Ischaemic optic neuropathy (ION) is the commonest adult optic neuropathy encountered in Southeast Asia and will increase in incidence with an ageing population. It occurs in two forms: arteritic and non-arteritic. The latter variety being by far the commoner encountered in the region and presenting as an anterior optic neuropathy with optic disc swelling. The clinical presentation of both varieties is described with particular reference to the hyperaemic disc appearance of the non-arteritic disease as opposed to the ischaemic, pale, swollen, infarcted disc seen in arteritic anterior ION. Essential visual field defects found in both varieties are emphasized; the prognosis and treatment are discussed. Pathological specimens are also illustrated. Posterior ION is briefly mentioned being a diagnosis of exclusion. The anatomy, especially the blood supply of the optic nerve head, is discussed along with its role in the production of the different varieties of ION.
Optic Nerve Diseases ; Pathology

The apex of the orbit is basically formed by the optic canal, the superior orbital fissure, and their contents. Space-occupying lesions in this area can result in clinical deficits caused by compression of the optic nerve or extraocular muscles. Evenvascular changes in the cavernous sinus can produce a direct mass effect and affect the orbitapex. When pathologic changes in this region is suspected, contrast-enhanced MR imaging with fat saturation is very useful. According to the anatomic regions from which the lesions arise, they can be classified as belonging to one of five groups; lesions of the optic nerve-sheath complex, of the conal and intraconal spaces, of the extraconal space and bony orbit, of the cavernous sinus or diffuse. The characteristic MR findings of various orbital lesions will be described in this paper.
Cavernous Sinus ; Magnetic Resonance Imaging* ; Muscles ; Optic Nerve ; Orbit* ; Pathology*

To evaluate characteristic CT findings of orbital pseudotumor and to define differentialpoints from other pathology, the authors retrospectively reviewed CT of 19 patients who were prooen to have orbital pseudotumor by clinical course and, in some cases, biopsy. A variety of CT findings including extraocular muscle thickening(11 cases), streaky infiltration of retroorbital fat(11 cases), mass formation(10 cases), optic nerve thickening (6 cases), conjunctival thickening (5 cases), scleral thickening(4cases), enlarged lacrimal gland(4 cases) and destruction of orbital bone (2 cases) were observed. Thickening of the anterior portion and irregular margin were characteristic findings of extraocular muscle and optic nerve lesions. Mass formation predominantly occurs in the anterior portion of the orbit. In most cases more than two orbital structures are involved by lesion.
Biopsy ; Humans ; Optic Nerve ; Orbit* ; Orbital Pseudotumor* ; Pathology ; Retrospective Studies

OBJECTIVETo establish the animal model of traumatic optic neuropathy similar to clinical feature by injuring the optic nerve of the pipeline through the ethmoid and sphenoid sinus. The electrophysiology and morphology were observed.

METHODSThe optic nerve in 2 cats was anatomically observed. Thirty healthy adult cats were divided into 1 h, 1 d, 3 d, 1 w, 2 w, 4 w injury groups. The right eye was selected as the experiment eye, and the left as the control. The optic canals were damaged by the injury instrument. The changes of optic nerve were observed using light and electron microscope. The pattern reversal visual evoked potential (PR-VEP) was used to determine the succeed model and pupil was monitored. PR-VEP and neural tissue morphology were examined at intervals of 1 h, 1 d, 3 d, 1 w, 2 w, 4 w after trauma.

RESULTSEight cats had Marcus-Gunn's pupil, and 22 cats did not have after injury. Neural tissue was physaliphorous degeneration in light microscope. The neural fibers swelled gradually and fibers physaliphorous degeneration in the first day after damage. At the seventh day, the bubble enlarged to be a big flat. After two weeks, the big flat bubble came out to be a bigger bubble. Under the electronic microscope, axons were physaliphorous degeneration, crack emerged between axon membrane and myelin sheath and myelin sheath were loose in the first day. At the third day, axon swelled, physaliphorous degeneration rose and myelin sheath were loose obviously. At the seventh day, axon and myelin sheath appeared loop in half cycle and bubble-like broke up. A lot of pieces came out and axon became physaliphorous and uniform. Microtubule and microfilament disappeared. After two weeks, myelin sheath became onion-like. On fourth week, myelin sheaths enlarged and squeezed to center. Axoplasm disappeared and neural tissues collapsed.

CONCLUSIONSThis animal model was similar to clinical optic nerve decompression through ethmoid and sphenoid sinus. The change of PR-VEP and neuromorphology were distinct before and after trauma. The pathological changes of optic nerve catching vibrated injury are mainly degeneration, so earlier decompression of optic nerve may improve the visual function.

Animals ; Cats ; Disease Models, Animal ; Evoked Potentials, Visual ; Optic Nerve ; pathology ; physiopathology ; Optic Nerve Injuries ; pathology ; physiopathology

PURPOSE: To evaluate the parameters of optic nerve head (ONH) and retinal nerve fiber layer (RNFL) in patients with large cup/disc ratio (CDR) and normal neuroretinal rim configuration who have normal perimetry (physiologic large cups, LC) and to compare these parameters with those of the normal and early glaucoma patients. METHODS: Using Heidelberg retinal tomography (HRT) and optical coherence tomography (OCT), 30 patients with LC, 29 normal subjects, and 31 early glaucoma patients were examined. One eye from each subject was randomly selected. RESULTS: Significant differences between LC and glaucomatous eyes (GE) were found in parameters indicating loss of nerve fibers, such as rim area, rim volume, and mean RNFL thickness. However, there was no difference between LC and normal eyes (NE) in RNFL thickness, rim area, and rim volume. LC was able to be defined as a normal central excavation with a large disc and large CDR with a normal rim area. CONCLUSIONS: HRT ONH parameters and RNFL thickness obtained with OCT may be useful for differentiating between glaucoma and LC eyes.
Retina/*pathology ; Optic Disk/*pathology ; Nerve Fibers/*pathology ; Middle Aged ; Humans ; Glaucoma/*pathology ; Adult ; Adolescent

A 59-year-old woman was referred to our clinic for a glaucoma evaluation. The visual acuity and intraocular pressure were normal in both eyes. However, red-free fundus photography in the left eye showed a superotemporal wedge-shaped retinal nerve fiber layer defect, and visual field testing showed a corresponding partial arcuate scotoma. In an optical coherence tomography examination, the macula was flat, but an arcuate-shaped peripapillary retinoschisis was found. Further, the retinoschisis seemed to be connected with a superotemporal optic pit shown in a disc photograph. After 3 months of a topical prostaglandin analogue medication, the intraocular pressure in the retinoschisis eye was lowered from 14 to 10 mmHg and the peripapillary retinoschisis was almost resolved. We report a rare case of an optic disc pit with peripapillary retinoschisis presenting as a localized retinal nerve fiber layer defect.
Female ; Humans ; Middle Aged ; Nerve Fibers/*pathology ; Optic Disk/*abnormalities/*pathology ; Optic Nerve Diseases/*diagnosis ; Retinal Ganglion Cells/*pathology ; Retinoschisis/*diagnosis/drug therapy ; Tomography, Optical Coherence

Hemangioblastoma ; metabolism ; pathology ; surgery ; Humans ; Male ; Middle Aged ; Optic Nerve ; pathology ; Optic Nerve Neoplasms ; metabolism ; pathology ; surgery ; Phosphopyruvate Hydratase ; metabolism ; Vimentin ; metabolism ; von Willebrand Factor ; metabolism

Alzheimer Disease ; Diabetic Neuropathies ; pathology ; Glaucoma ; pathology ; Humans ; Multiple Sclerosis ; pathology ; Nerve Fibers ; pathology ; Ophthalmoscopy ; Optic Nerve ; pathology ; Parkinson Disease ; pathology ; Retinal Neurons ; pathology ; Tomography, Optical Coherence

Interference with visual pathways is usually not caused by intracranial aneurysms. Aneurysms of the anterior communicating artery rarely produce visual symptoms and signs in spite of their proximity to the visual pathways. The reason may be that these aneurysms rupture and present with subarachnoid hemorrhage before becoming large enough to exert significant pressure on the chiasm or optic nerves. The visual symptoms would be presented as visual field defect or impaired vision. These can be explained as the result of direct compression of the optic pathways, ischemic changes in the visual pathways caused by severe vasospasm after subarachnoid hemorrhage, or intraocular pathology such as retinal hemorrhage. 2 cases of anterior communicating artery aneurysms associated with visual symptoms are presented with a brief review of literatures.
Aneurysm ; Arteries ; Intracranial Aneurysm* ; Optic Nerve ; Pathology ; Retinal Hemorrhage ; Rupture ; Subarachnoid Hemorrhage ; Visual Fields ; Visual Pathways

Apoptosis ; Extracellular Matrix Proteins ; metabolism ; Glaucoma ; pathology ; Glutamic Acid ; metabolism ; Humans ; Neuroglia ; pathology ; physiology ; Nitric Oxide Synthase ; physiology ; Optic Nerve ; physiology ; Optic Nerve Diseases ; pathology ; Retinal Ganglion Cells ; pathology ; Tumor Necrosis Factor-alpha ; physiology