This is my understanding of the background to the development of schizophrenia: its proximate cause.
Schizophrenia comes about because of an abnormal brain change in those people developing the illness.
The hippocampus area of the brain in schizophrenia , proliferates half only of what is the necessity for proliferating new cells in the normal hippocampus [ 700 new cells daily: Spalding et al Spalding et al ]
The consequence of this change is a failure to perform the essential process of selection, distinguishing that which is useful to know, out of all the incoming stimuli/information what is salient experience, personally useful to go into longterm store, disregarding what is already known or not useful .
[Note:- too much hippocampal GABA inhibition
[which may happen if there is too little new cell proliferation )
affects attention choice ]
Without the ongoing update of useful information, people developing schizophrenia are at a disadvantage when coping with day to day expectations requiring decision making, especially completing sequences with a changing background context. As in conversation there is 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.
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 cortex.
Hippocampal new cells encode incoming information stimuli temporarily, for eventual brain storage. They also retrieve such information , again temporarily, used to provide the changing context as working memory 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 likely to be overloaded with incoming stimuli.
Anxiety about these changes and the difficulties that ensue, are felt by sufferer as abnormal, before the florid illness develops.
What/who is making these adverse fears?
What can be done about it?
What explanatory account will enable them better to deal with what is happening.
Psychiatric Times link:- those patients. in whom psychosis developed later already had significantly worse attention, working memory abilities, and declarative memory abilities.
seidman plus reference link
That is what would happen when dentate gyrus fails in new cell proliferation. It points to the hippocampal failure occurring in the pre -illness years before the outcome of a delusional system.
idiosyncratic speech precedes schizophrenia
and 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 siblings move ahead and away, they are left behind. They lose natural support and mentoring. They are more anxious.
Their lives are liable to stimulus/ information overload before any signs of florid illness. That raises continual high anxiety
How and where would the brain deal with this surplus stimuli/information, pointless information,unwanted, that has some how 'got in' - been given dopamine high value, needing attention and a response.
abnormal salience especially when distractors are present
This is what happens during overload distraction in normal people.
Fuerte et al 2006: distraction
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 [ 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
Gazzaniga describes - " 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 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 response to 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 by influencing the priority of such
stimuli for the person concerned'. It also takes part in giving memories their longterm 'status'.
] It is dopamine that establishes the emotional value - fear or joy - in this case registers the continual anxiety 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 with what is going to come up in the day and the week; what to carry along in 'stand by' memory, whilst whatever else there 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