Anatomical Asymmetries in the Adult and Developing Brain and their Implications for Function

Abstract

The left cerebral hemisphere is dominant for language function. Thus, lesions involving this hemisphere in children and adults are more likely to cause disorders in language function than the same or even larger lesions in the opposite hemisphere. Lesions that interfere with language tend to be clustered around the Sylvian fissure. Two regions appear to be especially important: one in the posterior frontal opercular area, the other in the posterior third of the superior temporal gyrus and adjacent parietal operculum. Lesions in other language regions that occupy more posterior portions of the inferior parietal lobule appear to result in disorders of written language; supplementary motor and sensory areas located on the medial portion of the left hemisphere surrounding the cingulate gyrus appear to influence spontaneous language activity. Finally, lesions in the left posterior pulvinar may also produce short-lived aphasic disturbances. The brain exhibits both gross anatomical and microscopic asymmetries in the region of the language areas. Sylvian fissure asymmetries suggest a greater development of the posterior temporal region and of the parietal operculum on the left. The greater development of the left posterior temporal region is also illustrated by a larger posterior upper surface (planum temporale) on that side. Furthermore, the anterior speech area on the frontal operculum may be more convoluted and therefore larger on the left. Asymmetries in the Sylvian fissures and in the relative widths of portions of the hemispheres can be demonstrated during life by radiologic means. Gross anatomical asymmetries appear to reflect side differences in areas of distinctive microscopic structure (architectonic areas) and function. Thus, in the posterior speech area the auditory field Tpt is larger on the left, and in the frontal lobe an opercular motor field is also larger on the left. Area 39, an inferior parietal association cortex, may be thicker on the left side, and its corresponding thalamic projection nucleus, nucleus lateralis posterior, is also larger on the left. The normally occurring asymmetry may be altered in pathology and pathological lesions may be asymmetrically distributed. Thus, the analysis of a brain of a dyslexic patient has disclosed an abnormally large left hemisphere as well as cortical malformations restricted to the left side of the brain. Later-alized abnormalities may occur in other disease entities and may be linked to genetic abnormalities, as evidenced by the familial occurrence of some dyslexias as well as of similar brain malformations. On the other hand, lateralized abnormalities may result from early lesions, as illustrated by limb malformations in rats and reversals of habenular asymmetries in newts. Lateralized limb malformations with a male preponderance also occur in man, although genetic or environmental factors have not been identified. Finally, lateralized malformations in fiber connectivities may be the result of early lesions in the brain, as shown by experimental data from fetal monkeys and newborn hamsters. Thus, knowledge of functional and structural lateralization of the human brain has begun to play an increasingly important role in our understanding of the neurologic bases of normal language function and of some disorders of functional lateralization of which developmental dyslexia is an example. Future improvements in the anatomical model of language and related functions will come from additional studies of anatomical lateralization. It is likely that anatomical lateralization results from genetic and prenatal environmental influences, and that a clearer picture of the factors leading to normal and abnormal manifestations of asymmetry will come from animal models of lateralization. Until recently, lateralization in function has been thought to be an exclusively human trait. However, animal models appear to be emerging with the discovery of functional lateralization in rats35, 67 and monkeys.61 Furthermore, the effects of early lesions on recovery and laterality are under current investigation in these animal models.36, 66 Finally, the possible identification of intrauterine environmental insults leading in some manner to abnormalities in lateralization of structure and function provide additional hope for improvement of our ability to prevent and treat disorders of brain asymmetry.