Ever since Freud, the couch has been viewed as an important--some would argue essential--component of psychoanalysis. Although many theoretical papers and case reports have addressed the use of the couch in psychoanalysis, no empirical study has investigated its effect on psychoanalytic process or outcome. After a review of the literature, a number of research designs are proposed that might be used in such an investigation. Finally, preliminary empirical data are presented from archived audiotapes of two psychoanalyses: one in which the patient switched from lying down to sitting up, and one in which the opposite occurred. The aim is to stimulate research-oriented psychoanalysts to undertake empirical investigations of the theoretical concepts underlying use of the couch and, more generally, to present a specific example of research as a paradigm for a broader research agenda for empirical investigation of the key theoretical ideas underlying psychoanalysis.
Though maternal treatment with thyrotropin-releasing hormone (TRH) for prevention of hyaline membrane disease has been utilized, precise mechanisms of TRH in accelerating fetal lung maturation remain unclear. We studied the effect of maternally administered TRH or DN1417 (an analog of TRH) on functional and morphologic fetal rabbit lung maturation and the duration of survival after premature delivery. Because DN1417 retains the neurotransmitter but not the neuroendocrine effects of TRH, this study enables us to determine which of these effects was responsible for enhancement of lung maturation. TRH or DN1417 (0.2 mg/kg/dose) or saline was injected intravenously into New Zealand White rabbit does 48, 36, 24, 12 and 2 h prior to sacrifice on day 27 of gestation. Functional pulmonary maturity was assessed by pressure-volume hysteresis, and morphologic maturity was assessed by histologic techniques. Maternal administration of TRH or DN1417 enhanced both functional and morphologic fetal lung maturation as well as the duration of neonatal survival after premature delivery. We propose that the effect of TRH in fetal lung maturation is due to neurotransmitter rather than neuroendocrine effects.
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