Letter 1, May BJ PSych 2010 unpublished - declined

Fiona Gaughran and Shitij Kapur
Editorial: The Psychiatrist:

How change comes: translating biological research into care

Sir, "
Thousands of papers have been published on the biological associations with psychosis yet this has had a limited impact on the routine clinical care of people with psychosis"

Certainly not much has come to practising psychiatry from biological research but it is down to clinical disregard rather than irrelevance in the research.

Clinical studies [1] agree memory falters in continuing schizophrenia in the community. Cognitive weakness is linked to that, is a trait in the illness.
Memory management requires intact neurogenesis in the hippocampal area in the brain. It correlates with the level of neurogenesis in the hippocampus. [2]

This post-mortem study on banked material [3] looking for some connection between neurogenesis in the hippocampus and mood illness found no connection there,
but instead demonstrated depletion of neurogenesis in the hippocampus of a control sample, taken from sufferers with continuing schizophrenia.

There has been no attempt to replicate nor to foster interest in this crucial finding.
I can't imagine such indifference towards an equivalent possible discovery in cancer or arthritis.

Subsequent studies [4] [5] in the area of working memory give confirmation to the finding. They show poor working memory capacity in sufferers with continuing schizophrenia, sufficient to explain how and why they fail to cope with outside engagement.

They are unable – on that account - to move on, to rehabilitate themselves.
They need help, at present an unmet need.
With hippocampal neurogenesis failing at the onset of the illness , they are unable to acquire, to build on, new experience, to take from it so as to advance personal, domestic, and social supporting skills.

Their peers,friends, family, move on. They do not.

Where depleted neurogenesis in the hippocampus is there at the beginning of the illness, consequences follow that should receive clinical attention.

1. Those developing schizophrenia later have more built in experience than when the illness starts at the earlier age. Presentation and capability will be different.

2. Working memory capacity is required for recall. Without it, memory for previous illness behaviour is faulty.
Choice cannot be from full awareness.
If there is evidence of both illness and neglect it is not 'their choice'.

3. Estimation of capacity, of insight, of the degree of illness, during professional interview alone, will be inadequate.
'Not ill as I saw them' is insufficiently based.
If declared authoritatively, it is misleading when given without the benefit of access to other, different observation, from community and family.
That used to come from the history' taken by the Social Worker - who remained in touch and was the subsequent open contact for the family or community observer.

4. Although the studies on working memory capacity explain the failure in coping with ordinary living choices and decisions, this study (5)confirms the ability to 'automate' .

5. Automation - 'chunking' - allows working memory to build up internal stores of experience bit by bit, until a whole process can be managed.

6. Rehabilitation into outside activities can be established in this way at the pace suitable to the degree of disability.
Something like a regular 'normalising' routine of outside engagement can be achieved, giving meaningful breaks for those with residual schizophrenia, giving breaks away from the burden of care on community and family carers.

7. Family carers have long known that following a routine is what helps caring, and care and treatment most, retaining regular contact, preventing relapse by relieving uncertainty and unreconciled high emotional differences.

Service provision, divided as it is between Local Authority and NHS provision., is neglecting – it is neglect - to provide the sheltering resource that will allow those with continuing schizophrenia to go into recovery.

How many OT staff are there in after-care teams ?

References : -

1. Al-usri J. Bruce, MBChB, MRCPsych, S. Frost, MBBS, MRCPsych and D. Mackintosh, MBChB, MRCPsych
Measuring memory impairment in community-based patients with schizophrenia
B J PSYCHIATRY 2006 189 132-13

2. Florian A. Siebzehnrubl and Ingmar Blumcke in
the human hippocampus and its relevance to temporal lobe epilepsies
Epilepsia, 49(Suppl. 5):55–65, 2008

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

4. JM Gold, Ph.D., Hahn, Ph.D., Zhang, Ph.D. Robinson, , Kappenman, , Becket al
Reduced capacity but spared precision and maintenance of working memory representations in schizophrenia
Arch Gen Psychiatry. 2010 June ; 67(6): 570–577.

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

References : -

4.
Neurogenesis in the human hippocampus and its relevance to temporal lobe epilepsies
F.Siebzehnrubl and Ingmar Blumcke Epilepsia, 49(Suppl. 5):55–65, 2008
hippocampal neurogenesis
Low proliferation and differentiation capacities of adult hippocampal stem cells correlate with memory dysfunction in humans
Roland Coras,,* Florian A. Siebzehnrubl,,* Elisabeth Pauli,,* Hagen B. Huttner, Njunting,et al
Brain 2010: 133; 3359–3372

5.
Measuring memory impairment in community-based patients with schizophrenia
J. Bruce, MBChB, MRCPsych, S. Frost, MBBS, MRCPsych and D. Mackintosh, MBChB, MRCPsych
B J PSYCHIATRY 2006 189 132-13

6.
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.
Nithsdale Schizophrenia Surveys 20

Letter 2. BJPsych June 2017

It is a long time since schizophrenia was the core subject for clinical Psychiatry, if it ever was, or will be again, delivery of services lapsing under competing mental health conditions with prior political imperatives. Luckily academic studies have maintained interest, subsequent to HM's surgical hippocampal disaster, many corroborating the crucial importance of brain hippocampal neurogenesis status in managing experience into memory, although clinical practice interest lags.
Importantly, hippocampal neurogenesis in continuing schizophrenia is half only of what is required normally.

. [ If I had time to put in second thoughts I would have added.
There is a heavy genetic propensity to schizophrenia .
Hippocampal failure IS the proximate cause of schizophrenia .
What and where in the genetic code would be the genetic pathway instruction that would lead to hippocampal neurogenesis failure ? That is where academic research should go no . Time to prioritise all thse Grants !! ]

It is a disaster for those with schizophrenia. for, they do not, cannot reliably, call on updated experience to get through their daily living, nor prime themslves for their more immediate future,without much more time, and by restricting the flow of incoming stimuli /information .
They are overloaded.
This situation is worse if the illness arrives in adolescence.Those whose illness arrives later will have had the chance to accumulate some settled relationships, work and domestic skills.
Less reliable hippocapal memory management needs to be emphasised when providing a clinical service. Insufficiently informed community workers need more instruction, when they visit, on the imperfect memory and reduced capacity, that will likely be present in conversational interviews.
More time is needed to accommodate changes in daily living happenings, conversation.

Protected repetition in a simplified personal environment, is an unfulfilled treatment requirement at home and in community settings.

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