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Biomedical subjects

R M Burde

Publications and source records attributed to R M Burde.

At least 37 records · Page 2Linked to original sources
PubMed1990

Progressive visual field defects in patients with intracranial arteriovenous malformations.

Two men, aged 59 and 36 years, had large, intracranial arteriovenous malformations. Both patients developed severe, bilateral visual loss secondary to unrecognized chronic papilledema. Lumbar puncture disclosed increased intracranial pressure. Neuroimaging disclosed only vascular malformations. The patients were treated by embolization of the vascular malformations and ventriculoperitoneal shunting procedures. The malformation of one patient was excised.

Adult↗
PubMed1990

Optic neuropathy and central nervous system disease secondary to Sjögren's syndrome in a child.

The authors describe a 10-year-old girl in whom optic neuropathy and central nervous system (CNS) disease developed in association with primary Sjögren's syndrome. There was angiographic evidence of cerebral vasculitis and multiple infarcts present on neuroimaging. Results of parotid biopsy, cerebrospinal fluid, and serologic analyses showed abnormalities that were consistent with the diagnosis of Sjögren's syndrome. Although the patient had optic disc pallor on initial evaluation, her color vision and acuity improved with immunosuppressive therapy, as did her other neurologic symptoms. The authors believe this represents the first reported case of optic neuropathy and CNS disease associated with primary Sjögren's syndrome in the pediatric population. The possibility of improvement in visual function with early institution of immunosuppressive therapy makes prompt diagnosis essential.

Brain Diseases↗
PubMed1990

Yellow forelock--a new neuro-ophthalmological sign.

We examined a middle-aged man with a prominent yellow forelock who complained of loss of vision in both eyes. He smoked his pipe avidly and drank a little Bourbon whisky daily. The nicotine content of the forelock (21.7 ng/mg) was 10 times that of the hair on his occiput (2.23 ng/mg). A yellow forelock when associated with isolated painless visual loss suggests tobacco amblyopia.

Alcohol Drinking↗
PubMed1990

Visual loss following intranasal anesthetic injection.

Four patients had visual loss after nasal surgery. There was one instance each of branch retinal artery occlusion, central retinal artery occlusion, anterior ischemic optic neuropathy, and posterior ischemic optic neuropathy. The postulated mechanism is vasospasm. The submucosal injection, under pressure, of an anesthetic with epinephrine is deemed to be causative.

Adult↗
PubMed1989

Parasympathetic nuclei.

A series of experiments in monkeys using the fluorescent tracer substances Fast Blue and Nuclear yellow as well as wheat germ agglutinin-horseradish peroxidase injected into the ciliary ganglion has demonstrated labeling in 3 distinct regions of the mesencephalon: (1) anterior median nucleus; (2) Edinger-Westphal nucleus; and (3) the nucleus of Perlia. Further it was shown that the caudal extent of the Edinger-Westphal nucleus reaches the level of the central caudal nucleus of the somatic complex and that the lateral visceral column divided into a major and accessory column at the junction of the middle and posterior one-third of the somatic complex.

Amidines↗
PubMed1989

Acute oculomotor nerve palsy in childhood. Is arteriography necessary?

In the past, angiography was performed in all patients as part of the initial workup for isolated oculomotor paralysis, except patients older than 40 years with pupillary sparing. The pupil-sparing group was not subjected to angiography because of a low probability of cerebral aneurysm. It is believed that the case reported here constitutes the lower age limit (14 years) for documented, isolated oculomotor paralysis due to aneurysm. It is recommended that an angiogram not be a necessary part of the workup of patients 10 years old or younger.

Acute Disease↗
PubMed1989

Amaurosis fugax. An overview.

Amaurosis fugax is an all-inclusive term for all forms of transient visual loss. Clinically, it can be divided into four identifiable symptom complexes, each with its underlying pathoetiology: embolic, hypoperfusion, angiospasm, and unknown.

Blindness↗
PubMed1989

Breakdown of the blood--aqueous barrier in the rabbit eye by infrared radiation.

Breakdown of the blood-aqueous barrier was produced by infrared radiation (IR) at a heat flux from 24 to 44 J/cm2 in pigmented, but not in albino rabbits. Blood-aqueous barrier breakdown was inhibited by indomethacin and ketamine/xylazine anesthesia mixtures, but not by [D-Trp2,D-Pro7,9]-substance P. The degree of blood-aqueous barrier breakdown could be controlled by IR flux. Two models for accurate determination of the heat flux are presented.

Albinism↗
PubMed1988

Direct parasympathetic pathway to the eye: revisited.

Intraocular injections of wheat germ agglutinin horseradish peroxidase appeared to confirm previous experimental and clinical data supporting the existence of a direct, non-synapsing, parasympathetic pathway from the mesencephalon to the eye. Quantitative and qualitative differences between the two pathways were noted. The intraocular injection of the fluorescent dyes Fast blue and Nuclear yellow failed to provide mesencephalic labeling. The implications of these findings are discussed.

Amidines↗
PubMed1988

Disparate visceral neuronal pools subserve spinal cord and ciliary ganglion in the monkey: a double labeling approach.

The fluorescent dyes Nuclear yellow, a nuclear marker, and Fast blue, a cytoplasmic marker, were utilized in a double-labeling procedure. One or the other of these dyes was injected sequentially into the cervical spinal cords and ciliary ganglia of 6 cynomolgus monkeys. No double labeling of cells was noted in the anterior median nucleus, Edinger-Westphal nucleus, or nucleus of Perlia in the mid-brain.

Animals↗
PubMed1988

Retinocortical conduction time in diabetics with abnormal pattern reversal electroretinograms and visual evoked potentials.

Clinically evident retinal vascular disease in patients with diabetes mellitus may be preceded by an increase in visual evoked potential latency in electrophysiologic testing. This increase may indicate either retinal or optic nerve dysfunction. To determine the origin of the latency increase we initiated a cross-sectional study of simultaneous pattern-reversal electroretinograms and visual evoked potentials. We recorded transient (3.8 reversals/second) pattern electroretinograms and visual evoked potentials using both 15' and 60' high-contrast black-white checks. Fifty-five diabetic patients (34 with no retinopathy and 21 with background retinopathy) and 34 age-matched visual normals (controls) were tested. Group data in diabetics showed significant latency increases in both tests, but not significant differences in retinocortical conduction time were noted. These results suggest that the increases in visual evoked potential latency exhibited by diabetic patients with little or no retinopathy usually reflect altered retinal function rather than optic neuropathy. Two patients with background retinopathy exhibited retinocortical conduction times that exceeded the normal mean by more than two standard deviations, suggesting that optic neuropathy may occasionally occur in diabetic patients with background retinopathy.

Adult↗
PubMed1988

The relationship between hue discrimination and contrast sensitivity deficits in patients with diabetes mellitus.

In an attempt to elucidate more fully the pathophysiologic basis of early visual dysfunction in patients with diabetes mellitus, color vision (hue discrimination) and spatial resolution (contrast sensitivity) were tested in diabetic patients with little or no retinopathy (n = 57) and age-matched visual normals (n = 35). Some evidence of visual dysfunction was observed in 37.8% of the diabetics with no retinopathy and 60.0% of the diabetics with background retinopathy. Although significant hue discrimination and contrast sensitivity deficits were observed in both groups of diabetic patients, contrast sensitivity was abnormal more frequently than hue discrimination. However, only 5.4% of the diabetics with no retinopathy and 10.0% of the diabetics with background retinopathy exhibited both abnormal hue discrimination and abnormal contrast sensitivity. Contrary to previous reports, blue-yellow (B-Y) and red-green (R-G) hue discrimination deficits were observed with approximately equal frequency. In the diabetic group, contrast sensitivity was reduced at all spatial frequencies tested, but for individual diabetic patients, significant deficits were only evident for the mid-range spatial frequencies. Among diabetic patients, the hue discrimination deficits, but not the contrast sensitivity abnormalities, were correlated with the patients' hemoglobin A1 level. A negative correlation between contrast sensitivity at 6.0 cpd and the duration of diabetes also was observed.

Adult↗
PubMed1988

Autoimmune optic neuropathy: evaluation and treatment.

Fourteen patients, 12 of whom were women, with an age range from 26 to 56 years, presented with progressive or recurrent optic neuropathy, despite conventional doses of corticosteroid, and laboratory evidence of collagen vascular disease. The visual loss was severe and most had an acuity less than 20/200. Megadose corticosteroid therapy improved the vision in 11 of the 12 patients. Continued oral prednisone and cytotoxic drugs were necessary to maintain vision in nine patients. Patients with autoimmune optic neuropathy must be differentiated from cases with idiopathic optic neuritis or multiple sclerosis to facilitate the appropriate therapy.

Adult↗