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Biomedical subjects

C Ellenberger

Publications and source records attributed to C Ellenberger.

12 recordsLinked to original sources
PubMed1979

Ischemic optic neuropathy as a possible early complication of vascular hypertension.

Eighteen patients with idiopathic optic neuropathy lacked symptoms and signs of cardiovascular and cerebrovascular disease, especially when compared to three groups of patients with sudden visual loss caused by retinal infarction, transient ischemia, and cerebral infarction. Many patients in the latter groups had hypertension, carotid bruits, heart disease, transient ischemic attack, and stroke. But among the patients with ischemic optic neuropathy, hypertension was the only evidence of cardiovascular disease, affecting 44% of the patients. We argue that, in many cases, ischemic optic neuropathy represents a direct and early complication of hypertension arterial disease affecting small arterioles supplying the anterior part of the optic nerve. The pathologic process may thus be similar or identical to lacunar infarction of the brain.

Adult↗
PubMed1978

Electrical correlates of normal binocular vision.

Several characteristics of the visual stimulus determine the waveform of the visually evoked potential (VEP). Many of them must be controlled for the most efficient application of this technique as a clinical diagnostic test. We describe a simple system that demonstrates the effects of the VEP of adding structure to the stimulus, varying the size and clarity of its pattern elements, and presenting an image to the eye opposite the stimulated eye. We identify wave components of the VEP generated by a flashed pattern that reliably reflect each of these changes in stimulus properties.

Adult↗
PubMed1978

Papillophlebitis: benign retinopathy resembling papilledema or papillitis.

Three young adult patients are described to illustrate an uncommon syndrome, papillophlebitis. This entity, characterized by mild but protracted monocular visual impairment, edema of the optic disc, retinal venous engorgement, and perivenous retinal hemorrhages, resembles atherosclerotic occlusion of the central retinal vein in older patients. In younger individuals it is benign and self limited, but may be incorrectly diagnosed as optic neuritis or papilledema. These alternatives can usually be excluded if tests of visual function do not indicate an optic nerve conduction defect and if the clinical presentation and examination of the opposite ocular fundus do not disclose evidence of increased intracranial pressure. Because resolution usually occurs spontaneously, immediate neuroroentgenographic tests may be inappropriate. Effective treatment has not been established; local instillation of corticosteroids may hasten recovery.

Adult↗
PubMed1978

The visually evoked potential in Huntington disease.

The visually evoked potential was abnormal in 17 of 18 patients with Huntington disease. Both early and late wave components were affected, and the averaged amplitude for the patients was reduced in comparison with 50 normal control subjects. Despite striking attenuation and disorganization of the complex, latency of initial wave components was normal. The abnormality was not present in patients with a variety of other nonfocal cerebral disorders nor in 13 children of patients with Huntington disease.

Adolescent↗
PubMed1977

Perimetry.

Explore the source record for details and available documents.

Humans↗
PubMed1976

Perioptic meningiomas. Syndrome of long-standing visual loss, pale disk edema, and optociliary veins.

Three patients had a syndrome of progressive or long-standing visual loss, pale disk edema, and optociliary veins, indicating that a spheno-orbital meningioma had invaded the anterior perioptic meninges. To diagnose this syndrome, one must distinguish "disk edema" from "papilledema"; although both result from increased pressure within the perioptic subarachnoid space, disk edema is caused by a variety of lesions just behind the globe, whereas papilledema is caused by remote lesions that raise intracranial pressure. Optociliary veins reflect the slowness of progression of both processes. This ophthalmoscopic diagnosis carries important implications, namely, that the tumor grows very slowly and that surgical treatment will not improve vision. Therefore, excision may not be the treatment of choice.

Adult↗
PubMedDate not supplied

Moebius syndrome in association with hypogonadotropic hypogonadism.

The association between hypogonadotropic hypogonadism and multiple CNS lesions in a variety of disorders suggests a possible causative link between these clinical findings. Neural afferent input into the hypothalamus from higher CNS centers modulates GnRH secretion and derangements of these neural pathways could potentially result in diminished gonadotropin secretion and hypogonadism. This report describes a patient with multiple CNS defects secondary to Moebius syndrome and hypogonadotropic hypogonadism whose clinical features support the hypothesis that his CNS and endocrine defects may be causally associated. Comprehensive clinical evaluation in this patient revealed severe mental retardation; cranial nerve palsies; motor, reflex, and gait disturbances; and sexual infantilism secondary to hypogonadotropic hypogonadism. An MRI of the brain revealed atrophy or hypoplasia of the third cranial nerve and the olfactory gyri. Numerous syndromes including the Moebius syndrome are now described in which hypogonadotropic hypogonadism and CNS defects are associated. Detailed neuroanatomic and embryologic studies have demonstrated the important functional interrelationships between higher central nervous system centers and the hypothalamus. Taken together, these findings provide support for the causative association of multiple CNS defects and hypogonadotropic hypogonadism.

Abnormalities, Multiple↗