Clinical pupillary symptoms in lesions of the optic nerve, optic chiasm, and optic tract.
Explore the source record for details and available documents.
Disease↗
SEARCH · Search PubMed
Results for “OPTICS”
Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Human optic nerve fiber count and optic disc size.
In the optic nerve head, the optic nerve fibers are represented by the neuroretinal rim. The rim area showing a high interindividual variability is positively correlated with the optic disc size. This study was performed to address the question of whether, in addition to having a larger neuroretinal rim, eyes with large optic discs also have a higher count of optic nerve fibers compared to eyes with small optic nerve heads. Histologic semithin sections of 72 optic nerves of 56 cornea donors were histomorphometrically evaluated using a computerized image analyzer. The optic nerve fiber count increased significantly (P = 0.01) with enlarging optic disc size. The nerve fiber count was positively correlated with the retrobulbar optic nerve cross section area. It decreased with advancing age, with a mean annual loss of about 4,000 fibers. The nerve fiber density per disc area decreased with increasing optic disc area. Mean and median of the minimal nerve fiber diameter was larger in older subjects. The results may indicate that the optic nerve fiber count, and the anatomic reserve capacity in progressive optic neuropathies, are higher in eyes with large optic discs than in eyes with small optic nerve heads. The optic nerve fiber population decreased with advancing age. This is important for progression, pseudoprogression, and prognosis of optic neuropathies. Optic nerve fiber crowding is more marked in eyes with small optic discs than in eyes with large optic nerve heads. The age-related loss of predominantly small optic nerve fibers can potentiate the optic nerve atrophy in glaucoma and Alzheimer's disease, with both damaging preferentially large axons.
Adult↗
[Three essential elements of glaucomatous optic nerve damage and discrimination of optic nerve rim loss].
Three essential elements of glaucomatous optic nerve damages are optic nerve rim loss, retinal nerve fiber layer defects (RNFLD) and optic disc linear hemorrhages. It's suggested that if there are two positive signs detected among the three elements, the diagnosis of the glaucomatous optic nerve damages can be established. There is no definitely described how to identify optic nerve rim loss in the previous textbooks, therefore it is important to know about the morphological features of the physical optic nerve rim and influence factors before discrimination of optic nerve rim loss. Most of physical optic nerve rim are in accordance with ISNT rule, physical large optic cups are also accord with ISNT rule. Exceptional cases exist in two patterns, optic nerve rim loss or normal optic nerve rim morphological variances. The latter includes part of small discs, horizontally oval optic discs, the position of the central retinal vessel trunk and the titled optic discs which affect the morphological feature of optic nerve rim as well. In some small discs, the width of inferior rim is narrower than that of superior rim, therefore, the inferior or the superior rim loss can be evaluated by comparison with nasal rim width. Concerning horizontal oval optic discs, the width of inferior rim and superior rim should be compared to evaluate whether there is the optic nerve rim loss. If those patterns of normal optic nerve rim variances can be recognized, it is not difficult to find the presence of the optic nerve rim loss. However, not all of the optic nerve rim loss is due to glaucomatous optic nerve damages, non-glaucomatous optic nerve damage should be distinguished.
Diagnosis, Differential↗
Pseudophakic accommodation with translation lenses--dual optic vs mono optic.
PURPOSE: To investigate the pseudophakic accommodation effect in dual and mono optic translation accommodative intraocular lenses (AIOL) using linear matrix methods in the paraxial space. METHODS: Dual (anterior optic of power +32 D linked to a compensatory posterior optic of negative power) and mono lens power was determined in the non-accommodated state using linear geometric optics based on the Gullstrand model eye. The position of the AIOL was calculated from a regression formula. Pseudophakic accommodation was assessed with three systems: (1) forward shift of the mono optic lens, (2) anterior translation of the anterior optic in the dual optic lens system with an unchanged position of the posterior minus lens and (3) symmetrical anterior and posterior translation of the anterior and posterior lens. The Gullstrand model eye was modified by changing the axial length (and proportionally changing the phakic anterior chamber depth) to investigate the accommodative effect in myopic and hyperopic eyes. RESULTS: The dual optic lens system (2) yields a nearly constant accommodation amplitude of 2.4-2.5 D mm(-1) movement over the total range of axial lengths. The mono optic lens (1) provides a higher accommodative effect only in extremely short eyes (high refractive power of the lens), whereas for normal eyes (1.4-1.5 D mm(-1) movement) and for long (myopic) eyes the accommodative effect is much less than the dual optic lens. The dual optic lens system under condition (3) yields less accommodation amplitude compared with the dual optic system under condition (2) over the total range of axial length but provides higher accommodation amplitude compared with the mono optic lens system (1) with axial lengths greater than 22.3 mm (lens power 25.5 D). In the accommodated state, with lens translation of 1 mm, the absolute value of the lateral magnification increases with the refractive power of the mono optic lens (1) and decreases in both dual optic lens systems (under conditions 2 and 3). CONCLUSIONS: A mathematical strategy is presented for calculation of the accommodative effect of mono-optic and dual optic AIOL. The dual optic lens yielded a nearly constant accommodation amplitude of about 2.4-2.5 D mm(-1) translation, whereas the mono optic lens yielded an accommodative response of <2 D mm(-1) translation in long myopic or normal eyes. Only in extremely short eyes is the accommodative amplitude of the mono-optic lens higher than the dual optic lens.
Accommodation, Ocular↗
[Optic neuritis--from diagnosis to optic nerve transplantation].
Optic neuritis is a clinical syndrome resulting from inflammation, demyelination, or infection of the optic nerve. Its diagnosis and treatment are complicated. In 1884, Nettleship first reported 28 cases of optic neuritis whose clinical symptoms have been accepted up to the present without any change. On the other hand, the development of diagnostic procedures and steroid therapy have also altered the clinical features of optic neuritis. Among several developed diagnostic procedures, the visually evoked cortical potential (VECP) has become a good tool to prove the impairment of the optic nerve. In 1971, we reported a decrease of threshold intensity required to evoke VECPs in optic neuritis patients whose visual acuity was relatively well preserved. In the same year, Halliday et al. reported that pattern VECP (PVECP) was delayed in 93% of patients with multiple sclerosis (MS) without optic neuritis. Stimulated by this report, a great number of studies appeared to show the usefulness of PVECP in the diagnosis of MS. However, few of these studies gave descriptions of ophthalmic findings. PVECP later become known to be closely related with ophthalmic conditions. In the ophthalmological field, we reported the influence of pupillary size, accommodation power, refractive powers, eccentricity of stimulated retinal area, retinal luminance, contrast, wavelengths, spatial and temporal frequencies, stimulus field etc. On the basis of our results, we developed a television display system in 1975 and applied it clinically. In the present study, we reviewed the medical records of a total of 272 cases of optic neuritis who presented in our clinic between 1978 and 1999. In the diagnostic, therapeutic point of view in relation with the data of other countries, the study was important regarding the racial differences and recent conceptions of optic neuritis. The results showed that there were no racial difference in optic neuritis as had been thought. The development from optic neuritis to multiple sclerosis was not less than in Caucasian patients. Regarding steroid therapy, we found that the most effective method was sub-Tenon injection. For cases which recur and progress to optic atrophy, optic nerve transplantation will be needed. Therefore, we have been studying the reconstruction of the optic nerve in Wister rats. We experimentally damaged the ganglion cells by causing ischemic retina with ligation of the ophthalmic artery and cutting the optic nerve just behind the eyeball. To prevent the apoptosis of ganglion cells, we injected various neurotrophic factors such as BDNF, GDNF, and HSP 27 into the vitreous. For effective injection of DNA, electropolation was applied and the best condition for avoiding apoptosis was chosen. Further, in Mx-c-fos transgenic mice, we found that regeneration of ganglion cells was inhibited. Based on the rescue study of the ganglion cells, optic nerve transplantation was performed using an artificial graft in which cultured Schwann cells from the ischiatic nerve, BDNF, CNTF, insulin, and forscolin were compound and bridged to the superior colliculus. The results showed a regeneration rate of the optic nerve axon of 15%. This rate was much higher than in other reports. Keratoplasty and intraocular lens implantation had a relatively long history of research before achieving clinical success. We believe that optic nerve transplantation will one day be successful in clinical treatment in the same way.
Adult↗
The optic nerve sheath on MRI in acute optic neuritis.
Optic nerve sheath dilatation or gadolinium-enhancement on magnetic resonance imaging in acute optic neuritis have been previously reported but have been thought to be rare occurrences. This study recruited 33 patients with acute unilateral optic neuritis. All had their optic nerves imaged with fat-saturated fast spin-echo (FSE) imaging, and 28 had imaging before and after triple-dose gadolinium-enhanced fat-saturated T(1)-weighted imaging. Follow-up imaging was performed on 20 patients (15 following gadolinium). A dilated subarachnoid space at the anterior end of the symptomatic optic nerve on FSE imaging was seen in 15/33 cases. In three of these cases, dilatation was visible on short-term follow-up. Optic nerve sheath enhancement was seen in 21/28 cases acutely: seven at the anterior end of the lesion only, five at the posterior end only and nine at both ends. Optic sheath enhancement was seen in 13 patients on follow-up. This study suggests that optic nerve sheath dilatation on FSE images and optic nerve sheath enhancement on triple-dose gadolinium-enhanced images are common findings in acute optic neuritis. Optic nerve sheath dilatation may be due to inflammation of the optic nerve, with its associated swelling, interrupting the communication between the subarachnoid space of the diseased optic nerve and the chiasmal cistern. Optic nerve sheath enhancement suggests that meningeal inflammation occurs in optic neuritis, in agreement with pathological studies of both optic neuritis and multiple sclerosis.
Acute Disease↗
[Recovery of visual field defects in ischemic optic neuropathy and idiopathic optic neuritis].
Fifty-four eyes of 41 patients with optic nerve disease demonstrating acute visual field defects without any traumatic, compressive, or other known etiology were classified into four categories. Those showing poor recovery of visual field defects were ischemic optic neuropathy which was subclassified into either anterior ischemic optic neuropathy (AION) or posterior ischemic optic neuropathy (PION) according to the ophthalmoscopic changes in the optic nerve head. Those showing good recovery of visual field defects were idiopathic optic neuritis which was subclassified into either papillitis or retrobulbar neuritis according to the ophthalmoscopic pathology of the optic disc. Patients with ischemic optic neuropathy were significantly older than those with optic neuritis. All eyes with optic neuritis showed good recovery of vision, whereas those with ischemic optic neuropathy showed varying outcomes of vision. With regard to the pattern of field defect, central or paracentral scotoma was predominant in all but eyes with AION in which altitude defect predominated. Pale swelling of the optic nerve head and angiographic evidence of circulatory disturbance in the optic disc or adjacent choroid were common findings in eyes with AION, whereas such findings were never observed in eyes with papillitis. The amplitude of pattern visual evoked potential was significantly lower in eyes with PION than in those with retrobulbar optic neuritis. Four patients classified as optic neuritis developed into multiple sclerosis in the follow-up study. It was concluded that poor recovery of visual field defect is one of the most convincing evidences for the diagnosis of ischemic optic neuropathy.
Adult↗
Optic nerve fiber count and diameter of the retrobulbar optic nerve in normal and glaucomatous eyes.
BACKGROUND: The caliber of the retrobulbar optic nerve and the count of optic nerve fibers vary considerably in normals. The diameter of the retrobulbar optic nerve also decreases with optic nerve atrophy. This study aimed to determine the relationship between the caliber of the optic nerve and the optic nerve fiber count. METHODS: We counted the optic nerve fibers and measured the diameter of histological cross sections of the optic nerve for 56 normal subjects and 23 patients with absolute glaucoma. RESULTS: The optic nerve fiber count increased significantly (P < 0.0001) by 777,000 fibers for every millimeter increase in retrobulbar optic nerve diameter, starting at a baseline diameter of 1.89 mm. CONCLUSION: Using this linear regression equation, the optic nerve fiber count can be estimated in routine histology by measuring the optic nerve diameter. Taking into account a fixation-induced tissue shrinkage, this method may also give some indication of the optic nerve fiber count intravitally, when, for eyes with opaque optic media, the diameter of the retrobulbar optic nerve has been measured by imaging techniques. Greater retrobulbar optic nerve caliber may indicate greater structural reserve capacity.
Adult↗
A serial MRI study following optic nerve mean area in acute optic neuritis.
This study assessed optic nerve mean area on serial MRI in a cohort of patients with a first episode of acute unilateral optic neuritis to assess the effects of a single acute inflammatory demyelinating lesion. Twenty-nine patients with a median delay from onset of visual symptoms of 13 days (range 7-24 days) were recruited. After a clinical examination and visual evoked potential (VEP) measurement, each patient had their optic nerves imaged with a coronal fat-saturated short echo fast fluid-attenuated inversion recovery sequence. Twenty-one patients had serial examinations after 2, 4, 8, 12, 26 and 52 weeks. In addition, 32 control subjects had their optic nerves imaged up to three times. The mean cross-sectional area of the intra-orbital portion of each optic nerve was calculated by a blinded observer using a computer-assisted contouring technique. At baseline, the mean area of diseased optic nerves was 16.1 mm2 compared with 13.4 mm2 for healthy contralateral optic nerves (20.1% higher, P < 0.0001) and 13.6 mm2 for controls (18.4% higher, P = 0.0003). The diseased optic nerve mean area declined over time, from initial swelling to later atrophy. The mean decline at 52 weeks was -0.0018 mm2/day (95% confidence interval -0.0038 to -0.00051). At 52 weeks, the mean area of diseased optic nerves was 11.3 mm2 compared with 12.8 mm2 for healthy contralateral optic nerves (11.7% lower, P = 0.032) and 13.1 mm2 for controls (13.7% lower, P = 0.008). The 52 week diseased optic nerve mean area was not significantly affected by the baseline mean area. There was an association between baseline optic nerve mean area and logMAR visual acuity (rS = 0.46, P = 0.012) and visual field mean deviation (rS = -0.55, P = 0.002), but there was no evidence of an association between 1 year mean area and visual outcome. There was no evidence of association between baseline, rates of decline or 1 year diseased optic nerve mean areas and any of the baseline, 1 year or time-averaged VEP variables. The present study shows a consistent pattern of changes associated with individual inflammatory demyelinating lesions in the optic nerve. Acutely, there was swelling, consistent with the presence of acute inflammation, which was related to visual impairment. Over the longer term, there was loss of tissue. The lack of association between 1 year optic nerve mean area and visual outcome may reflect a mild loss of tissue, redundancy or remodelling of function.
Acute Disease↗
Imaging of the optic disc and retinal nerve fiber layer in acute optic neuritis.
PURPOSE: To demonstrate whether optical coherence tomography (OCT-3) and scanning laser ophthalmoscopy (HRT-2) can be used to measure changes of the optic disc and peripapillary retinal nerve fiber layer (RNFL) in eyes with acute retrobulbar optic neuritis that have no clinically apparent optic disc swelling. To correlate these findings with presentation magnetic resonance imaging (MRI) of the affected optic nerve. METHODS: Eight consecutive patients with acute retrobulbar optic neuritis, who had no prior optic neuritis in either eye, were prospectively investigated at presentation and at between 1 and 3 months with clinical examination, OCT-3, HRT-2. At presentation, MRI of the optic nerves were performed in 7/8 patients. RESULTS: Compared to unaffected eyes, affected eyes without clinically seen optic disc swelling at baseline, there was a non-significant trend to increased thickness in the total RNFL, superior and nasal measurements. Baseline HRT in affected eyes showed smaller mean cup to disc ratio (p=0.003) and a smaller cup area (p=0.002) compared with the unaffected eye. The MRI-demonstrated optic nerve lesion did not correlate with OCT RNFL thickening or HRT decrease of the physiological cup. Follow-up imaging of the affected eyes showed normalization of HRT cup size parameters and OCT RNFL thickness (p<0.04). At follow-up, the temporal RNFL had thinning in 7/8 affected eyes (46.8 mum, p=0.021) compared with fellow unaffected eyes (57.8 mum), which did not change. CONCLUSION: OCT-3 and HRT demonstrate mild RNFL thickening or optic disc swelling in acute optic neuritis, even when swelling is not seen clinically. OCT-3 appears to reveal measurable RNFL thinning in the temporal quadrant after retrobulbar optic neuritis, even though vision improves. RNFL imaging may be useful in future studies of residual injury after optic neuritis.
Acute Disease↗
Normal and regenerating optic fibers in goldfish tectum: HRP-EM evidence for rapid synaptogenesis and optic fiber-fiber affinity.
The distribution of normal and regenerating retinal fibers and synapses was studied on tectum in goldfish by light (LM) and electron microscopy (EM). Since labeling of the early regenerating fibers was previously reported to be difficult, a new 'cold-fill' HRP labeling protocol was developed, which labeled regenerating optic fibers and terminals on tectum as early as 14 days after nerve crush when they first arrive on tectum. In order to characterize the laminar distribution of optic afferents in normal fish and in fish regenerating for 14-240 days, EM photomontages of areas 14 microns wide by 160 microns deep through the HRP-labeled primary optic innervation layer (S-SO-SFGS) were constructed. The time points in regeneration that were examined spanned the period in which others have shown that an initially diffuse retinotopic map becomes spatially restricted. At the LM level regenerating optic fibers were restricted to the optic lamina. They reinnervated tectum in an anterior to posterior sequence as previously seen with autoradiography. In addition, at 14 days, some "pioneer" optic fascicles were found to have already grown to posterior tectum where they gave rise to branches with boutonlike terminations and growth-cone-like processes. Form the ultrastructural analysis it was clear that optic fibers and terminals observed strict laminar boundaries as they partitioned themselves in the optic laminae (S, SO and SFGS) in both normal and regenerating fish. The behavior of optic fibers was lamina specific with respect to synapse formation and the orientation of fiber outgrowth. As early as 14 days regeneration, optic fibers made synapses onto the four types of postsynaptic profiles observed in normal fish. Numerous optic terminals were labeled at 14 days, and there appeared to be no waiting period between fiber ingrowth to the SO and synapse formation in the S and SFGS. At 14-60 days, atypical synaptic contacts which appear to be nascent synapses were made by labeled optic fibers in fascicles and by growth-cone-like processes. By 21-30 days, the density of optic terminals was high and there were many more fasciculated optic fibers in the SFGS than normal as late as 350 days. These findings suggest that optic fiber lamination is highly constrained by tectal cues, that fibers rapidly regenerate many synaptic terminals before retinotopic map refinement is complete, and that fibers have a strong affinity for each other.
Animals↗
The distribution of axons according to diameter in the optic nerve and optic tract of the rat.
The distribution of axons according to diameter was examined in the optic nerve and optic tract of adult hooded rats. Observations were made on semithin sections, and measurements of axonal diameters were made on electron micrographs taken from various locations across thin sections through the optic nerve and tract. The distribution of axons by size differs markedly in the optic nerve and tract. Coarse (greater than 2 microns) and fine (less than or equal to 2 microns) axons are distributed throughout all regions of the optic nerve. In the optic tract, in contrast, coarse axons are especially dense dorsally, at the deep border of the tract, while they are absent ventrally, subjacent to the pial surface. No regions of the optic nerve contain densities of coarse axons as high as the deep nor as low as the superficial extremes of the optic tract. Nevertheless, even at the deep (dorsal) border of the optic tract, the coarse axons make up only a small minority (roughly 15%) of the total number of axons in that region. The axons 2 microns or smaller may be divisible into two overlapping, fine and intermediate, diameter classes, that are partially segregated within the optic tract, but not in the optic nerve: the distributions of axon diameters smaller than 2 microns are skewed to distinctly smaller diameters at the dorsal and ventral extremes of the optic tract, while in between, at mid-positions along the deep-to-superficial axis of the optic tract, the axon size distributions contain many more axons greater than 1 micron in diameter. These different axon diameter groups may arise from the morphologically distinct retinal ganglion cell types, and may underlie the components of the trimodal compound axon potential seen in the rat's primary optic pathway. Their partial segregation within the tract anticipates the partial segregation of their terminal arborizations within the laminae of the dorsal lateral geniculate nucleus. The rearrangement of axons into a partial segregation by size within the optic tract may indicate a chronology of axonal arrival during early development, proximity to the pial surface being an index of recency of arrival. As axonal outgrowth and neurogenesis appear to be directly related within the retinal ganglion cell population in mammals, the relative birthdates of the retinal ganglion cell types giving rise to the axon diameter classes in the rat may be inferred from the present results.
Animals↗
Vasculature and morphometry of the optic canal and intracanalicular optic nerve.
OBJECTIVES: To study the bony structure of the optic canal and the vasculature of the intracanalicular optic nerve in human cadavers. MATERIALS AND METHODS: Gross and microscopic examinations were performed in 25 optic canals from 13 cadavers to study the pattern of vascular supply of the intracanalicular optic nerve. Neoprene latex was injected through the most proximal part of the ophthalmic artery in seven optic canals. The intracanalicular branches from the ophthalmic artery were carefully identified and quantified. Quantitative measurements of the canal length, canal thickness, canal transverse area, optic nerve transverse area, and subdural space were done for the other 18 canals by means of semiautomated morphometric analysis system. Each canal was divided into anterior, middle, and posterior parts for better visualization and measurement. RESULTS: The ophthalmic artery gives off three branches that supply the intracanalicular optic nerve: medial collateral branch, lateral collateral branch, and ventral branch. Each branch pierces the dura and then supplies the nerve through the pia mater. The middle medial wall was the thinnest bony part of the canal (0.31 +/- 0.06 mm). The optic canal, optic nerve, and subdural space transverse area varied at different transection levels. The narrowest space was in the middle part of the optic canal. The mean subdural cross-sectional space was only 1.84 mm2. This, multiplied by the average canal length (11.79 mm), can be considered the potential space for hemorrhage, optic nerve edema, or hematoma. CONCLUSIONS: The vasculature within the bony canal is extremely delicate. Due to the limitation of this space, even a tiny amount of blood or swelling of the nerve (21.69 mm3) may cause optic nerve compression. It appears that these vessels could easily be disrupted in closed head injury by a shearing or concussive force, leading to ischemic infarction of the optic nerve. Since the narrowest portion of the canal is in the middle portion, it is the middle part of the optic canal that is most critical in doing an optic canal decompression.
Anthropometry↗
Optic radiation involvement in optic pathway gliomas in neurofibromatosis.
PURPOSE: Optic pathway gliomas (pilocytic astrocytomas) in neurofibromatosis type 1 (NF-1) typically involve some combination of the optic nerves, chiasm, or optic tracts. Involvement of the optic radiations is rare. DESIGN: This paper describes seven patients with NF-1 with gliomas involving the pregeniculate optic pathway in addition to the optic radiations. METHODS: A retrospective database review was made of all patients with NF-1 and optic pathway gliomas seen by one of the authors (G.T.L.) at the Children's Hospital of Philadelphia from July 1993 to October 2001. Patients with involvement of pregeniculate optic pathway and the optic radiations were identified. From November 2001 to February 2003, patients were sought prospectively. Cases were also identified from the practice of another author (M.C.B.) at Arkansas Children's Hospital. RESULTS: Four patients from Children's Hospital of Philadelphia (three of 83 total NF-1/optic pathway gliomas from July 1993 to October 2001 and one prospectively) and three from Arkansas Children's Hospital were identified. Two had expanding mass lesions within the white matter of the temporal or parietal lobes, which were histopathologically demonstrated to be pilocytic astrocytomas. The other five had radiographic involvement of the optic radiations but did not undergo biopsy. In three of the cases the vision was 20/200 or worse in each eye. CONCLUSIONS: Optic pathway gliomas in NF-1 may rarely involve the optic radiations. Optic radiation involvement may signal a more aggressive optic pathway glioma in patients with neurofibromatosis-1.
Child, Preschool↗
Optic nerve atrophy and retinal nerve fibre layer thinning following optic neuritis: evidence that axonal loss is a substrate of MRI-detected atrophy.
Magnetic resonance imaging (MRI) measures of brain atrophy are often considered to be a marker of axonal loss in multiple sclerosis (MS) but evidence is limited. Optic neuritis is a common manifestation of MS and results in optic nerve atrophy. Retinal nerve fibre layer (RNFL) imaging is a non-invasive way of detecting axonal loss following optic neuritis. We hypothesise that if the optic nerve atrophy that develops following optic neuritis is contributed to by axonal loss, it will correlate with thinning of the RNFL. Twenty-five patients were studied at least 1 year after a single unilateral attack of optic neuritis without recurrence, with a selection bias towards incomplete recovery. They had MR quantification of optic nerve cross-sectional area and optic nerve lesion length, as well as optical coherence tomography (OCT) measurement of mean RNFL thickness and macular volume, quantitative visual testing, and visual evoked potentials (VEPs). Fifteen controls were also studied. Significant optic nerve atrophy (mean decrease 30% versus controls), RNFL thinning (mean decrease 33% versus controls), and macular volume loss occurred in patients' affected eyes when compared with patients' unaffected eyes and healthy controls. The optic nerve atrophy was correlated with the RNFL thinning, macular volume loss, visual acuity, visual field mean deviation, and whole field VEP amplitude but not latency. These findings suggest that axonal loss contributes to optic nerve atrophy following a single attack of optic neuritis. By inference, axonal loss due to other post-inflammatory brain lesions is likely to contribute to the global MRI measure of brain atrophy in multiple sclerosis.
Adult↗
[Pits of the optic papilla in large optic nerve papillae. Papillometric characteristics in 15 eyes].
Fifteen optic nerve heads with pits measured by optic disk planimetry according to Littmann and Jaeger's method were significantly larger than previously determined normal optic nerve heads. Their area measured 4.84 +/- 1.42 mm2 (2.77-8.02 mm2), their horizontal diameter 2.42 +/- 0.42 mm (1.76-3.38 mm) and their vertical diameter 2.53 +/- 0.30 mm (1.14-3.06 mm). The quotients of minimum to maximum diameter and the angle between the maximum diameter and the horizontal line were similar to those in normal optic disks. Because of their enlarged area but normal form this pathologic entity forms a subunit of macrodisks. The pits were located in 14 optic disks on the temporal side on average 100 degrees from the upper disk pole, and in two optic disks on the nasal side about 85 degrees from the upper pole. In two cases they were double and in one bilateral. Their area and number were significantly correlated (p less than 0.001 and p less than 0.05) to the area of the optic disk. With increasing optic nerve head size the optic cup was less excavated. The largest optic disk seen in this study did not have one at all. There might be a stepless continuation from normal-sized optic disks to macrodisks with physiologic macrocups and to optic nerve heads with pits. These represent a maximum extreme in the spectrum of optic disk anomalies and diseases associated with optic nerve head size.
Adolescent↗
Optic nerve diffusion measurement from diffusion-weighted imaging in optic neuritis.
BACKGROUND AND PURPOSE: Increases in apparent diffusion coefficient (ADC) from diffusion-weighted (DW) imaging are thought to be due to axonal disruption, and changes have been well documented in multiple sclerosis lesions. DW imaging of the optic nerves, however, presents many challenges. The goal of this study was to measure ADC in patients with optic neuritis by using zonal oblique multisection echoplanar imaging. METHODS: The optic nerves of eighteen patients who had experienced an attack of optic neuritis 1 year previously and 11 control subjects were imaged with the diffusion sequence (usable data were available from 16 patients and 10 control subjects). The orbital optic nerves were segmented by a blinded observer by using a computer-assisted threshold-based contouring technique, and the mean ADC was determined. RESULTS: The mean ADC from diseased optic nerves was 1324 x 10(-6) mm2/s, compared with 990 x 10(-6) mm2/s from healthy contralateral optic nerves (P = .005 versus diseased optic nerves) and 928 x 10(-6) mm2/s from control optic nerves (P = .006 versus diseased optic nerves and P = .40 versus healthy contralateral optic nerves). The diseased optic nerve ADC correlated with both visual (e.g., r(S) = 0.73; P = .001 for logMAR visual acuity) and electrophysiological parameters (e.g., r(S) = -0.57, P = .021 for visual evoked potential central field amplitude [VEP]). CONCLUSION: It has been possible to apply DW imaging in a patient population, and, in the chronic phase following optic neuritis, the correlation of mean ADC with the clinical and electrophysiological parameters suggests that the ADC is giving a surrogate measure of axonal disruption in the chronic, postinflammatory optic nerve lesion.
Adult↗
Association of magnetic resonance imaging of anterior optic pathway with glaucomatous visual field damage and optic disc cupping.
PURPOSE: To investigate the association of magnetic resonance imaging (MRI) of anterior optic pathway with glaucomatous visual field damage and optic disc cupping. SUBJECTS AND METHODS: Twenty-three healthy volunteers (controls) and 31 glaucoma patients (14 with primary open angle glaucoma and 17 with normal tension glaucoma) were enrolled. All the participants showed no abnormal signs in their intracranial space and optic tract causing optic nerve atrophy and visual field defect, as confirmed by MRI. Multislice T1-weighted spin-echo imaging was performed in the sagittal plane followed by the coronal plane. MRI enabled the evaluation of the diameter of the optic nerve located in the retro-bulb space and the height of the optic chiasm in an observer-masked fashion. The MRI data were compared with the mean deviation (MD) score of the full threshold static visual field test and the optic cup-disc ratio (C/D ratio). RESULTS: The optic nerve diameter was significantly smaller in glaucoma patients (2.25 +/- 0.33 mm) than in controls (2.47 +/- 0.24 mm) and the height of the optic chiasm was significantly shorter in glaucoma patients (2.12 +/- 0.37 mm) than in controls (2.77 +/- 0.36 mm). The optic nerve diameter showed significant correlation with MD score (r = 0.547, P = 0.001) and C/D ratio (r = 0.407, P = 0.009). These correlations are similar to that between MD score and C/D ratio (r = 0.490, P = 0.001). The height of the optic chiasm showed significant correlation with MD score (r = 0.503, P = 0.01) and low correlation with C/D ratio (r = 0.339, P = 0.113). CONCLUSION: Glaucoma affects the anterior visual pathway anterogradely at least up to the optic chiasm, and these morphologic changes in the anterior visual pathway are correlated with glaucomatous optic nerve damage. MRI of the anterior visual pathway may be a good tool for evaluating glaucomatous damage objectively.
Adult↗