Unit2-VisualDisorders.pdf

1 Illusory contours illusion Illusory contours are visual illusions that evoke the perception of an edge without a luminance or color change across that edge. Illusory brightness and depth ordering frequently accompany illusory contours. Our ability to see this particular illusion relies upon a nor...

1 Illusory contours illusion Illusory contours are visual illusions that evoke the perception of an edge without a luminance or color change across that edge. Illusory brightness and depth ordering frequently accompany illusory contours. Our ability to see this particular illusion relies upon a normally developed visual cortex and knowledge of English letters. The retinal inputs are simply black lines on a white background. Higher-order visual cortex is providing the information to create the perception of a capital letter E. 2 Visual processing: From image, through eye, to primary visual cortex in posterior occipital lobe 3 Diagram of visual fields – note terms that we use to discuss different regions of the visual field Visual field – the entire area or field of view that can be seen when an eye is fixed straight at a point on space. Descriptions of the visual field include: vertical meridian – line dividing the field of view into left/right halves; horizontal meridian – line dividing field of view into top and bottom halves. Hemifield = ‘half the visual field,’ typically refers to left and right halves only (not top/bottom) Quarterfield – ‘one quarter or quadrant of the visual field,’ defined by the quadrant created by the vertical and horizontal meridian lines 4 Diagram of the eye cut in half. Iris is the part that is the color you can see. The middle black hole is the pupil. Light travels through the pupil to the retina at the back of the eye. The blind spot is the place in the visual field that corresponds to the lack of light-detecting photoreceptor cells on the optic disc of the retina where the axons of the retinal ganglion cells exit the retina and form the optic nerve. (Note that the cell bodies of the optic nerve axons are the retinal ganglion cells.) Because there are no cells to detect light on the optic disc, the corresponding part of the field of vision is invisible. Some process in our brains “fills-in” the blind spot with estimates of expected visual info based on surrounding detail and information from the other eye, so we do not normally perceive the blind spot. 5 Note that retina has photoreceptor layer that absorbs light at the back layer. Modulatory neurons include amacrine, horizontal, and bipolar cells. Retinal ganglion cells are sensory neurons that send outputs to the primary visual cortex. [In contrast, octopus and other cephalopod eyes are ‘inside out’: the light reaches the photoreceptor layer fist which connect to modulatory neuron layers and then to retinal ganglion cells at the back of the eyeball. Octopuses thus have no blind spot, as the retinal ganglion cells simply send axons out the back of the eyeball in a way that doesn’t overlap the photoreceptors.] 6 The fovea is responsible for sharp central vision (also called foveal vision), which is necessary in humans for activities where visual detail is of primary importance, such as reading and driving. EXTRA NOTES: The fovea is surrounded by the parafoveal belt, and the perifoveal outer region. The parafovea is the intermediate belt, where the ganglion cell layer is composed of more than five rows of cells, as well as the highest density of cones; the perifovea is the outermost region where the ganglion cell layer contains two to four rows of cells, and is where visual acuity is below the optimum. The perifovea contains an even more diminished density of cones, having 12 per 100 micrometres versus 50 per 100 micrometres in the most central fovea. This, in turn, is surrounded by a larger peripheral area that delivers highly compressed information of low resolution following the pattern of compression in foveated imaging. Approximately half of the nerve fibers in the optic nerve carry information from the fovea, while the remaining half carry information from the rest of the retina. The parafovea extends to a radius of 1.25 mm from the central fovea, and the perifovea is found at a 2.75 mm radius from the fovea centralis. Layers, from the bottom of image to the top: Outside eyeball Pigment epithelium Photoreceptors Outer limiting membrane Outer nuclear layer (rod, cone cell bodies) Outer plexiform layer (rod/cones to bipolar, horizontal cells) Inner nuclear layer (bipolar, horizontal, amacrine cell bodies) Inner plexiform layer (bipolar to ganglion cells) Ganglion cell layer Inner limiting membrane Image from Curcio & Rodieck 7 Left image: picture of the retina at the back of the eye as seen through the pupil Right image: Rods (R) and cones (C) seen through a scanning electron microscope. Each rod is about one micron across. Photoreceptors A photoreceptor cell is a specialized type of neuroepithelial cell found in the retina that is capable of visual phototransduction. The great biological importance of photoreceptors is that they convert light (visible electromagnetic radiation) into signals that can stimulate biological processes. To be more specific, photoreceptor proteins in the cell absorb photons, triggering a change in the cell's membrane potential. There are currently three known types of photoreceptor cells in mammalian eyes: rods, cones, and intrinsically photosensitive retinal ganglion cells. The two classic photoreceptor cells are rods and cones, each contributing information used by the visual system to form a representation of the visual world, sight. The rods are narrower than the cones and distributed differently across the retina, but the chemical process in each that supports phototransduction is similar. A third class of mammalian photoreceptor cell was discovered during the 1990s: the intrinsically photosensitive retinal ganglion cells (see upcoming slide). These cells do not contribute to sight directly, but are thought to support circadian rhythms 8 and pupillary reflex. Lower right image from http://webvision.med.utah.edu/photo1.html 8 Graph on right shows density of rod and cone photoreceptors across the retina. Note that the fovea has a very high concentration of cones and no rods in the center. There are major functional differences between the rods and cones: There are ~120 million rods. The rods are functional in low light (like starlight-level) – vision under these conditions is called ‘scotopic’. Even one photon can activate a rod photoreceptor. Each rod sends signals to many retinal ganglion cells (RGCs). Thus rods have a high sensitivity to light, but lower visual acuity due to the spreading of the rod signal across many retinal ganglion cells. The rods are good for night vision and movement. In contrast, the ~6 million cones are concentrated in the fovea (but do exist at a lower density across most of the retina). 10s to 100s of photons are needed for the activation of one cone, but each cone sends signals to just 1 or a few RGCs. Thus cones are less sensitive to light (better in day time), but have very good visual acuity as the cone signal does not spread across multiple RGCs. Vision under high-light conditions is called ‘photopic.’ In humans, there are three different types of cone cell, distinguished by their pattern of response to light of different wavelengths. Color experience is calculated from these three distinct signals, via an opponent process. This explains why colors cannot be seen at low light levels, when only the rod and not the cone photoreceptor cells are active. The three types of cone cell respond (roughly) to light of short, medium, and long wavelengths, so they may respectively be referred to as S-cones, M-cones, and L-cones. 9 Cones sometimes are called red, green, and blue cones (matching the L, M, and S cones, respectively), but this terminology is not as accurate. Note how each type of photoreceptor is responsive to a wide range of wavelengths, with a peak response at which that photoreceptor is most responsive. The data in the graph are from human photoreceptors. Bowmaker & Dartnall (1980) projected a known amount of light directly through the outer segments of photoreceptors and measured how much light was absorbed by the photopigment molecules. This procedure is called microspectrophotometry. They found four classes of photopigments as shown in the above graph. The colors of the curves do not represent the colors of the photopigments, but rather the approximate wavelength of maximum absorbance (420 nm for the short wavelength sensitive cones, 498 nm for the rods, 534 nm for the middle wavelength sensitive cones, and 564 curves is for the long wavelength sensitive cones). S-cone peak response: 420 nm M-cone peak response: 534 nm L-cone peak response: 564 nm Rods peak response: 498 nm In accordance with the principle of univariance, the firing of the cell depends upon only the 10 number of photons absorbed. The different responses of the three types of cone cells are determined by the likelihoods that their respective photoreceptor proteins will absorb photons of different wavelengths. So, for example, an L cone cell contains a photoreceptor protein that more readily absorbs long wavelengths of light (that is, more "red"). Light of a shorter wavelength can also produce the same response from an L cone cell, but it must be much brighter to do so. Principle of univariance: states that one and the same visual photoreceptor cell can be excited by different combinations of wavelength and intensity, so that the brain cannot know the color of a certain point of the retinal image without information from other photoreceptors. One individual photoreceptor type can therefore not differentiate between a change in wavelength and a change in intensity. Thus the wavelength information can be extracted only by comparing the responses across different types of receptors. The principle of univariance was first described by W. A. H. Rushton. The principle of univariance can be seen in situations where a stimulus can vary in two dimensions, but a cell's response can vary in one. For example, a colored light may vary in both wavelength and in luminance. However, the brain's cells can only vary in the rate at which action potentials are fired. Therefore, a cell tuned to red light may respond the same to a dim red light as to a bright yellow light. To avoid this, the response of multiple cells is compared. Both cone monochromats (those who only have 1 cone type) and rod monochromats (those with no cones – only rod vision) suffer from the principle of univariance – they have severe color blindness due to a lack of other photoreceptor types for comparison of color inputs. 10 Rod and cone photoreceptors are found on the outermost layer of the retina; they both have the same basic structure. Closest to the visual field (and farthest from the brain) is the axon terminal, which releases a neurotransmitter called glutamate (main excitatory neurotransmitter in the CNS) to the retinal bipolar cells. Farther back is the cell body, which contains the cell's organelles. Farther back still is the inner segment, a specialized part of the cell full of mitochondria. The chief function of the inner segment is to provide ATP (energy) for the sodium-potassium pump. Finally, closest to the brain (and farthest from the field of view) is the outer segment, the part of the photoreceptor that absorbs light. Outer segments are actually modified cilia that contain disks filled with opsin, the molecule that absorbs photons, as well as voltage-gated sodium channels. The membranous photoreceptor protein opsin contains a pigment molecule (a molecule that can absorb particular wavelengths of light; molecular structure determines what wavelength can be absorbed) called retinal (which is actually a form of vitamin A). In rod cells, these (pigment molecule plus retinal) together are called rhodopsin. In cone cells, there are different types of opsins that combine with retinal to form pigments called photopsins. Three different classes of photopsins in human cones react to different ranges of light frequency (i.e., different wavelengths of light), a differentiation that allows the visual system to calculate color. The function of the photoreceptor cell is to convert the light energy of the photon into a form of energy communicable to the nervous system and readily usable to the organism: This conversion is called signal transduction. 11 The Troxler Effect is named after Swiss physician and philosopher Ignaz Paul Vital Troxler (1780- 1866). In 1804, Troxler made the discovery that rigidly fixating one’s gaze on some element in the visual field can cause surrounding stationary images to seem to slowly disappear or fade. They are replaced with an experience, the nature of which is determined by the background that the object is on. This is known as filling-in (like the filling-in that happens with our blind spot). The Troxler effect illustrates the importance of saccades, the involuntary movements of the eye which occur even while one’s gaze is apparently settled. If we could perfectly fixate on some point in our visual field by suppressing saccadic movement, a static scene would slowly fade from view after a few seconds due to the local neural adaptation of the rods, cones and retinal ganglion cells in the retina. In brief, any constant light stimulus will cause an individual neuron to become desensitized to that stimulus, and hence reduce the strength of its signal to the brain. When we attempt to fix our gaze on an object, the eye undergoes extremely rapid and relatively large-scale sudden movements called microsaccades, in contrast to saccadic drifts or small oscillations. Microsaccades cause the pattern of activity which forms the retinal image to shift across hundreds of photoreceptors at a time, providing a constant “refreshing” of the image (Martinez-Conde 2010). The Troxler effect occurs with any stationary stimulus, but it is particularly fast-acting and noticeable with low-contrast stimuli (so note the persistence of the cat’s grin, which is of higher contrast than the rest of the image). https://www.illusionsindex.org/i/troxler-effect 12 Photoreceptor cells are typically arranged in an irregular but approximately hexagonal grid, known as the retinal mosaic. Retinal Images: Colorized images showing the arrangement of L (red), M (green), and S (blue) cones in the retinas of different human subjects. All images are shown to the same scale. Note how some retinas are visibly more green (M cones) than others. These are examples of how variable the numbers of different types of cones are among eyes. ++++++++++++++++ From Paper: Organization of the Human Trichromatic Cone Mosaic Heidi Hofer, Joseph Carroll, Jay Neitz, Maureen Neitz and David R. Williams Journal of Neuroscience 19 October 2005, 25 (42) 9669-9679; DOI: https://doi.org/10.1523/JNEUROSCI.2414-05.2005 Abstract: Using high-resolution adaptive-optics imaging combined with retinal densitometry, we characterized the arrangement of short- (S), middle- (M), and long- (L) wavelength-sensitive cones in eight human foveal mosaics. As suggested by previous studies, we found males with normal color vision that varied in the ratio of L to M cones (from 1.1:1 to 16.5:1). We also found a protan carrier with an even more extreme L:M ratio (0.37:1). All subjects had nearly identical S-cone densities, indicating independence of the developmental mechanism that governs the relative numerosity of L/M and S cones. L:M cone ratio estimates were correlated highly with those obtained in the same eyes using the flicker photometric electroretinogram (ERG), although the comparison indicates that the signal from each M cone makes a larger contribution to the ERG than each L cone. Although all subjects had highly disordered arrangements of L and M cones, three subjects showed evidence for departures from a strictly random rule for assigning the L and M cone photopigments. In two retinas, these departures corresponded to local clumping of cones of like type. In a third retina, the L:M cone ratio differed significantly at two retinal locations on opposite sides of the fovea. These results suggest that the assignment of L and M pigment, although highly irregular, is not a completely 13 random process. Surprisingly, in the protan carrier, in which X-chromosome inactivation would favor L- or M-cone clumping, there was no evidence of clumping, perhaps as a result of cone migration during foveal development. 13 The opponent-process theory was first developed by Ewald Hering. He noted that there are color combinations that we never see, such as reddish-green or yellowish-blue. Opponent-process theory suggests that color perception is controlled by the activity of paired opponent systems. The colors in each pair oppose each other. Red-green receptors cannot send messages about both colors at the same time. This is why you cannot see the colors blue-yellow, red-green. These are known as impossible colors. 14 These are simplified schematics of the two color-opponency circuits (red-green; blue- yellow) plus the luminance (brightness) circuit. [define abbrev.; add more about retinal circuitry and how to describe, note modulatory neuron layer info] Green vs. Red: To see RED, the retinal circuitry would be set up to have the L-cones have an excitatory input to the retinal ganglion cell, while the M-cones would have an inhibitory input. To see GREEN, the retinal circuitry would be set up to have the M-cone would have an excitatory input to the retinal ganglion cell, while the L-cone would have an inhibitory input. 15 These are simplified schematics of the two color-opponency circuits (red-green; blue- yellow) plus the luminance (brightness) circuit. Green vs. Red: To see RED, the retinal circuitry would be set up to have the L-cones have an excitatory input to the retinal ganglion cell, while the M-cones would have an inhibitory input. To see GREEN, the retinal circuitry would be set up to have the M-cone would have an excitatory input to the retinal ganglion cell, while the L-cone would have an inhibitory input. 16 These are simplified schematics of the two color-opponency circuits (red-green; blue-yellow) plus the luminance (brightness) circuit. Green vs. Red: To see RED, the retinal circuitry would be set up to have the L-cones have an excitatory input to the retinal ganglion cell, while the M-cones would have an inhibitory input. To see GREEN, the retinal circuitry would be set up to have the M-cone would have an excitatory input to the retinal ganglion cell, while the L-cone would have an inhibitory input. Blue vs. Yellow: The combined M+L-cone input acts as the ‘yellow’ signal (think red + green makes yellow). This input is combined via retinal circuitry set up to have L and M cones jointly activate To see BLUE, the retinal circuitry would be set up to have To see YELLOW, the opposite. In order to see BLUE, the S –(M+L) cone responses must be greater than 0. In other words, S-cone excitatory input must be greater than the inhibitory yellow (M+L) input. 17 These are simplified schematics of the two color-opponency circuits (red-green; blue- yellow) plus the luminance (brightness) circuit. Green vs. Red: To see GREEN, The M-cone would have an excitatory input to the retinal ganglion cell, while the L-cone would have an inhibitory input. Blue vs. Yellow: M+L is the ‘yellow’ signal (think red + green makes yellow). This yellow input is then compared to the blue input. To see YELLOW, the opposite. In order to see BLUE, the S –(M+L) cone responses must be greater than 0. In other words, S-cone excitatory input must be greater than the inhibitory yellow (M+L) input. 18 These are simplified schematics of the two color-opponency circuits (red-green; blue- yellow) plus the luminance (brightness) circuit. Green vs. Red: To see GREEN, The M-cone would have an excitatory input to the retinal ganglion cell, while the L-cone would have an inhibitory input. Blue vs. Yellow: M+L is the ‘yellow’ signal (think red + green makes yellow). This yellow input is then compared to the blue input. In order to see BLUE, the S –(M+L) cone responses must be greater than 0. In other words, S-cone excitatory input must be greater than the inhibitory yellow (M+L) input. To see YELLOW, the opposite will occur; the combined M+L cone (yellow) input must be greater than the S-cone (blue) input. Luminance: For luminance (which can approximately be thought of as brightness), the inputs from all three cones are combined. 19 Visual afterimages: When you stare at one colored spot, those photoreceptors that are responding (that have the receptive field covering that region of visual space) begin to adapt to the stimulus and become less sensitive. They will stop responding eventually. When you then look immediately at a blank white canvas, the surrounding photoreceptors that haven’t adapted send out a strong signal- this signal is as if you are looking at the other color- because the photoreceptors from the color you were looking at are weak, and there is a strong output around: so you get overall stronger response from the other photoreceptors. So the afterimage should be the output from the other two types of cells The receptive fields of the photoreceptors that provide inputs to a particular retinal ganglion cell combine to produce the receptive field of that ganglion cell. The RGC only processes color and luminance for that region of visual space. 20 Fun Fact: The common hippopotamus (Hippopotamus amphibius), or hippo, is a large, mostly herbivorous, semiaquatic mammal native to sub-Saharan Africa. After the elephant and rhinoceros, the common hippopotamus is the third-largest type of land mammal. Despite their physical resemblance to pigs and other terrestrial even-toed ungulates, the closest living relatives of the Hippopotamidae are cetaceans (whales, dolphins, porpoises, etc.) from which they diverged about 55 million years ago. 21 Fun Fact: The mantis shrimp has one of the most elaborate visual systems ever discovered. Compared to the three types of color-receptive cones that humans possess in their eyes, the eyes of a mantis shrimp carry 16 types of color receptive cones. It can see polarized light and multispectral images, has both serial and parallel visual processing, and each eye has trinocular and depth perception. The midband region of the mantis shrimp's eye is made up of six rows of specialized ommatidia. Four rows carry 16 differing sorts of photoreceptor pigments, 12 for color sensitivity, others for color filtering. Furthermore, some of these shrimp can tune the sensitivity of their long-wavelength vision to adapt to their environment. This phenomenon, known as "spectral tuning" is species-specific. Cheroske et al. did not observe spectral tuning in the mantis shrimp species Neogonodactylus oerstedii, the species with the most monotonous natural photic environment. In the mantis shrimp species N. bredini, a species with a variety of habitats ranging from 5-10m deep (although it can be found up to 20m deep), spectral tuning was observed, but the ability to alter wavelengths of maximum absorbance was not as pronounced as in the mantis shrimp species N. wennerae, a species with much higher ecological/photic habitat diversity. Fun Fact: http://theoatmeal.com Check out this link for more interesting and humorous discussions Retinal Cell Types Can Be Distinguished By Their Size And Branching Patterns (Dacey, 1993; Rodieck 1998) There are about 0.7 to 1.5 million retinal ganglion cells in the human retina. With about 4.6 million cone cells and 92 million rod cells, or 96.6 million photoreceptors per retina, on average each retinal ganglion cell receives inputs from about 100 rods and cones. However, these numbers vary greatly among individuals and as a function of retinal location. In the fovea (center of the retina), a single ganglion cell will communicate with as few as five photoreceptors. In the extreme periphery (ends of the retina), a single ganglion cell will receive information from many thousands of photoreceptors. 25 Retinal Cell Types Can Be Distinguished By Their Size And Branching Patterns (Dacey, 1993; Rodieck 1998) There are about 0.7 to 1.5 million retinal ganglion cells in the human retina. With about 4.6 million cone cells and 92 million rod cells, or 96.6 million photoreceptors per retina, on average each retinal ganglion cell receives inputs from about 100 rods and cones. However, these numbers vary greatly among individuals and as a function of retinal location. In the fovea (center of the retina), a single ganglion cell will communicate with as few as five photoreceptors. In the extreme periphery (ends of the retina), a single ganglion cell will receive information from many thousands of photoreceptors. 26 27 From Rodieck’s book, page 256 28 Retinal Cell Types Can Be Distinguished By Their Size And Branching Patterns (Dacey, 1993; Rodieck 1998) There are about 0.7 to 1.5 million retinal ganglion cells in the human retina. With about 4.6 million cone cells and 92 million rod cells, or 96.6 million photoreceptors per retina, on average each retinal ganglion cell receives inputs from about 100 rods and cones. However, these numbers vary greatly among individuals and as a function of retinal location. In the fovea (center of the retina), a single ganglion cell will communicate with as few as five photoreceptors. In the extreme periphery (ends of the retina), a single ganglion cell will receive information from many thousands of photoreceptors. 29 Retinal Cell Types Can Be Distinguished By Their Size And Branching Patterns (Dacey, 1993; Rodieck 1998) There are about 0.7 to 1.5 million retinal ganglion cells in the human retina. With about 4.6 million cone cells and 92 million rod cells, or 96.6 million photoreceptors per retina, on average each retinal ganglion cell receives inputs from about 100 rods and cones. However, these numbers vary greatly among individuals and as a function of retinal location. In the fovea (center of the retina), a single ganglion cell will communicate with as few as five photoreceptors. In the extreme periphery (ends of the retina), a single ganglion cell will receive information from many thousands of photoreceptors. 30 Separate processing pathways for visual information start in retina, project to LGN, and continue to primary visual cortex (V1). Midget retinal ganglion cells: Midget retinal ganglion cells project to the parvocellular layers of the lateral geniculate nucleus. These cells are known as midget retinal ganglion cells, based on the small sizes of their dendritic trees and cell bodies. About 80% of all retinal ganglion cells are midget cells in the parvocellular pathway. They receive inputs from relatively few rods and cones. In many cases, they are connected to midget bipolars, which are linked to one cone each. They have slow conduction velocity, and respond to changes in color but respond only weakly to changes in contrast unless the change is great (Kandel et al., 2000). They have simple center-surround receptive fields, where the center may be either ON or OFF while the surround is the opposite. Parasol retinal ganglion cells: Parasol retinal ganglion cells project to the magnocellular layers of the lateral geniculate nucleus. These cells are known as parasol retinal ganglion cells, based on the large sizes of their dendritic trees and cell bodies. About 10% of all retinal ganglion cells are parasol cells, and these cells are part of the magnocellular pathway. They receive inputs from relatively many rods and cones. They have fast conduction velocity, and can respond to low-contrast stimuli, but are not very sensitive to changes in color (Kandel et al., 2000). They have much larger receptive fields which are nonetheless also center-surround. Small bistratified retinal ganglion cells: Bistratified retinal ganglion cells project to the koniocellular layers of the lateral geniculate nucleus. Bistratified retinal ganglion cells have been identified only relatively recently. Koniocellular means "cells as small as dust"; their small size made them hard to find. About 10% of all retinal ganglion cells are bistratified cells, and these cells go through the koniocellular pathway. They receive inputs from intermediate numbers of rods and cones. They have moderate spatial resolution, moderate conduction velocity, and can respond to moderate-contrast stimuli. They may be involved in color vision. They have very large receptive fields that only have centers (no surrounds) and are always ON to the blue cone and OFF to both the red and green cone. 31 Melanopsin-containing retinal ganglion cells (also called intrinsically photosensitive retinal ganglion cells) are a recently discovered type of retinal ganglion cell that can directly absorb light. They contain the photopigment melanopsin, which allows them to function like the photoreceptors that transduce like for the rod and cone retinal ganglion cells. Compared to the rods and cones, the ipRGCs respond more sluggishly and signal the presence of light over the long term. They represent a very small subset (~1%) of the retinal ganglion cells (Berson, 2003). Their functional roles are non-image-forming and fundamentally different from those of pattern vision; they provide a stable representation of ambient light intensity. They have at least three primary functions. They play a major role in synchronizing circadian rhythms to the 24-hour light/dark cycle, providing primarily length-of-day and length-of night information. They send light information via the retinohypothalamic tract (RHT) directly to the circadian pacemaker of the brain, the suprachiasmatic nucleus of the hypothalamus. The physiological properties of these ganglion cells match known properties of the daily light entrainment (synchronization) mechanism regulating circadian rhythms. Photosensitive ganglion cells innervate other brain targets, such as the center of pupillary control, the olivary pretectal nucleus of the midbrain. They contribute to the regulation of pupil size and other behavioral responses to ambient lighting conditions. They contribute to photic regulation of, and acute photic suppression of, release of the hormone melatonin. In rats, they play some role in conscious visual perception, including perception of regular gratings, light levels, and spatial information. Photoreceptive ganglion cells have been isolated in humans where, in addition to regulating the circadian rhythm, they have been shown to mediate a degree of light recognition in rodless, coneless subjects suffering with disorders of rod and cone photoreceptors. Work by Farhan H. Zaidi and colleagues showed that photoreceptive ganglion cells may have some visual function in humans. The photopigment of photoreceptive ganglion cells, melanopsin, is excited by light mainly in the blue portion of the visible spectrum (absorption peaks at ~480 nanometers). The phototransduction mechanism in these cells is not fully understood, but seems likely to resemble that in invertebrate rhabdomeric photoreceptors. Photosensitive ganglion cells respond to light by depolarizing and increasing the rate at which they fire nerve impulses. In addition to responding directly to light, these cells may receive excitatory and inhibitory influences from rods and cones by way of synaptic connections in the retina. The axons from these ganglia innervate regions of the brain related to object recognition, including the superior colliculus and dorsal lateral geniculate nucleus. Figures taken from this paper: Melanopsin-expressing ganglion cells in primate retina signal colour and irradiance and project to the LGN Dennis M. Dacey, Hsi-Wen Liao, Beth B. Peterson, Farrel R. Robinson, Vivianne C. Smith, Joel Pokorny, King-Wai Yau and Paul D. Gamlin Nature 433, 749-754 (17 February 2005) doi: 10.1038/nature03387 Figure legend: Human vision starts with the activation of rod photoreceptors in dim light and short (S)-, medium (M)-, and long (L)- wavelength-sensitive cone photoreceptors in daylight. Recently a parallel, non-rod, non-cone photoreceptive pathway, arising from a population of retinal ganglion cells, was discovered in nocturnal rodents. These ganglion cells express the putative photopigment melanopsin and by signalling gross changes in light intensity serve the subconscious, 'non-image-forming' functions of circadian photoentrainment and pupil constriction. Here we show an anatomically distinct population of 'giant', melanopsin-expressing ganglion cells in the primate retina that, in addition to being intrinsically photosensitive, are strongly activated by rods and cones, and display a rare, S-Off, (L + M)-On type of colour-opponent receptive field. The intrinsic, rod and (L + M) cone-derived light responses combine in these giant cells to signal irradiance over the full dynamic range of human vision. In accordance with cone-based colour opponency, the giant cells project to the lateral geniculate nucleus, the thalamic relay to primary visual cortex. Thus, in the diurnal trichromatic primate, 'non-image-forming' and conventional 'image-forming' retinal pathways are merged, and the melanopsin-based signal likely also contributes to conscious visual perception. 32 Fun Fact: Damselflies are insects similar to dragonflies, but are smaller, have slimmer bodies, and most species fold the wings along the body when at rest. An ancient group, damselflies have existed since at least the Lower Permian (~300-250 million years ago), and are found on every continent except Antarctica. These ferocious aerobatic hunters are renowned for their enormous compound eyes, which give them the optical acuity necessary to seize prey in mid-air over open water. Both dragons and damsels have short antennae, so vision is their primary means of navigating and capturing food. Their eyes are made up of thousands of ommatidia (telescope-shaped clusters of photoreceptor cells) that resemble a honeycomb. These collect light and signals that, when they are processed by the brain, can produce a clearer and less pixilated image than in other smaller-eyed insects. Some dragonflies can also see colours that we can’t, such as ultraviolet. While dragons’ eyes are on the front of the head, damsels’ are on the sides. This may give less frontal vision for zoom-and-swoop attack, but allows all-round – including above and behind – perception of their aerospace. This is vital for hovering insects, especially damselflies, which often travel among the herbage rather than skimming the water or flying in the open. http://www.discoverwildlife.com/animals/bugs/why-do-dragonflies-and-damselflies-have-such-big- eyes 33 34 35 Damage to eye: Cornea, lens, retina Patient MM from next lecture was blinded by severe scarring of cornea (due to chemical burn). This scarring can prevent light from reaching the retina. 36 A cataract is an opacity in the lens that blocks light from reaching the retina. Cataracts can be congenital or can come with age, especially after a lot of UV light exposure (wear sun glasses!). 37 A cataract is a clouding of the lens in the eye that affects vision. Most cataracts are related to aging. Cataracts are very common in older people. By age 80, more than half of all Americans either have a cataract or have had cataract surgery. A cataract can occur in either or both eyes. It cannot spread from one eye to the other. The lens is a clear part of the eye that helps to focus light, or an image, on the retina. The retina is the light-sensitive tissue at the back of the eye. In a normal eye, light passes through the transparent lens to the retina. Once it reaches the retina, light is changed into nerve signals that are sent to the brain. The lens must be clear for the retina to receive a sharp image. If the lens is cloudy from a cataract, the image you see will be blurred. The lens lies behind the iris and the pupil. It works much like a camera lens. It focuses light onto the retina at the back of the eye, where an image is recorded. The lens also adjusts the eye's focus, letting us see things clearly both up close and far away. The lens is made of mostly water and protein. The protein is arranged in a precise way that keeps the lens clear and lets light pass through it. But as we age, some of the protein may clump together and start to cloud a small area of the lens. This is a cataract. Over time, the cataract may grow larger and cloud more of the lens, making it harder to see. Researchers suspect that there are several causes of cataract, such as sun (UV) exposure, smoking, and diabetes. Or, it may be that the protein in the lens just changes from the wear and tear it takes over the years. Age-related cataracts can affect your vision in two ways: Clumps of protein reduce the sharpness of the image reaching the retina. The lens consists mostly of water and protein. When the protein clumps up, it clouds the lens and reduces the light that reaches the retina. The clouding may become severe enough to cause blurred vision. Most age-related cataracts develop from protein clumpings. When a cataract is small, the cloudiness affects only a small part of the lens. You may not notice any changes in your vision. Cataracts tend to “grow” slowly, so vision gets worse gradually. Over time, the cloudy area in the lens may get larger, and the cataract may increase in size. Seeing may become more difficult. Your vision may get duller or blurrier. The clear lens slowly changes to a yellowish/brownish color, adding a brownish tint to vision. As the clear lens slowly colors with age, your vision gradually may acquire a brownish shade. At first, the amount of tinting may be small and may not cause a vision problem. Over time, increased tinting may make it more difficult to read and perform other routine activities. This gradual change in the amount of tinting does not affect the sharpness of the image transmitted to the retina. If you have advanced lens discoloration, you may not be able to identify blues and purples. You may be wearing what you believe to be a pair of black socks, only to find out from friends that you are wearing purple socks. 38 39 http://brainlagoon.com/wp-content/uploads/2012/12/Color-blindness.png People with dichromatic color vision have only two types of cones which are able to perceive color i.e. they have a total absence of function of one cone type. Lack of ability to see colour is the easiest way to explain this condition but in actual fact it is a specific section of the light spectrum which can’t be perceived. For convenience we call these areas of the light spectrum ‘red’, ‘green’ or ‘blue’. The sections of the light spectrum which the ‘red’ and ‘green’ cones perceive overlap and this is why red and green colour vision deficiencies are often known as red/green colour blindness and why people with red and green deficiencies see the world in a similar way. People suffering from protanopia are unable to perceive any ‘red’ light, those with deuteranopia are unable to perceive ‘green’ light and those with tritanopia are unable to perceive ‘blue’ light. People with both red and green deficiencies live in a world of murky greens where blues and yellows stand out. Browns, oranges, shades of red and green are easily confused. Both types will confuse some blues with some purples and both types will struggle to identify pale shades of most colours. However, there are some specific differences between the 2 red/green deficiencies. Protanopia Protanopes are more likely to confuse:- 1. Black with many shades of red 2. Dark brown with dark green, dark orange and dark red 2. Some blues with some reds, purples and dark pinks 3. Mid-greens with some oranges Deuteranopes Deuteranopes are more likely to confuse:- 1. Mid-reds with mid-greens 2. Blue-greens with grey and mid-pinks 3. Bright greens with yellows 4. Pale pinks with light grey 5. Mid-reds with mid-brown 6. Light blues with lilac Tritanopes The most common colour confusions for tritanopes are light blues with greys, dark purples with black, mid-greens with blues and oranges with reds. Monochromacy People with monochromatic vision can see no colour at all and their world consists of different shades of grey ranging from black to white, rather like only seeing the world on an old black and white television set. Achromatopsia is extremely rare, occuring only in approximately 1 person in 33,000 and its symptoms can make life very difficult. Usually someone with achromatopsia will need to wear dark glasses inside in normal light conditions. In approximately 1775, Typhoon Lengkieki struck and devastated the Micronesian atoll of Pingelap. The typhoon and ensuing famine left only around 20 survivors, one of whom was heterozygous for achromatopsia. Four generations after this population bottleneck the prevalence of achromatopsia is 5% with a further 30% as carriers. The people of this region have termed achromatopsia "maskun", which literally means "not see" in Pingelapese. Photophobia (fear of light) is a description of extreme light sensitivity. Nystagmus is a type of involuntary eye movement disorder that arises because a patient can’t fixate (hold eyes steady) normally. In the case of rod monochromats, the lack of central visions disrupts the patient’s ability to fixate. Normal retinal organization Gray overlays mark the cone photoreceptors that are inactive in rod monochromats. Note that the central vision is not functional. Colorblindness can be acquired, but more often it is inherited. As the name implies, this is colorblindness caused by defects in the retina of the eye, and more specifically, in the photoreceptive layer of the retina. Average rate of red-green color blindness is: 1/20 men, 1/400 women. L/M-conephotopsins are encoded on X chromosome; thus they are called ‘sex-linked’. With only one X chromosome, males (XY) are more susceptible to color blindness. The L photopsin is especially prone to mutations. Mutations in the L-cones create much of the variety of color vision. There is not as much variation (lower rate of mutation) in M cones. (See also slide 20.) S-cone photopsin mutations (causing tritanopia) are the most rare and are not sex-linked. 47 http://www.vischeck.com/examples/ This is a good website that will show you how images look in different disorders. This is important for advertising/webpages/etc. if you want to check that everyone will be able to read the info. You can upload your own images to the vischeck site to check them out. 48 Anomalous Trichromacy is the most common category of color blindness. It is an impairment of normal color vision, not a complete loss. This occurs when one of the cones is altered in its spectral sensitivity. It can be red/green or blue/yellow depending on which cone is altered.The ability of anomalous trichromats to distinguish between hues is better than dichromats but still not normal. Protanomaly is referred to as "red-weakness", an apt description of this form of color deficiency. Any redness seen in a color by a normal observer is seen more weakly by the protanomalous viewer, both in terms of its "coloring power" (saturation, or depth of color) and its brightness. Red, orange, yellow, and yellow-green appear somewhat shifted in hue ("hue" is just another word for "color") towards green, and all appear paler than they do to the normal observer. The redness component that a normal observer sees in a violet or lavender color is so weakened for the protanomalous observer that he may fail to detect it, and therefore sees only the blue component. Hence, to him the color that normals call "violet" may look only like another shade of blue. Deuteranomaly is a type of anomalous trichromatic vision in which the green-sensitive cones have decreased sensitivity. It is an X-linked trait, affecting about 5% of white males and 0.25% of females in the United States, and is the most common color vision deficiency. It is an inherited disorder of color vision, caused by a gene located on the X chromosome, in which a person has all three of the retinal pigments in the cones, but the sensivity of the green-sensitive cones is decreased. Tritanomaly is a rare type of anomalous trichromatic vision in which the third, blue-sensitive, cones have decreased sensitivity. Less than about 0.01% of people affected by it. However, it is known that reds and greens are unaffected, and some yellows may be visible on the lower end of the spectrum with this disorder. What is known about protanomaly and deuteranomaly suggests that tritanomaly is caused by defective S photopigment. It is known that persons affected by this condition have difficulty distinguishing between yellow and blue. A type of tritanomaly can also be acquired during one’s lifetime. Because the eye lens becomes less transparent with age, this can cause very light tritanomalous symptoms. Usually they are not serious enough for a positive diagnosis on color blindness. Among alcoholics a higher incidence rate of tritanopia could be counted. Large quantities of alcohol resulted in poorer color discrimination in all spectra but with significantly more errors in the blue-yellow versus the red-green color range. Mixtures of organic solvents even at low concentrations may also impair color vision. Errors were measured mainly in the blue-yellow color spectrum. An injury through a hard hit to the front of back of your head may also cause blue-yellow color blindness. Tritanopic deficits are on chromosome 7. Deuteranomoly is the most common form. Dichromacy is less common than anomolous trichromacy. Colorblind see 45; everyone else should see nothing Normal population: see a 6 Colorblindness: cannot see anything Normal vision should be 74 Colorblind should see 21 Total colorblindness: none Tetrachromacy is the condition of possessing four independent channels for conveying color information, or possessing four types of cone cells in the eye. Organisms with tetrachromacy are called tetrachromats. In tetrachromatic organisms, the sensory color space is four-dimensional, meaning that to match the sensory effect of arbitrarily chosen spectra of light within their visible spectrum requires mixtures of at least four primary colors. Tetrachromacy is demonstrated among several species of birds, fish, amphibians, reptiles, insects and some mammals. It was the normal condition of most mammals in the past; a genetic change made the majority of species of this class eventually lose two of their four cones. Variation in cone pigment genes is widespread in most human populations, but the most prevalent and pronounced tetrachromacy would derive from female carriers of major red/green pigment anomalies, usually classed as forms of "color blindness" (protanomaly or deuteranomaly). The biological basis for this phenomenon is X-inactivation of heterozygotic alleles for retinal pigment genes, which is the same mechanism that gives the majority of female new-world monkeys trichromatic vision. In other words, some human women may have one L-cone gene allele (type) on one X chromosome and a different L- cone allele on the other. Each cell of a human women randomly turns off 1 of the 2 X chromosomes in each cell. With a certain pattern of X chromosome inactivation, these women may end up with a color vision system in which they can functionally act as tetrachromats. 59 60 61 The optic radiation is a collection of axons from relay neurons in the lateral geniculate nucleus of the thalamus carrying visual information to the primary visual cortex (also called striate cortex due to a stripe in layer 4) along the calcarine sulcus in the posterior occipital lobe. Fibers from the inferior retina (also called "Meyer's loop“) : must pass into the temporal lobe by looping around the inferior horn of the lateral ventricle. ; Carry information from the superior part of the visual field Fibers from the superior retina : travel straight back to the occipital lobe and the primary visual cortex. Carry information from the inferior part of the visual field 62 Subcortical structures play roles in such things as orienting to visual stimulus, but will not be discussed in detail here. 63 Note how left visual field goes to half of each retina, and right to the other half. (Imagine the eyes fixated on a single spot). With the crossing of the fibers at the optic chiasm, each half of the visual field (hemifield) goes to the opposite hemisphere. 64 http://www.inma.ucl.ac.be/EYELAB/neurophysio/light_perception/LGN.html View of these visual pathways in a real brain. This is a ventral view of the brain with the temporal lobes removed to reveal the optic radiations. 65 Diagram of cortical layers in V1. Remember that the cortical sheet is made up of 6 layers. Key things to note are that the separate processing pathways (magno, parvo, koniocellular) all enter separately into different layers. And yes, ‘blob’ and ‘interblob’ are real terms which describe divisions of the upper layers of V1. EXTRA INFO – layers of primary visual cortex: The molecular layer I, which contains few scattered neurons and consists mainly of extensions of apical dendrites and horizontally-oriented axons; some Cajal-Retzius and spiny stellate neurons can be found The external granular layer II, which contains small pyramidal neurons and numerous stellate neurons The external pyramidal layer III, which contains predominantly small and medium-size pyramidal neurons, as well as non-pyramidal neurons with vertically-oriented intracortical axons; layers I through III are the main target of interhemispheric corticocortical afferents, and layer III is the principal source of corticocortical efferents The internal granular layer IV, which contains different types of stellate and pyramidal neurons, and is the main target of thalamocortical afferents as well as intra-hemispheric corticocortical afferents The internal pyramidal layer V, which contains large pyramidal neurons (as the Betz cells in the primary motor cortex), as well as interneurons; it is the principal source of efferent for all the motor-related subcortical structures The multiform layer VI, which contains few large pyramidal neurons and many small spindle-like pyramidal and multiform neurons; the layer VI sends efferent fibers to the thalamus, establishing a very precise reciprocal interconnection between the cortex and the thalamus (Creutzfeldt, 1995). 66 V1 = primary visual cortex 67 Fun facts: Coral sand magnified one-hundred times using transmission electron microscopy, brightfield mode. 68 Cornea, lens, retina, optic nerve The optic nerve exiting the eye causes the blindspot, as there is no photoreceptor layer to receive light in this location. Remember that the optic nerve is the bundled group of axons from the retinal ganglion cells. 69 A scotoma (plural: scotomas or scotomata) is an area of partial alteration in the field of vision consisting of a partially diminished or entirely degenerated visual acuity that is surrounded by a field of normal – or relatively well-preserved – vision. Image shows a diagram of visual field loss (scotoma) from retinal damage. Note that the patient usually does not see a black spot like this. For many locations of retinal damage, the brain fills in the missing region (like with the normal blindspot where the optic nerve exits the retina). This is called perceptual filling in. The patient cannot see in this region, so may notice that there is a problem with vision on the left, but not be able to specifically localize the region. If the damage is in the central fovea, the patient is more likely to notice even a small scotoma, as the high acuity vision used for reading will be disturbed. 70 Image from http://www.indiana.edu/~pietsch/hemianopsia.html 71 72 Remember normal visual pathway: retina – optic nerve – optic chiasm - optic tract – thalamus – optic radiations – primary visual cortex. Right images show what each eye sees: left eye sees the left image with Eiffel Tower, right eye sees partly overlapping image. The eyes would be fixated (held steady) in the middle. 73 There is no input from left eye if the optic nerve is severed. Note that as long as eye is attached to optic nerve, vision from this eye is still possible. (Name refers to location of visual field loss.) 74 Hemianopsia is a decreased vision or blindness (anopsia) in half the visual field, usually on one side of the vertical midline. The most common causes of this damage are stroke, brain tumor, and trauma. This image depicts vision with left hemianopsia: name refers to location of visual field loss. 75 76 77 78 Calcified carotid arteries physically press on the outside axons in the optic tract, ultimately destroying them and causing blindness. (Name refers to location of visual field loss.) 79 FYI: Pituitary tumor is a common cause of this. (The pituitary gland is part of the endocrine system that releases hormones like the growth hormone.) (Name refers to location of visual field loss.) 80 Damage can be anywhere along the path after the chiasm. Specific sites of damage that don’t cut all the axons from thalamus to V1 can lead to smaller sections of visual field loss, as well (e.g., quadrant/quarter field loss). (Name refers to location of visual field loss.) 81 http://artificialretina.energy.gov/howartificialretinaworks.shtml Found through Doheny eye institute Normal vision begins when light enters and moves through the eye to strike specialized photoreceptor (light-receiving) cells in the retina called rods and cones. These cells convert light signals to electric impulses that are sent to the optic nerve and the brain. Retinal diseases like age-related macular degeneration and retinitis pigmentosa destroy vision by annihilating these cells. With the artificial retina device, a miniature camera mounted in eyeglasses captures images and wirelessly sends the information to a microprocessor (worn on a belt) that converts the data to an electronic signal and transmits it to a receiver on the eye. The receiver sends the signals through a tiny, thin cable to the microelectrode array, stimulating it to emit pulses. The artificial retina device thus bypasses defunct photoreceptor cells and transmits electrical signals directly to the retina’s remaining viable cells. The pulses travel to the optic nerve and, ultimately, to the brain, which perceives patterns of light and dark spots corresponding to the electrodes stimulated. Patients learn to interpret these visual patterns. 82 83 84 Fun Facts: The emperor tamarin (Saguinus imperator), is a species of tamarin allegedly named for its resemblance to the German emperor Wilhelm II. The tamarins compose a family of squirrel-sized New World monkeys. 85 Size perception can be influenced by our understanding of depth and perspective in a scene. This is an example of Shepard’s Tables, an illusion first published by Roger Shepard as Turning the Tables, (see his book Mind Sights, 1990, pages 48 and 127-8). Here the tables are actually the same dimensions, but the different orientations cause a size illusion. The illusion is an example of size-constancy expansion – the illusory expansion of space with apparent distance. The receding edges of the tables are seen as if stretched into depth. With our use of perspective cues in our perception of size constancy, objects can appear wider with distance; the oblique edges of the tables seem to get a bit wider apart with distance. 86 Purple = human visual cortex. Images are lateral and medial views of a brain overlaid with the response to a full-field flickering checkerboard stimulus (one that maximally activates V1). Visual cortex composes about 20% of human cortex. 87  Dorsal pathway - Made up of multiple visual areas, it is one of two main visual processing streams after primary visual cortex. This pathway is involved in perception for action. Ventral pathway - Made up of multiple visual areas, it is one of two main visual processing streams after primary visual cortex. This pathway is involved in perception for recognition. 88 Models of parallel processing in primate visual system have focused on the innervation and contribution of M and P layers in the LGN. In their strictest form, these models propose that surface features of color and form are carried along the P pathway and divided in V1 into color and form subsystems, corresponding to blobs and interblobs (Livingstone & Hubel 1987, 1988). From there the path leads to ventral areas of cerebral cortex, eventually reaching inferior temporal cortex. The M pathway, by contrast, carries information relevant to motion and spatial aspects of vision through the upper part of layer IV in V1 to eventually reach areas of parietal lobe. 89 In the primate, visual information travels from the retina through the lateral geniculate nucleus (LGN) of the thalamus to primary visual cortex (area V1) in the posterior occipital lobe. One of the most powerful organizing principles in visual cortex is the presence of multiple visual areas. These areas are defined by their unique cytoarchitectonic structures, connectivity, functional processing, and visual field maps (Van Essen et al., 1984; Felleman and Essen, 1991; Van Essen, 2003). In the more anterior areas of the occipital lobe and in the parietal and temporal lobes, the definitions and functions of many of these areas are still being investigated. In human measurements, the most compelling evidence for visual areas in occipital cortex are visual field maps, commonly called retinotopic maps. The organization of these maps follows the organization of the retina; hence, retinotopic visual field maps are cortical regions in which nearby neurons analyze the properties of nearby points of an image on the retina. Each of the first few visual areas (V1/2/3) can be identified as containing a representation of a full hemifield of visual space, with each hemisphere representing the contralateral hemifield (Wandell, 1999[Wandell 2007]). Area V1 and the adjacent areas (V2 and V3) contribute to a confluent foveal representation at the occipital pole (Wandell, 1999; Wandell, et al., 2007). All of these areas have a lower visual field representation located on the dorsal part of the posterior occipital lobe and an upper visual field representation on the ventral surface. Beyond these early visual field maps in the posterior occipital lobe, visual cortex is loosely organized into anatomically distinct dorsal and ventral ‘streams’ (Morel and Bullier, 1990; Baizer et al., 1991). 90 Cortical magnification is a property of sensory and motor systems in which one part of a topographical representation is relatively larger than the rest, producing a region with higher acuity (better sensitivity) in the magnified region. In the visual system, cortical magnification describes how many neurons in an area of the visual cortex are 'responsible' for processing a stimulus of a given size, as a function of visual field location. In the center of the visual field, corresponding to the center of the fovea of the retina, a very large number of neurons process information from a small region of the visual field. If the same stimulus is seen in the periphery of the visual field (i.e. away from the center), it would be processed by a much smaller number of neurons. The increased number of neurons devoted to processing central vision helps make our central vision more sensitive than our peripheral vision. The magnification of central (e.g., foveal) is achieved in several steps along the visual pathway, starting in the fovea with densely packed cones and the midget retinal ganglion cells of the parvocellular pathway and continuing to the large region of cortex that receives information from the central vision. Other examples of cortical magnification include the expansion of the face and hand representations in the somatosensory and motor cortical regions. These body parts have sensitive touch and excellent motor control. From Wandell et al., Neuron 2007 Figure 1b This image illustrates the expansion of the foveal representation in the visual field map in V1. The image is a section of Godfrey Kneller’s 1989 portrait of Sir Isaac Newton. The figure illustrates how the visual field (left) is transformed and represented on the V1 cortical surface (right) using a mathematical description proposed by Schwartz (1977). The left visual field stimulates V1 in the right hemisphere; the image representation is inverted, and the center of the visual field, near the eye, is greatly expanded (cortical magnification). 91 Visual field map clusters describe a large-scale organization of visual field maps (representations of visual space) across cortex. Visual field map clusters 1) share a common circular or semi-circular eccentricity representation; 2) contain multiple angle representations within the shared eccentricity representation; 3) may share similar computational resources. Such clusters of sensory field maps are also seen in auditory cortex. [You will NOT need to understand how to identify these maps in an image for this class.] 92 This is not a macaw parrot. It is a lady painted to be the illusion a bird. Can you see her? 93 94 (Gestalt law of grouping) Do you see the cow? Our brain makes sense of the incoming black and white spots on the page once we can see the outline of the cow. Perception of the cow is based on knowledge about objects in the scene. 95 96 Depth perception can be upset when rules and knowledge are in conflict. This video demonstrates how our knowledge of faces can over-ride our perception of depth from shadows. http://www.richardgregory.org/experiments/index.htm Many of these illusions are not appreciated by patient MM (see slide 29), whose brain does not have normal object recognition pathways (and lacks a foundation of prior visual experience to cause the illusion). 97 This hollow face illusion is much like the hollow mask illusion in the last slide. This sculpture is actually concave; you are looking into the face just like you were looking into the hollow mask. In this case, as the viewer moves past the sculpture, the face appears to be convex – bending out toward the viewer – and to be moving. Disneyland uses pictures like this to create the moving faces in the Haunter Mansion. 98 In some cases of damage to V1, patients have no conscious knowledge that they can see (in all or part of the visual field), but may respond appropriately in certain situations that require vision. For example, if a ball is thrown at his head, a patient may raise his hand to catch the ball, but denies any reason for raising his hand. This condition is termed blindsight. It is thought that a small part of the visual pathway bypasses V1 (going in this case directly to the motion area of visual cortex, MT) 99 Medial views of normal (top) and patient MM (bottom) left hemispheres. Color overlay represents V1, V2, and V3 visual field maps. Note the full colors in the occipital lobe of the normal control. Note that MM has some remaining colors in his V1, but already some distortions can be seen ( rainbow of the map is wrinkled up more than normal). Lateral surface of MM’s occipital lobe (where object recognition occurs) lacks much normal visual cortex activity, except for some responses in the motion area (MT). 100 From the Discovery Channel – MM talks about seeing his footprints in the sand and having to figure out what they are 101 Visual agnosia is a disorder in which the patient suffers from the inability to recognize and identify objects, features of objects or scenes, faces or persons despite having knowledge of the characteristics of the objects, scenes, faces or persons. This condition can be loosely divided into two types that differ by severity: apperceptive and associative. It is not due to a deficit in vision (acuity, visual field, and scanning), language, memory, or low intellect. While cortical blindness results from lesions to primary visual cortex, visual agnosia is often due to damage to more anterior cortex such as the posterior occipital and/or temporal lobe(s) in the brain. Recognition of visual objects occurs at two primary levels. At an apperceptive level, the features of the visual information from the retina are put together to form a perceptual representation of an object. At an associative level, the meaning of an object is attached to the perceptual representation and the object is identified. If a person is unable to recognize objects because they cannot perceive correct forms of the objects, although their knowledge of the objects is intact (i.e. they do not have anomia), they have apperceptive agnosia. If a person correctly perceives the forms and has knowledge of the objects, but cannot identify the objects, they have associative agnosia. There are specific subgroups of visual agnosia, each of which selectively affects perception of one type of visual stimulus (e.g., object agnosia = objects, prosopagnosia = faces, simultagnosia = scenes). 102 Lateral and ventral occipital cortex is involved in object recognition. (Note that the division between occipital and temporal lobes is not the clear cut – you can think of this as lateral occipito-temporal.) Object perception occurs in both hemispheres. 103 May also be called simply ‘object agnosia’ It is a subgroup of visual agnosia in which only visual perception of objects is affected. Memory of the object can still be accessed through other senses; that is, a patient would not be able to recognize a key by sight, but could identify it when held in the hand. 104 105 106 Fun fact: This is a miniature goat standing on the head of a very chill capybara. The capybara is a mammal native to South America and is the largest living rodent in the world. Its close relatives include guinea pigs and chinchilla. 107 108 109 110 Activity in the Fusiform Face Area (FFA) is seen bilaterally (i.e., in response to face stimuli). However, there are case reports that unilateral (single hemisphere) lesions may also produce problems in face perception. Red = face Green = color Yellow = word form (alexia = problem with reading – we will discuss more in language section) Blue = motion 111 -Subgroup of visual agnosia in which only visual perception of faces is affected (apperceptive = without perception; amnesic = without memory) Prosopagnosia, also called face blindness, is a cognitive disorder of face perception in which the ability to recognize familiar faces, including one's own face (self-recognition), is impaired, while other aspects of visual processing (e.g., object discrimination) and intellectual functioning (e.g., decision making) remain intact. The term originally referred to a condition following acute brain damage (acquired prosopagnosia), but a congenital or developmental form of the disorder also exists, which may affect up to 2.5% of the United States population. The specific brain area usually associated with prosopagnosia is the fusiform gyrus, which activates specifically in response to faces. The functionality of the fusiform gyrus allows most people to recognize faces in more detail than they do similarly complex inanimate objects. For those with prosopagnosia, the new method for recognizing faces depends on the less-sensitive object recognition system. The right hemisphere fusiform gyrus is more often involved in familiar face recognition than the left. It remains unclear whether the fusiform gyrus is only specific for the recognition of human faces or if it is also involved in highly trained visual stimuli. 112 Capgras delusion is a disorder in which a person holds a delusion that a friend, spouse, parent, or other close family member (or pet) has been replaced by an identical-looking impostor. The Capgras delusion is classified as a delusional misidentification syndrome, a class of delusional beliefs that involves the misidentification of people, places, or objects (usually not in conjunction). It can occur in acute, transient, or chronic forms. Cases in which patients hold the belief that time has been "warped" or "substituted" have also been reported. The delusion most commonly occurs in patients diagnosed with paranoid schizophrenia, but has also been seen in patients suffering from brain injury and dementia. It presents often in individuals with a neurodegenerative disease, particularly at an older age. It has also been reported as occurring in association with diabetes, hypothyroidism, and migraine attacks. In one isolated case, the Capgras delusion was temporarily induced in a healthy subject by the drug ketamine. It occurs more frequently in females, with a female:male ratio of 3:2. 113 (Movie approximations include Mr. Smith in The Matrix and Being John Malkovich.) Image from http://radio.weblogs.com/0123486/myImages/malkovitch.jpg Fregoli syndrome (AKA the Fregoli delusion or the delusion of doubles) is a rare disorder in which a person holds a delusional belief that different people are in fact a single person who changes appearance or is in disguise. The syndrome may be related to a brain lesion and is often of a paranoid nature, with the delusional person believing themselves persecuted by the person they believe is in disguise. A person with the Fregoli delusion can also inaccurately recall places, objects, and events. This disorder can be explained by "associative nodes". The associative nodes serve as a biological link of information about other people with a particular familiar face (to the patient). This means that for any face that is similar to a recognizable face to the patient, the patient will recall that face as the person they know. The Fregoli delusion is classed both as a monothematic delusion, since it only encompasses one delusional topic, and as a delusional misidentification syndrome (DMS), a class of delusional beliefs that involves misidentifying people, places, or objects. Like Capgras syndrome, psychiatrists believe it is related to a breakdown in normal face perception. 114 -Subgroup of visual agnosia in which only visual perception of scenes is affected It is likely that damage to any of several cognitive mechanisms could result in simultagnosia (AKA simultanagnosia). Several theories have been proposed to account for simultagnosic symptoms, and while some focus on the disruption of a specific process, such as the speed of attentional processing, others focus on the disruption of a representational structure. Patients with simultanagnosia, a component of Bálint's syndrome, have a restricted spatial window of visual attention and cannot see more than one object at a time in a scene that contains more than one object. For instance, if presented with an image of a table containing both food and various utensils, a patient will report seeing only one item, such as a spoon. If the patient's attention is redirected to another object in the scene, such as a glass, the patient will report that they see the glass but no longer see the spoon. As a result of this impairment, simultanagnosic patients often fail to comprehend the overall meaning of a scene. In addition, patients note that one stationary object may spontaneously disappear from view as they become aware of another object in the scene. Simultanagnosic patients often exhibit a phenomenon known as "local capture" where they only identify the local elements of stimuli containing local and global features. 115 Elements bound into one object can be perceived together, as in the black star. If objects not bound together in some way – e.g., by space and color as seen in the top star, only one will be seen (e.g., red triangle). 116 117 Fun Fact: Giraffes live in herds of related females and their offspring, or bachelor herds of unrelated adult males, but are gregarious and may gather in large aggregations. Males establish social hierarchies through "necking", which are combat bouts where the neck is used as a weapon. 118 119 120 Color vision could be an entire class in itself – let’s just talk about the general pathway here. 121 Illusion from http://www.psy.ritsumei.ac.jp/~akitaoka/color-e.html Variation of Monnier-Shevell illusion There appear to be blue and green lines. Brain is making assumptions about the background color and perceiving the stripes as different colors. The actual color reaching the photoreceptors in each strip is the same color green – see following slides. 122 Color is dependent on the context of the scene such as the illumination and, in this case, the surrounding color. +++++++++++++++++++++++++ Ideally, a color constancy theory should also explain a closely related perceptual experience, color contrast. Color contrast refers to the change in perceived color of a colored patch as its local surround (within 2 degrees of visual field is changed. Color constancy, on the other hand, refers to the lack of change in the perceived color of a coloured patch as the global illumination changes. The Human Visual System does not exhibit perfect color constancy. It also performs poorly in lighting with abnormal spectral content (e.g. sodium arc, or early fluourescents). These remarkable effects show that the same targets can be made to look like very different colors, and that different colors can be made to look the same by manipulating the context. The standard stimulus for eliciting color contrast is two targets with the same spectral composition on differently chromatic backgrounds 123 124 We know how the retina processes color and how the initial color information is encoded (red vs. green, yellow (red+green) vs. blue) but we still don’t’ know how color is ‘read out’ after processing in visual cortex to give us the perception of specific colors. There is a lot of controversy about how much the brain processes info in specific modules or as a network. Think of these regions as key nodes in the color processing network. 125 126 127 128 129 It is now thought that both V1 and MT get input from the incoming optic pathways (thalamus). V1 and MT are seen most mammals – are evolutionarily old structures. Makes sense when you think about needing to at least see incoming, low resolution danger you need to run away from. MT stands for Middle Temporal – it is an area in lateral occipito-temporal cortex that is highly specialized for motion perception (or at least is a very key node in the motion perception network). MT contains neurons that respond preferentially to specific directions (direction-selective cells). Direct pathways to MT may be involved in blindsight - no concious perception of vision, as V1 is damaged, but retained ability to react to moving things. 130 hMT+: h = human MT = middle temporal (first described in monkey – homology/match to human is not absolutely clear) + because several areas may be embedded in here. 131 Rotating snakes illusion - Created by Akiyoshi Kitaoka This illusion activates direction selective cells in early visual cortex. Asymmetric luminance steps (irregular changes in brightness) are key – eye movements induce movement illusion. Brain assumes that such changes in brightness in this pattern must result from motion. 132 133 Individuals with akinetopsia can only perceive movement through a compilation of still images as if they were watching the world through a strobe light. This condition makes it hard to use vision to navigate through moving traffic, see people approaching, or see when the cup has filled with liquid. There is no treatment, but akinetopsia may improve as brain recovers from stroke or medications causing the symptoms are stopped. Patients are aware of the problem and can try to use aids to compensate. 134 Fun Fact: The Japanese dwarf flying squirrel is native to Japan where it inhabits sub-alpine forests and boreal evergreen forests on Honshu and Kyushu islands. It grows to a length of 20 cm (8 in) and has a membrane connecting its wrists and ankles which enables it to glide from tree to tree. 135