Mood, Motility and 17-Hydroxycorticoid Excretion; A Polyvariable Case Study

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Abstract
Since the initial observations of a relationship between depression and an increase in urinary adrenal glucocorticoids in psychiatric patients by Reiss (1953) and Rizzo et al. (1954), there have been a number of studies confirming this relationship using various chemical techniques (Board et al., 1957; Bunney et al., 1964 and 1965; Gibbons, Gibbons, Maxwell and Wilcox, 1960; Gibbons and McHugh, 1962; Gibbons, 1964; Kurland, 1964a and 1964b; Pryce 1964). One of the questions that immediately comes to mind in reviewing this work has to do with the specificity of this relationship. Perhaps the rise of urine corticoids in depression is a non-specific response to disturbance, as has been demonstrated in various forms of psychological stress (Hamburg, 1962) and in severe psychiatric disturbances such as acute schizophrenic episodes (Sachar et al., 1963). On the other hand it is tempting to hope that there may be a more specific relationship demonstrable between the complex psychobiological phenomenon of depression and some kind of neuroendocrine activation analagous to a syndrome like “periodic hypothalamic discharge” (Wolff et al., 1964). This syndrome is manifested by periodic episodes (lasting several days) of withdrawal and depression associated with marked elevations in 17-hydroxycorticoid excretion. Mandell et al. (1963) have recently demonstrated that subthreshold stimulation of limbic sites intimately related to hypothalamic modulation produces marked changes in plasma 17-hydroxycorticoids in man. Limbic areas have been related to affectual phenomena on a speculative basis since the classical papers of Papez (1937).