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 themselvesCarer getting nowhere with the Team .... go to Page 2.
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
go directly to what is the change in the brain that leads to schizophrenia
Caring for schizophrenia :- How to behave
1:- glutamate overactivity [ 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.
ready at rest
cognitive treatment reviewed
Klaus Conrad 'trema'
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.
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 forthe 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.
The hippocampus area of the brain in schizophrenia makes half only, of what is the rate for proliferating new cells in the normal hippocampus
Normally the hippocampus delivers 700 new cells daily: Spalding et al [ hippocampus neurogenesis ]Spalding et al
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 .
too much GABA inhibition may happen if there is too little new cell proliferation in the hippocampus dentate gurus
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.
The medial temporal lobes (MTL), and more specifically the hippocampus, are critical for forming mental representations of past experiences-autobiographical memories-and for forming other "nonexperienced" types of mental representations, such as imagined scenarios.
We interpret our findings as evidence that there are MTL-guided networks for forming distinct types of mental representations that align with functional distinctions within the hippocampus.
The perirhinal (PER) and lateral entorhinal (LEC) cortex form an anatomical link between the neocortex and the hippocampus. However, neocortical activity is transmitted through the PER and LEC to the hippocampus with a low probability, suggesting the involvement of the inhibitory network. This study explored the role of interneuron mediated inhibition, activated by electrical stimulation in the agranular insular cortex (AiP), in the deep layers of the PER and LEC. Activated synaptic input by AiP stimulation rarely evoked action potentials in the PER-LEC deep layer excitatory principal neurons, most probably because the evoked synaptic response consisted of a small excitatory and large inhibitory conductance. Furthermore, parvalbumin positive (PV) interneurons-a subset of interneurons projecting onto the axo-somatic region of principal neurons-received synaptic input earlier than principal neurons, suggesting recruitment of feedforward inhibition. This synaptic input in PV interneurons evoked varying trains of action potentials, explaining the fast rising, long lasting synaptic inhibition received by deep layer principal neurons. Altogether, the excitatory input from the AiP onto deep layer principal neurons is overruled by strong feedforward inhibition. PV interneurons, with their fast, extensive stimulus-evoked firing, are able to deliver this fast evoked inhibition in principal neurons. This indicates an essential role for PV interneurons in the gating mechanism of the PER-LEC network.
Hippocampal new cells encode
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.
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.
It points to the hippocampal proliferation failure occurring in the pre -illness years before hallucinations are present or a delusional system.
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
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,
[ locus coerulus or maybe hey! cortex - this has to get attention ... serotonin receptors] and is given emotional priority [ deal with this, please: striatal dopamine ]
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"
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 .
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
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.
Go to hippocampal striatum for an example of developing a delusion, and an explanation of the striatal memory route from Poldrack.
1. stem cell proliferation is decreased in schizophrenia, but not in depression
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
This study now confirmed :-
Koch et al Koch et al