Search PubMed⌕ Search

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.

At least 1,513 records · Page 84Linked to original sources

Optic neuritis. Doppler ultrasonography compared with MR and correlated with visual evoked potential assessments.

PURPOSE: To establish the role of Doppler ultrasonography (US) in the examination of patients with acute unilateral optic neuritis. MATERIAL AND METHODS: Twenty-five patients with a clinical diagnosis of optic neuritis were prospectively evaluated and 18 of them were included in the study. The inclusion criteria were MR findings of unilateral disease and age below 50 years. All patients were examined with MR in order to objectively detect, localize and measure the optic nerve lesions and in order to exclude patients with unidentifiable optic nerve involvement. Evaluation with US was performed to determine nerve morphology, nerve swelling, and resistance to flow in the central retinal artery. The patients' contralateral optic nerve served as an internal control. The US findings were correlated to the degree of visual impairment, both initially and at follow-up. Visual evoked potential (VEP) assessments were also performed in 16 patients. RESULTS: A statistically significant difference was found in the optic nerve diameter and in the resistance to flow in the central retinal artery between the affected and unaffected eyes. Patients with a prolonged impairment of visual acuity initially had a more swollen nerve and an increased resistance to flow in the affected optic nerve. Prognostic information was also gathered solely by evaluating the unaffected nerve diameter: patients who normally had thinner optic nerves had a more severe form of optic neuritis. VEP assessments were positive in all patients investigated. CONCLUSION: Doppler US can be used together with a VEP assessment as an indicator of the disease process in acute optic neuritis. These methods offer a potential for monitoring patients over time.

Adult↗

Choristoma of the optic nerve: case report.

OBJECTIVE AND IMPORTANCE: Optic nerve choristoma is a rare lesion composed of adipose tissue and smooth muscle involving the optic nerve. Few cases have been reported. CLINICAL PRESENTATION: A 20-year-old woman presented with a history of slowly progressive visual loss in the left eye. On T1-weighted magnetic resonance imaging studies, after frequency-selective fat saturation, an optic nerve mass was detected at the level of the optic canal with signal characteristics suggesting the diagnosis of optic nerve lipoma. INTERVENTION: At left frontotemporal craniotomy, the intracranial optic nerve appeared thin and atrophic proximally and was covered by abundant adipose tissue distally. Because no cleavage plane could be identified between the fatty lesion and the optic nerve, which appeared splayed within the adipose tissue, the nerve was resected after an intraoperative biopsy. The presence of two heterotopic mesodermal elements, a rim of adipose tissue admixed with bundles of mature smooth muscle, extending into the nerve septa, warranted a diagnosis of optic nerve choristoma. CONCLUSION: Optic nerve choristoma is an uncommon optic nerve lesion. Even if imaging studies are highly suggestive of the diagnosis, pathological confirmation is required because of the high adipose tissue content in the majority of cases. The lesion, most likely malformative and nonneoplastic in nature, can be the cause of progressive visual loss.

Adolescent↗

Visual manifestations of visible and buried optic disc drusen.

BACKGROUND: It has been reported that visible optic disc drusen are associated with decreased visual acuity and loss of peripheral visual field. Patients with buried optic disc drusen have not been as well characterized. METHODS: An observational, retrospective review was made of 92 eyes with funduscopic or ultrasonographic evidence of optic disc drusen. Demographics, presenting symptoms, visual acuity, refractive error, intraocular pressure, presence of an afferent pupillary defect, cup-to-disc ratio, appearance of the optic nerve, and visual field were recorded. RESULTS: Fifty-one (55%) of the eyes were symptomatic; among them, 63% had symptoms of visual acuity loss, and 49% had symptoms of visual field loss. Seventy-nine (86%) of the optic discs appeared abnormal on ophthalmoscopy, but only 42% of these had visible drusen. Forty-five (49%) of the eyes had a visual field defect, and 73% of these were nerve fiber bundle in type. Overall, 73% of optic discs with visible drusen had abnormal visual fields compared with only 36% of optic discs with buried drusen (P < 0.05). CONCLUSIONS: Among 92 eyes with optic disc drusen, only slightly more than 50% produced visual symptoms. Fewer than 50% of drusen were visible ophthalmoscopically. Buried optic disc drusen identified by ultrasound had a significantly lower frequency of associated visual field defects than did visible optic disc drusen.

Adolescent↗

Nonarteritic anterior ischemic optic neuropathy.

PURPOSE OF REVIEW: Nonarteritic anterior ischemic optic neuropathy remains a disease that is poorly understood in many aspects. The clinical presentation may diverge significantly from the classic unilateral, painless, sudden vision loss affecting patients over the age of 50 years. This variability might make nonarteritic anterior ischemic optic neuropathy hard to differentiate from optic neuritis and arteritic ischemic optic neuropathy. The course of nonarteritic anterior ischemic optic neuropathy is also variable, often sequentially affecting the other eye. RECENT FINDINGS: Visual recovery has been reported, but it is not the rule. Multiple risk factors have been proposed, including crowded disc, atherosclerosis, diabetes, hyperlipidemia, hypertension, hypotension, hemoconcentration, hemodilution, and hypercoagulable states. The optic nerve damage in nonarteritic anterior ischemic optic neuropathy appears to result from a perfusion insufficiency in the short posterior ciliary arteries leading to infarction of the retrolaminar portion of the optic disc. The underlying mechanisms are still unclear, however. Multiple medical and surgical treatment options have been investigated, including optic nerve sheath decompression, standard and megadose corticosteroids, levodopa, carbidopa, hyperbaric oxygen, and neuroprotective agents, but no proven effective treatment is currently available. SUMMARY: Intense investigations in humans and animals are under way. Hopefully these studies will enhance our understanding of the risk factors and pathophysiology of nonarteritic anterior ischemic optic neuropathy and aid in developing new strategies for prevention and treatment.

Arteritis↗

Subclinical optic neuropathy in multiple sclerosis. A neuro-ophthalmological investigation by means of visually evoked response, Farnworth-Munsell 100 Hue test and Ishihara test and their diagnostic value.

Affection of the optic nerves play a central role in multiple sclerosis (MS) symptomatology. In reported autopsy series the prevalence of optic neuropathy has approached 100%. In the present study subclinical affection of the optic nerves was investigated by visual evoked response (VER), Farnworth-Munsell 100 Hue test (FM 100 Hue test) and Ishihara plates in 17 patients with normal visual acuity and without a history of acute optic neuritis. Optic neuropathy was demonstrated in 72% of the eyes. The occurrence of optic neuropathy was also investigated by the same methods in 16 patients with previous acute optic neuritis, which was bilateral in 5 patients. Affection of the optic nerves was demonstrated in 95% in this group. The affection of also the fellow eye in patients with previous monolateral optic neuritis is unexplained. It may be an analogue to the symmetry of plaques found in the brain and the spinal cord. The cause of this peculiar distribution of lesions is, like the ethiology of MS, unexplained at present. In comparing the different methods of demonstrating optic neuropathy, VER is recommended as the method of choice.

Adult↗

Imaging characteristics of x-ray capillary optics in digital mammography.

Computed radiography (CR) has shown promise in digital mammographic screening due to its good low spatial frequency MTF and its relatively wide exposure latitude. The CR image format has not gained acceptance clinically because of reduced high spatial frequency resolution as compared to film-screen images. X-ray capillary optics, aligned between the breast and CR phosphor imaging plate, will capture primary x-ray photons almost exclusively. Due to the very small angle of acceptance, scattered photons angled more than about 1.6 x 10(-3) radians from primary trajectory will not be accepted at the capillary optic entrance. The virtual elimination of detected scatter means almost 100% of the possible primary contrast should be visible in the image. In addition, the image can be magnified without focal spot blurring. Effective resolution of CR images can be increased by a factor equal to that magnification. Clinical implementation of future capillary optics are expected to be either in the form of a large, stationary, post-patient optic that accepts primary from the entire breast or a fan-shaped optic that is scanned across the breast. Measurements of a test capillary optic showed a reduction of scatter fraction to 0.018. Images of a lucite contrast detail phantom revealed a corresponding increase in image contrast when compared to anti-scatter grid and no grid methods. Spectral transmission measurements using a high-purity germanium detector showed good primary transmission (45%-50%) in the mammographic energy range. The MTF measurements of both stationary and scanned capillary optics showed improvement at the 5% MTF level to 8.4 mm-1 for scanned optics and 9.2 mm-1 for stationary optics representing a 68% and 84% respective increase over the CR MTF without magnification or capillary optics.

Capillary Action↗

Linezolid-induced optic neuropathy: a mitochondrial disorder?

We report a case of bilateral mitochondrial optic neuropathies secondary to long-term linezolid treatment, show the nature of recovery, review the findings in the literature and propose a potential mitochondrial mechanism for linezolid-induced mitochondrial optic neuropathy. This is an observational case report and literature review with presentation of the clinical course of linezolid mitochondrial optic neuropathies through clinical and psychophysical documentation. Main outcome measures included: visual acuity, funduscopical examinations and peripapillary retinal nerve fibre layer (PRNFL) optical coherence tomography (OCT). A 6-year-old boy presented with bilateral optic neuropathies secondary to 1 year of linezolid treatment for osteomyelitis of the mandible. On presentation, visual acuities were 20/400 in both eyes, with considerable optic disc oedema, hyperaemia and PRNFL swelling confirmed by OCT. 2 weeks after the discontinuation of linezolid, visual acuities returned to 20/25 in both eyes, with reduction in the optic disc oedema, hyperaemia and PRNFL swelling. 3 months after the discontinuation of linezolid treatment, visual acuities were stable at 20/20 in both eyes, with a marked decrease in PRNFL swelling confirmed by OCT, and the development of mild temporal optic disc pallor in both eyes. Doctors should be aware of impairments of vision among patients on long-term linezolid treatment and promptly discontinue treatment to prevent irreversible vision loss. The development and resolution of bilateral optic neuropathies with considerable PRNFL swelling in this patient provide insight into the more general rubric of mitochondrial optic neuropathies.

Acetamides↗

Quantitative evaluation of the optic nerve head in early glaucoma.

AIMS: Progressive loss of neuroretinal rim tissue is known to occur early in glaucoma and measurement of the neuroretinal rim area is possible by magnification corrected analysis of optic disc photographs (planimetry). This study was performed to determine whether the facility to distinguish between glaucomatous and normal optic discs could be improved upon by: (a) taking into account the known relation between optic disc size and neuroretinal rim area, and (b) measuring rim area in a number of segments, in order to detect focal changes. METHODS: Planimetric examination of the optic disc photographs of 88 control subjects and 51 patients with early visual field defects was performed. In the control group, multiple linear regression analysis was performed between neuroretinal rim area and optic disc area, age, sex, eye side, refraction, and keratometry. This was repeated for the whole disc and for each of twelve 30 degree segments. Normal ranges were defined by the 98% prediction intervals of the regression analysis and the sensitivity and specificity for correct identification of optic discs in the two groups determined. RESULTS: Multiple linear regression demonstrated significant associations between the neuroretinal rim area and optic disc area and age in normal subjects. Sensitivity and specificity for glaucoma diagnosis, using the cut off derived from the 98% prediction intervals, was 37.7% and 98.9% respectively when total neuroretinal rim area alone was considered, and 88.7% and 94.3% respectively when the 30 degree segments were included. The most frequent pattern of neuroretinal rim loss was diffuse, followed by thinning in more than one sector and then by thinning in the inferotemporal sector alone. CONCLUSIONS: This method of optic disc analysis enables the examiner to identify glaucomatous optic discs at the stage of early perimetric loss with a high degree of precision. Optic disc photography is simple, and fundus cameras are widely available. This method for glaucoma case identification may therefore be suitable for the primary care setting as well as hospital practice.

Adult↗

Transforming growth factor beta isoforms in human optic nerve heads.

AIM: To determine if the isoforms of transforming growth factor beta (TGF-beta) are present in fetal, normal adult, and glaucomatous optic nerve heads. METHODS: To localise cells synthesising TGF-beta, optic nerve heads were stained using antibodies to TGF-beta 1, TGF-beta 2, and TGF-beta 3. To demonstrate synthesis, human optic nerve heads from fetal, glaucomatous, and normal age matched subjects were explanted, cultured overnight, and the culture supernatant was assayed for the presence of TGF-beta 1 and TGF-beta 2 by bioassay. In addition, semiquantitative RT-PCR was performed to determine the gene expression pattern of TGF-beta 2. RESULTS: Immunohistochemistry of glaucomatous samples revealed the presence of intense staining for TGF-beta 2 primarily in astrocytes, whereas TGF-beta 1 was localised to blood vessels. No TGF-beta 3 immunoreactivity was observed. There was little or no expression of TGF-beta in normal optic nerve heads. Optic nerve heads from glaucomatous eyes released 70-100-fold more TGF-beta 2 than normal age matched optic nerve heads. Fetal optic nerve heads released 90-100-fold more TGF-beta 2 than normal adult optic nerve heads. TGF-beta 1 was undetectable by bioassay in all samples tested. There was no apparent increase in TGF-beta 2 gene expression in glaucomatous and fetal eyes, suggesting post-transcriptional regulatory mechanisms. CONCLUSIONS: These results demonstrate that TGF-beta 2 is produced in high levels in the fetal and glaucomatous optic nerve heads, perhaps by a mechanism of post-transcriptional regulation. TGF-beta may be important during development of the optic nerve head and, in glaucoma, TGF-beta 2 may be a mediator of astrocyte reactivation and extracellular matrix remodelling in the lamina cribrosa.

Aged↗

Effect of indomethacin on the hypercapnia-associated vasodilation of the optic nerve head vessels: an experimental study in miniature pigs.

PURPOSE: To evaluate whether prostaglandins are mediators of the hypercapnia-associated vasodilation of the optic nerve head vessels. METHODS: We measured the PO(2) at intervascular areas of the optic disc in 9 anaesthetized miniature pigs using oxygen-sensitive microelectrodes placed at <50 mum from the optic disc. PO(2) was measured continuously under normoxia, hyperoxia (breathing of 100% O(2)), carbogen breathing (95% O(2), 5% CO(2)), and hypercapnia (40% increase in inhaled CO(2)). Similar measurements under these conditions were also done after intravenous administration of the prostaglandin inhibitor indomethacin. RESULTS: Before the injection of indomethacin, we observed a slight increase in the optic disc PO(2) during hypercapnia (DeltaPO(2) = 2.0 +/- 1.7 mm Hg; p < 0.001; n = 18) or hyperoxia (DeltaPO(2) = 3.4 +/- 1.6 mm Hg; p < 0.001; n = 23), but a much more important increase during carbogen breathing (DeltaPO(2) = 12.0 +/- 5.1 mm Hg; p < 0.001; n = 23). After the injection of indomethacin, the increase in the optic disc PO(2) was similar during hyperoxia (DeltaPO(2) = 5.6 +/- 2.2 mm Hg; p < 0.001; n = 9) or carbogen breathing (DeltaPO(2) = 5.8 +/- 3.2 mm Hg; p < 0.001; n = 9), while in hypercapnia the variation of the optic disc PO(2) was minimal (DeltaPO(2) = 0.5 +/- 1.9 mm Hg; p > 0.1; n = 6). CONCLUSIONS: Indomethacin inhibits the vasodilatory effect of increased systemic PaCO(2) on the optic nerve head vessels, leading to a similar moderate increase in the optic disc PO(2) during carbogen breathing as in hyperoxia. Indomethacin also inhibits the increase in the optic disc PO(2) seen during hypercapnia. Those results indicate that prostaglandins are mediators of the hypercapnia-associated vasodilation of the optic nerve head vessels.

Animals↗

Growth-associated expression of a membrane protein, neuropilin, in Xenopus optic nerve fibers.

Neuropilin (previously referred to as A5) is a neuronal cell surface protein which is widely distributed in such vertebrate species as Xenopus, chicken and mouse. In these vertebrate species, neuropilin is expressed in particular neuron circuits at particular developmental stages when axonal growth is active. To test whether the expression patterns of neuropilin is associated with axonal growth, we examined expression patterns of neuropilin in developing and regenerating Xenopus optic nerves. In embryos, a neuropilin-specific monoclonal antibody A5 (MAbA5) bound strongly to the optic nerves, and in situ hybridization signals for neuropilin mRNA were prominent in the retinal ganglion cells (RGCs), indicating that developing optic nerve fibers express neuropilin. The binding of MAbA5 to the optic nerve fibers was maximal at stages 41-43, then decreased in the subsequent tadpole life. In tadpoles after stage 50, the binding of MAbA5 to the optic nerves was extremely weak or almost nil, although RGCs expressed considerable amounts of neuropilin mRNA. When the tadpole optic nerves were crushed and prompted to regenerate, however, neuropilin protein reappeared in the optic nerve fibers. The binding of MAbA5 to the regenerating optic nerve fibers was detectable as early as the 5th day and maximal at the 2nd or 3rd weeks after the optic nerve crush, and declined thereafter. These findings suggest that the expression of neuropilin in the optic nerve fibers is regulated in an axonal growth-associated manner.

Animals↗

Responses of the optic tectum to telencephalic stimulation in catfish.

In order to test physiologically for cerebrotectal connections in a fish, averaged evoked potentials and unit responses were recorded from the optic tectum following electrical stimulation applied to the telencephalon in the siluroid teleost Ictalurus nebulosus. A single shock applied to the area dorsalis centralis (Dc) of the telencephalon, and only to this area, elicits a sequence of deflections in the ipsilateral optic tectum: an initial negative peak at about 8 ms, (= N8), a larger N25 and a slow P50-N95. The configurations, depth profiles, latencies and susceptibility to repetitive stimulation, together with the known tectal anatomy, suggest that the first wave is due to the afferent fibers from the telencephalon and that N25 is due to deep tectal neurons. Telencephalic input exerts a conditioning effect on the field potentials and unit responses evoked by direct optic nerve shock. Such a shock elicits, in the contralateral tectum, small negative, optic tract axon peaks followed by a large N6, believed to be postsynaptic, and a still later P12. As a first approximation it is argued that the telencephalic input and the retinal input are activating different sets of neuronal elements in the optic tectum, since the configuration and depth profile of the telencephalic and optic nerve shock-elicited potentials are different. A conditioning Dc stimulus has a long-lasting effect on the form of the optic nerve field potential, maximally when the pallial shock precedes the optic by about 90 ms. The effect, observed by subtracting the conditioned from the unconditioned tectal response to optic nerve shock, is a difference wave with N11 and P20. The unit activity from deep tectal laminae is either activated or accelerated following Dc stimulation, while superficially located neurons are not affected. In another group of tectal units, the optic nerve shock-induced response is depressed by a preceding pallial dorsalis centralis stimulus. The evidence is compatible with the assumption of direct projections from Dc to the deep layers of the tectum, but the timing could also permit indirect pathways. In any case, the influence is not simple or identical for different tectal cell classes.

Animals↗

Effect of carbogen breathing and acetazolamide on optic disc PO2.

PURPOSE: Acetazolamide was previously shown to increase optic disc partial pressure of oxygen (PO(2)). The study was conducted to evaluate optic disc PO(2) variations during normoxia, hyperoxia (100% O(2)), and carbogen breathing (95% O(2), 5% CO(2)), before and after intravenous administration of acetazolamide. METHODS: PO(2) measurements were obtained at intervascular areas of the optic disc in nine anesthetized minipigs using oxygen-sensitive microelectrodes (10-microm tip diameter) placed at <50 microm from the optic disc. PO(2) was measured continuously during 10 minutes under normoxia, hyperoxia, or carbogen breathing. Oxygen measurements were repeated under these conditions after intravenous injection of acetazolamide (500-mg bolus). RESULTS: In hyperoxia, optic disc PO(2) increased moderately (DeltaPO(2) = 4.81 +/- 1.16 mm Hg (mean +/- SD; 24%; P < 0.001) after a much larger increase in systemic PaO(2). Carbogen breathing induced a significant increase in both systemic PaO(2) and PaCO(2), which resulted in a large increase in optic disc PO(2) (DeltaPO(2) = 13.17 +/- 2.18 mm Hg; 67%; P < 0.001). Acetazolamide induced a slow and progressive increase in both systemic PaCO(2) and optic disc PO(2) (30 minutes DeltaPO(2) = 4.24 +/- 2.45 mm Hg; 24%; P < 0.04). However, it was when carbogen was simultaneously administered that optic disc PO(2) increased most substantially (DeltaPO(2) = 18.91 +/- 5.23 mm Hg; 90%; P < 0.002). CONCLUSIONS: Carbogen breathing increases optic disc Po(2) significantly in minipigs, more than hyperoxia. The association of acetazolamide injection with carbogen breathing could induce an additional increase in optic disc PO(2) through the effect of higher systemic PaCO(2).

Acetazolamide↗

Optic nerve hypoplasia: a review.

Optic nerve hypoplasia is a developmental anomaly of the retina and optic nerves in which there is a reduction in the number of ganglion cells in the retina and of their centripetal fibers projecting through the optic nerve to the lateral geniculate body. The condition may be unilateral or bilateral and is frequently misdiagnosed as optic atrophy. In about 25% of cases, bilateral optic nerve hypoplasia is associated with a variety of cerebral malformations of which the commonest single disturbance is absence of the septum pellucidum (septo-optic dysplasia). Cerebral malformations and their endocrine accompaniments are also seen, though less frequently, in unilateral hypoplasia. The endocrine disturbances that may accompany optic nerve hypoplasia include growth hormone deficiency, adrenal insufficiency, hypothyroidism, and disturbances of antidiuretic hormone production. Precocious puberty and hypogonadism have also been observed. The prognosis of optic nerve hypoplasia depends upon the severity of the changes in the optic nerves and especially the degree of associated cerebral malformation. The finding of optic nerve hypoplasia should lead to thorough ophthalmologic, neurologic, and endocrinologic evaluation of the patient.

Abnormalities, Multiple↗

Sarcoid masquerading as optic nerve sheath meningioma.

Sarcoid manifesting as an optic nerve tumor without evidence of systemic disease is uncommon. Throughout a 2-year period, a 22-year-old white woman had progressive monocular loss of vision to the level of no light perception. Optic atrophy but no uveitis was noted in the affected eye. Magnetic resonance imaging revealed thickening and enhancement of the apical optic nerve, with "tram-tracking." The presumptive diagnosis was optic nerve sheath meningioma; however, a biopsy specimen from the optic nerve revealed sarcoid. Extensive postoperative investigations revealed no systemic sarcoidosis. To our knowledge, 17 cases similar to ours, with the diagnosis proved by optic nerve biopsy, have been previously reported in the English-language literature. Most of these were mistaken preoperatively for optic nerve sheath meningioma. None of the patients had evidence of systemic sarcoidosis on initial postoperative testing. Neuroimaging, serum level of angiotensin-converting enzyme, and clinical characteristics such as age, race, sex, and optochoroidal collaterals do not distinguish optic nerve sheath meningioma from sarcoid of the optic nerve. In the absence of uveitis or systemic involvement, optic nerve sarcoid manifesting as an orbital tumor is virtually impossible to diagnose without results of biopsy.

Adult↗

[Unilateral visual field defect due to optic nerve compression by sclerotic internal carotid artery: a case report].

A case of unilateral visual field defect due to optic nerve compression by a sclerotic internal carotid artery was reported. A 71-year-old woman was admitted to our department because of constricted visual field of the right eye. MRI showed elevation of the right optic nerve compressed by an internal carotid artery. The right carotid angiography revealed elevation and distortion of the C1-2 portion. Frontal craniotomy was carried out and the optic nerve was visualized on this side. The right optic nerve was found to have been compressed by the sclerotic internal carotid artery. The optic canal was then unroofed. The post-operative course was uneventful. The visual field was improved. When last seen 6 months after surgery, her visual field remained in the improved condition. Nasal field abnormalities are most frequently encountered in retinal and anterior optic nerve pathology. Our success in improving the visual field disturbance may be accounted for by the fact that the preoperative period was short and the operation was performed before atrophy of ocular fundi occurred. Nasal field loss caused by intracranial lesions of the optic pathway is rare. It is probably impossible to determine degree of the symptomatology caused by direct-pressure compression as opposed to that caused by ischemia secondary to occlusion of small arterial supply branches. Vascular compressive neuropathy of optic nerve should not be diagnosed simply by the radiological finding of the optic nerve dislocation. However, optic nerve compression by surrounding arteries should be remembered as one of the possible causes of visual field defect which needs to be treated surgically.

Aged↗

Pre- versus post-anterior clinoidectomy measurements of the optic nerve, internal carotid artery, and opticocarotid triangle: a cadaveric morphometric study.

OBJECTIVE: Published morphometric data supporting the microsurgical advantages of anterior clinoidectomy are scant. The goal of this study was to quantify, with direct measurements, the improved exposure of the optic nerve, internal carotid artery (ICA), and opticocarotid triangle (OCT) after extradural removal of the anterior clinoid process. METHODS: Ten formalin-fixed adult cadaver heads were dissected bilaterally, and measurements were made both before and after anterior clinoidectomy. Twenty sets of pre- and post-anterior clinoidectomy measurements were collected, consisting of: 1) optic nerve length from the optic chiasm to the optic canal (pre) and to the anulus of Zinn (post); 2) ICA length from the ICA bifurcation to the distal limit of the anterior clinoid process (pre) and to the ICA distal dural ring (post); 3) OCT width, the widest in situ distance between the optic nerve and the ICA (pre) and the analogous measurement with allowable retraction on the mobilized ICA and optic nerve (post); and 4) OCT length from the point where the A1 segment crosses the optic chiasm to the optic canal (pre) and to the anulus of Zinn (post). RESULTS: The right and left combined mean values +/- standard error of the mean before and after removal of the anterior clinoid process, respectively, were: optic nerve length, 10.28 +/- 2.30 mm and 22.83 +/- 2.54 mm; ICA length, 10.48 +/- 2.39 mm and 14.78 +/- 3.02 mm; OCT width, 3.93 +/- 1.16 mm and 12.95 +/- 2.61 mm; and OCT length, 10.38 +/- 2.84 mm and 23.55 +/- 2.79 mm. CONCLUSION: Anterior clinoidectomy can provide a twofold increase in exposure of the optic nerve length and the OCT length, as well as a three- to fourfold increase in the maximum OCT width. This dramatically improves surgical exposure in the suprasellar and periclinoid regions.

Adult↗

[Optic neuropathy after proton-beam therapy for malignant choroidal melanoma].

Proton-beam irradiation is a conservative therapy commonly used for the treatment of uveal malignant melanomas. Some adverse effects such as optic neuropathy can compromise the visual outcome. We were interested in determining the risk factors for radiation papillopathy. Since there is currently no effective therapy, this is an interesting way to improve prevention of optic neuropathy. Six hundred sixty-two eyes had more than 24 month follow-up after proton-beam irradiation for uveal melanoma. In five hundred twenty-two cases, the clinical examination of the optic nerve head by ophthalmoscopy was possible. One-hundred eleven optic discs were pathologic, whereas 411 remained disease-free. Retrospective study of these two groups allowed to quantify the risk factors for optic neuropathy. The irradiation of more than 2mm of optic nerve at 30 Grays-equivalents appeared to be the major risk factor for optic neuropathy. For a given irradiation dose, the observed pattern of clinical responses was heterogeneous. These results are discussed and compared to the previous published reports. Visual results and life prognosis are also discussed, considering the optic nerve head status. Proton-beam therapy can preserve the optic nerve when the tumor location allows to keep it away from the irradiation-field. Patients must be informed about the risk of optic neuropathy after proton-beam irradiation.

Choroid Neoplasms↗