'To hold truth up to power' ... thank you, Marie Colvin.
"If you choose to use your influence and raise your voice on behalf of those who have no voice, if you choose to retain the ability to imagine yourself into the lives of those who do not have your advantages, then it will not only be your proud families that acknowledge your existence, but all of those people whose reality you have helped change. We do not need magic to change the world, we carry all the power we need inside ourselves already, we have the power to imagine better." (J. K. Rowling, The Importance of Imagination)
A UK website, for those caring about, and carers of schizophrenia; family, community, and the professional service support . 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 page for those beginning or reviewing their carer situation go to this link
[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
text me 07547 153 244
There is a limited general psychiatry section .... the link
The first and most important thing in any teaching to know about schizophrenia, is that although recognising it as a unified illness, the expression is different in the particular circumstance of the people it alters.
Especially by the the age it arrives: those after the age of 16 - 24, the ending of adolescence [shakespear], have built up competence in work and relationship experience, in domestic management, in personal success and failure.
Those where the illness shows itself in adolecence have already suffered from the cognitive failure that presages the florid illness, often clear in the difference in achievement between O-level results [ GCSE's ] and subsequent exams, and difficulty in the resolving issues of 'emancipation' between child and parenting.
The other separating difference in how the ilnness shows , is the effect on the underlying personality of the impending sufferer.
The introvert obsessional personality, will tend to negative behaviour - withdrawal: the extravert to outward abreactive behaviour.
Early onset is more governed by preceding thinking and memory management difficulties, a later onset by persistent delusional coherence together with an ability to behave in the real world that the early onset sufferers have not acquired..
What determines the age of onset is not known, it may be most governed by genetic influence.
NEW May 2019 Important unanswered questions about adult neurogenesis in schizophrenia. Weissleder C Shannon Weickert
Aberrant neurogenesis may contribute to the pathogenesis, pathophysiology and symptoms of schizophrenia. This review summarizes the state of knowledge of adult neurogenesis in schizophrenia and raises important unanswered questions. We highlight how alterations in signalling molecules in the local and peripheral environments in schizophrenia may regulate adult neurogenesis in the human subgranular zone of the hippocampus and the subependymal zone (SEZ).
Cell proliferation and density of mature neurons are reduced in the hippocampus, yet the extent of adult neurogenesis remains unexplored in the SEZ in schizophrenia. The human SEZ is a major source of postnatally migrating cortical and striatal inhibitory interneurons, indicating that aberrant neurogenesis may extend to the SEZ and contribute to inhibitory interneuron deficits in schizophrenia. Trophic factors and inflammatory cytokines regulate the generation of new neurons in rodents, suggesting that altered expression of these signalling molecules in the brain, peripheral vasculature and cerebrospinal fluid in schizophrenia may impact adult neurogenesis in both the hippocampus and the SEZ.
Knowledge about adult neurogenesis remains scant in schizophrenia. We propose that a more rigorous examination of adult neurogenesis in relation to regulatory signalling molecules will allow us to identify how abnormalities may contribute to the pathophysiology of schizophrenia.
neurons from adult neural stem cells
new adult neuron cells can be enacted, gives hope [ unwarranted, perhaps ]
go to my 'cause' of schizophrenia' not enough adult new neurons
[ early 2018, a careful study by Sorrell et al declared, [ for and against ] we found NO adult neurogenesis in the hippocampus,
something that hitherto was long generally accepted
[ and by me - it's failure in adolescence to proliferate enough hippocampus new cells , that I still see as the proximate cause of schizophrenia ]
and indeed, sorrell study contradicted in april 2018, adult neurogenesis is confirmed by Boldrini et al. April 2018[ I give the arguments on this page for and against]
UK:- THE CARE ACT.
a carer guide
Care Act sec 117
a Trust Carer Advisory Committee
Do You have one !?
You need it to make sure you, as carer, have access to the minutes of your local community team. to make sure your voice is heard at their weekly meetings.
write your trust Chief executive that they have one in cornwall - where carers struggle to get to a central point meeting - should be much easier in a Mental health urban Trust
Carer getting nowhere with the Team .... go to Page 2.
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: its proximate cause.
Of course there must be others, predisposing, matters :- genetics, birth damage, fathers, elderly at conception. infection by virus at a critical time in pregnancy
It is cognitive memory failure that leads to schizophrenia losing the ability to sort out incoming stimuli signals .
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 ...
[ but see March 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
The best evidence for the effect this has on potential sufferers comes from Al usri et al : Kelly et altwo studies into total catchment area patients in two different catchment areas of those with continuing schizophrenia; 80%plus had difficulty retrieving information given a short time earlier. see....memoryconsolidation Also the particular accounts of patients to their carers.
The hippocampal new cells are an essential part of the hippocampus, functioning as a hub, connecting updated incoming information to most of the brain networks dealing with 'what to attend to'that supports today's daily living and anything cropping up soon.
Awakening,it restarts your brain store of experience, matching that to the obligations for what is coming up to do today.[see prospective memory]
What is in the store is what you chose, depending on what information your brain memory store 'considers' it to be of use to know ; to reduce the work load, it set aside everything else.
My proximate 'cause' of schizophrenia is that those in schizophrenia have had insufficient new hippocampal neurons to do the functions of previous information selection, of restarting each day with the useful memories/experience previously consolidated.
[ N.B. The number of adult-generated neurons doubles in the rat dentate gyrus in response to experience on associative learning tasks that need deliberation, and thus require, the hippocampal connections ].
In contrast, training on associative learning tasks that do not require the hippocampus, that is habit learning done in the striatal proceduralmemory stream; it did not alter the number of new hippocampus cells....
this supports a good practice in giving those at risk of future schizophrenia regular practical experience in domestic management and shopping,]
Adult hippocampus new cell proliferation is to select into store from what's going on outside, is useful to know and therefore to store away, to be accessible at any particular moment of future need in daily living. With reduced hippocampal neurogenesis, this selection may go wrong.
Random stimuli/ information in overload circumstances [see Fuerte et al 2006: distraction] , which is not useful, escapes the hippocamus encoding, goes to the striatal memory route, gets dopamine validation , exacting an explanation as to why it has importance, so that a story is required to explain its importance -- the delusional belief - the delusional system taking over whenever anxiety dominates.
That is my explanation as to how an innocuous piece of information normally ignored, acquires attention, developing a delusional orientation, because it leads to a need for what has done this.
Gazzinga studying 'split'brains
What is the especial ability of hippocampus new adult cells, compared with the mature neurons already connected up.
This study labeled newborn neurons and used sophisticated electrophysiological and imaging techniques to
show that immature neurons integrate from a variety of different origins compared with mature neurons: mature neurons were highly input specific.
What makes neurogenesis cells so essential is that, whilst existing hippocampal mature neurons are already tied to particular connections, therefore not available for sorting and checking where new information needs to be encoded into memory ,
new cells are unencumbered, are available to assist the acquisition
Thus, immature neurons may represent a population of integrators that are broadly tuned during a transient period and may encode most features of incoming information.
After maturation, new granule cells display a high activation threshold and an input specificity to become good pattern separators .
The new adult hippocampus cells can hold new information until the information is analysed and accepted as having 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 to consolidation for long term experiencememoryconsolidation .....
Without enough memorising, learning from experience is incomplete.
Also, there is less keeping hold in memory about what is coming up in the near future. Hippocampus neurogenesis also refreshes old memories where the need is for a current background context.
The consequence of reduced hippocampus neurogenesis is the failure to perform an essential process in maturing. Maturing experience comes from taking in, out of all the incoming perceptions/ information the necessary consolidating into longterm store, of what it is useful to know, ignoring what is already known, or is not useful . Hippocampus neurogenesis and prefrontal cortex, together work out what sample to take in from all the incoming perceptual information/stimuli. the personal selection is useful to the current individual circumstance. This failure to discriminate is the disability that hinders those living with continuing schizophrenia.
Their reduced neurogenesis leads to a failure to encode selectively, to take in sufficiently, out of incoming material, only what they need, for their current circumstances, or soon coming future commitments
[ attention ...networking for Attention
Without this selective attention, useful information taken selectively from what is perceived, sufferer does not mature into a store of personal experience.
[ Note this:- Schizophrenia Bulletin april 2018 ... "
[ 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, they 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.for memory consolidation
Thus people developing schizophrenia are at a disadvantage when updating day to day experience 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 preceded 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 is often better in written form. ]
When schizophrenia arrives in adolescence that maturing experience is not encoded clearly enough.
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, memorising has to be able to select from 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 ?
Information/stimuli overload moves storage to the striatum memory route
see [see Fuerte et al 2006: distraction]
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 toGazzinga studying '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. [ GAZZANIGA see above ]
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 the time of recollection the hippocampus is integrating, 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 striatum .
Anxiety about these changes and the difficulties that ensue, are felt by sufferer as abnormal, before the florid illness develops, requirig a definite explanatory fall back allowing the issues to be dealt with..
These examples of early cognitive failure before any florid signs of schizophrenia are what would happen when the dentate gyrus fails in earier adolescence to proliferate enough new cell proliferation.
It points to the hippocampal proliferation failure occurring in the pre - illness years before hallucinations are present or a delusional system. [ one account of thought disorder -the Cloze procedure ]
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 continually anxious, subject to -
Sufferers need and take on an explanatory account that will enable them better to deal with what is happening to them
Recently, concepts similar to Conrad's concerning delusional ideas, ( i.e.... 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)
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."
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 systems ,
ending up instead in the basal ganglia mid-brain striatal memorising stream, going on to the networks where procedural skills are stored.
The striatum/putamen stream is where incoming stimuli carrying information are given significance.
[ the Locus coerulus or maybe hey! cortex - this has to get attention ... serotonin receptors] and is given emotional priority and [ 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?
when the brain is receiving confusing or conflicting information , the message from split brain 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 Gazzinga interview 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 .x
The striatum memory route is for routinised repetitived 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 schizophrenia 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.
The result of reduced neurogenesis in the hippocampus for schizopgrenia 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.
Those for and and against Human Adult hippocampus neurogenesis
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
Al-usri et al J. Bruce, MBChB, MRCPsych, S. Frost, MBBS, MRCPsych and D. Mackintosh, MBChB, MRCPsych
B J PSYCHIATRY 2006 189 132-13
Cognitive function in a catchment - area - based population of patients with schizophrenia
CIARA KELLY, VAL SHARKEY, GARY MORRISON, JUDITH ALLARDYCE, and ROBIN G. McCREADIE The British Journal of Psychiatry 2000 v. 177, p. 348-353.
Ciara Kelly et al
Nithsdale Schizophrenia Surveys 20
the most important findings.
karolinska frisen spalding
for and against is there human adult hippocampus neurogenesis
The result of reduced neurogenesis in the hippocampus 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.