Visual System Flashcards

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28
Q

Describe the pupillary light reflex.

A

Light enters through CN II which crosses at the optic chiasm and goes to the pretectal nucleus which projects bilaterally to the Edinger Westphal nucleus (CN III). The EW nucleus projects to the ipsilateral ciliary ganglion which acts on the pupillary contrictor muscle.

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29
Q

What is the near triad?

A

Convergence, miosis, and accommodation

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29
Q

What is the near reflex pathway?

A

The near reflex also allows for pupillary constriction but through a different pathway. Various areas of the cortex project to the Edinger-Westphal nucleus (to ciliary ganglion) instead of the pretectal nucleus.

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30
Q

Can the light reflex be impaired if the near response is normal? The reverse?

A

Yes, because only a fraction of the fibers in CN II account for the light reflex (6%) while the rest account for the near reflex. You can have a normal near response with an abnormal pupillary respose but the reverse is less likely.

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30
Q

What does an afferent pupillary defect generally imply?

A

Optic nerve problem–generally caused by damage to the optic nerve or bad retinal disease, not cataracts, vitreous, or corneal disease.

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31
Q

What is the term for unequal pupils? What is it a sign of?

A

Anisocoria is an indicator of an efferent problem, not an afferent problem.

Three potential causes:

  • Physiologic: 10-20% of the population have 0.4 mm anisocoria but they have normal light, near, and dark reactions
  • Horner’s syndrome: abnormal constricted pupil
  • CN III palsy: abnormal dilated pupil
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31
Q

Describe the symptoms of Horner’s syndrome.

A

Horner’s syndrome presents with an abnormally constricted pupil due to a loss of sympathetic signaling. It appears worse in the dark. Also presents with ptosis. To confirm that this is Horner’s syndrome, a cocaine test can be done to attempt to activate the sympathetic arm.

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32
Q

Describe how to localize a Horner’s syndrome.

A
  • First order neuron: descends from hypothalamus and synapses in spine–brainstem or spine injury
  • Second order neuron: Exits spinal nerve roots and synapses in the superior cervical ganglion–sign of an apical lung tumor (Pancoast tumor)
  • Third order neuron: ascends with the internal carotid artery to provide sympathetic innervation to the eye–sign of a carotid dissection which presents with pain

Use neurologic company to determine where the lesion is

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32
Q

What can cause an isolated pupillary dilation?

A
  • Trauma to the eye
  • Pharmacologically dilated (no near response or light response)
  • Environmental: motion sickness patches, blue night shade
  • Adie’s tonic pupil: damage to postganglionic fibers of parasympathetics to the eye (ciliary ganglion injury)–no light response, near response preserved but tonic
  • Oculomotor palsy
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33
Q

What are the symptoms of an oculomotor palsy? What can cause it?

A
  • Down and out eye: only lateral rectus and superior oblique still function
  • Dilated pupil (parasympathetics lost)
  • Can be caused by a PCOM aneurysm
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33
Q

What is an Argyll Robertson pupil?

A

Seen in neurosyphillis–pupils do not respond to light but do accommodate briskly. This is bilateral.

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34
Q

What path does light take through the eye? What are the two main refractive surfaces?

A

Light goes through the cornea, passes through the anterior chamber, the lens, and the vitreous and an optical image is formed in the plane of photoreceptors at the back of the eye. Change in membrane potential of the photoreceptors leads to phototransduction and activation of neural ciruits in the retina.

The main two refractive surfaces are the cornea and the lens.

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34
Q

What is the power of the lens expressed as? What is the power of a flat lens? How much of this is the cornea responsible for?

A

The power of a lens is expressed as 1/foal length (meters) and equals about 58 diopters in a nearly flat lens . The cornea is responsible for 52 of the 58 diopters, the lens accounts for the rest.

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35
Q

How does accommodation work? What happens to accommodation as we age?

A

At rest, the lens is stretched and flattened by the zonular fibers. When the eye accommodates, the ciliary muscle contracts which releases tension on the lens capsule allowing the lens to become spherical which increases the refractive power of the eye.

A young person can accommodate an additional 12 diopters for near vision but this diminishes as we age–the near point at which an object can be focused recedes (presbyopia).

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35
Q

Describe the structure of the retina.

A
  • Three cell layers: ganglion cell layer, inner nuclear layer (bipolar, horizontal, and amacrine cells), and outer nuclear layer (cell bodies of rods and cones)
  • Inner plexiform layer is between the ganglion and inner nuclear layers
  • Outer plexiform layer is between the inner nuclear and outer nuclear layers
  • Inner and outer segments of the photoreceptors are just below the choroid near the outside of the eye
  • The fovea is a pit of cones with long processes carrying signals to cells around the outside
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36
Q

Describe the distribution of rods and cones in the retina and the cells they project to.

A

Rods are highly sensitive to light but only see in grey scale, cones are less sensitive but contain three subtypes which respond to different wavelenghts to permit color vision. Cones are concentrated in the fovea and their density drops off as you move away. There are no rods in the fovea.

In the central fovea, each bipolar cell is driven by a single cone for maximal acuity but each cone contacts two bipolar cells.

In the parafovea, each bipolar cell receives signals from a single cone and a substantial number of rods.

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36
Q

Describe the mechanism of phototransduction in rods and cones.

A

Photoreceptors are always depolarized in the dark because they contain cytosolic cGMP and cGMP gated sodium channels. Therefore, in the dark, the rod is permeable to both sodium and potassium. When rhodopsin absorbs a photon it activates G proteins which activate cGMP phosphodiesterases which break down cGMP and stop them from releasing glutamate at their synaptic terminals. Light hyperpolarizes the photoreceptor, dark depolarizes the receptor. Cones are the same except for their absorption spectra.

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37
Q

How do bipolar cells respond to signals from rods and cone?

A

The response depends on the cell type. ON-bipolars are inhibited by glutamate so they are hyperpolarized in the dark and depolarized in the light. OFF-bipolars are excited by glutamate so they are depolarized in the dark and hyperpolarized in the light.

For every photoreceptor there is one postsynaptic ON-bipolar cell and one postsynaptic OFF-bipolar cell so this system is able to carry information about light increments as well as light decrements.

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37
Q

Describe the straight-through pathway of retinal computation.

A

The straight-through pathway is vertical–cones release glutamate to excite/inhibit ganglion cells and bipolar cells release glutamate to excite ganglion cells which generate action potentials (all other retinal cells communicate using graded synaptic release determined by changing membrane potentials)

Ganglion cells also have ON and OFF divisions

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38
Q

Describe the two major lateral pathways.

A

The inner plexiform layer contains amacrine cells which carry signals from bipolar cells to distant ganglion cells (function unclear).

The outer plexiform layer contains horizontal cells which are GABAergic and their action is always opposite to that of the photoreceptor input (antagonistic input). They collect the input from the photoreceptor and release an inhibitory signal back on them. The result is to enhance contrast between the center and the surround.

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38
Q

What is the consequence of this contrast based system?

A

Our visual systems are bad at representing absolute light levels

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39
Q

What does the neural image record as compared to the bipolar cells?

A

The neural image only shows the local contrast that is represented in a receptor field, not the absolute amount of light. It processes the difference in light between the center and the surround.

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39
Q

What classifications of ganglion cells are there?

A

The midget cells (P-cells) receives inputs from single bipolars and have tiny receptor field centers because they only get a single bipolar input. Many of them exhibit color specific responses (specifically red and green)

Parasol ganglion cells (M-cells) receive input from many bipolars so they have large receptor fields and an impoverished center-surround receptor field organization. They are particularly sensitive to motion.

40
Q

Where do M and P ganglion cells project to?

A

M-cells project to lamina 1 and 2 of the LGN while P-cells project to lamina 3 and 6 of the LGN.

40
Q

How is color vision coded?

A

Color is coded for by the ratio of activation of the three cone types over a small region of visual space. The outputs of the cones are recombined in a process that starts in the retina and continues in the visual cortex.

Channels:

Blue-yellow

Red-green

Black-white

41
Q

What are the central projections of the optic nerve?

A

Midbrain

  • Superior colliculus: generates orienting head and eye movements
  • Pretectal complex: efferents are to the Edinger-Westphal nucleus on both sides which controls the pupil
  • Accessory optic nuclei: reflex following movements

Hypothalamus

  • Suprachiasmatic nucleus: optic nerve input synchronizes circadian rhythms to the light-dark cycle

Thalamus

  • Lateral geniculate nucleus: thalamic relay nucleus for the primary visual cortex–main pathway for vision
41
Q

Projections from retinal ganglion cells in which hemiretina decussate in the optic chiasm?

A

Axons from retinal ganglion cells whose cell bodies lie in the nasal hemiretina cross at the chiasm while those from the temporal hemiretina do not cross in the chiasm.

42
Q

Where is each visual hemifield located? How does this relate to the half of the retina that the image is projected on to?

A

Each visual hemifield is represented in the contralateral visual cortex. Images in the right hemifield project onto the left temporal hemiretina (which don’t decussate) and onto the right nasal hemiretina (which do decussate), resulting in the entire right hemifield being represented in the left hemisphere.

42
Q

What part of the visual field is binocular? What hemiretina sees the monocular portions of the visual fleid?

A

The middle 120 degrees is binocular. The final 30 degrees on either side is seen by the extreme nasal retina of the eye on the same side.

43
Q

Which thalamic nucleus does the optic tract project to? What cell layers exist in that tract and what information do they receive?

A

The optic tract projects to the lateral geniculate nucleus ventrally. Layers 1 and 2 are magnocellular (M) and layers 3, 4, 5, and 6 are parvocellular (P) (midget and parasol cells are kept separate). Layers 1, 4, and 6 receive contralateral information while layers 2, 3, and 5 receive ipsilateral information (the eyes are kept separate). ON and OFF cells are separated in P layers, not M layers.

There are no binocular cells in the LGN receiving input from both eyes.

43
Q

Describe the retinotopic organization of the LGN.

A

Adjacent points on the retina are represented by adjacent points in the LGN–adjacent cells in the LGN will have receptor fields that are adjacent in space which produces a map of the contralateral hemifield in each LGN. Much more space, however, is devoted to the fovea and central visual field than is devoted to the periphery.

44
Q

How do LGN receptive fields compare to retinal fields?

A

They are identical to those of the RGCs–each LGN cell may be classified as a P-cell or M-cell. It is a relay nucleus that is gated to only permit information to reach the cortex during waking.

44
Q

How is are the visual fields represented in the striate cortex?

A

Striate cortex is the primary visual cortex (Brodmann area 17). The upper visual fields are represented on the lower bank of the calcarine fissure and the lower visual fields are on the upper bank. The fovea is represented at the occiptal pole.

45
Q

In what layers do thalamic inputs to the cortex terminate?

A

The thalamic input to area 17 is largely to layer IVC. M-cells terminate in the IVC-alpha and P-cells terminate in the IVC-beta. These inputs are still kept separate.

45
Q

Where does the M pathway terminate? The P pathway?

A

M pathway: Neurons in IVC-alpha project a short way to layer IVB which projects to two extrastriate areas–V2 (Brodmann’s area 18) and MT.

P pathway: neurons in IVC-beta project to layers II and III which send axons to extrastriate areas–V4 and V2.

They both send collaterals to layers V and VI which are the origins of major pathways to the pontine nuceli and the superior colliculus from layer V and the major feedback pathway to the LGN from layer VI.

46
Q

What unique processing happens in layer IVB?

A

Cells in IVB are orientation selective, direction selective, and stereoscopically selective. This means they will respond to an image component that is in a particular organization, moving in a specific direction, and located a certain distance from the organism (this requires binocularity).

Cell connections stop being one to one here. IVC-alpha cells project to many IVB cells and one IVB cell receives input from many IVC-alpha cells. These are a mixure of ON and OFF cells.

Transformation from IVC-alpha to IVB is responsible for finding the edges in a visible scene–they fire selectively for different orientations. They are the first cells with binocular recepive fields.

46
Q

Describe the modular organization in the visual cortex.

A

There is columnar organization for orientation selectivity, direction selectivity, ocular dominance, and color.

In layer IVC, all cells are driven either by the left eye or the right eye, but not both, so ocular dominance columns are absolute. In layers above and below, cells receive stronger input from one eye or the other but are dominated by the eye providing input to the layer IVC in that band.

Color module is in V1–layers II and III concentrate cytochrome oxidase in clusters. Cells in these clusters have center-surround RF’s, are color coded, and part of the P-pathway. CO clusters are centered on OD bands in layers below. Color information and eye dominance are respresented in an overlapping, coordinated set of cortical modules.

Orientation pinwheels are centered on CO clusters

47
Q

Does the cortex also have lateral processing pathways like the retina?

A

Yes–in some way it compares features extracted over adjacent and even distant parts of the scene. Neurons are capable of interacting with neurons whose receptive fields do not overlap with its own. They work in a space defined by orientation, motion, color, and stereoscopic depth.

47
Q

What is extrastriate cortex?

A

Any visual cortex outside V1

48
Q

Where are V1 and V2?

A

V1 and V2 are on the banks of the calcarine fissure with V2 surrounding V1. V4 is on the inferior surface of the occipital lobe.

48
Q

What are the two streams of visual processing?

A

Dorsal stream: where pathway

  • Arises from layer IVB in the striate cortex, proceeds through the thick CO stripes in V2, goes through MT and ends in the posterior parietal cortex
  • Represents the scene in a way suitable for guiding action (motion, depth)

Ventral stream: what pathway

  • Arises from layers II-III in the striate cortex, proceeds through the pale stripes in V2 and a series of areas including V4 to end in the inferotemporal cortex
  • Represents animate and inanimate objects
49
Q

What is MT? What does it recognize? What do lesions cause?

A

MT may be the homunculus for motion, which is a modality of vision analogous to color. MT cells are direction sensitive but not orientation sensitive.

Direction of motion is represented in a modular system in MT–columns of cells responding best to the same direction of motion

Lesions of the MT produce selective deficits in detecting/discriminating motion, called akinotopsia. Lesions of the MT abolish the ability to perceive structure from motion.

49
Q

What is the aperture problem?

A

The motion of an edge cannot be determined by a single orientation selective cell. MT cells combine the outputs of multiple V1 cells in such a way that MT cells are rendered sensitive to the true direction of motion regardless of the orientation of the edges.

50
Q

What is the ventral stream?

A

The cells in V4 are not sensitive to motion, but they are sensitive to color and shape and orientation.

Lesions to this area present achromatopsia.

50
Q

What do lesions to the posterior parietal cortex and the inferior temporal cortex result in?

A
  • Lesions to posterior parietal cortex produce contralateral neglect
  • Lesions to the inferior temporal cortex result in agnosias or prosopagnosia (inability to recognize objects or faces)
51
Q

What lesions produce each visual deficit?

A
51
Q

What visual deficit will an occlusion of the left inferior branch of the retinal artery produce?

A

Left eye superior altitudinal field defect

52
Q

What visual defect will a right optic nerve tumor produce?

A

No light perception in the right eye

52
Q

What visual defect will a pituitary adenoma produce?

A

Bitemporal hemianopsia

53
Q

What visual defect will a tumor in the right optic radiation produce?

A

Left homonymous hemianopsia

53
Q

What visual defect will a right temporal lobectomy produce?

A

Left homonymous quadrantanopsia

54
Q

What visual deficit will a left posterior cerebral artery stroke produce?

A

Right homonymous hemianopsia with macular sparing

54
Q

What visual defect will bilateral occiptal lobe stroke produce?

A

Cortical blindness

55
Q

What cortical visual disorders of the ventral pathway can occur?

A
  • Alexia without agraphia: unable to read, able to write, right homonymous hemianopsia due to lesion in left occipital lobe and left splenium of corpus callosum
  • Visual agnosias and prosopagnosia: inability to recognize objects or faces due to a lesion in the occipito-temporal lobe
  • Cerebral hemi-achromatopsia: lack of color vision in homonymous hemifield with upper quadrantonopsia due to lesions to fusiform and lingual gyri in the inferior occiptal lobe (V4)
55
Q

What cortical visual pathways of the dorsal pathway can occur?

A
  • Hemi-neglect: ignore or unaware of objects in left hemispace due to a lesion of the right parietal lobe
  • Balint’s syndrome: simultanagnosia (inability to put together a seam from its individual parts), ocular apraxia, optic ataxia due to a bilateral lesion in the parieto-occiptal lobe
  • Akinetopsia: inability to detect motion due to a lateral occipito-temporal lesion (V5)