What is it that we are trying to make up for in residual schizophrenia.?
Family carers know that an established routine helps for the day and the week ahead.
It is there as an anchoring reminder to prepare for daily living . An established routine for the week ahead helps by raising something definite for memory to be ready for.
Kraepelin wasn't so far out with calling it 'dementia praecox'
Many studies with patients indicate uncertain memory storage systems. Old stores and old interests are better kept, but are not always so accessible or relevant to current issues in living. Skills in current living don't seem to build on and hold.
It's a common ordinary observation:at times 'not all there'
There is no evidence that people with schizophrenia have more fleeting or off-the-mark memories than healthy subjects.
Rather, they are unable to simultaneously hold as many items at once in working memory. When you cannot at the relevant time call up the experience that is required to deal with something going on, hold on to it and update the background as you go along, that makes for mistakes in dealing with matters that have to be attended to along the way.
A routine in living arrangements reduces the amount of working memory needed.
If the working memory pool to be drawn upon is at times reduced, making and maintaining that routine yourself is more difficult, and may not be achievable.
The professional service has to help out.
If necessary with Community Treatment Orders - with the reciprocal benefit of being helped into an acceptable and working routine.
Working memory, the ability to briefly store and manipulate information, is the essential guide to completing purposeful behaviour
A more recent such investigation of 'working memory' has it that the 'available working memory pool' is reduced in schizophrenia.
Participants were clinically stable on medication.
They were presented with three or four different colors on a computer screen. After a pause when the screen went blank, subjects were to indicate the colour shown in a particular spot by selecting and clicking on it on a colour wheel. Subjects who stored the colour in memory and recalled it when tested should select those colours similar to those previously shown.
The results suggest that schizophrenia reduces working memory capacity, causing subjects with schizophrenia to store fewer items.
The length of delay made no difference in either the number of items recalled or the precision of recall for either control or patient group, contrary to expectations of less stable memories in schizophenia.
' Memory difficulty in schizophrenia is characterized primarily by reductions in storage capacity and not by an instability of the working memory representations '
There is not always enough memory available to deal with what is happening.
[ this is why conversation with sufferers is difficult and limited - there is little 'small talk' - it is literal ...concrete .... it follows leading, rather than leading - the pool of associations is not enough for making talk interesting and fresh, is not held in the background, there to be used for recall to initiative and association.
Where the talk is about things the sufferer knew well in the past before illness, the associations there are fixed enough before illness to help conversation along, and perhaps updating those associations is a route to helping engagement with others ]
How to expalin this reduced memory pool ? A most likely fault lies in the hippocampus where sufficient neurogenesis is needed to cope with the maturing in experience that comes from updating the information store
James Gold of the University of Maryland School of Medicine in Baltimore and colleagues questioned whether, as some theories suggest, working memory would be unstable and imprecise in schizophrenia.
Using novel methods that enabled them to tease apart different aspects of working memory,
they found no evidence
that people with schizophrenia have more fleeting or off-the-mark memories than healthy subjects.
Rather, they are unable to simultaneously hold as many items at once in working memory.
In light of these findings, Gold et al. recommend a trip back to the drawing board to revise current theories of the neurobiology of working memory deficits in schizophrenia.
Schizophrenia-related cognitive deficits hamper patients’ lives (see ), and
a recent meta-analysis found consistent evidence of large working memory deficits in subjects with schizophrenia as compared to healthy subjects ().
Working memory, the ability to briefly store and manipulate information, guides goal-directed behavior through other cognitive processes.
Several researchers have tried to explain the biological basis of cognitive symptoms in schizophrenia.
For instance, John Lisman and colleagues () suggest that reduced N-methyl-D-aspartate (NMDA) channel function impairs memory in schizophrenia by disinhibiting pyramidal cells in the hippocampus, thereby reducing gamma waves (see ).
Edmund Rolls and associates () suggest that reduced dopamine in schizophrenia decreases NMDA currents, causing neural networks to randomly fire, adding noise that drowns out information-carrying signals, rendering the networks unstable.
Daniel Durstewitz and Jeremy Seamans () propose that imbalanced activation of dopamine D1 and D2 receptors in the prefrontal cortex may result in excess noise and overly frail representations in memory.
These theories could lead one to expect imprecise or unstable working memory in schizophrenia.
Yet, when Gold and colleagues looked at previous findings regarding working memory in schizophrenia,
they found reason to doubt that schizophrenia causes faster-decaying or less accurate memories.
Members of the research team, Wei Zhang and Steven Luck, both of the University of California at Davis, had recently devised a way to separately examine the number of representations in memory, the precision of those memories, and their stability over time.
This provided an opportunity for the research group to test current theories of deficits in the workingmemory of individuals with schizophrenia.
The researchers’ approach involved a case-control design in which the researchers tested the working memory of 31 clinically stable patients who met criteria for schizophrenia or schizoaffective disorder.
They compared them with 26 mentally healthy subjects who had no history of psychosis.
Controls mirrored the patients in age, sex, ethnicity, and parental education.
All participants were presented with three or four different colors on a computer screen.
After a pause when the screen went blank, subjects were to indicate the color shown in a particular spot by selecting and clicking on it on a color wheel.
Subjects who stored the color in memory and recalled it when tested should select colors similar to those actually shown.
Those who did not would have to guess.
By examining the distribution of errors, Gold and colleagues
determined the probability that subjects held an item in memory at test time and the precision of that representation.
To check the stability of working memory representations, they tried both a one-second and a four-second delay.
They reasoned that if patients with schizophrenia have unstable memories,
they should perform worse than control subjects after a short delay.
A mixed bag
The results suggest that schizophrenia reduces working memory capacity,
causing subjects with schizophrenia to store fewer items.
Even so, patients recalled items that had been stored in memory with the same precision as healthy subjects.
Furthermore, the length of delay made no difference in either the number of items recalled
or the precision of recall for either group, contrary to expectations of less stable memories in schizophrenia.
“In our view, the recent biological accounts discussed above are at odds with much of the behavioral literature, and clearly at odds with the data presented here,” write Gold and associates.
While Gold et al. acknowledge that a longer delay might bring out unseen differences between the two groups of subjects,
they think that a four-second delay should be sufficient for detecting the disruptive working memory deficits expected in schizophrenia.
They cannot explain why the working memory of subjects with schizophrenia would hold fewer items,
although they note that neuroimaging studies point to the parietal cortex, perhaps in league with the prefrontal cortex,
in setting capacity for visual working memory.
They write, “Unfortunately, there is very little understanding of the origins of capacity limits in the basic cognitive neuroscience literature.”
All of the patients in the study were undergoing treatment with antipsychotic medication,
including clozapine in 18 cases, suggesting that other treatments had failed them
This indicates that clozapine may boost the signal-to-noise ratio
Gold and colleagues ' patients in the early stages of schizophrenia might show a different pattern of deficits.
They also caution that the results might not extend to other working memory tasks
that activate different neural pathways and/or do not involve color judgments.
Despite these findings, or maybe because of them, Gold and colleagues see a great need for models that explain the actual working memory deficits seen in schizophrenia.
Even so, they write, “these models must accurately capture the behavioral endpoint,
which is characterized primarily by reductions in storage capacity and not by an instability of the working memory representations.”—Victoria L. Wilcox.
Reference: Gold JM, Hahn B, Zhang WW, Robinson BM, Kappenman ES, Beck VM, Luck SJ. Reduced capacity but spared precision and maintenance of working memory representations in schizophrenia. Arch Gen Psychiatry. 2010 Jun;67(6):570-7.
back to schizophrenia:- uncertain memory storage systems
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