Five years ago, I reviewed some of the scientific literature on the neuroplasticity model of depression – a fascinating new way to think about mood disorders. Departing from the earlier, monoamine-based ideas – too little serotonin or dopamine – this model suggests that depressive states are associated with a reduction in the brain’s ability to change in response to experience. In my earlier review of neuroplasticity, I described how our brains are not fixed organs but are instead constantly changing in response to novel information and new learning. These changes involve strengthening or weakening of synaptic connections along with growth or shrinkage of neurons. In health, there is a constant growth, sculpting and refinement of neural pathways. This plasticity becomes impaired in depression: the brain becomes less malleable, there is reduced new learning and people become trapped in despair. The neuroplasticity model is a radically different way of thinking about mood disorders. What follows is an update on research on this area, which has focused on several major developments. These include the following: 1) investigations of brain plasticity based on visual evoked potentials (VEPs); 2) the use of learning and memory tests to evaluate structural change in the CNS and; 3) emerging research on the impact of antidepressants on neuroplasticity.
Continue reading » “Ch-Ch-Ch-Ch Changes! What Causes Depression and How Do Antidepressants Work, Part II”
We start with a powerhouse team of neuroscience researchers at the University of Wisconsin: Giulio Tononi and Chiara Cirelli. These two have been wrestling to understand the basic function of mammalian sleep: why do we do it? What critical functions does it serve? In 2003, using a collection of EEG, fMRI and some behavioral memory data, they formulated a new theory on the role of sleep: The Synaptic Homeostasis Theory, or SHY, for short . This theory asserts four main points:
Continue reading » “Neuroplasticity: What’s Sleep Got to Do with It?”
The connection between physical ailments and mood is not a new one. It is well-established that medical illness, ranging from infections to cardiovascular disease, can result in increased symptoms of depression, while depression can predispose people to become physically sick more often. Now, a growing body of evidence shows that depression and physical illness have something important in common: inflammation.
Continue reading » “Can Anti-inflammatory Drugs Treat Depression? Some Promising New Evidence But Not Yet Enough”
Many of us of a certain age will never forget the sage, one-word piece of occupational advice given to Benjamin Braddock in the movie, The Graduate: “Plastics.” In the early 1960’s, plastics were thought to be the next big area of economic growth. Benjamin, as we all remember, takes in this recommendation with alienated befuddlement. However from the vantage point of 21st century psychiatric research, this advice may have been unwittingly prescient.
Continue reading » ““Plastics””
The greater our understanding of an illness state, the better we are able to treat it. As one of the core disorders in our practice, we constantly review and update our knowledge on ADHD. In the course of a recent review, I came across a wonderful compilation issue on ADHD in Biological Psychiatry (Biol Psychiatry June 15 2011, vol. 69). The review issue covers a wide range of topics from psychostimulants as cognitive enhancers to the molecular genetics of ADHD. The most relevant and clinically applicable article, however, was Amy Arnsten’s paper on “Catecholamine Influences on Dorsolateral Prefrontal Cortical Networks” (Biol Psychiatry. 2011 June 15;69(12):e89-99). She does a masterful job of presenting complex material in a clear and elegant manner. Dr. Arnsten is able to capture the fluidity and dynamics of cortical functions associated with ADHD while still giving the reader anchor points that are useful in everyday clinical practice.
Continue reading » “Fine-Tuning our Understanding of the ADHD Brain”
The single most important research study in the past year in the area of clinical therapeutics of bipolar disorder was conducted by Geddes and colleagues at Oxford University in England. Using a randomized open-label design (no placebo control group and subjects knew which medications they were receiving), the BALANCE study sorted 330 subjects with bipolar disorder type I into three treatment groups: lithium alone, valproate (Depakote) alone, or combination treatment with both lithium and valproate. The outcome measures were time to recurrence of a major mood episode, either mania or depression. The study design allowed for an extended, two year follow-up on these subjects. This time frame allows for meaningful assessment of genuine prophylactic effects. The results found that combination therapy was most effective, marginally more so that lithium alone, but significantly greater than valproate monotherapy. The interpretation of the data supports the unique efficacy of lithium as the single-most effective mood stabilizer available.
Continue reading » “New Wonder Drug Remarkably Effective in Bipolar Disorder: Lithium (Yes, Lithium).”
In the past several years, two new studies have been published examining the efficacy (in pristine, experimental conditions; rigorous selection criteria, minimal comorbid conditions) and effectiveness (real world variability) of lamotrigine (Lamictal) in the treatment of acute bipolar depression [1, 2]. These and other studies were recently summarized in a review paper by Amann and colleagues in the Journal of Psychopharmacology. Attempting to synthesize disparate findings, Amann concludes that “…the antidepressant effect of LTG in acute bipolar depression, if it exists, is small.”
Continue reading » “Acute Antidepressant Effects of Lamotrigine: More and More Disappointing.”