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At least 73 records · Page 4Linked to original sources
PubMed2006

Optical integrator for optical dark-soliton detection and pulse shaping.

The design and analysis of an Nth-order optical integrator using the digital filter technique is presented. The optical integrator is synthesized using planar-waveguide technology. It is shown that a first-order optical integrator can be used as an optical dark-soliton detector by converting an optical dark-soliton pulse into an optical bell-shaped pulse for ease of detection. The optical integrators can generate an optical step function, staircase function, and paraboliclike functions from input optical Gaussian pulses. The optical integrators may be potentially used as basic building blocks of all-optical signal processing systems because the time integrals of signals may sometimes be required for further use or analysis. Furthermore, an optical integrator may be used for the shaping of optical pulses or in an optical feedback control system.

Journal Article↗
PubMed1998

Relationship of optic disc topography to optic nerve fiber number in glaucoma.

OBJECTIVE: To assess the relationship between in vivo measurements of optic disc topography and histomorphometric measurements of optic nerve fiber number in glaucoma. METHODS: Both eyes of 10 monkeys (Macaca fascicularis) with laser-induced glaucoma in the right eye were studied. Optic disc topography was measured in vivo with a confocal scanning laser ophthalmoscope. Histomorphometry was performed on optic nerve cross sections using bright-field microscopy with camera lucida. Nerve fiber density was estimated by unbiased random sampling. Nerve fiber number was estimated for each sector by multiplying nerve fiber density with neuroglial area. Nerve fiber count was compared with each of 13 global optic disc topographic parameters. RESULTS: For neuroretinal measurements in the glaucomatous eyes, rim area, retinal nerve fiber layer (RNFL) cross-sectional area, rim volume, and RNFL thickness correlated significantly with optic nerve fiber number. Differences in nerve fiber count between control and glaucomatous optic nerves showed the strongest correlation with differences in mean height contour; this was followed by RNFL cross-sectional area, RNFL thickness, rim volume, and differences in rim area. For cup measurements in the glaucomatous eyes, cup volume below reference, cup area, mean cup depth, the ratio of cup area to disc area, and cup shape correlated significantly with nerve fiber number. Differences in nerve fiber number between control and glaucomatous optic nerves showed the strongest correlation with differences in cup shape; this was followed by mean cup depth, cup volume below reference, the ratio of cup area to disc area, cup area, and differences in cup volume below surface. No association was found between optic nerve fiber number and optic disc area in glaucomatous eyes. CONCLUSIONS: In experimental glaucoma, most optic disc topography measures correlated significantly with optic nerve fiber number. The results of this histomorphometric study support the use of confocal scanning laser ophthalmoscopy to evaluate optic nerve damage in glaucoma.

Animals↗
PubMed1988

Optic synapse number but not density is constrained during regeneration onto surgically halved tectum in goldfish: HRP-EM evidence that optic fibers compete for fixed numbers of postsynaptic sites on the tectum.

The number of optic synapses in the half tectum of goldfish was counted by using an improved HRP-labeling protocol and a columnar sampling method that spanned the entire optic innervation layer, S-SO-SFGS. It was previously found by using this procedure in intact tectum that the normal number of optic synapses was regenerated by 30 days and maintained thereafter even in the absence of impulse activity. This suggested that the number of synapses in this system was intrinsically fixed. In order to examine whether this limit was imposed by optic fibers or by target cells, optic synapses were counted in surgically halved tecta which received compressed optic projections consisting of regenerating optic fibers from the entire retina. We reasoned that if synapse number is a function of the number of afferents, then there should be twice the normal number of optic synapses per column; on the other hand, if their number is fixed by target, then their number per column should be normal. We found that the number of optic (labeled) synapses was normal in sample columns from fish at 70 days and 160 days after optic nerve crush. Thus, retinal ganglion cells, on average, formed half as many synapses on the half tectum compared to intact tectum, indicating the number of optic synapses was limited by the tectum. The number of nonoptic (unlabeled) synapses was also found to be normal. By contrast, the S-SO-SFGS was found to be 88-103% thicker compared to normal fish, apparently because of a 20-fold increase in the number of optic fibers. As a result, the density of synapses was about half normal in half tecta, and so, in contrast to synapse number, synaptic density is not constrained during regeneration. We infer from these data that optic fibers compete for limited numbers of postsynaptic sites during regeneration and suggest that this competition promotes neural map refinement and the various plasticities described for this projection.

Animals↗
PubMed1975

An electron microscopic study on the blood-optic nerve and fluid-optic nerve barrier.

Utilizing horseradish peroxidase as a tracer, electron microscopic studies were done on the blood-optic nerve and fluid-optic nerve barrier to the peroxidase diffusion. Following intravenous injection the peroxidase was observed to fill the lumen of the capillaries of the laminar, prelaminar and orbital portions of the optic nerve but there was no penetratation of the capillary walls. The obstruction of the tracer diffusion out of capillary walls was attributed to the tight junctions between the endothelial cells. Peroxidase penetration was also absent in the capillaries of the pia and dura mater, however, was observed in pinocytotic vesicles of the endothelial cells. Lateral diffusion from the surrounding choroid into the optic nerve was detected but diffusion from the prelaminar optic nerve into the juxta-optic nerve retina was prevented by the Kuhnt intermediary tissue. Tight junctions which prevented peroxidase diffusion were found between the glial cells of the Kuhnt tissue, and this tissue was the barrier between the prelaminar optic nerve and the juxta-optic nerve retina. Peroxidase which was given into the lateral ventricle of the brain appeared in the subarachnoidal space around the optic nerve and penetrated freely into the optic nerve. The pial surface of the optic nerve possess no barrier activity. Peroxidase could be traced along the intercellular space between glial cells and optic nerve fibers. The basal lamina of the optic nerve capillaries was filled with peroxidase but diffusion into the capillary lumen was obstructured by the tight junctions between the endothelial cells.

Animals↗
PubMed1997

Effect of optic disc size or age on evaluation of optic disc variables.

AIMS/BACKGROUND: It has been reported that the number of optic nerve fibres decrease with age, and the cup/disc (C/D) ratio increases as the optic disc size increases. Consequently, the normal value of the optic disc variables measured by an optic disc analyser may change according to the optic disc size or age. The effect of individual variations in optic disc size or age on interpretation of optic disc variables was investigated. METHODS: Topographic optic disc variables of 104 normal Asian adults of both sexes aged 40 to 68 were measured using a confocal scanning laser ophthalmoscope (TopSS, Laser Diagnostic Technologies, Inc). Fourteen variables were evaluated according to the optic disc size or age. Statistical analysis was done by regression analysis. RESULTS: With an increase in optic disc size, the increase in cup shape, effective area, 1/2 depth area, C/D ratio, neuroretinal rim area, volume above, volume below, and 1/2 depth volume were statistically significant (p < 0.05). However, contour variation, mean contour depth, average depth, maximum depth, average slope, and maximum slope were not affected (p > 0.1). Age did not have any significant influence on optic disc variables (p > 0.1). CONCLUSION: Optic disc size, but not age, should be considered in the interpretation of optic disc variables.

Adult↗
PubMedDate not supplied

Optic neuropathy secondary to cat scratch disease: distinguishing MR imaging features from other types of optic neuropathies.

BACKGROUND AND PURPOSE: MR imaging characteristics of optic neuropathy caused by cat scratch disease have not yet been described; this lack of information may result in incorrect diagnosis and may contribute to initiation of inappropriate therapy. Our study was based on the hypothesis that cat scratch disease-related optic neuropathy has distinct MR imaging features compared with those of other types of optic neuropathies. METHODS: Eighty-two patients with various causes of optic neuropathy and available MR imaging examinations were included in this study. Two readers blinded to the diagnosis reviewed the MR images independently in regard to presence, location, and extent of optic nerve enhancement. The MR imaging findings were correlated with the final diagnosis. RESULTS: Eleven percent (9/82) of the patients received a final diagnosis of cat scratch disease. Optic nerve enhancement in patients with cat scratch disease (5/37) was localized to a 3- to 4-mm segment at the optic nerve-globe junction. All other patients with optic neuropathy (31/37) with one exception showed enhancement away from the optic nerve-globe junction or a long-segment enhancement when the optic nerve-globe junction was also involved. Four patients with cat scratch disease did not show any optic nerve MR abnormalities. CONCLUSION: Unilateral, short-segment enhancement localized to the optic nerve-globe junction is highly specific for cat scratch disease as the underlying cause of optic neuropathy and may help in establishing the diagnosis of this condition.

Adolescent↗
PubMed2004

Raldh2 expression in optic vesicle generates a retinoic acid signal needed for invagination of retina during optic cup formation.

Three retinaldehyde dehydrogenase genes (Raldh1, Raldh2, and Raldh3) expressed in unique spatiotemporal patterns may control synthesis of retinoic acid (RA) needed for retina development. However, previous studies indicate that retina formation still proceeds normally in Raldh1-/- mouse embryos lacking RA synthesis in the dorsal neural retina at the optic cup stage. Here, we demonstrate that Raldh2-/- embryos lacking RA synthesis in the optic vesicle exhibit a failure in retina invagination needed to develop an optic cup. This was also observed in Raldh1-/-:Raldh2-/- double mutants, which develop similarly. Both mutants retain RA activity in the lens placode associated with Raldh3 expression, but this RA activity is insufficient to induce optic cup formation. Maternal RA administration at the optic vesicle stage rescues optic cup formation in Raldh2-/- and Raldh1-/-:Raldh2-/- embryos, demonstrating that Raldh1 is not required during rescue of optic cup development. The optic cup of rescued Raldh1-/-:Raldh2-/- embryos exhibits normal RA activity and this is associated with Raldh3 expression in the retina and lens. Thus, RA signaling initiates in the optic vesicle in response to Raldh2 but can be maintained during optic cup formation by a gene other than Raldh1, most likely Raldh3. Loss of optic vesicle RA signaling does not effect expression of early determinants of retina at the optic vesicle stage (Pax6, Six3, Rx, Mitf). Our findings suggest that RA functions as one of the signals needed for invagination of the retina to generate an optic cup.

Aldehyde Oxidoreductases↗
PubMed2004

Optical coherence tomography can measure axonal loss in patients with ethambutol-induced optic neuropathy.

PURPOSE: To map and identify the pattern, in vivo, of axonal degeneration in ethambutol-induced optic neuropathy using optical coherence tomography (OCT). Ethambutol is an antimycobacterial agent often used to treat tuberculosis. A serious complication of ethambutol is an optic neuropathy that impairs visual acuity, contrast sensitivity, and color vision. However, early on, when the toxic optic neuropathy is mild and partly reversible, the funduscopic findings are often subtle and easy to miss. METHODS: Three subjects with a history of ethambutol (EMB)-induced optic neuropathy of short-, intermediate-, and long-term visual deficits were administered a full neuro-ophthalmologic examination including visual acuity, color vision, contrast sensitivity, and fundus examination. In addition, OCT (OCT 3000, Humphrey-Zeiss, Dublin, CA) was performed on both eyes of each subject using the retinal nerve fiber layer (RNFL) analysis protocol. OCT interpolates data from 100 points around the optic nerve to effectively map out the RNFL. RESULTS: The results were compared to the calculated average RNFL of normal eyes accumulated from four prior studies using OCT, n=661. In all subjects with history of EMB-induced optic neuropathy, there was a mean loss of 72% nerve fiber layer thickness in the temporal quadrant (patient A, with eventual recovery of visual acuity and fields, 58% loss; patient B, with intermediate visual deficits, 68% loss; patient C, with chronic visual deficits, 90% loss), with an average mean optic nerve thickness of 26+/-16 microm. There was a combined mean loss of 46% of fibers from the superior, inferior, and nasal quadrants in the (six) eyes of all three subjects (mean average thickness of 55+/-29 microm). In both sets (four) of eyes of the subjects with persistent visual deficits (patients B and C), there was an average loss of 79% of nerve fiber thickness in the temporal quadrant. CONCLUSIONS: The OCT results in these patients with EMB-induced optic neuropathy show considerable loss especially of the temporal fibers. This is consistent with prior histopathological studies that show predominant loss of parvo-cellular axons (or small-caliber axons) within the papillo-macular bundle in toxic or hereditary optic neuropathies. OCT can be a valuable tool in the quantitative analysis of optic neuropathies. Additionally, in terms of management of EMB-induced optic neuropathy, it is important to properly manage ethambutol dosing in patients with renal impairment and to achieve proper transition to a maintenance dose once an appropriate loading dose has been reached.

Aged↗
PubMed2002

Optic nerve degeneration and mitochondrial dysfunction: genetic and acquired optic neuropathies.

Selective degeneration of the smallest fibers (papillo-macular bundle) of the human optic nerve occurs in a large number of optic neuropathies characterized primarily by loss of central vision. The pathophysiology that underlies this peculiar pattern of cell involvement probably reflects different forms of genetic and acquired mitochondrial dysfunction. Maternally inherited Leber's hereditary optic neuropathy (LHON), dominant optic atrophy (Kjer disease), the optic atrophy of Leigh's syndrome, Friedreich ataxia and a variety of other conditions are examples of inherited mitochondrial disorders with different etiologies. Tobacco-alcohol amblyopia (TAA), the Cuban epidemic of optic neuropathy (CEON) and other dietary (Vitamins B, folate deficiencies) optic neuropathies, as well as toxic optic neuropathies such as due to chloramphenicol, ethambutol, or more rarely to carbon monoxide, methanol and cyanide are probably all related forms of acquired mitochondrial dysfunction. Biochemical and cellular studies in LHON point to a partial defect of respiratory chain function that may generate either an ATP synthesis defect and/or a chronic increase of oxidative stress. Histopathological studies in LHON cases and a rat model mimicking CEON revealed a selective loss of retinal ganglion cells (RGCs) and the corresponding axons, particularly in the temporal-central part of the optic nerve. Anatomical peculiarities of optic nerve axons, such as the asymmetric pattern of myelination, may have functional implications on energy dependence and distribution of mitochondrial populations in the different sections of the nerve. Histological evidence suggests impaired axonal transport of mitochondria in LHON and in the CEON-like rat model, indicating a possible common pathophysiology for this category of optic neuropathies. Histological evidence of myelin pathology in LHON also suggests a role for oxidative stress, possibly affecting the oligodendrocytes of the optic nerves.

Animals↗
PubMed2005

Optic nerve glioma and optic neuritis mimicking one another: case report.

OBJECTIVE AND IMPORTANCE: The clinical and radiographic presentations of optic nerve gliomas and optic neuritis are for the most part distinct and their diagnoses straightforward. We present two cases illustrating the occasional difficulty one can encounter in distinguishing neoplastic from inflammatory optic neuropathies. CLINICAL PRESENTATION: Patient 1 is a 17-year-old girl who presented with acute onset of pain and rapidly progressive visual loss in the right eye. Patient 2 is a 38-year-old man who presented with painless progressive visual loss in the left eye. INTERVENTION: Patient 1 was initially diagnosed with idiopathic retrobulbar optic neuritis. Interval increase of the optic nerve on magnetic resonance imaging prompted a biopsy of the optic nerve, which revealed a pilocytic astrocytoma. Patient 2 was found to have left optic nerve enhancement most consistent with an optic nerve glioma. Before a biopsy, the patient spontaneously improved without treatment, indicating an inflammatory process. CONCLUSION: Differentiating between optic nerve neoplasm and inflammation may be difficult. On occasion, the classic clinical finding of pain with eye movement and the radiographic finding of enlargement and enhancement of the optic nerve may be misleading. Open biopsy of the optic nerve is indicated only after a completely negative metabolic, infectious, and inflammatory workup; interval increase of the optic nerve on magnetic resonance imaging; and failure of the patient to recover vision.

Adolescent↗
PubMed2000

Ranking of optic disc variables for detection of glaucomatous optic nerve damage.

PURPOSE: To describe optic disc variables assessed by evaluation of clinical optic disc photographs and to compare sensitivity and specificity of these optic disc parameters in identifying patients with ocular hypertension who have nerve fiber layer defects and normal visual fields and patients with visual field defects. METHODS: The study included 500 normal subjects, 132 patients with ocular hypertension with retinal nerve fiber layer defects and normal visual fields (preperimetric glaucoma), and 840 patients with glaucomatous visual field defects. Color stereo optic disc photographs were morphometrically evaluated. RESULTS: Highest diagnostic power for the separation between the normal group and the preperimetric glaucoma group had the vertical cup-to-disc diameter ratio corrected for its dependence on the optic disc size, total neuroretinal rim area, rim-to-disc area ratio corrected for disc size, and cup-to-disc area ratio corrected for disc size. Diagnostic power was lower for rim area in the temporal inferior and temporal superior disc sector, cup area corrected for disc size, and horizontal cup-to-disc diameter ratio corrected for disc size. Less useful for the differentiation between the normal subjects and the preperimetric glaucoma group were size of zones alpha and beta of parapapillary chorioretinal atrophy, and ratios of neuroretinal rim width and rim area comparing various optic disc sectors with each other. CONCLUSIONS: In subjects with ocular hypertension with retinal nerve fiber layer defects and normal conventional achromatic visual fields, the vertical cup-to-disc diameter ratio corrected for optic disc size, total neuroretinal rim area, rim-to-disc area ratio, and cup-to-disc area ratio corrected for disc size are the most valuable optic disc variables for early detection of glaucomatous optic nerve damage. Correction for optic disc size is necessary for optic disc variables directly or indirectly derived from the optic cup. Parapapillary atrophy is less important in the early detection of glaucoma.

Adolescent↗
PubMed1985

Anterior optic nerve blood flow in experimental optic atrophy.

This study attempts to establish whether neurogenic optic atrophy induces changes in anterior optic nerve circulation and to determine how noninvasive techniques of measuring blood flow in vivo compare to microsphere distribution. Five cats underwent unilateral optic nerve transection in the orbital apex and a sham procedure in the contralateral eye. Two to three months later, no abnormalities were detected by fluorescein angiography. Laser Doppler measurements demonstrated a 53% decrease in red blood cell speed through the capillaries of the atrophic optic nerve heads in vivo. Optic disk reflectance measurements of anterior optic nerve blood volume in vivo demonstrated a 51% decrease in the estimated blood volume of the capillaries in atrophic optic nerve heads. Flow was calculated on the basis of these noninvasive measurements and demonstrated an average decrease of 74% in optic atrophy. Histologic studies of microsphere distribution demonstrated an average decrease of 80% in flow to the anterior optic nerve in optic atrophy. These results suggest that anterior optic nerve blood flow is significantly reduced in primary neurogenic optic atrophy. This study also demonstrates that the noninvasive measurements of blood flow are substantiated by histologic evaluation of microsphere distribution.

Animals↗
PubMed1998

Organization of retinal axons within the optic nerve, optic chiasm, and the innervation of multiple central nervous system targets Rana pipiens.

Light microscopic analysis of the optic nerve, chiasm, and optic tracts of Rana pipiens after the anterograde and retrograde transport of horseradish peroxidase has shown that retinal ganglion-cell axons reach the optic nerve head in chronotopically organized fascicles that form bands across the intraocular optic nerve. These bands of fascicles are divided along the midline in a "zone of reorganization" to create two full maps of the retinal surface; however, this map is discontinuous in that nasal and temporal quadrants are adjacent to one another. In the intracranial portion of the optic nerve, axons undergo another reorganization such that peripheral retinal axons shift position and become localized laterally and ventrally, whereas centrally placed axons become localized dorsally. Within this reorganization, the nerve is reconfigured into laminae of axons, and each lamina consists of age-related axons organized into two retinal maps. In the ipsilateral chiasm, axons diverge to form three central, optic tracts: the medial optic tract, the projection to the corpus geniculatum, and the basal optic root. Ipsilateral axons leave the chiasm at the same level of the chiasm as do their contralateral counterparts. The remaining axons converge in the lateral diencephalon to form a fourth fascicle, the marginal optic tract. Thus, within the optic chiasm, a sequence of positional transformations occur that result in the formation of multiple optic pathways. The various changes in axonal trajectory always coincide with changes in the orientation of cell groups that lie within the nerve and optic chiasm.

Animals↗
PubMed1983

Optic nerve axons and acquired alterations in the appearance of the optic disc.

The pathophysiologic events in optic nerve axons have recently been recognized as crucial to an understanding of clinically significant acquired alterations in the ophthalmoscopic appearance of the optic disc. Stasis and related abnormalities of axonal transport appear to explain most aspects of optic nerve head swelling, including optic disc drusen and retinal cottonwool spots. Loss of axoplasm and axonal death can be invoked to interpret optic disc pallor, thinning and narrowing of rim tissue, changes in the size and outline of the optic cup, laminar dots, atrophy of the retinal nerve fiber layer, and acquired demyelination and myelination of the retinal nerve fiber layer. It is speculated that the axons may also play a role in the mechanical support of the lamina cribrosa in resisting the pressure gradient across the pars scleralis of the optic nerve head. Axons and their associated glial cells may be involved in those cases where "reversibility" of cupping of the optic disc has been reported. The structure, physiology, and experimental pathologic findings of the optic nerve head have been reviewed. Many aspects concerning the final anatomic appearance of the optic nerve head have been explained. However, many questions remain concerning the intermediate mechanisms by which increased intracranial pressure retards the various components of axonal transport in papilledema and by which increased IOP causes axonal loss in glaucoma. Investigation of the molecular biology of axonal constituents and their responses to abnormalities in their physical and chemical milieu could extend our understanding of the events that result from mechanical compression and local ischemia. Moreover, we have identified a need to further explore the role of axons in the pathophysiology of optic disc cupping.

Animals↗
PubMed1982

Measurement of the optical density of the optic nerve head II: short-time fluctuations of the optical density of the nerve head.

The fluctuation of pallor with increasing IOP could be due to either insufficient reliability of the method or to an unrecognized pulsating phenomenon. A better arrangement should eliminate imperfection of the method. Coupling the release with the ECG should reveal a relationship to the arterial pulse rate. Neither condition could be demonstrated as the reason for the fluctuation. The connection of the fluctuation and its possible relationship to central venous pressure is discussed. The margin of error is shown, which is 9% on average.

Electrocardiography↗