Posted on Wednesday 4 May 2016
It may seem peculiar, but it makes sense to me. As a young guy in medicine, I was pulled in two directions – research into things we don’t yet know, and the application of things we do know. The former was where my mind naturally headed, but the latter was what gave me a sense of purpose. While it’s only in retrospect, it makes perfect sense to me that I would’ve ended up being a psychoanalytically oriented psychotherapist [n=1 research with a practical application] where every case is something new. Similarly, my retirement fun has been re·search·ing the post-DSM-III psychiatric research where I’ve stayed on the practical side – psychopharmacology, clinical trials, diagnosis. I’ve shied away from the neuro·anatomy, neuro·physiology, neuro·science side of things, I think because I’m not convinced we know enough yet for there to be a practical side to the equation.
The whole of the past decade in psychiatry might be called the Decade of Jumping the Gun.
The fact is that we simply don’t have good enough neuroscience tools yet to allow us to answer the clinically important questions. We just don’t. We might get there eventually but at the moment we are not there.Given which, any attempt to ‘translate’ our primitive neuroscience into clinical practice will be an effort to jump the gun.by Neuroskeptic…
Blood-oxygen-level dependent contrast imaging, or BOLD-contrast imaging, is a method used in functional magnetic resonance imaging [fMRI] to observe different areas of the brain or other organs, which are found to be active at any given time. Its proof of concept was provided by Seiji Ogawa and colleagues in 1990, following an experiment which demonstrated that an in vivo change of blood oxygenation could be detected with MRI. Other notable pioneers of BOLD fMRI include Kenneth Kwong and colleagues, who first used the technique in human participants in 1992.
Neurons do not have internal reserves of energy in the form of sugar and oxygen, so their firing causes a need for more energy to be brought in quickly. Through a process called the hemodynamic response, blood releases oxygen to them at a greater rate than to inactive neurons. This causes a change of the relative levels of oxyhemoglobin and deoxyhemoglobin [oxygenated or deoxygenated blood] that can be detected on the basis of their differential magnetic susceptibility.In 1990, three papers published by Seiji Ogawa and colleagues showed that hemoglobin has different magnetic properties in its oxygenated and deoxygenated forms, both of which could be detected using MRI. This leads to magnetic signal variation which can be detected using an MRI scanner. Given many repetitions of a thought, action or experience, statistical methods can be used to determine the areas of the brain which reliably have more of this difference as a result, and therefore which areas of the brain are active during that thought, action or experience…from Wikipedia…
The fMRI  and the mapping of the human genome  had the bio-medical psychiatrists
peeing in their pants filled with excitement at the turn of the century. And it was pretty exciting. Tom Insel became the Director of the NIMH and announced psychiatry was to become clinical neuroscience. The DSM-5 Task Force tooled up to add biomedical findings to their coming diagnostic manual. A new century and a new psychiatry based on solid brain science was just around the corner. They had already jumped the gun some in the Decade of the Brain [the 1990s], but this time, they forgot the adages, "look before you leap" "don’t count your chickens before they hatch", and dove into the deep end, and ended up with a long chain of disappointments fueling disillusionment and skepticism. So now we’re presented with a big NIMH Study, this time about neural circuits [see weary…].
Already we are seeing multiple approaches to identifying abnormal functional activity in the brain, from functional MRI to in vivo neurochemistry and studies of brain receptors. One approach uses functional imaging to identify differences in regional activity. For instance, evidence from several different approaches implicates circuitry involving ventral, medial prefrontal cortex [Area 25] with major depressive disorder… Individuals with the short allele of the serotonin transporter gene have reduced expression of the transporter and appear to be at a higher risk for developing depression following stressful life events. Recently, this short allele has been shown to be associated with reduced gray matter volume of Area 25 and uncoupling of an anterior cingulate-amygdala circuit necessary for extinction of negative affect, providing a model for linking genetic risk and environmental stress to a specific neural circuit implicated in depression. One might imagine that studies of this circuit could be used to predict response to treatment, just as imaging in cardiology or oncology can be used to predict treatment response.
But what I would’ve preferred from these articles would have been something solid and well referenced about the neural circuits themselves. Perhaps such things are widely talked about and known in neuroscience circles, but they’re not in the general population of practitioners, psychiatrists, or others who aren’t specifically immersed in the world of neuroimaging. The articles are so busy addressing possible translations that they give short shrift to the basics – basics that most readers [like me] don’t know much about. Since this study is essentially a data gathering exercise with the behavior of the neural circuits on the front burner, I ought to know more about that than I do after reading these papers repeatedly.