Persistently poor memory in continuing schizophrenia is recorded in Bruce: Kelly (1)
A crucial study Reif (2) in post mortem tissue, found neurogenesis in the hippocampus was reduced not as the hypothesis expected in mood illness but in schizophrenia.
Schobel (3) points to the loss being at the time of onset of the illness, and stays.
Siebzhenrubl in studies on human material, confirmed mice studies; that reduced neurogenesis in the hippocampus is associated with poor working memory.
Neurogenesis in the hippocampus is necessary for maintaining working memory capacity.
Gold (4). testing working memory capacity, finds reduced working memory capacity in schizophrenia.
Depleted working memory capacity accounts for sufferers being unable to create and sustain a domestic routine, or one of engagement in outside activities by themselves.
They cannot hold on to a purposed intention , deal with, or manage appropriately, distractions to what is going on, so as to be able to complete what has been intended.
Rehabilitating themselves is outwith them.
Raalten (5)
'When encouraged and accompanied, given the opportunity to practice, sufferers do store what they have memorised: equally as well as for 'control subjects'.
Our findings support the notion of inefficient WM function and reduced capacity in schizophrenia.
This was not related to a failure in automatization, but was a failure when processing continuously changing information'.
A supportive routine in outside activities of the sort that comes ordinarily from work patterns can be established in schizophrenia by rehearsal, led and adding bit by bit , till successfully built, with a primed internal expectation.
The absence of anchoring routine outside themselves, outside the illness, is an unmet need.
The absence of occupational activities for rehabilitation, open to those with schizophrenia in the community, is an unmet health treatment .which leads to relapse.
Staff should issue a Service Deficiency Form to the Mental Health Trust and the purchasing Trust.
Family and community carers know that following an established routine is what prevents relapsing.
To leave it to family and community carers to push sufferer for engagement in outside routine, risks face to face emotion between them that provokes recrimination, or breakdown.
Insight in schizophrenia uses a sufficient working memory capacity to recognise and learn from previous errors. Sufferers with insufficient capacity do not see the need to take part in re-mediation.
Rehabilitation, in best interests, can require some degree of persuasion. Community Treatment Orders deliver authoritative advice from experience, properly with resources to provide a supportive routine
Withholding authoritative professional intervention into situations of personal and domestic neglect , on the grounds that
'it was their choice ... 'they had capacity as I saw them ' .
.. should reflect that insufficient working memory capacity is likely a general, and persistent fault after the onset of schizophrenia..
(1)Bruce :BJPsych 2006 189 132-136
(2)Reif:Molecular Psychiatry (2006) 11, 514522
(3)Schobel et al [Arch Gen Psychiatry. 2009;66(9):938-946
(4)Gold:Arch Gen Psychiatry. 2010 June ; 67(6): 570577.
(5)Raalten: Schizophrenia Research 100 (2008) 161171
David H Yates FRC Psych: family carer.
Letter to a Consultant Psychiatrist
I hope you have time to read this. Or someone in your team ?
It's something about continuing schizophrenia that people have not taken on board as a basic consideration when delivering continuing care and treatment.
It's a study by Reif in 2006on tissue taken from ' post mortem brain banks'. Neurogenesis cells[ NG } in the the hippocampus were measured, in tissue from three kinds of subjects sources.:- mood illness; schizophrenia; controls.
The author was testing a thought that NG would be altered in mood illness.
That was not so but it was the case in the schizophrenia subjects.
Reif concludes [under Discussion ]
" Does the finding of decreased Adult Neurogenesis [ AN ] in Schizophrenia [SZ ] make sense?
Sz is known to go along with several cognitive deficits, which is stable over time, that is, trait rather than state dependent.
role of hippocampus is rather memory formation than affect regulation.
Thus, diminished Adult neurogenesis, [ AN ] which has been suggested to result in impaired memory formation, will contribute to the cognitive impairment seen in Sz; improvement of cognitive functioning in Sz by clozapine might be due to the increase of AN seen in animal studies.
As learning, exercise, and enriched environment all increase AN as well, this directly points toward non-pharmacological treatment of schizophrenics. The preliminary finding of reduced AN in Sz provided in the present study is thus worth being pursued further."
If the finding in Reif is general in schizophrenia, any aftercare has to carry in their planning and provision that since the illness descended on them, they have a smaller working memory capacity.
Scott et al state that the presence or absence of a form of turbulence in the hippocampus dental gyrus precedes and predicts which of potential young candidates for schizophrenia will go that way and which will not, adds something to looking at hippocampal failure as a core problem.
Gold et al: Reduced capacity but spared precision and maintenance of working memory representations in schizophrenia'confirms this
What was experience already 'in store' at the age the illness arrived will decide the level of personal, domestic, relationship, work and interest, activities, to be worked with.
The memory problem [ dementia praecox !] that is left with schizophrenia is not progressive as in alzheimers and similar conditions.
What was stored 'inside 'before the illness struck , still there to be connected to, is available to be enlarged upon, to start rebuilding connections to outside activities and therefore to accumulate experience relevant for now.
The reduction in hippocampal neurogenesis requires that this rebuilding can only take place at the 'pace' allowed by a reduced working memory capacity.
This will by no means always be recognised by the sufferer - the insight into, and the recall of, illness behaviour - is not enough to permit this - so that co-operation must be founded first. Or some form of acceptable coercion brought to bear.
[ Raalten et al : 'Automatization and working memory capacity in schizophrenia' ]
Introducing a routine of activities away from the domestic setting is best done by ' chunking ', proceeding bit by bit , in rehearsal with a lead professional companion accompanying a sufferer on the route into engagement, taking plenty of unhurried time over the introduction, making favourable circumstances, setting the scene carefully, for mutual acceptance, into a daily and weekly routine, that will act as an anchor place to turn to when 'adrift in illness '.
Such 'breaks' within the weekly days, gives community carers a time to themselves. reduces 'face to face ' opportunties for the emotional expression of tired rejections.
It is the absence of the kind of settings in the community, that would allow this re-introduction into activities, that thwarts rehabilitation.
Day centres have lost the outward direction, the bridging step towards maintaining 'outside' activities, relevant to the interests and abilities of those attending.
They are not decisively led by secondary mental health. The division and argument between Health and Social service in accountability, responsibility for this provision, and the source of funding for it, is what prevents service to residual schizophrenia developing.
Add that to the difficulty in obtaining engagement from the sufferer, and giving up on them is explicable, if unforgiveable.
Here is on extract from a very concerned leader of an Inquiry after a Homicide Report .....
"The failure to engage with Mr Gonzales, exemplified by individual and system failures, was influenced by the negative attitude about his care and treatment which existed throughout his contact with the service after he left the Oaktree clinic.
To succeed, the approach must be one of determined therapeutic optimism. Goals need to be achievable rather than unattainable dreams, and failures need to be treated as correctable mistakes.
Service-providers should not punish themselves for making mistakes, but see them as an opportunity to find out why the plan did not work and to make a better one.
If the next attempt fails, it again needs to be rectified by analysing the failure and trying something else. And so on until, if necessary, all the creative and professional resources of the trust have been brought to bear.
Front line staff should be given the resources to work in this way
That is the most telling comment.
A service delivering rehabilitation for this illness is best given on the basis that it is a fault in structural working memory capacity for which a remedy is to be found in continuing treatment and care?
Deciding not to intervene , on grounds of of 'it is their choice' ... 'they had capacity' must be decided not in a routine interview, but measured against what their current life behaviour, what the present support says about their circumstance, what their current life behaviour shows about their overall working memory capacity to rehabilitate themselves.
yours sincerely,
a letter to a research neuroscientist
Brit Elvevaag MD
....................................................................... D H Yates FRC Psych
National Institute of Mental Health
USA
44 01208 816035
davidwatch@bt.internet.com
16th May 2011
Dear M(r)s B Elevevaag,
I have re-read the review you did in 2003, with T Goldberg .... that ' Cognitive impairment in Schizophrenia is the Core of the Disorder ': a trait failure.
Reif 2006 seems to give it substantiation
[ stem cell proliferation is decreased in schizophrenia, but not in depression A Reif1,4, S Fritzen,4, M Finger, A Strobel, M Lauer, A SchmittK-P Lesch Molecular Psychiatry (2006) 11, 514522 ]
yet is neither quoted, nor given critical attention, nor taken into account in WM studies.
Reif found reduced hippocampal neurogenesis in banked material, not when looking for it in mood illness, but instead finding it in schizophrenia.
Scott at al
[ Scott et al http://archpsyc.ama-assn.org/cgi/reprint/66/9/938 ]
looking to see how to predict which out of people chosen as being more vulnerable would turn out to get the illness found that a 'commotion' in the hippocampal area when seen , is a great predictor, whereas when there was no such changes , the illness did not follow.
Siebzehnrubl
[ Neurogenesis in the human hippocampus and its relevance to temporal lobe epilepsies
Florian A. Siebzehnrubl and Ingmar Blumcke Epilepsia, 49(Suppl. 5):5565, 2008 ]
confirms what is known from 'knockdown' mice studies that hippocampal neurogenesis is crucial to working memory.
When seen in surgically removed tissue from subjects with temporal epilepsy that there was reduced hippocampal neurogenesis in surgically removed brain tissues from the hippocampus of epilepsy cases, it was from subjects that had poor memory.
issue from such people, in good memory,test taking had adequate neurogenesis.
What follows from poor working memory is failure in working capacity tests - shown many times and in prospective memory tasks and simulations of 'real' challenges.
As lessened neuro-genesis is a structural reduction, it is not likely to be open to retraining although particular areas can be accommodated, and stored, by 'chunking' - bit by bit building - rehearsal accumulations with lead companions on particular projects again as in your prospective study, and in Goldberg later
[
Terry E. Goldberg, PhD; et al 2007;64(10):1115-1122 ]
concludes that remediation in particular studies, only improves result in that area it does not generalise something confirmed in your later paper with on prospective memory on a pursuit game and in Raalten
This Gold study
[ Gold:Arch Gen Psychiatry. 2010 June ; 67(6): 570577.
]
fits in with what would expected to be a consequence of poor WM giving Reif some confirmation.
Surely Reif requires urgent ratification.
If reduced hippocampal neuro-genesis is the general finding in schizophrenia, happens at the time of the origin of the illness, stays that way , then your original Review is correct.
Study now should go into finding out how the reduction in neurogenesis at the onset of the illness is brought about.
If Reif is correct, sufferers cannot rehabilitate themselves, nor can remediation alter trait failure, but can bring about satisfactory living routines, by rehearsal, bit by bit, so adding on engagement in activities outside themselves, giving them the sort of support that routine of work schedules bring to ordinary weeks. [ Automatization and working memory capacity in schizophrenia Tamar R. van Raalten a,?, Nick F. Ramsey , J. Martijn Jansma , Gerry Jager a, Renι S. Kahn / Schizophrenia Research 100 (2008) 161171
BMC Psychiatry [ research article open access ]
It really is important that those dealing with after-care in schizophrenia change their expectations and their attitude to long term residual schizophrenia, no longer being put off by ... it's their choice ...or, it's too difficult to get them involved when they won't co-operate
it's not won't ...it's can't - without a genuine lead concern.
Do you know of any appreciation of the Reif study ? I can't find any ratification of his findings ?
D H Yates FRC Psych
family carer
References
Stem cell proliferation is decreased in schizophrenia, but not in depression A Reif1,4, S Fritzen,4, M Finger, A Strobel, M Lauer, A SchmittK-P Lesch Molecular Psychiatry (2006) 11, 514522
Differential targeting of the CA1 sub- field of the hippocampus by schizophrenia and related psychotic disorders.
Scott A. Schobel; Nicole M. Lewandowski; Cheryl M. Corcoran; Holly Moore; Truman Brown; Dolores Malaspina; Scott A. Small Arch Gen Psychiatry. 2009;66(9):938-946.
Neurogenesis in the human hippocampus and its relevance to temporal lobe epilepsies
Florian A. Siebzehnrubl and Ingmar Blumcke Epilepsia, 49(Suppl. 5):5565, 2008
JM Gold, Ph.D Hahn, Ph.D.1 Zhang, Ph.D Reduced capacity but spared precision and maintenance of working memory representations in schizophrenia Kappenman, , Beck, , and Luck, Ph.D Arch Gen Psychiatry. 2010 June ; 67(6): 570577.
Automatization and working memory capacity in schizophrenia Tamar R. van Raalten a,?, Nick F. Ramsey , J. Martijn Jansma , Gerry Jager a, Renι S. Kahn / Schizophrenia Research 100 (2008) 161171
BMC Psychiatry [ research article open access ]
prospective memory in schizophrenia
Brita Elvevaag, Elizabeth A Maylor, Abigail L Gilbert
article is available from: http://www.biomedcentral.com/1471-244X/3/9
Letter to a neurophysiologist at the Imperial College London - a neighbour of the Editor of thr BJ Psychiatry Journal
http://nervenklinik.uk-wuerzburg.de/fileadmin/uk/psychiatrie/Dokumente/Forschung/Psychiatric_Neurobiology_and_Bipolar_Disorder_Program/Adult_neurogenesis_in_schizophrenia.pdf
Reif et al 2006 found hippocampal neurogenesis to be reduced in brain bank tissue in schizophrenia. Do you know of any work that has confirmed this finding as a general fault in schizophrenia.
Memory is poor in schizophrenia.Working memory, working memory capacity, prospective memory are all insufficient to update experience in schizophrenia who remain stuck at the level of expereince when their illness arrived.
The hippocampus seems to work as a common choke point, a limiting factor, in working memory capacity tasks. In real life it means they cannot renhabilitate themselves.
They cannot take forward personal living matters - comparitive to co-ordinating the planning and taking forward to completion, cooking of a midday sunday meal.
But they can progress if they are allowed time and helped via small add on capabilities till they arrive at successful full engagements, from this rehearsal.
Surely a discovery of poor hippocampal neurogenesis in schizophrenia has to be established in some urgency with confirmatory study.
There is little point in further study of outcomes on tasks, if poor neurogenesis in the hippocampus of schizophrenia sufferers is there at the starting point. I am alarmed that there seems to be no confirmation , no attempt to do so , after Reif.
D H Yates FRC Psych
I am retired but have my son with schizophrenia living with me.
I have gathered relevant studies and links to papers at http://www.schizophreniawatch.co.uk/fresh%20page.
Letter to a neuropathologist with access to a 'brain bank'
Reif et al 2006
Reif et al 2006 found hippocampal neurogenesis to be reduced in brain bank
tissue in schizophrenia.
Do you know of any work that has confirmed this
finding as a general fault in schizophrenia.
Would your service hold brain from
people suffering with schizophrenia.
Memory is poor in schizophrenia. Working memory, working memory capacity,
prospective memory are all insufficient to update experience in schizophrenia.
They remain stuck at the level of experience when their illness arrived.They
can't move on.
The hippocampus seems to work as a common 'choke point, a limiting factor', in
working memory capacity tasks.
In real life it means they cannot rehabilitate
themselves. They cannot take forward personal living matters - comparitive to
co-ordinating their cooking of a midday sunday meal.
But they can progress if they are allowed time and helped via small add on
capabilities till they arrive at successful full engagements, by this
rehearsal.
Surely a discovery of poor hippocampal neurogenesis in schizophrenia has to be
established in some urgency with confirmatory study.
There is little point in
further study of outcomes on tasks in schizophrenia, if poor neurogeneisis in
the hippocampus in schizophrenia is there at the starting point.
I am alarmed
that there seems to be no confirmation , no attempt to do so , after Reif .
D H Yates FRC Psych
[ NB your predecessor was my brother ]
I am retired but have my son with schizophrenia living with me. I have gathered relevant studies and links to papers at
http://www.schizophreniawatch.co.uk/fresh%20page.html
E-mail to a working psychiatrist
...
I cannot understand how it is that the study by Reif in 2006 is neither referred nor taken into account in discussions about providing after-care service to schizophrenia.
Especially where someone decides a sufferer is choosing to live the way they do, choosing not to engage, choosing not to take part in activities found for them by Rehabilitation services, so should be left alone.
The Mayan Coomeraswame Inquest revealed an outcome that is disturbing.
There are enough studies noting poor memory in schizophrenia to require a further look at the study by Reif .
Looking for a failure of neuro-genesis in the hippo-campus in in bank tissue taken from brains from post mortems on sufferers from mood illness, instead he found reductions tissuetaken from people with schizophrenia.
Hippocampal neurogenesis is essential for working memory.
In tissue taken from surgical intervention, from subjects with epilepsy S found that as in many knockdown studies in mice that if subjects had poor memory the hippocampus showed reduction in neurogenesis. Conversely where memory was good neurogenesis is intact.
Gold recently concluded that people with schizophrenia have a restricted working memory capacity.
Without capacity ordinary personal and domestic matters can't be progressed.
It's not choice for them, it's that they do not have working memory capacity to hold all the contingencies in place to complete an intention.
And haven't been able to add and acquire experience because of that loss of capacity the since when the illness arrived.
They are stuck with the experience and capabilities they had when the illness struck.
If it happens after early adulthood they keep the personal and domestic and social skills they had realised and stored away then.
The illness starting in adolescence never reaches the level of personal competence.
Raalten gives hope and points to rehabilitation. When a new matter is approached, rehearsing, bit by bit, 'chunking' , the bits can be consolidated.
.
letter to the British Journal of Psychiatry - now amended above
..... ......
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