1
Q
What parts of the brain are involved in visual processing?
A
- Occipital cortex: perception
- Parietal and temporal lobes: visual memory
- Brain stem/spinal cord: visual reflexes
- Pineal gland and diencephalon: circadian rhythm, general metabolic rate, hormonal function, mood
2
Q
What is the utility of visual testing? What kinds of things can you test for?
A
- Easily administered and locates the lesion
- Cognitive status: visual memory
- Motor reflexes: postural reflex
- Autonomic function: pupil dilation
- Inner ear problem: eye movement
- REMEMBER: retinal is the only visible vascular system in the body
3
Q
What is the fovea for? How does light arrive there?
A
- Incoming light from objects of interest is focused on the fovea
- LIGHT: refracted by cornea,
1. Inverted through pupillary opening,
2. Variably refracted by the lens (under control of suspensory ligaments/ciliary mm; less effective with aging)
3. Projected on fovea (pit) in center of macula (yellow pigmented area) - DEVOID OF BLOOD VESSELS: if blood vessels grow here (as they do in macular degeneration), it affects vision bc blood distorts the image
4
Q
What do these arrows illustrate about visual processing?
A
- Arrow is upright outside of the eye, but SMALLER and INVERTED when it reaches the fovea
- Smaller due to refraction in the cornea and lens, but this INC the clarity of the image
- NOTE: lens refraction abilities are controlled by the ciliary mm, under SYM and PARA control
5
Q
What is the sclera?
A
- Protective layer for the retina and choroid
6
Q
What is the choroid?
A
- Vascular bed of the outer retina
- Has highest blood flow of any organ in the body based on size
- Provides BF and nutrients to photoreceptors and retinal pigmented epithelium (RPE) cells
7
Q
What provides the retinal blood flow?
A
- Supplied by CENTRAL RETINAL ARTERY that enters through the optic NN, and supplies about 20% of blood in human retina
- Rest is provided by the CHOROID
- NOTE: fovea is devoid of blood vessels
8
Q
What is responsible for maintaining the visual axis on the fovea?
A
Extraocular mm
9
Q
Describe the 10 layers of the retina and their associated cell types (image).
A
- Pigment cells = retinal pigmented epithelial (RPE) cells that provide a barrier to retina from the choroid
- Photoreceptors = cones and rods that come in contact with the RPE
1. Cell bodies of photoreceptors in outer nuclear layer, but projections in outer plexiform layer to bipolar cells (cell bodies in inner nuclear layer) - Final layer the retinal ganglion cells (ganglion cell layer) -> visual object transduced to these cells, then enters into Optic N to go to brain
10
Q
What is the role of the RPE?
A
- Support photoreceptors (line outermost surface), providing nutrients
11
Q
What is the retinal pathway?
A
- Photoreceptors to bipolars to ganglion cells
12
Q
What are the interneurons in the retina? Role?
A
- HORIZONTAL cells: outer plexiform layer
- AMACRINES: inner plexiform layer
- Help in convergence of the image from the millions of photoreceptors to hundreds of bipolar cells to tens of ganglion cells (signal can be modified)
1. Image ultimately sent through ganglion cells to the optic nerve - NOTE: optic nerve entry into retina is the blind spot
13
Q
How are the ganglion cells related to the Optic N?
A
- Ganglion cell axons coalesce to form the Optic N head
- REMEMBER: Optic N entry into retina is the blind spot
14
Q
What cellular elements are present in the fovea?
A
- All cellular elements except outer segments (cones) are displaced radially
1. CONES (outer segment) and the rest of their signaling pathway (bipolar cells, ganglion cells) project radially away - This allows for minimal distortion of the image
- NOTE: all cell types are in retina in all regions
15
Q
Describe the retinal pigmented epithelium and its 4 main functions.
A
- RPE: layer that separates choroid (vascular) from the retina (neural) -> main function
- Contains black pigment, MELANIN: helps absorb some of the light that comes to photoreceptors, protecting them from light damage
1. Reduction of this (blue-eye v. brown) may contribute to eye disease - Phagocytosis of rod outer segments every 10d, but less effective as we age: many proteins left in RPE, which can cause them to autofluoresce, aka DRUSEN (key factor in macular degeneration)
- Also provides retinal nutrition
- NOTE: diseases of retina often affect tight junctions bt RPE and retina, allowing substances to leak in & out
16
Q
What is macular degeneration?
A
- Results when blood vessels damage the RPE and break through their barrier, growing into macular region of the eye
- This causes visual distortion of the image
- As phagocytosis of rod outer segments gets less effective as we age, many fatty proteins left in RPE, which can cause them to autofluoresce, aka DRUSEN
1. While these likely do not cause age-related macular degeneration, their presence INC risk
17
Q
What are the key differences bt rods and cones?
A
18
Q
Describe the key features of the rod photoreceptors.
A
- Process black and white info (scotopic; night) info
- Light detected and transduced in outer segment
- Named for shape of outer segment, which reaches and lays against RPE cells
1. Undergo phagocytosis by RPE, w/new outer segment formed every 10 days - Synaptic expansion called the spherule
- Much simpler than cones
19
Q
Describe the key features of the cone photoreceptors.
A
- Process color (photopic) info; 3 types, each of which responds to different color of light:
1. L-cones: long wavelengths (red)
2. M-cones: medium wavelengths (green)
3. S-cones: short wavelength (blue) - Every color represented by a unique combo of L-, M-, and S- cones
- Named for shape of outer segment, which is smaller and shorter than rod outer segments
20
Q
How does color distribution work in cones? How is this inherited?
A
- L cones = red; M cones = green; S cones = blue
- If one type of cone is absent bc of genetic defects, person will be missing corresponding opsin = color-blind
- M- and L-cones carried on X chromosome: why men are often red-green color-blind (only 1 X, instead of 2 in F)
21
Q
What is the function of the photoreceptors? Why is it unique?
A
- Absorb quanta of light (photons) and convert to electrical signal
- Both cones and rods undergo HYPERPOLARIZATION in response to light -> ONLY sensory system in which hyperpolarization is response to the stimulus
22
Q
Describe the steps in visual transduction in rods.
A
- 1) Light comes in and converts 11-cis-retinal to all-trans-retinal, activating rod opsin -> rhodopsin
- 2) Active rhodopsin can activate GTP, which activates cGMP phosphodiesterase (PDE)
- 3) Active PDE (no INH subunit) lowers cGMP levels enough to hyperpolarize mem and close cGMP-gated Na+ and Ca2+ channels -> signal = visual response
- 4) Once enough Na+ and Ca2+ are stuck in mem, Ca begins to be pumped out through Na/Ca exchanger
- 5) As Ca reduced in mem, cGMP levels rise and repolarize mem to pre-stimulus levels, re-opening channel
- 6) Slowly, rhodopsin dephosphorylated and all-trans-retinal converted back to 11-cis-retinal
- 7) Rhodopsin kinase comes back to rephosphorylate rhodopsin, which is bound by arrestin to render it inactive
- 8) Once light stimulus occurs again, arrestin will be removed via conversion of 11-cis-retinal to all-trans-retinal
- NOTE: similar actions in cones, but 3 opsins instead of just rhodopsin (with e/corresponding to retinal in a specific manner)
23
Q
What are bipolar cells? Location? Function?
A
- High degree of convergence: 100 million receptor cells synapsing onto 1 million ganglion cells
1. Horizontal cells help converge signals from multiple rod photoreceptors to fewer rod bipolar cells - At bipolar-ganglion cell synapse, amacrine cells detect major changes in activity levels
- Cones and rods have their own bipolar cells, with cone bipolars in central retina, and rod in periphery
24
Q
What are the key features of alpha-ganglion cells?
A
- Predominate in peripheral retina -> most input from RODS
- Extensive dendritic trees, large axons, and little participation in color perception
- Project to MAGNOCELLULAR layer of lateral geniculate nucleus (LGN) -> location of object in space
- NOTE: categorized by physiological role/size, and activate based on image presented; the different ganglion cells project to different regions in brain
25
What are the key features of beta-ganglion cells?
- Found primarily in central retina -\> respond predominantly to CONES
- Small receptive fields, small dendritic arbors, and responsive to color stimuli
- Project to PARVOCELLULAR region in lateral geniculate nucleus (LGN) -\> _define color and texture of object_
26
What is unique about the photoreceptor - ganglion relationship in the fovea?
- _1 photoreceptor for each ganglion cell_: this allows for crisp image representation
- Unlike the rest of the retina, in the fovea, **convergence does NOT occur**
- IMAGE: one cone connected to one bipolar cell and 1 ganglion cell in right half of image -\> there are _NOT horizontal or amacrine cell interaxns_
27
This is the eye. Appreciate it.
Good job!
## Footnote
- Note how the blood vessels radiate from the optic disk (displaced nasally) and that the macula is in the center
28
Describe the central visual pathways, and projection of images to their final destination.
- Visual image _reversed and inverted_ due to pinhole effect of pupil
- Ganglion cell axons in Optic N partially decussate in optic chiasm (**only nasal fibers cross**)
- Optic tract projects to _lateral geniculate_
- Optic radiations carry geniculate fibers to primary visual cortex in occipital lobe; all fibers _retinotopically organized_
- LEFT VISUAL FIELD processed in RIGHT VISUAL CORTEX
- NOTE: 180o visual field viewed by both eyes, except 45o peripherally due to nose
29
Describe the M and P pathways for transfer of visual information from the ganglion cells to the occipital cortex.
- Cells that respond preferentially to input from 1 eye (ocular dominant) are _segregated into layers_ in the lateral geniculate and visual cortex
- _M pathway_ originates from magnocellular ganglion cells, projects to lateral geniculate layers **1 and 2**, then layer 4C-_alpha_ in cortex -\> space information
- _P pathway_ originates from parvocellular ganglion cells, projects to lateral geniculate layers **3-6**, to layer 4C-_beta_ in cortex -\> form information
30
What causes diabetic retinopathy (DR)?
- CHANGES IN VASCULATURE: angiogenic growth factors, loss of angiostatic growth factors
- CHANGES IN NEURONS: loss of photoreceptors, loss of ganglion cells
- We don't really know: high glu causes _damage to retinal endo cells_ and pericytes, eventually causing _hypoxia and activating growth factors_ (it also damages neurons)
- NOTE: attached image is what a pt with DR will see
31
What might be going on here?
- _Proliferative diabetic retinopathy_: light spots at the bottom of the image are likely areas w/o BF (due to damage)
- Inferior region (below the optic disk): blood vessel has been damaged, and there is edema
32
What might this be a symptom of?
Macular degeneration: this is what these pts will see
33
What happened here?
- _Advanced macular degeneration_: note all of the hyperfluorescence and areas of no vascularity
34
Compare and contrast macular degeneration (AMD) and diabetic retinopathy (DR).
- AMD: _choroid_ neovascularization (NV) that breaks through RPE cells and damages macula, age-induced, some genetic, lose CENTRAL VISION (due to damage to macula)
1. Leading cause of blindness in _older ppl_
- DR: _retina_ NV, no age effect, some genetic, lose ALL VISION
1. Leading cause of blindness in _working age adults_
35
What is the difference bt dry AMD and wet AMD?
- DRY AMD: drusen (fatty protein deposits under the retina), _little vision loss_, often in _1 eye_ -\> atrophic macular degeneration (**90%** of cases, anc can be tx'd with visual aids)
1. Can progress to wet
- WET AMD: sometimes drusen, vision loss, progresses to both eyes
36
What causes AMD? Txs?
- Age (biggest cause)
- Smoking (big contributor)
- Genetic predisposition due to altered inflammatory responses
- Changes in angiogenic/angiostatic factors
- _Treatments_: laser coagulation and anti-angiogenic therapies (Avastin and Macugen)
1. IV injections (1/mo) can block vascular growth
2. Does not restore vision in most pts, but often helps _maintain what vision they have_ -\> still eventually lose vision, but drugs much better than in the past
Clinical Neuro
flashcards
Decks in class (15)
# Cards
-
Alexandrov - Stroke77
-
Lennon/Sweatman - Sleep31
-
Levin - MS53
-
Khan - Brain Tumors47
-
Belland/Ryan - Fungal/Bacterial Meningitis31
-
Sweatman - Anesthesia150
-
Sweatman - Brain Tumors13
-
Ferrante - Radiculopathies15
-
Jacewicz - Dizziness16
-
Sweatman - Vertigo, Hearing Loss, N/V22
-
Sweatman - Epilepsy Drugs93
-
Levin - Myelopathy48
-
Jacewicz - Coma23
-
Adamolekun - Seizures59
-
Steinle - Visual System36
