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Notes
It will perhaps strike the reader as curious that Goldstein should have embraced so classical an approach. I have discussed more fully elsewhere Goldstein’s position in the history of aphasia (Geschwind 1964a) but can only comment here that he was in fact much more of a localizationist than is generally appreciated. His theoretical writings with their criticisms of classical ideas contain so many qualifications that they are often compatible with even the most extreme localizationist views. The reader who goes carefully through the “Special Part” of Goldstein’s 1927 monograph will repeatedly find in it an active defence of many classical ideas; indeed, many of Goldstein’s disagreements with other authors are primarily on details of localization. His later book on language (Goldstein 1948) continues to show his acceptance of many classical ideas, especially in his discussion of particular syndromes.
In the monkey there appears to be a bundle which is homologous to this structure in the rabbit and which perforates the splenium of the corpus callosum. There is, however, some question as to whether the bundle even in the rabbit does indeed rise in the visual cortex; for the monkey the site of origin of the corresponding tract is unknown, and it is certainly possible that it arises from retrosplenial cortex or from areas 18 or 19 on the medial surface. It is conceivable that this bundle may run directly from the visual cortex to the hippocampus in the rabbit while in higher forms these connexions must be made by way of association cortex. The analysis by Pribram and MacLean (1953) of the connexions of the mediobasal cortex of the monkey presents ample evidence for indirect pathways which could lead along the medial surface of the hemisphere from visual cortex to visual association cortex, hippocampal gyrus and hippocampus.
Petr et al. use the term “fusiform gyrus” for areas TF and even TH in the macaque. Bonin and Bailey (1947) note the great similarities of TF and TH. Papez (1929) uses the term “fusiform-hippocampal gyrus” and “pyriform area” for these two regions. It is likely that the fusiform gyrus in the human sense is not present in the monkey and that these two areas are probably most reasonably considered as hippocampal gyrus (now called parahippocampal gyrus by some authors). Whitlock and Nauta (1956) in reporting the results of Petr et al. substitute the term “hippocampal gyrus” for “fusiform gyrus” and we will follow their usage.
I use this term advisedly rather than “loss of visual discriminations.” The subsequent theoretical discussion will make the reason for this choice of words clear.
These elementary results have an important bearing on the question of cross-modal associations. Recent studies, e.g. those of Ettlinger and different co-workers have clearly demonstrated difficulties of tactile-visual or visual-auditory transfers in monkeys (Burton and Ettlinger 1960; Ettlinger 1961). The conclusion should, however, not be drawn that monkeys form no cross-modal associations. It is abundantly clear, in fact, that the majority of classical learning experiments with most organisms do in fact demonstrate formation of cross-modal associations, as long as the modality to which the association is made is a “limbic” modality, i.e. a reinforcer, such as food, water, etc. I will return to the question of the difficulty of transfer between “non-limbic” modalities at a later point.
The authors state that they ablated “areas 18 and 19,” but it is possible from their diagram that part of the association cortex posterior to the lunate sulcus was preserved. Bonin and Bailey (1947) place OB behind the lunate sulcus and Crosby et al. (1962) show area 18 as behind the lunate sulcus. It is not unlikely that some of area 18 was spared in the Ades and Raab experiments.
Since the writing of this section it has been called to the author’s attention that other experimenters have had results different from those of Downer. It will be important to ascertain the reasons for these discrepancies.
Meyer and Yates (1955) showed that patients with left temporal lobe lesions are likely to have verbal recall difficulties. Milner (1962) has confirmed their findings, showing that left anterior temporal lobectomy has a more profound effect on verbal memory than similar right temporal lobectomies. It is quite likely that the reason for this is that left temporal lobectomy cuts of connexions between the posterior speech area and the limbic system and thus leads to verbal learning deficit.
This mechanism for incomprehension of spelled words appears to Dr. Howes and myself to be more simply and more clearly based physiologically than the classical explanation, which simply invokes a new disturbance, “word-sound deafness,” to account for incomprehension of spelled words. By any standard the term “word-sound deafness” is a poor one. “Letter-name deafness” would have been closer to being a correct description. “Inability to understand words spelled orally” is the best descriptive term.
I am indebted to Sir Charles Symonds for having called Vialet’s monograph to my attention. It was in fact his paper (Symonds 1953) which alerted me to this interesting syndrome. I am also grateful to him for having read and criticized an earlier paper of mine on this topic.
It may be objected that the alexia in a half-field from a right parietal lesion is the result of “neglect” of that field. While I do not wish to discuss this problem extensively here, I would like to point out that what I am attempting to show is that one mechanism of “neglect” of a normal left visual field is disconnexion of the normal right occipital cortex from the speech area.
In an illiterate society a lack of visual-auditory associations would not seriously inconvenience anyone except in unusual situations; literacy makes this ability highly important. Other cross-modal association deficits may exist but might never be detected because they cause so little disturbance. It is conceivable that direct visual-tactile associations may be as badly developed in many humans as they appear to be in monkeys (Ettlinger 1960) but only specific testing will bring this out. It is important, of course, to study children as early as possible in the course of development.
These authors also found another group of parietal areas which responded to click with only slightly longer latency than the primary auditory region. They presented evidence that the response in these areas depended on collaterals from the medial geniculate body. These areas would not in my terms be “association” areas. I will not discuss their possible function here.
It should be added that the second temporal gyrus of man appears to be a phylo-genetically very late region of whose connexions we know very little. It may be a region of great importance and it is conceivable that the view of Wernicke’s area presented above is too narrow. I would, however, disagree with those authors who include in Wernicke’s area all the posterior regions involved in speech in both the temporal and parietal lobes.
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This article has been re-typeset for clarity but the content is unchanged from the original version published as Geschwind, N. (1965). Disconnexion syndromes in animals and man. I. Brain 88:237–294. Copyright 1965 by The Oxford University Press.
From the Aphasia Research Section, Neurology Service, Boston Veterans Administration Hospital and the Department of Neurology, Boston University Medical School. This work was supported in part by a grant (MH 08472, Professor Davis Howes, Principal Investigator) from the National Institutes of Health to the Boston University Medical School.
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Geschwind, N. Disconnexion Syndromes in Animals and Man: Part I. Neuropsychol Rev 20, 128–157 (2010). https://doi.org/10.1007/s11065-010-9131-0
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DOI: https://doi.org/10.1007/s11065-010-9131-0