Electrocorticographic (ECoG) spectral patterns obtained during language tasks from 12 epilepsy patients (age: 12-44 years) were analysed in order to identify and characterize cortical language areas. ECoG from 63 subdural electrodes (500 Hz/channel) chronically implanted over frontal, parietal and temporal lobes were examined. Two language tasks were performed. During the first language task, patients listened to a series of 50 words preceded by warning tones, and were asked to repeat each word. During a second memory task, subjects heard the 50 words from the first task randomly mixed with 50 new words and were asked to repeat the word only if it was a new word. Increases in ECoG gamma power (70-100 Hz) were observed in response to hearing tones (primary auditory cortex), hearing words (posterior temporal and parietal cortex) and repeating words (lateral frontal and anterior parietal cortex). These findings were compared to direct electrical stimulation and separate analysis of ECoG gamma changes during spontaneous inter-personal conversations. The results indicate that high-frequency ECoG reliably differentiates cortical areas associated with receptive and expressive speech processes for individual patients. Compared to listening to words, greater frontal lobe and decreased temporal lobe gamma activity was observed while speaking. The data support the concept of distributed functionally specific language modules interacting to serve receptive and expressive speech, with frontal lobe 'corollary discharges' suppressing low-level receptive cortical language areas in the temporal lobe during speaking.

Primary cultures of purified human cytotrophoblasts have been used to examine the expression of the corticotropin-releasing hormone (CRH) gene in placenta. We report here that glucocorticoids stimulate placental CRH synthesis and secretion in primary cultures of human placenta. This stimulation is in contrast to the glucocorticoid suppression of CRH expression in hypothalamus. The positive regulation of CRH by glucocorticoids suggests that the rise in CRH preceding parturition could result from the previously described rise in fetal glucocorticoids. Furthermore, this increase in placental CRH could stimulate, via adrenocorticotropic hormone, a further rise in fetal glucocorticoids, completing a positive feedback loop that would be terminated by delivery.Corticotropin-releasing hormone (CRH), one ofthe hypothalamic components of the hypothalamic-pituitary-adrenal axis (1, 2), is also present in human placenta, where its synthesis and secretion rise more than 20-fold in the 5 weeks preceding parturition (3, 4). The secretion of glucocorticoids by the adrenal gland of the human fetus also increases markedly during this same period (5), although the manner in which glucocorticoids interact with placental CRH is not known. Defining the nature of this interaction is a prerequisite to determining the role of these hormones in human pregnancy. To examine the effect of glucocorticoids on placental CRH gene expression, we have purified and characterized cultures of human cytotrophoblasts and performed blot hybridization analysis of RNA isolated from cultured cells. METHODSCytotrophoblast Purification and Immunocytochemistry. Full-gestation human placentae were obtained at elective Caesarean section, and cytotrophoblasts were enzymatically dispersed, purified by Percoll gradient centrifugation, and cultured as described (6). For immunocytochemistry, cultures were washed in several changes of cold 0.01 M phosphate, pH 7.4/0.9% NaCl (PBS), and fixed for 10 min in cold acetone/methanol (1:1, vol/vol) or 2% paraformaldehyde in PBS. Slides were air dried and stored at -70°C until immunocytochemistry was performed. Acetone/methanolfixed cells were allowed to react with anti-cytotrophoblast monoclonal antibody 18B/A5 (kindly provided by Y. W. Loke, Univ. of Cambridge) (7). Avidin-biotin-peroxidase (Vectastain, Burlingame, CA) and 0.05% diaminobenzidine (Sigma) were used to localize bound antibody. Paraformaldehyde-fixed cells were allowed to react with a polyclonal anti-placental alkaline phosphatase antiserum (Dako, Santa Barbara, CA) and horseradish peroxidase. All sections were lightly counterstained with Gill's hematoxylin. tTo whom reprint requests should be addressed. 5244The publication costs of this article were defrayed in part by page charge payment. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. §1734 solely to indicate this fact.

PFD, C1 laminectomy, and duraplasty for the treatment of Chiari I malformation may lead to a more reliable reduction in the volume of concomitant hydromyelia, compared with PFD and C1 laminectomy alone. However, there seems to be a subset of patients whose symptoms will resolve and whose hydromyelic cavity will decrease with the removal of bone only. These patients seem to undergo a volumetric increase in the posterior fossa. Further studies are needed to better characterize these patients, to determine which patients with Chiari I malformation are better served with bony decompression only, and which will require duraplasty to resolve their hydromyelia.

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