SchizophreniaWatch

A UK website, principally for carers 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 site is edited by a retired psychiatrist who has looked after someone with the schizophrenia condition, at home, affected by the negative form of schizophrenia, for the last twenty years. [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, email me

There is a limited general psychiatry section .... links


A.
go directly to academic studies on the schizophrenic brain

B.
THE CARE ACT
Care Act sec 117

Caring for schizophrenia :- How to behave with a sufferer

How to behave with the professionals

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

early days how to respond


New February 2018
1.
untreated leads to hippocampus size reduction
2.
networking for Attention

january 2018

1:- glutamate overactivityN.B. [ hippocampal failure in neurogenesis would lead to this - reduced neurogenesis means reduced inhibition on Ca3, to glutamate overactivity.
2 :-dentate neurogenesis

The hippocampus keeps the brain networks ready to deal withliving in theworld around them, by a steady alerting low wave distribution.
see ready at rest

Old News

1.
cognitive treatment reviewed

2.
Klaus Conrad 'trema'




November2017

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.

Howes

The Article


links to academic studies supporting that there is hippocampal failure in schizophrenia

the the brain in schizophrenia

Schizophrenia appears to be inexplicable. If there is an explanation for the illness, it removes the challenge of the unknown.

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

Brain is the organ of the mind

Schizophrenia comes about because of an abnormal brain change in those people developing the illness. A brain change will change mental behaviour.
Normally the hippocampus delivers 700 new cells daily: Spalding et al [ hippocampus neurogenesis ]Spalding et al
The hippocampus area of the brain in schizophrenia makes half only, of what is the rate for proliferating new cells in the normal hippocampus


The consequence of this change is the failure to perform the essential process of personal selection, from what is going on in the outside world,
The relevance of what is perceived to the store of personal experience .
That is, distinguishing that which it is useful to know, out of all the incoming perceptions, whilst not giving a reaction, to what is already known or not useful .


How could this hippocampus neurogenesis reduction let in a delusional explanation ?
The brain resolves ambiguity by settling for one explanation - see split brain resolution of information that appears unreconcilable. it comes up with an answer that the brain executor can move on from the ambiguity, the irreconcileable presentation between two differing incoming stimuli/information. go tostudying 'split'brains]


[ Schneider primary delusion ..... = abnormal salience ..... somthing normally insignificant is taken as significant by sufferer, is the basis for a delusional misbelief.
We know that different gamma waves sort out access to which new things are perceived. But how for example how does the amygdala give emotional value priority - how to 'click' on which of the gamma assignments should go into available longterm store for usefully held context enables an intention to proceed correctly.
Beta oscillations play at least two important roles in the processing of task stimuli in healthy subjects, the second of which is disrupted in schizophrenia.
First, both relevant and irrelevant task stimuli induce a rapid but transient phasic reduction in beta amplitude relative to baseline, probably due to the retuning of local excitatory–inhibitory encoding circuits from the beta to the gamma range.
Second, in response to task-relevant stimuli, there is enhancement of a more gradual phasic increase in beta amplitude relative to baseline, postulated to represent a beta signal implicated in integrating information across widely distributed brain regions. Together, these two opposing beta effects (early suppression of local beta in favor of gamma; more gradual increase in long-range beta integrative signal) sum to produce an initial net beta amplitude reduction (beta ERD) followed by a sharp increase (beta ERS).

In schizophrenia, we conclude, the local beta encoding signal, reflected in the early beta desynchronization, is not abnormal. However, in the insula network, the integrative beta signal showed an attenuated response to task-relevant stimuli while conversely actually showed a significantly increased response to irrelevant stimuli.

Taken together with robust evidence for grey matter deficits in the bilateral insula, this suggests that in patients with schizophrenia a faulty salience network fails to signal the salience of task-relevant stimuli, resulting in disruption to the integrative processes required for efficient evaluation of stimuli and appropriate response selection.

Such disruption could lead both to failure to recognize what is relevant, and to attribution of salience to what is irrelevant
See --- E B Liddle ..... suggest this happens when sufferer is in a conflictual situatio over a period, giving continual anxiety, that is settled, if abnormally by giving ... a resolving explanation ... something to ...go on with....



Note:- maybe too much hippocampal GABA inhibition ..... Bast studies ( Bast GABA disinhibition )revealed that 'faulty inhibitory neurotransmission in the hippocampus does not only disrupt aspects of memory typically supported by this brain region, but also impaired attentional function, which is highly dependent on the prefrontal cortex, a region that is strongly connected to the hippocampus.

too much GABA inhibition may happen if there is too little new cell proliferation in the hippocampus dentate gurus
It affects attention choice

Too few new Hippocampus dental granule stem cells will 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.


Without the ongoing update of useful information, people developing schizophrenia are at a disadvantage when coping with day to day expectations that require decision making, especially holding on to what todo, in an input of 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.

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 or drawing together different aspects of a memory .

. The hippocampus is like a hub, where a lot of information comes in and has to be redirected to the correct destination within the brain, especially to the executive brain cortex.



Hippocampal new cells encode
[ that is, they turn incoming perceptions into a form that the rest of the brain can respond to ]
incoming information stimuli temporarily , for accessible brain storage. The hippocampus can also retrieve such information , again temporarily, used to provide the changing context as memory at work proceeds.

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.
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.

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


.

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

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


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

salience


.

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 [ READ this article about when Gazzaniga :- BR> " the amazing capacities of the non-speaking 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.














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1. stem cell proliferation is decreased in schizophrenia, but not in depression
A Reif,, S Fritzen,, M Finger, A Strobel, M Lauer, A SchmittK-P Lesch Molecular Psychiatry (2006) 11, 514-522
Reif et al 2006

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

the most important findings. Subsequent studies [ see below ] give confirmation - as does 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

2.
Reduced capacity but spared precision and maintenance of working memory representations in schizophrenia
JM Gold, Ph.D., Hahn, Ph.D., Zhang, Ph.D. Robinson, , Kappenman, , Beck, , and Luck, Ph.D. Arch Gen Psychiatry. 2010 June ; 67(6): 570-577.
link to the Gold et al paper

3.
Automatization and working memory capacity in schizophrenia
Tamar R. van Raalten , Nick F. Ramsey , J. Martijn Jansma , Gerry Jager a, René S. Kahn / Schizophrenia Research 100 (2008) 161-171
Raalten

This study now confirmed :-

Koch et al Koch et al
"... First evidence from studies with schizophrenia patients indicates that the potential to profit from short-term practice under stable learning conditions

Confidentiality

Carers know a thing or two

The guide lines that professional service must respect
necessary for carers the Care Programme Approach

Basic ideas about schizophrenia

the Team