Addressing the Causality Gap in Human Psychiatric Neuroscience
- Type: #article
- Year read:#read2018
- Subject: (in brackets, can also bracket keywords in text)
- Bibtex: @etkin2017
- Bibliography: Etkin, A. Addressing the Causality Gap in Human Psychiatric Neuroscience. JAMA Psychiatry (2017). doi:10.1001/jamapsychiatry.2017.3610
Why and when I was reading this
- His main point is that neuroimaging methods like fMRI demonstrate correlation but not causation. We should therefore be very careful in interpreting these results, and move towards more experimental manipulation.
- Dysfunctions across disorders are more similar than previously thought. Demonstrating that OCD cases and healthy controls differ in imaging studies does not necessarily point to specific alterations in OCD but psychopathology more general.
- We do not know whether different treatments exert their effects through common or specific brain pathways.
- Transcranial magnetic stimulation (TMS) is one way to experimentally manipulate brain functioning.
- RCTs with mechanistic hypotheses and incorporation of neural mechanisms are needed
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In fact, neuroimaging meta- analyses across psychiatric disorders have found more neural similarities than differences between disorders, despite their divergent symptoms.
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Simply put, our dominant tool, neuroimag- ing, demonstrates correlations, ultimately revealing associations but not demonstrating by itself how a cir- cuit perturbation causes aberrant behavior and symp- toms.
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Causal neurostimulation tools such as transcranial magnetic stimulation (TMS) allow researchers to ma- nipulate the function of targeted regions and their con- nected neural networks for periods that range from mil- liseconds to weeks.
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Nonetheless, it is also important to realize that some of the strongest correlations may lack any causal rela- tionships
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s valuable as these de- velopments might be in providing patients with additional treatment options, it is nonetheless important to acknowledge that a great deal of effort has gone into treatment development without an understand- ing of whether the neural mechanisms they treat are indeed different.
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Greater use of mechanistic comparative trials is ethical and can advance clinical outcomes by revealing the true factors affect- ing who responds and why.