Posterior Callosal Infarction: Clinicopathological Correlations

Abstract

Clinicoanatomical observations on a patient with partial interhemispheric disconnection associated with complete ischaemic destruction of the splenium and of the posterior part of the body of the corpus callosum are presented. Neuropathological examination of the areas containing degenerated white matter indicated that the lesions affected the transcallosal fibres that link the cortex of the occipital lobes and the superior parietal lobules (SPL). The white matter situated in the temporal lobes was intact. This suggests that in man, and contrary to what has been described in the monkey, the callosal pathway followed by the temporal fibres is rostral to the one followed by the parietal or at least by the SPL fibres. The most prominent disconnection syndrome elements were left tactile anomia (in spite of a rather good tactile-motor integration between the hemispheres), left visual anomia, agraphia of the left hand and 'diagnostic' apraxia. The fact that the anterior part of the corpus callosum was intact accounts for the preservation of interhemispheric transfer of somatic sensory information and for the absence of left extinction during the dichotic listening test. An attempt is made to give a more detailed explanation of the results obtained during the different tests.

Somesthetic Disconnection Syndromes in Patients with Callosal Lesions

“…There were no deficits in either our cases or the case reported by Degos et al [10]in the transfer of simple joint-position sense involving a single joint, which might also be consistent with the findings of McCloskey [3], suggesting that simple joint-position sense could be transferred via subcallosal connections. The preservation of the transfer of directional cutaneous kinesthesia in cases 2 and 3 in our study suggests that it might also be transferred through pathways other than in the corpus callosum.…”

“…The cases reported in the literature with unilateral tactile anomia and/or somesthetic alexia showed a similar tendency [9, 10, 12, 13], suggesting that the somesthetic information necessary for tactile naming and somesthetic reading might pass via portions of the corpus callosum quite close to the regions via which the more basic discriminative sensations are transferred. Cases 1 and 2 in our study, and the cases with unilateral tactile anomia reported in the literature [9, 10, 12, 13]shared a common lesion site, the posterior truncus. Cases 1 and 2 in our study, and the cases reported in the literature with unilateral somesthetic alexia [12, 20]also demonstrate the importance of the posterior truncus.…”

“…Stereognosis, recognition of a solid object by active touch, might also require the transformation of compound somatosensory information into spatial images. Dimond et al [9], Degos et al [10], Habib et al [12]and the authors investigated pure stereognosis using controlled materials such as wooden blocks and geometrical forms, and the results suggest that such pure stereognosis might also be transferred via the corpus callosum. Cases with callosal lesions who exhibit transfer deficits of hand posture [10, 12, 13]and/or stereognosis [9, 10, 12], including cases 1 and 2 in our study, most commonly have lesions in the posterior truncus of the corpus callosum, suggesting that this callosal part might be important for the interhemispheric transfer of hand posture and stereognosis.…”

Examination of the split fovea theory in a case of pure left hemialexia

“…This pathway goes through the splenium of the corpus callosum, possibly its most ventral segment (Suzuki et al, 1998), and over the lateral ventricles (Molko et al, 2002). Several patients have been described with a left hemialexia, either accompanied by a left visual anomia (see Gazzaniga, Bogen, & Sperry, 1965) or pure, without deficits in naming objects in the LVF (Abe et al, 1986;Binder et al, 1992;Cohen & Dehaene, 1996;Damasio et al, 1980;Degos et al, 1987;Habib et al, 1990;Lausberg et al, 1999;Levine & Calvanio, 1980;Maspes, 1948;Sidtis et al, 1981;Sugishita et al, 1978Sugishita et al, , 1986Suzuki et al, 1998;Trescher & Ford, 1937;Wechsler, 1972). Most such patients had a lesion of the splenium of the corpus callosum.…”

“…Left hemialexia is invariably observed following posterior callosal lesions (Abe, Nakamura, Sugishita, Kato, & Iwata, 1986;Binder et al, 1992;Cohen & Dehaene, 1996;Damasio, Chui, Corbett, & Kassel, 1980;Degos et al, 1987;Habib, Ceccaldi, & Poncet, 1990;Lausberg, Göttert, Münßinger, Boegner, & Marx, 1999;Levine & Calvanio, 1980;Maspes, 1948;Sidtis, Volpe, Holtzman, Wilson, & Gazzaniga, 1981;Sugishita, Iwata, Toyokura, Yoshioka, & Yamada, 1978;Sugishita, Yoshioka, & Kawamura, 1986;Suzuki et al, 1998;Trescher & Ford, 1937;Wechsler, 1972). Patients with left hemialexia typically show impaired reading of LVF words, contrasting with a perfectly normal performance with RVF words.…”