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January 2018

Addressing the Causality Gap in Human Psychiatric Neuroscience

Author Affiliations
  • 1Department of Psychiatry and Behavioral Sciences, Stanford University, Stanford, California
  • 2Veterans Affairs Palo Alto Healthcare System and the Sierra Pacific Mental Illness, Research, Education, and Clinical Center (MIRECC), Palo Alto, California
JAMA Psychiatry. 2018;75(1):3-4. doi:10.1001/jamapsychiatry.2017.3610

As clinicians, we are accustomed to stories—those that our patients tell about their lives and struggles, and those that we tell about the causes of their difficulties. As scientists, especially clinical neuroscientists, we likewise tell stories about presumed neural mechanisms of illness and its treatment. Unfortunately, the truth behind these stories remains uncertain because our science remains descriptive. Simply put, our dominant tool, neuroimaging, demonstrates correlations, ultimately revealing associations but not demonstrating by itself how a circuit perturbation causes aberrant behavior and symptoms. By confusing this evidence with substantiation of causation, we risk creating “Just-So Stories”—internally consistent explanations that have no basis in fact.1 In the spirit of this series on pragmatic psychiatry, I outline several domains where causality at the level of brain circuitry is a critical missing link ready to be addressed. At the heart of the argument is the idea that understanding causal mechanisms, which are discoverable in a variety of ways, holds great promise not only for explaining illness, but also for furthering the efficiency and effectiveness of the pragmatic search for treatments.

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