Abstract
Agenesis of the corpus callosum results from partial or total failure of callosal axons to cross the midline during the first trimester of fetal development (Rakic and Yakovlev, 1968; Rauch and Jinkins, this volume). Although the resulting structural modifications of the brain are shared by all cases, the clinical expression of this malformation seems to depend on the extent of concomitant pathology of the nervous system (e.g. O’Brien, this volume; Wisniewski and Jeret, this volume). In most cases some neurological dysfunction can be observed. At the cognitive level there seems to exist, as would be expected, a strong relationship between the severity of co-existing CNS defects and level of functioning. Especially affected are those with multiple malformations, such as in Aicardi syndrome (Aicardi and Chevrié, this volume) and other syndromes described in this volume (see Andermann and Andermann; Geoffroy, Wisniewski and Jeret). Recent MRI studies by de Léon et al. (1987) and Atlas et al. (1986) have revealed extensive abnormalities of limbic structures, including absence of the hippocampal formation in some cases, and it has been suggested that these subcortical malformations may be at the basis of the mental deficiencies found in so many syndromes that include callosal agenesis (de Léon et al., 1987).
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Sauerwein, H.C., Nolin, P., Lassonde, M. (1994). Cognitive Functioning in Callosal Agenesis. In: Lassonde, M., Jeeves, M.A. (eds) Callosal Agenesis. Advances in Behavioral Biology, vol 42. Springer, Boston, MA. https://doi.org/10.1007/978-1-4613-0487-6_23
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