Medical Neuroscience explores the functional organization and neurophysiology of the human central nervous system, while providing a neurobiological framework for understanding human behavior. In this course, you will discover the organization of the neural systems in the brain and spinal cord that mediate sensation, motivate bodily action, and integrate sensorimotor signals with memory, emotion and related faculties of cognition. The overall goal of this course is to provide the foundation for understanding the impairments of sensation, action and cognition that accompany injury, disease or dysfunction in the central nervous system. The course will build upon knowledge acquired through prior studies of cell and molecular biology, general physiology and human anatomy, as we focus primarily on the central nervous system. This online course is designed to include all of the core concepts in neurophysiology and clinical neuroanatomy that would be presented in most first-year neuroscience courses in schools of medicine. However, there are some topics (e.g., biological psychiatry) and several learning experiences (e.g., hands-on brain dissection) that we provide in the corresponding course offered in the Duke University School of Medicine on campus that we are not attempting to reproduce in Medical Neuroscience online. Nevertheless, our aim is to faithfully present in scope and rigor a medical school caliber course experience. This course comprises six units of content organized into 12 weeks, with an additional week for a comprehensive final exam: - Unit 1 Neuroanatomy (weeks 1-2). This unit covers the surface anatomy of the human brain, its internal structure, and the overall organization of sensory and motor systems in the brainstem and spinal cord. - Unit 2 Neural signaling (weeks 3-4). This unit addresses the fundamental mechanisms of neuronal excitability, signal generation and propagation, synaptic transmission, post synaptic mechanisms of signal integration, and neural plasticity. - Unit 3 Sensory systems (weeks 5-7). Here, you will learn the overall organization and function of the sensory systems that contribute to our sense of self relative to the world around us: somatic sensory systems, proprioception, vision, audition, and balance senses. - Unit 4 Motor systems (weeks 8-9). In this unit, we will examine the organization and function of the brain and spinal mechanisms that govern bodily movement. - Unit 5 Brain Development (week 10). Next, we turn our attention to the neurobiological mechanisms for building the nervous system in embryonic development and in early postnatal life; we will also consider how the brain changes across the lifespan. - Unit 6 Cognition (weeks 11-12). The course concludes with a survey of the association systems of the cerebral hemispheres, with an emphasis on cortical networks that integrate perception, memory and emotion in organizing behavior and planning for the future; we will also consider brain systems for maintaining homeostasis and regulating brain state.
Visual Field Deficits
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Del curso dictado por Duke University
Medical Neuroscience
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De la lección
Sensory Systems: The Visual System
This module will provide lessons that are designed to help you understand the basic mechanisms by which light is transduced into electrical signals that are then used to construct visual perceptions in the brain. Your studies of the visual system will benefit you at this point in the course, but also in later studies when we use the visual system as a model for understanding general principles of developmental plasticity. Lastly, it is worth noting how much of the forebrain contains elements of the visual pathways. Thus, injuries and disease in widespread regions of the brain may have a clinically important impact on visual function. All the more reason to learn these lessons well as you progress in Medical Neuroscience.
Conoce a los instructores
Leonard E. White, Ph.D.Associate Professor
Department of Neurology, Department of Neurobiology, Duke University School of Medicine; Department of Psychology & Neuroscience, Trinity College of Arts & Sciences; Director of Education, Duke Institute for Brain Sciences; Duke University
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.
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