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Which out of eagle, rat, duck or owl has the widest angle of binocular vision?
I am pretty sure it's not rat and duck but I am confused between owl and eagle. Can anybody help me figure out which one would have the widest angle of binocular vision?
Take a look at some pictures of eagle and owl and observe their beaks. It will help you in concluding which might have the widest binocular vision angle.
A Novel Binocular Vision System for Wearable Devices
We present a novel binocular imaging system for wearable devices incorporating the biology knowledge of the human eyes. Unlike the camera system in smartphones, two fish-eye lenses with a larger angle of view are used, the visual field of the new system is larger, and the central resolution of output images is higher. This design leads to more effective image acquisition, facilitating computer vision tasks such as target recognition, navigation and object tracking.
Monocular vision loss represents the ideal testing situation, since it is difficult for the patient to separate out what each eye sees individually ( Bruce and Newman, 2010 Newman and Biousse, 2014 ). Truly monocular patients can still navigate a new environment with ease as long as there is useful vision in the unaffected eye. However, observation does have a role in the NOVL patient who complains of monocular vision loss. For example, these patients may attempt to close one eye during examination to simulate their complaint of monocular vision loss ( Bruce and Newman, 2010 Newman and Biousse, 2014 ). Patching the good eye (with a taped patch) of a patient with presumed profound monocular visual loss and observing the patient's behavior during the interview can be helpful. The success of many of the tests that will be presented in the rest of this chapter depends, in part, on the ability of the examiner to use sleight of hand, appropriate banter, and misdirection, much in the same way an illusionist misdirects an audience with hand or body motions or distracts the audience with skillfully engaging banter ( Bruce and Newman, 2010 Newman and Biousse, 2014 ).
Tests of stereopsis are a good way to prove useful binocular vision. Good stereopsis requires good vision in each eye individually and the ability to use the eyes in unison (fusion) ( Levy and Glick, 1974 Bruce and Newman, 2010 Newman and Biousse, 2014 ). When performing stereopsis with a patient suspected of monocular NOVL, the examiner should describe the test in a way that is truthful but does not give away the examiner's true intent, such as saying, “This is a test of your ability to see in 3D.” Table 29.1 shows the association between stereopsis and visual acuity in each eye for the degree of stereopsis recorded ( Levy and Glick, 1974 ).
Table 29.1 . Relationship of Snellen visual acuity and stereopsis *
|Stereopsis (arc seconds)||Visual acuity in each eye (Snellen)|
Adapted from Biousse and Newman (2009) , pp. 7 and 503.
Similarly, using glasses with colored lenses (one green lens and one red lens) or glasses with lenses which are polarized in different directions can help unmask the NOVL patient. Using specially designed eye charts with alternating green and red letters, in the former case, or with polarized letters, in the latter case, can allow the examiner to test the vision in each eye separately without the patient's knowledge ( Levy and Glick, 1974 Bruce and Newman, 2010 Newman and Biousse, 2014 ). In the case of using colored lenses, the patient will only be able to see red letters through the red lens and green letters through the green lens. Similarly, polarized lenses only allow light through them that is projected in the same axis as the lenses and no light will be seen if the axis of the light is 90° away from the axis of lens polarization.
Testing stereopsis and/or using glasses with colored lenses or polarized lenses are excellent choices in the NOVL patient reporting decreased vision in only one eye, because they work on principles that are typically not known to our patients. They allow the patient to keep both eyes open yet actually test each eye individually without altering/manipulating the vision in the “better-seeing” eye, they are quantifiable, and they can be replicated accurately among examiners.
A newly designed pocket eye card, developed for use with patients suspected of NOVL, contains objects of progressively decreasing size, but the minimum visual acuity necessary to see the largest objects on the card is the same as the visual acuity needed to see the smallest objects. Patients with organic visual loss are able to identify all objects on the eye card, while patients with NOVL have a tendency to only identify the larger objects ( Mojon and Flueckiger, 2002 Pula, 2012 ).
Another quantifiable test for determining vision in the reportedly worse eye is to fog (add a moderately high plus lens in front of) the “better-seeing” eye, effectively reducing the vision in that eye. The best vision obtained from the patient will then equal the vision from the nonfogged, “bad” eye ( Miller, 1973 Kramer et al., 1979 Smith et al., 1983 Keltner et al., 1985 Thompson, 1985 Bienfang and Kurtz, 1998 ). Although fogging typically requires the use of a phoropter, a specialized piece of equipment used for refraction in ophthalmology practices, holding up a loose lens in front of the patient has the same effect. Alternatively, fogging glasses can be made from over-the-counter reading glasses, where one lens of a moderately high-power pair of reading glasses (e.g., + 3.50 D) is removed and replaced with either a low-power plus lens (e.g., + 0.25 D) or a lens without any refractive power (plano). These glasses can then be placed on to the patient to obtain a quantifiable measure of vision from the eye in question. These tests have the advantage of not only being able to disprove dysfunction of the involved eye, but to quantifiably demonstrate the degree of function in that eye, thereby allowing the examiner to diagnose NOVL.
Less quantitative maneuvers also exist, such as the prism test or binocular visual field test. In the prism test an object, such as a letter on the eye chart, is presented to the patient and each eye is sequentially occluded. The object chosen for the test should be the largest object that the patient reports being able to see with the “good” eye but unable to see with the “bad” eye. A prism (e.g., 4-D prism) is placed vertically over the “good” eye and the patient is asked if he or she sees two objects ( Bienfang and Kurtz, 1998 Golnik et al., 2004 Chen et al., 2007 Bruce and Newman, 2010 Pula, 2012 Newman and Biousse, 2014 ). If the patient sees two objects, then the examiner has proven useful vision in the “bad” eye. A truly monocular patient would never be able to see two objects on a prism test.
A variation on this test involves occluding the “bad” eye and bisecting the visual axis of the “good” eye with a prism producing monocular diplopia in the “good” eye. The patient is then asked to open the “bad” eye and the prism is quickly shifted to completely cover the “good” eye (ideally, without the patient being aware that the prism has been moved). In patients with extremely poor vision in one eye, no diplopia will be present. However, a patient with NOVL will still claim to have diplopia ( Incesu, 2013 ). This is a useful variation of the prism test but does involve some sleight of hand and may be uncovered by the astute patient with NOVL. Although these tests are useful skills to have, one premise is that the “bad” eye must have profoundly worse vision than the “good” eye. These tests are not useful for patients complaining of subtle vision loss in one eye.
In patients claiming vision worse than 20/400 in one eye, an optokinetic nystagmus (OKN) drum can be used to assess vision in the “bad” eye. Once the “good” eye is occluded, the OKN drum is rotated in front of the patient. The presence of the appropriate fast and slow phase of nystagmus in response to the OKN drum in the “bad” eye demonstrates a visual acuity of at least 20/200 ( Weller and Wiedemann, 1989 Bienfang and Kurtz, 1998 Bruce and Newman, 2010 Newman and Biousse, 2014 ).
The binocular visual field test, another test best utilized with patients complaining of profound monocular vision loss, works by mapping the physiologic blind spot on formal visual field testing. With both eyes open the physiologic blind spot should not be apparent on the visual field display. However, if one eye has profound vision loss, then the blind spot will be present, even with both eyes open. The caveat is that mapping the blind spot even with one eye occluded requires the patient to have good fixation on the specified target throughout the test. If the patient is unable to fixate on the target then the blind spot will not be mapped even in a person with good visual acuity ( Bruce and Newman, 2010 Newman and Biousse, 2014 ).
Testing pupillary responses is essential in patients with monocular visual loss. The lack of a relative afferent pupillary defect (RAPD or Marcus Gunn pupil) implies functioning of the visual system from the retina to the optic chiasm. Ocular diseases responsible for profound visual loss are obvious on examination. When the ocular examination is normal, profound monocular visual loss suggests an optic neuropathy and an RAPD should be obvious. Occult retinal disorders must not be missed in this situation. Posterior to the optic chiasm, up to the level of the lateral geniculate body, a lesion of the optic tract will produce a subtle contralateral RAPD ( Bruce and Newman, 2010 Newman and Biousse, 2014 ).
The tests described in the following section on binocular visual loss can also be applied to patients with monocular visual loss however, in patients with monocular visual loss, the “good” eye must be occluded in order to prove useful vision in the “bad” eye. Astute patients with NOVL may tailor their responses to the eye being tested. Careful misdirection and sleight of hand are sometimes necessary to get a reliable examination in these situations.
This system allows the efficiency in online 3D-stream applications:
Automatic 3D-tracking of dynamic objects in the center of stereo-shooting and keeping in focus
Focusing viewers on the subject of analysis
3D-stereo video lesson recording
3D-stream video system included:
— Controllable cameras and remote controlled servo drive (focus, zoom, axis)
— Industrial box (Linux)
— Software Stereo-codec (Compression/Quality)
— Software 3D-tracking of dynamic object
User: On-line network, router
— Headset provides the best quality : 4K
— Scene management (Zoom, autofocus)
— The choice of the analysis dynamic object with controller
— Motion detection, 3D-Tracking, Camera stabilization
Eduard Lanovyk CEO/CFO
Senior manager/principal with a wide range of experience in asset management and investments.
Eduard has proven business development skills and strong entrepreneurial aptitude. His vast experience of relationship building and networking comes from professional career at SONY, some prominent American and Izraeli corporations.
Thanks to his involvement our company is equipped with a diversified arsenal of practical collaborations and professional contacts in prospective markets like UAE, UK, CEE and Taiwan.
Sergey Dubrovskiy founder and CTO
Sergey co-founded 3D-stream Binocular vision in 2020. From the very beginning of 3D-stream, Sergiy brought in his exhaustive expertise in field of audio/image/video/3D-flow encoding.
-Author of technical patents and scientific articles in the fields of:
— image/video encoding, motion detection and tracking algorithms and multimedia recognition
— optical video surveillance and Infrared systems, signal data processing, creation of radio systems, radars, direction finders.
CTO and COO in Ukrainian radio-telecom and R&D companies
Oleh Trofimiuk, R&D Head
Oleh is co-inventor of binocular 3D — stream technology.
Master degree in nuclear physics, specialist in mathematic, fuzzy logic algorithms, engineering, radar technologies, tracking systems, neural networks, programing and data analysis.
Possible Central Origins of Strabismus
As indicated above, it is the anatomo-functional maturation before and after birth of multiple neural networks from the eyes to the brain that subtend the normal development of visual perception. This occurs by implicating both genetic and epigenetic factors such as postnatal visual experience. Our driving hypothesis here is that any insult to this normal process of maturation may, in turn, generate strabismus. This applies evidently to any level of the sensory and/or motor networks that are involved in the elaboration of visual perception (cf. Figure 2). Some examples are provided below to illustrate this. How an abnormal development of any visual path or any neural activity somewhere within the visual system may lead to strabismus are considered in succession. How an abnormal neural activity in the oculomotor system may lead to strabismus is also discussed.
Abnormal Development of the Visual Paths
First, we hypothesize that any insult during the normal processes of neurogenesis, axonal growth, migration of neurons, synaptogenesis, myelination, apoptosis or even elimination of juvenile exuberant axons, may potentially lead to strabismus. For example, strabismus may be the consequence of the misrouting of some paths within the visual and/or the oculomotor networks.
Abnormal routing of ganglion cell axons
Interestingly, Siamese cats spontaneously display a convergent strabismus. They also have an abnormal predominance of the crossed retino-geniculo-cortical pathway compared to normal cats (Montero and Guillery, 1978 Shatz and Levay, 1979). This results from stagnation at an early stage of development, which itself recalls the development of visual pathways during phylogenesis. We propose that such abnormal predominance of the crossed retino-geniculo-cortical pathway may also be the cause of the early onset convergent strabismus in humans, in which the early asymmetry of the optokinetic nystagmus also persists with age.
Paradoxically, in case of divergent strabismus, it could also be hypothesized that a predominance of the crossed pathways could be the primum movens of strabismus. During evolution, the visual system is first an “only crossed fibers” network with lateral eyes and panoramic vision. It then evolves to a balanced system with equal importance between the direct pathway and the crossed pathway, and frontal eyes allowing binocular vision. We propose here that an abnormal routing of the retinal ganglion cell axons at the level of the optic chiasm might lead to a loss of balance between crossed and direct fibers and thus lead to strabismus. This might occur by an abnormal expression of ephrins, i.e., surface molecules which are specifically implicated in guiding the retinal ganglion cell axons at the level of the optic chiasm during the developmental process (Petros et al., 2009). The axons of ipsilateral projections from temporal retina (direct fibers) express the guidance receptor ephrin B1 (but not the axons of contralateral projections from the nasal retina, i.e., crossed fibers). At the optic chiasm, radial glia cells express ephrin B2, which repulses the ephrin B1 axons from crossing the midline, unlike the contralateral fibers from the nasal retina. Expressions of ephrins and of ephrin receptors are specific and precise timing is necessary to ensure the normal and balanced development of visual pathways. If this system was altered through an abnormal expression of ephrins and/or ephrin receptors during development, an asymmetrical neural network of crossed and uncrossed fibers would develop and could result in the development of strabismus.
Misrouting and abnormal retinotopy
During development, ganglion cell axons reach progressively central visual structures by respecting “retinotopy.” The visual field is thus encoded by neurons with precision from the retina up to the cortex (e.g., Tootell et al., 1998 for review), a necessary condition to ensure normal visual perception, including binocular visual perception. Guidance of axons creating retinotopy is also permitted by ephrins. Gradients of ephrins A and ephrins B, both in the retina and in the visual cortex, allow the creation of x and y coordinates (Cang et al., 2005a,b). This leads to the establishment of neuronal “retinotopic maps,” which are refined with age and visual experience. Again we propose here that abnormal guidance through abnormal levels of ephrins A or B and/or their receptors during development would alter retinotopy and would cause, in turn, strabismus. In some cases at least, distortions within retinotopic maps, which may lead to abnormal retinal correspondence in early onset strabismus (e.g., Wong, 2000 Popple and Levi, 2005 Mansouri et al., 2009 Wang et al., 2012), would therefore be a cause of strabismus rather than a consequence.
The subplate, i.e., mostly temporary cells located below layer VI of Area V1, plays a major role for growing axons to reach the visual cortical plate during development (Ghosh et al., 1980 McConnell et al., 1989). Any abnormality during such process would interfere with normal development of geniculo-cortical connections, thus with normal development of retinotopic maps in V1. Again, this could potentially induce strabismus.
Abnormal cortico-cortical connections
Strabismus is now well known to disrupt the development of numerous cortico-cortical connections implicated in visual perception. These cortico-cortical connections may be “short” and located within one given area or “long,” thus linking various areas which may be located very far from one to the other. Thus, for example, strabismus is known to stabilize normally transient intra-hemispheric cortico-cortical connections in V1, leading to interconnect larger cell groups driven through the same eye than in the normal case (e.g., Löwel and Singer, 1992 Schmidt and Löwel, 2008). It is also known to lead to drastic anatomo-functional changes in the organization of the interhemispheric callosal connections, which normally link reciprocally and homotopically various visual areas to “glue” both visual hemifields into a single scene (Payne, 1990, 1991 Payne and Siwek, 1991a,b Bui Quoc et al., 2012). In particular, in the case of strabismus, it leads to the development of asymmetrical interhemispheric connections which prevent the fusion of both visual hemifields along the vertical midline (Lund and Mitchell, 1979 Milleret and Houzel, 2001 Bui Quoc et al., 2012).
Our idea here is that abnormal anatomical cortico-cortical connections within or between visual cortical areas (whatever their origin) may conversely lead in turn to strabismus. Our hypothesis may be supported first by experiments which have consisted in cutting the CC of adult cats, who rapidly displayed a misalignment of their eyes and even strabismus (Elberger, 1979 Payne et al., 1981 Elberger and Hirsch, 1982). This is further supported by studies showing the implication of the CC during eye movements (e.g., Pasik et al., 1971 Tusa and Ungerleider, 1988 Zernicki et al., 1997). Our hypothesis is also strengthened by analyzing the deficits in visual and visuo-spatial developments that are present in young children with Williams syndrome. They are interpreted as the result of a split between the ventral and dorsal stream processing of visual information (see Figure 2), with a generalized deficit in dorsal stream processing (Atkinson et al., 2001). Of great interest here, the authors underlined that patients with such syndrome also display a much higher incidence of strabismus, visual acuity loss, amblyopia and reduced stereopsis than the general population.
Abnormal Development of Neuronal Activity
In addition to genes, axonal guidance cues and molecules, spontaneous and early visually evoked neural activity are necessary for anatomical and functional refinement of developing visual circuits (e.g., Huberman et al., 2008 for review). Appropriate synchronizations within the visual network then need to develop in order to elaborate visual perception optimally (e.g., Singer, 1999, 2013 Uhlhaas et al., 2009a,b Menon, 2013). Any abnormality in such neural activities from the retina to the visual cortex may also lead to strabismus. Some data in the literature strengthens this idea already. The same applies to neural circuits subtending eye movements.
Effects of an abnormal neuronal activity on visual system
Let us evaluate, in succession, the potential impacts on the alignment of the eyes of: (a) abnormal prenatal retinal waves (b) abnormalities during postnatal visual experience (c) abnormal excitation/inhibition balance and (d) pathological asynchrony of neural activity.
(a) Abnormal retinal waves. First, prenatal spontaneous neural activity in retina, discovered by Galli and Maffei (1988), must be absolutely normal to allow the visual system to organize with precision. It plays both permissive and instructive roles. Indeed, even if this activity is generated very early in life, before vision begins, it is a necessity for the proper development of functional properties of visual neurons and that of the various functional maps all along the visual system. The retinotopic organization of the retino-geniculo-cortical projections is affected first. Indeed, retinotopic maps in the SC, dLGN, and V1 all develop before photoreceptors can be driven by light. The same applies to eye-specific inputs to dLGN and ocular dominance columns in V1. Orientation-selective circuits in V1 also start to form before visual experience begins. The same applies to circuits encoding spatial frequency (Tani et al., 2012). This is possible because spontaneous neural activity in the retina is highly structured, and thus allows the transmission of very precise messages to the central nervous system. This is achieved through slow wave oscillations with very specific spatial and temporal characteristics (Rochefort et al., 2009). If retinal waves display abnormality, for any reason, this entire process of development will be disrupted. The segregation of inputs from both eyes and/or the development of retinotopic maps will be abnormal (e.g., Cang et al., 2005a,b Xu et al., 2011 Ackman et al., 2012 see also Huberman et al., 2008 for review Figure 1). The orientation and/or the spatial frequency maps might also develop incorrectly. In other words, prenatal neural bases for binocular integration and/or for acuity would be altered centrally. It must also be taken into account that such alterations may in turn lead to misalignment of the eyes. For example, this may occur through incongruent interactions with the oculomotor system. As discussed below, this may also occur during development of visual perception itself. Even if it is difficult to prove, such a possibility might unavoidably correspond to the etiology of some forms of strabismus at least.
(b) Abnormal visual perception may induce strabismus. Coming back to the normal process, once the visual system becomes capable of responding to light, sensory-evoked activity then stabilizes the nascent visual connections, refines them further or induces additional circuit properties (e.g., Huberman et al., 2008 for review). But any abnormality within the visual network (because of abnormal retinal waves prenatally or otherwise) will again lead to an abnormal visual perception, with a central origin. Thus, for example, an abnormal segregation of inputs from both eyes and/or an abnormal retinotopic map will lead to an abnormal binocular integration. Abnormalities in the orientation and/or the spatial frequency maps will lead to amblyopia, which may itself lead to strabismus, because of the poor ability to fixate of the amblyopic eye during binocular fixation. A decrease in vision is very well known to impair the proper alignment of the eyes (e.g., Quick et al., 1989). Amblyopia can also be responsible for abnormal saccades and pursuits (e.g., Niechwiej-Szwedo et al., 2010). Considering more extreme conditions, blind people also systematically display completely uncorrelated eye movements.
(c) Abnormal balance excitation/inhibition. The visual system is a complex network of neurons interconnected through excitatory or inhibitory synapses. Suppression is as important as activation, in particular postnatally. Thus, for example and of great importance here, it has been demonstrated that interocular suppression occurring in V1 of strabismic patients involves GABAergic-mediated inhibition (Sengpiel et al., 2006 see also Scholl et al., 2013). It has also been shown recently that it is the transformation of parvalbumin GABAergic (PV) interneurons from excitatory neurons to inhibitory ones that opens the critical period of visual development by internalizing the homeoprotein Otx2 (Sugiyama et al., 2008 Beurdeley et al., 2012). Reducing intraocular inhibition in the adult visual cortex has also been demonstrated to promote plasticity (e.g., Harauzov et al., 2010). In short, a balance between excitatory and inhibitory inputs from retina to cortex is required for elaborating correctly visual perception. Abnormality in this balance, either before or after birth, might lead to abnormal vision and/or uncorrelated eye movements.
(d) Abnormal synchronization of neural activity. The oscillatory pattern of neuronal responses and the synchronization of the oscillations from retina to cortex are now considered as playing a major role in elaborating visual perception (e.g., Gray et al., 1989 Engel et al., 1991 Neuenschwander and Singer, 1996 Castelo-Branco et al., 1998 Fries et al., 2002 see also Singer and Gray, 1995 Singer, 1999, 2013 Engel et al., 2001 for reviews). We propose here that any abnormality of this synchronization, at any level, may lead to strabismus (as well as binocular vision loss and/or amblyopia).
Visual cortex is a highly distributed system implicating more than forty areas distributed from the occipital lobe to the parietal and temporal lobes (Figure 2). To elaborate visual perception, these areas operate in parallel and interact with one another to complement each other. This is achieved through short and long cortico-cortical connections which allow synchronizing of oscillatory neuronal responses within each area and between different areas, mainly in the β and γ frequency range i.e., 20 Hz (Engel et al., 2001 Fries, 2005). Among other functions, this is considered as solving the 𠇋inding” problem which consists in assembling all the attributes of the visual scene (namely location in space, direction of movement, orientation, spatial frequency, disparity etc.) into a coherent form during visual perception in various contexts, attention states etc. (e.g., Singer, 1999, 2013 Fries, 2005 for reviews). Very recently, this has also been established to allow prediction of perception (Hipp et al., 2011).
Such synchronization develops with age, at least up to adolescence, in parallel to the maturation of cortico-cortical connections (including their myelinization) as well as excitatory and inhibitory circuits (Uhlhaas et al., 2009a,b). The maturation of the inhibitory PV neurons again plays a major role in this process since they serve as “pacemakers” for rhythmic neuronal activity, in particular in the γ frequency range (30 Hz). In other words, they assume a pivotal role in the temporal structuring and coordination of neuronal responses (Cardin et al., 2009 Sohal et al., 2009). Of interest, without going into details, all this developmental process of the brain rhythms occurs under strong genetic control (e.g., Buzsáki et al., 2013 for review). Simultaneously, visual perception also increases. Thus, for example, Csibra et al. (2000) measured γ band responses in EEG data in 6- and 8-month old infants during the perception of Kanisza squares that require the binding of contour elements into a coherent object representation. Based on prior behavioral studies that showed that infants up to 6 months of age are unable to perceive Kanisza figures, the authors hypothesized that perceptual binding in 8-month-old infants is related to the emergence of the γ band oscillations.
Not surprisingly, epigenetic factors also play a role in this. Thus, any abnormal postnatal visual experience such as the one resulting from strabismus modifies the normal development of synchronization within the visual system by altering both wiring and neural activity (e.g., Löwel and Singer, 1992 Schmidt and Löwel, 2008). Neuronal synchrony is reduced in visual cortex compared to normal (Roelfsema et al., 1994). Recent data from Hess and his group have strengthened this by establishing that interactions between cells in disparate brain regions are reduced when driven by the amblyopic eye of strabismic subjects, from dLGN to superior visual areas, via V1 (Li et al., 2011). They have also demonstrated that amblyopia (in strabismic patients) is associated to temporal synchrony deficits (Huang et al., 2012).
In turn, we postulate that any abnormality within one given visual area or between at least two visual areas, due to developmental anatomical and/or functional abnormalities somewhere in the visual system, may lead to strabismus (and amblyopia and/or binocular vision loss) by altering synchrony. Since abnormalities in synchrony may occur before or after birth (see above), this may lead to an early or a late strabismus. The same idea may be extended to the oculomotor system since it has been shown recently that it has its own dynamics (Gregoriou et al., 2012 Cordones et al., 2013) and that changes in neural synchrony also occur during development of the motor system (Kilner et al., 2000). Situations when the visual and the oculomotor systems need to interact to elaborate visual perception, i.e., during sensori-motor processing, are also affected. One may underline that our hypothesis is directly in line with increasing evidence that disturbances of synchrony in the developing brain, associated to aberrant neurodevelopment, subtend the cognitive dysfunctions associated to major brain pathologies such as schizophrenia and autism spectrum disorders (Uhlhaas and Singer, 2006 Uhlhaas et al., 2009a,b, 2011). As outlined above, genetics play a major role in that. Thus, for example, in schizophrenic patients, the GABA synthesizing enzyme GAD 65 and the calcium-binding protein parvalbumin are down-regulated in basket cells, while they are crucial for the generation of γ rhythms (Lewis et al., 2005 see also above).
Effects of abnormal neural activity on oculomotor system
Neuronal activity within the various structures implicated in the movement of the eyes also needs to be normal whatever the age. As illustrated below, any abnormality may induce strabismus.
(a) Abnormal extraocular proprioceptive afferents from EOMs to V1. Proprioceptive afferents from EOMs project to V1 (Buisseret and Maffei, 1977). They strongly contribute to the maturation of visual neurons in V1 during development, including their ability to perceive details. Thus, when removed in their entirety early in life, visual neurons do not develop their functional properties properly. It is as if they had never benefited from any visual experience. Also, if proprioceptive afferents in one plane are removed, a perpendicular meridian amblyopia develops (cf. Buisseret, 1995 for review). Since an amblyopia may induce strabismus (cf. above), we put forward the idea that any disequilibrium in the proprioceptive afferents from the EOMs might also induce strabismus. Note that such a process might be extended to any of the central structures which receive afferents from the EOMs, belonging to both the visual and the oculomotor systems (e.g., Donaldson, 1979 Donaldson and Dixon, 1980 Milleret et al., 1987).
(b) Abnormal activity of the vergence neurons and abnormal cortical control. Specific convergence neurons have been identified in the Medial Reticular Formation of the brainstem (Mays, 1984) and abnormal activity, either an excess of activity or a loss of activity, may also be responsible for a deviation of the eyes. Hyperactivity of these neurons could lead to convergent esotropia. Hyperexcitability of the neurons, enhancing the accommodation/convergence loop, may play a role in accommodative esotropia with an excess of convergence. On the other hand, a loss of activity of the neurons, premature apoptosis or a progressive degeneration of the neurons or axons may also induce exophoria and exotropia. Such a progressive insult to the system would explain the natural history of divergent strabismus, in which there is an increase in divergent deviation with time.
Similarly, divergent strabismus may result from an excess of positive inputs from the divergence neurons which have been identified in the Pontine Reticular Formation (cf. also Mays, 1984). It has been hypothesized that a lack of activity of those divergence neurons would induce esotropia.
Higher structures command eye movement and eye position. Our hypothesis here is that the genesis of strabismus may also result from abnormal inputs from those cortical structures which play a role in the triggering of ocular movements such as Frontal Eye Field, Supplementary Eye Field, and Parietal Eye Field (cf. Figure 2). Indeed, it has been shown by neuro-imaging that, in adult strabismic patients, the gray matter volume of those cortical eye fields can be abnormal, either larger or smaller (Chan et al., 2004).
(c) Abnormal activity in Superior Colliculus, cerebellum and vestibular pathways. The SC is a key structure in the control of eye movements. It is another structure that may potentially contribute to inducing strabismus. For example, it has been hypothesized that an insufficiently developed neuronal coupling between both superior colliculi would be implicated in vertical dissociated deviation, which is a particular form of strabismus that is associated with early onset strabismus (Brodsky, 2011 Ten Tusscher, 2011). Cerebellum and vestibular nuclei also control eye movements in normal visual conditions. An insult to those structures could also be hypothesized to be a central cause of strabismus. This is supported by the fact that an insult to the vestibulo-ocular input, through an attempt at the level of the otoliths, can cause this particular vertical strabismus, known as a “skew deviation” (Schlenker et al., 2009). Also, a malformation of the cerebellum, such as the one found in Joubert syndrome or in rhombencephalosynapsis, is associated with strabismus (Canturk et al., 2008 Keskinbora, 2008).
Binocular vision is vision in which both eyes are used together.  It can mean having two eyes instead of one, but more often it means having a visual field which is put together by the brain with input from both eyes. This is the standard equipment for vertebrates and many other types of animals.
Humans have a maximum horizontal field of view of about 200 degrees with two eyes. About 120 degrees make up the binocular field of view (seen by both eyes), and two side fields of about 40 degrees seen by only one eye.  
Our system of vision uses parallax to give precise depth information, called stereopsis.  Such binocular vision is usually accompanied by singleness of vision or binocular fusion, in which a single image is seen even though each eye has its own image of an object. 
Stereopsis is the impression of depth we get when we look at a scene with both eyes. Binocular viewing of a scene creates two slightly different images of the scene in the two eyes due to the eyes' different positions on the head. These differences give information that the brain uses to calculate depth in the visual scene. The term 'stereopsis' is often used as short hand for 'binocular vision', 'binocular depth perception' or 'stereoscopic depth perception', though strictly speaking, the impression of depth associated with stereopsis can also be got under other conditions, such as when an observer views a scene with only one eye while moving. Observer motion creates differences in the single retinal image over time similar to binocular disparity this is referred to as motion parallax.
Some animals, usually but not always prey animals, have their two eyes positioned on opposite sides of their heads to give the widest possible field of view. Examples include rabbits, buffaloes, and antelopes. In such animals, the eyes often move independently to increase the field of view. Even without moving their eyes, some birds have a 360-degree field of view.
Other animals, usually but not always predatory animals, have their two eyes positioned on the front of their heads, thereby allowing for binocular vision and reducing their field of view in favor of stereopsis. Examples include humans, eagles, wolves, and snakes.
Some predator animals, particularly large ones such as sperm whales and killer whales, have their two eyes positioned on opposite sides of their heads. Other animals that are not necessarily predators, such as fruit bats and a number of primates also have forward facing eyes. These are usually animals that need fine depth discrimination/perception for instance, binocular vision improves the ability to pick a chosen fruit or to find and grasp a particular branch.
In animals with forward-facing eyes, the eyes usually move together. Some animals use both strategies. A starling, for example, has laterally placed eyes to cover a wide field of view, but can also move them together to point to the front so their fields overlap giving stereopsis. A remarkable example is the chameleon, whose eyes appear to be mounted on turrets, each moving independently of the other, up or down, left or right. Nevertheless, the chameleon can bring both of its eyes to bear on a single object when it is hunting.
All About Goose Eyesight
Geese can see better, further and a wider range of colors than humans can. This helps to guarantee their survival against predators and to find food. Geese, like most other types of birds, rely mainly on their eyesight for survival.
In fact, eyesight is the dominant sense that a goose possesses, far more highly developed than their sense of taste or hearing.
As a result, goose eyesight is highly evolved - far more so than even human eyesight.
It might surprise you to discover that geese not only see in color, but that they can actually see a wider range of colors than even we can!
Because of the way their retina work, they see four primary colors, instead of the three that the human eye sees.
They can see red, yellow, blue plus green more vibrantly than we do. The green vision, I assume, helps them to find the most tender grasses, weeds and shoots to nibble on.
And thanks to an extra set of cones in their eyes, geese, like chickens, ducks and other birds, can see colors near the ultraviolet spectrum that are invisible to the human eye.
This aids them in choosing mates, identifying their healthiest offspring, detecting predators and finding food.
All super important if you're a goose!
Geese also see pretty well in the dark, with night vision that is more than ten times greater than ours.
Of course domestic geese can't fly, but wild geese will often fly at night because it's cooler, so that night vision comes in handy.
In addition to having good night vision, they also have excellent memories, being able to identify landmarks from previous flights.
Another difference in goose eyesight is that they have predominantly monocular vision instead of binocular vision like humans. Since their eyes are located on the side of the head instead of the front, only one eye can look at a single object at a time.
However, this monocular vision allows each eye to be used separately. This way they greatly increase their field of vision, however their depth perception is more limited.
Humans with binocular vision have better depth perception, but our range of vision does overlap considerably because our eyes are so close together.
That said, geese do have a very narrow field of binocular vision - basically just right in front of their bills.
Scientists have determined that geese have nerves in their eyes that are distributed in a way that enables them to see clearly over a wide range, and in fact, their vision is angled at a slight incline to the horizon.
This enables them to see both the ground and sky clearly at the same time and gives them near panoramic vision. This is very helpful when they're grazing out in an open field.
Geese can also see objects clearly up to three times further than humans can, although they have to tilt their head, for example to watch a plane or hawk flying overhead.
And they compensate for not being able to see the whole panorama ahead of them by quickly swinging their head from side to side.
This allows them to see the object in front of them with one eye from two different angles almost simultaneously.
Geese, like ducks, have a 360 degree range of vision. 180 degrees on each side, both horizontally and vertically. Conversely, most humans only have a 150 degree total range.
Geese Enjoy Unihemispheric Slow-Wave Sleep
Also like ducks (as wellas chickens), geese can let one hemisphere of their brain sleep and rest, while the other side stays wide awake to keep an eye out for predators. This is called Unihemispheric Slow-Wave Sleep.
Instead of closing both eyes and letting the brain lose consciousness, many aquatic and avian species including ducks and geese close one eye and let half of their brain go into a form of non-rapid eye movement deep sleep, while keeping the other eye open and the corresponding half of their brain alert.
Migrating birds and waterfowl use this technique during their migratory flights, basically the equivalent of the co-pilot flying the plane while the pilot naps! It also comes in handy to allow the birds to rest while still staying alert to possible predators.
They can also close both eyes and enjoy a "normal" sleep period giving both sides of their brain time to rest.
I guess the moral of the story is . good luck hiding from a goose!
Further Reading/References The Science Behind Waterfowl Eyesight Nighttime Geese Flights A Birds Eye View Canada Goose Eyes Adapted to Prairie Landscape
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Horses have very large eyes with very large pupils. The eyeballs are placed toward the side of the head, giving horses a wider field of vision. In contrast, dogs and coyotes have eyes placed toward the front of their heads, which narrows their total field of vision.
Horses (as well as some other animals such as sheep and cattle) have a much wider visual field than do dogs or coyotes. Horses can scan their entire surroundings with only slight head movement.
The horse uses only one eye–its monocular vision–to observe the width of its visual field. When a horse sees an object with monocular vision, it will tend to turn toward the object to better hear and also, with binocular vision, better see the object. Binocular vision–use of two eyes–results in better depth perception and a more concentrated field of vision. A brief visual shift sometimes occurs as the horse switches from monocular to binocular vision, which can cause an unexplained “spooking” of the horse.
The size of the pupil improves the ability of a horse to pick up movement. The large size provides the effect of a built-in wide-angle lens, which is further enhanced by the placement of the visual receptors in the retina. The total effect is better peripheral (side) vision. The horse can see movement well. However, it is believed that while the horse sees practically all the way around its body, the image is not as clearly defined as what humans see, especially within 4 feet.
In spite of a wide field of vision, there is a blind spot directly behind a horse. You should avoid approaching a horse from behind because your presence may not be easily detected, and it could startle the horse. Some horses may instinctively kick in this situation. When approaching a horse from the rear cannot be avoided, make a soothing noise to announce your presence. Do not sneak up on a horse from behind.
A question often asked is whether or not horses can see color. It was first thought that both horses and cattle were color blind. If horses can distinguish colors, it is unlikely that their ability to see color is equal to that of other species, such as humans.
How the Eye Works . The eye works like a camera. Light rays enter it through the adjustable iris and are focused by the lens onto the retina, a thin light-sensitive layer which corresponds to the film of the camera. The retina converts the light rays into nerve impulses, which are relayed to the visual center. There the brain interprets them as images.
Like a camera lens, the lens of the eye reverses images as it focuses them. The images on the retina are upside down and they are &ldquoflipped over&rdquo in the visual center. In a psychology experiment, a number of volunteers wore glasses that inverted everything. After 8 days, their visual centers adjusted to this new situation, and when they took off the glasses, the world looked upside down until their brain centers readjusted.
The retina is made up of millions of tiny nerve cells that contain specialized chemicals that are sensitive to light. There are two varieties of these nerve cells, rods and cones . Between them they cover the full range of the eye's adaptation to light. The cones are sensitive in bright light, and the rods in dim light. At twilight, as the light fades, the cones stop operating and the rods go into action. The momentary blindness experienced on going from bright to dim light, or from dim to bright, is the pause needed for the other set of nerve cells to take over.
The rods are spread toward the edges of the retina, so that vision in dim light is general but not very sharp or clear. The cones are clustered thickly in the center of the retina, in the fovea centralis. When the eyes are turned and focused on the object to be seen the image is brought to the central area of the retina. In very dim light, on the other hand, an object is seen more clearly if it is not looked at directly, because then its image falls on an area where the rods are thicker.
Color Vision . Color vision is a function of the cones. The most widely accepted theory is that there are three types of cones, each containing chemicals that respond to one of the three primary colors (red, green, and violet). White light stimulates all three sets of cones any other color stimulates only one or two sets. The brain can then interpret the impulses from these cones as various colors. Man's color vision is amazingly delicate a trained expert can distinguish among as many as 300,000 different hues.
Color vision deficiency (popularly called &ldquocolor blindness&rdquo) is the result of a disorder of one or more sets of cones. The great majority of people with some degree of deficiency lack either red or green cones, and cannot distinguish between those two colors. Complete color vision deficiency (monochromatic vision ), in which none of the sets of color cones works, is very rare. Most deficiencies of color vision are inherited, usually by male children through their mothers from a grandfather with the condition.
Stereoscopic Vision . Stereoscopic vision, or vision in depth, is caused by the way the eyes are placed. Each eye has a slightly different field of vision. The two images are superimposed on one another, but because of the distance between the eyes, the image from each eye goes slightly around its side of the object. From the differences between the images and from other indicators such as the position of the eye muscles when the eyes are focused on the object, the brain can determine the distance of the object.
Stereoscopic vision works best on nearby objects. As the distance increases, the difference between the left-eyed and the right-eyed views becomes less, and the brain must depend on other factors to determine distance. Among these are the relative size of the object, its color and clearness, and the receding lines of perspective. These factors may fool the eye for example, in clear mountain air distant objects may seem to be very close. This is because their sharpness and color are not dulled by the atmosphere as much as they would be in more familiar settings.
Patient Care. Visually handicapped persons who are visiting a clinic for the first time or being admitted to a hospital room require orientation to their environment. Ambulatory patients can be walked around to familiarize them with the location of the bathroom and any other facility they may need to use.
Patients who are in bed following surgery or for therapeutic rest should have articles on their bedside table arranged in the same way all of the time so that they can be found easily. If only one eye is affected, articles should be placed within reach on the unaffected side and persons communicating with the patient also should stand on that side. If peripheral vision is limited, objects and persons should be positioned in the patient's line of vision.
Some patients, especially the elderly, may experience increased sensitivity to glare. Wearing sunglasses outdoors, adjusting the window blinds to deflect the sun, and using indirect lighting can help avoid discomfort. This does not mean that the patient should be in a darkened room. For most, increased illumination makes it easier to see. It is the glare that impairs their vision.
Whenever it is necessary to do something for the visually impaired person, explain beforehand what will be done. This helps reduce confusion and establishes trust in the caregiver. (For patient care, see also blindness .)
Patients with impaired vision may also benefit from such low-vision aids as convex or magnifying lenses that are hand held or mounted on a stand or clipped to the eyeglasses. Adjustable lamps, large-print reading matter, reading stands, writing guides and lined paper, and felt-tipped pens can facilitate reading and writing and improve the quality of life of a person with limited vision.
Categories of nursing diagnoses associated with impaired vision include Anxiety, Ineffective Coping Patterns, Fear of Total Blindness, Impaired Home Maintenance Management, Potential for Physical Injury, Impaired Physical Mobility, Self-Care Deficit, and Self-Imposed Social Isolation.
Owl Eyes & Vision
Of all an owl's features, perhaps the most striking is its eyes. Large and forward facing, they may account for one to five percent of the owl's body weight, depending on species. The forward facing aspect of the eyes that give an owl its "wise" appearance, also give it a wide range of "binocular" vision (seeing an object with both eyes at the same time). This means the owl can see objects in 3 dimensions (height, width, and depth), and can judge distances in a similar way to humans. The field of view for an owl is about 110 degrees, with about 70 degrees being binocular vision.
By comparison, humans have a field of view that covers 180 degrees, with 140 degrees being binocular. A woodcock has an amazing 360 degree field of view, because its eyes are on the side of its head. However, less than 10 degrees of this is binocular.
An owl's eyes are large in order to improve their efficiency, especially under low light conditions. In fact, the eyes are so well developed, that they are not eye balls as such, but elongated tubes. They are held in place by bony structures in the skull called Sclerotic rings. For this reason, an owl cannot "roll" or move its eyes - that is, it can only look straight ahead!
The owl more than makes up for this by being able to turn its head up to 270 degrees left or right from the forward facing position, and almost upside down. There are several adaptations that allow this, outlined in the owl skeletal system article.
As most owls are active at night, their eyes must be very efficient at collecting and processing light. This starts with a large cornea (the transparent outer coating of the eye) and pupil (the opening at the centre of the eye). The pupil's size is controlled by the iris (the coloured membrane suspended between the cornea and lens). When the pupil is larger, more light passes through the lens and onto the large retina (light sensitive tissue on which the image is formed).
The retina of an owl's eye has an abundance of light-sensitive, rod-shaped cells appropriately called "rod" cells. Although these cells are very sensitive to light and movement, they do not react well to colour. Cells that do react to colour are called "cone" cells (shaped like a cone), and an owl's eye possesses few of these, so most Owls see in limited colour or in monochrome.
Since owls have extraordinary night vision, it is often thought that they are blind in strong light. This is not true, because their pupils have a wide range of adjustment, allowing the right amount of light to strike the retina. Some species of owls can actually see better than humans in bright light.
To protect their eyes, owls are equipped with 3 eyelids. They have a normal upper and lower eyelid, the upper closing when the owl blinks, and the lower closing up when the owl is asleep. The third eyelid is called a nictitating membrane, and is a thin layer of tissue that closes diagonally across the eye, from the inside to the outside. This cleans and protects the surface of the eye.