Regression & complex thinking

[Pilgrim]

Associations, as a primitive form of thought, are retained as a substructure in the development of the higher forms of thinking, but they are uncovered and begin to act independently in accordance with their own laws when the whole personality, for some reason, is disturbed. There is reason to believe that complex thought* is not a specific product of schizophrenia, but merely a cropping out of the older forms of thought, which are always present in a latent form in the psyche of the patient but which becomes apparent only when the higher intellectual processes become disturbed by illness. The regression to earlier forms of thought is observed also in other diseases in which there is interference with conceptual thinking. The process of thinking then becomes strikingly similar to thought in schizophrenia, and this probably accounts for the schizophrenic reaction in the course of physical illnesses. The other proof that these are earlier forms of thought can be found in the fact that associative thinking is latent in all of us and comes to the surface in connection with sudden emotional shocks and in a setting of fatigue, sleep and dreams. There is nothing impossible, then, in the assumption that regression of patients with schizophrenia to complex thinking is merely a reversion to earlier forms of thought. Each one of us carries schizophrenia in a latent form, i.e. in the mechanisms of thought which, when uncovered, become the central figure in the drama of schizophrenic thought. Thus, the history of the development of thought ought to be used as a means of reaching an understanding of the peculiarities of complex thinking in schizophrenia.

Lev Vygotsky, Thought in Schizophrenia.


*The factual bonds underlying complexes are discovered through direct experience. A complex, therefore, is first and foremost a concrete grouping of objects connected by factual bonds. Since a complex is not formed on the plane of abstract, logical thinking, the bonds that create it, as well as the bonds it helps to create, lack logical unity; they may be of many different kinds. Any factually present connection may lead to the inclusion of a given element into a complex. That is the main difference between a complex and a concept. While a concept groups objects according to one attribute, the bonds relating the elements of a complex to the whole and to one another may be as diverse as the contacts and relations of the elements are in reality.

Lev Vygotsky & Alex Kozulin, Thought and Language.

[Corey Browning]

Schizophrenia never ceases to amaze me. A delightfully interesting disorder, or disease, either work.

I would say, rather than observing the complex thought, perhaps a study at how this is disrupted might hold key?

However, this passage carries one big mistake, only those with a predespotition to schizophrenia hold the disorder, and not in a latent way either. Once symptoms become triggered, they usually don't end.

Even with the aid of anti-psychotics, these only stop the continuous flow of certain symptoms, never to end them. This won't be possible until we target ALL the sources of the symptoms, not only to pin-point single symptoms.

Anyhow, thank you for this. It's very interesting.

Edit: I do tend to think of schizophrenia in a biological light rather than a cognitive light. I tend to only research what triggers certain cognitive actions, such as the symptoms of this disease. I have to check and see if schizophrenia is 100% genetic, but I am sure it is. Just for reference, I am using the term schizophrenia as in the disorder, not of schizophrenic symptoms, which can be caused by many factors including cocain abuse.

[Pilgrim]

Risk & releasing agents.

Victorian studies [...] revealed that regular use of cannabis by adolescent girls could trigger long-term depression. And for those vulnerable to a psychotic disorder, even a small amount of cannabis could pose a threat. Professor Castle, author of the book Marijuana and Madness, has said that those people with this "psychotic proneness" were those who had a family history of mental illness or who had had a bad response on their first use of cannabis or to a tiny amount. Others at risk included those who had experienced a psychotic episode where they had paranoid thinking or heard a voice calling their name. Professor Castle said experiencing such a one-off episode was far more common than people thought. "People with such a vulnerability should avoid cannabis like the plague," he said. Without the effects of the drug, such a person might live their whole life without ever experiencing mental health problems. It has been estimated, for example, that between 8% and 13% of people that have schizophrenia today would never have developed the illness without exposure to cannabis.

http://www.schizophrenia.com/prevent...reetdrugs.html

...

English Wikipedia on twin studies relating to schizophrenia:

Estimates of the heritability of schizophrenia tend to vary owing to the difficulty of separating the effects of genetics and the environment although twin and adoption studies have suggested a high level of heritability (the proportion of variation between individuals in a population that is influenced by genetic factors).

Same subject, from German Wikipedia:

Twin studies have shown the genetic component, overemphasized by eugenically oriented researchers such as Rüdin or Manfred Bleuler, to be a relative influence. A closer genetic relation to someone suffering from schizophrenia means a higher probability of illness. Having a schizophrenic parent leads to a 5-10% probability, with a suffering sibling there is a 8-10% risk, by one-egged twins 45%, and by two-egged twins 21%. (If schizophrenia was a wholly genetically caused disease there would have to be a 100% probability by one-egged twins) The higher occurence among one-egged twins may also be attributed to the heightened probability of a single intrauterine infection affecting the two foetuses during a twin pregnancy.

From French Wikipedia, same subject:

Statistically, it has been observed that among most men the illness is becoming clinically apparent during late adolescence, whilst among women it appears somewhat later, and that a first-born or only child are statistically more often afflicted. None of which favour a genetic origin. One hypothesis is that heredity may predispose an individual for this illness: Among one-egged twins, if there is one person with schizophrenia, the other twin have a 40% probability. There is also a heightened risk if there is a case of schizophrenia in the same family, but this does not necessarily imply a genetic cause as twins also are exposed in utero to immune reactions caused by viral infections or to other environmental factors or co-factors. Certain genes, such as NRG1 or DTNBP1, have been identified as risk markers.

...

The English version also has further information on the various genetic components leading to a heightened risk of schizophrenia, all of which seem to make it quite clear that there is no single gene causing this illness, but rather a number of different markers combining towards a greater risk; a couple of these factors also overlapping with a greater probability of bipolar disorder.

My guess would be that, in this particular case, the heightened risk may very well have been caused by a combination of genetic factors (confirmed case(s) of suffering relative(s)) and birth trauma (as related by the mother), possibly even with cannabis/marijuana acting as the releasing agent (a sailor/harbour connection ?). As far as circumstantial evidence goes, I would not be very surprised if all of these circumstances turned out to be true.

My main purpose here, though, was merely to make a point of the regressive cognitive state typical of 'complex thinking', as it clearly seems to relate to the evidence in this case.

[Pilgrim]

...

As my last post might give the impression that a hereditary genetic component is a necessary, though not sufficient, factor in the development of schizophrenia, I may add that there also are non-familial cases caused by spontaneous genetic mutations leading to a similar heightened vulnerability. (Spontaneous Mutations Rife In Nonfamilial Schizophrenia). It might seem, then, to some extent comparable to cancer - as one may find hereditary as well as non-hereditary cases, the latter caused by spontaneous mutations induced by various environmental factors. It may also seem to some extent comparable to diabetes 1 and diabetes 2, the former showing - much as in schizophrenia - a 30-50% hereditary factor in identical twins with several genetic markers acting together; on the other hand, dietary influence of excessive fat and glucose on gene expression being a dominant causal factor in diabetes 2. So, it can seem there may be some reason to suspect that we do "each one of us carry schizophrenia in a latent form, i.e. in the mechanisms of thought (i.e. 'complex thinking') which, when uncovered, become the central figure in the drama of schizophrenic thought".