Southern California College of Optometry Solve Your Patient’s Visual Acuity Complaints by Prescribing NeuroVision Technology Peter Shaw-McMinn, OD Assistant Professor Southern California College of Optometry This is new technology that has been available in Singapore for 3 years. They are getting ready to enter the US market and you will be the first to know about it!

One of the advantages of our profession is we have the opportunity to improve the quality of our patient’s life on a daily basis.

We have the opportunity to improve the quality of life of: Patients Staff Ourselves Our professions The Eyecare Industry Society I’m especially thrilled to bring you a new technology that will change the way we view vision correction in the future! We can truly improve the lives of our patients with this…and the technology is just beginning…

Today’s Objectives Explain what limits visual acuity  You will be able to: Explain what limits visual acuity Describe the brain processes that allow us to see clearly Understand how the NeuroVision technology works Recognize how the NeuroVision program can benefit patients This is how I’m going to improve your lives today! I’m going to give you the science basis on how we can improve our patients vision. We’ve all had patients who could not see as well as others. I will tell you about new technology that can improve the vision of nearly every patient you see! And make you their hero!

What Determines Our Visual Acuity? How do we see? Ever answer that question? What do you say?

Retinal image + Neural Processing We’ve concentrated our efforts on getting a clear image on the retina…and with the correction of higher order aberrations we can do this better than ever…but what about the neural processing along the visual pathway?

Visual system Remember you neurophysiology classes in optometry school? We’ve got a lot more going on than just the eye when it comes to vision. We’ve got processing at the retina, the lateral geniculate nucleus and the visual cortex.

Cells in the retina At the retinal level, light strikes the photoreceptor causing a chemical reaction which sends electric charge to the bipolar cell which sends it on to the ganglion cells. The horizontal cells enable each photoreceptor to interact with others and with other bipolar cells. The signal transmitted via the horizontal cell results in the inhibition of neighboring receptor cells (lateral inhibition) and, hence, an enhancement in contrast. This synaptic connection, however, is modulated by the amacrine cells. These cells provide negative feedback and thus allow regulation of the sensitivity of transmission from the bipolar to ganglion cells to suitable levels, depending on the immediate past light levels. The amacrine cells enable the bipolar cells and the ganglion cells to interact with each other. We call these interactions, lateral interactions.

Neuronal morphology Dendrites: shaft, spines, specialized synaptic structures Extensions of cell body, with same membrane & organelles Shape and number characteristic of each type of neuron; shape determines number of synaptic sites, physiological properties Remember, our nerve cells have several sites at which to interact with other cells. The dendrites as well as the synaptic terminals.

Light hits photoreceptor You can see here how all the cells are interacting with one another through the dendrites…note the cones go to multiple bipolar cells. The horizontal and amacrine cells interconnect all three.

The initial step in the translation of light information from a spot of light into an electric signal propagating to the visual cortex takes place in the photoreceptors in a process known as transduction. This consists of the cis-trans isomerization of the carotenoid chromophore, which leads to a transient change in the membrane potential of the cell. The result consists of a graded response, seen as a hyperpolarization of the photoreceptor, and an electrotonic current linking the outer and inner segments. A photoreceptor is capable of transducing the energy of a single photon (about 4×10-12erg) into a pulsed reduction of axial current of about 1 pA lasting about 1 s with an energy equivalent of 2×10-7erg (Levick and Dvorak, 1986). Thus, a photoreceptor serves as a photomultiplier with an energy gain of some 105 times. So in anwsering “How we see”, you might say:

Chemical reaction releases glutamate At the retinal level the main connections are the photoreceptor to the bipolar cell to the ganglion cells by releasing the chemical glutamate with the horizontal cells and amacrine cells modulating the responses.

How we see - at the Retinal Level Photoreceptors use a biochemical process to convert light in electrical signals that are transmitted via bipolar cells to ganglion cells. The axons of the ganglion cells form the optic nerve that connects the retina with visual centers of the brain. This vertical signal transduction is mediated by the excitatory neurotransmitter glutamate, and is modulated laterally by horizontal and amacrine cells that use the inhibitory neurotransmitters γ-aminobutyric acid (GABA) and glycine. This horizontal inhibition causes a negative feed-back for the vertical excitatory signal pathway. This feed-back increases the signal to noise ratio of the light signal, regulates the light sensitivity of the retina (adaptation), causes selectivity in ganglion cell responses for the orientation of objects and the direction of their movements, and is important for the generation of receptive fields. In Summary: You might explain how we see biochemically:

Fig. 7-18. Receptive fields of two retinal ganglion cells Fig. 7-18. Receptive fields of two retinal ganglion cells. Fields are circuluar areas of the retina surrounded by an annulus of different properties. The cell in the upper part of the figure responds when the center is illuminated (on-center, a) and when the surround is darkened (off surround, b). The cell in the lower part of the figure responds when the center is darkened (off-center, d) and when the surround is illuminated (on-surround, e). Both cells give on- and off- responses when both center and surround are illuminated (c and f), but neither response is as strong as when only center or surround is illuminated. (Hubel DH: Sci Amer 209:54-62, 1963)

Receptive field Hartline introduced the concept of 'receptive field' to describe the spatial properties of retinal ganglion cells. He used 'spot mapping' to define such fields. Cells were found to respond to relatively dim spots when the stimulus was positioned in the 'center' of the receptive field but brighter stimuli were required as the spots were moved away from this region. Hartline concluded that ganglion cell receptive fields were fixed in space and immobile, typically did not extend beyond 1 mm in diameter, and were graded in sensitivity over this region. Receptive fields were much larger than expected of individual photoreceptors, suggesting signal processing and integration through retinal circuitry.

Receptive Fields and Contrast Sensitivity The characteristic 'spatial tuning' of ganglion cell receptive fields is reflected in peaked contrast sensitivity functions This tuning reflects in part the variable dendritic span in ganglion cells. Dendritic span is one of the factors allowing ganglion cells to collect visual signals over a broad reach of visual space. But dendritic field span in itself does not provide for a decline in sensitivity as stimulus sizes become large. Surrounds are required.

Contrast sensitivity is one measure of size selectivity in ganglion cells. Another measure is 'hyperacuity'. This is the ability to detect movements within the ganglion cell receptive field. Examples are: Researchers actually measure the response of cells to different contrasts and hyperacuity tasks. This tells them the activity level of the neurons.

Lateral Geniculate Body After the ganglion cells leave the retina, then make up the optic nerve. At the chiasm we know the optic n from each eye interchange half of the fibers resulting in the left visual field being seen by the right side of the brain and the right visual field being seen by the left side of the brain. This allows a larger opportunity for interactions.

LGN has six layers of cells The ganglion cells lead to the LGN where they are organized into 6 distinct layers. This allows lateral interactions among the cells. The M or parasol cells go to the Magnocellular layers which are peripheral retina. The P midget cells to the parvocellular layers which deal with foveal vision.

1 .3 million neurons same as number of ganglion cells The mangocellular layers process visual information concerned with low spatial frequencies, high temporal frequencies, low contrast and luminance. (Peripheral retina) The parvocellular layers process visual information concerned with high spatial frequencies, low temporal frequencies, high contrast and color. (Central retina) The parvocellular layers are the ones we are concerned with for sharp foveal vision.

Sharpest vision at fovea The specialized cone pathways of the central fovea of human and monkey retinas are designed to have the least convergence and the greatest resolution capabilities of the visual system. This is accomplished by making the connections as "private" as possible and narrowing them to a one to one relationship in the so-called midget pathways. Some ganglion cells are influenced by a lower number of photoreceptors than others.

The midget pathways consist of midget bipolar cells and midget ganglion cells, the latter of which project to individual parvocellular layer cells of the lateral geniculate nucleus in the brain. Because of the need for the high acuity midget pathways also to be organized into ON- and OFF-center channels like the diffuse cone pathways for maximization of contrast, it means that every cone of the fovea will have dual midget pathways. The two midget bipolars will be an ON-center type and an OFF-center type and will connect with ON-center and OFF-center midget ganglion cells respectively. This improves contrast sensitivity for high spatial frequencies.

Fig. 7-18. Receptive fields of two retinal ganglion cells Fig. 7-18. Receptive fields of two retinal ganglion cells. Fields are circuluar areas of the retina surrounded by an annulus of different properties. The cell in the upper part of the figure responds when the center is illuminated (on-center, a) and when the surround is darkened (off surround, b). The cell in the lower part of the figure responds when the center is darkened (off-center, d) and when the surround is illuminated (on-surround, e). Both cells give on- and off- responses when both center and surround are illuminated (c and f), but neither response is as strong as when only center or surround is illuminated. (Hubel DH: Sci Amer 209:54-62, 1963)

Striate Cortex We’ve got a lot more going on than just the eye when it comes to vision. We’ve got processing at the retina, the lateral geniculate nucleus and the visual cortex.

Striate Cortex has 6 layers 1.3 million ganglion and LGN cells diverge to 260 million neurons in the visual cortex Layers 5 and 6 project back to the LGN Layer 4 goes on to higher cortical layers Cells are arranged retinotopically as in the LGN, so cells located next to one another in the cortex process information from areas of the visual field located next to one another. More cortical cells are devoted to processing macular information than peripheral information. 50% of the striate cortex is devoted to processing information from the central 10 degrees of visual field. Borish.

Visual Cortical Cells In 1959 Hubel and Wiesal discovered that cortical cells responded to certain orientation of bar targets. All cells within a column through the 6 cortical layers have roughly the same orientation preference.

Receptive fields in V1 of visual cortex Recall that the receptive fields of both ganglion cells and LGN neurons were center-surround, and that they responded optimally to points of light. Neurons in the cortex, however, respond very poorly to points of light. The optimal stimulus for most cortical neurons turns out to be a bar of light, in a very specific orientation. How did this come about?

This is significant because if you want to maximally stimulate visual cortex neurons you would need to use a target that is bars…and you would need it at specific orientations

How we see Light strikes our retinal photoreceptors which converts chemicals into energy releasing electrical stimulation to the bipolar cells with lateral interactions modulated by the horizontal cells which releases energy to ganglion cells whose lateral interactions are modulated by amacrine cells. The 1.3 million ganglion cells compose the optic nerve which goes to the lateral geniculate nucleus and organized into 6 layers where lateral interactions occur between on/off midget cells. From there 1.3 million cells terminate in the striate cortex where lateral interactions occur in 260 million cells which further process the image allowing us to see.

What happens when something goes wrong with this? AMBLYOPIA

Amblyopia In amblyopia radiographic visual evoked response studies show that cells in the LGN and visual cortex are smaller and have fewer connections. Electrophysiologically, Amblyopic cells have decreased CSF with higher spatial frequencies. Temporal timing functions are also reduced, meaning they can detect slower moving targets versus faster moving targets.

Amblyopia Biochemically, autoradiographic analysis of enzymes used in transporting information show less energy production so there is less activity among neural connections. Less lateral interactions.

How does Patching work? Patching results in increased cell size and more connections by making pathway function more efficiently improving the response. It is important that the amblyopic eye looks at targets which stress the eye at the limit of it’s ability. I went through the neuroVision program with my left eye which was slightely amblyopic. I was born with 4 D astigmatism in my left eye, plo in the right eye. The word stress is a good one here. I was exhausted after 20 minutes of going through the treatment!

How does loss of the good eye affect the amblyopic eye? When good eye is lost, connections which were turned off by interactions with good eye are now allowed to turn on. The inhibiting connections from the good eye are gone, unmasking the good connections already present. The more connections, the better the acuity. We’ve all noticed amblyopic eyes improve in acuity once the good eye was lost. I never could understand how we can say nothing can improve an amblyopic eye after age 9 because of this. Partly this is semantics. Purists would say the eye was already developed to the max, just inhibited.

So, who is amblyopic? Could a 20/20 eye be amblyopic? During our developmental years, the visual pathway efficiency depends upon a sharp image on the retina. No sharp image, less cell interactions and decreased v.a. How many of us have sharp images on our retina during our formative years?

Refractive error and age Histogram of mean right eye spherical equivalent refractive error by age and gender ('2000s' data). Error bars represent standard error. Junghans et al. BMC Ophthalmology 2005 5:1   doi:10.1186/1471-2415-5-1

Lack of sharp image on retina Most kids are hyperopic, going into and out of focus. Many have uncorrected astigmatism. At age 4 2/3 have astigmatism. Borish Many have higher order aberrations. (20% of blur in average person.) Only a few of us have our visual pathways developed for maximal v.a. (Think Ted Williams) Remember Ted Williams the baseball player? Good baseball hitters generally have great visual acuities. How did they get them?

What if we could improve the visual pathway efficiency in the adult? What if we could increase the cell size and number of connections throughout the visual pathway in adults? What if we could reach into the brain and rewire it? Improve the connections and how the cells communicate with each other?

NV has been in Singapore improving the lives of people throughout the country. The military has gone through it as well as all children in school.

Scientific Basic Principles Enhance neuronal Lateral Interactions Neuronal Plasticity Perceptual Learning

Neuronal Network of Lateral Interactions Target excites cortical cells Area of lateral excitation provided by interaction of similar orientations Area of lateral inhibition (orientation of little relevance)

The Visual Cortex Cortical cells (neurons) are highly specialized and optimized image analyzers They respond only to a limited range of parameters (filters) of the visual image

The Visual Cortex (cont) Individual neurons respond to Precise location Specific orientation Specific spatial frequency Adapted from: Hubel & Wiesel (1959). Receptive fields of single neurons in the cat’s striate cortex. J Physiol (Lond) 148:574-591

The Visual Cortex (cont) To characterize an image, visual processing involves the cooperative activity of many neurons, these neuronal interactions are contributing both excitation and inhibition.

Neural Activity Determines CSF Contrast - activates neurons involved in vision processing Neural interactions determine the sensitivity for contrast at each spatial frequency The combinations of neural activities derive individual’s contrast sensitivity function

Neural Activity Determines CSF Responses of individual neurons to repeated presentations of the same stimulus are highly variable (noisy) CSF is limited by S/N ratio, as noise limits the detection and discrimination of visual signals by individual cortical neurons. The brain pools responses across many neurons to average out noisy activity of single cells, thus improving signal-to- noise ratio Patching gives targets with lots of noise. The images cannot optimally stimulate the neurons as in a controlled situation.

Gabor Patch “Gabor Patches” 1 are widely used in the field of visual neuroscience. Having been shown to efficiently describe the shape of receptive fields of neurons in the primary visual cortex they thus represent the most effective stimulation.2 Gabor (1946), Theory of Communication. Journal of the Institute of Electrical Engineers, London, 93, 429-457). Daugman. Two-dimensional spectral analysis of cortical receptive field profiles. Vision Res 1980; 20:847-56.

Precise Control of Variables Spatial Frequency Local Orientation Contrast Global Orientation Target-Flankers Separation Target Displacement

Excitation from outside the CRF Adapted from: Polat U., Mizobe, K., Kasamatsu, T., Norcia A.M. (1998). Collinear stimuli regulate visual responses depending on Cell's contrast threshold. Nature, 391, 580-584 Contrast response of a single neuron can be modulated by activity of neighboring neurons (single-unit recordings in cats and monkeys1) Chen, Kasamatsu, Polat, & Norcia, 2001; Kapadia, Ito, Gilbert, & Westheimer, 1995; Levitt & Lund, 1997; Mizobe, Polat, Pettet, & Kasamatsu, 2001; Polat, Mizobe, Pettet, Kasamatsu, & Norcia, 1998; Sillito, Grieve, Jones, Cudeiro, & Davis, 1995

Modulation of Contrast Response Contrast - activates neurons involved in vision processing Certain spatial arrangements of visual stimuli determine the balance of excitation and inhibition which control CSF (shown by psychophysics1 and visual-evoked potentials -VEP2) Contrast response of a single neuron can be modulated by activity of neighboring neurons (single-unit recordings in cats and monkeys3) Bonneh & Sagi, 1998; Chen & Tyler, 1999; Polat, 1999; Polat & Sagi, 1993; Polat & Sagi, 1994a; Polat & Sagi, 1994b; Polat & Tyler, 1999 Polat & Norcia, 1996 Chen, Kasamatsu, Polat, & Norcia, 2001; Kapadia, Ito, Gilbert, & Westheimer, 1995; Levitt & Lund, 1997; Mizobe, Polat, Pettet, & Kasamatsu, 2001; Polat, Mizobe, Pettet, Kasamatsu, & Norcia, 1998; Sillito, Grieve, Jones, Cudeiro, & Davis, 1995

Neural Plasticity Neural plasticity - relates to the ability of the nervous system to adapt to changed conditions, in acquiring new skills. The new required skills are retained for years Evidence for Neural plasticity - Visual acuity improvement in adults with amblyopia has been reported after prolonged patching1 or when the better eye’s vision has been lost2 or degraded, by age related macular degeneration3, cataract4 or trauma5 Birnbaum MH, Koslowe K, Sanet R. (1977) Vereecken EP, Brabant P. (1984) El Mallah MK, Chakravarthy U, Hart PM. (2000) Wilson ME. (1992) Rabin J. (1984)

Perceptual Learning & Neural Plasticity The phenomenon - Perception can be modified by experience. Visual performance improves with practice The technique - Repetitive performance of controlled and specific visual tasks Perceptual learning has been evidenced in a variety of visual tasks and was found to persist for years without further practice1 Clinical observations2 and experimental evidence3 indicate the presence of residual neural plasticity well after the critical period. I was talking to a neurophysiologist that teaches this at SCCO. He called it learning as if it was something bad. Whatever you want to call it, it works! Repetitive performance of specific visual tasks efficiently stimulates the specific neurons and effectively promotes spatial interactions among these neurons Enhanced spatial interactions reduce noise level in neuronal activity and increase signal strength, therefore improve neuronal efficiency inducing improvement of Contrast Sensitivity Function (CSF) Improved CSF induce improvement in Visual Acuity Gilbert, 1998; Sagi & Tanne, 1994). Moseley, Fielder (2001) Polat, Sagi(1994); Levi, Polat (1996); Levi, Polat, Hu (1997)

Lateral Masking – NVC Fundamental Technique This stimulation-control technique is called “Lateral Masking”, where collinearly-oriented flanking gabors are displayed in addition to the target gabor image, in a specific controlled manner Neuro scientists demonstrated that the contrast sensitivity function of adult subjects can be increased significantly through precise control of stimulus parameters

Few of us have maximally developed visual pathways. Summary Image quality depends both on the sharpness of the image on the retinal and the processing in the visual part in the brain (visual cortex) The visual system in the brain has mechanisms for further ‘enhancing’ the visual processing (lateral interactions) Amblyopia treatments enhance the under- developed neural processing to better process the clear image coming from the retina Few of us have maximally developed visual pathways. Neural Plasticity Relates to the ability of the nervous system to adapt to changed conditions, in acquiring new skills. The new required skills are retained for years Clinical observations and experimental evidence indicate the presence of residual neural plasticity Personalized Treatment In order to achieve optimal results, the treatment is specifically tailored to patients’ deficiencies / inefficiencies and visual abilities Treatment sequence is unique to each patient

What are the NeuroVision Treatments? The patient is examined and best prescription is determined. Baseline data is gathered on uncorrected v.a.s and best corrected v.a.s Baseline data on Contrast Sensitivity Function is obtained with uncorrected v.a.s and best corrected v.a.s Baseline data is entered into the NeuroVision system over the internet for the patient. This allows NeuroVision to determine at what level to begin the treatments.

FACT CSF chart and ETDRS Acuity chart

Treatment sessions The patient is seated at a computer 5 feet away. Each session lasts 25 to 30 minutes and is composed of 10 – 12 sections. During each session only one orientation of target is shown.

Treatment session The patient is asked to make a forced choice between flashes of targets. Which one had the target (limits on spatial frequency threshold) Which target was brighter (contrast differential) Which one was aligned higher or lower (vernier acuity)

Treatment Targets Spatial Frequency Local Orientation Contrast Global Orientation Target-Flankers Separation Target Displacement

Treatment sessions 1 treatment a day 2 to 7 treatments per week. 15 treatments give 85% of the gain 20 to 30 treatments total

Patient Management Treatment Set-Up Administration Customization Baseline Test by optometrist Computerized analysis of neural inefficiencies Administration Controlled home/clinic environment Sessions of 25-30 minutes each 20 to 30 Sessions (depending on the patient) Once a day or as few as two sessions per week Customization Treatment Progress Results automatically sent to Data Center Individualized sessions adjust to progress Interim tests by technician Each session directly treats neural inefficiencies Treatment end – When patient’s vision does not further improve

Results of Clinicals in US Amblyopia Low myopia Presbyopia

Visual Acuity Improvement in FDA Amblyopia Study – 2000 -0.1 0.1 0.8 0.7 0.6 0.5 0.4 0.3 0.2 0.0 LogMar 6/36 6/30 6/24 6/18 6/15 6/12 6/9 6/4.5 6/7.5 6/6 Snellen Equiv Individual VA Improvement – 44 Patients Completed

Stability of VA Improvement in FDA Amblyopia Study - 2000 6/18 6/15 6/12 6/9 6/4.5 6/7.5 6/6

Contrast Sensitivity Improvement in FDA Amblyopia Study - 2000 Before treatment At end of treatment 12 months post treatment

Binocular Functions (Worth-4dot) in FDA Amblyopia Study - 2000

NeuroVision On Going Trial Low Myopia and Presbyopia Dan Durrie, MD Peter Shaw McMinn, OD 15 Presbyopia Treatment Group Low Myopia Treatment Group 7 8 Presbyopia Control Group Low Myopia Control Group 45 Total Number of Subjects I have been interested in this since I graduated and when NeuroVision interviewed Ods to do their study I jumped at it. 50% of the Treated Patients are Doing the Treatment at Home and 50% in the Clinic The Control Patients are Only Doing Visual Exams without NeuroVision Treatment

NeuroVision On Going Trial Interim Results (As per October 1, 2007) US Trials (Updated on Oct 1, 2007) International Data Presbyopia Improvement in Unaided Near VA 2.2 Lines (22 Patients) 2.0 Lines Low Myopia Improvement in Unaided Distance VA (15 Patients) 2.6 Lines Controls 0.4 Lines (10 Patients) The Interim Results in the US Trials are Consistent with the International Results

NeuroVision On Going Trial Interim Results (As per October 1, 2007) Presbyopia Spatial Frequency UCVA=20/28 UCVA=20/54 UCVA=20/30 UCVA=20/36 UCVA=20/60 Low Myopia Spatial Frequency UCVA=20/25 UCVA=20/44 UCVA=20/30 UCVA=20/52 The Interim Results in the US Trials are Consistent with the International Results

Clinical Visual Acuity Improvement Contrast Sensitivity Improvement Retention of Improvement 1 Year Post Treatment Main Functional Outcome Myopia Up to -1.50D 2.7 Lines ETDRS (Distance) Above 100% in All Frequencies 90% of the Improvement Decrease Dependency on Spectacles Presbyopia Up to +1.5D 2.0 Lines ETDRS (Near) Average Of 100% in No Data Available Yet Delay The Need of Reading Glasses Post Refractive Surgery 2.3 Lines ETDRS (Distance) Increased Quality of Functional Vision Amblyopia 2.5 Lines ETDRS Quality of Vision, Improved Binocularity

Implications for our patients Amblyopes Low myopes, hyperopes, astigmats Early presbyopes Pathology patients Post LASIK Learning disabilities Individuals who require or desire excellent visual acuity

Product Line Existing Future Presbyopia (Up to Add +1.5D) Low Myopia (Up to -1.5DS + -0.75DC) Pediatric Myopia Post Refractive Surgery Adult Amblyopia (“Lazy Eye”) Future Super Vision—Sports Vision, Military, etc. IOL Enhancement Contact Lens Enhancement Early AMD Enhancement

attractive for all eye care market segments Optometry New Non-surgical Vision Improvement Treatment No Medical Degree Required to be Administered— An Optometric Alternative to LASIK Specs & Contact Lenses Do Not Always Provide Sharp Vision Presbyopia Treatment - Premium Revenue Generator People Do Not Invest Much in Reading Glasses Low Myopia Treatment will Generate Additional New Business

attractive for all eye care market segments (cont’d.) Optometry (cont) Can be Performed in Practice or at Home Home Option Minimizes Management Overhead Minimal “Chair Time” – Optometrist Needed Only for Baseline Examination. Other Examinations by Technician

For more information: www.neuro-vision.com

Solve Your Patient’s Acuity Problems by Prescribing NeuroVision Technology! Thank You for Attending the class! Peter Shaw-McMinn, O.D. shawmc@cox.net

Contrast Sensitivity

The luminance of peaks and troughs remains constant along a given horizontal path through the image. Therefore, if the detection of contrast is dictated solely by image contrast, the alternating bright and dark bars should appear to have equal height everywhere in the image. However, the bars appear taller in the middle of the image than at the sides. This inverted-U shaped envelope of visibility is your contrast sensitivity function. The exact location of the peak depends on the viewing distance. Try moving farther away from the display, and back closer. Note that the apparent position of the peak shifts as you do this. Therefore, the inverted-U shaped envelope is not in the image, but reflects the property of your visual system. UCB

Contrast sensitivity is a measure of the limit of visibility for low contrast patterns -- how faded or washed out can images be before they become indistinguishable from a uniform field? (Think of driving in a fog). It is a function of the size (coarse/fineness) of image features, or the spatial frequency.