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Results for “optic neuropathies”

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At least 19 recordsLinked to original sources
PubMed1997

Does optic disc appearance distinguish ischemic optic neuropathy from optic neuritis?

OBJECTIVE: To determine whether characteristics of optic nerve swelling assist in distinguishing between optic neuritis and anterior ischemic optic neuropathy. METHOD: Optic nerve stereophotograph review by masked observers. RESULTS: Altitudinal swelling, pallor, arterial attenuation, and hemorrhage are found more commonly in anterior ischemic optic neuropathy than in optic neuritis. CONCLUSION: Optic disc appearance does help to distinguish anterior ischemic optic neuropathy from optic neuritis, although there are overlapping features.

Acute Disease↗
PubMed2003

Suppression of complex I gene expression induces optic neuropathy.

Optic nerve degeneration is a feature common to diseases with mutations in genes that encode complex I of the respiratory chain. Vulnerability of this central nervous system tract is a mystery, because of the paucity of animal models used to investigate effects of the mutated DNA in tissues rather than isolated in cultured cells. Using a ribozyme designed to degrade the mRNA encoding a critical nuclear-encoded subunit gene of complex I (NDUFA1), we tested whether oxidative phosphorylation deficiency can recapitulate the optic neuropathy of mitochondrial disease. Injection of adenoassociated virus expressing this ribozyme led to axonal destruction and demyelination, the hallmarks of Leber hereditary optic neuropathy.

3T3 Cells↗
PubMed1991

Orbital and sinus inflammation with secondary optic neuropathy.

Optic neuropathy with simultaneous orbital and sinus inflammation is a diagnostic dilemma. Although sinus inflammation was described previously as causative in some cases of optic neuritis, the relatively high rate of asymptomatic sinus opacification in radiologic studies of the general population (as high as 13%) makes this a diagnosis of exclusion. We describe a patient who had optic neuropathy associated with simultaneous orbital and sinus inflammation. Although definitive determination of etiology may not be made without tissue biopsy, cases suspected of having a bacterial etiology may benefit from an initial 48-hour trial of intravenous antibiotics before initiation of systemic corticosteroids.

Adrenal Cortex Hormones↗
PubMed1984

Lymphomatous optic neuropathy.

Optic neuropathy as the first sign of a lymphoreticular neoplasm is rare. A 65-year-old man complained of initially transient and then progressive visual loss in the right eye for two weeks. Computed tomography demonstrated a mass in the region of the intracranial portion of the right optic nerve. Frontal craniotomy was performed and histopathologic examination of the tumor disclosed a granulomatous process. Regrowth of the mass and visual deterioration, despite systemic steroid therapy, prompted surgical reexploration. Histopathologic examination confirmed large cell lymphoma. After local radiotherapy (2,500 rad), the patient is well and free of local or systemic lymphoma one year later. Other reported cases of lymphomatous optic neuropathy are reviewed and the diagnostic difficulties encountered are discussed.

Aged↗
PubMed1996

Visual recovery following treatment with very high dose corticosteroid in traumatic optic neuropathy.

Optic nerve compression is a true ophthalmic emergency. In addition to causes such as tumours, infection, mucoceles and granulomas, the majority of cases are the result of orbitofacial or closed-head trauma. The appropriate management of such cases is controversial; with some authors favouring surgical decompression while others advocate medical treatment using very high-dose corticosteroids, or a combination of both. We report a case of traumatic optic neuropathy in which there was marked improvement in visual acuity following the administration of methylprednisolone.

Aged↗
PubMedDate not supplied

Effect of transcorneal electrical stimulation in patients with nonarteritic ischemic optic neuropathy or traumatic optic neuropathy.

PURPOSE: To determine whether transcorneal electrical stimulation (TES) can improve the visual function of patients with nonarteritic ischemic optic neuropathy (NAION) or traumatic optic neuropathy (TON). METHODS: Eight consecutive patients at the Osaka University Hospital were studied. TES (600-800 microA, 20 Hz, 30 min) was applied once each to three eyes with NAION and to five eyes with TON, using a contact lens-type stimulating electrode. The primary outcome measurement was the change in visual acuity at 1 to 3 months after TES. An improvement in visual acuity was defined as a change of > or =0.3 log (minimum angle of resolution) (logMAR) units. The side effects of TES were also investigated. RESULTS: After TES application, the visual acuity improved in two patients with NAION and in four patients with TON. Visual acuity did not worsen in any of the eyes. Only a mild superficial punctuate keratopathy was observed in all eyes immediately after TES, and it healed by the next day. CONCLUSIONS: Visual acuity can be improved after TES without major complications in some patients with NAION or TON. These results suggest that TES should be considered as a new treatment for eyes with optic neuropathy.

Adolescent↗
PubMed1980

Endocrine optic neuropathies.

Optic neuropathy is found as a primary disorder in a number of endocrinological diseases. The authors discuss in this respect dysfunction of the thyroid, parathyroid, suprarenals, pancreas, ovarian and hypophysis.

Adrenal Gland Diseases↗
PubMed2001

Magnetization transfer and diffusion tensor MR imaging of the optic radiations and calcarine cortex from patients with Leber's hereditary optic neuropathy.

Optic nerve abnormalities are easily detectable in patients with Leber's hereditary optic neuropathy (LHON), using magnetic resonance imaging (MRI). However, the presence of structural changes in the optic radiations and calcarine cortex of these patients is still an unresolved issue. In this study, we obtained magnetization transfer (MT) and diffusion tensor (DT) MRI to investigate the integrity of these structures in patients with LHON. Dual echo, MT- and DT-MRI scans of the brain were obtained from 10 men with LHON and 10 healthy sex- and age-matched controls. After image co-registration, we obtained MT ratio (MTR), average diffusivity (D) and fractional anisotropy (FA) maps. MTR, D and FA values for the white matter of the optic radiations and MTR and D values for the calcarine cortex were obtained using a region of interest (ROI) analysis. No macroscopic abnormalities were detected in any of the scans from LHON patients and controls. No statistically significant differences of MTR, D or FA values were found for any of the regions studied in LHON patients and healthy controls. Our results suggest that, in patients with LHON, the optic radiations and the calcarine cortex are spared from structural damage, both at a macroscopic and a microscopic level.

Adult↗
PubMed2001

Endoscopic optic nerve decompression for the treatment of traumatic optic neuropathy.

Optic nerve decompression has been accomplished by a variety of procedures. Since 1995, endoscopic optic nerve decompression (EOND) has been used to treat traumatic optic neuropathy (TON) patients in our hospital after medical treatment failed. To date, 17 TON patients have received EOND in our hospital and have been followed up for more than half a year. After decompression, vision improved in 9 patients, remained the same in 6, and became worse in 2. The dura was incidentally exposed during the operation in 1 patient. We conclude that it is easier and more precise to perform optic nerve decompression by EOND than by other optic nerve decompression procedures. However, its efficacy still needs further investigation.

Adolescent↗
PubMed2004

Visual failure caused by vitamin B12 deficiency optic neuropathy.

Optic neuropathy is a rare but recognised complication of vitamin B12 deficiency, which may proceed to visual failure if not diagnosed early enough. Clues to the possible diagnosis include a history of, or risk factors for, pernicious anaemia, or previous resective gastrointestinal surgery.

Adult↗
PubMed1989

Optic nerve decompression may improve the progressive form of nonarteritic ischemic optic neuropathy.

Optic nerve sheath decompression surgery improved visual function for 12 of 14 patients with progressive nonarteritic ischemic optic neuropathy (NAION). Visual recovery was maintained in all patients during a follow-up period of 6 to 18 months (average, 11 months). Seven patients had experienced a previous NAION in the eye that was not operated on that did not improve spontaneously. Surprisingly, 2 of these 7 eyes with long-standing decreased vision demonstrated some visual improvement after surgery on the contralateral, acutely affected eye. Spontaneous visual improvement did not occur in an age- and sex-matched control group of 12 patients with similar entry-level visual acuity and field loss. Only 1 of 3 patients with sudden, nonprogressive visual loss secondary to NAION improved after surgery. In a control group with nonprogressive NAION, 2 of 15 eyes (14 patients) demonstrated spontaneous improvement. Optic nerve sheath decompression improves visual loss due to progressive NAION, a disorder without any previously effective therapy. However, for acute, nonprogressive NAION, surgery for a small number of patients did not improve the natural history of the disease.

Adult↗
PubMed2004

Optic nerve head circulation in nonarteritic anterior ischemic optic neuropathy and optic neuritis.

PURPOSE: To quantify optic nerve head circulatory abnormalities in patients with unilateral nonarteritic anterior ischemic optic neuropathy (NAION) or optic neuritis (ON), and to assess the potential of such measurements to differentiate NAION from ON. DESIGN: Prospective, cross-sectional, observational study. PARTICIPANTS: Thirty consecutive patients with unilateral NAION, 22 consecutive patients with unilateral ON, and 50 healthy control subjects. METHODS: All subjects underwent a complete neuro-ophthalmologic evaluation. The widths of Doppler-broadened frequency spectra, which are directly proportional to the speed of blood cells flowing through the capillaries of the optic nerve head, were measured at multiple sites in both eyes of each subject. The variation of Doppler broadening (DB) with age was determined in the control subjects. Doppler broadening values in the patients were compared between similar sites in affected and contralateral eyes, and between both affected and contralateral eyes and the age-adjusted values determined in the control subjects. MAIN OUTCOME MEASURES: The differences in DB between (1) the affected and contralateral eyes of the patients, (2) the patients and the control subjects, and (3) the patients with NAION and those with ON. RESULTS: In NAION, DB was decreased at both temporal (-20.2% and -18.5%) and nasal (-12.8% and -12.4%) sites of the nerve head in affected eyes compared with contralateral eyes or eyes of control subjects. In ON, DB was also decreased at temporal sites (-11.3% and -9.2%) in affected eyes compared with contralateral or control eyes. At nasal sites, there were no significant differences in DB in affected eyes of ON patients compared with contralateral or control eyes. The DB decreases were significantly greater in NAION patients than in ON patients. CONCLUSIONS: Optic nerve head circulatory abnormalities are present in patients with NAION or ON. This is the first demonstration of such abnormalities in ON, a finding consistent with the recent attention given to the phenomenon of axonal loss in this disease. Although there are differences in the circulatory abnormalities between the 2 diseases that provide insights into the pathophysiological mechanisms at play, they are not large enough to enable the clinician to distinguish between ON and NAION in an individual patient.

Adolescent↗
PubMed1999

[Bilateral anterior acute ischemic optic neuropathy complicating optic nerve head drusen. Apropos of a case].

A case of bilateral Anterior Ischemic Optic Neuropathy (AION) which is related to buried optic nerve head drusen is presented. Such an etiology has rarely been described and is poorly-documented in the literature. This etiologic diagnosis is brought by the imaging techniques: fluorescein angiography, B-scan ultrasonography and computed tomography. The pathogenesis may be related to the compressive effects encountered in a small scleral canal. The other complications of optic nerve head drusen are described and their similar mechanisms discussed.

Diagnostic Imaging↗
PubMed2003

Correlation between optic disc atrophy and aetiology: anterior ischaemic optic neuropathy vs optic neuritis.

BACKGROUND: The morphologic features of swollen disc in the acute stage of optic neuritis and anterior ischaemic optic neuropathy (AION) have been extensively investigated in contrast to the morphologic features of optic disc atrophy after these events. OBJECTIVE: : A prospective study to evaluate the morphologic features of optic disc atrophy 6 months or more after optic neuritis and nonarteritic AION. PATIENTS AND METHODS: A total of 35 optic discs after nonarteritic AION (n=27) and 24 after optic neuritis (n=19) in otherwise healthy subjects have been evaluated by direct fundoscopic examination with a +90 diopters lens and optic disc photography. The average age of patients at the onset of AION was 57.8 years (range: 38-80) and at the onset of optic neuritis was 32.6 (range: 19-46). The female:male ratio was 18 : 17 in the former and 15 : 9 in the latter. The evaluated parameters included: degree of rim pallor (0 to +3), location of rim pallor, height of rim above the retina, depth and width of cup, peripapillary retinal artery to vein (A : V) ratio, and peripapillary pigment epithelial atrophy. A comparison was made also with 17 age-matched normal discs of 17 patients. Statistical significance was calculated with chi(2) and Fisher's exact test. RESULTS: Most of the discs after AION were paler (+2: 70%, +3: 26%) than after optic neuritis (normal colour: 8%, +1: 58%, P< or =0.007). Rim segmental involvement after AION was usually either superior 'altitudinal' (53%) or inferior 'altitudinal' (29%), whereas after optic neuritis, it was usually either temporal-central (papillomacular) (42%) or diffuse temporal (42%, P<0.0001). Discs had lower A : V ratio (1 : 3, 40%) after AION compared with optic neuritis (1 : 3, 8%) (P=0.007). There were no significant differences between the two groups in height of the rim, cupping, and peripapillary atrophy. CONCLUSIONS: : A combination of the degree of rim pallor, location of rim pallor, and A : V ratio may be of value in assessing the aetiology of optic disc atrophy when no previous clinical data are available and a compressive lesion has been ruled out.

Acute Disease↗
PubMed1978

Quantitative perimetry in compressive optic neuropathy and optic neuritis.

The Goldmann perimetric defects in 20 cases of compressive optic neuropathy and 54 cases of optic neuritis were analyzed. While defects involving the papillomacular bundle were the rule in both compressive and neuritis cases, sparing of the fixational area occurred in 24% of neuritis eyes but in none of the eyes with compressive neuropathy. The most reliable differential perimetric sign was the presence of a hemianopic defect; at least one eye of 15 (75%) cases of compression showed such a defect, which was not found in any neuritis cases. The I2e was the largest kinetic isopter to demonstrate the hemianopic defect in a substantial proportion of cases. These defects were corroborated with sequential static presentation of the I2e to I4e stimuli to either side of the vertical meridan, and with similar techniques using 18/1,000 red test objects at the tangent screen.

Adolescent↗
PubMed1981

Anterior ischemic optic neuropathy. V. Optic disc edema an early sign.

Four unusual patients had bilateral anterior ischemic optic neuropathy (AION). In all four cases, AION developed in the first eye with the classic presentation. The fellow eye had symptomless optic disc edema (ODE) with no subjective or objective visual loss initially, but the classic AION clinical picture developed later on. The findings indicate that symptomless ODE may precede the visual loss in AION and could constitute the earliest sign of this disease. Since ODE in AION is due to axoplasmic flow stasis that, by itself, does not produce visual loss (this is produced by disruption of visual impulse transmission), this would suggest that mild optic nerve head ischemia interferes with axoplasmic flow without disrupting the visual impulse; however, more severe ischemia would disrupt both. Possible effects of various grades of acute optic nerve head ischemia are discussed.

Aged↗