The expanding role of the minister as community health services develop

Conclusion In summary, we have suggested in this brief discussion that (1) clinical pastoral training has established itself firmly in our culture and will be an important resource in the function of community mental health centers; (2) there will also be need for many clinically trained pastoral ministers who will serve importantly in the prevention of mental illness and promotion of mental health; (3) that standards of training in the clinical pastoral field are very much needed and should be nationally unified and coordinated; and (4) that the Association of Mental Hospital Chaplains might well exercise the leadership in developing a national resurgence of interest in a dynamic religion which will better meet the needs of our people as we move forward in this complex scientific age. For myself, I have no doubt that religion can provide many of the positive elements of good mental health, and I believe that this concept will grow to full maturity in the years ahead.Delivered at Annual Anton T. Boisen Banquet, Association of Mental Hospital Chaplains, Los Angeles, California May 6, 1964.     

A model for narcolepsy.

A model for narcolepsy is developed on the basis of data obtained from brains collected at post mortem from three patients with narcolepsy. The concentration of dopamine, noradrenaline, and serotonin and their metabolites was measured in many brain regions. The number and affinity of the 3-H-spiperone and 3-H-prazocin binding sites was also measured in many of these regions to characterize the D-2 dopamine and alpha-1-noradrenergic receptors, respectively. Evidence for significantly increased serotonin levels and serotonin turnover was found in many brain regions. Noradrenaline turnover was increased in the frontal cortex. DOPAC/DA was significantly reduced in the striatum. The number of D-2 dopamine receptors, however, was markedly increased in this region. The number of alpha-1-noradrenergic receptors was significantly decreased in the frontal cortex and amygdala. Our neurochemical data demonstrating increased NA and 5-HT turnover suggest that locus coeruleus noradrenergic neurones and raphe serotonergic neurones are overactive in narcolepsy. Current evidence posits that increased activity in these neurones depresses the activity of cholinergic pedunculopontine (PP) REM sleep effector neurones. PP neurones project to and stimulate the dopaminergic substantia nigra compacta neurones. Decreased PP activity in narcolepsy, thus, could lead to pontine cholinergic supersensitivity and could also reduce the firing rates of dopaminergic neurones, as the low striatal ratio of DOPAC/DA suggests. An increase in the number of D-2 dopamine receptors in the striatum may result. The reason for the increased activity of the noradrenergic and serotonergic neurones remains to be determined, but immune inactivation of alpha-1-noradrenergic receptors may be the initiating event. Low alpha-1-noradrenergic receptor numbers may account for the chronic drowsiness of narcolepsy. The repeated entry into sleep, and into REM sleep in particular, may represent a homeostatic response to increase these receptor numbers and, thus, to increase alertness. Some therapeutic implications of this model are presented in the discussion.