary with angle of tilt. However, the results of an ANOVA demonstrate a highly significant tilt-dependent modulation of the amplitude of the test reflex for the initial inhibitory phase of the contralateral tibialis anterior. We propose that this tilt-dependent effect on the crossed cutaneomuscular reflex originates from activity in the otolith organ receptors.

Human optokinetic afternystagmus. Charging characteristics and stimulus exposure time dependence in the two-component model.

The dependence of human optokinetic afternystagmus (OKAN) velocity storage (charging) and optokinetic nystagmus (OKN) characteristics on optokinetic (OK) stimulus exposure time was investigated, using the two-component double exponential model for OKAN decay. Results are compatible with our previously proposed concept of two velocity storage integrators, one responsible for the short time constant decay (pursuit-mediated) and the other for the long time constant decay (OK system-mediated). The dependence of the long time constant integrator of OKAN on stimulus exposure time was clearly demonstrated. The short time constant integrator appeared to be independent of stimulus exposure time within the range studied. We conclude that the charging time-course of each component is distinct from that of the other. The time constants of each component decay were found to be invariant. A left-right asymmetry observed in both OKN and OKAN responses suggests that the integrators are direction sensitive.

Human optokinetic afternystagmus. Stimulus velocity dependence of the two-component decay model and involvement of pursuit.

The dependence of human OKAN characteristics on optokinetic (OK) stimulus velocity was examined using the two-component double exponential model for OKAN decay. Drum velocities studied were between 10 degrees and 70 degrees deg/sec over a constant exposure period of 60 sec. Results reveal two distinct types of response: a 'low'-level response at lower drum velocities (10 degrees, 20 degrees, 30 degrees/sec) and a 'high'-level response at higher drum velocities (40 degrees, 60 degrees, 70 degrees /sec). These findings support our previous proposal that OKAN decay is a two-component process, and extend it by demonstrating that these two components have differing stimulus velocity sensitivities, as would be predicted if it were assumed that they represented direct (pursuit) and indirect (non-pursuit) pathways respectively.

Initiation of locomotion from the mesencephalic locomotor region: effects of selective brainstem lesions.

The effects of selected brainstem lesions on controlled treadmill locomotion produced by stimulation of the mesencephalic locomotor region (MLR) in postmamillary cats were determined in these experiments. The importance for the initiation of locomotion of projections from the MLR to rostral brainstem structures, described in a preceding paper, were examined by selective lesioning or by adjusting the level of the decerebration. The role played by the lateral vestibulospinal tract (LVST) in the initiation of locomotion was examined by lesioning Deiters' nucleus bilaterally. Contrary to previous claims, the results of the present experiments show that areas of the brainstem rostral to the MLR are not required for the initiation of locomotion by MLR stimulation. This finding eliminates the ventral tegmental area of Tsai and the substantia nigra, both implicated in the initiation of locomotion, as required participants in MLR stimulated locomotion. Bilateral Deiters' nucleus (DN) lesions did not significantly affect the initiation of locomotion from the MLR, nor did such lesions alter in a systematic fashion the amplitude or timing of EMG activity in flexor or extensor muscles of the hindlimb during MLR evoked walking. Joint angle changes during the locomotor cycle were also essentially unaltered by DN lesions. The significance of these findings regarding the brainstem structures which must be involved in the initiation of locomotion are discussed.

Human optokinetic afternystagmus. Effects of repeated stimulation.

Normal human subjects were exposed to repeated optokinetic afternystagmus (OKAN) testing in either one direction or alternating directions of stripe movement. Sessions were conducted at intervals of either one week or several weeks. Repeated exposure to OKAN stimulation in one direction produced significant response decrements in cumulative displacement, short time constant, long time constant, and the coefficient of the long time constant component (C). The data suggest that the decrease in C and cumulative displacement occurred most noticeably between trials 3 and 4 of the first session. Retesting after 1 week, and up to 8 weeks later revealed no recovery. Repeated exposure to alternating leftward and rightward stimuli resulted in response decrement in both cumulative displacement and C. Responses to leftward stimuli were indistinguishable from responses to rightward stimuli.

Human optokinetic afternystagmus. Slow-phase characteristics and analysis of the decay of slow-phase velocity.

Events following the extinction of lights after 1-minute exposures of naive, normal subjects to an optokinetic stimulus at 40 deg/sec have been closely examined and quantified. Mean eye displacement in each slow phase decreased from 10.12 +/- 1.61 deg during optokinetic nystagmus (OKN) to 3.36 +/- 2.32 deg during optokinetic afternystagmus (OKAN). Slow-phase duration increased from 0.26 +/- 0.03 sec during OKN to 0.45 +/- 0.195 sec during OKAN. Eye displacement per slow phase remained fairly constant during OKAN, suggesting a spatial reference for the resetting of gaze. OKAN decay is a two-component process which can be closely approximated by a sum of two exponentials, one with a short time constant of 1.15 sec and the other with a long time constant of 48.8 sec. OKAN decay commenced at a time after lights out which depended upon the presence and timing of an intervening fast phase. When a fast phase intervened, OKAN decay commenced about 230 msec after it, and about 460 msec after lights out. When lights out occurred during the fast phase, OKAN decay commenced about 340 msec later.

Reversible cooling of the brainstem reveals areas required for mesencephalic locomotor region evoked treadmill locomotion.

The evidence suggests that the mesencephalic locomotor region (MLR) may not be a unitary region since anatomical and functional variations in the descending projections are clearly indicated. Reversible cooling of midline reticular structures can effectively block locomotion evoked by stimulation of lateral MLR (L3.5-4) sites while not significantly affecting the locomotion evoked from more medial MLR (L2-2.5) sites. In contrast, locomotion evoked by stimulation of the medial MLR sites is blocked by cooling of the ipsilateral lateral brainstem region which corresponds to the pontomedullary strip (PLS). Ipsilateral PLS cooling was not effective for blocking lateral MLR evoked locomotion, and contralateral PLS cooling was not effective for blocking either medial or lateral MLR evoked stepping. The evidence indicates that the lateral MLR relays through medial reticular nuclei while the medial MLR sites relay largely through the lateral brainstem structures often referred to as the PLS.

Symmetrical optokinetic after-nystagmus loss in Wallenberg's syndrome and multiple sclerosis.

We have demonstrated abolition of OKAN in either horizontal direction with retention of caloric responses in 3 patients with unilateral brain stem infarcts. In one further patient with diffuse brain stem disease, we have been able to show bilateral loss of horizontal OKAN in the acute phase, with recovery during remission. These findings support the conclusion that the velocity storage mechanism or connections to it, are permanently disabled by unilateral medullary infarcts and may be temporarily disabled by demyelinating disease. Retention of caloric responses in the absence of OKAN would appear to be of assistance in the differential diagnosis between peripheral and central vestibular pathway lesions.