Hello again. Welcome to this tutoral on visual field deficits. We're going to be talking about the complexilty of the visual pathways and how that complexity can be simplified if you understand the basic framework for the central visual projections. That will be of great assistance to you as you examine patients that have visual field deficits. We're going to be basing our knowledge on genetically constructed circuits that are the foundation for visual function in the nervous system. And understanding these visual pathways and using that knowledge to properly localize lesions or disease in your patients will go a long way towards promoting healthy living and the treatment of disease. Well my learning objectives for you today are to describe the distribution of the axons of retinal ganglion cells to the major processing centers in the fore brain and in the brain stem. I want you to be able to discuss the topographic representation of visual space in the primary visual cortex and its anatomical basis in the organization of the visual projections.. Now, both of these objectives carry over from their previous session. On the distribution of information from the retina, to the brain. If you've not yet viewed the tutorial on the central visual pathways, then now's the time to do that, before proceeding onto this session. But if you've done so, great. my final goal for you at the conclusion of this tutorial, would be to characterize, in appropriate clinical terms, the visual field deficits that are associated with damage or disease along the central visual pathways. Well just to be sure you recall what I'm talking about. The central visual pathways are the distribution of retinal ganglion cell axons, from the retinas to the brain and that distribution goes to both sides of the brain with the nasal retina giving rise to axons across the optic chiasm. The temporal retina giving rise to axons that remain on the ipsilateral side of the brain. Running into the ipsilateral optic tract. Once axons grow posterior to the optic chiasm, they supply various targets in the diencephalon such as the suprachiasmatic nucleus of the hypothalamus and the lateral geniculate nucleus which is the major destination. Of visual information that's going to be used for the construction of visual percepts. In addition to those diencephalic targets visual information is relayed to the mid brain, specifically to the region known as the Pretectum, which is really just between the mid brain and the diencephalon and the superior colliculus. Well, our focus today is going to be on the image forming pathway. That is the pathway from the retina to the lateral geniculate nucleus. And then from the lateral geniculate nucleus back into the primary visual cortex and beyond into extrastriate visual cortex. Here from the lateral view, again we find our lateral geniculate nucleus. Which gives rise to the optic radiations. the optic radiations sweep around the lateral ventricle. those that run through the parietal white matter. Are representing the lower visual field. And those axons, travel and terminate in the cuneus gyrus, on the upper bank of the calcarine sulcus. Whereas, a portion of the optic radiation that emerges from the more ventral aspect of the geniculate. Sweeps around the temporal horn of the lateral ventricle, through the white matter of the temporal lobe, terminating on the inferior bank of the calcarine sulcus in the lingual gyrus. These axons that are running through the white matter of the temporal lobe represent the upper portion of the contralateral visual field. So what we have, then, is an inversion of the representation of the world in the brain, such that the opposite side of the visual field is represented in one hemisphere, and the upper bank of the calcarine sulcus is representing the contralateral inferior quadrant of space. Whereas the, lower bank of calcarine sulcus is representing the contra lateral, upper field. So with that background in mind let's turn our attention now to the analysis of injury or disease that afflicts some local region along this visual pathway. And before we actually look at representation of such injury, I want to get some terms out in front of you that will be useful. as we describe these lesions, and, these terms, seem a li-, a little bit burdensome, but actually they're quite descriptive. And I think if you can understand the meaning of the terms, then their proper clinical use will quickly become second nature. So let's begin with the term Anopsia. Anopsia refers to a large area of blindness in one eye. So hemianopsia means blindness in one hemifield, that is half field that is seen just by one eye. Quadrantanopsia means blindness in one quadrant within a hemifield that's seen by an eye. Now we modify these words with a term homonymous and a complimentary term heteronomous. So homonymous means same side so this refers to the same visual hemifield that is seen in each eye. For example, one can have a lesion in the central visual pathway that produces blindness on the left side of the visual field for one eye and the left side, or the same side, of the visual field for the other eye. That's an example of a homonymous hemianopsia. So if the regions of blindness are not on the same side of the mid line for the views of each eye, then we call that a Heteronymous hemianopsia. So Heteronymous means different side, this refers to opposite vision hemifields being impacted in the field of view of each eye. And then, finally, the word, scotoma refers to a much smaller lesion. a small area of blindness somewhere within a visual field. The blind spot that we each bear in our visual hemispheres. Due to the fact that the optic nerve head has no photoreceptors overlying it. Is one example of a natural[SOUND] scotoma. But, of course, scotomas can arise because of focal[SOUND] injury to their visual pathways. Or to the cortex itself. [SOUND] Now here's an important figure that I want you to spend some time studying. This figure relates a series of locations[SOUND] along the visual pathways. That potentially could be the location of injury or disease to a reprensentaion of the visaul fields of each eye. And the convention in this representaion is to use black shading to indicate blindness. So let's walk through each of these. locations and visual field deficits in turn. First of all, let's orient ourselves to the brain. We are looking down through the brain from above. So notice that we have the right eye on the right side of this illustration. And the left eye on the left side of the illustration. That seems quite fundamental. But it will be critical when you're studying and you're learning to be certain that you know which side of the brain you're considering. So in this figure, right is right and left is left. OK, so let's consider what happens if there were to be an injury. In the right eye or the right optic nerve. Well that should be pretty straightforward. The right eye would be blind so this would be simply blindness in the right eye. Now, let's imagine that we had a lesion. Not in the optic nerve, but right in the middle of the optic chiasm. this can happen sometimes when there is a traumatic injury that induces a sharing force along the midline of the hemispheres. Or perhaps with a tumor that's growing out of the pituitary gland. Gland, which attaches right below the optic chiasm. Well, a lesion of the optic chiasm, would cut the axons of the nasal retina that cross in the midline. And that results in blindness, in the peripheral parts of our visual world. Specifically. The line is in what the nasal retina's C and the nasal retina of the left eye sees the lateral or the temporal part of the visual world. The nasal portion of the right eye sees it's lateral retina. We have preservation of central visual space but blindness to the left and right sides of our visual fields. And that's an example of bitemporal hemianopsia, or specifically a heteronymous hemianopsia. So, let's see how we use those terms. Hemianopsia means half visual field blindness for what an eye sees. And then the further modifiers talk about whether it's concordant for the field of view of each eye. And in this case, it's not. It's the left visual field that is lost for the view of the left eye. And the right visual field for the view of the right eye. That's a bilateral, or bitemporal heteronymous hemianopsia. Now let's consider the remaining lesions here and let's continue to work our way back. So, lesion C is a lesion of the right optic tract. So, at this location we have sorted out the. Principal of contralateral representation such that in the right optic tract, we have the axons from the two eyes that see the left side of the midline. So the image to the right optic tract produces blindness in the left side of the visual fields that are seen by each eye. So here is also a hemianopsia but now its a homonymous hemianopsia. Specifically a left sided homonymous hemianopsia. The left side of mid-line is lost for the field of view of each eye. The same would essentially be the case if we jump all the way back now, and look at what happens with damage to the right occipital cortex. If we imagined that this was a widespread lesion in the right occipital cortex, we would likewise produce damage to the field of view that's seen on the left. Now notice there's a little bit of a carved region of visual preservation just around the central part of the visual field there on the left side of the midline. This is called macular sparing. And there are a couple of ideas as to why this comes about. One idea is simply the fact that we have such a large representation of the macular region in the visual cortex. A brain injury following, let's say, a stroke or a trauma very well may damage a wide region of the visual cortex, but potentially there is preservation of some small region that very well may be representing the macula and what it sees. Just because this is the part of the visual field that is given the most cortical circuitry. Well should that be the case then we might expect there to be some sparing of that region of the visual field. Well, perhaps there's another explanation that has to do with how the retina sorts out what's called the line of decussation. Which means where exactly is the division between the temporal and the nasal retina. But that's a story more for the aficionados out there. So if we wanted to kick that into the discussion forum that would be fine, but I won't take the time to talk about that story here. So let's, complete our analysis of this figure by considering lesion D. Now lesion D is taken to, effect the axons of Meyer's loop. And as you recall, the axons that are growing out to contribute the inferior portion of the optic radiation have to loop around the temporal horn of the lateral ventricle. They do so by forming this very distinctive array of axons that sweep, first inferior and laterally around the temporal horn of the lateral ventricle. And then, posterior and, inferior, along the white matter of the inferior temporal lobe back into the occipital lobe. These axons terminate in the lingual gyrus. And they're representing the contra lateral upper part of visual space. So if we have damage to these axon, then what we would see is loss of the representation of the contra lateral superior quadrant of the visual world. So this would be an example of a left sided Homonymous quadrantanopsia. Do you see how we used all of those terms, so it's left of midline. It's a quadrant that's lost. So a quadrant, quadrantanopsia. And it's homonymous. That is, it's the same side of the midline that's lost in the visual field of each eye. Okay. I'm going to leave you with a couple of study questions that will ask you to think about two patients who have problems that you suspect maybe related to visual field deficits. So, consider these patients and the options that I'm giving you to work through and see what you think. I'll see you next time.
