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Review of diseases of the optic nerve, optic tract, and visual cortex: 1975-76.

The ophthalmic literature dealing with diseases of the optic nerve, the optic tracts, and the visual cortex was reviewed for the period November 1975 through November 1976. Twenty-nine papers on topics of interest to optometrists were abstracted. The main areas of interest include: papilledema and optic atrophy (with ophthalmoscopic signs of both optic atrophy and papilledema); giant-cell arteritis; papillitis; interesting malformations of the face, palate, and orbital position that occur in conjunction with microphthalmus, situs inversus, and hypoplasia and aplasia of the optic nerve; the proposed association of myopia with unusual eyebrows; myelinated nerve fibers at the nerve head; pigment anomalies; the continuing discussion of nerve-head blood supply; an unexpected cause for nerve-head neovascularization; the importance of the swinging-flashlight test in the diagnosis of glaucoma; an unusual type of glaucomatous cupping; doubts about the peripapillary "halo" as a sign of glaucoma; new uses for old field tests; and new methods of ocular photography.

Abnormalities, Multiple

Experimental injury of the optic nerve with optic disc swelling.

An ultrastructural study utilizing horseradish peroxidase was performed to determine the mechanism and consequences of leakage of vascular protein following injury of the optic nerve. Unilateral optic nerve injuries were produced in four rhesus monkeys by making a cautery lesion on the retrobulbar portion of the optic nerve. Optic disc changes were followed with stereo fundus photography and fluorescein angiography. Three to 14 days after injury horseradish peroxidase was given intravenously and the tissue was prepared for electron microscopy, including serial sections of selected tissue blocks. Fundus photography and fluorescein angiography showed edema of the optic disc in two animals. There was leakage of horseradish peroxidase into the optic nerve head from the optic nerve lesion and the peripapillary choriocapillaris. Although the pathway of horseradish peroxidase leakage in the injured optic nerve was not entirely clear, serial sections indicated intraendothelial channels as one possible route. Alterations of the optic nerve head were confined to the axon segments anterior to the injury, and included aggregation of mitochondria, disruption of neurotubules, and swelling. These findings suggest that optic nerve injury produces damming of axoplasmic flow and that swelling of the optic nerve head is the result of axon enlargement.

Animals

Surgical lesions of the intracranial optic nerves and optic chiasm.

Compressive tumors and vascular lesions affecting the intracranial optic nerves and optic chiasm are of interest to both the neurosurgeon and the neuro-ophthalmologist. Common types of tumors that occur in the chiasmal and parasellar regions are discussed in terms of their course, neuro-ophthalmologic implications, and surgical treatment by the transsphenoidal approach as opposed to the standard subfrontal approach. Vascular lesions that cause visual distrubances, including intracranial aneurysms and arteries acting as compressive lesions of the chiasm and nerves or in conjunction with tumors, are discussed.

Aneurysm

An electron microscopic study on the blood-optic nerve and fluid-optic nerve barrier.

Utilizing horseradish peroxidase as a tracer, electron microscopic studies were done on the blood-optic nerve and fluid-optic nerve barrier to the peroxidase diffusion. Following intravenous injection the peroxidase was observed to fill the lumen of the capillaries of the laminar, prelaminar and orbital portions of the optic nerve but there was no penetratation of the capillary walls. The obstruction of the tracer diffusion out of capillary walls was attributed to the tight junctions between the endothelial cells. Peroxidase penetration was also absent in the capillaries of the pia and dura mater, however, was observed in pinocytotic vesicles of the endothelial cells. Lateral diffusion from the surrounding choroid into the optic nerve was detected but diffusion from the prelaminar optic nerve into the juxta-optic nerve retina was prevented by the Kuhnt intermediary tissue. Tight junctions which prevented peroxidase diffusion were found between the glial cells of the Kuhnt tissue, and this tissue was the barrier between the prelaminar optic nerve and the juxta-optic nerve retina. Peroxidase which was given into the lateral ventricle of the brain appeared in the subarachnoidal space around the optic nerve and penetrated freely into the optic nerve. The pial surface of the optic nerve possess no barrier activity. Peroxidase could be traced along the intercellular space between glial cells and optic nerve fibers. The basal lamina of the optic nerve capillaries was filled with peroxidase but diffusion into the capillary lumen was obstructured by the tight junctions between the endothelial cells.

Animals

[Correlation between conduction velocities in fibers of the optic nerve and optic radiation in cats].

The responses of dorsal lateral geniculate body units to striate cortex and optic chiasm stimulation were examined in cats immobilized with d-tubocurarine. A high correlation between antidromic responses to striate cortex and orthodromic responses to optic chiasm stimulation was found (r=0.895; P=0.01). 9% of neurons responded antidromically to optic chiasm stimulation indicating the existence of centrifugal fibres in the optic nerve. The functional significance of time dispersion of the afferent volley in visual system is discussed.

Animals

Electron microscopy of the mouse optic nerve: a quantitative study of the total optic nerve fibers.

The total number of myelinated and unmyelinated nerve fibers was counted in a montage of electron micrographs prepared to cover the entire profile of the mouse optic nerve in transverse section. Many astrocytic processes form a barrier structure all around the optic nerve. As a whole, the mouse optic nerve consists of one fascicle where the nerve fibers, the glia cells and their processes, and the capillaries are fitted closely together to fill substantially all of the available space. No tissue space accompanied with connective tissue septa penetrates into the fascicle, except for those situated around the arteriole and venule. The total number of 64,746 myelinated nerve fibers in the optic nerve in one side was counted. This corresponds to about 98.8% of the total number of the optic nerve fibers. The total number of 807 unmyelinated nerve fibers was also counted. This corresponds to about 1.2% of the total nerve fibers. The external diameter of every myelinated fiber, including the myelin sheath, was measured on the montage micrograph and its frequency distribution was examined. The diameter of the myelinated fibers ranges from 0.3 to 4.2 mu and its mean value is 0.96 mu. The frequency distribution of fiber diameter is unimodal with a peak at 0.7 to 0.9 mu. A regional heterogeneity in fiber size is found in the optic nerve. The nerve fibers in the peripheral area of the nerve are relatively small and uniform in diameter, whereas those in the central area show a fairly wide range in diameter.

Animals

Cavernous hemangioma of optic chiasm, optic nerves and right optic tract. Case report and review of literature.

Diminishing right ocular visual acuity for three weeks in a 30 year old man was confirmed by examination. Bilateral scotomata and bitemporal hemiachromatopsia indicated a chiasmal lesion; reduced visual acuity and Marcus Gunn pupil of the right eye and left relative temporal hemianopia indicated asymmetric involvement. Erythrocytes in the CSF verified a suspected subarachnoid bleed; contrast-enhanced CAT scan demonstrated a suprasellar mass. A cystic, multiloculated, bluish mass distorted the right optic nerve, tract, and chiasm. A hematoma was evacuated and biopsy revealed a cavernous hemangioma of the right optic nerve. Post-operatively, visual acuity has recovered in the right eye but a left homonymous temporal hemianopia has developed.

Adult

Electrical potentials from the eye and optic nerve of Strombus: effects of electrical stimulation of the optic nerve.

1. Photic stimulation of the mature eye of Strombus can evoke in the optic nerve 'on' activity in numerous small afferent fibres and repetitive 'off' bursts of afferent impulses in a smaller number of larger fibres. 2. Synchronous invasion of the eye by electrically evoked impulses in small optic nerve fibres (apparently the 'on' afferents, antidromically activated) can evoke a burst of impulses in the larger 'off' fibres which propagate away from the eye. Invasion of the eye via one branch of optic nerve can evoke an answering burst in another branch. 3. Such electrically evoked bursts are similar to light-evoked 'off' bursts with respect to their impulse composition, their ability to be inhibited by illumination of the eye, and their susceptibility to MgCl2 anaesthesia. 4. Invasion of the eye by a train of repetitive electrically evoked impulses in the absence of photic stimulation can give rise to repetitive 'off' bursts as well as concomitant oscillatory potentials in the eye which are similar to those normally evoked by cessation of a photic stimulus. 5. The electrically evoked 'off' bursts appear to be caused by an excitatory rebound following the cessation of inhibitory synaptic input from photoreceptors which can be antidromically activated by electrical stimulation of the optic nerve. 6. The experimental results suggest that the rhythmic discharge of the 'off' fibres evoked by the cessation of a photic stimulus is mediated by the abrupt decrease of inhibitory synaptic input from the receptors.

Action Potentials

Spectrum of optic nerve hypoplasia.

Optic nerve hypoplasia is a non-progressive condition characterised by subnormal vision and a subnormal number of optic nerve axons. It may be unilateral or bilateral, isolated or combined with other defects. Analysis of fundus photographs from a series of 7 patients with a stationary abnormality of different degrees showed that the functional defects could be closely correlated with defects in the retinal nerve fibre layer. Our observations show that the condition has a wide range of both functional and anatomical defects and that a subnormal diameter of the optic disc is not a requisite for the diagnosis. Presumably, there is also a wide variety of causes, not only a primary failure of development of retinal ganglion cells. We suggest that optic nerve hypoplasia can be viewed as a non-specific manifestation of damage to the visual system, sustained any time before its full development.

Adolescent

Optic nerve hypoplasia.

Optic nerve hypoplasia is rarely met in otherwise normal eyes. Three unilateral cases of patients with small optic disks, reduced visual acuity, and convergent squint on the affected eye are presented. The anomaly is probably caused by failure of development of the ganglion cell layer of the retina causing a small optic nerve head with normal central vessels. Inheritance or induction by drugs could not be found in our cases.

Child

[Hypoplasia of the optic nerve head].

Optic nerve hypoplasia is not a rare eventuality in children. This report discusses the clinical features of 10 new cases on a multiple point of view including optic canal tomography, fluorescein angiography and cat's examination. Optic nerve hypoplasia is not always accompanied by decreased visual acuity: sector fields are often identified in these cases.

Adult

Altitudinal field defects and retinal nerve fibre degeneration in optic nerve lesions.

Altitudinal visual field defects in five cases with optic nerve lesions due to optic glioma, compression, and trauma are correlated to retinal nerve fibre degeneration, recorded with ophthalmoscopy and photography in red-free light. In one case the optic nerve was damaged at operation. Repeated fundus photography was used to record the evolution of descending optic atrophy. The results suggest that the findings in funduscopic examination of the retinal nerve fibre layer should be cautiously judged and the method cannot replace careful perimetry in cooperative patients.

Adult

Elimination of cobalt from the frog brain introduced into the optic centres through the optic nerve.

One optic nerve in several frogs was filled with cobaltous-lysine complex, and the animals were left to survive from 1 day to 52 days. Degenerated cobalt-filled retinal fibres were phagocytosed by ependymo-glial, and microglial cells. The cobalt appeared in the ependymo-glial cells in the 4th postoperative day, and its amount was greatly reduced by the 52nd day. Within 12 days the labelled axons were replaced by cobalt-loaded microglial cells in the termination sites of optic fibres. By the end of the experimental period, the number of labelled cells increased in the periventricular layers, and decreased in places where retinal fibres had terminated. These processes were accompanied by the appearance of cobalt in the choroid plexus. It is supposed that glial cells dischargd the cobalt into brain ventricles, and the metal left the nervous tissue via the cerebrospinal fluid.

Animals

Centrifugal nerve fibers in the adult human optic nerve: 16 days after enucleation.

The optic nerve stump of a 56-year-old patient was removed 16 days after enucleation of the corresponding eyeball. The stumps of numerous centrifugal (efferent) nerve fibers are demonstrated histologically in this optic nerve central to the 16-day old surgical cut. Electron-microscopic views of the centrifugal nerve fibers are offered for the first time. The findings are further evidence for the existence of centrifugal fibers in the human optic nerve. The nerve fiber stumps exhibit reactive terminal swellings pointing towards the surgical cut indicating axoplasmic flow in that direction. It is of special interest that the centrifugal nerve fibers of this 56-year-old patient lack any evidence of attempted regeneration that has been observed under similar conditions in th optic nerve stump of a child.

Age Factors