at Austin and the Austin Neurological Clinic Studies of corpus callosum dysfunction in schizophrenia have typically relied on measures that reveal impairment in commissurotomy patients, but measures that distinguish people with callosal agenesis may be more appropriate. Four of these indexes were included in the present study. Tests of associated movements, cross-localization of touch, interocular transfer of spiral aftereffect, and transfer of blind formboard learning were administered to 18 chronic schizophrenics, 19 schizoaffectives, and 20 normal volunteers. Both schizophrenics and schizo-affectives were impaired on all measures except transfer of blind formboard learning. Schizophrenics also made significantly more associated movements than schizo-affectives and exhibited a different pattern of cross-localization deficit. These results support the hypothesis of developmental callosal dysfunction in schizophrenia and schizo-affective disorder, although the nature of this dysfunction differs in part from that exhibited by acallosals.Several studies have indicated that two related functions of the corpus callosum, conduction and inhibition of nerve impulses, may be disrupted in schizophrenics. Tress, Kugler, and Caudrey (1979) and Jones and Miller (1981) compared contralateral and ipsilateral somatosensory-evoked potentials (SEPs) in schizophrenics and in normal people (normals). Normals' SEPs from the ipsilateral cortex were delayed relative to their contralateral responses. Jones and Miller attributed this delay to the predominance of contralateral pathways in the normal brain, which cause ipsilateral potentials to be produced by crossing over the callosum and then back to the original hemisphere. Because only one crossing is required for contralateral SEPs, they show a reduced latency relative to ipsilateral responses in normals. In contrast to the normal pattern, both of the aforementioned studies found that schizophrenics' ipsilateral and contralateral SEP latencies were identical, implying that ipsilateral responses were being produced by ipsilateral pathways. Absence of an ipsilateral latency delay may thus be secondary to impaired callosal conduction in the schizophrenic subjects, which in turn may be related to failure of ipsilateral pathway inhibition.Gulman, Wildschiodtz, and Orbaek (1982) also found a significantly reduced latency delay between contralateral and ipsi-This study was completed in partial fulfillment of the requirements for Suzanne Craft's doctoral degree from the University of Texas at Austin.