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PubMed2000

[Diagnosis of swollen optic disks using color Doppler ultrasonography] .

The Goal of this study was prospective evaluation of the blood flow parameters-maximal systolic velocity (MSV), minimal diastolic velocity (MDV) and Pourcelot's resistivity index (RI) in patients with swollen optic dis. 63 patients (79 eyes) were examined with swollen optic disc-10 patients (17 eyes) with intracranial hypertension, 12 patients (14 eyes) with pseudoedema of disk of the optic nerve, 7 patients (7 eyes) with inflammation swollen optic disc, 3 patients (6 eyes) with pseudotumor cerebri, 8 patients (12 eyes) with arteritic anterior ischemic optic neuropathy (A-AION) and 23 patients (23 eyes) with nonarteritic anterior ischemic optic neuropathy (N-AION) and 23 patients (23 eyes) with nonarteritic anterior ischemic optic neuropathy (N-AION). All patients had ophthalmological examinations and Color Doppler ultrasonography in central retinal artery (CRA), posterior ciliary artery (PCA), ophthalmic artery (OA) and in central retinal vein (CRV). The blood flow parameters of the swollen optic disc and normal optic disc were not significant changed at intracranial hypertension, pseudooedema cerebri, inflammation swelling, and at pseudotumour od the optic disc. A-AION and N-AION acallocated significant changes of the blood velocities and resistivity index. A-AION: significant increasing resistivity index at CRA, CPA, significant decrease of MSV and MDV and difficult mapping of the CPA in Color doppler mapping. At the fellow eye (without swollen optic disc) was significant decreasing of the blood velocities of the CRA, CPA, but not so much as at the defective eye with swollen optic nerve disk. N-AION: defective eye with swollen optic disc--there were: nonsignificant decreasing of MSV, MDV, significant decreasing of MSV, MDV and increasing of resistivity index of the CRA, CPA at the fellow eye. AO was without significant changes. Color Doppler information allowed to specify diagnosis of A-AION and N-AION.

Blood Flow Velocity↗
PubMed1990

Optic nerve hypoplasia. Identification by magnetic resonance imaging.

High-resolution magnetic resonance images of the intracranial optic nerves and chiasm were obtained in 15 patients with severe optic nerve hypoplasia. These were compared, in a double-blind manner, with similar images from 30 age-matched controls. On both coronal and sagittal images, hypoplastic optic nerves were thin and demonstrated signal attenuation when compared with normal optic nerves. All patients with severe bilateral optic nerve hypoplasia also had diffuse chiasmal hypoplasia, which was seen best on coronal images. Patients with unilateral or asymmetrical optic nerve hypoplasia had variable chiasmal abnormalities. The degree to which the magnetic resonance diagnosis of optic nerve hypoplasia matched the clinical diagnosis was highly significant (P less than .001, Fisher's Exact Test) for both coronal and sagittal views of the intracranial optic nerves. Oblique axial and coronal views of the orbital optic nerves did not reliably distinguish optic nerve hypoplasia from normal optic nerves. High-resolution magnetic resonance imaging is a useful diagnostic modality to identify small optic nerves neuroradiologically.

Adolescent↗
PubMed1998

Influence of optic disc size on the sensitivity of the Heidelberg Retina Tomograph.

PURPOSE: The aim of this study was to evaluate the influence of optic disc size on the ability of variables generated by the Heidelberg Retina Tomograph, software version 1.11, to distinguish glaucoma patients from normals in a cross-sectional study. PATIENTS AND METHODS: For evaluation of the optic disc with the Heidelberg Retina Tomograph, eyes of 87 normals and 61 glaucoma patients were selected. Disc area, volume above reference, rim area, cup area, cup volume, third moment in contour and the mean retinal nerve fibre layer thickness at the border of the optic disc were selected for evaluation. The sensitivity at 80% specificity of these variables was calculated under three conditions: (1) no correction for disc size; (2) calculation in the following disc size ranges: class I (1.0-2.0 mm2), class II (2.0-2.5 mm2), class III (2.5-3.15 mm2) and class IV (3.15-5.0 mm2); (3) calculation globally, taking into account the different disc sizes of the four classes. RESULTS: Neuroretinal rim area, cup area and volume, third moment and nerve fibre layer thickness were significantly and positively correlated with optic disc size in normals. Neuroretinal rim volume measurements were statistically independent of optic disc size. Sensitivity was lowest when the size of the optic disc was not considered. Sensitivity increased when evaluated in four optic disc size classes. With growing optic disc size sensitivity of the retinal nerve fibre layer increased and third moment value decreased. Cup volume and area had their lowest sensitivity for large optic discs. The area of the neuroretinal rim was the only variable which showed similar sensitivity values under all three conditions. CONCLUSIONS: The sensitivities of HRT variables varied with optic disc size. Evaluation of their sensitivity requires the definition of optic disc classes or statistical correction for the size of the optic disc.

Adult↗
PubMed2004

Serial magnetization transfer imaging in acute optic neuritis.

In serial studies of multiple sclerosis lesions, reductions in magnetization transfer ratio (MTR) are thought to be due to demyelination and axonal loss, with later rises due to remyelination. This study followed serial changes in MTR in acute optic neuritis in combination with clinical and electrophysiological measurements to determine if the MTR changes over time mirror the picture in multiple sclerosis lesions, further validating MTR as a marker of tissue integrity. Twenty-nine patients were recruited who had acute optic neuritis for a median of 13 days (range 7-24 days) since the onset of visual symptoms. A clinical examination and measurement of visual evoked potentials (VEP) was performed on each patient. Their optic nerves were imaged with a fat-saturated fast spin echo (FSE) sequence and a magnetization transfer sequence. Twenty-one had multiple subsequent examinations over the course of 1 year. In addition, 27 control subjects had their optic nerves imaged up to three times over 1 year. A blinded observer segmented the optic nerves from the MTR maps. Lesions were defined on the acute FSE images and, from the coordinates, the ratio of mean lesion MTR : healthy nerve MTR (lesion ratio) was calculated for each dataset. The time-averaged mean MTR in control optic nerves was 47.7 per cent units (pu). In diseased optic nerves, baseline mean MTR was 47.3 pu, with a mean lesion ratio of 0.98. The diseased optic nerve MTR and lesion ratio declined over time with a nadir at about 240 days at a mean MTR value of 44.2 pu and mean lesion ratio of 0.91. Subsequently, diseased optic nerve MTR appeared to rise; after 1 year the diseased optic nerve mean MTR was 45.1 pu (mean lesion ratio 0.93), although the difference was not significant compared with the nadir value. For each 0.01 increase in time-averaged lesion ratio logMAR visual acuity recovery improved by 0.03 (95% CI, 0.002, 0.08, P = 0.02). Time-averaged VEP central field latency was shorter by 6.1 ms (95% CI 1.5, 10.7, P = 0.012) per 1 pu rise in time-averaged diseased optic nerve MTR. The early fall in diseased optic nerve MTR is consistent with demyelination and Wallerian degeneration of transected axons. The late nadir compared with studies of multiple sclerosis lesions may have been due to slow clearance of myelin debris. Remyelination may have influenced subsequent MTR changes. The observations support using MTR to monitor symptomatic demyelinating lesions.

Acute Disease↗
PubMed1992

Management of traumatic optic neuropathy--a study of 23 patients.

Twenty three patients with traumatic optic neuropathy were managed by medical and surgical treatment as follows. High dose intravenous steroids were initiated in all patients. If visions did not improve significantly after 24 to 48 hours decompression of an optic nerve sheath haematoma by medial orbitotomy and neurosurgical decompression of the optic canal were considered based on computed tomographic scan findings. Nine of 16 patients who received steroids only showed significant improvement. One of three showed improvement on optic nerve decompression after steroid failure; three or four showed improvement on optic nerve decompression after steroid failure; three or four showed improvement with combined optic nerve sheath decompression by the medial orbitotomy and decompression of the optic canal by frontal craniotomy. A lucid interval of vision after injury and an enlarged optic nerve sheath were associated with an improved prognosis. Five of the 23 patients had a lucid interval and all five had a final improved vision, while only five of 18 patients without a lucid interval improved. Similarly seven of the nine with an enlarged optic nerve sheath showed improvement while only three of 10 patients (three bilateral cases) who presented with no light perception improved with medical and surgical treatment. While a prospective controlled study of the management of traumatic optic neuropathy is necessary this preliminary study suggests that treatment of traumatic optic nerve sheath haematoma by optic nerve sheath decompression should be considered in selected patients.

Adolescent↗
PubMed2006

Proper patterning of the optic fissure requires the sequential activity of BMP7 and SHH.

The optic disc develops at the interface between optic stalk and retina, and enables both the exit of visual fibres and the entrance of mesenchymal cells that will form the hyaloid artery. In spite of the importance of the optic disc for eye function, little is known about the mechanisms that control its development. Here, we show that in mouse embryos, retinal fissure precursors can be recognised by the expression of netrin 1 and the overlapping distribution of both optic stalk (Pax2, Vax1) and ventral neural retina markers (Vax2, Raldh3). We also show that in the absence of Bmp7, fissure formation is not initiated. This absence is associated with a reduced cell proliferation and apoptosis in the proximoventral quadrant of the optic cup, lack of the hyaloid artery, optic nerve aplasia, and intra-retinal misrouting of RGC axons. BMP7 addition to organotypic cultures of optic vesicles from Bmp7-/- embryos rescues Pax2 expression in the ventral region, while follistatin, a BMP7 antagonist, prevents it in early, but not in late, optic vesicle cultures from wild-type embryos. The presence of Pax2-positive cells in late optic cup is instead abolished by interfering with Shh signalling. Furthermore, SHH addition re-establishes Pax2 expression in late optic cups derived from ocular retardation (or) embryos, where optic disc development is impaired owing to the near absence of SHH-producing RGC. Collectively, these data indicate that BMP7 is required for retinal fissure formation and that its activity is needed, before SHH signalling, for the generation of PAX2-positive cells at the optic disc.

Aldehyde Oxidoreductases↗
PubMed1998

Acquired mitochondrial impairment as a cause of optic nerve disease.

BACKGROUND: Blindness from an optic neuropathy recently occurred as an epidemic affecting 50,000 patients in Cuba (CEON) and had clinical features reminiscent of both tobacco-alcohol amblyopia (TAA) and Leber's hereditary optic neuropathy (Leber's; LHON). Selective damage to the papillomacular bundle was characteristic, and many patients also developed a peripheral neuropathy. Identified risk factors included vitamin deficiencies as well as exposure to methanol and cyanide. In all 3 syndromes, there is evidence that singular or combined insults to mitochondrial oxidative phosphorylation are associated with a clinically characteristic optic neuropathy. PURPOSE: First, to test the hypothesis that a common pathophysiologic mechanism involving impairment of mitochondria function and, consequently, axonal transport underlies both genetic optic nerve diseases such as Leber's and acquired toxic and nutritional deficiency optic neuropathies. According to this hypothesis, ATP depletion below a certain threshold leads to a blockage of orthograde axonal transport of mitochondria, which, in turn, leads to total ATP depletion and subsequent cell death. Second, to address several related questions, including (1) How does impaired energy production lead to optic neuropathy, particularly since it seems to relatively spare other metabolically active tissues, such as liver and heart? (2) Within the nervous system, why is the optic nerve, and most particularly the papillomacular bundle, so highly sensitive? Although there have been previous publications on the clinical features of the Cuban epidemic of blindness, the present hypothesis and the subsequent questions have not been previously addressed. METHODS: Patients in Cuba with epidemic optic neuropathy were personally evaluated through a comprehensive neuro-ophthalmologic examination. In addition, serum, lymphocytes for DNA analysis, cerebrospinal fluid (CSF), sural nerves, and eyes with attached optic nerves were obtained from Cuban patients, as well as from Leber's patients, for study. Finally, we developed an animal model to match the low serum folic acid and high serum formate levels found in the CEON patients, by administering to rats low doses of methanol after several months of a folic acid-deficient diet. Optic nerves and other tissues obtained from these rats were analyzed and compared with those from the Cuban patients. RESULTS: Patients from the Cuban epidemic of optic neuropathy with clinical evidence of a selective loss of the papillomacular bundle did much better once their nutritional status was corrected and exposure to toxins ceased. Patients with CEON often demonstrated low levels of folic acid and high levels of formate in their blood. Histopathologic studies demonstrated losses of the longest fibers (in the sural nerve) and those of smallest caliber (papillomacular bundle) in the optic nerve, with intra-axonal accumulations just anterior to the lamina cribrosa. Our animal model duplicated the serologic changes (low folic acid, high formate) as well as these histopathologic changes. Furthermore, ultrastructural examination of rat tissues demonstrated mitochondrial changes that further matched those seen on ultrastructural examination of tissues from patients with Leber's. CONCLUSION: Mitochondria can be impaired either genetically (as in Leber's) or through acquired insults (such as nutritional or toxic factors). Either may challenge energy production in all cells of the body. While this challenge may be met through certain compensatory mechanisms (such as in the size, shape, or number of the mitochondria), there exists in neurons a threshold which, once passed, leads to catastrophic changes. This threshold may be that point at which mitochondrial derangement leads to such ATP depletion that axonal transport is compromised, and decreased mitochondrial transport results in even further ATP depletion. Neurons are singularly dependent on the axonal transport of mitochondria. (

Adult↗
PubMed2000

Hypovolemic ischemic optic neuropathy.

BACKGROUND: Ischemic optic neuropathy refers to an acute event of ischemia, or decreased blood flow, to the optic nerve resulting in varying degrees of vision loss and visual field defects. Typically this disease affects the elderly population who experience systemic diseases that compromise the blood flow efficiency of the optic nerve head (e.g., giant-cell arteritis, hypertension, diabetes, etc.). However, cases of blood loss to the optic nerve, secondary to traumatic injuries or surgeries, have also been shown to result in ischemic optic neuropathy, regardless of age. It seems that in these cases, the resulting anemia and hypotension play contributing roles in the development of ischemic optic neuropathy. METHODS: A 41-year-old black man came to us with optic nerve head pallor O.S., count-fingers vision O.S., positive afferent pupillary defect O.S., and a central scotoma O.S. after being hospitalized and treated for a stab wound to his left neck that severed his left carotid artery at the bifurcation. RESULTS: This patient had been seen in the Optometry Clinic two years before the stab-wound incident. At that time, he had 20/20 vision in his left eye and no remarkable neurological deficits. His ocular presentation after the traumatic hypovolemic event was probably a direct result of the hypoperfusion to the left optic nerve head. This patient was diagnosed with a hypovolemic, or blood loss-related, ischemic optic neuropathy (O.S.). CONCLUSIONS: Patients who experience large amounts of blood loss due to trauma, surgery, internal bleeding, etc. and report vision loss should be screened for possible optic nerve ischemia. As eye care providers, when we are presented with patients who have optic nerve head atrophy, we should inquire about events that may have precipitated blood loss, potentially triggering ischemic optic neuropathy.

Adult↗
PubMed1985

Regeneration of peptide-containing retinofugal axons into the optic tectum with reappearance of a substance P-containing lamina.

Twenty-five specimens of Rana pipiens were subjected to a unilateral crush of the optic nerve. Substance P (SP)-, leucine enkephalin (LENK)-, cholecystokinin octapeptide (CCK8)-, and bombesin (BOM)-like immunoreactivities were analyzed in the retinae, optic nerves, and optic tecta, 9 days to 9 months postoperatively, by means of immunohistochemical methods. Peptide-like immunoreactivity was observed in axons within the optic nerve stump retinal to the crush, as in previous studies (Kuljis and Karten, '83b, Kuljis et al., '84). Peptide-containing retinofugal axons began traversing the lesion site between 10 and 20 days postoperatively, in progressively increasing numbers. Ten to 20 days following crush of the optic nerve SP-, LENK-, and CCK8-containing axons could be found in the cerebral stump of the optic nerve and in the optic chiasm, advancing to the side of the brain deafferented by the crush. The number of axons displaying peptide-like immunoreactivity within the optic nerve, retinal or cerebral to the crush, and within the optic chiasm gradually decreased after 2-3 months. The optic nerve contralateral to the procedure displayed only occasional isolated peptide-containing fibers, as in normal optic nerves. The retinae ipsilateral and contralateral to the crush exhibited no change in the normal pattern of peptide-like immunoreactivity, including the absence of demonstrable peptide-like immunoreactivity in the somata of retinal ganglion cells. The optic tectum deafferented by the procedure underwent modifications in the pattern of peptide-like immunoreactivity identical to those reported following unilateral eye enucleation (Kuljis and Karten, '82a, '83a). The patterns of LENK-, CCK8-, and BOM-like immunoreactivities in the tectum were identical to those following irreversible retinal deafferentation as long as 9 months postoperatively. SP-like immunoreactivity, however, was gradually restored in layer 11 of Ramón y Cajal ('46; layer D of Potter, '69) of the superficial (retinorecipient) neuropil 4-6 months postoperatively. The persistence of lamina-specific depletion patterns of LENK-, CCK8-, and BOM-like immunoreactivities in reafferented tecta represents a puzzling observation. The latter findings contrast sharply with the recovery of SP-like immunoreactivity, which occurs long after apparently complete restitution of the retinofugal projection, as shown by anatomical (Stelzner et al., '81), physiological (Maturana et al., '59), and behavioral (Sperry, '44) methods.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMedDate not supplied

Morphometric analysis of the optic disc surface. The level of smoothness as a diagnostic parameter for glaucoma.

PURPOSE: Since the glaucomatous loss of nerve fibers changes the appearance of the optic disc, we evaluated the morphology of the surface of the optic disc in normal and glaucomatous eyes by using a computerized system to provide the reciprocal position of a large number of points placed on its surface in order to study the clinical significance of differences in the 'smoothness' of optic disc surface. METHODS: The morphology of the optic disc surface was evaluated by means of simultaneous stereoscopic videographic pictures (IMAGEnet X Rev-3.51b-Topcon Europe, The Netherlands): the reciprocal distribution of a large number of points located on the surface of one eye of 100 subjects randomly chosen (45 normal and 55 glaucoma patients) was studied. In order to define the level of 'smoothness' of the optic disc surface, the differences of the relative position of each surface point were studied by measuring the standard deviation (SD) from the average heights of the points (n. ranging from 623 to 1916 depending on the size of the disc area) that identify the optic disc surface. RESULTS: The coefficient of variation of the reciprocal location of the points, placed on the optic disc surface at the different measurements performed by a single operator was 10.4%. The differences in Optic Disc Surface Smoothness (ODSS) between glaucoma and normal group were statistically significant (p < 0.0001 using Mann-Whitney U test). No correlation was detectable between age and standard deviation. The best threshold value, calculated using ROC methodology, able to separate the two groups was: normal group: SD < or = 17.79 (-1 x 10(-2) mm); glaucoma group: SD > -17.79 (-1 x 10(-2) mm). Such threshold value had a sensitivity of 82.1%, a specificity of 92.2% and a diagnostic precision (DP) of 86.5% in dividing the glaucoma group from the normal group. CONCLUSION: ODSS is a global index of optic disc conditions based on quantitative measurements of the morphology of the optic disc surface. As such it does not provide information about the location and the characteristics of optic disc damage. Nevertheless, ODSS measurement is able to separate normal from glaucomatous optic disc with a rather interesting sensitivity, specificity and diagnostic precision (DP). As such it could be useful both for research and clinical applications.

Female↗
PubMed2006

Pattern electroretinography and visual evoked potentials in optic nerve diseases.

BACKGROUND: To evaluate transient pattern electroretinography (PERG) and pattern visual evoked potential (VEP) for the diagnosis, differential diagnosis and follow-up of optic nerve diseases. METHODS: Twenty-nine consecutive patients (14 female, 15 male) with the diagnosis of ischaemic optic neuropathy (n=14) and optic neuritis (n=15) were included in this study. Mean age of the patients with ischaemic optic neuropathy was 63.3+/-3.3 (60-78) years and the mean age of the patients with optic neuritis was 28.3+/-8.4 (19-43) years. In each patient ophthalmological examination and systemic evaluation were done and VEP and PERG were recorded. As a control group, VEP recordings of 35 healthy subjects were included. RESULTS: In the ischaemic optic neuropathy group (group 1), mean VEP amplitude (+/-SD) (1.96+/-0.95 microV) was found to be decreased significantly in the affected eyes in comparison to the control group and the unaffected eyes. The delay in latency (116.3+/-20.14 msec in the affected eyes compared with 101.31+/-6.19 msec in unaffected eyes) was statistically significant when compared with the healthy subjects. In the optic neuritis group (group 2), VEP amplitude was decreased (4.13+/-4.04 microV vs 6.97+/-3.35 microV and 6.97+/-4.43 microV) and latency was increased (122.59+/-20.09 msec vs 101.31+/-6.19 msec and 108.76+/-13.57 msec) in affected eyes significantly in comparison to the unaffected eyes and control group, respectively. Even though there were no significant differences for P50 latency and N95/P50 ratios between affected and unaffected eyes in both groups, N95 amplitude decreased significantly in the affected eyes of the ischaemic optic neuropathy patients and N95 latency was found to be decreased in optic neuritis patients. There was no correlation between VEP and PERG findings in both groups. CONCLUSION: VEP amplitude decreased significantly in ischaemic optic neuropathies while latency delay was more significant in patients with optic neuritis. PERG findings showed decreased N95 amplitude in ischemic optic neuropathy without associated latency changes.

Adult↗
PubMed2005

Three-dimensional morphological characterization of optic nerve fibers by atomic force microscopy and by scanning electron microscopy.

A comparative study of scanning electron microscopy (SEM) and atomic force microscopy (AFM) imaging of the healthy human optic nerve was carried out to determine the similarities and the differences. In this study we compared the fine optic nerve structures as observed by SEM and AFM. The fibers of the right optic nerve of a 61-year-old man show different arrangements in transverse sections taken from the same individual 5 mm central to the optic canal and 5 mm peripheral to the optic chiasma; this difference can be recognized by light microscopy (LM), SEM, and AFM. AFM revealed such typical optic nerve fibers (taken from a point 5 mm central to the optic canal) with annular and longitudinal orientations, which were not visible by SEM in this form. By contrast, LM and SEM visualized other structures, such as pia mater and optic nerve fibers loosely arranged in bundles, none of which was visualized by AFM. The images, however, taken 5 mm peripheral from the optic chiasma show shapeless nerve fibers having a wavy course. Our results reveal that more detailed information on optic nerve morphology is obtained by exploiting the advantages of both SEM and AFM. These are the first SEM and AFM images of healthy human optic nerve fibers, containing clear representations of the three dimensions of the optic nerve.

Aged↗
PubMed2001

Optic neuritis in an urban black African community.

PURPOSE: To describe the clinical profile of idiopathic optic neuritis in South African blacks. METHODS: South African black patients with acute isolated idiopathic optic neuritis, treated and followed for at least 3 months at a large medical centre, were studied. Exclusion criteria were other causes of optic neuropathy (such as ischaemic optic neuropathy, toxins or Leber's hereditary optic neuropathy); all causes of optic neuritis (such as HIV, neurosyphilis, sarcoid or connective tissue disease); neurological disease outside of the optic nerves; and any race other than South African black. Patients underwent extensive ophthalmic, neurological, radiological, cerebrospinal fluid and blood assessment. RESULTS: Eighteen eyes of 10 patients were studied. The mean age was 35.7 years and 9 patients were female. Only 2 patients had truly unilateral optic neuritis, the other 8 having either bilaterally simultaneous or consecutive disease. Presenting visual acuity (VA) was less than 6/60 in 17 of 18 eyes, with severe dyschromatopsia in all eyes. Fifteen eyes had optic disc swelling. All patients were treated with corticosteroids. After at least 3 months follow-up only 6 eyes recovered VA of 6/12 or better, with only 3 eyes recovering colour vision of 10/13 or better on Ishihara plate testing. No patient had multiple sclerosis (MS) on presentation, nor developed MS on follow-up. CONCLUSION: Idiopathic optic neuritis in black South Africans differs from that in whites. The higher prevalence of bilateral cases and of optic disc swelling, the weaker association with MS and the extremely poor visual outcome distinguish optic neuritis in black South Africans.

Acute Disease↗
PubMed2003

Optic disc morphology in south India: the Vellore Eye Study.

AIM: To evaluate the morphology of the optic nerve head in an unselected population group in south India. METHODS: The study included 70 subjects forming a population based sample, selected in a random manner. Mean age was 47.5 (SD 8.7) years, mean refractive error measured -0.07 (1.11) dioptres (range -4.50 to +2.50 dioptres). Optic disc slides were morphometrically analysed. RESULTS: Mean optic disc area measured 2.58 (0.65) mm(2). It was statistically independent of age and refractive error. Optic disc shape was slightly vertically oval. Mean neuroretinal rim area was 1.60 (0.37) mm(2). It was significantly and positively correlated with optic disc size and optic cup size. It was independent of age, sex, refractive error, and axial length. In all subjects included in the study, the rim was smallest in the temporal horizontal optic disc sector. Mean horizontal cup/disc diameter ratio (0.66 (0.07)) was significantly (p<0.001) higher than the mean vertical cup/disc diameter ratio (0.56 (0.08)). Both ratios were highly significantly (p <0.001) and positively correlated with optic disc size. The alpha zone of parapapillary atrophy (0.84 (0.29) mm(2)), and beta zone (0.13 (0.38) mm(2)), respectively, occurred in 69 (98.6%) subjects and in eight (11.4%) subjects, respectively. They were significantly larger in the temporal horizontal sector. The alpha zone was significantly (p<0.001) larger and occurred significantly more often than beta zone. Retinal arterioles and venules were wider, and in spatial correlation, the visibility of the retinal nerve fibre layer was significantly better, in the temporal inferior disc arcade and the temporal superior arcade than in the nasal superior arcade and the nasal inferior vessel arcade. Except for the absolute size measurements these optic nerve head parameters did not differ markedly (p >0.05) from the values found in white people. CONCLUSIONS: South Indians and white people do not show marked differences in the morphology of the optic nerve head as measured by morphometric optic disc parameters, with the possible exception of the absolute optic disc dimensions.

Adult↗
PubMed2005

Dynamic atypical optic nerve coloboma associated with transient macular detachment.

PURPOSE: Macular schisis or detachment is frequently observed in eyes with optic pits or colobomas. Although spontaneous resolution of the maculopathy has been reported, concurrent changes in the optic nerve coloboma have not. We report three cases of atypical optic nerve colobomas in which dynamic optic nerve changes coincide with the development and subsequent resolution of the associated maculopathy. METHODS: We reviewed the records of three patients with dynamic optic nerve changes associated with maculopathy. All patients were observed for at least 6 months. Fundus photography and fluorescein angiography were used to document the optic nerve and macular changes. RESULTS: Three patients were noted to have macular detachments without apparent optic nerve excavation. With observation, the maculopathy spontaneously resolved in each case. We documented concurrent optic nerve changes whereby atypical optic nerve colobomas became apparent over several months in all cases. In one case, we noted the simultaneous development of maculopathy in association with obscuration of a prior disc anomaly. None of the eyes had a posterior vitreous detachment. We could not identify any associated systemic conditions or reproduce the findings with external stimulation. Initial Snellen acuity ranged from 20/60 to 20/200. Final Snellen acuity ranged from 20/20 to 20/40. CONCLUSIONS: Fluctuating optic nerve changes may occur in the setting of atypical optic nerve coloboma and associated maculopathy. In cases of macular schisis or detachment where an optic nerve coloboma is not readily apparent, and no other causes are identified, consideration of a period of observation prior to therapeutic intervention seems appropriate.

Adult↗
PubMed1990

Specific routing of retinal ganglion cell axons at the mammalian optic chiasm during embryonic development.

During development of the mammalian CNS, axons encounter multiple pathway choices on their way to central target structures. A major pathway branch point in the visual system occurs at the optic chiasm, where retinal ganglion cell axons may either enter the ipsilateral or the contralateral optic tract. To investigate whether embryonic mouse retinal ganglion cell axons, upon reaching the optic chiasm, selectively grow into the correct pathway, developing retinal ganglion cells were retrogradely labeled using either 1,1'-dioctadecyl- 3,3,3',3'-tetramethylindocarbocyanine perchlorate (Dil) or fluorescent microspheres placed into the optic tract on one side. The distribution of ipsilaterally and contralaterally projecting ganglion cells in the embryo was then examined and compared to that of the adult animal. Results show that axon routing at the chiasm is already extremely adult-like as early as embryonic day 15 (E15), shortly after retinal axons arrive at the chiasm. [Retinal ganglion cell neurogenesis = E11-E18 (Drager, 1985); birth = E21.] Throughout the development of this pathway, routing errors are infrequent and are on the order of only about 3-8/1000 retinal ganglion cells. Thus, embryonic retinal ganglion cell axons do not project randomly at the optic chiasm but instead appear to be highly specific in their choice of pathway. To learn how correct pathway choices are made, retinal axons were retrogradely labeled with Dil and their trajectories at the optic chiasm were reconstructed. Results show that ipsilaterally and contralaterally projecting axons are highly intermixed as they enter the chiasm region but selectively grow into the correct pathway. For example, a contralaterally projecting axon near the entrance of the ipsilateral optic tract will turn and bypass this pathway and grow towards the midline to head into the contralateral optic tract. Similarly, axons far away from the ipsilateral optic tract frequently turn abruptly at right angles to enter the ipsilateral tract, directly crossing over contralaterally projecting axons heading to the opposite side. The sorting out of intermixed ipsilaterally and contralaterally projecting retinal axons into the appropriate optic tracts strongly suggests the presence of specific guidance cues at the optic chiasm during embryonic development. Together, results from this study demonstrate that the pattern of axon projection at the adult mammalian optic chiasm is gradually built upon a highly specific pattern of axon routing laid down early during development.

Animals↗
PubMed1988

Transient expression of laminin in the optic nerve of the developing rat.

The optic nerve of the developing rat was examined for the presence of laminin, an adhesive glycoprotein, to assess whether it might serve as a substrate for retinal axon growth in vivo. The optic stalk and nerve of developing rats were screened immunohistochemically for the presence of laminin before, during, and after the period of retinal axon growth. On embryonic day 14 (E14), laminin immunoreactivity was present in the ventral portion of the optic stalk, the same region in which the first retinal axons grow. Between E16 and postnatal day 10 (P10), cells positive for laminin were distributed throughout the cross-sectional area of the nerve. There was a progressive appearance of glial fibrillary acidic protein (GFAP) immunoreactivity, a marker for astrocytes, from the optic nerve head towards the chiasm beginning on E20. At the advancing front of GFAP immunoreactivity, cells were positive for both laminin and GFAP. Behind the front, laminin immunoreactivity disappeared from the cells. By P12, the only laminin immunoreactivity that remained within the optic nerve surrounded the vasculature. This is a time after the last retinal axons grow through the optic nerve. Monolayer cell cultures were prepared from perinatal rat optic nerves and processed for immunohistochemistry to determine which astrocyte type was laminin-positive. Type 1 astrocytes, which primarily compose the immature nerve, are GFAP-positive, A2B5-negative, and laminin-positive. Type 2 astrocytes, a major component of the mature optic nerve, were GFAP-positive, A2B5-positive and laminin-negative. An extract of developing optic nerve was analyzed by immunoblot along with laminin purified from Engelbreth-Holm-Swarm (EHS) sarcoma. Purified laminin ran with SDS-PAGE under reducing conditions as 2 bands with Mrs of 200,000 and 4000,000. Both bands reacted with antibodies to laminin. A low-salt extraction of whole optic nerve from E18 rats resulted in 2 bands with the same Mr as seen with laminin from EHS sarcoma. When only the inside of the optic nerve (which lacked the basal lamina and meninges that surround the outside) was processed, there was a dark 200,000 D band, but the 400,000 D band was virtually absent. These results are consistent with the hypothesis that laminin, or a variant form of laminin, serves as a substrate for retinal axon growth in the developing rat optic nerve.

Animals↗
PubMed1987

Standardized A-scan echography in optic nerve disease.

This study documents the results of standardized A-scan examinations performed in 59 cases of optic nerve lesions (15 perioptic meningiomas, four gliomas, 15 acute neuritides, ten optic atrophies, five ischemic optic neuropathies, five acute central retinal vein occlusions, five traumatic optic neuropathies), as compared with 73 normal optic nerves. Analysis included the assessment of reflectivity (spike height) and nerve width (maximal diameter) with the patient fixating in primary gaze and 30 degrees of eccentric gaze; measurements were obtained from the anterior one third and posterior one third of the optic nerves. Increased nerve diameters could be distinguished as noncompressible (a negative 30 degrees test) when due to tumor, or compressible (a positive 30 degrees test) when due to increased subarachnoid fluid, as exemplified by inflammatory optic neuritis or traumatic neuropathy. Moreover, reflectivity patterns regularly differentiated meningioma (medium reflectivity) from optic glioma (low reflectivity). Neither ischemic neuropathy nor vein occlusion altered optic nerve diameter. These results indicate that echographically defined optic nerve diameter, compressibility in eccentric gaze, and reflectivity patterns can be used to effectively distinguish among causes of chronic optic atrophy (tumor vs remote neuropathy) and disc edema (tumor vs neuritis vs ischemic neuropathy).

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