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PubMed1986

Involvement of posterior visual pathways by optic nerve gliomas.

We describe the computed tomographic (CT) findings in seven children with optic nerve gliomas extending posterior to the chiasm. These tumors spread along the optic tracts and in five of seven cases, involved the lateral geniculate bodies and adjacent optic radiations. The propensity for these tumors to extend along both the anterior and posterior visual pathways aids in their diagnosis. An MR scan was obtained in one patient and identified an unexpected site of tumor extension as well as the mass seen by CT.

Child↗
PubMed1982

Ingrowth of optic nerve fibers and onset of myelin ensheathment in the optic tectum of the trout (Salmo gairdneri).

The early differentiation of the optic pathway of the trout was studied by means of autoradiography, silver impregnation and electron microscopy. Ingrowth of the optic nerve fibers into the optic tectum was consistently shown by tracer application and Golgi studies to occur at stage 28, about one week before hatching. Fibers being arranged in discrete bundles were rapidly growing through the longitudinal axis of tectum and at stage 33 reached its posterior end. Cross sections of these fiber bundles at different positions revealed myelin ensheatment to be initiated at the end of stage 34 at the anterior pole of the tectum. Since in the optic nerve of the trout the onset of myelination occurred even earlier (stage 33), it is assumed that this differentiation process follows a rostro-caudal gradient during development of the optic pathway.

Animals↗
PubMed1984

Target selection by surgically misdirected optic fibers in the tectum of goldfish.

This study tested the capacity of regenerating optic fibers to read tectal markers and thereby grow to their appropriate tectal loci when initial position, optic pathway, and interfiber interactions are eliminated as useful cues. The stability of these markers with long-term optic denervation of the tectum was also examined. In adult goldfish optic fibers innervating lateroposterior optic tectum were dissected free of tectum and inserted into the medial anterior region of the opposite "host" tectum. Normally, fibers at this position either innervate medial anterior tectum or follow the medial division of the optic pathway into medioposterior tectum. Host tectum was denervated of all other optic fibers by enucleating its contralateral eye either at the time of the deflection or at various times up to 18 months prior to deflection. The regeneration of these deflected fibers into host tectum was examined by autoradiography and electrophysiology at 1 to 11 months later. At the insertion site deflected fibers split into two groups of roughly equal size. One group directly entered the optic layers of medial tectum and grew posterolaterally across the medial half of tectum into the lateral half. The second group followed an almost direct path to the lateral tectum, sometimes traversing through the deep cell layers of tectum in which optic fibers are not usually found. These fibers subsequently entered the optic layers at the lateral edge of tectum and grew posteriorly. This second path was not seen in controls in which optic fibers from medioposterior tectum were similarly deflected. Instead growth was almost entirely posteriorly directed. On the average by 1.5 months deflected lateroposterior fibers were preferentially distributed in the lateral half of the tectum. Densitometric measurements indicated nearly a 4-fold difference in lateroposterior compared with medial posterior labeling. By contrast, controls in which medial posterior fibers were deflected had 4 times more grains medially than laterally. There was also a posterior over anterior preference, but this was weak. There was no suggestion that long periods of optic denervation prior to deflection or long postoperative periods after deflection of lateroposterior fibers diminished the lateral over medial preference. These findings support the idea that stable tectal markers exist which are differentially read by medial and lateral optic fibers. However, in no case was the innervation by deflected fibers as selective as in the normal projection.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1980

Nasal visual field loss with intracranial lesions of the optic nerve pathways.

Five patients developed nasal visual field defects as a result of involvement of the intracranial portion of the optic nerves. The cause in each patient, respectively, was as follows: (1) dolichoectatic carotid arteries, (2) optochiasmatic arachnoiditis, (3) meningioma of the olfactory groove, (4) pituitary apoplexy, and (5) pituitary chromophobe adenoma. The common factor in these cases was probably impaired circulation in the prechiasmal arterial anastomotic network. The nasal visual field loss present in these cases was characterized by a pattern similar to that seen in glaucoma but with impairment of visual acuity. The superior nasal visual field was usually normal and the lower temporal visual field often defective.

Adenoma, Chromophobe↗
PubMed2004

Expression of phosphacan and neurocan during early development of mouse retinofugal pathway.

We have investigated whether the two major brain chondroitin sulfate (CS) proteoglycans (PGs), phosphacan and neurocan, are expressed in patterns that correlate to the axon order changes in the mouse retinofugal pathway. Expression of these proteoglycans was examined by polyclonal antibodies against phosphacan and N- and C-terminal fragments of neurocan. In E13-E15 mouse embryos, when most optic axons grow in the chiasm and the optic tract, phosphacan and neurocan were observed in the inner regions of the retina. In the chiasm and the tract, phosphacan but not neurocan was expressed prominently at the midline and in the deep parts of the tract. Both proteoglycans were observed on the chiasmatic neurons, which have been shown to regulate axon divergence at the chiasmatic midline and the chronotopic fiber ordering in the tract, but phosphacan appeared to be the predominant form that persists to later developmental stages. Intense staining of both proteoglycans was also observed in a strip of glial-like elements in lateral regions of the chiasm, partitioning axons in the stalk from those in the tract. We conclude that phosphacan but not neurocan is likely the major carrier of the CS glycosaminoglycans that play crucial functions in axon divergence and age-related axon ordering in the mouse optic pathway. Furthermore, localization of these carrier proteins in the optic pathway raises a possibility that these two proteoglycans regulate axon growth and patterning not only through the sulfated sugars but also by interactions of the protein parts with guidance molecules on the optic axons.

Animals↗
PubMed1986

Cell surface changes in the developing optic nerve of mice.

A recently defined antibody to a cell surface protein, M6, inhibits neurite outgrowth in culture (Lagenaur, Fushiki, and Schachner: Soc. Neurosci. Abstr. 10:739, '84). In the developing mouse, the antibody stains all parts of the primary optic pathway at birth. Over the next week, staining is lost from the proximal segment of the optic nerve and a week later from the more central part of the nerve. By contrast staining persists through adulthood in the optic fiber layer of the retina. This means that single axons in the mature optic nerve express the antigen over only the proximal few millimeters of their course and over their terminal region. The results are discussed in relation to the overall maturation of the optic pathway and to the processes of membrane maturation and myelination.

Animals↗
PubMed2003

MR imaging study of edema-like change along the optic tract in patients with pituitary region tumors.

BACKGROUND AND PURPOSE: Edema-like change along the optic tract commonly occurs in association with craniopharyngiomas. The aim of this study was to clarify whether it occurs in association with other common pituitary region tumors and to elucidate its mechanism as seen on MR images. METHODS: Fifty patients with pituitary region tumors that were touching or compressing the optic pathway underwent heavily T2-weighted MR imaging before and after treatment. RESULTS: Edema-like change along the optic tract was visible on the images of four of 25 pituitary adenomas, eight of 11 craniopharyngiomas, one germ cell tumor, and one malignant lymphoma and was not visible on the images of seven meningiomas and five Rathke's cleft cysts. After therapeutic decompression of the optic pathway, the edema-like change disappeared and large Virchow-Robin spaces, present under normal conditions, became visible along the optic tract. Comparison of pre- and post-treatment coronal and axial view MR images revealed that the edema-like change had been located at, along, and/or around the large Virchow-Robin spaces along the optic tract. CONCLUSION: Edema-like change occurs in association with pituitary region tumors other than craniopharyngiomas. It is related with distension of normally present large Virchow-Robin spaces adjacent to the optic tract. Because Virchow-Robin spaces are speculated to be a drainage route of interstitial fluid into the subarachnoid space, their distension may be related to the fluid retention in and along the Virchow-Robin spaces, the outlet of which into the subpial and/or subarachnoid space(s) is blocked by pituitary region tumors.

Adenoma↗
PubMed1976

Differential central distribution of optic nerve components in the rat.

The distribution of Fink-Heimer positive degeneration and neurofibrillar proliferation has been examined in the dorsal lateral geniculate nucleus (dLGN) and superior colliculus of albino and pigmented rats following enucleation between post-natal days 12 and 30 and as adults. With survival times of 6 h to 5 days following enucleation, the location of maximum degenerative reaction stained by the Fink-Heimer method changes with increasing survival time in both regions. In the dLGN contralateral to the eye removal the earliest degeneration appears in a lamina occupying the medioventral extent of the nucleus and is rapidly removed; later degeneration fills a central lamina of the nucleus with a patch of degeneration extending to the outer surface of the nucleus at the mediodorsal margin. The latest occurring degeneration fills the outermost lamina and is still obvious when degeneration is largely dispersed from the inner and central laminae; this outer lamina shows an early filamentous degenerative reaction in the adult. The uncrossed optic pathway occupies a portion of the central lamina of the nucleus, and in albino animals it shows a rapid degeneration and dispersion similar to the innermost lamina on the crossed side; in the pigmented animals degeneration of the uncrossed projection starts as early as that of the albino but persists as long as the degeneration of the central lamina on the crossed side. The degeneration time of the sprouted, uncrossed pathway resulting from unilateral enucleation at birth is similar in albino and pigmented rats and resembles in timing the normal uncrossed pathway of pigmented rats. These results suggest that there are at least 3 different fiber populations in the rat optic nerve with different distribution in the dLGN. The uncrossed optic pathway of albino and pigmented rats appears to differ in fiber composition; this may relate to aberrations in mapping of uncrossed projections in the albino.

Age Factors↗
PubMed2003

Posterior ocular malformations in children: somatic, neuroradiological and cognitive aspects.

AIM: To investigate associated neurological, endocrinological and cognitive dysfunctions in children with visual impairment caused by optic nerve hypoplasia or optic nerve/fundus coloboma and/or microphthalmus. METHODS: Forty children born between 1990 and 1998 were assessed by neurological examination, re-evaluation of neuroradiological investigations, review of medical records and examination of cognitive levels. RESULTS: Neurological dysfunctions (epilepsy and/or motor impairment) were found in 13/28 children with optic nerve hypoplasia and in 3/12 children with coloboma/microphthalmus. The optic pathways were thin in 22/24, an abnormal posterior pituitary gland and/or thin infundibulum was found in 16/22 and absence of septum pellucidum in 14/27 children with optic nerve hypoplasia. Other types of cerebral abnormalities occurred in 9/26 children. Among children with coloboma/microphthalmus, the optic pathways were thin in 4/8 children but none had pituitary or cerebral midline abnormalities. Sixteen children with optic nerve hypoplasia were receiving hormone substitution but none of the children with coloboma/microphthalmus. Thirteen of the 16 children with optic nerve hypoplasia and with an abnormal pituitary region had endocrinological deficiencies. Mental retardation was found in 9/24 of the children with optic nerve hypoplasia and in 5/10 of the children with coloboma/microphthalmus. CONCLUSION: Endocrinological. neurological and neuroradiological defects seem more common in children with optic nerve hypoplasia than in children with coloboma. A pituitary region that appears abnormal in magnetic resonance imaging seems to predict endocrinological deficits in children with optic nerve hypoplasia.

Blindness↗
PubMed1983

Visual-evoked responses in children with optic gliomas, with and without neurofibromatosis.

Gliomas of the optic pathway are considered to be slowly growing, potentially benign neoplasms. Association of this tumor with neurofibromatosis has been well established. We have recently evaluated 7 children with putative evidence of optic glioma, 6 of whom had additional evidence of neurofibromatosis. All children had CT scans and visual-evoked responses. CT scan allows anatomic assessment of the optic nerve mass while evoked responses offer the possibility of identifying functional abnormalities in the optic pathway. It is felt that both these modalities will add in the early diagnosis of optic gliomas and help to further establish the true natural history of this tumor.

Adolescent↗
PubMed1997

Wilbrand's knee of the primate optic chiasm is an artefact of monocular enucleation.

PURPOSE: The anterior chiasmal syndrome consists of a temporal hemianopia or complete visual field loss in one eye, plus a superior temporal hemianopia in the other eye. The superior temporal hemianopia in the other eye is thought to result from injury to Wilbrand's Knee of the optic chiasm. Wilbrand's Knee is a loop of decussating fibers which detours into the contralateral optic nerve before entering the optic tract. I studied the organization of fibers in the optic chiasm of monkeys and humans to verify the existence of Wilbrand's Knee and to elucidate further the pattern of visual field loss seen from lesions of the sellar region. METHODS: The primary optic pathway was labelled in monkeys by injection of [3H] proline into one eye, followed by autoradiography. There were 8 intact Rhesus monkeys and 3 intact squirrel monkeys. In addition, the optic pathway was studied in the Rhesus monkey 6 months and 4 years after monocular enucleation. The optic chiasm was also examined using myelin stains in specimens obtained post-mortem from 3 patients. The patients had lost 1 eye 5 months, 2 years, and 28 years prior to their deaths. Finally, clinical observations were recorded in 3 patients with the anterior chiasmal syndrome. RESULTS: In normal Rhesus and squirrel monkeys, optic nerve fibers crossed the optic chiasm without entering the contralateral optic nerve. After short-term monocular enucleation, fibers from the normal optic nerve were drawn closer to the entry zone of the degenerating optic nerve, but Wilbrand's Knee was still absent. After long-term enucleation, a typical Wilbrand's Knee was induced to form. In the human, Wilbrand's Knee was absent 5 months after monocular enucleation, but emerged in the two cases involving long-term enucleation, in a fashion analogous to the monkey. The case reports describe 3 patients with variants of the anterior chiasmal syndrome from parasellar tumors. CONCLUSIONS: Wilbrand's Knee does not exist in the normal primate optic chiasm. It forms gradually over a period of years following monocular enucleation, presumably from shrinkage of the optic chiasm caused by atrophy of fibers from the enucleated eye. Therefore, the superior temporal hemianopia in the "other eye" seen in the anterior chiasmal syndrome cannot be due to compression of Wilbrand's Knee. I propose that it occurs from combined compression of the optic chiasm and one (or both) optic nerves.

Aged↗
PubMed2000

Magnetic resonance findings and ophthalmologic abnormalities are correlated in patients with neurofibromatosis type 1 (NF1).

In subjects with neurofibromatosis type 1 (NF1), we show that a reduction in the visual field is the most sensitive indicator of gliomas along the optic pathway. Therefore, we conclude that a visual field evaluation is the most sensitive clinical test among those evaluated to predict the presence of optic pathway pathology on an MRI examination. These data may contribute to the establishment of more precise guidelines for the evaluation and treatment of children with NF1.

Adolescent↗
PubMed1995

Efficacy of herpes vaccine and acyclovir (ACV) in a rabbit model following intraocular inoculation of herpes simplex virus.

It has been shown that injection of herpes simplex virus (HSV) type I into the vitreous body of the eye in 18-day-old albino rabbits consistently induced encephalitis. In the untreated group the lesions followed a defined anatomical pathway in the central nervous system and produced a chronic progressive disease with 95% survival. Detailed observations in the spread of HSV along the optic pathway determined the extent of damage at any given day. Some of the old rabbits developed typical herpetic lesions on nose and lips. HSV was demonstrated from these lesions by electron microscopy and also by tissue culture isolation. The combined efficacy of heat-killed herpes vaccine prepared from the same isolate and acyclovir (ACV) in this animal model was studied by starting treatment four days before or four days after the challenge. Ten animals immunised before the challenge were protected. However, immunisation after the challenge not only did not confer protection, but surprisingly, appeared to enhance the primary disease. All 10 rabbits immunised after the challenge developed weakness of the hind legs and progressed very rapidly to paralysis. ACV treatment alone did not completely abrogate the HSV infection, there appears to be reactivation of HSV which produced fresh small lesions. However, a combination of immunisation and treatment with ACV after the challenge of the 10 rabbits in the group prevented the development of weakness of the hind legs or paralysis. Detailed observations on the spread of HSV along the optic pathway revealed that pathological lesions and damage were limited in the ACV and combined treatment with ACV and vaccine group.

Acyclovir↗
PubMed2002

Neurofibromatosis type 1 and the pediatric neurosurgeon: a 20-year institutional review.

Children with neurofibromatosis type 1 (NF1) undergo costly surveillance scanning for a variety of asymptomatic central nervous system lesions whose natural history is poorly understood. We performed a 20-year retrospective chart review of 25 patients with clinically proven NF1 who required surgery (group A) and contrasted this cohort with 150 NF1 patients who did not require surgery (group B). In group A, 52% of patients underwent multiple procedures for more than one lesion (p = 0.043). Group A patients were further distinguished from those in group B by exhibiting a greater number of optic gliomas (p = 0.015), nonoptic intracranial tumors (p = 0.006), cranial nerve (p = 0.000), paraspinal (p = 0.0062), craniofacial (p = 0.001) and visceral (p = 0.03) neurofibromas and moyamoya disease (p = 0.00), as well as a higher frequency of seizure disorder, sphenoid wing dysplasia and poor academic performance. Gadolinium enhancement occurred in 43% of optic gliomas, 50% of parenchymal gliomas, 100% of cranial nerve, 100% of plexus, 67% of paraspinal, 50% of craniofacial and 50% of visceral neurofibromas in group A, while only 1 group B tumor enhanced. In group A, radiological progression occurred after a median of 4 years from initial diagnosis for optic gliomas as well as cranial nerve, plexus and visceral neurofibromas, 2 years for paraspinal neurofibromas and brainstem gliomas and 2.7 years for craniofacial neurofibromas. Only 1 tumor progressed in group B. Therefore, a small subgroup of NF1 patients (12.5%) who require treatment are at risk of subsequently needing further surgical attention, whereas a larger group of NF1 patients (87.5%) carry an indolent form of the disease. We recommend imaging for asymptomatic, gadolinium-enhancing lesions every 2 years for optic pathway and parenchymal gliomas and cranial nerve and visceral neurofibromas, and every year for brainstem gliomas and paraspinal as well as craniofacial neurofibromas. Nonenhancing optic pathway lesions could be followed up radiographically much less often since they do not show progression.

Brain Neoplasms↗
PubMed1978

Malignant optic gliomas in adults.

Malignant gliomas of the optic pathways are uncommon in adults and are rarely diagnosed in life. In three cases of such tumors, the diagnosis was not suspected during life. Neuropathological examination showed involvement of the optic nerves, chiasm, and tracts with extensive involvement of contiguous structures in all of the cases. In view of the consistent clinical features, it is stressed that in adults with progressive visual failure, malignant gliomas of the optic pathways be included in the differential diagnosis.

Aged↗
PubMed1996

Cellular localisation of metabotropic glutamate receptors in the mammalian optic nerve: a mechanism for axon-glia communication.

It has been proposed that neurotransmitter signalling can occur between axons and glia in the mammalian optic nerve in the absence of synaptic specialisations, and that this may be glutamate mediated. Here, the cellular distribution of five metabotropic glutamate receptors (mGluR's 1a, 1b, 1c, 2/3 and 5) have been assessed in the rat optic pathway using specific antibodies. Positive immunoreactivity is found for mGluR2/3 and 5. Both are found in axons, although only mGluR5 is present in the majority of these. Strong immunoreactivity for mGluR2/3 is found in cells in the optic pathway and thalamus. The cellular morphology and distribution is consistent with their being astrocytes. Examination of brain sections stained for mGluR2/3 is consistent with this notion, with many cells having end-feet processes terminating on blood vessels or the pial surface. The axonal immunoreactivity could represent the presence of these receptors on axons, but it is more probable that the receptor protein synthesised in the ganglion cell soma is being transported to the cell terminal in sufficient concentration to be revealed by immunohistochemistry. The reason for the axon-astrocyte signalling is unclear, and may be associated with metabolic coupling. In development, communication between axons and glia mediates a range of functions including pathway selection and myelination. It is probable that in the adult this form of signalling underpins a range of functions that have yet to be described.

Animals↗
PubMed1987

Anterograde tracing of retinal axons in the avian embryo with low molecular weight derivatives of biotin.

Several reactive biotin esters were injected into the eyes of chick and quail embryos at various stages of development. Four of the biotin esters reacted with molecules of the eye tissue and were detected with light and electron microscopy in fluorescein isothiocyanate and peroxidase-avidin incubated sections and whole mounts. Intra and extracellular components of the lens, the vitreous body, and the retina were labeled to different degrees. Three of the biotin esters (biotin-N-hydroxysuccinimidester, biotin-epsilon-aminocaproic acid-N-hydroxysuccinimidester, and desthiobiotin-N-hydroxysuccinimidester) prominently marked the optic fiber layer in the retina and the biotin labels were transported along the optic pathway. The tracers were detected up to the growth cone of axons 24 to 36 hr after injection. Explants from biotin marked retinas were cultured on collagen or basal laminae. During culturing axons grew out from these explants into the substratum showing that labeled tissue and nerve fibers were viable. The development of the optic pathway at the chiasma of quail embryos was studied using the biotin/avidin tracing. The bulk of fibers emerging from the retina crossed as shown by double labeling of both optic nerves in a complex pattern of segregated and interdigitizing axon bundles at the chiasma toward the contralateral side of the brain. From stage 25 onward a minor ipsilateral projection was found. At the same developmental stage a few fibers traveled into the contralateral optic nerve and grew retrogradely toward the contralateral eye. The percentage of specimens having this retino-retinal projection increased during development from 53% (stage 24 to 27; E3.5-E5.5) to 89% (stage 29 to 35; E6-E8) and declined to 40% at late embryogenesis (stage 37 to 41; E9-E12). The fact that all retinal axons were found within predictable pathways with some of them running in the wrong direction suggests that nerve fiber pathways provide accurate positional information, but at best weak directional information for growing nerve fibers.

Animals↗
PubMed2003

Optic gliomas: a retrospective analysis of 50 cases.

PURPOSE: Gliomas of the optic pathways are rare childhood central nervous system tumors. The treatment approach is controversial because of its rarity and the slow and unpredictable growth rates of these lesions. METHODS AND MATERIALS: We reviewed 50 patients with the diagnosis of optic pathway low-grade gliomas treated between January 1980 and December 1995 at King Faisal Specialist Hospital and Research Center, Saudi Arabia. Thirty-five patients presented with chiasmatic/hypothalamic (posterior tumors), and 15 with optic nerve gliomas with or without chiasmal involvement (anterior tumors). Evidence of neurofibromatosis was present in 18 patients. Twenty-nine patients underwent surgery (total or partial resection), and 12 of these received postoperative radiotherapy (RT). Sixteen patients were treated with primary RT. The radiation dose varied between 42 and 54 Gy (median dose 50). RESULTS: The overall actuarial survival rate was 87.5% at 5 years and 75% at 10 years, and the corresponding progression-free survival (PFS) rates were 69% and 62%. Patients with anterior tumors fared better than those with posterior tumors, with a 10-year PFS rate of 72% and 58%, respectively; the difference, however, was not statistically significant (p = 0.58). A PFS advantage was found in favor of patients with posterior tumors treated with RT (primary or postoperative) compared with no RT, with 5-year PFS rates of 68% vs. 42% (p = 0.03). This, however, did not translate into a survival advantage because of the success of salvage treatment. CONCLUSION: In multivariate analysis, age (<3 vs. >3 years) emerged as the only significant determinant for PFS with patients <3 years old faring worse (p = 0.03). Neurologic and endocrine dysfunction are significant problems that need to be addressed.

Adolescent↗