A second group of patients with color agnosia have no difficulty with color perception (i.e., they can match seen colors), but they cannot reliably name them or point out colors in response to their names. They have a color anomia, of which there are at least two varieties. One is typically associated with pure word blindness, that is, alexia without agraphia, and is best explained by a disconnection of the primary visual areas from the language areas (see further on). In the second variety, the patient fails not only in tasks that require the matching of a seen color with its spoken name but also in purely verbal tasks pertaining to color naming, such as naming the colors of common objects (e.g., grass, banana). This latter disorder is probably best regarded as a form of anomic aphasia, in which the aphasia is more or less restricted to the naming of colors (Meadows, 1974b). According to Damasio and associates, the lesion has involved the medial part of the left hemisphere at the junction of the occipital and temporal lobes, just below the splenium of the corpus callosum. All their patients also had a right homonymous hemianopia as a result of destruction of the left lateral geniculate body, optic radiation, or calcarine cortex.
Visual simultanagnosia This describes an inability to grasp the sense of the multiple components of a total visual scene despite retained ability to identify individual details. Wolpert pointed out that there was an inability to read all but the shortest words, spelled out letter by letter, and a failure to perceive simultaneously all the elements of a scene and to properly interpret the scene, which Wolpert called simultanagnosia. A cognitive defect of synthesis of the visual impressions was thought to be the basis of this condition. Some patients with this disorder have a right homonymous hemianopia; in others, the visual fields are full but there is one-sided extinction when tested with double simultaneous stimulation. This is an integral part of the Balint syndrome described below.
Through tachistoscopic testing, Kinsbourne and
Warrington (1963) found that reducing the time of stimulus exposure permits single objects to be perceived, but not two objects. Rizzo and Robin proposed that the primary defect is in sustained attention to incoming visuospatial information. There is consistent localization; Nielsen has described it with a lesion of the inferolateral part of the dominant occipital lobe (area 18). In a patient who presented with an isolated “spelling dyslexia” and simultanagnosia, Kinsbourne and Warrington (1962) found the lesion to be localized within the inferior part of the left occipital lobe. In other instances, the lesions have been bilateral in the superior parts of the occipital association cortices.
Balint syndrome (See also Chap. 12.) In this not uncommon syndrome, the appreciation of a coherent and detailed visual world is disrupted and the patient perceives only disconnected individual parts of the scene, as in the visual simultanagnosia described earlier. While it is due to lesions that span the occipital and parietal lobes, it is presented here for ease of exposition. Balint, a Hungarian neurologist, was the first to recognize this constellation. The defect is noted when the patient describes a complex scene in a disjointed way, single objects being pointed out, others missed entirely, the relationships and context of parts of the picture remaining unappreciated.
The entire syndrome consists of (1) a disorder of visual attention mainly to the periphery of the visual field, in which the totality of a scene is not perceived despite preservation of vision for individual elements (visual simultanagnosia as discussed earlier); (2) difficulty in grasping or touching an object under visual guidance, as though hand and eye were not coordinated (called by Balint optic ataxia); and (3) an inability to project gaze voluntarily into the peripheral field and to scan it despite the fact that eye movements are full (termed psychic paralysis of fixation of gaze by Balint, incorrectly called optic apraxia).