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Section of Neurology, Mayo Clinic Scottsdale, Scottsdale, AZ.
Five somatosensory cortices have distinctive somatotopic representations, cytoarchitecture, and connectivity: primary somatosensory cortex (SI), ventrolateral association cortices (SII, SIII, and SIV), and dorsomedial association cortex (supplementary sensory area). Patients with focal lesions of ventrolateral (n = 5) and dorsomedial (n = 6) somatosensory association cortices (SACs) and hemiparetic (n = 8) and neurologically normal control patients (n = 14) underwent detailed somesthetic testing that encompassed basic, intermediate, and complex (tactile object recognition) somesthetic functions. Dorsomedial lesions acutely caused severe disruption of somesthetic processing and severe apraxia when the area of damage was extensive and involved anterior and posterior cortices. In contrast, ventrolateral lesions caused tactile agnosia. Chronically, sensorimotor function following dorsomedial damage improved considerably. Tactile agnosia following ventrolateral damage, however, was readily detectable for years following onset. Functional differences between ventrolateral and dorsomedial SACs may reflect parallel processing in dual somatosensory systems.
Presented in part at the 44th annual meeting of the American Academy of Neurology, San Diego, CA, May 1992.
Address correspondence and reprint requests to Dr. Richard J. Caselli, Section of Neurology, Mayo Clinic Scottsdale, 13400 E. Shea Boulevard, Scottsdale, AZ 85259.
Supported in part by a grant from the Mayo Foundation.
Received April 8, 1992. Accepted for publication in final form August 12, 1992.
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