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PubMed2004

Regional optic nerve damage in experimental mouse glaucoma.

PURPOSE: To assess the relationship between regional variation of axon loss and optic nerve head anatomy in laser-induced experimental glaucoma in the mouse. METHODS: Experimental glaucoma was induced unilaterally in eight NIH Swiss black mice. Intraocular pressure (IOP) was measured for 12 weeks, and the mice were killed. The eyes were enucleated, and both optic nerves were dissected and processed conventionally for electron microscopy. Low- and high-magnification images of the optic nerve cross sections 300 microm posterior to the globe were collected systematically and masked before analysis. For each nerve, cross-sectional area was measured in low-magnification micrographs. Axon number and density were determined in the high-magnification micrographs. Loss of axonal density was compared between the superior and inferior and nasal and temporal areas of the optic nerve cross section. Additional cross-section micrographs were collected at 10- or 20-microm intervals throughout the optic nerve head. RESULTS: In the treated (glaucoma) eyes, mean IOP was 44% higher than that in the control eyes. The optic nerve cross-sectional area, mean axonal density, and total axonal number were significantly less than those in the control eyes (P < 0.01 for each). Axon loss in the superior optic nerve was greater than in the inferior optic nerve in each glaucomatous eye (P = 0.012). The ratio of axonal density in the superior and inferior optic nerve (superior-to-inferior [S/I] ratio) in all treated eyes was <1.0 and significantly lower than that in the control eyes (P = 0.012). The central retinal vessels occupied approximately 20% of the central optic nerve head cross-sectional area, gradually shifted position ventrally as they progressed toward the scleral foramen (the mouse does not have a lamina cribrosa), and exited the inferior retrobulbar optic nerve adjacent to the posterior of the globe. CONCLUSIONS: Ocular hypertension in the mouse eye sufficient to cause optic nerve damage induces preferential loss of superior optic nerve axons. Optic nerve axon loss appeared less among the axons that were near the major optic nerve blood vessels at the scleral foramen. Topographic differences in optic nerve axon loss should be considered when evaluating optic nerve damage in experimental laser-induced glaucoma in the mouse.

Animals↗
PubMed1994

Optic nerve invasion of retinoblastoma. Metastatic potential and clinical risk factors.

BACKGROUND: Optic nerve invasion is one of the predictors for retinoblastoma metastases. This study was designed to investigate the risk of optic nerve invasion and clinical features that may identify those children with optic nerve invasion. METHODS: We reviewed the charts of 289 children with retinoblastoma treated initially with enucleation. Logistic regression analysis was performed to assess the risk for metastases from varying degrees of optic nerve invasion and to assess the clinical and histopathologic predictors of optic nerve invasion. RESULTS: There were 84 eyes (29%) with optic nerve invasion. The invasion was prelamina cribrosa in 44 cases (15%), up to but not posterior to the lamina cribrosa in 21 cases (7%), posterior to the lamina cribrosa but not to the cut end of the optic nerve in 17 cases (6%), and to the site of optic nerve transection in 2 cases (1%). Patients with optic nerve invasion were more likely to develop metastasis (P = 0.0016), particularly those with invasion to the postlaminar and cut section of the optic nerve (P = 0.0001). Development of metastasis was not statistically associated with laminar or prelaminar involvement. If those patients with choroidal invasion simultaneous with optic nerve invasion were excluded from evaluation, the presence of optic nerve invasion alone was not significant for development of metastasis. The clinical factors found to be predictive for optic nerve invasion from a univariate analysis included exophytic growth pattern (P = 0.011), elevated intraocular pressure (> 22 mm Hg) (P = 0.02), and tumor thickness greater than or equal to 15 mm (P = 0.03). The histopathologic factor significantly associated with optic nerve invasion (univariate analysis) was simultaneous choroidal invasion (P = 0.001). A trend toward an association with optic nerve invasion was found with vitreous hemorrhage (P = 0.06), iris neovascularization (P = 0.10), and poorly differentiated retinoblastoma (P = 0.07). A multivariate analysis showed the most significant clinical factors to be exophytic growth pattern (P = 0.002), tumor thickness greater than or equal to 15 mm (P = 0.01), and vitreous hemorrhage (P = 0.05). CONCLUSIONS: Optic nerve invasion of retinoblastoma beyond the lamina cribrosa is associated with a greater metastatic risk. Large exophytic retinoblastoma with secondary glaucoma is at highest risk for optic nerve invasion.

Child, Preschool↗
PubMed2006

Taurine trophic modulation of goldfish retinal outgrowth and its interaction with the optic tectum.

Goldfish retinal explant outgrowth in the presence of fetal calf serum is stimulated by taurine. In the absence of it, but with glucose in the medium, length of neurites is still elevated by the amino acid. Using the medium in the presence of glucose, but in the absence of fetal calf serum, we explored the effect of optic tectum medium from cultures of them coming from goldfish without crush of the optic nerve or 3, 5, 10, 14 and 20 days after crush. Retinal explants, intact or from goldfish with crush of the optic nerve 10 days prior to starting the culture, were employed in order to measure the possible effect of optic tectum media and the inter action with taurine. In other type of experiments the optic nerve was crushed 1, 2, 4, 7 and 10 days before dissection of the optic tectum, and then co-cultured with intact or 10 days post-crush retinal explants. Optic tectum media produced a time-dependent effect on outgrowth in lesioned retinas with a maximum effect around 5 days after the lesion for the corresponding optic tectum. Taurine, 4 mM, did not further affect the outgrowth in the presence of optic tectum media, but did significantly increase length of neurites either in intact or in post-lesion retinas. Co-culture of optic tectum at different days post-lesion and retinas at 10 days post-lesion increased the outgrowth around 4 days post-lesion, in a preparation resulting in mutual effects of both types of tissues. The addition of taurine in these conditions did not further increase outgrowth, rather inhibited it according to the time after lesion of optic nerve corresponding to the co-cultured optic tectum. The effect of taurine was concentration-dependent, since 0.2 mM was more effective than 2 or 4 mM in the presence of optic tectum with lesion of 2 days. These results demonstrate the time-course of the regeneration processes in the visual system of goldfish, indicating the crucial periods after crush in which the tectum could produce stimulation and later decrease or no effect on outgrowth from the retina. In addition, they are evidences of the interaction between taurine and optic tectum production of time-produced specific agents. The mechanisms underlying these effects are closely related to calcium, as it was demonstrated by the addition of extracellular or intracellular chelators to the medium, which inhibited the effects of the optic tectum and the trophic properties of taurine in this system. The inhibitor of taurine transport, guanidoethylsulfonate, also decreased the stimulatory effects of the optic tectum and of taurine, indicating an interaction of substances produced by the tectum with taurine, and an effect of taurine mediated through its entrance to the cells. Overall, retinal explants outgrowth in the absence of fetal calf serum, the interaction of agents of the optic tectum and taurine modulates outgrowth from the retina, and these effects are mediated by calcium levels and by the levels of intracellular taurine.

Animals↗
PubMed1988

Axon diameter distributions across the monkey's optic nerve.

The distribution of axons according to diameter has been examined in the optic nerve of old world monkeys. Axon diameters were measured from electron micrographs, and histograms were constructed at regular intervals across a section through the optic nerve to reveal the local axon diameter distribution. The total axon diameter distribution was also estimated. Fine-calibre optic axons (less than 2.0 micron in diameter) are found at all locations across the optic nerve. They are most frequent centrotemporally, where very few coarse optic axons can be found, but also make up the majority at the optic nerve's periphery. Coarse optic axons (greater than 2.0 microns in diameter) are increasingly common at progressively peripheral positions in the nerve. Around the nerve's circumference, these coarse optic axons are least numerous temporally, and most common dorsonasally. The axon diameter distribution peaks around 1.25 microns at most locations across the optic nerve, but there are more, slightly larger (1.5-2.0 microns), optic axons dorsally than ventrally. The estimated total axon diameter distribution is unimodal, peaking at 1.0-1.25 microns, with an extended tail towards larger diameters. This centroperipheral gradient of increasing axon diameters across the optic nerve is not substantial enough to account for the partial segregation of axons by size in the monkey's optic tract: there, coarse optic axons form a conspicuously greater proportion of the local axon diameter distribution along the tract's superficial (sub-pial) border, and fine optic axons are the only axons present near the tract's deep border. Hence, the fibre distribution in the optic tract cannot be formed by a simple combination of the fibre distributions of the two respective half-nerves, as described in the classic neuro-ophthalmologic literature. Rather, the present results, in conjunction with previous results from the optic tract, demonstrate that there must be a reorganization of axons by size in or near the optic chiasm.

Animals↗
PubMed1997

Wilbrand's knee of the primate optic chiasm is an artefact of monocular enucleation.

PURPOSE: The anterior chiasmal syndrome consists of a temporal hemianopia or complete visual field loss in one eye, plus a superior temporal hemianopia in the other eye. The superior temporal hemianopia in the other eye is thought to result from injury to Wilbrand's Knee of the optic chiasm. Wilbrand's Knee is a loop of decussating fibers which detours into the contralateral optic nerve before entering the optic tract. I studied the organization of fibers in the optic chiasm of monkeys and humans to verify the existence of Wilbrand's Knee and to elucidate further the pattern of visual field loss seen from lesions of the sellar region. METHODS: The primary optic pathway was labelled in monkeys by injection of [3H] proline into one eye, followed by autoradiography. There were 8 intact Rhesus monkeys and 3 intact squirrel monkeys. In addition, the optic pathway was studied in the Rhesus monkey 6 months and 4 years after monocular enucleation. The optic chiasm was also examined using myelin stains in specimens obtained post-mortem from 3 patients. The patients had lost 1 eye 5 months, 2 years, and 28 years prior to their deaths. Finally, clinical observations were recorded in 3 patients with the anterior chiasmal syndrome. RESULTS: In normal Rhesus and squirrel monkeys, optic nerve fibers crossed the optic chiasm without entering the contralateral optic nerve. After short-term monocular enucleation, fibers from the normal optic nerve were drawn closer to the entry zone of the degenerating optic nerve, but Wilbrand's Knee was still absent. After long-term enucleation, a typical Wilbrand's Knee was induced to form. In the human, Wilbrand's Knee was absent 5 months after monocular enucleation, but emerged in the two cases involving long-term enucleation, in a fashion analogous to the monkey. The case reports describe 3 patients with variants of the anterior chiasmal syndrome from parasellar tumors. CONCLUSIONS: Wilbrand's Knee does not exist in the normal primate optic chiasm. It forms gradually over a period of years following monocular enucleation, presumably from shrinkage of the optic chiasm caused by atrophy of fibers from the enucleated eye. Therefore, the superior temporal hemianopia in the "other eye" seen in the anterior chiasmal syndrome cannot be due to compression of Wilbrand's Knee. I propose that it occurs from combined compression of the optic chiasm and one (or both) optic nerves.

Aged↗
PubMed2004

Tenascin-R as a repellent guidance molecule for newly growing and regenerating optic axons in adult zebrafish.

In adult fish, in contrast to mammals, new optic axons are continuously added to the optic projection, and optic axons regrow after injury. Thus, pathfinding of optic axons during development, adult growth, and adult regeneration may rely on the same guidance cues. We have shown that tenascin-R, a component of the extracellular matrix, borders the optic pathway in developing zebrafish and acts as a repellent guidance molecule for optic axons. Here we analyze tenascin-R expression patterns along the unlesioned and lesioned optic pathway of adult zebrafish and test the influence of tenascin-R on growing optic axons of adult fish in vitro. Within intraretinal fascicles of optic axons and in the optic nerve, newly added optic axons grow in a tenascin-R immunonegative pathway, which is bordered by tenascin-R immunoreactivity. In the brain, tenascin-R expression domains in the ventral diencephalon, in non-retinorecipient pretectal nuclei and in some tectal layers closely border the optic pathway in unlesioned animals and during axon regrowth. We mimicked these boundary situations with a sharp substrate border of tenascin-R in vitro. Optic axons emanating from adult retinal explants were repelled by tenascin-R substrate borders. This is consistent with a function of tenascin-R as a repellent guidance molecule in boundaries for adult optic axons. Thus, tenascin-R may guide newly added and regenerating optic axons by a contact-repellent mechanism in the optic pathway of adult fish.

Animals↗
PubMed2001

Interobserver variability of optic disk variables measured by confocal scanning laser tomography.

PURPOSE: To assess the interobserver variation of confocal laser scanning tomographic measurements of the optic nerve head and to address the question of whether the addition of clinical optic disk photographs is helpful in outlining the optic disk margin and in reducing the observer-related variation of the measurements. PATIENTS AND METHODS: Optic disk variables for 16 eyes of 16 patients with glaucoma, generated by confocal laser scanning laser tomography (Heidelberg Retina Tomograph), were independently evaluated by four experienced glaucoma specialists, and the interobserver variability was calculated. A second separate review by the same observers included the use of clinical stereoscopic color optic nerve head photographs to aid definition of the optic disk margin. RESULTS: Optic disk parameters with the smallest interobserver variation were cup shape measure, maximum cup depth, height variation contour, and mean height contour. The intraobserver variation of these parameters did not increase when clinical optic disk slides were additionally available. Parameters with the highest interobserver variation were volume below surface, volume below reference, volume above surface, and volume above reference. The observer variation of these optic disk parameters increased significantly for two of the four examiners when clinical optic disk slides were additionally available for outlining the optic disk margin. CONCLUSION: Confocal laser scanning tomography of the optic nerve head can be improved significantly if clinical optic disk photographs are additionally available to help in outlining the optic disk margin. Because interobserver variation in the tomographic optic disk measurements can be significant, even if experienced observer are involved, tomographic optic disk measurements may be centralized in reading centers in the case of multicenter studies.

Diagnostic Techniques, Ophthalmological↗
PubMed1982

Retinotopic and temporal organization of the optic nerve and tracts in the adult goldfish.

In order to investigate the role of the different factors controlling the pathways and termination sites of growing axons, selected optic fibers were traced from the eye to the tectum in adult goldfish either by filling them with HRP, or by severing a group of fibers and tracing their degeneration in 2 micrometers plastic sections stained with toluidine blue. Some fish received more than one lesion and others received both lesions and HRP applications. Two major rearrangements of the optic fibers were identified, one at the exit from the eye, the other within the optic tracts. Near the eye the optic fibers appear to be guided by the conformation of the underlying tissue planes that they encounter. The most recently added fibers, from the peripheral retina, grow over the vitread surface of the older fibers toward the blood vessel in the center of the optic nerve head. Behind the eye the fibers follow this blood vessel until it leaves the side of the optic nerve, and the fibers from peripheral retina are left as a single group on the ventral edge of the optic nerve cross section. As a consequence of this pattern of fiber growth the fibers form an orderly temporal sequence in the optic nerve, with the oldest fibers from the central retina on one side of the nerve and the youngest from peripheral retina on the other. In addition, the fibers are ordered topographically at right angles to this central-to-peripheral axis, with fibers from ventral retina on each edge of the nerve, dorsal fibers in the center, and nasal and temporal fibers in between. This arrangement of the optic fibers continues with only a little loss of precision up to the optic tracts. A more radical fiber rearrangement, seemingly incompatible with the fibers simply following tissue planes occurs within the optic tracts. Each newly arriving set of fibers grows over the surface of the optic tracts so that the older fibers come to lie deepest in the tracts. This segregation of fibers of different ages ensures that the rearrangement is limited to each layer of fibers. The abrupt reorganization of the fibers occurs as the tracts split around the nucleus rotundus to form the brachia of the optic tracts. The fibers are then arranged with temporal fibers nearest the nucleus rotundus and nasal fibers on the opposite edges of the brachia. From this point the fibers grow out over the tectal surface to their termination sites with only minimal rearrangements. Therefore the optic fiber rearrangements show evidence of several different sorts of constraints acting on the fibers at separate points in the optic pathway, each contributing to the final orderly arrangement of the fibers on the optic tectum.

Animals↗
PubMed1985

Topography of the goldfish optic tracts: implications for the chronological clustering model.

Both the dorsal and ventral optic tracts of goldfish have similar shapes when they are sectioned perpendicularly to their longitudinal axes. Each tract is pear-shaped, consisting of a narrow and a deep apex, a wide midspan, and a progressively curved and tapered superficial base. The tracts differ in that the apex of the dorsal optic tract points caudally, while the apex of the ventral optic tract points medially. In addition, upon segregating from the main optic tract, the dorsal optic tract courses dorsally while the ventral optic tract courses caudally. Thus, the two optic tracts have similar shapes and are orthongonal to one another. The topography of the retinal fibers within the optic tracts was determined either by ablating part of the retina and subsequently filling the axons from the intact hemiretina with cobaltous-lysine or by applying cobaltous-lysine to a slit in the retina. Both optic tracts contain a similar arrangement of optic fibers. Axons of central retinal ganglion cells (RGCs) are in the apex of each tract and optic fibers of peripheral RGCs are located along the base of each tract. Axons of temporal RGCs are located dorsally in the ventral optic tract and laterally in the dorsal optic tract, while axons of nasal RGCs are located ventrally in the ventral optic tract and medially in the dorsal optic tract. These findings indicate that the optic axons are organized as laminae. Deeper laminae contain the axons of older annuli of RGCs and superficial laminae contain the axons of younger annuli of RGCs. This type of chronological organization appears to be consistent across vertebrates.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Retinotopic organization of central optic projections in Rana pipiens.

The retinotopic organization of the anuran visual system has been investigated with the method of selective anterograde transport of horseradish peroxidase (HRP) following retinal lesions. The course of optic axons to specific structures was also confirmed by retrograde transport in the optic tract following HRP injections in the tectum and pretectum. As the optic nerve reaches the optic chiasm, the fibers from each of the four retinal quadrants appear as bands with the nasal (n) quadrant entering the chiasmal anterior pole, followed by ventral (v), temporal (t), and dorsal (d) quadrants. The preoptic nucleus is the first structure to be innervated, followed by the suprachiasmatic nucleus; both are innervated directly from fibers in the dorsal part of the optic nerve, which contains fibers from all the retinal quadrants. Each quadrant expands across the dorsoventral extent of the chiasm at the point where it enters. At this level the quadrants are arrayed along the rostrocaudal axis (as they are later in the marginal optic tract) in the sequence n-v-t-d. Optic fibers then spread across the chiasm, the nasal quadrant splits, taking up positions in the rostral and caudal margins of the optic radiation. Following the split in the nasal representation, the optic tract is transformed into topographically arranged sheets in the marginal optic tract. In the other retinorecipient nuclei, the sheet of optic axons is transformed back into the shape of the retinal hemisphere. Topographic maps of this kind display one of two possible orientations: (1) in the tectum and the nucleus lentiformis mesencephali (nLM), the temporal retina is represented in the anterior portion of the nucleus, whereas the nasal quadrant is found in the posterior portion; (2) in the thalamus, the retinotopic map is organized as a mirror-image reversal of that seen in the tectum and nLM (i.e., the nasal pole is anterior, whereas the temporal pole is in the posterior portion of the nucleus). Structures with this type of retinal map include the rostral visual nucleus, the corpus geniculatum, the nucleus of Bellonci, and the posterior thalamic nucleus. A third type of innervation occurs in the nucleus of the basal optic root (nBOR), which is the only mesencephalic visual nucleus not innervated by the marginal optic tract. The basal optic root is formed by the fibers exiting most caudally from the optic chiasm. All the retinal quadrants contribute to the basal optic root, but no evidence of retinotopy was found in nBOR.4+ target nuclei.

Animals↗
PubMed1992

Sodium channel expression in optic nerve astrocytes chronically deprived of axonal contact.

Immunocytochemical and electrophysiological methods were used to examine the effect of retinal ablation on the expression of sodium channels within optic nerve astrocytes in situ and in vitro. Enucleation was performed at postnatal day 3 (P3), and electron microscopy of the enucleated optic nerves at P28-P40 revealed complete degeneration of retinal ganglion axons, resulting in optic nerves composed predominantly of astrocytes. In contrast to control (non-enucleated) optic nerve astrocytes, which exhibited distinct sodium channel immunoreactivity following immunostaining with antibody 7493, the astrocytes in enucleated optic nerves did not display sodium channel immunoreactivity in situ. Cultures obtained from enucleated optic nerves consisted principally (greater than 90%) of glial fibrillary acidic protein (GFAP)+/A2B5- ("type-1") astrocytes, as determined by indirect immunofluorescence; GFAP+/A2B5+ ("type-2") astrocytes were not present, nor were GFAP-/A2B5+ (O-2A) progenitor cells. Sodium channel immunoreactivity was not present in GFAP+/A2B5- astrocytes obtained from enucleated optic nerves; in contrast, GFAP+/A2B5- astrocytes from control optic nerves exhibited 7493 immunostaining for the first 4-6 days in culture. Sodium current expression, studied using whole-cell patch-clamp recording, was attenuated in cultured astrocytes derived from enucleated optic nerves. Whereas 39 of 50 type-1 astrocytes cultured from intact optic nerves showed measurable sodium currents at 1-7 days in vitro, sodium currents were present in only 6 of 38 astrocytes cultured from enucleated optic nerves. Mean sodium current densities in astrocytes from the enucleated optic nerves (0.66 +/- 0.3 pA/pF) were significantly smaller than in astrocytes from control optic nerves (7.15 +/- 1.1 pA/pF). The h infinity-curves of sodium currents were similar in A2B5- astrocytes from enucleated and control rat optic nerves. These results suggest that there is neuronal modulation of sodium channel expression in type-1 optic nerve astrocytes, and that, following chronic loss of axonal association in vivo, sodium channel expression is down-regulated in this population of optic nerve astrocytes.

Animals↗
PubMed2004

Alterations in neurofilament light in optic nerve in rat kainate and monkey ocular hypertension models.

The purpose of this study is to evaluate the changes in neurofilament light (NF-L) protein in the optic nerve in rat kainate and monkey ocular hypertension models. In the rat model, optic nerve damage was induced by kainate injection into the vitreous body. In the monkey model, photocoagulation of the trabecular meshwork led to laser-induced ocular hypertension. NF-L in optic nerve extract was quantified by quantitative immunoblot using an imaging analyzer. The amount of NF-L in optic nerve was compared between normal and kainate-treated groups at 7 days after kainate injection. Specimens from rat optic nerves and retinas were evaluated histologically to examine the correlations between damage and amount of NF-L in the optic nerve. In monkeys, the amount of NF-L in the optic nerve was compared between control fellow and ocular hypertensive eyes. Injection of kainate induced morphological optic nerve and retinal damage in rats. The amount of NF-L in the optic nerve was significantly reduced in kainate-treated eyes (vs. normal eyes). The amount of NF-L correlated with the cell count in the ganglion cell layer and the axon number in the optic nerve at 7 days after kainate injection. Further, 6-cyano-7-nitro-quinoxaline-2,3-dione, a non N-methyl-D-aspartate receptor antagonist, suppressed the kainate-induced reduction in NF-L and retinal damage. In the monkey model, ocular hypertension and morphological optic nerve damage were shown by laser-treated eyes. The amount of NF-L in the optic nerve was reduced in laser-treated eyes. In conclusion, in rat kainate and monkey ocular hypertension models, immunoblot evaluation of NF-L shows the reduction of the amount of NF-L in the optic nerves of treated-eyes. The amount of NF-L correlated with the morphological retinal and optic nerve damage in rats. These findings indicate that immunoblot evaluation of NF-L in the optic nerve may provide a quantitative index of optic nerve damage.

6-Cyano-7-nitroquinoxaline-2,3-dione↗
PubMed1988

Laminar histochemical and cytochemical localization of cytochrome oxidase in the goldfish retina and optic tectum in response to deafferentation and during regeneration.

Cytochrome oxidase (C.O.) histochemistry and cytochemistry were used to examine the effects of optic denervation and subsequent optic fiber regeneration on oxidative metabolism in the retina and optic tectum of the goldfish. In the tectum, there was a dramatic and rapid decrease in C.O. activity within the optic layers 3-4 days after contralateral eye removal or optic nerve crush. At the E.M. level this was correlated with an initial decrease in mitochondrial reactivity within optic terminals followed by the subsequent degradation of mitochondria and phagocytosis of optic terminals. By 1 month after optic nerve crush, the entire tectum was reinnervated. However, the normal dark reactivity of the stratum fibrosum et griseum superficialis (SFGS), the main optic innervation layer, was not restored until after 3-4 months postcrush. The normal intense reactivity of the large-diameter optic axons and terminals at the bottom of the SFGS required an even longer period, about 7-8 months, for full recovery. The delayed restoration of C.O. reactivity was not due to a delay in synaptogenesis or in mitochondrial accumulation within optic terminals but to a delay in the maturation of mitochondrial reactivity. Following regeneration, the normal sublaminar stratification of C.O. bands was reestablished, suggesting that metabolically distinct classes of optic fibers may reinnervate at their original sublaminae. By using a distinct and persistent C.O. reactive sublamina, a of stratum griseum centrale (SGCa), just subjacent to the SFGS, it was possible to measure the thickness of the SFGS following optic denervation and subsequent reinnervation. At 1 week after optic nerve crush, the SFGS shrank by 35%. During regeneration, the thickness of the SFGS gradually increased to about 23% above normal at 2 months postcrush and this was maintained indefinitely. In the retina, ganglion cells were hypertrophic by 1 month postcrush and exhibited elevated levels of C.O. during the same period of time when optic terminals were unreactive. This indicates that oxidative metabolic activity within perikarya and axon terminals of the same neuron may be locally and independently regulated. It also suggests that in spite of the well-known elevation of axonal transport during the initial period of axon elongation and synaptogenesis, that oxidative metabolic energy production within the optic fibers is less than that of the mature projection.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1982

[On the CT-diagnosis of optic nerve lesions. Differential diagnostic criteria (author's transl)].

Computed tomograms of 166 optic nerve lesions were analyzed: 97 were mainly orbital and 69 mainly intracranial. The criteria were clinical course, size, density and delineation of the optic nerve shadow, orbital and cerebral soft tissue abnormalities, and bony changes in the optic canal. Characteristic CT features are described of individual disease entities such as optic gliomas, optic nerve sheath meningiomas, neoplastic and inflammatory infiltrations. The differential diagnostic importance of individual CT criteria is evaluated and discussed. Simultaneous visualization of orbital and intracranial soft tissue changes as well as bony changes in the optic canal allow the location and identification of the majority of optic nerve lesions based on the criteria mentioned above, and optic nerve tumors can be differentiated. In 9 patients with optic neuritis due to clinically proven encephalitis and in 17 patients with total optic atrophy, no changes in the size of the optic nerve could be found. CT evaluation of the intraorbital portion of the optic nerve requires special examination techniques. Oblique computer reformations through the optic canal provide excellent visualization of bony changes in the optic canal. The exclusion of intracranial causes of optic nerve lesions requires intravenous injection of contrast material.

Diagnosis, Differential↗
PubMed1995

The 1994 Von Sallman Lecture. The optic nerve head circulation in health and disease.

This is a brief overview of multifaceted anatomical, experimental and clinical studies conducted by the author since 1955 on the optic nerve head circulation in health and disease. Conclusions, based on the accumulated information provided by these studies, are summarized. The studies on the pattern of blood supply of the optic nerve head have shown that: (a) its main source of blood supply is the posterior ciliary artery circulation, with retinal circulation supplying only the surface nerve fiber layer, (b) there is marked interindividual variation in the blood supply pattern, and (c) the blood supply in the optic nerve head has a sectorial distribution. The various factors which produce interindividual variation in the blood supply of the optic nerve head are discussed, particularly those in the posterior ciliary artery circulation; this is because all available evidence indicates that it is derangement in the posterior ciliary circulation in the optic nerve head that is primarily responsible for the common ischemic disorders of the optic nerve head, e.g. anterior ischemic optic neuropathy and glaucomatous optic neuropathy. Factors that may derange the blood flow in the optic nerve head include defective autoregulation of blood flow in it, vascular changes in its feeding arteries, hematologic abnormalities, systemic arterial hypertension and hypotension, and intraocular pressure; their roles are discussed. For better understanding and management of optic nerve head ischemic disorders, there is an urgent need for an accurate clinical method of assessment of blood flow in the posterior ciliary circulation in optic nerve head, since no satisfactory method is currently available. Redness or pallor of the optic disk on ophthalmoscopy is not a true guide to the optic nerve head vascularity as it gives no information about the state of the posterior ciliary circulation. Fluorescein fundus angiography, though far superior to the optic disk color for evaluation of optic nerve head vascularity, has a number of limitations. All these topics and various controversies about them are discussed briefly.

Animals↗
PubMed2006

A family with X-linked optic atrophy linked to the OPA2 locus Xp11.4-Xp11.2.

Autosomal dominant optic atrophy (ADOA) is the most common inherited optic atrophy. Clinical features of ADOA include a slowly progressive bilateral loss of visual acuity, constriction of peripheral visual fields, central scotomas, and color vision abnormalities. Although ADOA is the most commonly inherited optic atrophy, autosomal recessive, X-linked, mitochondrial, and sporadic forms have also been reported. Four families with X-linked optic atrophy (XLOA) were previously described. One family was subsequently linked to Xp11.4-Xp11.2 (OPA2). This investigation studied one multi-generation family with an apparently X-linked form of optic atrophy and compared their clinical characteristics with those of the previously described families, and determined whether this family was linked to the same genetic locus. Fifteen individuals in a three-generation Idaho family underwent complete eye examination, color vision testing, automated perimetry, and fundus photography. Polymorphic markers were used to genotype each individual and to determine linkage. Visual acuities ranged from 20/30 to 20/100. All affected subjects had significant optic nerve pallor. Obligate female carriers were clinically unaffected. Preliminary linkage analysis (LOD score = 1.8) revealed that the disease gene localized to the OPA2 locus on Xp11.4-Xp11.2. Four forms of inherited optic neuropathy, ADOA, autosomal recessive optic atrophy (Costeff Syndrome), Leber hereditary optic neuropathy, and Charcot-Marie-Tooth disease with optic atrophy, are associated with mitochondrial dysfunction. Future identification of the XLOA gene will reveal whether this form of optic atrophy is also associated with a mitochondrial defect. Identification of the XLOA gene will advance our understanding of the inherited optic neuropathies and perhaps suggest treatments for these diseases. An improved understanding of inherited optic neuropathies may in turn advance our understanding of acquired optic nerve diseases, such as glaucoma and ischemic optic neuropathy.

Chromosomes, Human, X↗
PubMed2004

The distributions of mitochondria and sodium channels reflect the specific energy requirements and conduction properties of the human optic nerve head.

AIM: To study the normal distributions of mitochondria and voltage gated Na+ channels in the human optic nerve head in order to gain insight into the potential mechanisms of optic nerve dysfunction seen in the inherited optic neuropathies. METHODS: Five fresh frozen human optic nerves were studied. Longitudinally orientated, serial cryosections of optic nerve head were cut for mitochondrial enzyme histochemistry and immunolabelling for cytochrome c oxidase (COX) subunits and voltage gated Na+ channel subtypes (Na(v) 1.1, 1.2, 1.3, and 1.6). RESULTS: A high density of voltage gated Na+ channels (subtypes Na(v) 1.1, 1.3, and 1.6) in the unmyelinated, prelaminar, and laminar optic nerve was found. This distribution co-localised both with areas of high COX activity and strong immunolabelling for COX subunits I and IV. CONCLUSIONS: Increased numbers of mitochondria in the prelaminar optic nerve have previously been interpreted as indicating a mechanical hold up of axoplasmic flow at the lamina cribrosa. These results suggest that this increased mitochondrial density serves the higher energy requirements for electrical conduction in unmyelinated axons in the prelaminar and laminar optic nerve and is not a reflection of any mechanical restriction. This could explain why optic neuropathies typically occur in primary inherited mitochondrial diseases such as Leber's hereditary optic neuropathy, myoclonic epilepsy with ragged red fibres (MERRF), and Leigh's syndrome. Secondary mitochondrial dysfunction has also been reported in dominant optic atrophy, Friedreich's ataxia, tobacco alcohol amblyopia, Cuban epidemic optic neuropathy, and chloramphenicol optic neuropathy. These diseases are rare but these findings challenge the traditional theories of optic nerve structure and function and may suggest an alternative approach to the study of commoner optic neuropathies such as glaucoma.

Adult↗
PubMed2003

Optic neuritis: characteristics and visual outcome.

OBJECTIVE: To determine clinical characteristics of patients with optic neuritis and visual outcome after intravenous methylprednisolone treatment. METHOD: A total of 81 patients with optic neuritis were reviewed retrospectively with regard to their clinical characteristics by dividing into two groups as follows: group I had isolated optic neuritis and group II had optic neuritis with demyelinative disease. The visual outcome in these patients before and after intravenous methylprednisolone treatment was analyzed. RESULTS: Of 81 patients with optic neuritis, 63 patients (77.8%) had isolated optic neuritis and 18 (22.2%) patients were optic neuritis with demyelinative disease. The ages of the patients ranged from 16 to 59 years (mean = 35.3 years) in patients with isolated optic neuritis and from 16 to 73 years of age (mean = 35.8 years) in patients with optic neuritis with demyelinative disease. After treatment, 45 patients (52 eyes) with isolated optic neuritis and 14 patients (25 eyes) with optic neuritis with demyelinative disease who were followed-up for more than 10 days were studied. After treatment, 60 per cent of the isolated optic neuritis patients and 24 per cent of the optic neuritis patients with demyelinative disease had a visual acuity of 6/12 or better respectively. The isolated optic neuritis who had an onset interval to treatment of less than 8 days had a visual acuity better than 6/9 in 75 per cent. CONCLUSION: The final visual outcome in patients with isolated optic neuritis who received earlier treatment was better than those who received treatment later.

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