Bruce Charlton linked me to a paper he wrote about structural imaging and the brain about two decades ago a few weeks ago. He noted that neuroimaging would not be able to mimic physiology.
It is uncertain exactly what level of spatial resolution is required of an imaging technique to accomplish such fractionation, because the necessary size of neural structures needed for intermediate processing is not yet properly established (probably, the more complex the computational task, the larger the necessary size of neural circuitry).
However, many specialized cortical areas are some millimetres in diameter, so a resolution of at least tenths of a millimetre would seem to be necessary.
And temporal recording of neural activity would need millisecond resolution in order to discriminate the steps of neural activation involved in cognitive processing.
Unfortunately, none of the currently available techniques for functional imaging of the brain are able to provide the minimum necessary structural and functional discrimination of neural activation
We have managed to get resolution down to around the millimeter, perhaps to the micrometer. We cannot estimate events in scanners millisecond by millisecond. So we use proxies: blood flow, neurochemical markers (fMRI) and more recently summation models.
For neuroimaging has not added to clinical knowledge.
Despite the enduring efforts and the impressive number of MRI studies published in patients with schizophrenia (more than 5000), there are no clinical biomarkers for structural MRI in psychosis. Recent systematic reviews and meta-analyses of the available evidence have identified specific cortical and subcortical alterations in patients with psychosis as compared to healthy controls. Yet, after four decades of research, the conclusion of the first 1988 study included in our database ‘none of the findings from CT or MRI explained clinical observation or led to a change in treatment’ is still valid. As recently confirmed by positional statements by leading authors, imaging research has yielded no clinical advancement for patients with psychosis
This is further confirmed by our empirical analysis, which uncovered only one study satisfying the basic requirement for some potential clinical applicability of biomarkers in psychosis . This study suggested that neuroanatomical classification could provide generalizable diagnostic tools distinguishing schizophrenia from mood disorders early in the course of psychosis. However, it is important to note that the assessment of the theoretical clinical applicability per se does not assure real-world clinical utility. Indeed, proper randomized clinical trials (of this biomarker vs standard care) should be carried out so that additional factors such as cost of administration, potential risks and side-effects, inconvenience, and delays associated with testing can be balanced and a decision on its real-world clinical utility can then be made [23]. Because of this, the clinical utility of the biomarker described by this unique study is still in need of additional converging support. This is particularly relevant given that the brain areas implicated by this study are only partially consistent with the largest MRI analysis in patients with schizophrenia . Similarly, structural imaging is not clinically recommended for the differential diagnosis of incidental organic psychoses due to underlying brain abnormalities. A recent review of 1379 MRI scans found that none of the neuropathological findings observed in the patients represented a possible substrate for organic psychosis, concluding that MRI brain scans should not be an essential part of routine screening for patients with psychosis. On the basis of these findings, the current NICE guidelines do not recommend the use of structural neuroimaging to routinely examine all patients who have suffered from a first episode of psychosis.
I was discussing this with one of my statistical colleagues. He said that if he’d predicted this in 1995, and now, twenty years later, is proven correct, he would be smug. Every time he walked past the scanner — which has never become used routinely for people with psychosis — he would gloat.
I would enjoy Schadenfreude.
Bruce is far nicer than I am. He has just continued to move on.
That’s generous of you! Am I allowed to feel smug for a few minutes?
The reason I did this careful evaluation of functional imaging was that I am a theoretical biologist, and was working on the ideas that I later published in Psychiatry and the Human Condition
http://www.hedweb.com/bgcharlton/psychhuman.html
and I needed to make the strategic decision of whether or not to use functional imaging results in my theorising. I concluded that this research was without any value (except to careerism – there it was of immense value; but I have not had any career, so that didn’t affect me personally), and I never used functional imaging at all – not to contrinute to, and neither to confirm nor to refute my hypotheses: I just ignored it!
You would not be human if you were not humming “I told you so”. I would be smug indeed: you are correct. The issue of functional networking and how this affects the brain is still open — my boss showed be a paper on this last week, but I haven’t read it yet.
In my view, the issue of brain and mind beyond is a philosophical question. There is such a thing as madness, and we don’t understand it. We may never understand it: the logical positivists who think that if they throw a high enougn N at the problem forget that no brute force approach works if you don’t have good hypotheses.
The best hypotheses at present involve synaptic reconstruction, neural networks, and the physiology of this. But these things are quite hard to nove to the point where they have clinical utulity and BDNT is moderately hard to manipulate. Which is what I’m interest in at present.
Because I’m sick of seeing psychosis burn lives out too young