A lot of us are investigating the pathophysiology associated with mental disorders. One popular method is fMRI, which would be one example of measuring macro properties of the brain, at the regional / circuit level.
Research in differentiating many disease and disease states from each other took a great leap forward with the advent of fMRI. However, much of this leap forward is in diagnostics and breaking mono-disease states in reclassifications of multi-disease states. Showing different patterns of acitivity (increased or decreased) of certain regions of the brain does not explain the pathology. A similar view can be held of EEG/LFP recordings at the macro levels which sum the activity of many many cell assemblies, which also has been around for much longer. To really understand the pathophysiology, as well as the impact of an intervention, one must go to the micro level, or single unit analysis. The traditional methods of single wire single unit recording however, are also inadequate for disease state unravelling, as one still needs to work at a network or cell assembly level. Cell assembly is even a better term in my mind, as it indicates that important players in the network are heard from, and not just any population of cells. Pathophysiology may involve both interneurons, and a host of projection or principal cells from multiple structures.
logothetis in his workup to recording from cell assemblies, while monkeys were in an fMRI did a great job of differentiating the fMRI BOLD signaal from single unit signals and LFP signals. Indicating what can be brought to the table by each, and how they capture different aspects.
There is the larger 2002 Phil. Trans paper. and a much shorter summary in J. Neursci around that time.
A 2006-2007 Trends in Cognitive Sciences (TICS) Vol.11 No.2 p84. review by Myishita's monkey lab in Japan does a decent job of assessing the literature comparing neurophys results to fMRI results across sensori-motor visual cortices and more complex computations in higher more diffuse cortical areas.
Came across most of these articles and summaries as we worked on our own manuscript comparing Maccaque LFP and Human fMRI in a near identical competer generated learning task, while I was in Wendy Suzuki's lab at NYU.
Hargreaves et al., Neuron, 74, p7430-752.
Bassett, D. S., and Gazzaniga, M. S. (2011). Understanding complexity in the human brain. Trends in Cognitive Sciences, 15, 200-209. doi:10.1016/j.tics.2011.03.006 provided an interesting discussion along these lines. We have now published a series of articles suggesting the appropriate level to understand higher cortical functions is based on dynamic cortical columns that are in circuits. These in turn interact with subcortical structures, consistent with Luria's views that higher functions can only be understood as whole brain activity. The same theory provides information on serious neuropsychiatric disorders, depression/anxiety, the metatraits of plasticity and stability of the Big 5, the process variables in psychotherapy, and a structured approach in dealing with influential relationship-based negative emotional memories. I have attached one article from June that discussed the microcircuitry allowing the theorized manner of column formation. The other articles are available at my page, with the first being in 2006.
Article The Role of Dynamic Columns in Explaining Gamma-band Synchro...
Interesting points from all!
It seems to me, that the results from fMRI studies involving patients with mental disorders are not terribly specific to that particular disorder. You see that researchers working with distinct mental disorders often talk about the same brain regions/circuits. The same is probably the case (?) for other macro-measures as well, such as EEG. If our goal is to understand the etiology, or specific psychophysiology of these disorders, it seems that we should be able to detect differences between disorders.
I take Shanna's point about reductionism; it makes sense to study properties that resemble the net total you are interested in (i.e. combination of symptoms which we label a 'mental disorder'). On the other hand, I think that in order to understand etiology, and the specific mechanisms behind the development of a disorder, you have to zoom in and dismantle. To use your vacuum example; if the vacuum cleaner does not start, and you want to understand why (because you are curious or because you want to fix it), you would have to do some dismantling (unless it becomes obvious that you forgot to plug in the electrical cord). However, I do agree that when adopting a single-unit approach, as Eric suggests, there is a risk that you "lose" the properties that are only evident at higher levels of analysis (e.g. delusions, phobic fear). Despite this, I suspect that such micro-properties might be where the differences between mental disorders reside.
Robert, thank you for the article, sounds really interesting! I will download it now.
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