The rods, although highly sensitive to light, play no role in color discrimination and give very poor visual acuity, owing to the complexity and multiplicity of their connections with the bipolar and amacrine cells of the inner nuclear and molecular layers of the retina. They are absent in the fovea and their density increases as one passes toward the periphery, until a critical distance from the fovea is reached, after which the density decreases. In the extreme periphery, only rods may be observed microscopically; cones are absent.
The sensitivity of the eye to light may be extraordinarily great. Hecht and his colleagues have adduced evidence which indicates that the absolute threshold to light corresponds to stimulation by only a few quanta when the retina is dark-adapted.
The absolute threshold depends on many variables. Shifts in any of them will produce measurable differences in the magnitude of the threshold.
State of Adaptation. The most important variable is the sate of adaptation of the eye. When the eye is light-adapted to the high level of illumination found outdoors on a bright day and the absolute threshold is measured immediately, it will be as much as 10,000 times greater then the value obtained if the eye has been resting in complete darkness for a period of thirty or forty minutes. The change in sensitivity which occurs as the eye remains in the dark proceeds very rapidly for the first two to three minutes, and then at a slower rate for from five to six minutes. During this first period of adaptation the cones have become dark-adapted. A second period of adaption then begins, at first rapidly then at a decelerated pace. This second phase, which accounts for the major parts of the increase in sensitivity, is attributable to the adaptation of the rods, and is associated with concentration of rhodopsin within those cells. The threshold obtained when dark adaptation is complete is the absolute terminal threshold. Figure 101 presents a dark-adaptation curve showing the progress of dark adaptation in normal and abnormal retinas. Part of this change in sensitivity can be attributed to dilatation of the pupil occurring concurrently with the earlier phases of dark adaptation, but this is only a small part. It is defective dark adaptation and low sensitivity of the rods which is ordinarily associated with nyctalopia1 or night blindness; relatively few studies have been made of the adaptation of the cones.
The rate at which dark adaptation proceeds depends upon the intensity and duration of previous exposure to light. Those who work outdoors in the summer, when sky brightness is high, may show a deficit of dark adaptation for several days after exposure to sunlight and will not show absolute thresholds within normal range until the use of some such device as dark sunglasses has permitted recovery. Those, on the contrary, who work under artificial illumination may become completely dark-adapted in from fifteen to twenty minutes. A rapid recovery ensues after exposure to very short flashes of high brightness but recovery is slower after more prolonged exposure to a lower intensity. Wald has related this to the cycle of regeneration of rhodopsin in the retina.
Stimulus Variables.–Other variables which will alter the value of the absolute threshold relate to the characteristics of the stimulus flash used in the threshold measurement. These are its (1) distribution of energy throughout the spectrum, (2) area, (3) duration, (4) position in the visual threshold and (5) shape. Each of these must be controlled precisely if reasonable reliable threshold measurements are to be obtained. An ultimate limit on the precision of control of the stimulus is placed by the probability of arrival at the retina of the requisite number of quanta within the flash duration.
Methodological variables.–Even though precise control of the stimulus is possible and the other relevant variables are kept physically constant, variations in the threshold may appear with variation in the technic of measurement. Such factors as instruction and cooperation of the subject, skill of the subject in observing, and stimulations and reporting procedures will produce variations in the results.
Variability of the Sensitivity of the Retina.–The sensitivity of the retina has been observed to shift from day to day, providing yet another limitation on the reproducibility of any measure of the visual threshold.
In all, the characteristics of night vision are so different from those of day vision that a special technic of observation is required, and special training and practice are necessary for those who must see well under low levels of illumination.
However, a sharp distinction must be made between night blindness as indicated by such reported difficulties and nyctalopia, or true night blindness, which may be diagnosed only on the basis of an accurate measurement of retinal sensitivity. Many, if not most, of those individuals who report difficulty in seeing at night prove to be psychoneurotic. Many who have unusually insensitive retinas, on the other hand, do not report special difficulties in seeing at night, either because they assume that others have the same difficulties, or because they fail to note them in out well-illuminated urban culture, which offers few situations in which intact rod function is required. To establish the presence of nyctalopia, it is essential to use an instrument of established validity for the measurement of retinal sensitivity.
Incidence of Nyctalopia.–No definitive data on the occurrence of nyctalopia in the population are available, since measurements have never been made on a representative sample of the population. From the studies which have been made of selected groups (e.g. school children, service men), it is known that the normal population will include a small percentage of persons of low visual sensitivity whose performance will be as poor as or poorer than that of many individuals whose nyctalopia is associated with disease or degenerative processes. About 2 per cent of the Navy men were disqualified for night duties as “night blind” on this basis. Those so disqualified seldom if ever showed symptoms other than a relatively high absolute terminal threshold, and their reduced sensitivity must be taken as the consequence of the normal variability in the density in the retinal rods and the efficiency of the process whereby rhodopsin, the visual purple, is regenerated.
The incidence of nyctalopia as part of a distinct clinical pattern is not well understood. It has been observed frequently in several diseases, and may appear in certain unusual conditions such as:
(1) Idiopathic Nyctalopia.–Idiopathic nyctalopia is an hereditary absence of rod function, which has been traced through several generations of certain families. Although typically it appears alone, it may be associated with color blindness and myopia. There is no effective treatment.
(2) Oguchi’s Disease.–This rare hereditary syndrome, first reported in Japan and later observed in Europe, has its primary symptom nyctalopia with marked contraction of the visual field under low levels of illumination. Ophthalmoscopic examination shows a remarkably gray appearance of this fundus which disappears with dark-adaptation. Day vision is not affected. No treatment as proved of value.
(3) Retinitis Pigmentosa.–Nyctalopia is the first and invariable symptom of retinitis pigmentosa. In the early stages of the disease, dark adaptation takes place, but at a retarded rate. As the disease advances, rod function is progressively lost, and the absolute terminal threshold is elevated. Diagnosis of retinitis pigmentosa is based upon ophthalmoscopic examination.
(4) Glaucoma.–Early impairment and progressive loss of rod sensitivity is observed in glaucoma.
(5) Retinitis Punctata Albescens.–The earliest symptom of this disease is the complete absence of rod function. Often nyctalopia is the only symptom associated with the altered state of the retina.
(6) Other syndromes of the Visual System.–Nyctalopia has been observed as one symptom of each of the following pathologic conditions: myopia, disseminated chorioretinitis, pregnancy, nicotine poisoning, the Lawrence-Moon-Biedl syndrome, gyrate atrophy of the choroid and retina, choroideremia and atrophy of the optic nerve. Nyctalopia may be simulated by opacities of the ocular media.
(7) Overexposure to Sunlight.–Mild transient nyctalopia may appear in persons who have been overexposed to bright sunlight for several days. It will disappear within a few days if the persons will protect their eyes from the sun wither by remaining indoors or by the use of dark sun glasses.
(8) Avitaminotic Nyctalopia.–Epidemics of night blindness have been observed in populations subject to a vitamin A deficient diet. This phenomenon has been related to the important role played by vitamin A in the cycle of regeneration of rhodopsin. Nyctalopia has been considered the classical symptom of this deficiency and the presence of an elevated terminal threshold has been erroneously taken by some as sufficient basis for diagnosis, even in the absence of other signs of the deficiency.
Although much work has been done on experimentally induced vitamin A deficiency and the terminal rod threshold, the data are still inconclusive. Some investigators have been able to produce night blindness experimentally (See Fig. 101) and to reproduce remarkably rapid recoveries through the administrations of rapid of massive doses of vitamin A, e.g., 100,000 I.U. Others have found recovery slow or absent in some cases after several months of its administration. Others have not been able to produce nyctalopia in all subjects through the manipulation of the diet. The conclusions are that vitamin A deficiency may or may not produce nyctalopia and that administration of vitamin A may or may not lead to recovery from it. Ingestion of the provitamin carotene was conspicuously unsuccessful in improving night visual performance of American service personnel, although it seems to have somewhat improved that of less well-nourished armies, as the Japanese. If an individual complains of difficulty in seeing at night and such pathologic conditions as retinitis pigmentosa have been ruled out, the administration of massive doses of vitamin A may lead to improvement, and hence to the conclusion that the nyctalopia was produced by a vitamin A deficient diet.
(9) Faulty Vitamin A Metabolism.–In such diseases as cirrhosis of the liver, reduced retinal sensitivity may appear. Massive dosage with vitamin A is followed by partial or complete return of sensitivity to the normal range. It is believed that such nyctalopia may be referred to altered intermediary metabolism of vitamin A.
Tests for Detecting Nyctalopia.–Since the first measurements of absolute visual thresholds were made and the clinical significance of night-blindness noted, several adaptometers or photometers have been developed for this purpose. Of the early ones, those of Nagel and Foerster were perhaps best known. In recent years new devices and methods, with decided advantages, have been developed as a consequence of the need to eliminate from certain duties military and Naval personnel unable to perform efficiently at night. Screening tests, designed only to detect the night-blind, were produced. Adaptometers capable of measuring the terminal rod threshold with great precision were widely distributed. Any of these instruments has a definite clinical value in the detection of nyctalopia, and may take its place in the medical laboratory. Certain precautions, however, must be taken before any importance is attached to the results obtained with any of them; these precautions are based both on the essential properties of the tests and on the behavior of the patients, as for example:
(1) The instruments are difficult to keep in proper calibration. Since the intensity of light delivered by the instrument may shift considerably from the prescribed values, with consequent erroneous measurement of the threshold, leading to an incorrect diagnosis of nyctalopia or a failure to detect it, the instrument must be calibrated at regular intervals.
(2) Slight departure from the method of testing prescribed by the designers may similarly yield erroneous results. Errors in the placement of the patient with respect to the instrument, in the position of the fixation point and in details of stimulating the subject or recording of test performance may be misleading. Each instrument must be used strictly according to directions.
(3) The greatest care must be taken to ensure that the subject is fully dark-adapted before the test is administered. Each of the acceptable tests2 assumes that such is the case, and the administration of the test to one who is not fully dark-adapted is most certain to lead to a diagnosis of night blindness. It is, then, essential that the test be made when the retina has reached its final stable level of adaptation. Satisfactory dark-adaptation may be achieved by seating the patient in a completely light-tight dark room for at least one half-hour, or by allowing the patient to wear read dark adaptation goggles3for twenty minutes before a final ten minute period in the dark room. The greatest care should be taken to ensure that no white light leaks in around the goggles and that the patient’s eyes are not exposed to light when in the dark room.
(4) The classification of an individual as “normal” or “night blind” must be based upon the norms established with a particular instrument.
(5) The measured sensitivity of the retina of light may vary considerably in the same individual from time to time. This may be because of psychologic factors, slow physiologic changes, or exposure to strong illumination during the days proceeding the test. It is therefore urged that any diagnosis be based upon the results of two tests spaced at least twenty four hours apart.
As an example of the serious consequences of failure to use a properly designed instrument and a reliable method of measuring the threshold, the results on one adaptometer may be cited. This instrument, widely publicized, invariably found 25 per cent of those tested “night blind”. However, it did so without consistency, so that the individual taking the test 10 times was classified “night blind” three times, and “normal” seven.
These important sources of error make the administration of makeshift tests extremely misleading. It has been suggested frequently that adequate results may be obtained by comparing the performance of a patient in reading a standard Snellen chart under dim illumination with that of the physician. Such a method can be useful only if both individuals have had the same immediate history of light and dark adaptation, if the physician possesses normal sensitivity, and if there is definite assurance that the level of illumination is sufficiently low that rod vision is required for the performance. (This is of great importance; many such tests investigate cone functions alone, and are consequently quite without validity in the diagnosis of nyctalopia.) It is almost impossible to be sure that these conditions are all satisfied, so that such procedures must be discarded.
Acceptable Instruments.–During and immediately proceeding World War II, a number of satisfactory adaptometers were developed.
Hecht-Shlaer Adaptometer.–This device permits extremely accurate measurement of the terminal rod threshold for form and light sensitivity. The most sensitivity retinal area for scotopic form is approximately 4 degrees from the fovea whereas the similar area for light is about 20 degrees from the fovea. The Hecht-Shlaer instrument is small and convenient to use. A circular stimulus patch of violet light, 3 degrees in diameter, is presented 7 degrees from a fixation point. The patch is flashed on for a duration of 0.2 seconds at regular intervals, and its intensity is systematically variable. Several models have been manufactured. High absolute terminal thresholds, as measured by this device, warrant a diagnosis of nyctalopia.
Wald Adaptometer.–This portable device also measures the absolute terminal rod threshold. It is perhaps more convenient to use than the Hecht, but is not quite so easily and accurately calibrated.
Radium Plaque Adaptometer.–This inexpensive and simple instrument is capable of detecting only gross deficiencies in rod performance. It was developed by the U.S. navy as a screening device to single out the worst 2 to 4 per cent of the population, a percentage which certainly includes all those who are clinically night blind. Failure to pass after at least two tests indicates night blindness.
AAF-Sam Night Vision Tests.–Similar to the Radium Plaque Adaptometer, this device permits a more complete classification of personnel with respect to rod performance, and is similarly able to select out the night blind.
Livingston Screen.–Essentially this is the familiar tangent screen employed in perimetry. The test consists in determining the visual field of the dark-adapted eye for small spots of radioactive material of very low brightness. Cases of night blindness show, at levels of illumination well above the terminal threshold, a restricted visual field and an enlarged central scotoma. The test is extremely difficult to administer and requires considerable time.
General Remarks.–A wide variety of adaptometers has been developed. Properly used, any of them which has been used in research will adequately detect nyctalopia. Commercially produced models should be employed with caution, and only after a critical examination of the scientific literature on them.
The utility to the clinician of any rapidly administered clinical test may be questioned (1) because a diagnosis of night blindness can never be taken as unequivocal evidence of one or another pathologic state of the organism in the absence of other, more easily observable signs, and (2) owing to the extreme difficulty of properly administering tests of dark adaptation without special training.
2. Duke-Elder, W.S.: Textbook of Ophthalmology, St. Louis, C.V. Mosby Co., 19 38, p.2094.
3. Elwyn, H.: Diseases of the Retina, Philadelphia, The Blakinston Co., 1946, p. 587.
4. Epstein, E., and Lesser, S.A.H.: A trick Test to Detect Night Blindness “Malingerers,” Brit. M.J., 2: 644, 1945.
5. Feldman, J.B.: Light Threshold: Its Clinical Evaluation, Arch. Ophth., 26: 466, 1941.
6. Fridericia, L.S., and Holm, E.: Experimental Contribution to the Study of the Relation between Night Blindness and Nutrition, Am. J. Physiol., 73: 63, 1925.
7. Gates, R.R.: Human Genetics, Vol.I., New York, The Macmillian Co., 1946, p.742.
8. Hecht, S.: The Quantum Relations of Vision, J. Opt. Soc. Amer., 32: 42, 1942.
9. Hecht, S.: Sunlight Harms Night Vision, Air Surg. Bull., 2: 45, 1945.
10. Hecht, S., and Mandelbaum, J.: Dark Adaptation and Experimental Human Vitamin A Deficiency, Am. J. Physiol., 130: 651, 1940.
11. Hecht, S., Shlaer, S., and Pirenne, M.H.: Energy, Quanta, and Vision, J. Gen. Physiol., 25: 819, 1942.
12. Hinn, G.J., and Montano, R.A.: A Case of Night Blindness, Air Surg. Bull., 2: 287, 1945.
13. Hoff, E.C.: Night Vision Selection, Hosp. Corps Quart., 18: 16, 1945.
14. Manelbaum, J.: Dark Adaptation: Some Physiologic and Clinical Considerations, Arch. Ophth., 26: 203, 1941.
15. Patek, A.J., Jr., and Haig, C.: The Occurrence of Abnormal Dark Adaptation and its Relation to Vitamin A Metabolism in Patients with Cirrhosis of the Liver, J. Clin. Inv., 18: 609, 1939.
16. Steven, D., and Wald, G.: Vitamin A Deficiency. A Field Study in Newfoundland and Labrador, J. Nutrition, 21: 461, 1941.
17. Pinson, E.A., and Chapanis, A.: AML Portable Radium Plaque Night Vision Tester, Air Surg. Bull., 2: 285, 1945.
18. Wald, G.: Caroteniods and the Visual Cycle, J. Gen. Physiol., 19: 351, 1935.
19. Wald, G.: A Portable Visual Adaptometer, J. Opt. Soc. Amer., 31: 234, 1941.
20. Wald, G., and Steven, D.: An Experiment in Human Vitamin A Deficiency, Proc. Nat. Acad. Sci., 25: 344, 1939.
21. Wittkower, E.; Roger, T.F.; Scott, G.I., and Semeonoff, B.:”Night Blindness”-A Psychological Study, Brit. M.J., 2: 571, 1941.
2 Certain tests have been designed for administration during the first few minutes of adaptation. Such tests have consistently proved to be unreliable, owing to the rapid changes taking place during this period.
3 Made by the Polariod Corporation.