Explaining the Antidepressant Effect
December 19, 2011
In addition to blog postings related to the business of psychotherapy and psychiatric practices I occasionally address clinical matters here. I have found the information in this piece to be very useful in offering a plausible explanation of how antidepressants work and the expected time course of that effect. Providing this information is good for the patient’s treatment and for your business.
I tell my patients about at least two mechanisms of action – an early calming, likely due to amygdalar modulation (a simmering down of the brain’s threat assessment circuitry) and a later one entailing improving mood, sleep, and functioning in general due to the gradually increasing concentration of BDNF – brain derived neurotrophic factor – which promotes neurogenesis and a “healthier” functioning brain, especially the massive network of dendritic trees.
From “Stress, Depression, and Neuroplasticity: A Convergence of Mechanisms” published in Neuropsychopharmcology Review we read:
“Increasing evidence demonstrates that neuroplasticity, a fundamental mechanism of neuronal adaptation, is disrupted in mood disorders and in animal models of stress. There is evidence that chronic stress, which can precipitate or exacerbate depression, disrupts neuroplasticity, while antidepressant treatment produces opposing effects and can enhance neuroplasticity. We discuss neuroplasticity at different levels: structural plasticity (such as plastic changes in spine and dendrite morphology as well as adult neurogenesis), functional synaptic plasticity, and the molecular and cellular mechanisms accompanying such changes. Together, these studies elucidate mechanisms that may contribute to the pathophysiology of depression. Greater appreciation of the convergence of mechanisms between stress, depression, and neuroplasticity is likely to lead to the identification of novel targets for more efficacious treatments.”
Antidepressants help our patients in many ways. I will discuss other proposed mechanisms of action in later postings. A more sophisticated understanding of their mechanisms of action will help us combat what I heard an imminent psychoanalyst say at a dinner gathering of other analysts – “My God, patients there (a local psychiatric residency program) are more likely to get Prozac than psychotherapy!” This was an old greybeard spouting dogma. This position now should be considered malpractice. Certainly Freudian psychotherapy was a tremendous advance over applying electrical shocks to hysterical patients but that was such a long time ago.
More accurately, antidepressants – given that there are indications for their use and the patient can tolerate the possible adverse effects – can quickly begin the process of helping our patients move out of the dark pit of depression. They work quickly but the full bloom of their effect takes several weeks. And understanding the various ways they effect our patients’ brain and social functioning will help us more convincingly inform and engage them.
So – What do you tell your patients about how these medications can help them?