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Biomedical subjects

D A Robinson

Publications and source records attributed to D A Robinson.

At least 127 records · Page 7Linked to original sources
PubMed1976

Slow saccades in spinocerebellar degeneration.

Two patients with spinocerebellar degeneration made abnormally slow horizontal refixations. One patient produced quick phases of nystagmus with identical maximum velocities, suggesting her refixations were abnormal saccades and not voluntary pursuit movements. In response to double target jumps, neither patient showed an obligatory refractory period after each saccade; they responded to every target movement after one reaction time. Their slow refixations were not preprogrammed since they could be modified in flight. To reconcile these observations with normal saccadic behavior, we hypothesized a neural network that made saccades by driving the eyes to an orbital position rather than preprogramming a distance for movement. Computer simulation of this model produced both realistically appearing normal saccades and, when appropriately "lesioned" to simulate a loss of saccadic "burst" neurons in the pontine reticular formation, slow saccades that could be modified in flight.

Adolescent↗
PubMed1976

An explanation of eye movements seen in internuclear ophthalmoplegia.

Recent findings in experiments on monkeys show that a horizontal saccade is made by a pulse-step of neural activity, part of which rises to medial rectus (MR) motoneurons on the fibers of the medial longitudinal fasciculus (MLF). If inhibitory as well as excitatory fibers run in the MLF, then the data show that each MLF must carry both the excitatory and inhibitory activity required for contralateral, horizontal saccades. Therefore, interruption of these fibers removes not only excitation from the ipsilateral MR but inhibition from the contralateral MR. Such a lesion also disturbs the correct relationship between the pulse and the step and creates abnormal saccades. These facts make it possible to explain why, in internuclear ophthalmoplegia, the eye on the side of the lesion adducts slowly and inadequately, while the opposite eye has nystagmus in abduction.

Abducens Nerve↗
PubMed1976

Ocular motor abnormalities in hereditary cerebellar ataxia.

Twelve members of a family with hereditary cerebellar ataxia of late onset were examined and, in 5, quantitative recording of eye movements were obtained. The initial and most severe symptom in all patients was ataxia of gait, followed by dysarthria and later by dysmetria of the limbs. Clinical examination did not reveal involvement of structures other than the cerebellum. Ocular motor examination showed: (1) inability to hold eccentric gaze resulting in gaze-paretic nystagmus; (2) downward beating nystagmus, accentuated on lateral gaze; (3) defective smooth pursuit, with relative preservation of optokinetic nystagmus induced by full-field stimulation; (4) rebound nystagmus; (5) enhanced gain (eye velocity/head velocity) of the vestibulo-ocular reflex during rotation in darkness; (6) decreased ability to suppress the vestibulo-ocular reflex during fixation of an object rotating with the patient; (7) saccadic dysmetria, especially downward overshoot; and (8) square wave-jerks. Although each of these signs can probably occur with lesions elsewhere in the brain, in combination they are highly suggestive of cerebellar involvement. With the reservation that we do not yet have pathological confirmation of the location of our patients' lesions, our results support the suggestion that the cerebellum specifically: (1) helps maintain eccentric gaze; (2) produces smooth pursuit eye movements; and (3) modulates the amplitude of saccadic eye movements. Many of the characteristics of the altered vestibulo-ocular responses and rebound nystagmus could be explained by the underlying anomaly in the smooth pursuit system.

Adult↗
PubMed1976

Adaptive gain control of vestibuloocular reflex by the cerebellum.

1. The gain of the vestibuloocular reflex (slow-phase eye velocity/head velocity) was measured in 17 adult cats. 2. The gain of the reflex, in the dark, was 0.90 (+/-0.15 SD) over the frequency range 0.03-1.2 Hz. 3. In the range 0.01-0.15 Hz, the phase behaved as though the overall reflex time constant were 12 s or greater. The cupula time constant is 4 s. Therefore, the central part of the reflex must manipulate the canal signal to improve its low-frequency response by a factor of at least three. 4. When the cats wore left-right reversing prisms chronically and were also rotated for 2 h every day, the reflex underwent large, plastic changes. The gain, tested in the dark, decreased by 93% at 0.05 Hz and 55% at 1.2 Hz. In effect, the low-frequency response was abolished. The process took about 8 days. 5. In the light, with reversed vision, the gain decreased further and, at low frequencies, the eye movements did reverse in direction. 6. When the vestibulocerebellum was removed, the gain, in the dark, rose to about 1.17 and the plastic changes caused by reversing prisms were completely abolished. 7. Reversing prisms create vestibuloocular dysmetria. The change in gain they produce is considered to be an adaptive response designed to reduce image motion on the retina during head movements. The vestibulocerebellum is necessary for this adaptive process. It is proposed that detecting and repairing dysmetria (of natural origin) is an important cerebellar function.

Adaptation, Physiological↗
PubMed1975

The irreversible binding of acetylcholine mustard to muscarinic receptors in intestinal smooth muscle of the guinea-pig.

1. Acetylcholine mustard (N-2-chloroethyl-N-methyl-2-acetoxyethylamine), a potent muscarinic agonist, binds virtually irreversibly to muscarinic receptors in longitudinal muscle strips from guinea-pig small intesting, as shown by the inhibition of the binding of E13-H]-propylbenzilycholine mustard ([3-H-PrBCM), an affinity label for the muscarinin receptor. 2. A value for the apparent binding affinity of acetylcholine mustard and a value for the rate constant for the receptor alkylation reaction have been deduced from the rate of onset of the inhibition of [3-H]-PrBCM binding. 3. The kinetic constants obtained may refer largely to the interaction between acetylcholine mustard and the desensitized receptor. 4. At high concentrations acetylcholine mustard practically abolishes the contractile response to carbachol. At the concentrations acetylcholine mustard appears to have multiple actions on the tissue.

Acetylcholine↗
PubMed1975

A quantitative analysis of extraocular muscle cooperation and squint.

The mechanical properties of human extraocular muscles have recently been described. This allows one to use the force-balance equation of mechanics to solve for the complete mechanical state of all six extraocular muscles and the passive orbital tissues in any eye position. This includes each muscle's force, length, innervation, and unit action vector, which describes how its force is distributed to act horizontally, vertically, and in torsion. Most important, this calculation method allows one to predict the tropias that occur in an eye subject to any imaginable form of peripheral pathology. It also permitts, by calculation, an estimation of the correction that might be expected from any sort of muscle surgery. The tight lateral rectus syndrome is used to illustrate the application of the method in diagnosis and surgery. It also offers, for the first time, a quantitative estimate of the multitude of ways in which muscles can interact and interfere with each other when they hold the globe. Two of the results are interesting: because muscles have different lengths and sizes, their innervational participation in a movement can appear to be quite different than their mechanical participation. From an innervational standpoint, the vertical recti and obliques participate equally in vertical gaze. Muscles interfere with each other a good deal and necessitate changes of innervation to counteract these cross-couplings. This causes unexpected dependencies of innervation on eye position and leads, for example, to the fact that the superior rectus innervation in up gaze is just as large in adduction as in abduction.

Biomechanical Phenomena↗