e.g.

Once doing a ward round - the first two days, new patients were in or around their beds, getting used to medication, and the nurses, as nurses - I introduced myself 'Dr Y I will be looking after you here - what's your name ,,,, to be answered by a patient three beds down suffering from schizophrenia who answered as though it was a Q. addressed to her . It was 'forced' out of her; she could not find the context that showed to be inappropriate and set it asid Some sufferers put fingers in their ears, some play music - to keep out a takeover/ - others make hooting noises to do the same.The intrusions are less when sufferer is concentrating on the cues at hand. Concentration lapses in time and oddities creep in .

Primary Delusion ..... perceptual delusion .... arises out of passivity

Something is observed , is the same that anyone else would observe, but to the sufferer , it has an indiosyncratic meaning, which carries conviction into an extended misbelief.

e.g. an white adolescent stated his father was not his real father: the freckles on his arm indicated that he was a rastafarian and his real father was haile. . He later called the police 'pigs' and got beaten up; he tried to join in a group of caribbean peers 'yo' showing them the 'fives' - and they beat him up for mockery.

Thought Disorder [ deduced from speech ]

Cloze paragraph

The initial starting point to what will become a sequence of conversational exchange is not borne along in the conversation, so that odd words , odd associations creep in, the thread is then lost. Or, the conversation is restricted , lacks some associations that would make it a personal presentation- is tightly held together so that it seems formal and pedantic without taking into account who is being spoken to and the context for that.
Literal- concrete speaking. Boring.

'Voices'

So that the the person knows what is inside behavior from what is outside, there is a self monitoring service.

When action is self generated in the brain, a sensory area also receives a signal from the that active area informing them of the intended action, allowing a prediction of what should be expected as sensory feed back. The process is called a 'corollary discharge' or an 'efferent copy'.
The prediction can be used to explain away the sensation that would be normally be fed back, or cancel it.
Normally we distinguish between someone else speaking, from seaking inside - thoughts - depending on how well we can predict the sensory input they put in.
When thinking is 'voiced' inside, it is preceded by an internal notification triggered by a coro llary discharge from the feed back prediction about the expected sensory consequences of that action, a corollary message precedes the thinking 'voices'.,the prediction being substracted from the actual sensory input.
Aberrant corollary discharges may so impair the perceptual inference, leading to 'voices' seeming to come from outside.
Some how this faculty is weakened or lost for some thinking and it is 'heard' as though from outside. Perhaps the thinking in the delusional 'field' is not so well managed by, or integrated in, the corollary work.

Why now ?

in puberty through adolescence to early adulthood - 24 years - full insulation of brain inner connections has not settled, particularly those of the hippocampus [ dealing with new experience ] to the pre-frontal area which at 24 becomes the mature executive brain;
pruning of neuronal connections takes place from the back brain onwards, finally to the prefrontal region. Does it go awry ?

[ from a Feinberg letter BJ Psych February 2010: The changes in sleep EEG are particularly prominent and were an important stimulus to the model of adolescent brain reorganization driven by synaptic pruning ; a corollary of this hypothesis was that errors in post-natal brain developmental processes might cause mental illness.

We are carrying out a longitudinal study of sleep EEG in normal children aimed at defining the trajectories of adolescent brain reorganization.
NREM delta power is unchanged between ages 6 and 11.5 years. It begins a massive decline at 11.5-12 years, falling 65% by age 17, when the decline slows markedly.
NREM delta EEG appears to reflect frontal lobe electrophysiology.
Abnormalities in the functional development of frontal cortex could impair both neural integration and emotional control.
More Why now ?
a team of researchers led by Elizabeth Thomas of the Scripps Research Institute has taken a novel approach to this problem, performing a gene network-based analysis that revealed surprising insight into schizophrenia development.

The group analyzed gene expression data from the prefrontal cortex, a region of the brain associated with schizophrenia,
sampled post-mortem from normal individuals and schizophrenia patients ranging from 19 to 81 years old.

However, instead of just looking at genes individually, Thomas and colleagues considered interactions between genes,
as well as groups of genes that showed similar patterns of expression, to identify dysfunctional cellular pathways in schizophrenia.

"Once gene co-expression networks are identified," said Thomas, "we can then ask how they are affected by factors,
such as age or drug treatment, or if they are associated with particular cell types in the brain."

The gene network analysis suggested that normal individuals and schizophrenia patients have a unexpectedly similar connectivity between genes,
but the most surprising finding was a significant link between aging and gene expression patterns in schizophrenia.
The team identified several groups of co-expressed genes
that behaved differently in schizophrenia patients compared to normal subjects when age was considered.

A particularly striking age-related difference in co-expression was found in a group of thirty genes related to developmental processes of the nervous system.
Normally these genes are turned off as a person ages, but in schizophrenia patients the genes remain active.
This critical finding strongly suggests that age-related aberrant regulation of genes important for development
can explain at least part of the manifestation of schizophrenia.

Thomas explained that these findings help to refine the developmental hypothesis of schizophrenia, which states that one or more pathogenic "triggers" occur during critical periods of development to increase risk of the disease.

Specifically, this work indicates that abnormal gene expression in developmentally related genes might be a significant pathogenic trigger,
occurring over a broader time-scale than expected.

"Rather than a pathological trigger occurring at a critical developmental time point," said Thomas, "the trigger is ongoing throughout development and aging."

Furthermore, Thomas noted that their study supports early intervention and treatment of schizophrenia.
Treatment approaches aimed at averting gene expression changes and altering the course of the disease,
could be specifically tailored to the age of the patient.

Scientists from the Scripps Translational Science Institute (La Jolla, CA), the Mental Health Research Institute (Parkville, Australia), and the Scripps Research Institute (La Jolla, CA) contributed to this study.

This work was supported by the Scripps Translation Science Institute Clinical Translational Science Award, the National Institutes of Health, and a Scripps Dickinson Fellowship.
Both schizophrenia and major mood disorders have their onsets during or shortly after the period of adolescent brain reorganization.
Since pubertal development is taking place at the same time, it is tempting to attribute adolescent brain changes to sexual maturation.

However, we have demonstrated 4 that NREM delta maturation is strongly related to age when sexual maturation is statistically controlled; conversely, when age is controlled, the delta decline is unrelated to pubertal changes.

It is more likely to be related to the declining effect of growth hormone as sexual maturation butts in, rather than a direct effect of the secondary sex homones themselves.

The explanation then goes something like this. [ perhaps ]

some previous happening on brain development sets the stage - e.g difficult labour with anoxia after first pregnancy - or with jaundice after birth where there is some minor blood group incompatibility between parents. [ my own eccentric view is that there is an argument between the direction of personality hard lining when one parent contribution is towards extraversion, and the other is towards introversion: the contributions cannot 'live' together ] Growth hormone maintains brain development as other body development for those neurons and connections that have found a use.

Growth hormone declines; pruning of those connections and neurons not used , occurs on a brain development made more vulnerable after thehappenings around birth, so that the rpruning goes awry. Schizophrenia follows because there are not enough cells or not enough connected up cells in place to sustain a network that gives the necessary and sufficient access to the stored experience, or to continue assimilate and accomodate to the updated experience at the level that comes with and is required for progress through adolescence.
Research involves DISC 1 as a dendrite connector missing or weakening in Schizophrenia
In some the pruning leaves sufficient cells and connections, but the brain vulnerable to the further shedding of neurons and connections that is part of ageing: schizophrenia then arrives later, ith a better prognosis because by that time sufficient adult experience has accumulated for personal maintenance and some occupational experience.

There are no abnormal dying brain cells as in alzheimers and other dementias. A lack of brain 'volume', enlarged fluid chambers, and a reduction in dendrites and white connections is reported, without a specific pattern. ] [ see Hippocampus bits ]

Recovery - a nice word ?

Recovery occurs when sufferer with some residual impairment has a routine in place for daily and weekly activities, regular and supported. Wandering out of normality is checked by having an anchoring programme to return to.