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Chapter 15: Visual Processing: Cortical Pathways

Valentin Dragoi, Ph.D., Department of Neurobiology and Anatomy, The UT Medical School at Houston

(content provided by Chieyeko Tsuchitani, Ph.D.)

Reviewed and revised 07 Oct 2020
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The visual system is unique as much of visual processing occurs outside the brain within the retina of the eye. The previous chapter described how the light-sensitive receptors of the eye convert the image projected onto the retina into spatially distributed neural activity in the first neurons of the visual pathway (i.e., the photoreceptors). Within the retina, the receptors synapse with bipolar and horizontal cells, which establish the basis for brightness and color contrasts. In turn, the bipolar cells (the 2° visual afferent) synapse with retinal ganglion cells and amacrine cells, which enhance contrast effects that support form vision and establish the basis for movement detection. The information from the eye is carried by the axons of the retinal ganglion cells (the 3° visual afferent) to the midbrain and diencephalon. This chapter will provide more information about visual pathway organization and the visual processing that occurs within the brain.

15.1 The Visual Pathway from Retina to Cortex

As noted previously in the somatosensory sections, all sensory information must reach the cerebral cortex to be perceived and, with one exception, reach the cortex by way of the thalamus. In the case of the visual system, the thalamic nucleus is the lateral geniculate nucleus and the cortex is the striate cortex of the occipital lobe.

The Optic Nerve

Figure 15.1 The visual pathway with the course of information flow from the right (green) and left (blue) hemifields of the two eye's visual fields.

The axons of the 3° visual afferents (the retinal ganglion cells) form the optic nerve fiber layer of the retina on their course to the optic disc. At the optic disc, the 3° visual afferents exit the eye and form the optic nerve. The fibers of the optic nerve that originate from ganglion cells in the nasal half of the retina (i.e., the nasal hemiretina) decussate in the optic chiasm to the opposite optic tract (Figure 15.1). Consequently, each optic tract contains retinal ganglion cell axons that originate in the nasal half of the contralateral retina and the temporal half of the ipsilateral retina. Recall that the ipsilateral temporal hemiretina and the contralateral nasal hemiretina have projected on them the images of corresponding halves of their visual fields. For example, the temporal (left) hemiretina of left eye and the nasal (left) hemiretina of right eye both have projected on them the right halves of their respective visual fields. Consequently, each optic tract has within it axons representing the contralateral half of the visual field.

The axons in the optic tract terminate in four nuclei within the brain (Figure 15.2):

• the lateral geniculate nucleus of the thalamus - for visual perception;
  
• the superior colliculus of the midbrain - for control of eye movements;
  
• the pretectum of the midbrain - for control of the pupillary light reflex; and
  
• the suprachiasmatic nucleus of the hypothalamus - for control of diurnal rhythms and hormonal changes.

Figure 15.2 The inferior surface of the brain illustrating the visual pathway. The termination sites of the retinal ganglion cell axons in three nuclei that are not considered a part of the visual pathway are also illustrated. They include the hypothalamus, pretectum and the superior colliculus.

The Lateral Geniculate Nucleus

The vast majority of optic tract fibers terminate on neurons in the lateral geniculate nucleus (LGN) of the thalamus (Figure 15.3A).

Like the retina, the lateral geniculate nucleus is a laminated structure, in this case, with six principal layers of cells (Figure 15.3B).

• The largest cells form the deepest two (magnocellular) layers
  
• Smaller cells form the upper four (parvocellular) layers
  
• Thin layers of the smallest cells (i.e., the koniocellular neurons) are interposed between these principal layers.
  

The optic tract fibers (3° visual afferents) from each eye synapse in different layers of the LGN. Consequently, each LGN neuron responds to stimulation of one eye only.

Figure 15.3 Structures of the visual pathway (A). The neurons of the lateral geniculate nucleus form 6 layers that are visible when stained for Nissl substance (B). The magnocellular layers (1 and 2) appear darker as the cells in these layers are larger and contain more Nissl substance than the cells in the parvocellular layers (3 through 6).

The functional properties of LGN neurons are similar to those of retinal ganglion cells.

The LGN neurons are monocular (i.e., respond to stimulation of one eye only) and have concentric (center-surround) receptive fields. The LGN neurons are segregated into three major groups:

• The neurons in the magnocellular layers (mLGN cells)
  
  • process M-retinal ganglion cell inputs
    
  • behave like M-retinal ganglion cells
    
  • have relatively large center-surround receptive fields
    
  • are color insensitive
    
  • are most sensitive to movement of visual stimuli
    
• The neurons in the parvocellular layers (pLGN cells)
  
  • process P-retinal ganglion cell inputs
    
  • behave like P-retinal ganglion cells
    
  • have relatively small center-surround receptive fields
    
  • are color sensitive
    
  • are well suited for detecting contrasts that form the basis for shape/form discrimination.
    
• A third group, the koniocellular neurons (kLGN)
  
  • process P-retinal ganglion cell inputs
    
  • behave like P-retinal ganglion cells
    
  • have the smallest concentric receptive fields
    
  • have stronger color sensitivity than P-retinal ganglion cells
    
  • are well suited for detecting colors that aid in shape/form discrimination.
    

The axons of these different types of LGN neurons terminate in different layers or sublayers of the primary visual cortex.

Visual Cortical Areas

The primary visual cortical receiving area is in the occipital lobe. The primary visual cortex is characterized by a unique layered appearance in Nissl stained tissue.

Figure 15.4 Nearly the entire caudal half of the cerebral cortex is dedicated to processing visual information. A lateral view of the left cerebral hemisphere (A). A view of the medial surface of the right hemisphere (B). The primary motor cortex (i.e., the precentral gyrus), and the primary somatosensory receiving area (i.e., the postcentral gyrus) are represented in red and blue, respectively. The numbers provide the Brodmann Area designation.

Consequently, it is called the striate cortex. It includes the calcarine cortex, which straddles the calcarine fissure, and extends around the occipital pole to include the lateral aspect of the caudal occipital lobe (Figure 15.4, Area 17).

Figure 15.5 The course of the optic radiations from the lateral geniculate nucleus of the thalamus to the striate cortex of the occipital lobe is illustrated in a lateral view of the left side of the brain.

The LGN neurons (4° visual afferents) send their axons in the internal capsule to the occipital lobe where they terminate in the striate cortex (Figure 15.5).

• The LGN axons fan out as the optic radiations of the internal capsule and travel through the temporal, parietal and occipital lobes.
  
• The LGN axons in the sublenticular segment of the optic radiations pass below the lenticular nuclei, loop around the inferior horn of the lateral ventricle within the temporal lobe and swing posteriorly to form Meyer’s loop.
  
  • Once around the inferior horn, they travel up to the inferior bank of the striate cortex, where they terminate.
    
• The LGN axons in the retrolenticular segment of the internal capsule pass superiorly through the parietal lobe to end in the superior bank of the striate cortex.

The striate cortex (Figure 15.6) is considered to be the primary visual cortex or V1, as

• most LGN axons terminate in V1
  
• all V1 neurons respond to visual stimuli exclusively
  
• ablating V1 results in blindness
  
• electrical stimulation of V1 elicits visual sensations.
  

The striate cortex is involved in the initial cortical processing of all visual information necessary for visual perception and its damage results in loss of vision in the contralesional hemifield.

Figure 15.6 The topographic map of the left halves of the visual fields in the medial aspect of the right striate cortex. Note that the neurons representing the visual field center extend around the occipital pole into the lateral surface of the occipital lobe. This results in a disproportionate representation of the central field when compared to the cortical area representing the peripheral visual field.

The color (kLGN), shape (pLGN) and movement (mLGN) information from the thalamus are sent to different neurons within V1 for further processing in V1 and then sent onto different areas of the extrastriate visual cortex.

Figure 15.7 The responses of a "shape-form" type primary visual cortex neuron is recorded while a light bar is flashed on and off the screen. For each of the frames, the light bar has a different orientation. The neuron displays a preference (i.e., produces a maximal response) for a light bar centered and parallel to the long axis of the receptive field.

V1 blob cells: Some V1 cells resemble kLGN neurons. They are

• monocular (i.e., respond to stimulation of one eye only).
  
• color sensitive.
  
• characterized by small, concentric receptive fields.
  
• found in clusters (.e., blob cells).
  
• a special target of the kLGN axon terminals.
  

The P-stream information processed by the V1 blob cells is used in color perception, color discrimination and the learning and memory of the color of objects. The blob cells are the "color" processing cells of V1.

V1 interblob cells: Most V1 interblob cells are

• binocular (i.e., respond to stimulation of either eye).
  
• not color sensitive.
  
• characterized by elongated (rectangular-shaped) receptive fields that may or may not have a center-surround type organization.
  
• found around the clusters of color-sensitive V1 blob cells.
  
• exhibit ocular dominance (i.e., respond best to stimulation of a preferred eye).
  
• exhibit orientation specificity (i.e., respond best when the stimulus is oriented in a particular plane).
  

Location specific V1 interblob cells: One subset of V1 interblob cells responds best when the stimulus is in a specific location of the receptive field (i.e., they also exhibit location specificity).

The P-stream information processed by the V1 interblob cells that exhibit orientation and location specificity but are not motion sensitive is used in object perception, discrimination, learning and memory or in spatial orientation. These interblob cells are the "shape/form" processing cells and the "location" processing cells of V1.

Movement sensitive V1 interblob cells: A second subset of interblob cells respond best to moving stimuli (i.e., exhibit movement sensitivity, Figure 15.8) without a preference for the direction of movement.

Figure 15.8 The responses of a "motion sensitive" primary visual cortex neuron recorded in response to movement of a light bar across the neuron's receptive field from left to right.

Figure 15.9 The responses of a "motion sensitive" primary visual cortex neuron recorded in response to movement of a light bar across the neuron's receptive field. The neuron responds vigorously to movement in one direction (i.e., from left to right as in Figure 15.8) and poorly to movement in the opposite direction (i.e., from right to left). Consequently, this neuron exhibits directional sensitivity.

Direction specific V1 interblob cells: A third subset displays a preference for movement in a particular direction (i.e., some also exhibit directional sensitivity, Figure 15.9).

The M-stream of information processed by the motion sensitive V1 interblob cells is used to detect object movement and direction/velocity of movement and to guide eye movements. These motion-sensitive interblob cells are the "motion detecting” cells of V1.

Extrastriate Visual Cortex. The extrastriate cortex includes all of the occipital lobe areas surrounding the primary visual cortex (Figure 15.4, Areas 18 & 19). The extrastriate cortex in non-human primates has been subdivided into as many as three functional areas, V2, V3, and V4. The primary visual cortex, V1, sends input to extrastriate cortex and to visual association cortex. The information from the “color”, “shape/form”, "location" and “motion” detecting V1, neurons are sent to different areas of the extrastriate cortex (Figure 15.10).

Damage to extrastriate cortex does not result in a “simple loss of vision”; rather it results in higher order visual perceptual deficits including the failure to recognize objects, colors and/or movement of objects.

Figure 15.10 The flow of visual information from the primary visual cortex to other cortical areas depends on the type of information being processed. Information used to locate objects and detect their motion is sent to more superior cortex (a.k.a. the dorsal stream). Information necessary to detect, identify and use color and shape information is sent to inferior cortical areas (a.k.a., the ventral stream).

Visual Association Cortex. The visual association cortex extends anteriorly from the extrastriate cortex to encompass adjacent areas of the posterior parietal lobe and much of the posterior temporal lobe (Figure 15.4, Areas 7, 20, 37 & 39). In most cases, these areas receive visual input via the extrastriate cortex, which sends color, shape/form, location and motion information to different areas of the visual association cortex (Figure 15.10).

The Dorsal Stream: The neurons in the parietal association cortex and superior and middle temporal visual association cortex (Areas 7 and 39 and the superior part of Area 37 in Figure 15.4) have binocular receptive fields and process P-channel information about object location and M-channel information about object movement.

These dorsally located visual association neurons are responsible for producing our sense of

• spatial orientation
  
• binocular fusion/depth perception
  
• the location, the movement and the movement direction and velocity of objects in space.
  

The dorsal stream processes information about the “where” of the visual stimulus (Figure 15.10).

Damage the dorsal visual association cortex results in deficits in spatial orientation, motion detection and in guidance of visual tracking eye movements.

The Ventral Stream: The neurons in the inferior temporal visual association cortex (Area 20 and the inferior part of Areas 37 & 39 in Figure 15.4) process P-channel information about object color and form.

These ventrally located visual association neurons are responsible for processing information necessary for our abilities to

• recognize objects and colors
  
• read text and
  
• learn and remember visual objects (e.g., words and their meanings)
  

This ventral stream processes information about the “what” of the visual stimulus (Figure 15.10).

Damage to the inferior visual association cortex produces deficits in complex visual perception tasks, attention and learning/memory.

15.2 Retinotopic Organization in the Visual Pathway

Clinical Examples

The topographic (spatial) relationships of retinal neurons are maintained throughout the visual system, which preserves the retinotopic map of the visual world. That is, the retina is mapped onto the LGN and striate cortex in an organized (topographic) fashion. Consequently, neighboring parts of retina project to neighboring parts of LGN and neighboring parts of LGN project to neighboring parts of the striate cortex. This retinotopic organization in the visual pathway results in a spatial representation of the visual field in the LGN and visual cortex.

Spatial Representation of the Retinal Image

You should recall the following regarding the spatial representation of the retinal image within the visual pathway.

• The optic image on the retina is upside-down and left-right reversed.
  
• The monocular visual fields of the two eyes overlap partially to form the binocular visual field .
  
• The temporal hemiretina of one eye and the nasal hemiretina of the other eye have projected on them the images of corresponding halves of their visual fields (Figure 15.1). For example, the temporal (left) hemiretina of left eye and the nasal (left) hemiretina of right eye both have projected on them the right half of the visual fields of each eye.
  
• Beyond the optic chiasm, the corresponding visual hemifields of the two eyes are represented in the contralateral side of the visual pathway (Figure 15.1). For example, the left hemifield of both eyes are represented in the right optic tract, right lateral geniculate nucleus, right optic radiations and right striate cortex.
  
• The fibers of the optic radiation fan out into the temporal, parietal and occipital lobes on their course to the striate cortex. Those forming the sublenticular optic radiations carry information about the superior hemifield, whereas those forming the retrolenticular optic radiations carry information about the inferior hemifield (Figure 15.5). The optic radiation fibers traveling the most direct course back to the striate cortex carry information about the central visual field.
  
• There are many more receptor cells in the fovea and many more bipolar and ganglion cells in the macula than in the periphery of the retina. Consequently, the central visual field is disproportionately represented in the visual system. That is, more visual receptors, more optic nerve fibers and more LGN and cortical neurons are involved in processing and carrying information about that portion of the retinal image representing the center of the visual field.
  

Visual Field Defects

Visual field defects are areas of loss of vision in the visual field. Visual field defects are detected by perimetry testing, during which the patient fixates his eyes on a target and his ability to detect a small object in specific positions in space is determined.

Figure 15.11 The binocular visual field (top panel), perimetry testing results for the monocular visual fields (middle panel) and a simplified version of the monocular visual fields (bottom panel) of a person with normal vision. In this panel, the blind spot is illustrated as a dark oblong spot, whereas the central visual field is illustrated as a larger yellow circle.

Figure 15.11 illustrates perimetry test results for the two eyes of someone with normal vision. The bottom panel of Figure 15.11 is a simplified illustration of the monocular visual fields used in the following examples of visual field defects. A visual field defect provides clues to the structure(s) affected. That is, the area(s) of visual field loss and eye(s) exhibiting the visual field loss offer clues about the site of the damage. The following examples of visual field losses should help you determine how well you can utilize what you have learned thus far about the visual system.

15.3 Clinical Example #1

Figure 15.12 Ophthalmoscope examination of the fundus detects an abnormality in the nasal hemiretina in the left eye of a diabetic patient. Notice that the fundus of the patient's left eye appears to the right, just as it appears on the right side of the physician viewing the fundus.

Symptoms: The patient is having his semiannual physical examination. As he is diabetic, the physician examines his retinas and performs a confrontation test of his visual fields. An abnormality is detected in his left fundus (Figure 15.12) but the confrontational field test detects nothing.

Perimetry testing is requested.

Perimetry Test Results: The results indicate the right eye's visual field is normal and that there is peripheral a scotoma (i.e., loss of vision that does not follow the boundaries of the visual field quadrants) in the left eye's temporal hemifield (Figure 15.13).

Figure 15.13 The fundus of each eye as seen by the physician (A). The perimetry map of the monocular visual fields as viewed by the patient (B). The perimetry test result for the left eye indicates a small loss of vision in the temporal hemifield. The scotoma appears smaller in B as the view of the retina in A is limited to approximately 35 degrees, which extends from the nasal edge of the macula to slightly beyond the temporal edge of the optic disc.

Side & Retinotopicity of damage: The visual loss

• is limited to the left eye
  
• is in the temporal (left) hemifield
  
• is associated with retinal abnormalities in the nasal hemiretina of the left eye
  

So you conclude that the visual defect involves

• retinal damage in the left eye
  
• damage located in the nasal half of the left retina (Figure 15.14, Lesion 1)
  
• damage related to the patient's diabetes - diabetic retinopathy
  

Figure 15.14 This cartoon illustrates the central visual pathway (right panel) and the effects of lesions in the pathway (left panel). The numbered lesions in the right panel produce the correspondingly numbered visual field defects in the left panel.

Retinal Damage: A defect involving only the visual field of one eye indicates possible damage in the retina or optic nerve. If the visual loss is confined to one eye, it is called a monocular visual field defect. Often retinal lesions are small and do not follow the boundaries of the visual field quadrants. Such a visual field disorder is called a scotoma. A retinal visual field defect is most severe when vision in the central field is affected, as in the case of macular degeneration. In macular degeneration, the patient will report difficulty reading and seeing clearly and visual field testing will demonstrate that the patient has a central scotoma (i.e., is blind in the visual field center).

15.4 Clinical Example #2

Figure 15.15 The perimetry test results indicates a loss of vision over most of the visual field of the left eye - with no loss in the right eye's visual field. Notice that the central visual field for the left eye is represented by a black spot, indicating a loss of central field vision.

Symptoms: The patient complains of a sudden headache and loss of vision in his left eye. Ophthalmoscope examination does not reveal abnormalities in the left eye¹. However, confrontation testing indicates a severe loss of vision in the left eye.

The patient is referred for immediate neuroradiographic tests and perimetry testing.

Perimetry Test Results: The results indicate the right eye's visual field is normal and that there is a large visual loss encompassing nearly all of the left eye's visual field (Figure 15.15).

Side & Retinotopicity of damage: The visual loss

• does not appear to relate to changes in the retina of the left eye
  
• is limited to the left eye
  
• encompasses nearly the entire the visual field of the left eye
  

So, you conclude that the visual defect is

• retrobulbar (beyond the retina or eye) (Figure 15.14, Lesion 2)
  
• probably limited to optic nerve damage (only one eye affected)
  

Neural imaging results indicate an aneurysm on the left ophthalmic artery, which is compressing the left optic nerve (Figure 15.16). Compression of the nerve prevents action potentials from the retina to travel to the lateral geniculate nucleus of the thalamus. Long-term compression may damage the nerve, however, of greater concern is the potential rupture of the aneurysm, which could cause extensive brain damage.

Figure 15.16 A view of the inferior surface of the brain illustrating an aneurysm in the left ophthalmic artery, which is compressing the left optic nerve.

Optic Nerve Damage: Each optic nerve contains the axons of retinal ganglion cells from one eye, e.g., the right nerve from the right eye. Damage to one optic nerve will produce a monocular visual field defect. Destruction of one optic nerve (e.g., crushed by a tumor on the orbital surface of the frontal cortex) will result in the total loss of vision in the ipsilesional eye.

15.5 Clinical Example #3

Figure 15.17 The perimetry test results for Example 3 indicate a bitemporal hemianopia (i.e., a bilateral visual defect involving the temporal hemifields of both eyes). Notice that only the temporal halves of the two central areas exhibit a visual loss (i.e., appear as dark hemicircles).

Symptoms: At his annual physical exam, the patient complains of a general malaise and changes in his vision that he noticed while playing soccer. He said he was often "blindsided" on the playing field because he "couldn't see players approaching him from the side". Ophthalmoscope examination does not reveal abnormalities in either eye². Confrontation field testing indicates a constriction of the temporal hemifields of both eyes. The patient is referred for neuroradiographic tests and perimetry testing.

Perimetry Test Results: The results indicate a bitemporal hemianopia, i.e., loss of vision in the temporal hemifields of both eyes (Figure 15.17).

Side & Retinotopicity of damage: The visual loss

• is not related to changes in the retina of either eye
  
• involves vision in both eyes
  
• encompasses only the temporal hemifields
  

You conclude that the visual field defect is related to damage that

• is retrobulbar (beyond the retina)
  
• involves the optic chiasm (Figure 15.14, Lesion 3)
  

Neural imaging results (Figure 15.18) indicate a pituitary adenoma that is compressing the optic chiasm. Compression of the decussating nerve fibers prevents action potentials from the nasal hemiretina to reach the contralateral lateral geniculate nucleus of the thalamus. As the tumor grows larger it will crush the optic chiasm, destroying it and eventually compromising the remaining optic nerve fibers.

Figure 15.18 A view of the inferior surface of the brain illustrating a pituitary tumor, which is compressing the optic chiasm.

Optic Chiasm Damage: The fibers of the optic nerve that originate from ganglion cells in the nasal half of the retina decussate in the optic chiasm to the opposite optic tract (Figure 15.1). The crossing fibers of the optic chiasm may be crushed by a pituitary tumor. Damage to the optic chiasm produces a unique form of visual field deficit, a bitemporal hemianopia (Figure 15.17). Recall that the fibers of the optic chiasm carry information about objects in the temporal hemifields of both eyes (i.e., the right hemifield of the right eye and the left hemifield of the left eye). Consequently section of the optic chiasm produces a visual loss in only the temporal half of the visual field of each eye. When the patient views the world out of both eyes, the boundary of his binocular visual field is narrower than normal.

15.6 Clinical Example #4

Figure 15.19 The perimetry test results indicate a right homonymous hemianopia (i.e., a binocular visual defect involving the right hemifields of both eyes) with macular sparing (i.e., central field vision was not affected).

Symptoms: A patient is brought to the emergency room complaining of a severe headache and nausea. He is conscious and coherent when examined in the ER. Ophthalmoscope examination does not reveal abnormalities in either eye. Confrontation field testing indicates a visual loss in the right hemifield of both eyes.

The patient is referred for neuroradiographic tests and perimetry testing.

Perimetry Test Results: The results indicate a right homonymous hemianopia with macular sparing (Figure 15.19).
Side & Retinotopicity of damage: The visual loss

• is not related to changes in the retina of either eye
  
• involves field losses for both eyes
  
• involves the right hemifields
  
• is homonymous or congruent
  
• spares the central visual field
  

You conclude that the visual field defect is related to damage that

• is retrobulbar (beyond the retina)
  
• is retrochiasmatic or postchiasmatic (beyond the optic chiasm)
  
• involves the left calcarine cortex
  
• may involve hemorrhage from a branch of the left posterior cerebral artery
  
• spared the more caudal and lateral parts of the striate cortex, which receives collateral blood flow from branches of the middle cerebral artery
  

Neural imaging results indicate injury to the rostral half of the left calcarine cortex, which receives blood from the left posterior cerebral artery (Figure 15.20). Recall that the rostral calcarine cortex processes information from the visual field periphery, whereas the caudal and lateral striate cortex process information derived from the visual field center.

Figure 15.20 The perimetry test results indicate a right homonymous hemianopia with macular sparing. The medial and inferior portions of the occipital lobe receives blood from branches of the posterior cerebral artery.

Calcarine Cortex Damage. An infarct created by obstruction of, or a hemorrhage in, branches of the posterior cerebral artery may result in damage to the rostral calcarine cortex. Damage to the calcarine cortex on one side may produce a binocular, contralateral homonymous hemianopia with macular sparing (Figure 15.20). A collateral blood supply from branches of the middle cerebral artery is believed to spare the cortical neurons in the caudal and lateral regions of the striate cortex, which receive information from the macular area.

15.7 Clinical Example #5

Figure 15.21 The cortical areas involved in color perception and face recognition are illustrated in the left hemisected brain with cerebellum removed (A). Distribution of the major branches of the anterior and posterior cerebral arteries viewed on the inferior and medial surfaces of the brain with the cerebellum removed (B). The location of the lesion is colored red.

Symptoms: A patient, who is stabilized after suffering a stroke two months earlier, is referred to a neuro-ophthalmologist for evaluation. The patient does not appear to be blind but has problems with processing visual information. For example, the patient cannot describe the color of an object presented to him or recognize faces. He has normal spatial orientation and motion detection.

The patient is referred for perimetry testing.

Perimetry Test Results: The results indicate no consistent loss of vision. However, it is difficult to obtain consistent results because the patient tires easily and his attention appears to wander.

Side & Retinotopicity of damage: The patient

• is not blind in either eye
  
• does not have deficits in detecting the location or movement of objects
  
• does not exhibit the symptom of "neglect" (i.e., visual inattention)
  
• exhibits deficits in higher visual processing involving color and object recognition
  

You conclude that the neurological defect is

• not related to damage in the visual pathway from the eye to the striate cortex
  
• not related to damage in the middle or superior temporal gyrus
  
• not related to damage in the parietal lobe
  
• related to damage in the inferior temporal gyrus (Figure 15.21)
  
• involving branches of the posterior cerebral artery that supply the inferior temporal gyri
  

Neural imaging results indicate damage to the caudal portion of the inferior temporal lobe, which normally receives blood from branches of the posterior cerebral artery.

Extrastriate or Association Cortex Damage: While destruction of the primary visual cortex produces blindness in the contralesional hemifield, damage to cortical areas surrounding the striate cortex does not Instead, they may produce profound deficits in the higher order-processing of visual information. For example, bilateral damage to a small area of the inferior temporal gyrus (Figure 15.21) produces a loss in the ability to recognize faces. Damage to more superior areas of the temporal lobe (area 39 in Figure 15.4) produces an inability to recognize or comprehend written words and/or passages. Damage to areas in the parietal cortex may result in the inability to see motion (i.e., a moving object will be seen in “frames’’ in one place at one point in time and at another place in a following period of time). The object does not appear to move; rather it appears to have jumped from one place to the next. Damage to large areas involving the posterior parietal cortex and superior temporal cortex may result in the symptom of "neglect", wherein objects in parts of the visual field are ignored or denied existence.

15.8 Summary

In this chapter, you have learned how the visual system is organized in the brain. You have learned that stimulus features extracted by the retinal neurons (color, brightness contrast, movement) are kept segregated in separate “information channels” and processed in parallel by different cells at all levels of the visual system. Information coded and carried by one million retinal ganglion cells are distributed to hundreds of millions of cortical neurons in the occipital, parietal and temporal lobes. The perception of a coherent visual image is recomposed out of these fragments of information by the simultaneous activation of large areas of cortex. You have also learned how the spatial representation of the visual image is maintained by the retinotopic organization of the visual system and learned how this information is useful in determining the location and extent of damage to the visual system by examining the visual fields. Finally, you have learned that neuronal responses in visual cortex exhibit plasticity at different time scales, short term (as adaptation and dynamics) and long term (as learning) – this plasticity allows visual cortex to construct an accurate picture of the world that can rapidly adapt to match the changes in the environment.

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