Idiopathic inflammation of optic nerve simulating optic nerve sheath meningioma: CT demonstration.
Explore the source record for details and available documents.
Cranial Nerve Neoplasms↗
SEARCH · Search PubMed
Results for “optic nerve”
Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
[Koyanagi's retrolaminar angiomatous cavern formation in the optic nerve ("angiomatous optic nerve malformation"). Review of the literature and suspected pathogenesis].
Explore the source record for details and available documents.
Child↗
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↗
Harris P. Mosher Award thesis. The recovery potential of the optic nerve.
Optic nerve dysfunction can be secondary to mass lesions, osseous compression states, inflammatory disorders, ischemia, increased cerebrospinal fluid pressure, and trauma. Representative clinical material from each of these areas is described, with an institutional review of 70 cases that were managed surgically. It is evident that compromise of optic nerve function can resolve with medical and surgical therapy. This clinical review is designed to highlight factors that favor this recovery. Although each condition has unique characteristics, an evaluation of clinical disorders that affect the nerve from globe to optic chiasm is presented as a comprehensive review of optic neuropathy. It is apparent from the literature that many questions need to be answered concerning the pathophysiology of optic nerve injury and the factors that influence recovery. A basic animal model for the analysis of these questions has been developed. An optic nerve injury produced in the cat leads to progressive loss of myelin but preservation of axons, the precise theoretic state that may be reversible with corticosteroid therapy or surgical management. Finally, the model may allow future study of the biochemical mediators of injury and the factors that promote recovery.
Animals↗
Idiopathic inflammation of optic nerve simulating optic nerve sheath meningioma.
Explore the source record for details and available documents.
Cranial Nerve Neoplasms↗
A histopathologic and morphometric differentiation of nerves in optic nerve hypoplasia and Leber hereditary optic neuropathy.
OBJECTIVES: To characterize and quantitate optic nerve histopathologic and morphometric differences between optic nerve hypoplasia (ONH) as an early and congenital form of intrinsic axonal loss and Leber hereditary optic neuropathy (LHON) as a late and acquired form of intrinsic axonal loss. MATERIALS AND METHODS: Optic nerves from 3 sources were examined: a 42-year-old healthy woman (control), a 53-year-old woman with ONH diagnosed postmortem, and a 74-year-old woman with LHON. The optic nerves were processed, embedded, and stained with a 1% solution of paraphenylene diamine. Histopathologic and morphometric analyses were performed via light microscopy and a semiautomatic computer image analysis system. RESULTS: The ONH showed severe axonal depletion without degenerated profiles in an inferonasal sector, with only a small superotemporal sector having a near normal appearance. The LHON revealed general axonal depletion centrally, fibrocytic scarring, scattered "degeneration dust," and evidence of minimal inflammation, with residual axons limited to superior and temporal peripheral clusters. Morphometric analysis revealed total fiber populations of 98,000 in the ONH optic nerve and 48,000 in the LHON optic nerve, representing 90% and 95% reductions, respectively, compared with the control optic nerve (1.2 million fibers). CONCLUSIONS: Optic nerve hypoplasia and LHON present 2 distinguishable and distinctive patterns of nerve fiber distribution and axonal dropout. The lack of degenerated axons in ONH indicates that any axonal death probably occurred through apoptosis during development. In LHON, degenerated axons and minimal grade of inflammation were obvious, implicating a more "active" pathologic process. This study describes distinctions between these 2 optic neuropathies.
Adult↗
The fine structure of the astroglia in the human optic nerve and optic nerve head.
Explore the source record for details and available documents.
Animals↗
The distribution of axons according to diameter in the optic nerve and optic tract of the rat.
The distribution of axons according to diameter was examined in the optic nerve and optic tract of adult hooded rats. Observations were made on semithin sections, and measurements of axonal diameters were made on electron micrographs taken from various locations across thin sections through the optic nerve and tract. The distribution of axons by size differs markedly in the optic nerve and tract. Coarse (greater than 2 microns) and fine (less than or equal to 2 microns) axons are distributed throughout all regions of the optic nerve. In the optic tract, in contrast, coarse axons are especially dense dorsally, at the deep border of the tract, while they are absent ventrally, subjacent to the pial surface. No regions of the optic nerve contain densities of coarse axons as high as the deep nor as low as the superficial extremes of the optic tract. Nevertheless, even at the deep (dorsal) border of the optic tract, the coarse axons make up only a small minority (roughly 15%) of the total number of axons in that region. The axons 2 microns or smaller may be divisible into two overlapping, fine and intermediate, diameter classes, that are partially segregated within the optic tract, but not in the optic nerve: the distributions of axon diameters smaller than 2 microns are skewed to distinctly smaller diameters at the dorsal and ventral extremes of the optic tract, while in between, at mid-positions along the deep-to-superficial axis of the optic tract, the axon size distributions contain many more axons greater than 1 micron in diameter. These different axon diameter groups may arise from the morphologically distinct retinal ganglion cell types, and may underlie the components of the trimodal compound axon potential seen in the rat's primary optic pathway. Their partial segregation within the tract anticipates the partial segregation of their terminal arborizations within the laminae of the dorsal lateral geniculate nucleus. The rearrangement of axons into a partial segregation by size within the optic tract may indicate a chronology of axonal arrival during early development, proximity to the pial surface being an index of recency of arrival. As axonal outgrowth and neurogenesis appear to be directly related within the retinal ganglion cell population in mammals, the relative birthdates of the retinal ganglion cell types giving rise to the axon diameter classes in the rat may be inferred from the present results.
Animals↗
Distribution of membrane phospholipids in the rabbit neural retina, optic nerve head and optic nerve.
Since diseases of the neural retina and optic nerve can result in alteration of biological membranes, this study determines similarities and differences in the membrane phospholipid content of the neural retina, optic nerve head, and optic nerve to serve as baseline data. Neural retina, optic nerve head, and optic nerve were dissected, isolated as 5 sets from 20 rabbits and frozen in liquid N2. Separate pooled-tissue extracts were prepared for each set of tissues and phosphorus-31 nuclear magnetic resonance (31P NMR) analyses performed. Ten phospholipids were quantified (respective neural retina, optic nerve head, and optic nerve mole % are given for the 5 major phospholipids detected): phosphatidylcholine (PC), 44.61, 27.67, 26.40; PC plasmalogen or alkylacyl PC (CPLIP); phosphatidylinositol (PI); sphingomyelin (SM); phosphatidylserine (PS), 12.63, 14.77, 15.09; phosphatidylethanolamine (PE), 21.21, 9.59, 8.69; PE plasmalogen (EPLAS), 11.07, 30.96, 33.93; an unidentified (unknown) phospholipid (U) at the chemical-shift value of 0.13 ppm; diphosphatidylglycerol (DPG); and phosphatidic acid (PA), 0.46, 2.92, 1.57. Significant differences between the various tissues were determined by the one-way analysis of variance, using a Scheffé range value of P < 0.05. The neural retina in all phospholipids detected except for the uncharacterized (unknown) phospholipid was significantly different from the optic nerve head tissue. The optic nerve head was significantly different from the optic nerve in PC, CPLIP, PE, EPLAS, U, DPG, and PA. The data provide a baseline for studies on pathologically changed neural retina, optic nerve head, and optic nerve.
Animals↗
Evulsion of the optic nerve.
Optic nerve evulsion is an uncommon traumatic event, which may result from various orbital or facial injuries. Two patients in whom clear media permitted prompt diagnosis are described. The possible mechanisms are not quite clear, but extreme rotation of the globe seems to play an important role.
Adult↗
Effect of different illumination conditions and ionic environment on the guanylate cyclase activity in retina, optic nerve and optic chiasm of the rat.
Guanylate cyclase is sensitive to changes of light and dark periods in incubated extracts obtained from soluble fractions of the retina, optic nerve and optic chiasm. The changes in guanylate cyclase activity found, about 100-fold between dark and light periods in those tissues, indicate a key role for this enzyme. The results showed that light inhibits strongly the retinal guanylate cyclase activity, while it increases the activity of this enzyme in the optic nerve. A generalized photo-inhibited response of guanylate cyclase was observed in all studied tissues in animals adapted to the dark. This suggests that light could act as a double stimulus gating the central circuit which promotes the hydrolysis of cGMP via cGMP phosphodiesterase-rhodopsin-transducin cascade, and by direct inhibition of the retinal guanylate cyclase activity. Finally, different responses have been observed in the guanylate cyclase activity in relation with the ion exposure depending on the studied tissue. In summary, all indicate an important role for the soluble guanylate cyclase activity in retina, and other tissues involved in the visual process such as optic nerve and optic chiasm, which have not been examined until now.
Adaptation, Physiological↗
The response of regenerating peripheral neurites to a grafted optic nerve.
Optic nerves, both viable (fresh or pre-degenerate) or non-viable (frozen-thawed) were grafted between the proximal and distal stumps of freshly transected sciatic nerves, using either 10/0 sutures or strips of nitrocellulose paper. The majority of regenerating peripheral neurites, always in association with Schwann cells, avoided the viable optic nerve grafts, growing along the outside of the grafts in well vascularized minifascicles until they gained the distal stumps. A very small number of axons entered the grafts and grew, for distances typically less than 2 mm, between layers of astrocyte processes. The number of axons entering was not increased by using predegenerate grafts or by blocking Schwann cell proliferation in the proximal stumps by pre-treating the latter with mitomycin C. There was no evidence of a continuous cellular-acellular partition between graft and host during the outgrowth phase of the neurites: it was concluded that axons failed to enter the grafts as a result of inhibitory interactions between Schwann cells and astrocytes. When grafts were rendered acellular, all structured debris, including recognizable components of the extracellular matrix, was rapidly removed and the space thus vacated was invaded by manifascicles of Schwann cells and regenerating neurites. Glial fibrillary acidic protein-positive astrocytes and carbonic anhydrase II-positive oligodendrocytes persisted within viable grafts for 17 months; they did not migrate into the surrounding nerve.
Animals↗
Pharmacological sensitivities of two afterhyperpolarizations in rat optic nerve.
Optic nerves were removed from 4-8-week-old rats and studied in a modified sucrose gap chamber in order to examine the pharmacological sensitivities of two afterhyperpolarizations (AHPs), an early and a late one. The peak latency of the early AHP, which occurred immediately after the action potential, was 6-12 ms, and its duration was 44-75 ms. The early AHP was present at resting potential in about 75% of recorded nerves. In the nerves in which an early AHP was not present at resting potential, an AHP was present during delivery of constant current depolarization through the sucrose gap. The early AHP was increased in amplitude by depolarization of the nerve, decreased in amplitude or reversed in polarity by hyperpolarization, was not affected by tetraethylammonium (TEA) or Co2+, and was obliterated by 4-aminopyridine (4-AP) concomitant with action potential broadening. The late AHP followed a broadened action potential in the presence of the potassium channel blocker 4-AP. Its peak latency ranged from 112 to 254 ms and its duration from 336 to 710 ms. It was increased in amplitude with repetitive stimulation, was reversibly obliterated by TEA, but was not significantly altered by Co2+, Cd2+, Ca2+ removal, charybdotoxin or apamin. The results demonstrate the presence of two AHPs mediated by pharmacologically distinct potassium conductances in rat optic nerve, neither of which is calcium-dependent.
4-Aminopyridine↗
Guanylate cyclase activity in retina optic nerve and optic chiasm of rats under different illumination conditions.
In the present work we have measured the guanylate cyclase activity in soluble fractions from several tissues relevant to the visual response under different illumination conditions. Guanylate cyclase was sensitive to changes of light/dark periods in incubated extract obtained from soluble fractions of retina, optic nerve and optic chiasm. The changes in soluble guanylate cyclase activity found, about 100 fold between dark and light periods in those tissues, indicate a key role for this enzyme. The results showed that light inhibit strongly the soluble retinal guanylate cyclase activity; while it increases the activity of this enzyme in the optic nerve. A generalized photoinhibited response of soluble guanylate cyclase was observed in all studied tissues in prolonged dark adapted animals. The effect of Na+ 1 and 10 mM, and free Ca++ 28 eta M and 2.8 microM on the guanylate cyclase activity was performed in the studied tissues. The enzymatic activity appeared to be inversely related in the retina and optic nerve with regard to the ion exposure, which may involve different ionic control mechanisms. All indicate an active role for the soluble guanylate cyclase in the phototransduction process not only in retina, also in other tissues relevant in the visual response.
Adaptation, Ocular↗
GABA immunopositive axons in the optic nerve and optic tract of macaque monkeys.
Using an antibody to gamma-aminobutyric acid (GABA), we examined the optic nerves and optic tracts from macaque monkeys at the light and electron microscopic levels to determine if there is a possible inhibitory projection from the retina to the brain. All of the monkeys (n = 5) had GABA immunopositive axons that were evenly distributed in their optic nerves. These immunopositive axons were slightly larger than the axons around them and comprised an average of 2.6% of the axons in the nerves. Thus, their estimated total was about 44,000 axons per nerve. In the optic tracts, the GABA immunopositive axons were not distributed evenly, but were concentrated mostly in the ventromedial part, indicating that this retinal pathway probably goes to a midbrain destination such as the superior colliculus. The present findings provide further evidence that there is a GABAergic retinal projection to the brain in primates with currently unknown physiological influences.
Animals↗
Visual system of the channel catfish (Ictalurus punctatus): III. Fiber order in the optic nerve and optic tract.
In channel catfish the ganglion cell axons leave the retina via a ring of approximately 13 separate optic papillae. Each papilla serves an area of retina extending from the central zone of the retina to the periphery. Papillae located at a dorsal position in the ring serve exclusively dorsal retina. Ventrally located papillae, however, have an exaggerated peripheral retinal representation, so that they serve mostly ventral retina but also some areas of peripheral retina dorsal to the nasal and temporal poles. The ganglion cell axon bundles departing from the retina via individual papillae were labelled with horseradish peroxidase, and sections of the optic pathway were examined to reveal the topographic organization of the fibers. The topographic order of the optic nerve was dissimilar to that of cichlids and goldfish. Fibers from individual papillae remained together throughout the optic nerve. Close to the optic nerve head, the papillae were arranged as a continuum around the U-shaped optic nerve, without the discontinuity in the representation of the ventral retina seen in other fish. Fibers associated with the dorsal papillae were located at the tip of the caudolateral arm of the U, and fibers from ventral papillae were on the rostromedial arm. Fibers from nasally and temporally located papillae were found on the base of the U. By the level of the optic chiasm the U shape had flattened out but retained the relative ordering of the papillae. Rotation of the nerve as it became the optic tract brought the representation of the ventral papillae to the dorsal pole of the tract, and the dorsal papillae to the ventral tract. It was only in the optic tract that rearrangement of fibers became apparent. As described above, the axons of some ganglion cells in dorsal, peripheral retina left the retina and travelled through the optic nerve with axons from extreme ventral retina. In the optic tract, these dorsal fibers joined the main body of fibers from the dorsal retina. The significance of these observations for theories of fiber rearrangement is discussed.
Animals↗
[Transcranial optic nerve decompression for optic nerve injury].
OBJECTIVE: To discuss the operative indications and advantages of transcranial optic nerve decompression in treatment of optic nerve injury resulted from skull base fracture. METHODS: The data, such as the site of impact, vision, ocular movement, characteristic of CT, and pathologic changes during operation, and the extent of operative decompression of 118 patients with optic nerve injury. According the site of impact on the head, 87 of lateral superciliary arch type, 18 of medial superciliary arch type, and 13 of zygomatic type, undergoing transcranial optic nerve decompression were analyzed retrospectively. The patients were followed up for 6 months after operation. For the purpose of evaluation, the postoperative outcome of visual acuity was classified into five grades: blindness, hand movement, finger count, light perception and visual acuity > 0.05. The visual acuity improvement reaching one grade or more was defined as effective. The improvement of visual field was also considered effective. RESULTS: After follow-up of 6 months, effect was shown in 35 out of the 72 patients with pre-operative blindness (48.6%), and all the 46 patients with residual vision (100%). The total effective rate was 68.6%. The post-operative effective rate was 64.4% in patients with lateral superciliary arch type, 83.3% in patients with medial superciliary arch type injury and 76.9% in patients with zygomatic type injury. CONCLUSIONS: Transcranial optic nerve decompression is worthy recommending to the patients with traumatic optic neuropathy. The operative indications include patients with residual vision; patients with bilateral optic nerve injury; and patients with blindness less than 3 days.
Adolescent↗
[MRI lesions of the optic nerves in optic neuritis].
Magnetic resonance imaging (MRI) was performed in 14 patients with optic neuritis. Three patients suffered from multiple sclerosis but the etiologies of the remaining 11 cases could not be identified. They were bilateral in 6, and unilateral in 8. The MR images were compared with the symptomatic lesions of optic neuritis and pattern reversal VECP. The STIR mode (short time inversion recovery), was employed for the MRI in the orbit and T2-weighted mode in the brain. In 11 eyes with hyperemia of the optic disc, 7 eyes showed a high signal in the optic nerve with the MRI, and 9 eyes showed an abnormal pattern VECP. Seven eyes with normal disc and two eyes with a pale disc showed a high signal in the optic nerve with MRI, those 9 eyes had abnormal pattern VECP. The high signal in the optic nerve was not related to visual acuity or visual field abnormalities of patients. However, the degree of the high signal of the optic nerve lesion in MRI was associated with the clinical course and prognosis of the optic neuritis. The degree of the high signal of the optic nerve lesion decreased with the recovery of visual acuity in optic neuritis.
Adolescent↗