Blood supply of the optic nerve head and its role in optic atrophy, glaucoma, and oedema of the optic disc.
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Adolescent↗
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Topographic disorganization of the optic tracts following long-term optic nerve regeneration: a quantitative image analysis study.
Experiments were designed to find the degree to which regenerated optic axons occupied their previous locations in the optic tracts. Following optic nerve crush and regeneration, either the dorsal, ventral, peripheral, temporal, or nasal part of the retina was ablated. The axons of the remaining retinal ganglion cells (RGCs) were labeled with cobalt. Density of the regenerated dorsal and ventral axons in the dorsal vs. ventral optic tracts was determined digitally. In addition, we determined the density of temporal and nasal axons in the temporal vs. nasal compartments of each optic tract and the density of central axons in the central vs. peripheral compartments of both optic tracts. Regenerated axons were not distributed randomly in the optic tracts. Instead, they were slightly but, significantly biased toward growing through the tract or compartment that they had occupied previously. Still, the pathway specificity exhibited by the regenerated axons was closer to random than it was to the pathway specificity seen in normal animals. Dorsal, ventral, and central RGC axons were significantly better localized to their correct tract or compartment than were temporal or nasal RGC axons. Also, over time, dorsal and ventral axons tended to disappear from incorrectly chosen optic tracts. The slight bias toward choosing the appropriate optic tract or optic tract compartment may be enough to account for the topographic specificity of the regenerated retinotectal projection. Near-randomness of the axonal positions in the tracts argues against the presence of any specific guidance cues in the optic tracts of adult animals. Axonal density was highest in the correct compartment and diminished progressively with increasing distance into the incorrect compartment. Such a gradient of axonal density suggests that regenerating axons "drift" away from their previous positions in the optic pathways.
Animals↗
Distribution of membrane phospholipids in the rabbit neural retina, optic nerve head and optic nerve.
Since diseases of the neural retina and optic nerve can result in alteration of biological membranes, this study determines similarities and differences in the membrane phospholipid content of the neural retina, optic nerve head, and optic nerve to serve as baseline data. Neural retina, optic nerve head, and optic nerve were dissected, isolated as 5 sets from 20 rabbits and frozen in liquid N2. Separate pooled-tissue extracts were prepared for each set of tissues and phosphorus-31 nuclear magnetic resonance (31P NMR) analyses performed. Ten phospholipids were quantified (respective neural retina, optic nerve head, and optic nerve mole % are given for the 5 major phospholipids detected): phosphatidylcholine (PC), 44.61, 27.67, 26.40; PC plasmalogen or alkylacyl PC (CPLIP); phosphatidylinositol (PI); sphingomyelin (SM); phosphatidylserine (PS), 12.63, 14.77, 15.09; phosphatidylethanolamine (PE), 21.21, 9.59, 8.69; PE plasmalogen (EPLAS), 11.07, 30.96, 33.93; an unidentified (unknown) phospholipid (U) at the chemical-shift value of 0.13 ppm; diphosphatidylglycerol (DPG); and phosphatidic acid (PA), 0.46, 2.92, 1.57. Significant differences between the various tissues were determined by the one-way analysis of variance, using a Scheffé range value of P < 0.05. The neural retina in all phospholipids detected except for the uncharacterized (unknown) phospholipid was significantly different from the optic nerve head tissue. The optic nerve head was significantly different from the optic nerve in PC, CPLIP, PE, EPLAS, U, DPG, and PA. The data provide a baseline for studies on pathologically changed neural retina, optic nerve head, and optic nerve.
Animals↗
Synchrony dual-optic accommodating intraocular lens. Part 1: optical and biomechanical principles and design considerations.
PURPOSE: To describe a dual-optic accommodating intraocular lens (IOL) based on theoretical considerations. SETTING: University and independent research group. METHODS: Ray-tracing analysis using optical modeling software (ZEMAXTM, Focus Software Inc., Tucson, Ariz) in a theoretical model eye was used to analyze lens configurations to optimize the accommodative and magnification effects of axial lens displacement. Finite-element modelling using a commercially available PC-based software package (COSMOS DesignSTAR) was applied to design the biomechanical parameters of the inter-optic articulations and optics. RESULTS: Ray-tracing analysis indicated that a dual-optic design with a high plus-powered front optic coupled to a minus posterior optic produced greater change in conjugation power of the eye compared to a single-optic intraocular lens and that magnification effects were unlikely to account for improved near vision. Finite-element modelling indicated that the 2 optics can be linked by spring-loaded haptics that allow anterior and posterior axial displacement of the front optic in response to changes in ciliary body tone and capsular tension. CONCLUSION: A dual-optic design linked by spring haptics increases the accommodative effect of axial optic displacement with minimal magnification effect and has promise for improving the performance of accommodative intraocular lenses.
Accommodation, Ocular↗
Optical coherence tomography in optic disk pit maculopathy treated by the macular buckling procedure.
PURPOSE: To report optical coherence tomography in optic disk pit maculopathy treated with macular scleral buckling procedure. METHODS: Twenty six eyes (26 patients) with optic disk pit maculopathy were treated with macular buckling procedure and evaluated with optical coherence tomography. In group 1, five eyes were evaluated with optical coherence tomography before and after macular buckling procedure. In group 2, 21 eyes were evaluated with optical coherence tomography after macular buckling procedure. With optical coherence tomography, cross-sectional, horizontal retinal images were obtained through the fovea and optic disk pit. RESULTS: In group 1, four of five eyes showed absorption of intraretinal fluid 7 to 9 months after macular buckling procedure. After absorption of fluid, retinal thickness in the foveal center ranged from 128 to 178 microm. In one eye the channel from optic disk to fovea reopened and fluid reappeared. In group 2, 20 of 21 eyes showed absorption of intraretinal schisis and subretinal fluid after macular buckling procedure. After absorption of fluid, retinal thickness in the foveal center ranged from 119 to 216 microm. CONCLUSIONS: In optic disk pit maculopathy, optical coherence tomography enabled morphologic assessment of the retina before and after macular buckling procedure. In the successfully treated cases the permanent closure of the connection between the optic disk pit and the intraretinal schisis was demonstrated. Eventual disappearance of schisis and subretinal fluid was depicted. It was also proved that the thickness of the macula returned to normal and visual acuity improved.
Adolescent↗
Long-term outcome of optic nerve encasement and optic nerve decompression in patients with fibrous dysplasia: risk factors for blindness and safety of observation.
OBJECTIVE: Fibrous dysplasia (FD) of bone may occur solely as a skeletal condition or it may occur in association with extraskeletal manifestations, including growth hormone (GH) excess. Uncertainty exists as to the management of FD involving the optic nerves. In an effort to clarify management, the authors studied a large population of patients. METHODS: One hundred four patients underwent an evaluation that included review of records, endocrine testing, cranial computed tomography, and neuro-ophthalmological examination. RESULTS: Ninety-one of 104 patients had craniofacial FD; complete records were available for 87 patients (174 nerves). Seventeen percent of the optic nerves were less than 50% encased, 22% were 50 to 99% encased, and 61% were 100% encased. Twelve percent of the nerves that were 100% encased showed evidence of optic neuropathy, but 88% did not. The group with optic neuropathy was not older than the group without. Patients with GH excess were significantly more likely to have nerves that were 100% encased (relative risk, 4.1; 95% confidence interval, 1.5-11.1; P = 0.0017) and to have optic neuropathy (relative risk, 3.8; 95% confidence interval, 2.0-7.1; P = 0.0019). Six prophylactic optic nerve decompressions were performed; in five patients, vision was stable after surgery, and one patient was blind after surgery. Thirteen interventional optic nerve decompression procedures were performed; six of the 13 patients showed some improvement and seven of the 13 showed no improvement or worsened vision. CONCLUSION: The vast majority of optic nerves encased with FD do not exhibit symptoms of optic neuropathy and seem to be stable over time. GH excess is associated with increased risk of nerve encasement and optic neuropathy. Patients with craniofacial FD should be screened for GH excess, and optic nerve decompression should be performed only when there is objective evidence of progressive optic neuropathy.
Adolescent↗
Evaluation of inducible nitric oxide synthase in glaucomatous optic neuropathy and pressure-induced optic nerve damage.
PURPOSE: To determine whether inducible nitric oxide synthase (NOS-2) is involved in glaucomatous optic neuropathy. METHODS: Chronic elevation of rat intraocular pressure (IOP) leading to optic nerve damage was induced by episcleral injection of hypertonic saline, which caused sclerosis and blockade of aqueous humor outflow pathways. Expression of NOS-2 in the retina and optic nerve head (ONH) was evaluated by immunohistochemistry, gene array analysis, and quantitative PCR (Q-PCR). Immunohistochemistry was also used to assess the NOS-2 level in the ONH from primary open-angle glaucoma (POAG) and nonglaucomatous human eyes. Finally, an NOS-2 inhibitor, aminoguanidine, administered orally in the drinking water, was tested for its effect on optic nerve injury in rats with ocular hypertension. RESULTS: Chronically elevated IOP in the rat produced optic nerve damage that correlated with pressure change (r(2) = 0.77), but did not increase NOS-2 immunoreactivity in the optic nerve, ONH, or ganglion cell layer. Retinal and ONH NOS-2 mRNA levels did not correlate with either IOP level or severity of optic nerve injury. Similarly, there was no difference in NOS-2 immunoreactivity in the optic nerve or ONH between POAG and nonglaucomatous eyes. Furthermore, aminoguanidine treatment did not affect the development of pressure-induced optic neuropathy in the rat. CONCLUSIONS: As demonstrated by several independent methods, glaucomatous optic neuropathy was not associated with a significant change in the expression of NOS-2 in the retina, ONH, or optic nerve.
Aged↗
High-resolution magnetic resonance imaging of the intraorbital optic nerve and subarachnoid space in patients with papilledema and optic atrophy.
OBJECTIVE: To evaluate the orbital portion of the optic nerve and the subarachnoid space using fast spin-echo magnetic resonance imaging in normal subjects and in patients with papilledema or optic atrophy. DESIGN: Measurements of the optic nerve complex on coronal images were made using high-resolution magnetic resonance imaging with fast spin-echo sequences. PATIENTS: Twenty-one patients, including 5 patients with papilledema due to congenital hydrocephalus, intracranial tumors, or meningitis, as well as 16 patients with optic atrophy, were studied. Sixteen healthy volunteers served as controls. MAIN OUTCOME MEASURES: The longitudinal diameter of the optic nerve, the longitudinal outer diameter of the subarachnoid space, the diameter ratio, and the area of the subarachnoid space were determined. RESULTS: In normal subjects, the ring-shaped area of high signal intensity that represented the subarachnoid space was widest behind the globe, then narrowed toward the orbital apex. In patients with papilledema, the area of the subarachnoid space was markedly dilated, the optic nerve was compressed, and the nerve sheath was widened, resulting in a small diameter ratio compared with that of controls. Patients with pallor of the temporal aspect of the optic disc appeared to exhibit dilation of the subarachnoid space; the size of the optic nerve was decreased more than that of the nerve sheath, resulting in a small diameter ratio compared with controls. Patients with complete pallor of the disc, however, exhibited hyperintense optic nerve complexes without a ring-shaped appearance toward the orbital apex. CONCLUSION: Fast spin-echo magnetic resonance imaging appears useful for objectively evaluating the optic nerve and surrounding subarachnoid space in patients with papilledema and optic atrophy.
Adolescent↗
Visual system of the channel catfish (Ictalurus punctatus): III. Fiber order in the optic nerve and optic tract.
In channel catfish the ganglion cell axons leave the retina via a ring of approximately 13 separate optic papillae. Each papilla serves an area of retina extending from the central zone of the retina to the periphery. Papillae located at a dorsal position in the ring serve exclusively dorsal retina. Ventrally located papillae, however, have an exaggerated peripheral retinal representation, so that they serve mostly ventral retina but also some areas of peripheral retina dorsal to the nasal and temporal poles. The ganglion cell axon bundles departing from the retina via individual papillae were labelled with horseradish peroxidase, and sections of the optic pathway were examined to reveal the topographic organization of the fibers. The topographic order of the optic nerve was dissimilar to that of cichlids and goldfish. Fibers from individual papillae remained together throughout the optic nerve. Close to the optic nerve head, the papillae were arranged as a continuum around the U-shaped optic nerve, without the discontinuity in the representation of the ventral retina seen in other fish. Fibers associated with the dorsal papillae were located at the tip of the caudolateral arm of the U, and fibers from ventral papillae were on the rostromedial arm. Fibers from nasally and temporally located papillae were found on the base of the U. By the level of the optic chiasm the U shape had flattened out but retained the relative ordering of the papillae. Rotation of the nerve as it became the optic tract brought the representation of the ventral papillae to the dorsal pole of the tract, and the dorsal papillae to the ventral tract. It was only in the optic tract that rearrangement of fibers became apparent. As described above, the axons of some ganglion cells in dorsal, peripheral retina left the retina and travelled through the optic nerve with axons from extreme ventral retina. In the optic tract, these dorsal fibers joined the main body of fibers from the dorsal retina. The significance of these observations for theories of fiber rearrangement is discussed.
Animals↗
Optic cup deepening spatially correlated with optic nerve damage in focal normal-pressure glaucoma.
PURPOSE: To evaluate whether deepening of the optic cup in patients with focal normal-pressure glaucoma is correlated with the location of most marked loss of neuroretinal rim and visual field. METHODS: Using morphometric evaluation of color stereo optic disc photographs of 102 eyes of 65 patients with focal normal-pressure glaucoma, the superior half of the optic disc was compared with the inferior half. RESULTS: In eyes in which the optic cup was deepest in the inferior half of the disc, the most pronounced rim loss was located inferiorly significantly more often than superiorly, and the most marked visual field loss was located superiorly significantly more often than inferiorly. In eyes in which the optic cup was deepest in the superior half of the disc, the most pronounced rim loss was located superiorly significantly more often than inferiorly, and the most marked visual field loss was located inferiorly significantly more often than superiorly. Correspondingly, in eyes in which the most marked rim loss was located inferiorly, the deepest optic cup part was located inferiorly significantly more often than superiorly, and vice versa. CONCLUSION: In focal normal-pressure glaucoma, location of the most marked deepening of the optic cup is spatially correlated with the location of most pronounced neuroretinal rim loss and visual field damage. Because high-pressure glaucoma is typically associated with optic cup deepening and vascular optic nerve damage is associated with optic cup flattening, the spatial correlation between focal optic nerve damage and focal cup deepening may suggest the presence of a pathogenetic aspect in both high-pressure glaucoma and focal normal-pressure glaucoma.
Adult↗
Postembryonic changes in the optic primordia and optic bud in the flesh fly Sarcophaga ruficornis fabr. (Diptera: Sarcophagidae).
Differentiation of the optic lobe anlagen begin in the brain of second instar. Each is an elongated disc of cortical cells placed on the dorsolateral border of each protocerebrum. In the late second instar the disc elongates and its two ends bend inwards which gradually separate from the central region, thus giving three imaginal discs. The protocerebral neuropile extends into these discs and medulla interna and externa are formed. The rudiments of compound eyes (cephalic complex) appear in the early laid larva. These are attached with the brain and pharyngeal wall separately. The posterior portion of cephalic complex (optic bud), after establishing a nervous association with the central optic lobe anlage (lamina ganglionaris), forms the compound eye. Ech optic bud is attached to the brain by a non-nervous stalk. The epiblast cells of the optic bud do not migrate into the brain and the lamina is formed by the proliferation of the central imaginal disc. The reorientation of the optic lobe anlagen starts in the late third instar and the medulla interna divides into two unequal lobes. In 2 day pupa the nerve fibres from the lamina travel into the optic stalk and the optic nerve is formed. The epiblast cells of the optic bud differentiate to form a peripheral epithelial layer which becomes pigmented and gets apposed to the lateral boundary of the brain. The central epiblast cells of the optic bud form several ommatidia. The optic nerve degenerates gradually and various components of the compound eye are formed by the epiblast cells. Chiasm internum is present but chiasm externum is absent.
Animals↗
Experimental injury of the optic nerve with optic disc swelling.
An ultrastructural study utilizing horseradish peroxidase was performed to determine the mechanism and consequences of leakage of vascular protein following injury of the optic nerve. Unilateral optic nerve injuries were produced in four rhesus monkeys by making a cautery lesion on the retrobulbar portion of the optic nerve. Optic disc changes were followed with stereo fundus photography and fluorescein angiography. Three to 14 days after injury horseradish peroxidase was given intravenously and the tissue was prepared for electron microscopy, including serial sections of selected tissue blocks. Fundus photography and fluorescein angiography showed edema of the optic disc in two animals. There was leakage of horseradish peroxidase into the optic nerve head from the optic nerve lesion and the peripapillary choriocapillaris. Although the pathway of horseradish peroxidase leakage in the injured optic nerve was not entirely clear, serial sections indicated intraendothelial channels as one possible route. Alterations of the optic nerve head were confined to the axon segments anterior to the injury, and included aggregation of mitochondria, disruption of neurotubules, and swelling. These findings suggest that optic nerve injury produces damming of axoplasmic flow and that swelling of the optic nerve head is the result of axon enlargement.
Animals↗
Regeneration in the optic nerve of adult rats: influences of cultured astrocytes and optic nerve grafts of different ontogenetic stages.
We have studied the effects of transplanted optic nerves of different ontogenetic stages (E19 to adult), and cultured astrocytes from P2 cerebral cortex on the regeneration of axons in the optic nerve of adult rats. Regeneration was visualized by anterograde tracing with rhodamine-iso-thiocyanate. Grafts were identified with Nuclear Yellow. Astroglia within both the cut optic nerve and the transplants were detected by anti-glial fibrillary acidic protein staining. In control animals (cut optic nerve, 2-3 mm behind the optic disc), only a few neurites were found 15 days after the operation which grew randomly for short distances into the surrounding meningeal sheaths. Perinatal (E19 to P2) optic nerves induced a massive outgrowth of RITC-filled axons from the host optic nerve. The regenerating fibres grew for up to 3 mm towards the graft, ahead of glial fibrillary acidic protein-positive astroglia emanating from the host optic nerve that seemed to follow them. Although the regenerating fibres reached the grafts, they did not penetrate them. Optic nerve grafts of increasing age elicited smaller growth responses; e.g. grafts from P8 promoted only a very limited (several 100 microns) growth response, grafts from P12 and later induced outgrowth comparable with that of control animals. Grafted astrocytes from P2 donors that had previously been grown in culture, were also capable of promoting outgrowth of rhodamine-iso-thiocyanate-filled axons from the host optic nerve. These findings suggest that only astrocytes at an immature stage of differentiation are capable of inducing axon growth from the adult optic nerve. Furthermore, the absence of an obvious cellular bridge between host and graft suggests that the graft effect is probably mediated by the release of astroglia-derived diffusible neurite growth promoting factors.
Animals↗
Macrophages during retina and optic nerve development in the mouse embryo: relationship to cell death and optic fibres.
We compared the spatial and temporal patterns of distribution of macrophages, with patterns of naturally occurring cell death and optic fibre growth during early retina and optic nerve development, in the mouse. We used embryos between day 10 of embryogenesis (E10; before the first optic fibres are generated in the retina) and E13 (when the first optic fibres have crossed the chiasmatic anlage). The macrophages and optic axons were identified by immunocytochemistry, and the apoptotic cells were detected by the TUNEL technique, which specifically labels fragmented DNA. Cell death was observed in the retina and the optic stalk long before the first optic axons appeared in either region. Subsequently, specialized F4/80-positive phagocytes were detected in chronological and topographical coincidence with cell death, which disappeared progressively. As development proceeded, the pioneer ganglion cell axons reached the regions where the macrophages were located. As the number of optic fibres increased, the macrophages disappeared. Therefore, cell death, accompanied by macrophages, preceded the growth of fibres in the retina and the optic nerve. Moreover, these macrophages synthesized NGF and the optic axons were p75 neurotrophin receptor (p75(NTR))- and TrkA-positive. These findings suggest that macrophages may be involved in optic axon guidance and fasciculation.
Animals↗
Hypoplastic optic nerves studied with B-scan ultrasonography and axial tomography of the optic canals.
Radiologic studies of the optic foramina in cases of optic nerve hypoplasia have been inconsistent, some authors reporting normal foramina, others finding small foramina. The technique of axial tomography of the optic canals has been found more useful in this regard than plain foramen views, and has demonstrated small canals in cases of optic nerve hypoplasia. A case of bilateral hypoplasia is presented in which the discs were one half normal size, the optic nerves measured 2 mm in diameter on B-scan ultrasonography, and the optic canals were about 4 mm in diameter radiographically on the axial tomograms. These measurements are compared with normals of 4 to 4.5 mm for scans of the optic nerve, and a reported average optic canal width of 5.5 mm. A second case of less severe hypoplasia also presented a small ultrasonic nerve pattern of 3.5 mm. With the techniques of ultrasonography and axial tomography, the course of hypoplasic nerves can be followed from the level of the retina to the optic chiasm posteriorly. It is suggested that the optic canal dimensions correspond closely to the size of the optic nerve in cases of hypoplasia. When the nerve is only slightly hypoplastic the radiographic change in foramen or canal dimensions may not be detectable. Reasonably accurate measurements of the nerve may be more easily obtained with ultrasound.
Adolescent↗
Detection of optic nerve atrophy following a single episode of unilateral optic neuritis by MRI using a fat-saturated short-echo fast FLAIR sequence.
We describe an MRI technique for quantifying optic nerve atrophy resulting from a single episode of unilateral optic neuritis. We imaged 17 patients, with a median time since onset of optic neuritis of 21 months (range 3-81 months), using a coronal-oblique fat-saturated short-echo fast fluid-attenuated inversion-recovery (sTE fFLAIR) sequence. The mean cross-sectional area of the intraorbital portion of the optic nerves was calculated by a blinded observer from five consecutive 3 mm slices from the orbital apex forwards using a semiautomated contouring technique and compared with data from 16 controls. The mean optic nerve area was 11.2 mm2 in the affected eye of the patients, 12.9 mm2 in the contralateral eye (P = 0.006 compared to the affected eye) and 12.8 mm2 in controls (P = 0.03 compared to the affected eyes). There was a significant negative correlation between disease duration and the size of the affected optic nerve (r = -0.59, P = 0.012). The measurement coefficient of variation was 4.8%. The sTE fFLAIR sequence enables measurement of optic nerve area with sufficient reproducibility to show optic nerve atrophy following a single episode of unilateral optic neuritis. The correlation of increasing optic nerve atrophy with disease duration would be consistent with ongoing axonal loss in a persistently demyelinated lesion, or Wallerian degeneration following axonal damage during the acute inflammatory phase.
Adult↗
Hereditary optic neuropathies: from the mitochondria to the optic nerve.
PURPOSE: To review our current knowledge of inherited optic neuropathies. DESIGN: Perspective. METHODS: Literature review. RESULTS: The hereditary optic neuropathies consist of a group of disorders in which optic nerve dysfunction figures solely or prominently and direct inheritance is clinically or genetically proven. The most common of these disorders are autosomal dominant optic atrophy (Kjers' disease) and maternally-inherited Leber's hereditary optic neuropathy. Other inherited neurologic and systemic syndromic diseases will frequently manifest optic neuropathy. A selective vulnerability of the optic nerve to perturbations in mitochondrial function may underlie a final common pathway among these disorders. CONCLUSIONS: The ophthalmologist should be familiar with the clinical characteristics and diagnosis of the hereditary optic neuropathies. Recent advances in our understanding of the underlying pathophysiology of the inherited optic neuropathies may provide insight into their treatment and the treatment of acquired optic nerve disorders.
Humans↗
Use of magnetic resonance imaging to differentiate optic neuritis and nonarteritic anterior ischemic optic neuropathy.
OBJECTIVE: To determine if magnetic resonance imaging (MRI) of the optic nerves obtained during the acute phase can distinguish patients with optic neuritis (ON) from those with nonarteritic anterior ischemic optic neuropathy (NAION). DESIGN: Retrospective, neuroradiologic, observational study. PARTICIPANTS: Sixty-four patients diagnosed as having either ON or NAION who were diagnosed by clinical criteria and imaged by MRI. METHODS: Demographic information on the MRI scans was masked and the patients were presented randomly and in a blinded fashion to a neuroradiologist (JDR) for determination of abnormalities. Reproducibility was assessed by presenting 10 of the scans a second time to the same neuroradiologist. MAIN OUTCOME MEASURES: The presence or absence and location of abnormal MRI signals of the optic nerve. RESULTS: Evaluation of reproducibility revealed identical interpretations of the ten scans submitted a second time. The optic nerve was abnormal in the clinically affected eye in 31 of the 32 ON patients but in only 5 of the 32 NAION patients. Thirty of the 31 ON patients who received gadolinium had enhancement, and 27 of the 32 ON patients had increased short T(1) inversion recovery signal in the clinically affected optic nerve. The five NAION patients with abnormal scans in the clinically affected eye had increased short T(1) inversion recovery signal, and in two of these, there also was enhancement of the optic nerve. For the ON patients, enhancement involved the entire length of the intraorbital optic nerve in 18 cases and the intracranial segment of the optic nerve in 19 cases. CONCLUSIONS: Our study shows that MRI scanning of the optic nerve shows significantly different results between patients clinically diagnosed with either ON or NAION.
Acute Disease↗