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Biomedical subjects

R D Yee

Publications and source records attributed to R D Yee.

At least 109 records · Page 6Linked to original sources
PubMed1977

Experimental myelin intrusion in the nerve head.

On the assumption that myelin intrusion into the papilla and peripapillary region might occur with traumatic lesions of the optic nerve, a study was made of the clinical and histopathologic changes that might be expected. Nine monkey eyes were subjected to hemostat compression of the nerve close to the globe and studied over variable periods up to 28 days. Myelin was demonstrable ophthalmoscopically, followed by variable and increasing amounts of hemorrhage. The myelin was demonstrable histopathologically only during the first 2 weeks after the manipulation and was then masked by the associated hemorrhage and gliosis. The optic nerve showed expected myelinolytic reactions.

Animals↗
PubMed1977

Management of a patient with orbital varices, visual loss, and ipsilateral glaucoma.

A man with congenital orbital varices developed progressive ipsilateral visual loss beginning at age 62. Work-up demonstrated elevated intraocular pressure, decreased outflow facility, and mildly elevated episcleral venous pressure in the affected eye. Initiation of adequate glaucoma treatment was associated with interruption of declining visual acuity and with expansion of the constricted visual field. Medical control of coexisting glaucoma should be attempted prior to consideration of surgical intervention in any patient with visual loss and an ipsilateral orbital varix.

Epinephrine↗
PubMed1976

Ophthalmoplegia and dissociated nystagmus in adetalipoproteinemia.

A characteristic pattern of acquired exotropia, progressive paresis of the medial rectus muscles, and dissociated nystagmus on lateral gaze was found in three patients with abetalipoproteinemia. Study with electronystagmography of the eye movements of one patient revealed abnormally slow voluntary saccades and slow or absent fast components of vestibular nystagmus, optokinetic nystagmus, and jerk-type, disassociated nystagmus. Defects in central nervous system centers generating saccadic eye movements are postulated.

Abetalipoproteinemia↗
PubMed1976

Rapid eye movements in myasthenia gravis. I. Clinical observations.

Rapid eye movements, having high velocity and low amplitude, are described in 11 patients with myasthenia gravis. These movements occur with various degrees of ophthalmoplegia. To distinguish them from the somewhat similar lid-twitch phenomenon, they are called quiver movements. We believed that their presence is pathognomonic of myasthenia and results from a differential involvement of the two myoneural mechanisms that are peculiar to the extraocular muscles.

Adolescent↗
PubMed1976

Rapid eye movements in myasthenia gravis. II. Electro-oculographic analysis.

Voluntary saccades were studied by electro-oculography in ten patients with myasthenia gravis (MG) and in eight patients with other types of ophthalmoplegia. Despite limited range of eye movements, maximum velocities of 20 degree and 40 degree saccades in patients with MG were not significantly different from those in normal individuals, whereas maximum velocities in patients with other types of ophthalmoplegia were significantly decreased. In some myasthenic patients, small amplitude saccades were hypermetric and had high velocities, appearing clinically as "quiver" movements characteristic of MG. In MG the preservation of saccades with high initial velocities, even in the presence of severe ophthalmoplegia, suggests that muscle fibers generating rapid movements during saccades (twitch fibers) can be relatively spared when muscle fibers responsible for maintenance of excentric gaze (tonic fibers) are severely affected.

Adolescent↗
PubMed1976

Ocular manifestations of acute pandysautonomia.

A 33-year-old white man developed premature presbyopia and anisocoria as initial manifestations of acute pandysautonomia. Nine months later signs and symptoms of generalized, severe autonomic dysfunction developed, and six years later only paralysis of pupillary reactions, presbyopia, and orthostatic hypotension were unresolved. Pharmacologic testing of the pupils demonstrated no mydriasis to cocaine 4% or hydroxyamphetamine 1% and hypersensitivity to epinephrine 0.1%, methacholine 2.5%, and pilocarpine 0.0625%, suggesting the presence of sympathetic and parasympathetic, postganglionic blockage of autonomic innervation of the iris.

Adult↗
PubMed1976

Plasma cell infiltration of the conjunctiva associated with pancytopenia, dermatitis, and polyclonal gammopathy.

A 73-year-old man developed conjunctivitis, epiphora, pancytopenia, dermatitis, and a polyclonal gammopathy. Diffuse infiltration and thickening of the conjunctiva and lacrimal canaliculi by plasma cells was present. Histopathologic examination suggested a reactive, chronic inflammatory response rather than neoplasia. The patient's ocular manifestations appeared to be related to his pancytopenia, dermatitis, and polyclonal gammopathy.

Aged↗
PubMed1976

Atypical retinitis pigmentosa in familial hypobetalipoproteinemia.

Of three patients with familial hypobetalipoproteinemia, a 42-yeear-old white woman, who was homozygous for this autosomal dominantly inherited disease, had no detectable serum betalipoprotein and had a marked retinal pigmentary degeneration characterized by ring scotomas by Goldmann perimetry, extinguished electroretinographic responses, delayed responses and elevated thresholds during dark adaptometry, and abnoramal cone thresholds. A 4-year-old daughter and a 28-year-old niece of the first patient, who wer heterozygous, had reduced but detectable levels of serum betalipoprotein and no significant retinal pigmentary degeneration. Unlike patients with autosomal recessively inherited abetalipoproteinemia (the Bassen-Kornzweig syndrome), none of our patients had significant neurologic of cardiac defects. Although the level of serum betalipoprotein might be correlated with retinal pigmentary degeneration in familial hypobetalipoproteinemia and abetalipoproteinemia, it appears that neurologic and cardiac defects are dependent on other factors.

Abetalipoproteinemia↗
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

A study of congenital nystagmus: waveforms.

Eighteen patients with congenital nystagmus were studied with the techniques of electronystagmography and computer analysis. We found several complex wave forms of congenital nystagmus in the primary position of gaze above those of jerk and pendular nystagmus as defined clinically. An etiologic classification of motor fixation defect and sensory fixation defect nystagmus based on waveforms is not justified. Ocular tracking studies demonstrate that the smooth pursuit system is operational in congenital nystagmus and substantiate the belief that the fast component of jerk nystagmus is a corrective movement generated by the saccadic system. Patients with congenital nystagmus are able to produce voluntary saccades with normal velocity-amplitude relationships.

Adolescent↗
PubMed1975

Corneal intrastromal cyst following lamellar keratoplasty.

A case is reported documenting formation of an intrastromal corneal cyst following lamellar keratoplasty. A patient with keratoglobus sustained trauma to the left eye. The trauma resulted in rupture of the cornea, which was repaired with an overlay conreal graft. Two and one-half years later, an intrastromal fluid-filled cyst of the cornea was found in the visual axis. Cytologic examination of the aspirated cyst fluid revealed epithelial cells.

Adolescent↗