PTSD and Complex PTSD can seriously affect the default mode network in the brain and cause faulty neuronal connections that can lead to psychotic symptoms.  The failure to perceive this as an injury rather than a disease causes bio-psychiatrists to employ medications that cause further injury to this complex structure of inter brain communication, which consequently causes cognitive dysfunction and psychosis.  

Bob Johnson has focused on this and the concomitant decreases in oxygenated blood in the brain.  

Neuroleptics will not treat PTSD but merely depress the more florid symptoms of it.  The problem is that they also cause the disruption in the DMN to get worse.

Bob’s comments on the effects in Broca’s area of the brain is fascinating.  This is the centre for language processing and damage there might account for the word fixation that is seen in some patients incorrectly diagnosed as psychotic.  

“Dr Richard Ngomba and I are also looking into disruptions in the mesocortical pathways potentially caused by brain inflammation.”  Decreases in oxygenated blood may well cause the triggering of inflammation in the temporal horn.    We saw in Martin Harrow’s study that neuroleptics have caused a marked decrease in cognitive function in patients prescribed these drugs long term.   Precisely what you would expect in patients with damage to neural pathways (mesocortical pathways) 

Professor Roderick Orner, who is an international authority on complex PTSD is in our research group.  

Subject: What is complex PTSD? – Mind

Disruption in the default mode network (DMN) has been implicated in numerous neuropsychiatric disorders, including posttraumatic stress disorder (PTSD).

My work has focussed on trauma recall.
This is blocked 100% in severe, untreated cases.
If the DMN is “autonomic’, then it is less significant clinically, than
voluntary, or insight driven cerebral

DMN abnormalities in patients with severe PTSD symptoms
are characterized by decreased overall inter connections.
Absolutely – but especially, as mentioned in Broca’s area, and the
frontal cortex. Decrease is an understatement – the blank look on the
faces is underpinned by Kolk’s PET scans when trauma tapes are played.

Those decreased interconnections are another potential reason why
patients incorrectly diagnosed with psychosis who are actually suffering
from PTSD are treatment refractive.
2 points –(1) beneath every psychotic symptom I have examined, there is a
fiercely blocked trauma. In one transcribed dialogue a 40 year old
verbalises the difficulty she has thinking. PTSD in spades.
(2) If the treatment envisaged is neuroleptics, then, as Harrow showed,
it makes things worse. In my view it does this by blocking even the
beginnings of reactivation of frontal cortical blockage, which is intimately
linked to Broca. Drug induced zombies cannot begin to pull themselves

The decreased interactions will interfere with the uptake of psychopharmaceutical medications by creating an effective block in neurotransmitter receptors in the mesocortical pathways.
Is the assumption here that better uptake is clinically beneficial? Clinical
evidence does not support this, though bio-psychiatrists swear by it.
And, yes, the blockages noted by Kolk were arterial, oxygen supply related, I
imagine, which implies the whole frontal area shows decreased activity.
DR Bob Johnson Page 2 of 2 Your 6 points – 1MAY22

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