Ralph M. Jell

Responses of hypothalamic neurones to local temperature and to acetylcholine, noradrenaline and 5-hydroxytryptamine

(1) Extra-cellular unit activity has been recorded from the preoptic and anterior hypothalamic area of unanaesthetized cats while local temperature was varied using implanted thermodes, and while ACh, NA and 5-HT were applied locally by microelectrophoresis. The thermal and drug responses of 222 spontaneously firing neurones were classified and tabulated. (2) No significant differences were found in the distribution of drug responses of any thermal response type, except that among type D cells (thermosensitive with hysteresis), significantly more (P < 0.01) ACh excitations than NA or 5-HT excitations were observed. (3) Distributions of drug excitations and depressions were found to be essentially independent of thermal response type. (4) Examination of cell responses to combinations of drugs suggests that cells not responding to drugs tend to be non-thermosensitive, and that cells responding to only one drug tend to be thermosensitive. (5) The implications of these results are discussed in terms of current theories of preoptic and anterior hypothalamic contributions to body temperature regulation.

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.

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.

Spinal Cord Concussion

A reliable experimental model using decerebrate frogs has been developed by which a measured cutaneous stimulus to the right forelimb produces a single electrical response from the left sciatic nerve. Using this model, the minimal concussing force necessary to abolish the propagation of the nerve impulse down the spinal cord was established by trial and error. The mean recovery time was 31.2 seconds, with a standard deviation of 1.32 seconds. Recovery of function of the spinal cord, as measured this method, was complete following single and multiple concussions.

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.

Spinal-cord concussion in frogs: a study of reflex changes

A reliable experimental model of the spinal frog, employing the flexor withdrawal reflex to a noxious stimulus, has been used to study the response to single and repeated concussing blows over the spinal column. It is evident that caudally placed blows depress the reflex response, whereas more cephalad blows facilitate the response. The results of studies using repeated concussing blows support the concept that neuronal units may completely lose their function without suffering permanent structural damage.

Modification of Vertical OKN and Vertical OKAN Asymmetry in Humans During Parabolic Flight

Characteristics of human vertical optokinetic nystagmus (OKN) and afternystagmus (OKAN) were examined by ISCAN imaging system on the ground and on board NASAs KC-135 aircraft in a parabolic flight study. The aircraft produced alternating periods of micro-(ca. 10(-2) G) and hyper-(ca. 1.8 G) gravitoinertial forces. Each phase lasted approximately 20 to 25 s. As compared to the baseline data on the ground, there was a significant increase of downward OKN/OKAN, whereas the upward OKN/OKAN did not change significantly in either micro- or hyper-G. As a consequence, the asymmetry of vertical OKN/OKAN, normally seen on the ground, was lost. It is postulated that the increase of downward OKN/OKAN in non-1-G conditions was governed by two different mechanisms. In micro-G, the normal inhibition effect in 1 G on the downward eye movement mediated by otolith organ activity to vertical velocity storage was removed. In hyper-G, downward OKN/OKAN was facilitated by augmented otolith-ocular reflex because of increased gravitoinertial force, so as to produce enhanced compensatory downward eye movement.

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.

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.

Multisensory Integration in the Human Vestibular Velocity Storage Mechanism

To test the hypothesis that auditory inputs can interact with the optokinetically or vestibularly-charged human VSM, we examined the effects of sound on rotational nystagmus and HOKAN. Subjects were rotated at 60 degrees/s, in either clockwise (CW) or counterclockwise (CCV) direction, for a total of 3 min. After 1 min of constant rotation, the optokinetic surround (7 ft dia., 2 degrees stripes at 18 degrees intervals) was illuminated for 60 s and the ensuing HOKAN was recorded for 60 s (standard DCEOG). The chair was stopped 60 s later and the post-rotatory nystagmus (PRN) was recorded. The acoustic stimulus (4/s, 10 ms pulses) was presented to the subject by a loudspeaker in 4 randomized test conditions: (1) fixed to the surround-on during OKN, off during OKAN (2) fixed to the surround-off during OKN, on during OKAN (3) rotating with the subject-on during OKN, off during OKAN (4) rotating with the subject-off during OKN, on during OKAN. In all conditions, the sound was on during per- and post-rotatory nystagmus. Each test was performed on a different day and consisted of 4 randomized control and test trials (CW and CCW). Under none of the above conditions was the rotatory or optokinetic decay affected by the presence of stationary or rotating sound. This absence of alteration of PRN by sound cues contradicts that reported by Kollar et al. (1988). Our evidence that neither HOKAN nor post rotatory nystagmus decay is affected by sound cues supports the conclusion that, under our conditions, multisensory interaction does not occur in the human VSM.