Therapy of Depressive Illness

The term depression is used for a variety of states that are characterized by downswings in mood varying from slight to most severe. The principal types are  

It would be a major therapeutic error to administer a drive-enhancing drug such as amphetamine to a depressed patient with psychomotor inhibition (A). Suicide would be an expected consequence. 

The antidepressant effect of thymoleptics manifests after a prolonged latency usually 1-3 weeks pass before subjective or objective improvement becomes noticeable (A). In contrast, somatic effects are immediately evident specifically, the interference with neuronal transmitter/modulator systems (norepinephrine, serotonin, acetylcholine, histamine, dopamine). Reuptake of released serotonin, norepinephrine, or both is impaired (— elevated concentration in synaptic cleft) and/or receptors are blocked (example in A). These effects are demonstrable in animal studies and are the cause of acute adverse effects. 

The importance of these phenomena for the antidepressant effect remains unclear. Presumably, adaptation of receptor systems to altered concentrations or actions of transmitter/modulator substances plays a role. 2005 Thieme and conditions of license. 

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CINP Task Force Impact of neuropharmacology in the 1990s strategies for the therapy of depressive illness. Eur. Neuropsychopharmacol. 3. 153-156, 1993. 

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