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Biomedical subjects

D B Reingold

Publications and source records attributed to D B Reingold.

8 recordsLinked to original sources
PubMed1983

Clinical studies of color vision with Gunkel's chromagraph.

Color thresholds in a series of patients with local or systemic diseases were determined by a chromagraph method and subjected to computer analysis. When compared with normal persons, those with optic nerve disease (multiple sclerosis, optic neuritis, and optic atrophy) showed an overall weakness for all colors (enlarged neutral areas), with an additional specific defect in the orange-cyan (greenish blue) axis. Those with the two retinal diseases studied (macular degeneration and retinitis pigmentosa) also showed threshold elevation for all colors, but with a special defect in the yellow-blue axis. The general elevation was greater for patients with retinitis pigmentosa than for those with macular degeneration, regardless of the visual acuity. In patients undergoing treatment for systemic lupus erythematosus and rheumatoid arthritis, there was a mild elevation of the color threshold, especially for yellow.

Arthritis, Rheumatoid↗
PubMed1983

Blink-saccade synkinesis.

We studied two patients who could make saccades of normal velocity and amplitude only in association with a simultaneous blink. In one patient, the initiation of saccades was also facilitated by blinks. Both patients had signs of cerebellar or brainstem dysfunction, suggesting a posterior fossa localization for blink facilitation of saccadic velocity and amplitude.

Adult↗
PubMed1982

Ocular signs of cerebellar disease.

Ocular signs of cerebellar disease have been increasingly appreciated with the advent of means for quantitative recording of eye movements. The graphs in this article illustrate ocular flutter, dysmetria, abnormal (nonsmooth) pursuit, instability of fixation, faulty vestibular suppression, impaired optokinetic response, end-position nystagmus, and rebound nystagmus. The signs may be categorized as follows: (1) proprioceptive abnormalities manifest by flutter, dysmetria, and instability of gaze and (2) defects of vision-dependent functions manifest by abnormalities of pursuit, vestibular suppression, optokinetic response, and nystagmus.

Basal Ganglia↗
PubMed1979

Alpha-adrenergic hyper-responsiveness in asthma.

Because alpha-adrenergic stimulation causes bronchoconstriction, the alpha-adrenergic responsiveness of 21 subjects with allergic asthma was compared with that of 16 subjects with allergic rhinitis and 38 normal control subjects. None of the patients had taken medications for at least 30 days before study. Alpha-adrenergic responsiveness was measured by the capacity of phenylephrine to constrict the cutaneous vascular bed and to dilate the pupillary sphincter muscle. Asthmatic subjects required 4.0 +/- 0.6 ng to reduce their cutaneous blood flow by 50 per cent, whereas normal controls required 32.0 +/- 7.5 ng (P less than 0.005) and subjects with allergic rhinitis required 23.7 +/- 9.4 ng (P less than 0.02). The pupils of asthmatic subjects dilated by greater than 0.5 mm in response to 1.8 +/- 0.14 per cent phenylephrine, patients with allergic rhinitis required 2.4 +/- 0.16 (P less than 0.01), and normal controls needed 2.7 +/- 0.07 (P less than 0.00001). Therefore, the patients with allergic asthma had significantly enhanced alpha-adrenergic responses when compared both to normal subjects and patients with allergic rhinitis; the possibility that increased alpha-adrenergic activity contributes to the asthmatic diathesis warrants further exploration.

Adolescent↗
PubMed1979

The eye movement disorders of progressive supranuclear palsy.

In addition to the gross disturbances of vertical gaze, patients with progressive supranuclear palsy may show abnormalities in the saccadic and pursuit subsystems of horizontal gaze. Saccades are slower and smaller than normal. An attempt to elicit a large amplitude saccade will often result in a series of "fractionated" saccades. Pursuit eye movements become saccadic. The quick phases of vestibular and optokinetic nystagmus are of low amplitude. In the study presented, eye movements of 13 patients were recorded clinically and by electro-oculography, and data from the two methods, compared.

Adult↗
PubMed1979

Neural correlates of nystagmus in abducens nerve.

1. The firing rates of action potentials of abducens nerve single fibers were recorded in the cat's orbit during a variety of vestibular and optokinetic stimulations. 2. Comparison was made of the neural firing rates associated with agonist and antagonist responses during slow and fast components of vestibular and optokinetic nystagmus. It was found that the relationship between the motoneuron firing rates and the eye motion was independent of the reflex with which they were associated--vestibular or optokinetic, or the type of response--agonist or antagonist. No neurons were observed that responded only during the fast or only during the slow nystagmus phase. Motoneuron firing rates were proportional to both velocity and position of the eye in a ratio of 1 (spikes/s)/(deg/s) to 7.2 (spikes/s)/deg. The behavior of the motoneurons was compatible with the hypothesis that thier firing rates are sufficient to overcome both elastic and viscous forces by which the muscles and ligaments hold the eye in the orbit. 3. For low-frequency head rotations, eye displacement and neural responses showed a small phase angle difference. At higher frequencies, however, while the eyes maintained a fixed relationship to the head rotation, the neural responses showed an increasing phase lead. One component of this phase lead compensated for the phase lag introduced by the orbital mechanics. The other was modeled as a constant delay of approximately 70 ms, which may be accounted for by neuromuscular transmission and transduction.

Abducens Nerve↗