I pulled the post after re-reading it because it does not make physiological sense. (I am wondering if the person who wrote the story about the research actually understood it. This is not unusual in science stories reported by under-educated lay people.)
I was right. The article about the new research was egregiously in error. Here is a synopsis from the JAMA Journal itself, followed by an explanation of why this matters.
Severe neuropsychiatric conditions, such as schizophrenia, affect distributed neural computations. One candidate system profoundly altered in chronic schizophrenia involves the thalamocortical networks. It is widely acknowledged that schizophrenia is a neurodevelopmental disorder that likely affects the brain before onset of clinical symptoms. However, no investigation has tested whether thalamocortical connectivity is altered in individuals at risk for psychosis or whether this pattern is more severe in individuals who later develop full-blown illness.
To determine whether baseline thalamocortical connectivity differs between individuals at clinical high risk for psychosis and healthy controls, whether this pattern is more severe in those who later convert to full-blown illness, and whether magnitude of thalamocortical dysconnectivity is associated with baseline prodromal symptom severity.
Design, Setting, and Participants
In this multicenter, 2-year follow-up, case-control study, we examined 397 participants aged 12-35 years of age (243 individuals at clinical high risk of psychosis, of whom 21 converted to full-blown illness, and 154 healthy controls). The baseline scan dates were January 15, 2010, to April 30, 2012.
Main Outcomes and Measures
Whole-brain thalamic functional connectivity maps were generated using individuals’ anatomically defined thalamic seeds, measured using resting-state functional connectivity magnetic resonance imaging.
Using baseline magnetic resonance images, we identified thalamocortical dysconnectivity in the 243 individuals at clinical high risk for psychosis, which was particularly pronounced in the 21 participants who converted to full-blown illness. The pattern involved widespread hypoconnectivity between the thalamus and prefrontal and cerebellar areas, which was more prominent in those who converted to full-blown illness (t173 = 3.77, P < .001, Hedge g = 0.88). Conversely, there was marked thalamic hyperconnectivity with sensory motor areas, again most pronounced in those who converted to full-blown illness (t173 = 2.85, P < .001, Hedge g = 0.66). Both patterns were significantly correlated with concurrent prodromal symptom severity (r = 0.27, P < 3.6 × 10−8, Spearman ρ = 0.27, P < 4.75 × 10−5, 2-tailed).
Conclusions and Relevance
Thalamic dysconnectivity, resembling that seen in schizophrenia, was evident in individuals at clinical high risk for psychosis and more prominently in those who later converted to psychosis. Dysconnectivity correlated with symptom severity, supporting the idea that thalamic connectivity may have prognostic implications for risk of conversion to full-blown illness.
Okay. Now: The reason this is significant is that thalamus figures in control of both rumination (thinking something to death) and acting upon such thoughts. If the little sucker isn’t adequately connected to the first area cited above, but is overly connected to the second and third, one will have problems with “crazy ideas” and impulses to act on them.
There are known ways to stimulate growth of the neural links to and from the pre-frontal cortex that involve psychotherapy and behavioral conditioning. I’m not sure about what to do with the latter two problems other than use anti-Ps to block some of the Da receptors along those chains.
I had a counselor who used to have me thump my chest to stimulate my Thalamus.
Now I am not at home in neuro-lingo, but would you expect this thalamic connectivity to be different in so-called double bookkeeping patients? I.e. patients who voice extraordinairy delusions but do not seem to act consistently on them? These patients seem to pose an especially hard problem to the understanding, where action and firmly held “belief” seem to come apart.
I would expect it to be exactly as described in the research article; yes. Under-connected in the pathways up to and back down from (especially the latter) the medial pre-frontal cortex (that would otherwise be able to limit and control impulsivity), and over-connected to the seats of impulsive reactivity, including the insula > amygdala > hypothalamus > pituitary > adrenal (the “HPA”) that sets off the sympathetic branch of the autonomic nervous system into “fight or flight.” And if those latter pathways are continuously fired, into “freak and fry.”
This may be the physiological mechanism of converting the behaviorally conditioned predisposition for paranoid interpretation into the PTSD manifestations so commonly observed in sz pts.
Yeah I know a person, who is very annoying, who makes my conscious thinking happen less and make me take more action before I think. So even though I can’t avoid this person, I have less delusional thoughts but its just very bothersome and I want this person to go away. Anyways the reason I post this is I think it related to the thalamocortical network disorder.