You will need the following pictures in front of you as you read this section.            From your Course Pack: CP#67, #68, #83. From your Picture (loaner) Pack: LP#13 & 43.

Now that you understand the basic anatomy, you have a foundation for understanding what happens to a person's vision when parts of the visual system are destroyed. Losing one eye is very simple to understand -- you are blind in that eye. But what happens if there is a lesion (area of destruction) in the optic nerve, or tract, or radiations, or in the cortex? Do all of these lesions produce blindness? The answer is that damage anywhere in the visual projection system produces blindness, as does a lesion to V1, but beyond V1 there is a great deal of visual cortex and much of that cortex can lost without blindness. Losing a part of the cortex outside of V1 will cost you the loss of some visual ability , however. For example, if you lose the disparity detecting neurons, you will no longer have stereognosis and will be no better at perceiving depth than a one-eyed person.

Let's trace throught the visual system to see the varying effects of lesions at different points along this information-processing route. In all of the following, remember that the entire nervous system is bilaterally symetrical and that each side is the mirror image of the other. That means that there is two of everything: two frontal lobes, two occipital lobes, two thalami, two eyes, etc.

A lesion that cuts the right optic nerve would produce the same result as loss of the right eye. However, loss of the right optic tract would produce blindness in the left visual field of each eye. (Verify this for yourself by tracing the path in CP #83.) Losing the optic radiations (the axons of LGN cells that run from LGN to the visual cortex) in one hemisphere would produce blindness in the contralateral field of each eye. A tumor growing at the midline of the brain at its base could invade the optic chiasm, killing all the fibers in the contralateral projections, (but leaving the ipsilateral) and result in tunnel vision (vision only in the center of the combined right and left fields). The loss of peripheral vision occurs because the each half-field is seen only by the contralteral eye. The left eye can see some of what is in the right visual field but cannot see as far around the right side of the head as can the right eye (and vice versa for the right eye and left field). (Check this out on CP #67. and 83.) So peripheral vision is lost in both fields.

After you study CP #83, you should be able to tell where a lesion might be if you are told the nature of the deficit. For example, if a person with both eyes intact and functioning were blind in the left eye but sighted in the right, the lesion would have to be in the _____ (choose between: left eye, left optic nerve, left optic tract, right optic tract).

Note that to get homonymous hemianopia, an entire half of the visual projections must be cut at some level. For example, an entire optic tract (not just some of its fibers) or an entire LGN, or all of the radiations in one hemisphere. This latter, however, is such an extensive lesion that it is unlikely to be seen in the clinic. More likely is the loss of some of the radiations, leaving the person blind in roughly one quadrant (quarter) of the visual field. This is protrayed in "D" in the chart of CP#83.

Now test your knowledge. Is it possible to produce hemianopia by cutting one of the optic nerves? Can you name the blindness caused by loss of an entire V1 in one hemisphere? (Hint: losing a V1 is just like losing the tract on that side.) We will have a practice session on these ideas that should help give you some practice in answering such questions.

V1 is a crucial area in that it seems to be somewhat of a bottleneck in the system; almost all the information from the retina must flow through this one zone. It is not unexpected then that the loss of a part of V1 causes a loss of all visual functions for the particular patch of the visual field handled by that portion of V1. Such a scotoma is experienced by the patient as a black area in a zone of vision. If the entire V1 area is lost in one hemisphere, the person is blind for the entire contralateral visual field and is said to suffer from hemianopia. Thus, loss of the right occipital lobe leaves one blind in the left visual field, a disorder called left-side hemianopia.

When the lesion occurs farther forward in the occipital lobe, outside of V1, however, blindness does not result. An area such as MT, for example, receives input from V4 but is not absolutely dependent on that route. It also gets information from V1 and V3 as well as several other areas (see CP #68). Although the loss of V4 input must hamper MT in performance of its analysis, the input coming from the other areas contains much of the same information as would have come from V4, so MT is not totally incapacitated. This means that the patient with a lesion in V4 will show visual peculiarities but not blindness. What are some of these peculiarities? That is, what are some of the symptoms of visual cortex damage outside of V1?

Another patient could not name the object on the table in front of him (a glass of water) and could not describe its function. However, a few more minutes into the interview, he reached over and took a drink from it. This does not mean he was lying when he claimed not to recognize what it was. it simply meant that the routes from the visual analyzers to his language cortex (the part of the brain that would answer the psychologist's question) were damaged whereas the pathways carrying visual information to the motivational circuits in the limbic system were still working. The patient may have been more surprised by his behavior than was the interviewer.

Small areas of damage may disrupt the function of only a few analyzers and leave the patient with a highly specific problem. Stengel, for example, reported on a patient (in Williams, 1979) with no visual problems other than color identification. In a standard color test, the patient was given a collection of colored yarns and asked to pick out the one that was the same color as grass (he chose a light green), sky (he chose a dark green), blood (red yarn), tomato (he hesitates, points to purple, then to orange, adding the the latter was probably more correct). The lesion, in this case, was probably in V4, as that area seems to be the final stage of color processing.

The above examples have been from patients who probably suffered more disruption of the object vision path (ventral stream) than of the spatial vision path (dorsal stream). When the lesion is in the dorsal stream (parietal cortex), some loss of spatial abilities is noted. Cleland and coworkers (1981), for example, report the case of a woman who suffered a stroke in the right posterior parietal region that left her with a tendency toward perseverative perception of movement sequences. The first time this happened, "a man walked in front of her window and she continued to see him in her left field of vision but his walking was speeded up. She described the sensation as though she was watching a film being shown at the wrong speed, that speed being about twice normal. The amplitude of the movements was unchanged. On the second occasion she continued to see a child waving but, as on the previous occasion, the action was speeded up. On the third occasion, her brother put his hand through his hair. She continued to see him repeatedly perform this action at a faster rate. Each episode of perseveration lasted about ten minutes with the image gradually fading although there was no diminution of the movement." Notice that she had no trouble seeing objects (like the man); her difficulty was locating them accurately in space.

This seems to be a problem in separating the figure (the visual elements to which one is attending) from the ground (all of the unattended, background elements). Either the patient could extract only one figure from the confusion of overlapping images or, having chosen one set of lines to use as a figure and relegating all the others to the status of ground, he was unable to shift attention to a different figure. Notice that this attention problem seems less related to spatial location (which is a parietal lobe function) than to a figure-ground problem. The task requires one to first see one set of lines as the figure (and the rest as the ground) and then to shift attention to the lines that were the ground - making them into the current figure.

Could some of the attentional problems of agnosia result from a problem with scanning (eye movements)? We Know that such neglect is a subtle attentional problem with complex causation but, perhaps a percentage of patients who fail to report the left ends of printed sentences simply never move their eyes to the point on the page where the beginning of the sentence would fall on their foveas. Peculiarities of scanning are fairly clear in some patients. For example, patients have been observed to enter an unfamiliar room with unusual caution, turning head from side to side and peering about. Head movements might be taking the place of missing eye movements. An important part of scanning is the fixation at the end of each eye movement. One patient failed to fixate objects normally and his eyes could be pulled away from a needed fixation by any new stimulus entering the field of view (Williams, 1979). Scanning problems of this sort could arise because the motor "machinery" that allows cortical circuits to direct eye movements is no longer connected to the visual system. Voluntary eye movements are directed by the frontal eye fields of the frontal cortex, just posterior to the prefrontal cortex. It is likely that some lesions of the parietal lobes might have severed the loop that runs between the visual processors and those eye fields. Thus, when frontal lobes recalled an object that should be looked at next and queried the parietal cortex for the location of that object, no answer came back and the frontal eye fields were unable to move the eyes to the object's location.

Luria, a famous Russian neuropsychologist, has devoted much of his career to finding ways to help brain damage patients (Luria, 1963). In the case of agnosia he has discovered some useful strategies for the patient that can help to compensate for the loss of visual functions. Frequently there is more than one way to accomplish a perceptual task, and just because one method has been lost to brain damage doesn't mean that all have been. Since brain damage patients may feel so defeated by their loss of abilities that they fail to find ways to compensate, one of the most important things a neuropsychologist can do is to motivate the patient to discover alternate strategies and use them. For example, if someone shows you some common object, they will expect you to identify it in a fraction of a second and make some intelligent reply immediately. Having behaved this way for years, the agnosia patient tries to make the identification faster than his limited processing capacity is able and this haste frequently produces a mislabeling of the object.

If you show a drawing of a spider, for example, the patient may call it a crab. A narrowing of the focus of attention, similar to that seen in the overlapping-images test, has led the patient to focus on the legs and kept him from seeing the body. Perhaps the eye movements needed to shift the foveas away from the "leg" region of the picture never occurred. Having perceived legs but little else, the patient names the first creature that comes to mind that has 6 or 8 legs. When shown a picture of eyeglasses, one patient called them scissors. He had perceived the two circles at the ends of the handles but little else.

The task of the therapist then, is to get patients to slow down and persist in their attempts to recognize the object. According to Luria, this frequently pays off with an eventual correct identification. He quotes from the response of a patient interviewed by Gelb and Goldstein who at first claimed to be completely unable to understand the test picture at all: "Something pink.....on top of it there's something black, and underneath something white, and then more black........ and the pink on top is probably a face......and the black......well, of course, it is quite obvious, it's a man! (cited in Luria, 1963). Persistence pays.

Another basic strategy is to relearn how to scan a scene. One of Luria's patients could write sentences easily from dictation but could not copy them from printed form. Obviously, this was a visual problem rather than a language disability. Luria had the patient practice tracing letters with his finger and follow his finger with his eyes. Since tracing activated the unharmed kinesthetic sense in the muscles and joints, the patient was immediately able to perceive the letters with that method. Making the eye movements simultaneously seemed to create new associations between these perceptions and the visual sense for he became faster and faster at letter identifications. Finally, Luria had the patient drop the finger tracing and rely solely on tracing the letters with eye movements (a detailed form of scanning). Eventually, the patient was able to recognize each letter without even the eye-movement tracing.

There is an interesting similarity between this example of relearning visual perceptions and the original learning of such perceptions reported by von Senden (described in Hebb, 1949) who examined surgery patients (without brain damage) who had just been given the ability to see for the first time in their lives. These people had been born with cataracts (clouded lenses) that allowed only diffuse light to reach their retinas. They had never experienced a visual image prior to the surgery that removed the cataracts. They strongly resembled agnosia patients in their inability to identify faces and objects visually even after several days of experience. One interviewer observed that the only way his patient eventually learned to perceive the difference between a triangle and a square was to move his eyes around the shape, counting the corners. In a few days, however, this detailed scanning apparently became unnecessary and the object could be immediately perceived as a whole as soon as it was presented. It is possible that Luria's teaching of scanning may represent a retraining procedure that mimics the way in which the brain originally built up the visual engrams lost when the occipital lobes were damaged.

Recent studies of visual agnosia have shown several different types. Theoretically, there must be a different type of agnosia for each different type (location) of lesion. For example, a lesion that removes V2 should produce different symptoms than one that eliminates MT. Since each module in the visual cortex gives you a different visual ability, there should be as many agnosias as there are visual abilities. However, lesions from strokes and accidents rarely remove completely any one module from both hemispheres and rarely confine themselves to a single module. And, areas like V2, V3, MT and MST may each contain five or more different modules. So, cataloging types of agnosias is a very crude business and shouldn't be pushed to more than a few very broad, loose categories. We recognize two such categories: apperceptive agnosia and associative agnosia.