Optic ataxia (Garcin-Rondot) observed in four patients with cerebrovascular disease was evaluated clinically and radiologically (CAT), and its possible mechanism was proposed on the basis of the analysis of our cases and the cases in literature ( Table 1.). The optic ataxia of Garcin-Rondot is charactereized by the inability to grasp an object presented in the peripheral visual field, while retaining the ability to grasp an object the patient is looking at. This could be explained by the failure of retinal information to reach the PG area of Economo-Koskinas (angular gyrus or Brodmann's 39 area in man), which is shown by an arrow pointing upwards to the left in Fig. 1.. In other words, this means the disturbance of visuo-somatosensory coordination. On the other hand, in the optic ataxia of Bálint syndrome, grasping of an object is difficult even when the patient is looking at the object, This may be explained by the failure of extraretinal oculomotor information (the upward arrow in Fig. 1 .) to reach the PG area, although in addition retinal information may not reach it. Possible mechanism of the two types of optic ataxia explained above is summarized in Fig. 6.. The mechanism may be comparable with that of Parinaud syndrome which also has two types, absolute and dissociative. The mechanism of the optic ataxia of Garcin-Rondot can be mostly explained by the disconnexion theory as mentioned above except for the difference in the symptoms depending on the side of the lesion. In the left cerebral hemisphere lesion, the symptom appears in the right hand in the right homonymous hemivisual field, whereas in the right-sided lesion, it appears in both hands in the left homonymous hemivisual field (Fig∂.5., lower half). Thus, there seems to be right cerebral hemisphere dominance in the normal visuo-motor coordination (Fig. 5., upper half), as the right cerebral hemisphere is known to be dominant in space perception and body skill.
The present paper deals with crticocortical connections of the posterior association cortex in cats, monkeys and man with particular empha sis on the most “developed” cortical region ; particularly the angular gyrus in man. Organization patterns of association fibers to the posterior association area are basically identical on several points in cats and monkeys. Thus, for example, convergence of association fibers from the somatosensory, auditory and visual cortical areas to a certain region in the posterior association area ( MSs, middle suprasylvian sulcus area in cat; STs, superior temporal sulcus area in monkey) is evident in both animal species. However, several dissimilarities, reflecting evolutionary development from carnivores to primates, do exist within the formation of some long association bundles, which have been revealed from a comparison of the findings obtained from the two kinds of animals. The angular gyrus (area 39) together with its adjacent areas can be considered from the evolutionary point of view as being homologue of part of the MSs and STs in the cat and monkey, respectively. Some aspects of the angular gyrus are discussed with relation to the monkey and crossmodal association (Geschwind, 1965), and the possibility of cortical connections between the angular gyrus and Broca's area is also commented with reference to our new findings obtained with the HRP method in monkeys.
The author investigated first the clinical significance of so-called “Gerstmann syndrome” and secondly the anatomoclinical correlation between Gerstmann syndrome and left angular gyrus lesion. Conclusions obtained are as follows : 1) Gerstman syndrome may not necessarily homogeneous. This point has already been indicated by many authors. 2) Left angular gyrus lesionmight not be necessary and sufficient condition of manifestation of the Gerstmann syndrome, because of existence of cases with angular lesion without Gerstmann syndrome and of cases without angulra lesion with Gerstmann syndrome. However, it is not doubtful that almost all cases of Gerstmann syndrome have left parietooccipital lesions including angular gyrus. 3) Why bilateral asomatognosia (Gerstmann syndrome and autotopagnosia) do appear with dominant parieto-occipital lesions is the problem which may be worth while to reexamine from neuropsychological point of view. 4) A few cases reported of Gerstmann syndrome with frontal lobe lesions may suggest the presence of certain roles played by frontal lobe in somatognosic and spatial-gnostic processes, in contrast to that played by parietal lobe. We must investigate in the future this difficult problem which remains unsolved.
Five cases of alexia with agraphia were reported. Analysis of symptoms showed that the syndrome can be independent of aphasic disturbance on the one hand and of alexia without agraphia on the other. Alexia in the syndrome is characterized by (1) preserved visual capacity of graphem perception, (2) tendency to read by impression witout analytical correction and (3) lack of kinesthetic facilitation. Agrahia is characterized by (1) preserved graphem output capacity. This is reflected by their attitude of letter copying. They would write down model letters according to their own penmanship even when they could not read the model letters. They never copied the models like non-meaningful letters as in the case of alexia without agraphia. It is also characterized by (2) presence of paragraphia. and (3) hesitancy and lack of confidence in spontaneous writing. Thus it seems that visual system, motor system of writing and auditory linguistic system are all preserved. What is at fault is an integrative process of these three functions. Lesions detected by CT scan all converged into an area of temporo-parieto-occipital junction of the left hemisphere. All were situated in the deep white matter. They cannot be attributed to a certain gyral area. i. e. angular gyrus.
Three cases of cerebral infarction were described with special references to the neuropsychological symptoms due to “minor cerebral hemisphere” damage. In each case, low density area relatively restricted to the right posterior parietal region, involving angular gyrus and its closely surrounding regions, was disclosed on CT scan. Visual disorientation, unilateral visual spatial agnosia, visual constructonal disability caused by hemineglect, and hemiasomatognosia were the neuropsychological symptoms noted in these three cases. The author discussed these symptoms and suggested that the observations of these cases seemed to support the generally accepted hypothesis, that the lesions of the right cerebral hemisphere, localized to the posterior parietal region were responsible for the development of most of the symptoms of so called the syndrome of “minor hemisphere” damage. These neuropsychological symptoms were slight and / or transitory in these three cases. It is likely that the more widespread lesions are necessary for the development of severe and lasting impairment.
Two cases with markedly constricted visual field defect nearly except macular vision due to acute carbon monoxide poisoning have had no trouble in daily life such as riding on a bicycle or catching a ball during about past eighteen years from the accident in 1963. Their visual capacities were cinematographically analysed and with EOG. The both patients were able to “see” objects in movement and moreover to reach their hands to the static targets in the peripheral “blind” field presented from the back of them. CT findings showed or suggested prdominately bilateral parietal lobe lesions. It is infered from the clinical facts that they are compensated the loss of vison with old primitive extrageniculostriate visual system, especially in reaching the hand to the static target in the blind field, though occipital lobe might possibly facilitate the visual function in seeing objects in movement. We have also discussed Balint's syndroms and optic ataxia in constrast with the above-mentioned cases.
A typical case of nonaphasic misnaming (Weinstein and Kahn) was reported. The patient, 65 year-old right-handed male, suffered from right putaminal hemorrhage exibiting left hemiplegia. A month after the stroke, a difficulty in object naming was developed. Paticularly, he showed a selective difficulty in naming things related to his illness such as doctor, nurse and medical instruments. There were marked neologims and perseverations. His spontaneous speech was fluent,and articulation, comprehension, repetition, reading and writing were normal. At the same time, he showed marked denial of his illness and marked cofabulation as seen in Korsakoff's syndrome, though he was fully alert and not amnesic. There was neither unilateral spatial neglect nor hemiasomatognosia. The lesion confirmed by CT scan was in the right basal ganglia and in the subcortical white matter extending inferiorly into the right mesial temporal lobe. EEG demonstrated focal slow wave focus in the posterior part of the right hemisphere. It is speculated that nonaphasic misnaming has a common defect with the phenomena such as denial of illness and confabulatory responses. One possible explanation is a disconnection hypothesis proposed by N. Geschwind (1965), in this paticular case, disconnection of the left hemisphere speech area from the right-sided limbic region (the right mesial temporal lobe) and / or from the right parietal lobe. Thus the disconnnected speech zone might be responsible in responding with misnaming, cofabulation and denial of illness.