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Results for “optic nerve”

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At least 19 recordsLinked to original sources
PubMed1978

Experimental injury of the optic nerve with optic disc swelling.

An ultrastructural study utilizing horseradish peroxidase was performed to determine the mechanism and consequences of leakage of vascular protein following injury of the optic nerve. Unilateral optic nerve injuries were produced in four rhesus monkeys by making a cautery lesion on the retrobulbar portion of the optic nerve. Optic disc changes were followed with stereo fundus photography and fluorescein angiography. Three to 14 days after injury horseradish peroxidase was given intravenously and the tissue was prepared for electron microscopy, including serial sections of selected tissue blocks. Fundus photography and fluorescein angiography showed edema of the optic disc in two animals. There was leakage of horseradish peroxidase into the optic nerve head from the optic nerve lesion and the peripapillary choriocapillaris. Although the pathway of horseradish peroxidase leakage in the injured optic nerve was not entirely clear, serial sections indicated intraendothelial channels as one possible route. Alterations of the optic nerve head were confined to the axon segments anterior to the injury, and included aggregation of mitochondria, disruption of neurotubules, and swelling. These findings suggest that optic nerve injury produces damming of axoplasmic flow and that swelling of the optic nerve head is the result of axon enlargement.

Animals↗
PubMed1979

Cavernous hemangioma of optic chiasm, optic nerves and right optic tract. Case report and review of literature.

Diminishing right ocular visual acuity for three weeks in a 30 year old man was confirmed by examination. Bilateral scotomata and bitemporal hemiachromatopsia indicated a chiasmal lesion; reduced visual acuity and Marcus Gunn pupil of the right eye and left relative temporal hemianopia indicated asymmetric involvement. Erythrocytes in the CSF verified a suspected subarachnoid bleed; contrast-enhanced CAT scan demonstrated a suprasellar mass. A cystic, multiloculated, bluish mass distorted the right optic nerve, tract, and chiasm. A hematoma was evacuated and biopsy revealed a cavernous hemangioma of the right optic nerve. Post-operatively, visual acuity has recovered in the right eye but a left homonymous temporal hemianopia has developed.

Adult↗
PubMed1977

Electrical potentials from the eye and optic nerve of Strombus: effects of electrical stimulation of the optic nerve.

1. Photic stimulation of the mature eye of Strombus can evoke in the optic nerve 'on' activity in numerous small afferent fibres and repetitive 'off' bursts of afferent impulses in a smaller number of larger fibres. 2. Synchronous invasion of the eye by electrically evoked impulses in small optic nerve fibres (apparently the 'on' afferents, antidromically activated) can evoke a burst of impulses in the larger 'off' fibres which propagate away from the eye. Invasion of the eye via one branch of optic nerve can evoke an answering burst in another branch. 3. Such electrically evoked bursts are similar to light-evoked 'off' bursts with respect to their impulse composition, their ability to be inhibited by illumination of the eye, and their susceptibility to MgCl2 anaesthesia. 4. Invasion of the eye by a train of repetitive electrically evoked impulses in the absence of photic stimulation can give rise to repetitive 'off' bursts as well as concomitant oscillatory potentials in the eye which are similar to those normally evoked by cessation of a photic stimulus. 5. The electrically evoked 'off' bursts appear to be caused by an excitatory rebound following the cessation of inhibitory synaptic input from photoreceptors which can be antidromically activated by electrical stimulation of the optic nerve. 6. The experimental results suggest that the rhythmic discharge of the 'off' fibres evoked by the cessation of a photic stimulus is mediated by the abrupt decrease of inhibitory synaptic input from the receptors.

Action Potentials↗
PubMed1979

[Hypoplasia of the optic nerve head].

Optic nerve hypoplasia is not a rare eventuality in children. This report discusses the clinical features of 10 new cases on a multiple point of view including optic canal tomography, fluorescein angiography and cat's examination. Optic nerve hypoplasia is not always accompanied by decreased visual acuity: sector fields are often identified in these cases.

Adult↗
PubMed1979

Elimination of cobalt from the frog brain introduced into the optic centres through the optic nerve.

One optic nerve in several frogs was filled with cobaltous-lysine complex, and the animals were left to survive from 1 day to 52 days. Degenerated cobalt-filled retinal fibres were phagocytosed by ependymo-glial, and microglial cells. The cobalt appeared in the ependymo-glial cells in the 4th postoperative day, and its amount was greatly reduced by the 52nd day. Within 12 days the labelled axons were replaced by cobalt-loaded microglial cells in the termination sites of optic fibres. By the end of the experimental period, the number of labelled cells increased in the periventricular layers, and decreased in places where retinal fibres had terminated. These processes were accompanied by the appearance of cobalt in the choroid plexus. It is supposed that glial cells dischargd the cobalt into brain ventricles, and the metal left the nervous tissue via the cerebrospinal fluid.

Animals↗
PubMed1979

Electron microscopic demonstration of centrifugal nerve fibers in the human optic nerve.

Electron microscopic views of centrifugal nerve fibers in the optic nerve stump of a 56-year-old man are presented. These nerve fibers had survived for 16 days after removal of the corresponding eyeball and exhibited terminal swellings pointing in a distal direction and indicating axoplasmic flow towards the removed eye. The centrifugal nerves in this adult lack any evidence of attempted regeneration that has earlier been observed under similar conditions in the optic nerve stump of a child.

Humans↗
PubMed1979

Vasculature of the optic nerve in anencephaly.

The optic nerves and globes obtained from 6 anencephalics were studied histologically and compared to normal specimens obtained from 4 stillborn infants as well as 1 case of septo-optic dysplasia. Special emphasis was placed on examination of the optic nerve, and it was found that an average of 48 vessels per high-power field were seen posterior to the lamina cribrosa in anencephalics. In contrast, control globes had an average of 12 vessels per high-power field. This suggested that an increase in the vasculature of the hypoplastic optic nerve is a characteristic feature of anencephalics.

Anencephaly↗
PubMedDate not supplied

Growth and myelination of goldfish optic nerve fibers after retina regeneration and nerve crush.

Axonal regeneration in the optic nerve and tectum of the goldfish was studied both after retina regeneration and nerve crush. The retina regeneration was evoked by ouabain-induced damage of at least the ganglion cells and cells of the inner nuclear layer. The necrotic retinal neurons are substituted by mitotic processes in the outer nuclear layer and the marginal growth zone at the ora serrata. The axons of these newly developed retina ganglion cells grow through the degenerating, but mechanically undamaged, optic nerve into the tectum, establishing there synaptic contacts already 16 days after the intraocular ouabain-injection. The fibers were myelinated at first in the tectum, later on in the optic nerve. Thus, the myelination process proceeds in retrograde direction. About 60--80 days after injection the myelination has become nearly normalized. On the contra-lateral side of the same animal, the optic nerve was crushed near the eye-bulb. The axons of the original retina ganglion cells grow out into the degenerating optic nerve and tectum. They also find synaptic contacts and are myelinated in retrograde direction, but to a much lesser extent than the axons of the regenerated retina ganglion cells. An axonal factor is discussed, which would influence the oligodendroglial myelination activity. The effectiveness of this factor is probably dependent on the neuronal age and suggested to be triggered by the establishment of synaptic contacts.

Animals↗
PubMed1978

Maternal anticonvulsants and optic nerve hypoplasia.

Seven patients with optic nerve hypoplasia, born of epileptic mothers, are presented. All the mothers took anticonvulsants during pregnancy. The possibility that maternal anticonvulsant therapy may play a role in the genesis of optic nerve hypoplasia is discussed in the light of what is known about the teratogenicity of these agents.

Abnormalities, Drug-Induced↗
PubMed1976

A light microscopic, autoradiographic study of axoplasmic transport in the normal rhesus optic nerve head.

A systematic study of axoplasmic transport in the normal optic nerve head is essential to the understanding of the role of this process in the pathogenesis of disease of the optic nerve. Twenty-one eyes from normal adult rhesus monkeys were subjected to intravitreal injections of tritiated leucine (3H) or proline (3H). Light microscopic autoradiographs were prepared on these eyes and optic nerves six hours to 60 days after injection. The isotope that was incorporated in cytoplasmic components associated with the slow phase of axoplasmic transport (3H leucine) became concentrated in the temporal region of the optic nerve head, unevenly distributed within axons in the axonal bundles, and apparently accumulated in axons or glial cells, or both, in the lamina choroidalis and scleralis as a broad pulse of isotope moved across the optic nerve head. Several anatomic factors, including the distribution of macular fibers, increasing amounts of glial cells within the same axonal bundles as the optic nerve passed from the lamina retinalis to the lamina scleralis, and the abrupt addition of myelin sheaths to axons behind the lamina scleralis, contributed to the complex distribution of isotope in the normal optic nerve head. Glial cell labeling was especially prominent with 3H proline.

Animals↗
PubMed1978

A combined lateral and medial orbitotomy for exposure of the optic nerve and orbital apex.

A technique for exposure and direct visualization of the optic nerve and medial apex of the orbit is presented. The technique involves an initial lateral orbitotomy or Krönlein procedure followed by a nasal conjunctival peritomy, detachment of the medial rectus muscle, and outward rotation of the globe to expose the optic nerve and apex of the orbit. With relaxing incisions in the conjunctiva, the globe can be rotated approximately 45 degrees with visualization of the optic nerve from its exit from the globe to its disappearance into the origin of the rectus muscles. This technique may be used for exposure of the optic nerve and orbital apex for the optic nerve decompression for chronic papilledema in indicated cases, biopsy of lesions of the orbital apex, or excisional biopsies of tumors of the optic nerve.

Cranial Nerve Neoplasms↗
PubMed1977

Aplasia of the optic nerve and disk.

To clarify the nature of aplasia of the optic nerve and disk, a rare congenital anomaly defined as absence of the optic nerve and disk, retinal ganglion cells, and retinal blood vessels, we evaluated all the cases with this designation in the files. Thirteen cases demonstrated that optic nerve aplasia typically occurs uniocularly in an otherwise healthy person. There was no sexual or racial predilection, or any evidence of an inherited factor. We believe typical aplasia of the optic nerve results from abnormal invagination of the ventral fissure and that the multiple associated ocular anomalies may also be attributed in part to this same mechanism. Two cases were atypical: they were bilateral, there was an associated hydrocephalus in one case and a possible familial history in the other, they apparently had a different pathogenesis from the typical cases, and possibly represent an extreme form of hypoplasia of the optic nerve.

Adolescent↗
PubMed1975

Slow axonal protein transport and visual function following retinal and optic nerve ischemia.

Retinal ganglion cell protein synthesis and slow axonal protein flow have been measured in eight optic nerves from four macacus rhesus monkeys after producing ganglion cell ischemia. Comparison of the slow axonal protein flowing into the two optic nerves of the same control animal reveals a variability of up to 27 per cent. Following central retinal artery ligation, infarction of the retinal ganglion cells was reflected by a 97 per cent reduction in the radioactively labeled protein within the optic nerve. This profound reduction in labeled protein within the nerve confirmed that only ganglion cell dependent intra-axonal protein flow was being measured. Ischemia to the ganglion cell axons, with preservation of blood flow to the cell soma, was obtained in two optic nerves from different animals by severing all the posterior ciliary vessels entering about the optic nerve. Six weeks later, only a modest histologic loss of axons was present in these optic nerves. However, a profound reduction (up to 97 per cent) in labeled optic nerve protein was found at four days following intravitreal leucine injection. This is the time when the optic nerve slow axonal protein flow is dominated by the foveomacular ganglion cells. The reduction in slow axonal protein flow corresponds histologically to a preferential retrograde degeneration of the foveomacular ganglion cells, suggesting increased sensitivity of the smaller foveal axons to the induced ischemia. Electrophysiologic measurements support this conduction.

Animals↗
PubMed1977

Descending optic nerve degeneration in primates.

We cut the optic nerve at the orbital apex in squirrel monkeys to study the descending degeneration of optic nerve axons and their ganglion cell bodies. We could not detect progressive disintegration of the axon from the site of injury back to the cell body. Instead, the entire length of individual axons seemed to degenerate simultaneously as early as 3 weeks and as late as 6 weeks after injury, as judged both by ultrastructural integrity and by continued slow axonal transport, a reflection of local physiologic function. We could not relate the time of degeneration to the distance of the injury from the cell body. Evidently there is a signal of injury to the cell body after axotomy, though the nature of the signal and the mechanism by which it leads to cell death are unknown.

Animals↗
PubMed1976

Transfer RNA may be axonally transported during regeneration of goldfish optic nerves.

If [3H]uridine is injected into the eyes of goldfish during optic nerve regeneration, then the return of fibers to the optic tectum is accompanied by the appearance of [3H]RNA in the tectum. The amount of [3H]RNA arriving in the tectum is consistently greater than in non-regenerating controls and reaches maximum levels (more than 10 times controls) 24 days after optic nerve crush. When [14C]uridine is injected subarachnoidally 1 day prior to sacrificing, the amount of [14C]RNA in the tectum is approximately doubled throughout the regeneration period. In order to characterize the radioactive tectal RNA in these experiments, we have crushed the optic nerves of 15 fish, and 18 days later injected [3H]uridine into both eyes. Five days later [14C]uridine was injected subarachnoidally and all fish were sacrificed a day later. RNA was extracted and fractionated in 2.0% polyacrylamide gels. The amounts of 3H- and 14C-labeled ribosomal as well as small molecular weight RNAs were increased during regeneration. Analysis of the area under the 28S, 18S and 4-7S RNA peaks indicated a small increase in 14C radioactivity in each peak (1.2, 1.5, and 1.5 times control, respectively). On the other hand, 3H radioactivity showed the greatest increase in the 4-7S fraction (8.0 times control) whereas large molecular weight ribosomal fractions were approximately 3 times control. Electrophoresis of the RNA on 10% polyacrylamide gels demonstrated that all of the small molecular weight RNA was confined to the 4S (tRNA) peak. These results suggest that when optic nerves of goldfish regenerate, they may enter the tectum carrying 4S (transfer) RNA.

Animals↗
PubMed1977

Autoregulation of the blood supply to the anterior optic nerve and lamina cribrosa.

In the optic nerve an axial arterial system of peripheral origin is present; several intraneural collaterals of the central retinal artery are absent in the majority of cases while a rich pial network always exists. The question whether the central retinal artery should be considered as an important axial nutritional artery for the anterior optic nerve has to be answered in the negative. One or two large centrifugal collaterals running to the pial sheath-network probably play an autoregulatory role, protecting the laminar region from a temporary lack of blood supply during moderate rises in intraocular pressure.

Collateral Circulation↗
PubMed1977

Age changes of the human optic nerve head. A neurohistologic study.

Eleven human optic nerves from subjects in different decades ranging from the fifth to the ninth were investigated with the silver carbonate method to establish the pattern and frequency of age changes within the optic nerve head and their relationship with the glaucomatous excavation. It has been found that despite the occurrence of age degeneration at the same level of the cribriform lamina, there are definite anatomical differences as compared with glaucoma changes, especially regarding the distribution of axonal damage.

Age Factors↗