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Background: The primary goals of this paper are to describe the collection and evaluation of various nonpharmacological treatment options for depressive disorders and to establish a basis for the development of a standard for the treatment of patients with depressive disorders. Method: To identify evidence-based treatment elements, a comprehensive investigation of national and international guidelines was conducted. The extracted guidelines were then assessed with regard to aspects of methodological quality and evidence-based treatment elements. In a further step, specific and systematic literature searches for residual treatment elements were conducted. For the corresponding literature search, a hierarchical approach was chosen in which current guidelines were reviewed first and systematic reviews and meta-analyses second. Psychopharmacological treatments were excluded from the analysis because this is covered by specific guidelines. Results: The treatment elements with an adequate level of evidence were identified as follows: psychotherapeutic interventions, marital/couples/family therapy and counseling, inclusion of family members, psycho-education, exercise, problem solving therapy, guided self-help and behavioral activation treatments. Further evidence-based methods include diagnostic treatment elements, participative decision-making, development of the therapeutic alliance, Cognitive Behavioral Analysis System for Psychotherapy, computerized cognitive behavior therapy, psychopharmacological therapy, combined psychopharmacological and psychotherapeutic therapy, electroconvulsive therapy, phototherapy, sleep deprivation, repetitive trans-cranial magnetic stimulation (rTMS) and acupuncture. Conclusion: In summary, using a hierarchical approach, it was possible to assign different levels of evidence to the various treatment options for depression.

Synaptic activation of γ‐aminobutyric acid (GABA)Breceptors at GABA synapses causes (a) postsynaptic hyperpolarization mediating a slow inhibitory postsynaptic potential/current (IPSP/C) and (b) presynaptic inhibition of GABA release which depresses IPSPs and leads to paired‐pulse widening of excitatory postsynaptic potentials (EPSPs). To address whether these effects are mediated by pharmacologically identical receptors the effects of six GABABreceptor antagonists of widely ranging potencies were tested against each response.Monosynaptic IPSPBs were recorded in the presence of GABAA, AMPA/kainate and NMDA receptor antagonists. All GABABreceptor antagonists tested depressed the IPSPBwith an IC50based rank order of potency of CGP55679CGP56433=CGP55845A=CGP52432>CGP51176> CGP36742.Paired‐pulse EPSP widening was recorded as an index of paired‐pulse depression of GABA‐mediated IPSP/Cs. A similar rank order of potency of antagonism of paired‐pulse widening was observed to that for IPSPBinhibition.Comparison of the IC50values for IPSPBinhibition and paired‐pulse EPSP widening revealed a close correlation between the two effects in that their IC50s lay within the 95% confidence limits of a correlation line that described IC50values for inhibition of paired‐pulse EPSP widening that were 7.3 times higher than those for IPSPBinhibition.Using the compounds tested here it is not possible to assign different subtypes of GABABreceptor to pre‐ and post‐synaptic loci at GABAergic synapses. However, 5–10 fold higher concentrations of antagonist are required to block presynaptic as opposed to postsynaptic receptors when these are activated by synaptically released GABA.

Abstract: Objective: Parasitic infestations are known to elicit T-helper lymphocyte type 2 (Th-2) reactions, characterized by a pronounced eosinophila and high IgE levels. In humans both elevated specific IgE levels and eosinophil counts are associated with resistance to reinfection with schistosomiasis. This study aimed to establish whether the Th-2 reaction could be enhanced with calcitriol (vitamin D3). Calcitriol has been shown to cause a shift from Th-1 to Th-2 type reactions when applied locally to the skin. Methods: Fifty-nine patients with Schistostomahaematobium infection were randomized to one of four treatment modalities, i.e. (a) praziquantel (PZQ) 60 mg · kg−1 orally on day 1, (b) PZQ 60 mg · kg−1 on day 1 plus calcitriol 1 μg per day orally for 5 consecutive days, (c) calcitriol 1 μg per day for 5 consecutive days or (d) placebo. Blood for differential counts, eosinophil cationic protein (ECP), specific IgE and IgG to whole-worm antigen, as well as urine samples for egg counts, were collected on days 0 and 21. Results: Baseline values did not differ significantly between the groups. Calcitriol alone resulted in significant increases in circulating lymphocytes (median increase of 5.5%) and the percentage of eosinophil vacuolization (mean increase 28%). It, however, significantly decreased ECP levels (mean decrease 46%). PZQ in combination with calcitriol significantly enhanced production of specific IgE (mean increase 213%) and IgG (mean increase of 170%) and tended to increase eosinophil vacuolization (mean increase 22%). All these changes also differed significantly from those in the placebo group. The specific IgE and IgG levels were also significantly higher than the already increased levels seen with PZQ treatment only. ECP levels were, however, not significantly affected by combination therapy, whereas PZQ alone significantly enhanced ECP production (mean increase 93%). Conclusions: The increases in specific IgE responses and percentage of eosinophil vacuolization favour a Th-2 type of reaction. The ECP values viewed in isolation may, paradoxically, indicate a Th-1 response; this could, however, have been an artefact due to the method of ECP detection ex vivo. Finally, it would seem that calcitriol does cause some immune augmentation when combined with PZQ therapy in patients with schistosomiasis. However, long-term follow-up is needed to prove that these findings would translate into resistance against reinfection.

Summary Vincamine, hydergine and piracetam are used for the treatment of memory disturbances as well as for the treatment of various other brain dysfunctions seen in the elderly patient.

The locus coeruleus is one of the most thoroughly investigated mammalian brain areas. Its fibers innervate large parts of the neuraxis, in particular, areas involved in cognitive functions such as the cortex and the hippocampus. A role of locus coeruleus has been proposed in such processes as memory, the control of vigilance, blood pressure and others. Results obtained in this and other laboratories demonstrate that the firing rate of locus coeruleus neurons is affected by a great number of psychoactive agents such as antidepressants, minor tranquillizers, neuroleptics, psychostimulants and certain psychogeriatric drugs. We have attempted to correlate the data obtained on the cell bodies of locus coeruleus with studies reporting effects on terminal areas and thereby gain an overall view of the action of the above mentioned drugs on this cell system. The activity of noradrenergic neurons in locus coeruleus is thought to correlate with the level of cortical vigilance. Special emphasis is placed on the finding that a number of drugs which exert a positive effect on cognitive functions in man and animals increase the firing rate of the rat locus coeruleus neurons.