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Visual System


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Why is "pie in the sky" right quadrantinopsia often associated with language disorders?
Upside down and backwards - the visual system is wired this way (like most cameras). So the Meyers loops that carry visual information for the rightupper hemispace run through the LEFT lower temporal lobe (top of the visual field is represented in the BOTTOM of the temporal lobe). Language and right upper visual field wiring runs through the same areas and can therfore be lesioned together easily.
Is it possible to be able to know where something is by "sight" without knowing what it is?
Absolutely. This is called "blind sight" and is not at all uncommon. There are 2 visual systems in the brain - the "what" system which ends in the visual cortex and the "where" system which ends in association visual and motor cortices and the brainstem. Coritcally blind individuals have no conscious awareness of the "where" system, but can ususally catch or deflect a ball thrown directly at them (or at least will flinch / duck) because the where system that tracks movement is still working.
Why will alligators and snakes strike at limbs or other non-edible moving objects are readily as they will at prey? Why can you sometimes avoid their notice if you are still?
The cortical visual system, which handles "what" an object is (visual identification) is rudimentary in lower animals (they have little cortex). The "where" movement system is their primary visual system. So movement is what they respond to, not visual identification of prey. If you are still, you "disappear". Cortical damage in humans can mimic this lower animal visual system.
What are the 2 major recptor cells in the human eye?
1) rods, much more numerous (20:1) but poor spatial resolution , no color, mostly useful in low light conditions. Think of 20 guys in grey suits groping around in the dark.

2) Cones - very specific about location, size, shape, color. Fewer of them because they only live in the best areas for catching the light (the fovea). Think of a few very wealthy guys living in the center of town in high rises, taking in the sun on their balconies and roof top terraces while below a vast sea of the groping grey guys spread all around, searching for any bit of light they can find. Cones are definitely upper middle management. Lots of lower critters have no cones (and therefore don't see colors as we do - just shades of grey).
How close is a camera analogy to the actual visual system?
Not bad, really.
1) Image comes in through the lens of the eye. Muscles surrounding the eye (run by cranial nerves 3, 4, and 7) move the eyeball up, down and obliquely to point the lens and sympathetic / parasympathetic muscles manage the thickness and opening of the lens. At the lens, incoming information is inverted (top to bottom and left to right).

2) This doubly inverted image is focused, not on a photographic medium (as in the camera) but on a "medium" of photorecptors in the fovea. In bright light, all the image concentrates well, the aperture is small and the picture is clear. In poorer light, the lens opening is bigger, the light is more dispersed, the image is "grainier" and the rods are working as well as the centrally located cones. Black and white film works better for low light shots just as the black and white rods are needed in their vast numbers to absorb all the stray light in low light settings.
3) In a digital camera, the focused image is carried by wire back to the dock (or computer) for storage. In the visual system, there are wires leading the image to 2 further processors. The where system runs back from the fovea to the optic chiasm (where the information is sorted so all right hemispatial info goes to the left and all left hemispatial attention goes to the right) and through the lateral geniculate (some via the superior colliculus) and a few go on to the brainstem, the association areas and the frontal eye fields (to turn the head and eyes automatically for following the stimulus); the majority go to the primary and secondary visual cortex (Broadmann areas 17 & 18 mostly) for careful processing and identification - then the info goes to the verbal cortex for verbal identification (confrontation naming)
What is homonymous hemianopsia?
Homonymous refers to the fact that all of the information coming from a particular visual field (not a particular eye) is affected. Although clients often say they can't see out of the "right eye" for instance, what they may mean is that all information from the right side of space has been obliterated. That can only happen after the information is sorted at the optic chiasm, so their lesion would be on the left side of the brain and hits both halves of the optic radiation (the upper radiation and the lower or Meyer's loop) in the temporal lobe or is even more massive farther back in the brain to the point of injury to the entire left occipital pole. Hemianopsia refers to an acquired defect of vision, usually only or mostly the what system, for an entire hemispace.
What are pie in the sky or pie on the floor qudrantanospias? Where is the lesion?
A quadrantanopsia is the loss of the "what" system (primarily) for all information coming from a particular quadrant (1/4) of space. Pie in the sky means you lost the top quarter of the visual space (a Meyer's loop lesion usually), pie on the floor means the bottom quarter. Since the visual system is "upside down and backwards", pie in the sky lesions are in the BOTTOM of the temporal lobe opposite (low left lesions create high right quadrantanopsias) and pie on the floor lesions are high temporal and low parietal, more likely to be associated with reading and praxis (for the right pie on the floor) or praxis / spatial deficits (for the left pie on the floor) than with primary language disorders and memory problems.
The photoreceptors differ from all other neurons in the way they transmit signals. How?
Photorecptors (and the bipolar cells they connect to) do not fire in an all or none fashion, like neurons throughout the rest of the nervous system do. There is a threshold of light below which they can't operate at all, but above that threshold they will respond (rods to much less light than cones). No color information is avialable if only the rods can pick up the light. If the cones can respond, the neurochemicals are conducted passively and the amount of neurochemical conducted (graded potential) and released at the synapse determines the amount of potential (information) transmitted. So a "really yellow" stimulus releases lots of chemical messenger compared to a barely yellow stimulus. (Close your eyes or look away and you see the "echo" of the opposite color for a moment while the chemicals equalize). By combining the 3 different types of cones/bipolar cells, we create the range of hues and intensities of color experience we can manage. Loose a cone type (the red/green appear to be really fragile) and you are colorblind (can't distinguish those 2 hues). Usually congenital and usually male. Acquired colorblindness is rare and usually total (an occipital lesion).
Why is acquired colorblindness usually total and not red/green or blue /yellow?
Because it is hard to damage just one population of the tightly packed cones / bipolar cells in the fovea and optic nerve without affecting the other. An acquired color loss would probably be an occipital problem / lesion, affecting all color processing.
Why do people sometimes call the eyes the visible part of the brain?
The eyes are actually an extension of the brain to the body surface (and therefore one of the best ways, along with sinuses nearby, of infecting the brain). The optic tracts are not true "nerves" because they are entirely surrounded by the central nervous system tissues. The optic tract is the set of ganglia leading from the retina back to the crossing at the optic chiasm.
What happens when there is damage to or pressure on the optic tracts (before the crossing at the chiasm)?
This is not an uncommon happening if the anterior pituitary in particular develops a growth (benign or malignant). If the pressure is to the optic tract, there is a monocular (one eye only) loss of information for the viual field opposite the lesion. Since pituitary tumors are often fairly round, you usually get pressure on the inside of both tracts at the bottom so you have binasal information loss but only of the information from the top portion of vision in the opposite eye. So you get right hemispace information only from the right eye and left hemispatial information only from the left eye for information in the upper visual fields both left and right. Probably not very noticeable to the client unless they notice the world seems dimmer or less clear above the horizon. Might complain about reading overhead signs at night. Incidentally, this often puts pressure on the globes of the eyes so they may tend to bulge a bit.
What happens if there is pressure on the optic nerves right behind the chiasm?
This is the more common place for pituitary and other midline tumors to play havoc with vision. Because the visual information has already crossed, you see bitemporal (upper visual field on both outsides) visual deficits. It is noticeable because all the visual information is gone from the top outside quarter on both visual fields (the pressure comes from below). Overhead signs are usually ok but street signs at the sides of the road are gone or very pale. Unless the tumor is really large, the position of the globes of the eyes may not be affected.
Where do the optic tracts go after the crossing?
To the lateral geniculate bodies of the thalamus, then through the temporal lobes as the optic radiations (Meyers loops on the bottom) and to the optic cortex. Lesions anywhere after the chiasm will produce contralateral homonymous (only one side of space) defects.
What are the 2 potential pathways the optic tracts follow?
1) the Retino - geniculo-triate pathway. Most cone fibers follow this primary path. From the retina to the lateral geniculate to the optic cortex (called striate because it looks striped). Many of the rod fibers also follow htis pathway, but mostly in a supporting cast role (they don't help much with discrimination).

2) Retino-pulvinar-extrastriate cortex path: also called the extrageniculate visual pathway) - from the retina to the superior colliculus to the pulvinar and lateral posterior nucleaus of the thalamus, to brainstem and association visual and motor cortices (including the frontal eye fields); this is the where system, lots of rod data and less cone - far less conscious awareness - probably involved in "blindsight" (cortical blindness)
Where is the primary visual cortex? What happens if it is lesioned?
The primary visual corties (areas 17 and 18) lie "on the banks" of (both above and below) the calcarine fissure at the occipital pole of the brain. The medial occipital lobe up is wedge shaped (above the calcarine) and is called the "cuneas". It receives the upper optic radiations so lesions create lower contralateral visual field defects. The bottom part of the visual cortex is called the "lingula" (literally little tongue) and is below the calcarine fissure. It receives Meyer's loop so lesions result in upper quadrantaopsias of the opposite visual field.
Odd tid bits - the "grandmother monkey cells"
It appears that there are particular cell groups in the striate cortex that respond only to very particular visual stimuli (like letters, faces, colors). At one time it was thought that there was an area so precise it would only respond to the face of the (monkeys were the experimental subjects) monkey's paternal grandmother. Turns out it isn't quite that specific, probably, but close.
How is visual acuity measured? Do brain lesions affect it?
Visual acuity is measured on the Snellen index - comparing the subject's ability to see clearly at 20 feet objects clearly visible by an individual with "normal vision" at what distance. So if I can see this letter 20 feet away and "normals" can see it 600 feet away, my vision is 20/600 (which is accurate for me). Usually measured separately for the right eye (labelled the OD - d for dexter or right) and the left eye (labelled OS - s for sinister or left) and then for both labelled OU
Brain lesions do not typically affect acuity. So a standard optometry visit won't often pick up subtle brain problems. A Behavioral optometry eval is needed.
What does a client report of blurry vision usually mean?
$64000 question. Typically, clients say they have a problem with one eye when it is really one visual field. Often they can't remember the difference between neglect of an arm and neglect of that visual hemispace (and, to be fair, they often occur together). Monocular visual problems are often reported as "blurry", but so is failure of tear production (like for Horner's syndrome). When in doubt, send them out - get a neuro-optometry eval before using such reports to try to localize.
What is visual extinction to double simultaneous stimulation?
This is a phenomenon that occurs when the client can see fingers (and finger movement) on either side if only one visual field is stimulated at a time, but if you move or display fingers on both sides, they only report one (usually the side contralateral to the damage or the "healthy side"). So, for example, a person with a left lower occipital injury might lose stimulation of the right upper visual field if the left upper visual field was simultaneously stimulated. Unfortunately, the localization isn't that specific and parietal lesions or lesions in the brainstem pathways can create total or partial extinctions when the cortex is fine.
What are "negative visual symptoms" or "negative visual phenomena"? What would the client report?
Field defects and scotoma. We all have a scotoma or "blind spots" in our peripheral visual field but it is only evident under odd circumstances. It is where the optic nerve exits the retina and deforms it, leaving a spot that we don't see. The brain "fills in" the missing information as best it can from the surrounding visual field info. But if there is a passing car in the "blind spot" you are completely unaware of it - that's why Driver's Ed instructors tell you to look over your shoulder when changing lane (so you can foveate the car - bring the image into the area that you can see).
After a brain injury, there may be scotoma all over the visual field of which the client is unaware. They may show up on Neuropsych testing (usually sustained cancellation tasks or CPT tasks). Similarly, there may be a quadrantonopsia or even a hemianopsia the client doesn't know about because the brain fills in and they aren't driving or performing other skilled tasks in a rapidly changing visual array.
What are positive visual phenomena and what gets reported?
The scotoma post-TBI are somewhat similar to the scotoma of migraines except migraines usually produce both negative and positive visual effects - some lost information and some inaccurate or exaggerated information. Fortification scotoma are often seen in migraine and there is an area of loss with a nearby zigzag of neon-like or scintillating (changing and bright) lights - sort of like little leds of different shades. If you look carefully, the colors in the scintillations are often present in the environmental surround so the brain is "filling in" even during the flashing, trying to make the odd areas make some sense. If you have pain with the scotoma, you avoid light (photophobia). If you have antalgic migraine or migraine aura, you can watch them without pain.
Anywhere along the pathway from the eyes to the calcarine cortex you can have lesions or vascular problems resulting in positive phenomena. With pulsating colored lights or miving geometric shapes, the most likely cause is electrical activity in the calcarine cortex (e.g. seizures). Formed visual hallucinations (people, animals, spirits that are recognizable as people) usually arise from temero-occipital association cortex (Myers loop into the occipital areas) electrical activity. Cuases are often toxins, metabolic problems, substances (esp. withdrawal), focal seizures and complex migraines. Narcolepsy and psychiatric disturbance can do it too (though psychiatric is usu. more auditory than visual). Pressure to the eyeballs (like rubbing them) can produce little sparkles of light.
Why do cortically blind clients often report "seeing things"? Why are they often unaware they are blind?
This is a release phenomenon. Deprive any sensory system of input long enough and it will start creating formed hallucinations, especially early in the process leading ot the deprivation. So the clients are having visual impressions that are as "real" as anything they saw before the lesion (since all vision is "imaginary" in that it is electrical and chemical activity in the brain and only corresponds to the environment if the system is working well". The brain will try to "fill in" the whole world, especially if hte surroundings are familiar and the sounds, smells, textures and tastes are right. Essentially, the brain provides "visual re-runs" in familiar places for a time, fooling the client into thinking he or she can still see.
What is Bonnet syndrome?
Elderly folks whose vision is slowly degenerating may have visual hallucinations of everyday objects and places due to the brain trying to help interpret the degraded visual data. Imagine someone with a large old fashioned Bonnet cutting most of the light from the eyes trying to peer under it to recognize places and people.
What is refractive error?
Indistinct vision (20/60 or above usually) that is correctible with corrective lenses
What are photopsias?
Bright, unformed flashes, streaks or balls of light.
What are phosphenes
Photopsias formed as the result of retinal shear or optic nerve disease (not just frm rubbing your eyes).
Entopic phenomena are what?
Seeing the structures in one's own eyes (usually while a bright light source is around, like seeing the vessels while having an eye exam).
Visual illusions are?
Distortions or misinterpretations of actual stimuli present in the visual field (e.g. the curtains blow and you "see" a ghost.
Visual halluncinations are?
Visual perception of things not present but without another misinterpretted stimulus (e.g. you are in an empty room and "see" your deceased brother). This can be organic (from brain damage) or psychiatric (which is just a way of saying organic with a particular set of symptoms best dealt with by antipsychotic medications).
How do you test for problems with visual fields?
1) confrontation testing: involves standing or sitting facing the client and holding your arms outstretched so your fingers fall into the client's peripheral visual fields. Test 3 sets (upper, middle and lower fields). Take care not to move the arm or sleeves more proximal to your body. Client is to focus on your nose or upper lip; if they can't maintain fixation, you can't test (often the case with the elderly). Ask them to tell you if your finger move to their left or their right. You actually do several left only, several right only, and several trials in which both move, randomly mixed. Watch for extinction to double simultaneous stimulation (often present in the neglected visual field).

2) formal Goldmann perimetry
What is a retinal lesion and what defect would it cause?
A retinal lesion usually affects only the retina of one eye. It occurs before the crossing of visual information, so it creates a monocular lesion (scotoma or field loss). A tear or detatchment of the retina or a stroke affecting the blood supply can cause this).
What is an optic nerve lesion and what defect of vision would it cause?
This is damage to or dysfunction of the optic nerve before the crossing of the visual informaiton at the chiasm, so it will create a unilateral defect. This can be a scotoma (limited) or a all vision to that eye. Common causes would be glaucoma (increased pressure in the fluid of the eye), optic neuritis (infection / inflammation of the optic nerve itself), or elevated intracranial pressure (putting pressure on the optic nerve and pinching it).
What would damage to or dysfunction of the optic chiasm cause functionally?
Once the visual information crosses at the chiasm, the deficit created become bilateral. The information carried along the interior paths of the chiasm is the information sent by the temporal side of each optic field, so this sort of lesion or dysfunction typically produced a bitemporal hemianopsia. A tumor of the pituitary (such as an adenoma) will produce this pattern (because all the pressure is from below).
WHat about damage or dysfunction behind the chiasm; what sort of functional affect would that have?
Again, from the chiasm back deficits tend to be homonymous (all information from only one side of space is affected). So lesions of the optic tract produce contralateral quadrant (if only half is damaged) or hemianopsia (if both Meyer's loop in the temporal and the upper optic raditations are damaged). Damage to the lateral geniculate of the thalamus also produces contralateral homonymous hemianopsia. Both would likely be from strokes. Harm Meyer's loop (for instance due to an inferior MCA storke) and you get pie in the sky quadrantinopsia. Harm the upper radiations (like from an upper division MCA stroke) and you get pie on the floor quadrantanopsia. A big MCA stroke could cause a contralateral homonymous hemianopsia. Lots of things (PCA infarcts, tumors, hemorrhages and infections, trauma to the occipital pole) can cause damage to the primary visual cortex. If only the upper bank of the calcarine cortex is harmed, you get a contralateral inferior quadrantanopsia. If only the lower section (the little tongue) is damaged, you get contralateral superior quadrantanopsia. Take out the whole cortex and you get contralateral hemianopsia.
How do quadrantanopsias differ from quandrantopias?
They don't. It is a spelling issue (like the British say grey and Americans spell the word gray).
What is macular sparing?
The macula or center of the focal area is represented so heavily in hte cortex (lots more cells per millimeter than in more outlying areas, kind of like downtown Manhattan residence per square mile versus upstate New York) that sometimes a lesion of the cortex (or other places along the radiations) will not affect the very central areas of the visual field as badly as the more peripheral areas. So you may have someone who can't see much outside of a tunnel of vision right in front of their eyes.
What is macular degeneration and what effect does it have on vision?
As you might expect, macular degeneration is an eye problem, not a brain issue. The macula itself, with all its tightly packed cells, is damaged (usually starved of blood) and slowly dies. The patient can see peripherally, but cannot read or sew or even eat eventually because what is right in front of them is blank. They need more light to see anything because the peripheral vision is poor (very spread out, detail is not crisp) and illumination really helps. They trip and stumble because they cannot see what is in front af their feet.
What blood vessels supply the various regions of the visual system?
1) The opthalmic artery supplies the retina.
2) the small perferating branches of the ACA, MCA, anterior and posterior communicating arteries perfuse the optic tracts, chiasm, a intracranial optic nerves
3) the Lateral geniculate nucleus of the THalamus is perfused differently in deifferent people; a stroke that affects its supply may also produce contralateral hemiparesis or hemisensory loss due to starving the posterior limb of the iternal capsule adn thalamic somatosensory radiations
4) the optic radiations pass through the parietal and temporal lobes so MCA strokes can affect them
5) the posterior communicating artery supplies the primary visual cortex and the basilar arteries supply the PCAs [bilateral altitudinal scotoma suggests vertebrobasilar insufficiency with reulsting TIAs)
6) PCAs also supply the inferior occipitotemporal visual association cortex (the "what system for identifying objects seen)
7) The MCA and PCA watershed areas (perfused by the farthest reaching capillaries of both) supplies the lateral parieto-occipital visual association cortex (the where system for tracking movements)
What is optic neuritis? How does it affect vision? What is its course?
Optic neuritis is an inflammatory demylenating disorder of the optic nerve; it is both causally and statistically related to MS; 50% of folks who have an incident of optic neuritis eventually develop MS. Onset is usually eye pain and monocular visual changes. Can be acute or gradual. Recovery is ususally complete in 6-8 weeks. There may be permanent visual loss, however.
Extraoccular weakness can affect vision. How? What are the symptoms? How do you distinguish this from problems in the visual system proper?
Weakness in the extraoccular eye muscles can produce diplopia (double vision) and ptosis (drooping eyelids). Double vision and blurring are reproted. The client may develop neck adn shoulder pain from tilting the head back in an exaggerated manner to see from under drooping lids.
The forehead may be contracted and furrowed from trying to use facial muscles to align visual images. Patients may complain that new glasses prescriptions are still "not working". If closing one eye corrects the visual problem, it is the extraocular muscles rather than the visual system at fault.
The Glasgow Coma Scale included eye movements as one of its scales. What are the numerical values assigned to various eye movements?
Spontaneous eye opening =4; eye opening to speech =3; eye opening to pain = 2; no eye opening =1.
What are "eye signs" related to traumatic brain injury?
The eyes reveal a lot about how serious a brian injury is and where it is, as well as whether it is becoming life threatening. Different levels of lesion produce different functional presentations.
1) a thalamic lesion can produce small, reactive pupils (also called diencephalic pupils)
2) hypothalamic and other sympathetic pathway lesions cause Horner's syndrom (ptosis - droopy lid), anhydrosis - no sweating, miosis - little pupils;
3) Midbrain lesions are more varied in presentation. a) lesions of the dorsal tectum produce "midposition eyes" that are fixed to light
b) lesions of the nuclear midbrain produce eyes that are fixed and pupils that are irregular /unequal
4) lesions of the 3rd cranial nerve or outside the brainstem create wide pupils that are unresponsive to light
5)pontine lesions create pinpoint pupils that are responsive to light

In general, all lesions above the level of the thalamus or below the pons yiled normal sized pupils (except the medulla which yields Horner's)

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