The concept of blindness has been changing rapidly in the last decade of the 20th Century. Prior to that time, blindness was usually thought of as an absolute condition. Lesser conditions were usually thought of in terms of poor eyesight (with respect to resolution) or color blindness.
The current understanding of blindness can be placed in a broader framework with a stronger conceptual and theoretical foundation. Within the framework of this overall work, blindness can be categorized into one of three major types of visual inadequacy. The broadest historical type is that of blindness due to non-neurological causes related to the physiological optical system. Physiological blindness includes the effects of cataract, glaucoma, retinal separations from its substrate and similar physical problems of the ocular globe. It also includes the failure of the Precision Optical System to cause tremor of the ocular globes through the action of the ocular muscles. These problems can be of genetic origin or due to disease, or trauma. In recent years, two separate categories of neurological blindness have become better defined. The first type involves perceptual blindness. Perceptual blindness involves problems in the signaling system between the retina and the stellate cells of the cortex. There are many sources of this type of blindness that can be easily described. The most recent form of blindness to become prominent is cognitive blindness. This type of blindness involves failures in the feature extraction engines and the recognition facilities of the cortex. Until the development of the MRI and CAT scanners, failures of this type could only be diagnosed based on traumatic injury to the brain, primarily through accident. More recently, these new techniques have allowed localization of the neural failures within the brain related to a given syndrome. To date most of these localizations are based on abnormal circulatory or metabolic system operation and not specific failures of the neurological system. Most recently, a new technique of visual evoked potential measurement has allowed localization of specific failures in the signaling system within the cortex. Although still of limited spatial resolution, it does provide new insights into cognitive failures.
By subdividing blindness according to the above classification system, it is possible to improve the definition of a specific form of blindness. Color blindness is a specific example. The sources of various forms of color blindness can be found throughout the neurological elements of the visual system. Because of the breadth of failures related to color blindness, it is highly unlikely that a simple genetic explanation of the problem can be based on only three or four artifacts in the genes of an individual.
Besides color blindness, the advent of the more sophisticated requirements on the visual system of modern living has surfaced a broad range of additional visual shortcomings. At the current time, as many as 32 different insufficiencies have been clinically documented. Although the technical language is still evolving, these conditions are being discussed in terms of "blindsight."
Blindsight includes the widely distributed diagnoses of individuals;and other situations suggestive of different types of cognitive blindness. Many of these are being encountered after cerebral accidents (strokes). The source of the problem is being localized within a millimeter or two on the surface of the cortex. Some of the conditions are found to be temporary, probably due to pressure on, rather than destruction of, neurons of the cortex. Alternately, the syndrome may be due to inadequate circulation of the metabolites required for the electrostenolytic processes on the surface of individual neurons. There are no common power supplies in the brain. Every individual neuron must receive the necessary metabolites.
Severe cases of blindness are obvious and easy to identify. However, many of the less severe cases of "blind sight" are frequently not recognized until the subject is placed in a demanding situation. In between these extremes is a large range of visual abnormalities that can be identified.
The current level of technology available allows a very precise definition of the cause and location of nearly every form of blindness that can be identified. Where recovery from a temporary condition is possible, the time profile of the recovery can often be provided to the patient. If the condition is permanent under current conditions, the subject can be provided a more assuring explanation of his situation than has been previously possible. In many cases, the location of a fault in the visual system can be located to within a few millimeters without any invasive procedure.
Color blindness is found in many absolute forms and a wide range of relative failures. Only a few rare forms can be attributed to the lack of one or more chromophores within the photoreceptor cells of the retina. Most chromatic inadequacies of the visual system are found within the signal manipulation and signal projection stages of the visual process. Some are found within the cortex.
If a subject exhibits a normal luminous efficiency function at nominal radiant intensities and at a spectral resolution of less than 10 nm wavelength interval, it is can be assumed that all of his spectral channels are operating properly. This condition indicates that all of the expected chromophores are present in the prescribed amounts and that all of the photoreceptors are operating normally up to their pedicels. It also suggests that the distribution of the three spectral types of photoreceptors are present in nominal densities within the retinal mosaic.
A subject exhibiting chromatic visual failures who passes the above test of luminous efficiency can be considered to be suffering perceptual or cognitive blindness. The number of locations, related to failures within the perceptual signal processing portion of the visual system, is large. The list begins with a failure of one or more of the connections between the pedicels of the photoreceptors of the retina and the horizontal cells of the 1st lateral processing matrix. The list continues with a failure of the 1st lateral matrix to generate the appropriate chrominance signals. Finally, failures can occur in the signal projection neurons responsible for the retinal encoding, transmitting, and cortical decoding the proper signals. The ganglion cells associated with part of the encoding function are particularly susceptible to failure because of their unique operating mode.
The 1st lateral matrix is the primary source of color information that is relayed to the cortex. The actual matrixing requires the proper operation of the Activas within the lateral cells in order to compute the P- & Q-channel signals. There are a variety of possible failures associated with the electrical performance of the horizontal cells. Many of these relate to the electrical biasing of these cells via an electrostenolytic process.
The midget ganglion cells of the retina are responsible for the encoding and initial transmission of the electrically bipolar chrominance signals to the brain. These cells are virtually identical to the parasol type ganglion cells that process only electrically monopolar luminance signals. The only distinguishing functional difference is the bias voltage applied between the emitter and base of these cells. If they are improperly biased, they will encode and transmit a data stream that favors one polarity of the bipolar signal. Such a failure will cause abnormal discrimination of the "red-green(azure)" or blue(violet)-yellow" type. The abnormality can be complete or one of degree.
Both the stellate cells of the cortex and the midget ganglion cells of the retina are dependent on the bias voltage between the emitter and base terminals of their Activas for proper operation. If either of these biases is incorrect, the recovered P- and Q-channel signals will be incorrect. The result will be some degree of color blindness. The most likely candidate for the source of this type of color blindness is the midget ganglion cell. This is because of a property of direct coupled analog circuits. A bias error of only a few millivolts is significant in this circuit. In these circuits, a bias error in one stage propagates through the following circuits. Besides its own potential bias error, the midget ganglion cell bias is impacted by potential bias errors in two photoreceptor cells, one horizontal cell, and possibly a bipolar cell. Most engineers avoid direct coupled circuits of more than two stages because of this design challenge. On the other hand, operation of the stellate cells depends only on the bias and other properties within the cells own circuits.
Science is on the verge of being able to trace the source of color blindness to specific malfunctions within the cortex. It can do this by demonstrating the presence of the appropriate P- and Q-channel signals within specific local areas of the occipital lobe of the brain. If these signals are received within the cortex, it can be assumed that the stellate cells of the signal projection system are operating properly and the color vision failure can be assumed to be cognitive in origin. A prime suspect would be the feature extraction engines providing signals to the saliency map that is shared with the higher cognitive centers of the brain. However, the feature extraction engines for color would appear to be relatively simple based on the tasks assigned to other feature extraction engines.
The next few years should see great progress in localizing the failure modes of the visual system by category. Watch for the signal projection system to be the primary source of failures related to color vision. Both the midget ganglion cells of the retina and the appropriate class of stellate cells of the cortex are primary suspects.