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This article presents the clinical and imaging aspects of some common and important orbital and optic pathway lesions occurring in childhood. Lesions that arise outside of and encroach on the orbit and visual pathways are included. Abnormalities intrinsic to the globe are covered elsewhere in this issue.
To analyze the Electrically evoked response (EER) in relation to the central visual pathway, the authors studied the properties of wave patterns and peak latencies of EER in 35 anesthetized adult cats. The cat EER showed two early positive waves on outward current (cornea cathode) stimulus and three or four early positive waves on inward current (cornea anode) stimulus. These waves were recorded within 50 ms after stimulus onset, and were the most consistent components in cat EER. The stimulus threshold for EER showed a less individual variation than amplitude. The difference of stimulus threshold between outward and inward current stimulus was also essentially negligible. The stimulus threshold was higher in early components than in late components. The peak latency of EER became shorter and the amplitude became higher, as the stimulus intensity was increased. However, this tendency was reversed and some wavelets started to appear when the stimulus was extremely strong. The recording using short stimulus duration and bipolar electrodes enabled us to reduce the electrical artifact of EER. These results obtained from cats were compared with those of humans and rabbits.
We have studied the microglial cells in the normal and regenerating visual pathways of Tinca tinca (Cyprinid, Teleost) by using the lectin from Lycopersicum esculentum (tomato), which, in our case, has been demonstrated as a specific marker for teleost microglia. In the normal fish, there are tomato lectin positive microglial cells in the retina, optic nerve, and optic tectum. Following optic nerve crush, we observed a more extensive labeling of the microglia in the crushed optic nerve and in the contralateral optic tectum affecting the stratum opticum and stratum fibrosum et griseum superficiale. In both cases, there was an increase of rounded and less ramified microglial cells, and granular cells. This response of a more extensive labeling of microglial cells increases to a maximum at 2-3 weeks after the crush; the density of labeled microglial cells decreases after 3 months after crushing. However, in the retina no changes were observed after optic nerve crush. These results suggest that the microglial cells could play an important role in regeneration of fish optic pathway, as other neuroglial cells do.
To analyze the electrically evoked response (EER) in relation to the central visual pathway, the response characteristics of the lateral geniculate neurons (LGNs) of the EER in 35 anesthetized adult cats were studied. Responses of the LGNs showed interindividual variation of more than one log unit in terms of the stimulus threshold for electrical stimuli. As the stimulus intensity increased, the spikes with constant latencies were recorded, which showed bursts with much stronger stimuli. The latencies of the spikes were closely correlated with those of negative components of EER. The LGNs were divided into two major groups by the latency. The periodical and alternative excitation of these neurons contributed to form the first negative wave of EER. The latency of these two major groups of LGNs was reversed when the electrode polarity was changed. At higher stimulus intensities, the components with short latency became dominant and those with longer latency were suppressed. The above results suggested that the periodical excitation of LGNs and the formation of the prominent EER components may result from the interaction between on- and off-type retinal ganglion cells and amacrine cells. It was also suggested that the origins of the wavelets in negative waves of EER at strong stimuli are the bursts of the spikes of the visual cortex neurons.
Studies on critical frequency of photic driving were performed on patients with optic atrophy, moderately expressed suprachiasmal lesions and normal subjects. A reduction was present only in optic atrophy patients. The critical frequency of photic driving showed significant correlations with visual acuity and differential light sensitivity of the areas located within 15 degrees from the fixation point. The correlation proved higher for foveal sensitivity expressed in non-logarithmic rather than in logarithmic units, the opposite being the case for the sensitivity of parafoveal areas. It may be concluded that critical frequency of photic driving is conditioned by the cortical projection zones and visual pathways corresponding to the central 15 degrees of the visual field, but with predominant role of foveal projections.
The presence of bone and fat in the orbit provide high contrast with normal structures on both CT and MR images. In patients with visual deficits or oculomotor paralysis, imaging studies should include the intracranial cavity to evaluate the visual pathways back to the occipital cortex and the cranial nerves within the cavernous sinuses and brainstem. Magnetic resonance images display the intracranial anatomy in exquisite detail. Fat-suppressed magnetic resonance sequences should be used in conjunction with gadolinium enhancement.
The present paper begins with a brief discussion of general clinical features found in patients with lesions of the posterior visual pathways. The author goes on to discuss various mechanisms of restitution of function in the central nervous system, including activation of neural pathways subserved by spared neurons, metabolic modulations, and neural plasticity.
Localized patterned visual stimulation was used in rats to investigate the feasibility of stimulus-dependent induction of the immediate early gene c-fos in neurons of cortical and subcortical visual centers of this mammal. Moving and stationary visual patterns, consisting of gratings and arrays of dark dots, induced Fos-like immunoreactivity in populations of neurons in retinotopically corresponding stimulated regions of the dorsal and ventral lateral geniculate nucleus (dLGN, vLGN), stratum griseum superficiale of the superior colliculus, nucleus of the optic tract, and primary (striate) visual cortex. Only moving stimuli induced Fos-like immunoreactive (FLI) neurons in extrastriate visual areas, particularly in the anterolateral (AL) visual area. This suggests that area AL is equivalent to the motion sensitive areas MT and PMLS of the monkey and cat. Stimulus-induced FLI neurons in the striate cortex were predominantly distributed in layers 4 and 6, while few labeled neurons were present in layers 2-3, and almost none in layer 5. The laminar distribution of stimulus-induced FLI cells in the extrastriate cortical area AL was similar to that of the striate cortex, with the exception that more FLI cells were present in layer 5. Statistical comparison of somata size of the stimulus-induced FLI neurons in dLGN with that of Cresyl violet stained neurons in the same sections revealed that the population of geniculate FLI neurons is composed of relay cells and interneurons.
We have used antisera directed against glial cytoskeletal proteins to examine the distribution and organization of astrocytes in the visual pathways of the goldfish. We describe two different types of cells, which may be distinguished by their unique cytoskeletal proteins. Antibodies raised against a 48 Kd optic nerve protein react with stellate astrocytes in the optic nerve but virtually no glial cells in the brain (although blood vessels and the meninges in the brain were stained). The optic nerve astrocytes form a dense meshwork of processes through which the optic fibers pass. The intraorbital and intracranial segments of the nerve are divided into fascicles, each bounded by a glia limitans, which extend across the optic chiasm. Astroglial cells in the brain bind antibodies raised against a 50 Kd brain cytoskeletal protein. These antibodies show a very limited cross-reactivity with optic nerve cells. Brain astrocytes have filiform profiles and most appear to be deployed as radial glia. The glial fabric of the brain, as revealed by these antibodies, is far more loosely woven than that of the optic nerve. There is a sharp boundary between the two types of glial cells, immediately behind the optic chiasm. Glial processes in the optic tracts arise from cells in the preoptic area, whereas those in the optic tectum arise from cells that reside locally. In the optic tract, a glia limitans was often difficult to discern, whereas in the tectum one was always evident and composed of endfeet at the pial extremities of radial glial processes. These findings are discussed both in the context of previous observations by other workers as well as with regard to their possible functional implications.
A 42-year-old man had progressive distal weakness and muscle atrophy, stocking-type sensory loss, upper motor-neuron and visual pathway lesions, and dysautonomia. Electrodiagnostic tests revealed a generalized sensorimotor peripheral neuropathy that largely involved axons. Low recumbent and upright norepinephrine levels implied a peripheral autonomic defect. Sural nerve biopsy showed mild abnormalities of medium and small size fibers. The patient's mother and two brothers were also affected. Other causes of peripheral motor, sensory, and autonomic failure were eliminated. This kinship does not fit any generally accepted classification of hereditary neuropathies.
"White"tigers show an inherited reduction of pigment, produced by an autosomal recessive gene. The brain of one of these tigers shows an abnormality of the visual pathways similar to abnormalities that are associated with albinism in many other mammals. There is a close relationship between the reduced pigment formation, the pathway abnormality, and strabismus.
Eighty rats received 10 light-shock pairings on two successive days. Seventy-two h after the final training session, subjects received lesions directed at the primary visual areas (deep and superficial layers of the superior colliculus, dorsal lateral geniculate nucleus, pretectal nuclei, visual cortex and thalamic reticular nucleus) and at the nuclei of the lateral lemniscus and reticularis pontis caudalis, proposed components of a primary acoustic startle circuit in the rat. Control animals were sham operated. One day later, all animals were tested for startle by presenting noise bursts of 3 different intensities in the presence or absence of the light conditioned stimulus. Potentiated startle (the difference between light-noise vs noise-alone trials) was significantly attenuated or eliminated by lesions directed at the dorsal nucleus of the lateral geniculate, deep layers of the superior colliculus, visual cortex, and the posteroventral region of the nucleus of the lateral lemniscus. Lesions directed at pretectal nuclei, superficial layers of the superior colliculus, thalamic reticular nucleus, nucleus reticularis pontis caudalis or dorsal nucleus of the lateral lemniscus did not attenuate potentiated startle. The results suggest that the visual pathway that mediates potentiated startle goes from the retina to the dorsal lateral geniculate nucleus to visual cortex to deep layers of superior colliculus and down to the postero-ventral region of the lateral lemniscus where acoustic startle is modulated.
In order to arrive at a quantitative understanding of the dynamics of cortical neuronal networks, we simulated a detailed model of the primary visual pathway of the adult cat. This computer model comprises a 5 degrees x 5 degrees patch of the visual field at a retinal eccentricity of 4.5 degrees and includes 2048 ON- and OFF-center retinal beta-ganglion cells, 8192 geniculate X-cells, and 4096 simple cells in layer IV in area 17. The neurons are implemented as improved integrate-and-fire units. Cortical receptive fields are determined by the pattern of afferent convergence and by inhibitory intracortical connections. Orientation columns are implemented continuously with a realistic receptive field scatter and jitter in the preferred orientations. We first show that realistic ON-OFF-responses, orientation selectivity, velocity low-pass behaviour, null response, and responses to spot stimuli can be obtained with an appropriate alignment of geniculate neurons converging onto the cortical simple cell (Hubel and Wiesel, 1962) and in the absence of intracortical connections. However, the average receptive field elongation (length to width) required to obtain realistic orientation tuning is 4.0, much higher than the average observed elongation. This strongly argues for additional intracortical mechanisms sharpening orientation selectivity. In the second stage, we simulated five different inhibitory intracortical connection patterns (random, local, sparse-local, circular, and cross-orientation) in order to investigate the connection specificity necessary to achieve orientation tuning. Inhibitory connection schemes were superimposed onto Hubel and Wiesel-type receptive fields with an elongation of 1.78. Cross-orientation inhibition gave rise to different horizontal and vertical orientation tuning curves, something not observed experimentally. A combination of two inhibitory schemes, local and circular inhibition (a weak form of cross-orientation inhibition), is in good agreement with observed receptive field properties. The specificity required to establish these connections during development is low. We propose that orientation selectivity is caused by at least three different mechanisms ("eclectic" model): a weak afferent geniculate bias, broadly tuned cross-orientation inhibition, and some iso-orientation inhibition. The most surprising finding is that an isotropic connection scheme, circular inhibition, in which a cell inhibits all of its postsynaptic target cells at a distance of approximately 500 microns, enhances orientation tuning and leads to a significant directional bias. This is caused by the embedding of cortical cells within a columnar structure and does not depend on our specific assumptions.(ABSTRACT TRUNCATED AT 400 WORDS)
OBJECTIVE: Our experience in children with visual pathway glioma (VPG) was reviewed to delineate its clinical characteristics. DESIGN: The charts and imaging studies of 21 children with VPG who were followed up in our centre during the last 12 years were reviewed and summarised. RESULTS: VPG accounted for 13.1% of all brain tumours treated during this period. Sixty two per cent of the children with VPG had neurofibromatosis type 1 (NF-1). Among these, more than 60% were detected as part of routine work up. In some cases decreasing visual function preceded the appearance of the VPG on imaging studies. Tumour growth rate was markedly unpredictable. All treatment modalities employed led to tumour shrinkage and stabilisation for a variable period, but none was successful in totally eradicating the tumour. Complications were less severe after chemotherapy compared with radiotherapy. Three children died, none with NF-1, with a globular hypothalamic/chiasmatic tumour and accompanying electrolyte abnormalities. CONCLUSIONS: NF-1 is a favourable prognostic marker for VPG. Whenever possible a period of observation is necessary before treatment is initiated, during which time tumour size and visual function should be closely followed up; an untoward change in either of these is an indication for the start of treatment, preferably chemotherapy first. The combination of a globular hypothalamic/chiasmatic glioma and electrolyte abnormalities in a child without NF-1 are related to a poor prognosis.
The visual cortex of macaque monkeys has been divided into two functional streams that have been characterized in terms of sensory processing (color/form vs motion) and in terms of behavioral goals (object recognition vs spatial orientation). As a step toward unifying these two views of cortical processing, we compared the behavioral modulation of sensory signals across the two streams in monkeys trained to do a visual short-term memory task. We recorded from individual neurons in areas MT, MST, 7a, and V4 while monkeys performed a delayed match-to-sample task using direction of motion as the matching criterion. This task allowed us to determine if sensory responses were modulated by extraretinal signals related to the direction of the remembered sample. We sorted neuronal responses as a function of the remembered direction and calculated a modulation index, MI = (maximum response--minimum response)/(maximum response + minimum response). In the motion pathway, we found virtually no extraretinal signals in MT (average MI = 0.11 +/- 0.01 SE, 66 cells), but progressively stronger extraretinal signals in later stages, that is, MST (average MI = 0.17 +/- 0.01 SE, 57 cells) and 7a (average MI = 0.23 +/- 0.02 SE, 46 cells). In contrast to MT, strong extraretinal signals for direction matching were found in V4 (average MI = 0.28 +/- 0.02 SE, 94 cells), a relatively early stage of the color/form pathway, even though this pathway is not generally viewed as playing a major role in motion processing. Some cells in V4 were also tested while the animals performed a color matching task. These cells showed memory-related modulation of their response when either color or direction was used as the matching criterion. We conclude that extraretinal signals related to the match-to-sample task may be stronger in the temporal (color/form) pathway than in the parietal (motion) pathway, regardless of the stimulus dimension involved. Furthermore, our results indicate that the temporal pathway is capable of making a significant contribution to motion processing in tasks where motion can be considered as a cue for the identification of object attributes.
While the anatomy of the human brain is well defined, the functional connectivity of its structures is far less understood. Modern neuroimaging techniques offer the unique opportunity of visualizing physiologic activation in central nervous structures and of identifying the elements underlying distributed networks for information processing. Following improved spatial resolution of deoxyhemoglobin-sensitive magnetic resonance imaging, we were able to detect simultaneous signal changes in the lateral geniculate nucleus and primary visual cortex during periodic photic stimulation. Visualization of coupled activation by cross-correlation analysis resulted in the first demonstration of thalamocortical interaction in the primary visual pathway of the intact human brain.
Recordings were made from depth electrodes placed in medial temporal and occipital lobes for the localization of seizure foci in patients with medically intractable psychomotor epilepsy. Electrodes were located in the amygdala and at three rostrocaudal levels of the hippocampal formation including the posterior hippocampal gyrus, which lies medial to the portion of the geniculostriate pathway which passes through the temporal lobe. 1. Approximately 10 per cent of single units recorded from microelectrodes chronically implanted in medial temporal sites were visually responsive. Some of the units in the posterior hippocampal gyrus displayed receptive field characteristics similar to those reported in lower primates, including circular or linear shape, monocular or binocular response, variable (1 to 10 deg) receptive field size, retinotopic organization and sustained or transient response. 2. Visually responsive units were also recorded from lateral geniculate nucleus, pulvinar nucleus and occipital cortex, and their basic response form and latencies compared with the short latency visually responsive cells in medial temporal lobe. 3. The heterogeneity of receptive field characteristics in the medial temporal lobe is consistent with the existence of more than one visual input to this region, while their retinotopic relationship differentiates these receptive fields from those of units studied in the inferior temporal lobe of lower primates. 4. Properties of visual pathways in this region are discussed in relation to several types of temporal lobe function and to memory. Recordings from these neurons offer a rare opportunity for comparison of central visual response properties and receptive field characteristics of humans with those reported in animal studies.
Therapeutic strategy and clinical course of 28 low grade gliomas of the anterior visual tract were analyzed and compared with results of quantitative microscopic examination. Children operated on between 1978 and 1987 were divided into four groups according to the tumor site. DNA microfluorometry and image analysis of bioptic material were used for an objective differentiation between morphologically almost identical gliomas classified as pilocytic astrocytomas (grade I). Six cases of posttraumatic gliosis were examined as controls. Results were tested with factor analysis and by multiple comparison procedures. Significant differences between quantitative parameters of tumors located along the visual pathway were found with the use of computer-aided microscopy. These results corresponded with the clinical experience and patient's outcome. A radical surgical intervention (without additional oncologic therapy) was recommended for patients with intraorbital gliomas which revealed favorable quantitative microscopic features.