An essential feature of the Balint syndrome appears to be a failure to properly direct oculomotor function in the exploration of space. This psychic paralysis of gaze is apparent when the patient is unable to turn his eyes to fixate an object in the right or left visual field or to consistently follow a moving object. The pattern in which the patient scans a picture is haphazard and fails to encompass on entire areas. Normal individuals accomplish visual scanning in a fairly uniform manner beginning paracentrally and moving clockwise, then to the corners. Thus, the mechanism of simultanagnosia may be in part the result of this abnormality of eye movements as pointed out by Tyler.
Optic ataxia is detected when the patient reaches for an object, either spontaneously or in response to verbal command. To reach the object, the patient engages in a tactile search with the palm and fingers, presumably using somatosensory cues to compensate for a lack of visual information. The disorder may involve one or both hands and give the erroneous impression that the patient is blind. In contrast, movements that do not require visual guidance, such as those directed to the body or movements of the body itself, are performed naturally. The presence of visual inattention is tested by asking the patient to carry out tasks such as looking at a series of objects or connecting a series of dots by lines; often only one of a series of objects can be found, even though the visual fields seem to be full.
In almost all reported cases of the Balint syndrome, the lesions have been bilateral, mainly in the vascular border zones (areas 19 and 7) of the parietooccipital regions, although instances of optic ataxia alone have been described within a single visual field contralateral to a right or left parietooccipital lesion, and visual simultanagnosia, as noted earlier, has had variable localization. The neuropsychologic aspects of the syndrome and several interesting historical notes, including the attribution of original reporting to Inouye, can be found in the review by Rizzo and Vecera.
The effects of disease of the occipital lobes may be summarized as follows:
I. Effects of unilateral disease, either right or left
A. Contralateral (congruent) homonymous hemianopia, which may be central (splitting the macula) or peripheral; also homonymous hemiachromatopsia
B. Elementary (unformed) hallucinations—usually because of irritative lesions
II. Effects of left occipital disease
A. Right homonymous hemianopia
B. If deep white matter and splenium of corpus callosum is involved, alexia without agraphia
C. Visual object agnosia
III. Effects of right occipital disease
A. Left homonymous hemianopia
B. With more extensive lesions, visual illusions (metamorphopsias) and hallucinations (more frequent with right-sided than left-sided lesions)
C. Loss of topographic memory and visual orientation
IV. Bilateral occipital disease
A. Cortical blindness bilateral hemianopias
B. Anton syndrome (visual anosognosia, denial of cortical blindness)
C. Loss of perception of color (achromatopsia)
D. Prosopagnosia (impaired face recognition, bilateral temporooccipital including fusiform gyrus)
E. Balint syndrome (bilateral dorsal parietooccipital)
A line of disagreement, as old as neurology itself, pertains to the relationship between the two cerebral hemispheres. Fechner, in 1860, speculated that since the two hemispheres, joined by the corpus callosum, were virtual mirror images of one another and functioned in totality in conscious life, separating them would result in two minds. William McDougall rejected this idea and is said to have offered to have his own brain divided by Charles
Sherrington should he have an incurable disease. He died of cancer, but the callosotomy was considered unnecessary, for already there were indications from the work of Sperry and colleagues that when separated, the two hemispheres had different functions.