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Night Vision: Current Research and Future Directions, Symposium Proceedings (1987)
Commission on Behavioral and Social Sciences and Education (CBASSE)

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PHOTORECEPTOR PROPERTIES

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INTRODUCTION Eliot L. Berson Night blindness disorders represent a significant cause of visual loss to people all over the world. The incidence of these conditions, sometimes grouped under the heading of retinitis pigmentosa, has been estimated to be 1 in 3,500 births in the United States. Affected pa- tients can be asymptomatic and have normal visual acuity and yet have considerable compromise in visual function due to abnormalities in dark adaptation and loss of midperipheral visual field. These patients can perform visual tasks under bright daylight conditions but fall to per- form the same task under starlight or moonlight conditions and, in some cases, under dim daylight conditions as well. This variability in per- formance, depending on the conditions of illumination, poses hazards to those affected as well as to those with whom they work. Some can have 20/20 vision but are legally blind due to the profound loss of their peripheral visual field with consequent "tunnel vision." Most of these disorders occur as a consequence of malfunction and loss of rod and cone photoreceptors. Considerable progress has been made in our understanding of normal photoreceptor function, and this has provided us with a framework for understanding the pathophysiology of different types of retinal dis- eases associated with night blindness. Sensitive tests of retinal function have made it possible to diagnose these conditions in their earliest stages, sometimes many years before the patient is symptomatic or changes can be seen on routine ocular examination. Two rare heredi- tary diseases associated with night blindness and retinitis pigmentosa are treatable if detected in the early stages. Electrooptical techno1- ogy has resulted in development of the night vision pocketscope that can be used to alleviate the symptom of night blindness. The papers in this section provide examples of the wide range of approaches that are being used to understand normal and abnormal pho- -toreceptor function. These include psychophysics, electrophysiology, biochemistry, electron microscopy, and molecular genetics. Current knowledge of the mechanism of visual excitation is reviewed, as is our understanding of how conditions of illumination affect visual function. The disorders themselves are considered in the context of early diagno- sis and some aspects of pathogenesis and management. It is hoped that these papers will encourage the continued examination of methods for assessing these patients and further research on causes and possible treatments. 25

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PHOTOTRANSDUCTION AND DARE NOT SE IN l ROD PHOTORECEPTORS David R. Copenhagen and Tom Reuter A study of night vision necessarily confines itself to an examina- tion of seeing mediated by rods and the rod visual pathways. In the rod system, high spatial and temporal resolution and color vision are sacrificed for an extremely high sensitivity to very dim lights. Under optimal conditions, fewer than 100 photons striking the eye are suffi- cient for rod-mediated vision. In equivalent terms, the dimmest detec- table visual stimulus corresponds to the light from a candle placed some 17 miles away. Certainly, there are mechanisms to enhance visual sensitivity as the signals travel along the rod pathways to cortical centers in the brain. However, the rod photoreceptors themselves are responsible for much of the high sensitivity of rod-mediated vision. The conversion of each photon absorption by a rod into an electrical signal is a high-gain biochemical process. This paper discusses cur- rent hypotheses related to how the rod photoreceptors transduce light into electrical energy and how they achieve their high sensitivity. One must keep in mind, however, that high gain alone does not guarantee optimum detection of a dim light. Seeing dim objects also involves an optimization of the signals with respect to the noise. This paper also addresses the origin of biological noise sources in the retina that limit night vision. TRANSDUCTION OF LIGHT IN THE RODS Structure of a Typical Rod The rods of vertebrates are cylindrical in shape and are perhaps the most structurally specialized class of neurons in the nervous system. See Figure 1 for a schematic drawing of a typical rod photo- receptor. In-depth reviews of rod transduction have recently been published (Korenbrot, 1985; Schwartz, 1985; Stryer, 1986~. The outer segments of the rods are embedded in the retinal pigment epithelium at the most distal margin of the retina. These outer segments function as the sole lock s for transduction. The inner segments of the rods are connected via a ciliary bridge to the outer segments. The inner segment of the rod contains m itochondr ia, Golgi apparatus, rough endoplasmic reticulum and, in many poikilotherms including reptiles and amphibians, 26

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27 Retinal Pigment Epithelium - Outer Segment Inner Segment Rh G . PDE t~ ~ . - Light ~ ~ GMP chat / \ . ,. . ) cGMP ~ ~ I 4 Dark Current NatI,/ ¢~ C>,/ Synaptic / O 1° Tern~inal ~ Oo fig _ Horizontal Cells K+ Bipolar Cells FIGURE 1 Schematic diagram of rod and mechanisms under ying the light responses. Abbreviations: Rh, rhodopsin; PLE, phosphodiesterase; GAP, guanosine monophosphate; cGhiP, cycl ic GAP .

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28 a store of glycogen. The inner segment is the site of cellular metabo- lism and protein synthesis. The synaptic terminal, at the proximal end of the inner segment, is the site specialized for communication with the second-order cells. Here, synaptic transmitter molecules are pack- aged within vesicles and secreted into the thin cleft separating the rods from the horizontal and bipolar cells, the neurons immediately postsynaptic to the rods. The outer segment consists of a plasma membrane which forms an envelope around a stack of pancake-like disks. These disks float inside the outer segment and are structurally and electrically iso- lated from the plasma membrane. They do appear to be tethered by slender strands that reach from the edges of the disks to the inside wall of the plasma membrane (Roof et al., 19821. The membrane of each disk, which is probably more correctly visualized as a flattened bal- loon, contains the photopigment rhodopsin. The absorption of incident photons by rhodopsin is the initial step in transduction. A total of 10 -10 of these protein molecules (240,000 molecular weight) are em- bedded in the membranes of the ~103 stacked disks. The wavelength at which rhodopsin exhibits its peak absorption ranges from 500 to 525 nm, depending on the species--this peak wavelength confers on the rod system an optimal sensitivity to lights in the green section of the visible spectrum. New disks are generated continuously at the base of the outer seg- ment, while the older disks are shed continuously from the tip of the outer segment where they are broken down by macrophagic and lysosomal degradation In the pigmented epithelium. Disk shedding f rom rods ap- pears to be circadian, with a peak of activity at the onset of morning light. A typical disk has a lifetime of about 10 days. Electron microscopic studies of disk membranes reveal 60-~-diameter bumps on the intradisk surface at densities of 30,000/pm2. These bumps correspond to the rhodopsin molecules. Examination of the extradisk side of the disk membrane shows large particles projecting above the surface and randomly distributed with a density of 2,000/m. These particles are believed to be the G protein, which is activated by bleached rhodopsin and is involved in the regulation of phosphocies- terase (PDE) (see below). Electrical Properties of the Rod in Darkness and in Light The generation of the electrical signal in the rods results from closure of specific ion channels located within the plasma membrane envelope of the rod's outer segment. Before covering the specific hypothesis linking the absorption of rhodopsin to the closure of these channels, it would be good to review the quiescent properties of the dark-adapted rod. In darkness, the rod is principally permeable to Na+ and K+ ions and moderately permeable to C1 and Cam. The trans- membrane potential in the dark is typically about -40 mV. The K and C1- permeability is conf ined primarily to the inner segment, while the flat permeabili ty is loca ~ ized to channels in the plasma membrane of the outer segment. Calcium ions can flow through channels in the inner and

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29 outer segments. Due to the spatial separation of these selectively permeable ionic channels, a net positive current flows extracellularly along the outside of the rod from the inner segment to the outer seg- ment, enters the rod through the Na+-selective (and probably C1 - and Ca+~-selective) channels of the outer segment, and returns to the inner segment through the ciliary bridge. This ionic current is termed the dark current. The ionic gradients across the rod membrane that serve as batteries for the ion flow are maintained by an ouabain-sensitive, ATP-dependent Na+/K+ exchange pump in the inner segment membrane. This pump clears Na+ from the intracellular cytosol and pumps Kay into the interior of the rod from the extracellular space. The magnitude of the dark current is species dependent and ranges between 10 x ~o~12 and 70 x 10 12 A. Monkey rods have dark currents of 12 pA (Baylor et al., 1984), while tiger salamander rods exhibit dark currents of 55 pA; The Na+ influx into the outer segment during darkness is about 10 Na ions/rod/s in toad and frog rods. On the assumption that each of these Na+ channels has a conductance of about 60 x 10-15 Q. that the membrane potential is -40 mV, and that the reversal potential for Nat ions is 0 my, this would indicate that the 20-pA dark current is conducted through about 5 x 103 open ionic channels in the plasma membrane of the outer segment. The absorption of an individual photon by a single rhocopsin mole- cule causes an isomerization of the rhodopsin molecule from a cis to a bans configuration. This single isomerization in a rod's outer seg- ment initiates ~ cascade of events that results in the closure of 2-4 percent of the channels conducting the dark current (Baylor et al., 1979b). In toad rods, the single photon signal represents the cessa- tion of 1 pA of the dark current or about 4 percent of the total. This single-photon response corresponds to the cessation of 106 to 107 Na+ ions/e resulting from the simultaneous closing of about 200 ionic c hannel s . B iochemical L ink between Photon Absorption and Channel Closings Given the ultrastructural picture of the rod and the need to explain the amplif ication f rom the single-photon absorption to the closure of 200 channels, two requirements for transduction are evident: ( 1) there must be one or more processes which amplify the effects of a single pho- toninitiated rhodopsin isomerization. The transformation of a single molecule cannot easily explain how 200 spatially separate channels can be modulated; and (2) there must be an internal, diffusible transmitter linking the photon absorption by rhodopsin on the disk membrane with the closing of channels in the electrically isolated plasma membrane. Intense research into the mechanisms mediating the generation of the electrical signal has been going on for the last 20 or more years. Originally, Ca++ was hypothesized as the internal transmitter (Yoshikami and Hagins, 1973~. Stores of Ca++ believed to be seques- tered within disks, were thought to be released on ~somerization of the rhodopsin. Many hundreds or thousands of Ca++ ions were thought to diffuse into the plasma membrane and subsequently block the ionic

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30 channels carrying the dark current. Recent experiments with C a++ buf- fers injected into outer segments (Matthews et al., 1985) and a lack of correspondence between Ca++ fluxes and the time course of the electri- cal response seriously undermine the validity of the Ca++ hypothesis (Gold, 1985~. Recent evidence indicates that the monophosphonucleotide cyclic guanosine monophosphate (cGMP) may be the internal transmitter. On this idea, cGMP levels are believed to be relatively high inside the outer segment in the dark. The presence or binding of cGMP to the cytosolic surface of the ionic channels of the plasma membrane is believed to hold these channels open to current flow. On photoiso- merization, the bleached rhodopsin is thought to activate a G protein Lasso called transducing, which in turn activates PDE molecules. The activation of PDE hydrolyzes cGMP to GMP, thereby reducing the intra- cellular concentrations of cGMP. This decrease causes the ionic chan- nels to close and thus suppress some of the dark current. Several recent results support this hypothesis. These include the demonstra- tion that cGMP can act on conductances in the plasma membrane (Fesenko, 1985; Nakatani and Yau, 1985), that cam injected into the outer seg- ment increases the dark current, and that the injection of PDE evokes a change in the rod's dark current (and membrane potential) which mimics light. Thus, cGMP is a satisfactory candidate for an internal trans- mitter. The amplification afforded by this process can be seen in an exam- ination of the number of intermediate molecules activated by each step. Under optimum conditions rhodopsin can activate 104 G prote~ns/s. One G protein can, in turn, under optimum conditions, activate 500 PDE mole- cules/s. The details of the reactions w' thin the cells themselves are still unclear, but it is known that in rods, one photoactivated rhodop- sin molecule can destroy 105 cGM~ molecules/s. Once the channels are closed by the reduction of cGMP, the cessa- tion of dark current causes the transmembrane potential to become more negative thyperpolarize). This hyperpolarization modulates the release of synaptic transmitter molecules from the synaptic terminal. This change in transmitter release signals the photon absorption to the second-order neurons in the rod pathways. These changes are relayed by similar modulatory schemes from neuron to neuron up to the higher vis- ual centers. SIGNAL DETECTION AND DARK NOISE IN THE UTICA As discussed above, a reasonable hypothesis exists for the trans- duction mechanism. Further studies are required for validation. Ir- respective of which mechanisms may be proven to underlie transduction, however, there are many additional aspects of visual processing that one must consider to understand the limits of night vision. The high- gain mechanisms of the rod are not sufficient by themselves to ensure that a photon or a group of photons get "seen." To illustrate this point, one car, visualize the problem of trying to listen to one con- ~-ersation across a crowded rood f illed with many other conversations.

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31 Being able to increase the gain on a microphone (unless it is a airec- tional one) will amplify the conversation of interest and all the other conversations which for these purposes could be considered noise. So detection of a selected conversation or a dim light is a signal-to-noise task, whereby a signal of potential interest must be extracted from on- going noise. In the following sections, noise sources that limit detec- tion of dim lights by the retina are discussed. At the levels of light used for night vision, there appear to be two main noise sources that limit detection: (1) random fluctuations in the stimulus itself, and (2) biological noise in the retina. Photon Noise Light, being composed of independent photons, is random in nature and therefore inherently noisy. If one considers a brief flash of light, the randomness of the photon fluxes is evident. For a series of identical flashes, there will be a mean number of photons per flash (m). In any one flash there may be fewer or more photons than the mean. The statistical variation of the photon actually delivered per flash follows a Poisson distribution in which the probability of obtaining photons is related to the mean by: P(x = n, = beam mn'/n, Where P (x = n) is the probability that each flash will contain exactl y n photons, g iven that the mean number is m. I t can be shown that the variance of the number of flashes is equal to the mean for such a dis- tribution and the standard deviation (~) is equal to the square root of the mean. For dim lights delivering an average of 1,000 photons per flash to the rods of the eye, the standard deviation of the photon count is 31. 6. For a much dimmer light delivering 10 photons, the standard deviation is 3.16 photons. This points out an important limitation in vision. Namely, the variance/mean ratio increases for dimmer lights. For very dim lights there is a large percentage of uncertainty as to how many photons are delivered per flash. For brighter lights, e.s., where 104 photons are incident on the cornea, the ratio of the standard deviation or variance to the mean is much less. Hence, the photon noise is less prevalent. Hecht et al. (1942), in their classical experiments measuring the absolute dark-adapted sensitivity of human vision, found close agreement between the randomness of seeing, as would be predicted by photon noise, and the estimated number of photons reaching the roast Their results implicitly assumed that vision at absolute threshold was limited strict- ly by photon noise. Barlow ( 1956) disputed the photon noise assumption and postulated that a second sou rce of noise imposed severe limitations on the relia- bility with which very dim 'ights could be detected. Barlow's (1956) assertion rested on results of some of his own experiments and a recal- culation of the number of photons that actually struck the retina in

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32 experiments similar to those of Hecht et al. (1942~. Barlow called this second noise source dark light and likened it to spontaneous photon-like events in the dark. That is, on a random basis the retina would wrongly register the arrival of a photon. The task of detecting an actual dim light was complicated by these spontaneous dark events. In an attempt to substantiate or rule out the Barlow (1956) hypothe- sis that these dark events limited detection in the retina, an endeavor was made to record threshold responses from ganglion cells in the retina of a rod-dominated animal and test whether the detection of dim lights was indeed influenced or limited by dark events. Recording was done extracellularly from ganglion cells in the retina of Bufo marines. The retinas of these animals can be maintained for several hours in an open eyecup preparation under an atmosphere of pure, moistened O2. This pre- paration offers several advantages. Since the anterior portion of the eye can be dissected away, light calibration is made easier. Further- more, intracellular recordings can be made of the light responses in the rods and other cells distal to the ganglion cells. Figure 2 shows typical data from ~ ganglion cell in Bufo marinus retina. Very dim flashes were presented multiple times at intensities below, at, or above those which elicited an action potential, the a) c o Q ~ 0.8 c: = o ._ ct - - ._ ce Q 1 .0 0.6- 0.4- 0.2 __-~' ~ .... X_ · / . /X . f.' :~. X - ~I I ~ -oo 0.5 1.0 1.5 Log Intensity FIGURE 2 Frequency of response functions for a ganglion cell. Abscissa plots the log (mean) flash intensity where 1. a = lo flash-indu~ed ~so- merizations within the recpetive field. The ordinate shows the fraction of flashes elicting an action potential in the ganglion cell with 2 s following the flash. Ten flashes (at interstimulus intervals of 30 s) were resented at each intensity. The dotted and solid continuous curves plot, as a function of mean intensity, the probability that the number of events, X, exceed a criterion value, c. The steeper dotted curve, the abscissa values denote flash-induced isomerizations. The flatter curves assume that the number of events is comprised of photon-elicited events plus dark events. The solid curve is plotted assuming that the rate of dark events was 0.06/rod and s. The shallowest dotted curve shows the curve assuming there were 0.24 dark events/rod and s.

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33 threshold response, in the ganglion cell. The ordinate plots the per- centage of flashes causing a response at each respective intensity. The steeper dotted line plots the predicted frequency of response func- tion on the assumption that the threshold responses were responding only to the photons in the light stimulus. This curve is a cumulative Poisson distribution (Barlow, 1964~. The actual data points fell along a shallower curve. Following the example of Barlow (1964), it was assumed that there is a continuous rate of ongoing photon-like events indistinguishable from the photon events. By altering the presumed rate of these events, the best curve was fitted to the data. For Figure 2, the best fit was obtained for a dark rate equivalent to 0.05 dark events/rod and s. These data and the results from other cells indicate that threshold detection is not limited strictly by photon noise and that a second source of noise exists which can be attributed to spontaneous dark events in the rods. If there were dark events in the rods, one might expect to find evidence in horizontal cells for fluctuations caused by these dark events. Figure 3 shows intracellular recordings from a horizontal cell in Bufo marines retina. The membrane potential is seen to fluctuate in darkness, and the magnitude of the fluctuations is increased by the background light which produces 0.58 photoisomerizations/rod and s. Figure 3B is a power spectral density curve calculated by a fast Fourier transform (FFT) method. This shows the power inherent in the fluctuations as a function of frequency. Both the background and dark curves display a prominent low-frequency component (<1 Hz). A differ- ence spectrum (background-dark) is shown in Figure 3C. This difference spectrum shows the power added by the background light. Also shown ~ pluses) is the power spectral density of very dim flash responses in the same celle The overlap of the difference spectrum and the flash spectrum strongly suggest that the background fluctuations are com- prised of many single-photon events which sum linearly together. Having established the likelihood that the background fluctuations originated with photon events, the key question then becomes whether the fluctuations in the dark originate with the photon-like dark events. Since the low-frequency components of both power spectral density curves overlap with a vertical scaling (Figure 3B), it is reasonable to assume that the dark fluctuations are caused by photon-like events occurring at a frequency substantially less than the 0.58 photoisomerizations/rod and s evoked by the background light. A comparison of the total vari- ance (area under the curve) of the low-f requency components indicates that the dark fluctuations would result from a spontaneous dark rate of 0.02 photoisomerization-like events rod and s. This rate of dark events compares favorably with the rate deduced from the frequency of response curves obtained from the ganglion cells. Within the last several years, the technology of recording currents flowing into and out of individual neurons has evolved. Baylor and colleagues, by using suction-type microelectrodes, recorded the dark currents of individual rods (Baylor et al., 1979a, 1979b, 1984~. They found a stereotyped response to light flashes that elicited single pho- toisomerizations. When the rods were kept in absolute darkness for per- iods of several minutes, spontaneous photon-like responses were observed

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- 5 70 , w mu - w u, - lo . TESt - `~, as BAt!GROUBO : 491 .R DURATION ~ 200 RSEt DItAY: 400 RSEt ~ Be A/ - 1 ~1 i f . ~1 1 1 1 I I -A S -` -I -2 -1 0 IOC BAt`GROUBD INlENSlT' IRE: 1.0 ERC/SEC'DECREE SQUARED) ~ Off it. FIGURE 9 Threshold just before and just after extinction of a back- ground field. The difference between the two is attributed to noise under steady illumination. Source: Krauskopf and Reeves (1984~. SOME PRACTICAL CONSIDERATIONS Limits of Sensitivity Whatever the reason, the human visual system falls short of sev- eral ideals. This leaves room for enhancement of visual performance through various aids. Telescopes and microscopes are classic examples. Knowing how the eye compares with various instruments intended to do similar tasks may help to determine the best combination of eye and instrument, and knowing the specific ways in which human performance deviates from an ideal may help to design aids that will bring the entire system closer to the ideal. It was argued above that even when the eye is at its best, it adds noise to that which inevitably accost panics the signal, and that in a variety of tasks human observers do about 10 times worse than an ideal quantum detector. This suggests that the signal-to-noise ratio can be increased by amplifying the stim- ulus, noise and all, for it would reduce the relative contribution of the noi se that is intr insic to the visual system. This is no secret to those who have worked with image intensif iers. According to the

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71 measurements of van Meeteren (1978), improvements of quantum eff ciency by image intensifiers are typically 100 to 1. Binocular Vision Same military applications require monocular viewing, as in sighting through optical devices and heads-up displays. Evidence presented above suggests that vision is likely to be best if light adaptation of the nonviewing eye is maintained. Transient Visual Adaptation The brief period of reduced sensitivity lasting about a second following large changes of illumination, referred to as transient visual adaptation and sometimes as neural adaptation, is of con- siderable practical importance. Therefore, it has been treated extensively in the illumination engineering literature (cf. Kaufman and Christensen, 1972) and so needs no further treatment here. Screening Procedures Human Factors and Testing Some of the issues relating to screening for night vision are not specific to vision and can be handled by specialists in testing or human factors or by reference to data in the literature on human factors, such as the text by Bailey (1982) or the reference works of Van Cott and Kinkade (1972) or Woodson (1981~. Duplicity A long-standing dogma of visual science is that the rod and cone systems form not one but two largely independent visual systems, each specialized to function under different conditions, but sharing the same retina and visual pathway. As the specialized functions of the cone system demand a high density of receptors, the small part of the retina const ituting the fovea is 9 iven over entirely to the cone sys- tem, and a ref ined eye movement mechanism has evolved the capability to bring this part of the retina to coincide with interesting parts of the retinal image. However, the proportion of the retina numer ically dominated by cones is exaggerated by our subjective experience and actually occupies less than 0.02 percent of the retina. As the two systems are specialized to operate under different levels of illumina- tion, one system tends to lie dormant while the other system is doing the work of vision, and so perhaps to save resources, both use the same pathway to the brain and the same neural machinery to process the information that their separate receptor systems gather. As the same

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72 optic nerve fibers carry the information for both systems, except in the fovea, the signals from the two systems are bound to interact under some circumstances, yet under most conditions the systems operate with astonishing independence. Several practical implications follow. Insofar as the systems have different functions, and to the extent that they compete for space and access to the brain, testing one will tell little about the other, and performance that depends more on one system could even vary inversely with that which depends more on the other system. Other fac- tors, such as optical quality of the eye, affect one system more than the other, and so would tend to make performance that depends more on one system somewhat independent of performance that depends more on the other systems Conversely, insofar as the same central mechanisms are used by both systems, measures that depend primarily on central processing are likely to correlate well with one another. My own impression is that cone sensitivity, as reflected by the level of the cone plateau of dark adaptation curves, is more variable than rod sensitivity, as reflected by the dark-adapted absolute threshold. Equivalent Backgrounds One of the significant findings about light and dark adaptation is that the state of the visual system under an enormous range of condi- tions can be characterized by a single parameter referred to as the equivalent background (Crawford, 19471. Hence, to measure an indi- vidual's adaptive state, there is seldom a need to test with more than one kind of test probe. Crawford successfully generalized his finding from the simple geometric shapes of the laboratory to natural objects, such as a zeppelin over Hamburg, a small boat in a harbor, and a dis- tant house on the horizon. SUMMARY Through a consideration of human performance at the absolute threshold for detecting light, I have tried to illustrate the value of comparing human performance with ideal systems and to stress the limits on vision attributable to noise. I have pointed to the many different sites at which adaptation to changing illumination occurs and estimated the magnitude of each under different illumination. Finally, I have discussed ways of reducing the limits that intrinsic noise places on visual performance and the implications that the mechanisms of visual adaptation might have for night vision screening procedures.

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73 REFERENCES Adelson, E.H. 1977 Transient rod saturation with moderate stepped backgrounds. Investigative Ophthalmology and Visual Science 16(Suppl.~:28. 1982 Saturation and adaptation in the rod system. Vision Research 22:1299-1312. Aguilar, M., and W.S. Stiles 1954 Saturation of the rod mechanism of the retina at high levels of stimulation. Optica Acta 1:59-65. Ahumada, Jr., A.J.A., and A.B. Watson 1985 Equivalent-noise model for contrast detection and discrimination. Journal of the Optical Society of America A 2:1133-1139. Auerbach, E., and N.S. Peachey 1984 Interocular transfer and dark adaptation to long-wave test lights. Vision Research 24:1043-1048. Bailey, R.W. 1982 Human Performance Engineering: A Guide for System Designers. Englewood Cliffs, N.J.: Prentice-Hall. Barlow, H.B. 1956 Retinal noise and absolute threshold. Journal of the Optical Society of America 46:634-639. 1962 A method for determining the over-all quantum efficiency of visual discriminations. Journal of Physiology 141:337-350. 1977 Retinal and central factors in human vision limited by noise. Pp. 337-358 in H.B. Barlow and P. Fatt, eds., Vertebrate Photoreception. New York: Academic Press. Barlow, H.B., and J.M.B. Sparrock 1964 The role of afterimages in dark adaptation. Science 144:1309-1314. Baylor, D.A., B.J. Nunn, and J.L. Schnapf 1984 The photocurrent, noise and spectral sensitivity of rods of the monkey Macaca fascicularis. Journal of Physiology 357:575-607. Crawford, B.H. 1947 visual adaptation in relation to br ief conditioning stimuli . Proceedings of the Royal Society (London) B134 :283-302. Denton, E.J., and M.H. Pirenne 1954 The absolute sensitivity and functional stability of the human eye. Journal of Physiology 123: 417-442. de Vries, H. 1943 The quantum character of light and its bear ing upon threshola of vision, the differential sensitivity ana visual acuity of the eye. Physica 10: 553-564 . Geisler, W.S. 1984 Physical limits of acuity and hype racu ity. Journal of the Optical Society of America A 1: 775-782 . Geisler, W.S., and K.D. Davila 1985 Ideal d iscriminators in spatial vis~on: Tw~ point stimuli. Journal of the Optical Society of America A 2 :1483-1497.

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74 Geisler, W.S., and D.B. Hamilton 1986 Sampling-theory analysis of spatial vision. Journal of the Optical Society of America A 3 :62-70. Hallett, P .E . 1969 Quantum eff iciency and false positive rate. Journal of Physiology 202: 4 21-43 6 . Hecht, S., S. Shlaer, and M.H. Pirenne 1942 Energy, quanta, and vision. Journal of General Physiology 25: 819-840. Kaufman, J .E ., and J .F . Chr istensen, eds. 1972 IES Lighting Handbook, 5th ed. New York: Illuminating Engineer ing Society. Kelly, D.H. 1972 Flicker. Pp. 273-302 in D. Jameson and L.M. Hurvich, eds., Handbook of Sensory Physiology: Visual Psychophysics. New York: Springer. Krauskopf, J., and A. Reeves 1980 Measurement of the effect of photon noise on detection. Vision Research 20 :193-196. . . MacLeod, D.I .A., D.R. Williams, and W. Makous 1985 Difference frequency gratings above the resolution limit. Investigative Ophthalmology and Visual Science 26(Suppl.) :11. Makou s, W., D . Telle r , and R. Boothe 1976 E3 inocular interaction in the dark. Vision Research 16 :473-476. Makous, W., D.R. Williams, and D.I.A. MacLeod 1985 Nonlinear transformation in human vision. Annual Meeting, Optical Society of Amer~ca, Digest of Technical Papers 2 :90. Nachmia s, J . 1972 Signal detection theory and its application to problems in vision. Pp. 56-77 in D. Jameson and L.M. Hurvich, eds., Handbook of Sensory Physiology: Visual Psychophysics. New Yor k: Spr inge r . Pell i, D .G . 1985 Uncertainty explains many aspects of visual contrast detec- tion and discr imination. Journal of the Optical Society A 2: 1508-1532. Peterson, W.W., T.G. Birdsall, and W.C. Fox 1954 Theory of signal detectability. IRE Transactions on Infor- mation Theory PGIT-4 :171-212. Pirenne, M.H., and F.H.C. Marriott 1959 The quantum theory of light and the psychophysiology of vision. Pp. 288-3 61 in S . Koch, ea., Psychology : A Study of a Science. New York: McGraw-Hill. - Pulos, E., and W. Makous 1982 Changes of visual sensitivity caused by on- and off transients. Vision Research 22 :879-887. Rose, A. 1948 The sensitivity performance c~f the human eye on an abso'ute scale. Journal of the Optical Society of America 38 :196-208.

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75 Rushton, W.A.H. 1963 1965 Increment threshold and dark adaptation. Journal of the Optical Society of America 53:104-109. The sensitivity of rods under illumination. Journal of Physiology 178:141-160. Sakitt, B. 1971 Configuration dependence of scotopic spatial summation. Journal of Physiology 216:513-529. 1972 Counting every quantum. .~, anal of Phvsioloav 223:131-150 Valeton, J.M., and D. van Norren 1983 Light adaptation of primate cones: An analysis based on extracellular data. Vision Research 23:1539-1547. Van Cott, H.P., and R.G. Kinkade 1972 Human Engineering Guide to Equipment Design. New York: McGraw-H ill. van Meeteren, A. . . 1978 On the detective quantum eff iciency of the human eye. Vision Research 18: 257-26 7. - van Meeteren, A., and J.J. Vos 1972 Resolution and contrast sensitivity at low luminances. Vision Research 12: 825-833 . Wood son, W.E. 1981 Human Factors Design Handbook. Wyszecki, G., and W.S. Stiles 1982 Color Sc fence: Formulas. New York: Zacks, J.L. 1970 New York: ~IcGraw-Hill. Concepts and Methods, Quantitative Data and John Wiley & Sons. Temporal summation phenomena at absolute coresnoxc~: Their relation to visual mechanisms. Science 170:197-199. Zuidema, P., W. Roest, M.A. Bouman, and J.J. Koenderink 1984 Detection of light and flicker at low luminance levels in the human peripheral visual system. I. Psychophysical experi- ments. Journal of the Optical Society A 1:764-774 . . ~. . . ~. ~ .

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GENERAL DISCUSSION BERSON: Does anyone feel that normal rod function would be enhanced by taking vitamin A every day? PITTS: The work that has been done on this shows that if a person has sufficient amounts of vitamin A, additional amounts of vitamin A are not going to help them. But we do know that if vitamin A is not in their diets, they're going to get an elevated threshold. A. MENENDEZ: I 'm with Technology Incorporated. It has come to our attention that the Air Force Office of Scientific Research is inter- ested in funding ways to improve normal vision through pharamacolog ical research--"super-vision," as we call it. That raises the question of whether normal vision is limited not so much by the physiological prom cess as by the actual quantum nature of light. If we believe in the doctrine of quantum limitation, then it seems that normal vision could not be improved and that the limiting factor is the physics of the light involved. I think that's related to the question of vitamin A in a general sense. BERSON: Dr. Copenhagen, would you like to comment on that? Do you think we have the most visually efficient system we could possibly have? COPENHAGEN: I would think selective evolutionary pressures would make it optimal. There is some dispute still over whether we are photon-limited at the absolute threshold. But the point is that you cannot get any better from the physics of the light. That's what the ideal observer can do. So you can build no machine that's better than that. There's no drug that you can take that's going to somehow change the physical properties of light. That's as far as we can go. So if that's super-vision, that would be the definition of super-vision. MACLEOD: I'd like to mention one interesting experiment concerned with super-vision and dietary vitamin A deprivation. One way to improve vision--even if the vision system is currently quantum-limited--is to absorb more quanta. I understand that during the war an effort was made to develop super-vision in the infrared by substituting vitamin A2 for vitamin Al in the diet, which should give a redward shift in the visual pigment absorption spectra. Experiments were done in Britain during World War II, but the project turned out to be infeasible with humans because it was difficult to induce sufficient vitamin A depriva- tion without endangering the general health of the observer. The ex- periment, however, has been made successfully using rats (S. Yoshikami, J . Pearlman, and F . Crescitelli, Vision Research 9: 633-646, 1969) . 76

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77 MAKOUS: I do want to add one thing to that. When we talk about "optimum," it depends on what "optimum" you're talking about. At abso- lute threshold, detecting quanta is certainly what the organism needs to do, but at high levels of illumination, it is more important to make discriminations of fine differences in the environment than simply to detect quanta. It is important to keep in mind what "optimum" you're comparing performance against. JOHNSON: I'd like to introduce the subject of individual differ- ences, particularly with regard to the ideal observer and the limiting factors on vision. There are considerable individual differences in the normal population. I was wondering if any of you would like to comment upon these individual differences. I'd also like to ask how the various clinical and psychological measures of photopic and sco- topic visual function compare in terms of the individual variations. What kind of correlations do you find among the various tests in normal individuals? MAKOUS: Crawford measured dark adaptation among 26 nonclinical subjects and found that the standard deviation of their time to a given point in dark adaptation was about 60 percent of the mean, which I would consider substantial variation among a nonclinical population. Another issue has to do with the relationship between cone dark adaptation and rod dark adaptation, but I don't have any data on it. I expect from our research that rod adaptation wouldn't tell you much about cone sensitiv- ity, or rate of cone dark adaptation or vice versa. They are factors that would tend to make the two systems competitive, and other factors would lead to independence of the two estimates. MASSOF: I want to respond to Chris's fJohnson] question on individ- ual differences. We've been doing studies with the electroretinogram [ERG] in normals to look at sources of variability. If you look across normal observers with the electroretinogram and look at a number of dif- ferent intensities so you're varying the amplitude across observers, the standard deviation of the between-observer distribution is a constant proportion of the mean amplitude. And the proportionality constant, the coefficient of variation, is 18 percent. So what that means is that across the normal population you expect to see a standard deviation of approximately 18 percent on the amplitude of the electroretinogram, on the dark-adapted eye. However, the within-observer coefficient of var~- ation is approximately 11 percent. So a large portion of the between- observer variability can be attributed to within-observer variability. The cetween-eye variables' coefficient of variation--recording the res- ponses of both eyes to the same flash--is about 3 percent. FISHMAN: Regarding visual f ield reproducibility, we have had the opportunity to look at it in the same individual repeated three times over a per lad of approximately 3 weeks. The visual field reproducibil- ity can be extremely poor, particularly in patients with ocular disease. In some patients with retinitis pigmentosa, the visual field area can vary by as much as 50 percent on short-term retest. BERSON: We found that the intervisit variation for 24 patients with retinitis pigmentosa was such that one had to have a change of greater than 33 percent in the ERG response to a single flash of white light to be certain with 99 percent confidence that the change had

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78 really occurred. We have not done intervisit variability of normals. But we have done yearly follow-ups of normals and find that they are not varying too much. MASSOF: I'd like to add to your comment, Jerry [Fishman], that the ERG numbers I'm using apply to Ganzfeld stimulation, so you're integrating over the entire retina. To talk about individual dark adaptation curves or individual measures of points, you have to add to that sampling errors and inhomogeneity of thresholds in terms of dis- tribution of sensitivity across the retina, so you would expect varia- bility to be higher. HARVEY: There really Is more to vision than detecting light. A lot of the uses that people want to optimize are not detecting small spots for which the ideal observer can be fairly well defined. So in tasks that require pattern observation there really is not a good theory of an ideal observer. It is really difficult to know whether there is not some sort of observable physical limit on an ideal observer for identi- fying or recognizing the target, rather than just detecting it. And since there are at least two psychological processes that go on, one involving sensory representations and the other involving decision, it would seem to me to be an open question whether you could have training strategies or some sort of intervention strategy that would lead to a substantive improvement. This is a possibility that should not be ruled out on theoretical grounds alone. MAKOUS: I'd like to comment on that. Bill Geisler has recently published two papers for which he's described an ideal observer for more complex tasks such as localization and Vernier acuity. I'd like to add a comment about dark adaptation, ERG variability, and psychophysical var lability. Of course, the ERG is of enormous value in clinical evaluations, but it' s hard to go directly f rom the variability of an ERG to variability of a psychophysical process such as afar k adaptation. MASSOF: I'd like to add to what Walt [Makous] just said. The ERG numbers I just gave you apply to the amplitude of the ERG, which is of course in all cases a suprathreshold stimulus. The other way you can look at the ERG is to take an intensity ser. ies. I f you plot amplitude versus log intensity and then look at the half-saturation constant, the variability across observers on that half-saturation constant is comparable to what you would get psychophysical. MACLEOD: I'd like to raise a question about the reproducibility of the course of dark adaptation for a given observer. I am very struck that in the lab when we try to measure dark adaptation curves of normal individuals, they are really disappointing in their reproducibility. Other psychophysical functions reproduce very well. Dark adaptation curves reproduce very poorly by comparison. There must be an underlying reason for that, in terms of a fluctuation over time and the dynamics of a given individual's dark adaptation process. I think it would be very interesting to try to do some analytical work on the systemic fac- tors that underlie this fluctuation with time in a given individual's dark adaptation characteristics, whether it's related to eating pat- terns, caffeine, or diurnal rhythms and body temperature, and in the latter case, whether sensitivity is optimal during the night phase or during the daytime phase when body temperature is higher.

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79 MONACO: I'd like to digress to what General Doppelt said and what I interpreted as him asking: What are the kinds of tests that are cur- rently available--diagnost~c tests, screening tests--that will answer some of the questions that the military has about operating under re- duced levels of illumination. FISHMAN: I'm not clear whether to make the screening procedures more efficient so that you could administer them to the 750,000 recruits that need to be screened for night-blinding disorders or whether you want to qualitatively improve the tests to discern the difference be- tween ~better" and "best" for a group of normal recruits, so that some could be optimized for night vision tasks while the rest would be deter- mined as adequate to perform the majority of night vision tasks. If the latter case is the goal, I think that's very difficult because I don't know how to solve it with any clinical techniques that are currently available; in other words, how to discern the individual that would be superlative at a potentially critical task done under dim illumination as opposed to other individuals that would be considered "good." TREDICI: That's one of the reasons we set up this conference. Yes, we need to know the true pathologic ones and separate those out at the very beginning. We do have methods for that, which you've all done. The other aspect, I understand, would be difficult. BERSON: I'd like to make one comment: The family history and a history of symptoms of cliff faulty with adaptation are, o' course, important in deciding which individuals should have an ERG to see if they have retinitis pigmentosa. I would also like to suggest for your consideration that the optics of the patient--the pair of glasses that they're wearing--should be a red flag, particularly if there's astig- matism. We analyzed the patients with ret~nitis pigmentosa and their normal relatives -with 20/20 to find out if the refractive errors in the retinitis pigmentosa patients differed from those in their normal rela- tives. We found that astigmatism of two or more diopters in the less astigmatic eye was seen in a sample of approximately 10 percent of 160 patients who had retinitis pigmentosa. When we compared this to the normal relatives, we found that only 1 to 2 percent of normal relatives had this refractive error and 20/20. I'm confining my remarks now to patients who have 20/20, for if their acuity is reduced, which is more often the case when they come to our hospital, that's a separate issue. If you want to obtain a higher yield of people who might have retinitis pigmentosa, we would suggest ERG testing of individuals who have two or more diopters of astigmatism. We suspect that the yield per examination of patients with retinitis pigmentosa would be greater for those with this refractive error. JOHNSON: Just a comment relative to rapid screen tests. Everybody wants a quick test that will give them all the answers. With a quick test you have very limited information. Since very little is presently known about the relative parameters of night vision for job performance, I think that a quick screening test is a bit preliminary. In order to establish a relationship between task performance and visual parameters, a great deal of work must be done. Only after these relationships have been established and the visual parameters have been fully characterized should a rapid screening test be contemplated.

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80 BERSON: I'd like to state that most of the disease states are symmetrical in both eyes. In terms of economy of time and effort, a patient can be dilated and dark-adapted in the waiting room with a patch over one eye and can do other tasks with the other eye, whether it's questionnaires or whatever. The patient can be led into the room to record a dark adaptation threshold, then have an ERG lens placed on the topically anesthetized cornea, have a few flashes of light adminis- tered, thus doing a very comprehensive and definitive examination in 10 or 15 minutes. So I think screening programs could be very definitive and run in a short period of time. The advantage of doing the testing this way also is that if the person is normal by ERG testing, our avail- able evidence is that they're not going to develop these diseases later. If you're going to pass someone, it would be helpful to know that they are going to be normal for the next 20 years. Therefore, it seems if you have a high-risk individual--high astigmatism, symptoms of night blindness or difficulty with adaptation, positive family history of retinitis pigmentosa--I would do ERG testing even though it may take an extra few minutes. I think this will be cost-effective in the end.

Representative terms from entire chapter:

dark adaptation