Directional plasticity of the vestibuloocular reflex in the cat.
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Biomedical subjects
Publications and source records attributed to D A Robinson.
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In an attempt to determine the clinical severity and prognosis of children admitted to hospital with whooping cough, 127 patients were studied prospectively during a 12-month period. Clinical and laboratory criteria were used and the impression gained was that most cases were mild, although 3 children were dangerously ill and at least 30% had symptoms lasting 2 months or longer. There were no deaths, and no permanent sequelae were noted. The mean age of patients was higher than in other series, which might have accounted for the fairly low severity. Although there was some evidence of a decline in severity and mortality, whooping cough is still an unpleasant and protracted illness.
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The gain (eye velocity/head velocity) of the vestibulo-ocular reflex (VOR) of cats was measured in the dark and light for sinusoidal head oscillations at 0.05 and 1.2 Hz with peak velocity of about 30 deg/sec. Animals wore visual reversing prisms chronically and were also subjected to forced oscillation in the light at 0.05 Hz for 2 h per day. Such experience produced adaptive reduction in VOR gain in the dark from 0.85 to 0.10 within about 4 days; qualitatively similar effects were observed at 1.2 Hz. In 4 cats, the dorsal cap of the inferior olive was located electrophysiologically by its responses to visual motion, and bilateral electrolytic lesions were made in or near this structure. The location of lesions was subsequently identified by histology. After lesions, 3 cats were unable to make adaptive changes in VOR gain when confronted with the same reversing prism paradigm; the fourth exhibited appreciable retardation of adaptation. These results imply that the dorsal cap is essential for plastic adaptation of the VOR. However, all cats retained the ability to use reversed vision to reduce VOR gain in the light after lesions. Optokinetic nystagmus (OKN) and optokinetic after nystagmus (OKAN) were measured in a striped optokinetic drum, before and after dorsal cap lesions, at drum velocities of 20 and 40 deg/sec. Lesions of the dorsal cap in 4 cats did not impair either OKN or OKAN. This result indicates that the climbing fiber system reaching the flocculus from the inferior olive is not essential for such optokinetic movements.
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1. The ability of the central nervous system to compensate for saccadic dysmetria was demonstrated in rhesus monkeys. The behavior of this adaptive mechanism after cerebellar ablations was examined. 2. Monkeys were trained to fixate small target lights. Eye movements were monitored while the animals were seated, with their heads fixed, in a rotating magnetic field. The horizontal recti muscles of one eye were weakened by tenectomy. Saccades made by this weakened eye were hypometric and followed by postsaccadic drift. 3. When the patch was switched so that the weak eye was viewing, the hypometric saccades made by the weak eye gradually became larger, until after 3 days they were essentially orthometric. This indicated that the central nervous system could compensate for a peripheral weakness. 4. The tenectomy operation reduced the strength of the muscles, creating hypometria, and upset the ratio of viscosity to elasticity in the orbit, creating postsaccadic drift in the weak eye. The innervation required to make a saccade has both phasic and tonic components, the so-called pulse and step. The sacccadic repair mechanism increased both the pulse and the step to compensate for the hypometria and also adjusted the ratio of the pulse to the step to eliminate postsaccadic drift. 5. Total cerebellectomies were performed on two monkeys, each of which had one tenectomized eye. These ablations created an enduring saccadic hypermetria and postsaccadic drift in the unoperated eye of both animals. The total cerebellectomy abolished all adaptive repair of the saccadic system. 6. Partial cerebellectomies were performed on two monkeys, each of which had one tenectomized eye. Lesions of the vermis and paravermis (lobes IV-IX) and the fastigial nuclei created an enduring saccadic hypermetria without postsaccadic drift in the unoperated eye of both animals. These lesions abolished adaptive control of the pulse of innervation. Adaptive changes in the step of innervation still occurred, so that postsaccadic drift was always eliminated in the experienced, viewing eye. Thus the midline cerebellum (vermis, paravermis, and fastigial nuclei) appears to be important for repair of saccadic dysmetria, but not for repair of postsaccadic drift. Additional evidence that postsaccadic retinal slip cannot be compensated for in flocculectomized monkeys suggest that the adaptive control of the step may depend on the flocculus. 7. After cerebellar lesions the monkeys were able to make saccades of all amplitudes and directions. The principal deficit in these animals seemed to be that the pulse and step of innervation were no longer appropriate to the target displacement. We conclude that the cerebellum's principal contribution to saccadic eye movements is the adjustment of the gains of the pulse- and step-generating mechanisms. Hence this study supports the hypothesis that repair of dysmetria is a general function of the cerebellum.
In October and November 1978 two outbreaks of enteritis occurred in the north of England. Symptoms lasted two to over eight days but in no case necessitated admission to hospital. Faecal specimens from most of the patients were found to contain thermophilic Campylobacter sp. Inquiry disclosed that all patients had consumed unpasteurised milk from local farms. Examination of rectal swabs from the cattle concerned and milk socks yielded strains of Campylobacter sp indistinguishable from those isolated from the patients. It was therefore concluded that, since campylobacters are not known to be excreted in milk, faecal contamination of the milk had probably occurred and had led to these outbreaks. Evidence suggests that thermophilic Campylobacter sp is an occasional contaminant of milk. So long as unpasteurised milk continues to be distributed further outbreaks will probably occur.
Eye movements in a patient with saccadic oscillations (ocular flutter) were recorded and analyzed. Findings were related to recent microelectrode studies in the monkey pontine reticular formation which have identified three types of premotor neurons related to saccadic eye movements: burst, tonic, and pause cells. We incorporated these cell types into a hypothetical circuit that generates saccades by rapidly driving the eye to a designated orbital position rather than preprogramming a distance for movement. Physiological measurements suggest that this neural network is unstable and that the burst neurons must be tonically inhibited to prevent saccadic oscillations during periods of fixation. Pause cells, which discharge tonically except during saccades, when they pause, appear to inhibit burst cells and prevent such saccadic oscillations. Analysis of our patient's behavior indicates that many types of saccadic oscillations can be explained and classified by assuming an abnormality of pause cell control over saccadic burst neurons.
The vestibuloocular relfex of the cat was studied during step and sinusoidal head velocity stimuli. A model is presented which simulates the observed slow phase and quick phase behavior. The model is constructed to be compatible with neurophysiological observations of the behavior of neurons in the pons. Emphasis is placed on the amplitude and timing of quick phases which are active orienting movements that drive the eyes into the direction of turning. It is proposed that quick phases, like saccades, are generated by a local feedback loop in the pons which rapidly drives the eyes to a point in the orbit specified by a vestibular signal. It is suggested that two internal signals specify the eye positions at which quick phases start and end. The statistics of the fluctuations of these signals was measured and correlation between them was discovered and incorporated in the model.
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A simple model of the vestibuloocular reflex and the optokinetic system was used to simulate recent data on visual and vestibular responses of neurons in the vestibular nucleus. Contrary to a previous interpretation, the results support the hypothesis that the optokinetic and semicircular canal signals are combined simply by linear addition on the cells of the vestibular nucleus.
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