"Watch with me".... Isaiah

A UK website, principally for about and carers for schizophrenia; family, community, and professional service caring, who should - must ! - give voice for the best interests of those cared for: they can't, they won't, they don't, voice for themselves

[The blue highlit links take you to another page.. ] You return via the back arrow at the top of your screen or from a link at the bottom of a page

contact me if you want to help me out with my views,

or text me 07547 153 244

There is a limited general psychiatry section .... the link

my 'cause' of schizophrenia' go to


a carer guide

Care Act sec 117


there is no human adult neurogenesis

a previous study agrees

Sorrels et al reply

worth another look
cognitive treatment reviewed

Klaus Konrad .... the developing illness 'trema' ... revisitedanxiety and schizophrenia

November 2017

Is this a new treatment or a false hope.
So, why not have a go ??

the treatment is offered to those with continuing schizophrenia.
But surely the pruning has already taken place. The treatment will not reverse that.


The Article


Carer getting nowhere with the Team .... go to Page 2.

How to behave to sufferers


a Trust Carer Advisory Committee
Do You have one !?

the Team - its weekly agenda

early days how to respond

How to behave with the professionals

Carers know a thing or two

Caring tragedy

an example

lessons to be learnt

violence in Schizophrenia

Schizophrenia appears to be inexplicable.

When there is an explanation for the illness, it removes the continual worrying about the unknown.
Knowing what has gone wrong , can lead to a more rational support to the sufferer.

This is my understanding of the background to the development of schizophrenia: is its proximate cause.

Brain is the organ of the mind

The mental illness schizophrenia comes about because of an abnormal brain change in those people developing the illness. Commonly in adolescence, already an unsettling social change.

Normally the hippocampus delivers 700 new cells daily: Spalding et al ...
hippocampal neurogenesis

*****!! ( but see 'New1.' above - I hope the Karolinska team quickly substantiate their case )

If there is no new hippocampus neurogenesis, my stated comments on how schizophrenia comes about are on false assumptions.

The Adult human hippocampal dentate gyrus stem cell area of the brain in schizophrenia makes half only, of what is the rate for proliferating new cells in the normal hippocampus
see adjoining column

( How might this neurogenesis loss come about )

These new cells are an essential part of the hippocampus, functioning as a hub, connecting updated incoming information to most of the other brain networks.

New adult hippocampus cells can hold new information until the information is analysed and accepted for useful salience, following which it is transferred to the appropriate brain networks that gather together the useful experience into store, allowing that experience to be retrieved when relevant responses to changes in living practice are required.

[ cp Suarez Carron;
In MICE ...Using a novel fast X-ray ablation protocol to deplete neurogenic cells, we demonstrate that immature adult hippocampal neurons are required for hippocampal learning and long-term memory formation.
Adult newborn hippocampus neurons are Involved in acquiring learning .... then transferring it from acquisition to consolidation for long term experience..... accessed May 27 2018 ]

Without enough memorising, learning from experience is incomplete.

Hippocampus neurogenesis also refreshes old memories where the need is for current background context.


The consequence of reduced hippocampus neurogenesis is the failure to perform an essential process in maturing; the personal selection out of what is useful to the individual circumstance, from what is going on in the outside world

This is the disability that hinders those living with continuing schizophrenia; a failure to deal with changing life matters whilst pursuing a personal intention in their situation living

They are distracted by incoming stimuli/information overload.
The answer is to simplify their environment, give them time in that to develop satisfactory routines, to a level of sufficient basic 'automated' life style which will allow a pursuit of more interesting interests, and ongoing companionships.

[ attention ...networking for Attention
Bast GaBa attention

Without this selective attention, useful information taken from what is perceived, sufferer does not mature a store of personal experience.

[ Note this:- Schizophrenia Bulletin april 2018 ... " Performance on the verbal memory task was significantly worse in the patients than in the controls after 24 hours. ... although the patients had similar pre-sleep performance to the controls, their forgot much faster than the latter group ...(11.5 vs. 3.5% ) ]
Maturing comes from the necessary consolidating into longterm store, out of all the incoming perceptions/ information, what it is useful to know, ignoring what is already known, or is not useful . Hippocampus and prefrontal cortex, together work out what sample to take in from all the incoming perceptual information/stimuli.

[ Note this:- Schizophrenia Bulletin april 2018 ... " Performance on the verbal memory task was significantly worse in the patients than in the controls after 24 hours. ... although the patients had similar pre-sleep performance to the controls, their forgot much faster than the latter group ...(11.5 vs. 3.5% ) ]

To generalise from this, memories of daytime experiences do not consolidate 'into store' overnight, so are not available for maturing skills.
Thus people developing schizophrenia are at a disadvantage when updating with day to day expectations that require decision making, especially holding on to what to do, when there is a change of circumstance, i.e. changes in incoming information.
For example in conversation there is a veering off the subject, forgetting the context in the beginning, so that there are intrusions of idiosyncratic words and associations, leading to an eventual peetering out of talk

In retrospective analysis those patients, who went on to show schizophrenia, already had significantly worse attention, working memory abilities, and declarative memory abilities.
seidman plus reference linkSee also ...
see also idiosyncratic speech precedes schizophrenia

[ Giving advice/information to people suffering from schizophrenia needs to be confirmed by rehearsal and repetition, to sustain a necessary automation of the material, so often better in written form. ]

The hippocampus coordinates with the prefrontal lobe of the brain in deciding what in perception, perceived happening, will be taken in as having useful in reference, will go into longterm memory. That is, experience that can be drawn upon in daily living decisions; acquiring maturity

When schizophrenia arrives in adolescence that maturing experience does not happen so well.
They are stuck with the interests, social skills, work experience, friendship relationships ( friends move away, move on in life ): sufferers stay at the age the illness struck with what they depended on before the illness arrived.
To get hold of perceived information, useful for up-lifting into long term practical experience, memorying has to be able to select attention .
A reduced hippocampus neurogenesis will constrain this choice of what is personally important incoming information/stimuli, leading to the delusional explanation of a misplaced abnormal salience.
How does this hippocampus neurogenesis failure lead to the accepting of a delusional explanation
The brain resolves uncertainty by settling for one explanation

It comes up with an answer with which the brain 'executor' frontal lobes can resolve the ambiguity, the irreconcileable presentation of two opposing incoming stimuli/information. [ for an account:- go tostudying 'split'brains]

[ Schneider describes aprimary delusion ..... = abnormal salience ..... something normally considered insignificant is taken on as significant by sufferer, then becomes the basis for a delusional belief.

..... I suggest this happens when sufferer is already in unresolved conflictual situations over a period, with continual anxiety, that is settled, if abnormally, by giving ... a resolving explanation .... the delusion.

Too few new Hippocampus dental granule stem cells bring a tendency to veer off the point allowing the encoding of new perceptions that are not 'salient', letting them into the longterm store of experience.

Another drawback following the hippocampal neurogenesis reduction is the inability to 'rehearse in mind' what is to be done in the future. That is 'Prospective memory

At a time of recollection the hippocampus is integrating or drawing together different aspects of a memory .

The hippocampus is a hub with connections to most other brain networking areas

Hippocampal new cells encode;
[ that is, they turn incoming perceptions into a form that the rest of the brain can respond to ]
The crucial point of thehippocampus neurogenesis is to hold incoming information/stimuli temporarily , to allow for selection of salient only information into accessible brain storage, preventing the overload that would come from encoding every incoming. In schizophrenia when the hippocampus fails to proliferates enough new cells, the hippocampus connections cannot cope with sorting out of all the stimuli/information coming in.
This is the disability to be addressed in treatment and rehabilitation in those with continuing schizophrenia. The reduced hippocampus neurogenesis lessens the ability to carry and engage in working memory, a background of ever changing perceptions.
It is drawn to new perceptions and fails to sort them for 'salience'
It is overloaded with incoming stimuli.
Incoming information overload brings in an alternative memory route - the striatal habit forming system. [ Fuerte et al 2006: distraction ]

Anxiety about these changes and the difficulties that ensue, are felt by sufferer as abnormal, before the florid illness develops.


It points to the hippocampal proliferation failure occurring in the pre -illness years before hallucinations are present or a delusional system.
As does the inability of continuing sufferers to accumulate maturing experience after the age at which the developing illness began.
They stick in the area of interest and at the level of personal domestic and social competence they had before the illness - their friends and siblings move ahead and away, they are left behind. They lose natural support and mentoring. They are more anxious.
Conrad's 'trema'

Their lives are liable to stimulus/ information overload before any signs of florid illness. That raises continual high anxiety
anxiety schizophrenia

What explanatory account will enable them better to deal with what is happening to them

Recently, concepts similar to Conrad’s concerning delusional ideas (i.e., that they are an attempt to restore meaning in a chaotic, frightening word) have been expressed by various authors. According to Freeman et al., for example, “it is hypothesized that individuals prone to paranoid ideation are trying to make sense of feelings of oddness caused by internal anomalies (e.g. hallucinations, perceptual anomalies, arousal).” [101, p. 1122], and according to Marwaha et al., in forms of psychosis: “the world comes to seem persistently unsafe. The sense that emotional experiences are out of one’s personal control may prompt a search for meaning that may find explanations in terms of external influence.”[from grillo 2018]

This is what happens during overload distraction in normal people.
Fuerte et al 2006: distraction

How and where would the brain deal with this surplus stimuli/information, pointless information, unwanted, that has some how 'got in' to the striatal memory route, where it will have to be checked for salience, been given dopamine high value, needing attention and a response.

abnormal salience especially when distractors are present



What is going on in overload is a bypassing of the selecting process of the hippocampal networking,
ending up instead in the basal ganglia mid-brain striatal memorising stream, going on to the networks where procedural are stored.
The striatum/putamen stream is where incoming stimuli carrying information are given significance

[ Locus coerulus or maybe hey! cortex - this has to get attention ... serotonin receptors] and is given emotional priority [ deal with this, please: striatal dopamine ]
Then off to the cortex that receives, and deals with, any other relevant experience.
An explanation, a stabilising coherent account of 'why' this abnormal incoming stimuli has got in to the striatal route, is required, a 'sense'of dealing with it, leading to the delusional story.

The brain needs a narrative explanation; who/what/where decides that?
Who's the boss?

when the brain is receiving confusing or conflicting information , the message from split brasin studies is that the dominant frontal lobe makes sense of the 'argument' by providing and acccepting an explanatory position that it will accept as an ongoing solution.[ READ this article about split brain reconciled
Gazzaniga :- " the amazing capacities of the non-speaking perceptual right cerebral hemisphere, and the wild confabulations of the speaking left hemisphere when asked to explain actions and decisions of its disconnected partner"
Gazzaniga found that if the right brain was given an ambiguous set of perceptions - or a situation so opposite that it was difficult to make it coherent, the left brain always made a narrative solution that put sense into the conflicting positions

Hence forward, sufferers have to live in two somewhat different worlds: reality, and the variably intrusive influence of the delusional account.

How is it that sufferers do not argue against the delusional story? I think this comes from 'the story' having been developed through the striatal memory route, and consolidated like a procedural experience .
? an example That route is for routinised repetition behaviour, belief that has become habituated , automated , less open to flexibility.
Suitable for enduring stability, as in learning a skill, such as riding a bicycle or relying on a basic structure of grammar. They don't have to be learnt again and again.
In schizophrenia, with a much reduced hippocampus new cell prioliferation, 'consolidation' of this overload of stimuli/information coming to the rest of the brain via this striatal route might be less open to reflection, less open to what the brain with normal hippocampal neurogenesis can do using 'second thoughts': so that a delusional narrative is made, can persist, uncorrected.
One explanation might be that it is consolidated during REM sleep where left over emotional stuff is dealt with: where 'overflow' from the slow wave night sleep review of unusual information is dealt with.

Why do people with shizophrenia hear 'voices'.
My explanation is that this is what happens, in many normal people during 'brain idling' or 'mind wandering': there will be people heard 'talking'.It is often critical , commenting adversely, threatening, intrusive and commanding in effect.
In active schizophrenia this kind of 'mind wandering' for the sufferers, comes out of the delusional narrative, the delusional explanation created outwith the way 'the brain' exercises it's usual internal checking scrutiny system ?

I also think the delusion comes similarly from 'mind wandering' during which 'the brain' seeks a narrative that is prepared to address fear difficulties. From whatever aberrant stuff has got into the striatal stream the 'cortex' will pick up on what yields an explanatory narrative that gives a focus, and relieves the continual uncertainty that comes from having to live with half only of hippocampal new cell proliferation; so, the filtering system in the hippocampus is ineffective
Perhaps the narrative is a reaction during the process of consolidation during REM sleep, That seems to be where emotional concerns are dealt with ?

How is it that all medications that help and prevent relapse are dopamine blockers? [ 'dopamine's role is in influencing the priority of such stimuli for the person concerned'. It also takes part in giving memories their longterm status, 'approval'. ] It is dopamine that establishes the emotional value - fear or joy - in this case it registers the continual anxiety from when reduced hippocampal neurogenesis makes the stimuli recognition world an uncertain place for the sufferer.
Clinically it is unresolved anxiety that leads to relapse, particularly if it comes out of a lack of confidence where there is unclear support from carers, family and professionals.

Bear in mind that a basic, continuing, fault in schizophrenia is how and what to hold on standby, when and where to use it, as context to what is going to come up in the day and the week; what to carry along in 'stand by' memory, whilst reacting to whatever is going on in any transaction.
New cell production in the hippocampus does that job normally.
With reduced neurogenesis, now they do not produce enough to hold and provide context
They are stuck with skills, interests and stored experience that they held before the age when the illness started: those with some continuing schizophrenia , have to try and make do with less new cells , less quick 'stand by' context. They do not 'move on' from the age when the illness presents

Go to hippocampal striatum for an example of developing a delusion, and an explanation of the striatal memory route from Poldrack.

back to top

A Reif,, S Fritzen,, M Finger, A Strobel, M Lauer, A SchmittK-P Lesch Molecular Psychiatry (2006) 11, 514-522
neurogenesis is reduced in schizophrenia
Reif et al 2006

Allen et al Confirmed.!!! nine years later.
In a different cohort Allen et al find there was a 60% hippocampal proliferation failure

the most important findings.
The result is the inability of continuing sufferers to accumulate maturing experience after the age at which the illness - they stick in the area of interest and at the level of personal domestic and social competence they had before the illness - their friends and family move ahead and away, they are left behind.: they lose natural support and mentoring.