I’m flying out to Salt Lake City tomorrow for a month of thinking about neuroscience; I process ideas by writing, so I’m kicking off an open-ended series of pieces dealing with the stuff I’m thinking about.
Part 1: Neurobiology, psychology, and the missing link(s)
Part 2: Gene Expression as a comprehensive diagnostic platform
Part 3: Neural resonance + neuroacoustics
The central problem of neuroscience is that despite all the advancements happening in medical science, we have embarrassingly few ways to quantify, or talk quantitatively about, mid-level functional differences between peoples’ brains.
It’s not that we have no tools at all for quantifying function and individual differences: we can draw correlations between specific genes and certain behavioral traits or neurophysiological features. We have the DSM IV (and soon, DSM V) as a sort of handbook on the symptoms of common brain-related problems. We have the Myers-Briggs and related personality-typing tests, we have psychometric tests, we have various scans that pick up gross neuroanatomy (and we can sometimes correlate this with behavioral deficits), and we have the fMRI, which can measure raw neural activity through the proxy of where blood flows in the brain.
The problem is that these methods of understanding brains are heavily clustered in two opposite areas: the reductionist neuroanatomical approach, which is great as far as it goes, but doesn’t go far enough up the ladder of abstraction to explain much about everyday behavior, and the symptom-centric psychological approach, which may be a great description of how various people behave, or some common neural equilibria, but really explains very little. There’s a great deal of room in neuroscience for an ontology with which to talk about, and mid-level tools which attempt to measure and correlate things with, this underserved middle-level of brain function.
Of course, the natural question regarding these mid-level approaches to understanding the brain is whether we can find ontologies and tools which can be said to “carve reality at its joints,” or not be based on a terribly leaky level of abstraction (as, for example, the DSM IV fails at), yet have direct relevance to psychological events as we experience them in ourselves and in others (as, for example, the DSM IV does). I don’t have any answers! But I do have ideas.
 To paraphrase Sir Karl Popper, implicit in any true explanation of a phenomenon is a prediction, and implicit in any prediction about a phenomenon is an explanation. So a good way to figure out how much of a field is true scientific explanation vs. ‘mere stamp-collecting’ is to check how much it deals with predictions, whether explicit or implicit. Psychology seems to be a primarily descriptive field that’s attempting to translate its rich (yet predictively shallow) descriptive ontology into a more prediction-based science.
 This point on the fuzziness of psychiatry was made rather eloquently in an Op-Ed by Simon Baron-Cohen (the famous autism researcher, and the first cousin of British comedian Sasha Baron-Cohen) in this week’s New York Times:
This history reminds us that psychiatric diagnoses are not set in stone. They are “manmade,” and different generations of doctors sit around the committee table and change how we think about “mental disorders.”
This in turn reminds us to set aside any assumption that the diagnostic manual is a taxonomic system. Maybe one day it will achieve this scientific value, but a classification system that can be changed so freely and so frequently can’t be close to following Plato’s recommendation of “carving nature at its joints.”
Part of the reason the diagnostic manual can move the boundaries and add or remove “mental disorders” so easily is that it focuses on surface appearances or behavior (symptoms) and is silent about causes. Symptoms can be arranged into groups in many ways, and there is no single right way to cluster them. Psychiatry is not at the stage of other branches of medicine, where a diagnostic category depends on a known biological mechanism. An example of where this does occur is Down syndrome, where surface appearances are irrelevant. Instead the cause — an extra copy of Chromosome 21 — is the sole determinant to obtain a diagnosis. Psychiatry, in contrast, does not yet have any diagnostic blood tests with which to reveal a biological mechanism.
 I realize this is somewhat vague. I plan to expand this description of what I think of as “mid-level functional attributes” and the sorts of concepts and tools I think may be useful for dealing with them. One example of a mid-level measurement that struck me as promising was a work correlating lack of microstructural integrity in the uncinate fasciculus with psychopathy.