Schizotype

obyvatel

The Living Force
Schizophrenia is a psychiatric disorder that has been studied quite extensively. Its prevalence rate is estimated to be around 1% in populations over the age of 18 years. It is believed that schizophrenia has a genetic component. Related to schizophrenia are personality disorders like schizoid and schizotypal disorders along with others which belong to the schizoid spectrum. Research on the cause (etiology) of schizophrenia has revealed some interesting insights. Here I will make an attempt to summarize the speculative theory put forward by Paul E Meehl, former professor of psychology in the University of Minnesotta. His publications are available at the university site (http://www.tc.umn.edu/~pemeehl/). I would also include some info on the schizoid and schizotypal personality disorders.

The question would come "why this topic?" I came across this topic while looking into schizoidal psychopathy in Political Ponerology. I was confused by some terms of a descriptive nature and wanted to see what was the basis of these terms. This is a complex topic - but I think it is worth getting a basic idea as it may have a pretty wide ranging effect on the population and is related to stuff we discuss here. I will be quoting and paraphrasing from Meehl's papers as well as other material.

Meehl's Theory

Schizophrenia involves both powerful genetic factors, and powerful environment factors. Any theory purporting to explain why some persons fall ill and others do not, that considers only one of these two classes of factors, is radically defective. Some humans have a talent for schizophrenia, just as some have a talent for playing the violin. But not everybody with violin talent becomes a violinist, and not everybody with a talent for schizophrenia becomes a schizophrene.

[quote author=Meehl]
Clinical schizophrenia (under which I include pseudo-neurotic as well as disintegrated degrees of decompensation) has a specific etiology, a sine qua non, a condition which is necessary but not sufficient for the production of the disease. This specific etiology I postulate to be a dominant gene, the ‘schizogene.’ Nobody can get schizophrenia if he lacks the schizogene, nobody in fact avoids schizotypy if he carries the schizogene, but many people — I postulate most, well over half — who carry the schizogene avoid schizophrenia, i.e., they remain compensated or at lease semi-compensated and at no point become psychiatrically diagnosable even by the currently enlarged standards of American psychiatry for the use of the schizophrenia label.”
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So there is a dominant gene termed schizogene which is passed on through inheritance. Theorists and researchers have suggested that the milder pathologies, such as personality disorders, represent undeveloped or minimally expressed defective genes; for example, the schizoid personality may possess a schizophrenic genotype, but in this case the defective gene is weakened by the operation of beneficial modifying genes or favorable environmental experiences which would include life experiences as well as diet related factors ( gluten and schizophrenia ). Meehl’s theory includes a dominant schizogene with polygenic potentiators like introversion, anxiety, hypohedonia (lower ability to experience positive emotions) which can be treated as temperamental factors.

According to Meehl, a single dominant gene produces a basic cognitive and cognitive-emotional “slippage” by altering some function of the synapse at all points in the nervous system, but in an extremely subtle way. The term used is “hypokrisia” which means neural integrative defect or “insufficiency of separation, differentiation or discrimination”. This schizotaxic gene is “silent” in most cases and its owners cannot be identified on the basis of hallucinations or delusions.

Schizotaxia, Hypokrisia, Schizotypy

The term schizotaxia is coined by Meehl. It is derived from schizo - schism or break and ataxia - disturbance in arrangement, array, marshalling, ordering.

[quote author=Meehl]
I conjecture that whatever is wrong with the schizotaxic CNS (central nervous system) is ubiquitous, a functional aberration present throughout, operating everywhere from the sacral cord to the frontal lobes. More specifically, this “something wrong at all levels” is something wrong about the way individual neurons work, a functional parametric aberration of the synaptic control system. The integrative defect in schizotaxia is ubiquitous instead of being localized to cerebral subsystem defects.
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As mentioned earlier, hypokrisia is the term used for this ubiquitous functional control problem at the level of synapses in a neuron. Meehl used the word "parametric" in this regard which indicates that it can be quantitatively bigger or smaller rather than a present or absent kind of situation. The word hypokrisia means an insufficiency of separation, differentiation, or discrimination.

Schizotypy is the resultant state of this defect. The form and content of this state is influenced by environmental conditioning and life experiences. So schizotypy is not inheritable but what is inheritable is schizotaxic central nervous system . Only a minority of persons with the CNS defect decompensate to the point of being diagnosable by psychiatric criteria. So in this respect most schizotypes are like men with the genome for gout who do not develop clinical gout throughout their entire life.

What is meant by hypokrisia or defect of integration?

[quote author=Meehl]
By saying that the defect is integrative, I mean that it is not a defect of input, storage, or retrieval, but it is analogous to (but different from) some other well recognized integrative defects: dyslexia, tone deafness, the specific spelling defect in some persons of normal intelligence and verbal ability, nonanatomic dysarticulation syndrome, attention deficit disorder, and perhaps some extreme degrees of poor motor control in persons free of neurological injury.
[/quote]

Why so many terms?
[quote author=Meehl]
I have been faulted for needless proliferation of language in distinguishing schizotaxia from schizotypy, since on my theory they are perfectly correlated in the population. Suffice it to point out that a correlated extension of two attributes does not collapse them into one attribute. As logician Quine likes to point out, the taxonomic fact that every animal with a heart has a kidney does not mean that the terms “heart” and “kidney” are synonyms to the biologist! Here we have different levels of analysis, one (schizotypy) in terms of psychisms, a second (schizotaxia) as an open concept about the integrative function of the brain, and a third (hypokrisia) as a specific conjecture about the neuron level process that underlies the schizotaxia. They are three distinguishable concepts, which is why a theorist could buy one of them and not the other two, or two of them and not the third. So we need a semantics adequate to discuss them.
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Base Rates

Based on empirical statistical data about the incidence of schizophrenia and inheritance , Meehl hypothesizes that the rate of incidence of schizotypy is 10% . This is a high base rate. Meehl comments

[quote author=Meehl]
If one thoroughly assimilates Rado’s concept of schizotypy, and thinks about the fairly contented and highly achieving schizotypes like “Kepler and Newton, Calvin and Kant, Schiller and Rousseau, Erasmus and Spinoza, Whistler and Goldsmith, Wagner and Chopin, Robespierre and George Washington…” (Menninger, 1930, p. 76), matters appear differently. Naturally the schizotypes one knows as a clinician are more or less distressed, at least part of the time, or we wouldn’t find them in our practice. For someone with my views, who finds many schizotypal nonpatients among colleagues, neighbors, students, it seems evident that there are a lot of schizotypes who lead relatively contented and fulfilling lives, especially if their polygenic situation is favorable, (e.g., not too much anxiety parameter or hypohedonia), and if they have good fortune in their occupational choices and their choices of a mate.
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How can such a high base rate be possible for a genetic defect through evolution when it is known from empirical data that diagnosed schizophrenes have low fertility rates? Shouldn't the deviant gene have long disappeared from the gene pool?

[quote author=Meehl]
Since schizotypy is not the same as schizophrenia, we cannot move directly from the impaired fertility of diagnosed schizophrenes to an equal impairment for schizotypes. The development of psychotic symptoms early in life is presumably a more severe impairer of reproductive fitness than merely having a schizoid personality makeup. It is well known that the fertility impairment is considerably lower in female schizophrenes than in males. I think a semicompensated female schizotype sometimes combines a certain carelessness about contraception with a special kind of erotic attractiveness (alluded to briefly in my 1962 paper), especially for neurotic males. In my 1962 paper I conjectured (although I have no quantitative support) that a plausible family constellation genetically for a schizophrene consists of a nonschizotypal father with anxiety or introverted polygenes, attracted to a compensated schizotypal mother, so that the proband gets the specific genetic loading from the mother’s side and the adverse polygenic potentiators from the father’s side.

If schizotypy had in past time some survival value for individuals, this could countervail a somewhat lower reproductive rate for those that survive. It has been suggested to me by a student that the narcissistic element of the schizotype could quite possibly have a survival value in the individual refusing to engage in group conflict such as war, raiding parties, etc., which are dangerous. Then there is a fairly good likelihood that in some preliterate cultures the shaman becomes so because of schizotypal characteristics such as hallucinations, dissociative tendencies, and the peculiar charisma of some bright, dominant schizotypes (Hitler, Wittgenstein). But I agree that this kind of speculation is dangerously ad hoc...
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Decompensation of schizotypy

The link between schizophrenia and shamanic and messed up shamanic capacities based on diet has been discussed in a C session here . Meehl discusses (other) potent environmental factors that can cause decompensation of a schizotype.

[quote author=Meehl]
One can divide environmental influences into those that were operative during the formative period of the psyche and current stressors on the adult. The decline of the schizophrenogenic mother theory has led to dismissal of her theoretical importance, so I will go out on a limb and forecast that when we have better data, requiring high-validity personality measures, she will be found to play a causal role, and one larger than father. The most malignant parental pattern for male schizotypes is a dominant, controlling, hypohedonic, ambivalent, character armored, compensated schizotypal mother (who transmits the schizogene and provides an aversive reinforcement schedule) and an anxious, insecure, passive, introverted, ineffectual father (who transmits the potentiating polygenes and provides a poor role model and no protective buffering from mother). This combination is bad genetically and environmentally, and maximizes the probability of adult decompensation. As a colleague put it, harshly but conveying the family flavor, “The worst setup is a schizy battleaxe mother and a Caspar Milquetoast father.”
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With some stretching of language, I subsume under the heading of “trauma” both major single traumata (e.g., childhood rape, witnessing violent death of a parent) and accumulative small traumata such as double bind rejections, unfavorable comparisons with preferred siblings, rejection by the peer group in school, effects of grinding poverty, and the like. I believe that cumulative small traumata or one major trauma raise the odds of adult decompensation. More broadly, I conjecture that almost any insult organic or social, suffices to raise the odds.
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With regard to the precipitating stressors of adult life, I am inclined to lay great weight upon the “luck factor.” I agree with Sir Karl Popper that sheer luck, happenings that befall us that are not attributable even to some unconscious selection of our friends or occupations and which have nothing to do with the repetition compulsion, play a crucial role in human happiness, health, and achievement. Social scientists underestimate the sheer luck factor because it does not lend itself very readily to inclusion in our predictive and explanatory equations (Meehl, 1978, p. 811 and references cited thereat). The difference between a schizotype who wins the Pulitizer Prize for poetry, and his MZ twin who ends up as a chronic deteriorated schizophrene in the state hospital may not always be understandable by some kind of systematic factor of the sort that psychologists and sociologists are accustomed to putting into their equations, such as a strong parental preference for one twin, or one twin having been dropped on its head as a baby.
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To be contd.
 
If the schizophrenia is bound(connected) to this gene, the "schizogene", which 10 % of the population possesses, it would mean that the rest of the population would be protect or even immunized by the typical attacks "illusions" by the entities 4 STS? Because you seem to say that the disorders(confusions) bound to this gene are activities only by a social environment, in particular the parents who favor a twin and not the other one! Are not there far more powerful strengths who influences the behavior? Or maybe I badly understood?
 
Kisito said:
If the schizophrenia is bound(connected) to this gene, the "schizogene", which 10 % of the population possesses, it would mean that the rest of the population would be protect or even immunized by the typical attacks "illusions" by the entities 4 STS? Because you seem to say that the disorders(confusions) bound to this gene are activities only by a social environment, in particular the parents who favor a twin and not the other one! Are not there far more powerful strengths who influences the behavior? Or maybe I badly understood?

I think you didn't really understand the text. Why would the rest of the population be "protected" or "immunized" against "attacks" by 4D STS? There are so many other genetic problems among them that just because they missed this one doesn't mean they don't have another. Further, for all we know, the issues of neuronal "slippage" of different types can be caused by other things including environmental factors.

So, just notice that this discussion is about ONE particular disorder and is not saying anything about others, or lack of disorders.

What strikes me is that the presence of this gene might be far more widespread than 10% though without co-factors that lead to obvious dysfunction. Consider the Authoritarian Follower type of individual, for example.
 
Laura said:
Kisito said:
If the schizophrenia is bound(connected) to this gene, the "schizogene", which 10 % of the population possesses, it would mean that the rest of the population would be protect or even immunized by the typical attacks "illusions" by the entities 4 STS? Because you seem to say that the disorders(confusions) bound to this gene are activities only by a social environment, in particular the parents who favor a twin and not the other one! Are not there far more powerful strengths who influences the behavior? Or maybe I badly understood?

I think you didn't really understand the text. Why would the rest of the population be "protected" or "immunized" against "attacks" by 4D STS? There are so many other genetic problems among them that just because they missed this one doesn't mean they don't have another. Further, for all we know, the issues of neuronal "slippage" of different types can be caused by other things including environmental factors.

So, just notice that this discussion is about ONE particular disorder and is not saying anything about others, or lack of disorders.

What strikes me is that the presence of this gene might be far more widespread than 10% though without co-factors that lead to obvious dysfunction. Consider the Authoritarian Follower type of individual, for example.
Because my brother is schizophrenic, sometimes he has language alien aggressive or unknown alien on earth (or a disappeared language), his voice is completely different and her personality also. Thus I do not know if it is " just the disorders " schyzotypes bound to the genes, to the neuronal dysfunction or the 4D STS who penetrate in him thanks to this genetic disturbance.
We are all attacked(affected), but the attacks which we undergo are not they bound to our genetics, as openings showing our vulnerability in STS? Every genetic vulnerability, in an attack STS different!
Maybe that it would be more difficult for the 4D STS to penetrate into a body if he had no this schizogene?
 
Kisito said:
Because my brother is schizophrenic, sometimes he has language alien aggressive or unknown alien on earth (or a disappeared language), his voice is completely different and her personality also. Thus I do not know if it is " just the disorders " schyzotypes bound to the genes, to the neuronal dysfunction or the 4D STS who penetrate in him thanks to this genetic disturbance.
We are all attacked(affected), but the attacks which we undergo are not they bound to our genetics, as openings showing our vulnerability in STS? Every genetic vulnerability, in an attack STS different!
Maybe that it would be more difficult for the 4D STS to penetrate into a body if he had no this schizogene?

If your brother has it, then you have a high probability of having it too. So, what differences do you observe between yourself and your brother? How do you know you are immune to attacks? How do you know that they are not just more subtle and hidden in yourself, and more easily accessible to the conscious mind in your brother?
 
obyvatel said:
Schizophrenia is a psychiatric disorder that has been studied quite extensively. Its prevalence rate is estimated to be around 1% in populations over the age of 18 years. It is believed that schizophrenia has a genetic component. Related to schizophrenia are personality disorders like schizoid and schizotypal disorders along with others which belong to the schizoid spectrum. Research on the cause (etiology) of schizophrenia has revealed some interesting insights. Here I will make an attempt to summarize the speculative theory put forward by Paul E Meehl, former professor of psychology in the University of Minnesotta. His publications are available at the university site (http://www.tc.umn.edu/~pemeehl/). I would also include some info on the schizoid and schizotypal personality disorders.

The question would come "why this topic?" I came across this topic while looking into schizoidal psychopathy in Political Ponerology. I was confused by some terms of a descriptive nature and wanted to see what was the basis of these terms. This is a complex topic - but I think it is worth getting a basic idea as it may have a pretty wide ranging effect on the population and is related to stuff we discuss here. I will be quoting and paraphrasing from Meehl's papers as well as other material.

....

To be contd.
Thanks for the info Obyvatel. It's interesting info indeed. Looking forward to the next section.
 
Meehl's Theory

Schizophrenia involves both powerful genetic factors, and powerful environment factors. Any theory purporting to explain why some persons fall ill and others do not, that considers only one of these two classes of factors, is radically defective. Some humans have a talent for schizophrenia, just as some have a talent for playing the violin. But not everybody with violin talent becomes a violinist, and not everybody with a talent for schizophrenia becomes a schizophrene.


Quote from: Meehl
Clinical schizophrenia (under which I include pseudo-neurotic as well as disintegrated degrees of decompensation) has a specific etiology, a sine qua non, a condition which is necessary but not sufficient for the production of the disease. This specific etiology I postulate to be a dominant gene, the ‘schizogene.’ Nobody can get schizophrenia if he lacks the schizogene, nobody in fact avoids schizotypy if he carries the schizogene, but many people — I postulate most, well over half — who carry the schizogene avoid schizophrenia, i.e., they remain compensated or at lease semi-compensated and at no point become psychiatrically diagnosable even by the currently enlarged standards of American psychiatry for the use of the schizophrenia label.”

So there is a dominant gene termed schizogene which is passed on through inheritance. Theorists and researchers have suggested that the milder pathologies, such as personality disorders, represent undeveloped or minimally expressed defective genes; for example, the schizoid personality may possess a schizophrenic genotype, but in this case the defective gene is weakened by the operation of beneficial modifying genes or favorable environmental experiences which would include life experiences as well as diet related factors ( gluten and schizophrenia ). Meehl’s theory includes a dominant schizogene with polygenic potentiators like introversion, anxiety, hypohedonia (lower ability to experience positive emotions) which can be treated as temperamental factors.

According to Meehl, a single dominant gene produces a basic cognitive and cognitive-emotional “slippage” by altering some function of the synapse at all points in the nervous system, but in an extremely subtle way. The term used is “hypokrisia” which means neural integrative defect or “insufficiency of separation, differentiation or discrimination”. This schizotaxic gene is “silent” in most cases and its owners cannot be identified on the basis of hallucinations or delusions.

This theory fits with some of my thoughts over the past few weeks, the basic idea that a certain percentage of people (some environmental factors I imagine would differ from certain regions across the planet) could have one or more "silent" anomalies within their genes that were either lacking a yet to be found catalyst, or having one with a diminished role. I was reading up on RNA because of the pathways of some diseases & mutations but I hadn't yet stretched my thoughts to make the full connection with synapses, (if I had I would probably have started at the neural net - a usual suspect) & hypohedonia although I didn't know of that word, has been another prevalent thought of mine looking for a right place to sit.

I had been pondering whether schizophrenia was really a part of the autistic spectrum of disorders or vice versa when I first looked into autism in a serious way, but recently I haven't been able to acquire the info that could have shed a light on that idea one way or the other.

So if a person with a schizotaxic CNS produce offspring is it right to say that the offspring will inherit the same? Or maybe the foundations for it? How is that affecting the neuroception process of the nervous system? If the neural circuits have been damaged & environmental risk assessment along with it, then the normal cues go out of the window. For children of schizophrenics & whatever is inherited, they will likely down regulate the social engagement system, (due to stress, trauma) & begin to gain more clinical disorders that may only be adaptive responses that can be brought back around so to speak, with the right kind of stimuli apparently.
So to say that this is (possibly) ubiquitous, a " functional parametric aberration of the synaptic control system" is pretty big, to me at least. What of paranoia, hysteria (from a personality development perspective) hypokrisia (underlying schizotaxia) possibly forming the bases of some authoritarian followers?

Is it incorrect to say limbic resonance can be altered by "the parametric aberration" (of the synaptic control system) & that this could add to emotional over-excitability in some with good positive disintegration on one side (of potential AF' s/authoritarian followers) & sensual-psychomotor O.E./over-excitability on the other?
If the polygenic situation is unfavourable for schizotypes (& epistasis is fairly complex) & they interact with say, characteropaths or another "heavy" pathological deviant (propagating a strong psychological contagion) how much will that change those individuals given that it's commonplace to find adults at a child-like emotional level?

Thanks to obyvatel for this thread.
 
obyvatel said:
Meehl’s theory includes a dominant schizogene with polygenic potentiators like introversion, anxiety, hypohedonia (lower ability to experience positive emotions) which can be treated as temperamental factors.

Laura said:
What strikes me is that the presence of this gene might be far more widespread than 10% though without co-factors that lead to obvious dysfunction. Consider the Authoritarian Follower type of individual, for example.

This reminds me of an analogy on brain programming and rewiring explained on the video Your brain in porn. He was explaining that addiction changes the brain like a process of creating a path in the grass as you walk more and more through it. If the process was coupled or due to strong emotions, i.e. anxiety, shock, humiliation, shame, guilt... it was the equivalent of creating a path with a weed wacker. The path is very strong and every time you feel shame or guilt, you run the program that makes you crave the addiction and walk through the path of less resistance. This was the reason why it was important not to feel shame or guilt, but to realize that the addiction was simply not helping.

So I was thinking that perhaps those who regardless of anything, still can't let go feelings of hypohedonia or anxiety, shame or guilt that make them walk the path of less resistance are those who are the Authoritarian Follower types.
 
Psyche said:
So I was thinking that perhaps those who regardless of anything, still can't let go feelings of hypohedonia or anxiety, shame or guilt that make them walk the path of less resistance are those who are the Authoritarian Follower types.

Well, it has been noted by various "authorities" that the fundie type individual is more likely to be guilty of sexual perversions than non-believers. Maybe there is something about "belief" that is mixed up in here?
 
Schizotype Signs

Hypokrisia manifests as “associative loosening” and “aversive drift”.

Associative loosening results in a failure to bring different aspects of a problem together and leads to cognitive slippage in thought and speech.

Aversive drift is a steady progression of an individual towards a negative tone of affect leading to a gloomy pessimistic attitude towards life.

How does a schizotype appear? The answer to that question depends on how well he is compensated. It can be manifested through thought disorders, interpersonal fear or through laboratory tests measuring psychosomatic and neurological dysfunctions some examples of which would be eye tracking dysfunction, working memory impairment, motor dysfunctions etc. What is described is for people who were brought into treatment - which implies some level of decompensation.

It is important to note that schizotypy is not the same as either schizophrenia or schizotypal or schizoid personality disorders though there are points of overlap. Schizotypy is a broader construct which can manifest in various ways including schizotypal, schizoid, paranoid, obesssive and other symptoms. Like mentioned earlier, schizotypy is not inherited. What is inherited is a schizotaxic nervous system which then manifests as schizotypy based on environmental conditions and other polygenic potentiators.

Aversive Drift

Regarding aversive drift, Meehl writes

[quote author=Meehl]
As one learns more about the patient he is struck by the fact that with the passage of time everything tends to get some negative loading. You get the feeling that all activities and relationships are somehow subtly “poisoned” as soon as the patient tries to make them his own. No person remains a “good figure”; no idea remains clearly acceptable; no interest or hobby can retain its appeal. The patient’s psyche seems to have kind of a “reverse Midas touch”—everything he touches turns to garbage…
Even a voluntarily under-taken new hobby gradually becomes boring, then irksome, and then even anxietous or shameful (e.g., “I haven’t practiced my cello lately. I hate the sight of it.”).
[/quote]

How does this differ from a normal or even a neurotic outlook? Success in what is undertaken would maintain the behavior in a normal and neurotic people; for the schizotype, activities tend to take on a burdensome, negative emotional charge with time even if they are successful.

Meehl mentions some special negative affective states.
[quote author=Meehl]
A striking and baffling manifestation of aversive drift is the occurrence of intensely negative affective states not clinically identifiable as variants of the commonly recognized aversive emotions. Although I lack quantitative evidence and cannot cite supportive clinical literature—surely there must be reports of it?—my psychotherapeutic experience suffices to convince me. Once a clinician has noticed it and learns to probe for it, the phenomenon is unmistakable, showing up in a sizable minority of pseudoneurotic patients and in the majority of disintegrated schizotypes. I have treated bright, introspective, and psychologically sophisticated individuals with Hoch-Polatin syndrome who complained of an acutely unpleasant mental state but steadfastly refused to accept my proffered labels (e.g., “anxiety,” “shame,” “guilt,” “grief” [object loss], “depression”). I am persuaded that this is not a semantic or defensive matter; rather it reveals the existence of a special kind of negative affective state that I, a nonschizotype, cannot empathize with because I have never experienced anything close to it in phenomenal space. I wish I (lazy!) had been systematically recording exemplary verbal expressions of it over the years, but here are some I can recall: “My whole mind just hurts” (this from the woman—a psychology student—in whom I first noted the symptom some 45 years ago); “It’s a bad pressure in the head” (query: a headache?), “No, in my mind, a stress”; “There’s a kind of friction in the brain when it works”; “I am mentally stretched on a rack”; “It’s this perpetual damned strain, strain, strain”; “There’s a sort of tension going on inside, a pulling and hauling”; “My thoughts are an intense irritation, like a sore.”
[/quote]
Interestingly, the examples Meehl gave relate to the schizotype’s propensity to use physical sensation words with reference to the mind while rejecting feeling words even when they are offered.

Cognitive slippage

It is difficult to give an exact definition of cognitive slippage and the term has some vagueness about it. Meehl describes it as a person with cognitive slippage is unusually aberrated in regard to how accurately he perceives and thinks about reality. This description would not make much sense if someone subscribes to post modern relativistic beliefs or the new age YCYOR (you create your own reality) beliefs. The meaning of the term hinges on the difference between fantasy and reality. Cognitive slippage manifests as thought disorders at various levels - from the most obvious delusions and hallucinations of schizophrenics and paranoids to increasingly subtle forms in well compensated schizotypes.

[quote author=Meehl]
The clear clinical forms of cognitive slippage represent those gross breakdowns of ego-function which are well-recognized among the accessory symptoms of florid psychotic schizophrenia—i.e., delusions and hallucinations. I do not suppose there is much that needs to be said about these, other than the importance of attempting to distinguish, if necessary by persistent and probing “cross-examination” whether or not the patient has started to cross that fine line between an obsessional idea and a delusional belief. Sophisticated and cagey patients may at times pay lip-service to the abstract possibility of their being mistaken when careful questioning (with special attention to the patient’s manner) will show that this is purely a matter of lip-service and that, experientially and behaviorally speaking, the patient has a pretty strong belief, or at least “quasi-belief,” in the content of his aberrated ideation.

Example: A usually well-compensated schizotype calls me up in a state of panic to make a special emergency appointment. Upon entering the office, she remains standing while telling me that her husband, who has taken a short trip away from the city, is having her followed by a private detective. She immediately adds the “insightful” comment, “Do you think I am going crazy or something? People have told me that I am paranoid, and of course it is quite possible that I am reading too much into the things that have been happening.” This comment shows that the patient is managing to retain a considerable criticality toward her own ideation and has a grasp, however tenuous, of external reality; but it would be quite incorrect to conclude from this that the patient is therefore, by virtue of her insight, free of cognitive slippage. She is deathly afraid to leave my office for that the hypothetical detective may be lurking in the corridor. As she recounts the particular incidents which led her to formulate this idea—incidents which individually and collectively could not possibly impress a rational mind and which, a few days hence, she retrospectively sees rationally—it is evident that by most of the usual standards of “genuine belief” she momentarily believes in the private detective hypothesis. Her comments about her own possible over-interpreting are a sop to her rational ego, and an attempt to show herself (and the therapist) that she is quite capable of being reasonable and engaging in critical thought. But she does not really, substantively, at the feeling and acting level, entertain very strong doubts about the truth of her momentary private detective notion. In what she sees and hears, in how she feels, and in how she acts, it is “as if” she fully believed in the existence and menace of the detective. The critical, self doubting comments are not insincere; but they are the only indicators of disbelief. She makes them because her rational ego is not utterly shattered or suspended, and therefore she can hardly avoid having at least the thought that “error may occur,” even to her. But she is, momentarily, at least a 75% believer in the detective.
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A second form of cognitive slippage is a subtle manifestation of a disturbance in association which is hard to describe in general terms. Certain verbal responses appear odd to a listener even though the right rules grammar and semantics are being followed. . Meehl writes that words appear in certain contexts which are not likely to be used by a normal mind.

[quote author=Meehl]
It may not involve anything more than the occurrence of a word at a certain point in a sequence of words which in the normal non-schizoid laws of association would have a very low transitional probability of appearing at that precise locus. So that when we look at the individual sentence it is hard to say exactly what is “wrong” with it and yet hearing such a person talk for an hour one has a very strong clinical impulse to say, “This individual somehow speaks ‘differently,’ ‘strangely,’ ‘oddly,’ or ‘unusually,’ but I don’t know just why I say that.”
[/quote]

Meehl gives some examples
[quote author=Meehl]
I still like my 1962 example of the patient who explained his presence in the institution by saying, “Well, doctor, naturally I am growing my father’s hair,” which would not leave a first-year medical student or undergraduate psychology major in doubt as to the psychiatric diagnosis.

I recall a patient I tested on my internship with the Healy Picture Completion II who had placed an alarm clock (instead of a book) in the picture where the boy is spilling his books on the way to school. Asked in the inquiry why he did that, he replied, “So he will have time to get to school.” Nobody but a schizophrene would say such a thing.

The Healy Pictorial Completion Test I was devised by William Healy in Chicago. It detected juvenile ‘delinquents’ or ‘defective and aberrational individuals’ as Healy termed them. It is an aptitude test. These were important in psychological testing during the 1920s. Children were given an illustrated scene with parts of the image missing. These parts could be replaced with a variety of imagery options. The child’s choice was scored and assessed.


Or consider the patient who, when asked why his conversation was sometimes hard to follow by others, replied, “Oh, that’s because I usually speak Echo Monster Head Affair Language.”

A fainter one, but which I find classified immediately by experienced clinicians, a patient (responding during the inquiry as to the aliveness of the usual lateral animals on Rorschach VIII) said, “Oh, yes, these images have the true resembling properties of live animals.”

One must distinguish between the rambling quality of some schizophrenic discourse (as in many of the examples in Bleuler’s book), which can be understood primarily as a lack of a guiding, overarching goal, so that the patient speaks like somebody free associating on the couch or trying to write a “stream of consciousness novel,” and the strange aberrations in syntax and semantics that can appear in discourse that preserves normal relevance, focusing, and goal-orientation.
[/quote]

Another example of cognitive slippage comes from the person who complains of getting perplexed and confused and mixed up in his thinking with such a high frequency that it represents a major feature of their personality. This type of confusion does not refer to being conflicted between different options which can be clearly articulated. Cognitive slippage applies when the thoughts and ideas are separately vague, scrambled or unclear. Thought deprivation or the mind going blank quite often would indicate cognitive slippage.

Regarding irrationality or distortion of reality Meehl writes
[quote author=Meehl]
I agree with Albert Ellis and Bertrand Russell that irrationality (illogical deductions plus faulty collection and evaluation of data) is not a rare aberration but pretty much the normal human condition. Cognitive, clinical, and social psychologists tell us that cognitive mistakes do not require that powerful motivational–affective distorting influences be at work (Dawes, Faust, & Meehl, 1989; Faust, 1984; Nisbet & Ross, 1980; and see references cited by Meehl, 1990c). Of course such counterrational forces, whether psychodynamic or ideological, often act to potentiate the garden-variety slippage to which our cerebral computers are prone. Further, even hyperrationalist Bertrand Russell makes the point that most of what we believe is believed on authority, since no one has the time or competence to investigate all the subjects on which he entertains opinions. Reliance on others is not irrational, so long as one picks the right (?) others and gives them the proper (?) weights. The relevance of this consideration for psychopathology is that attenuation of social bonds may be expected to reduce the search for consensual validation which normally serves as a check on cognitive slippage.

I conclude that delusions, in general, do not require an abnormal brain. This is of course compatible with conjecturing that an abnormal brain is sometimes the source, and that some kinds of delusions may be hard to come by if the brain’s chemistry and microstructure are normal.

One can analogize to a crazy computer printout. The transistors may be defective (like having schizotaxic neurons). Or a saboteur may have pounded it or poured acid into it (like a concussion or lead poisoning). Or the program may have bugs in it (like being raised to think oddly by a malcommunicative pathological family). Or the mechanism and program may be all right, but the data fed in are incorrect (like news propaganda or a trusted friend deceiving one). All of these are “physical” in the metaphysician’s sense, but they are obviously not all “organic disease” in the conventional sense of the neurologist.
……………………………
I tend to order secondary thought disorder on a scale running from least to severest pathology (with increasing probability of primary slippage due to cellular level malfunction involved) thus: Depressive delusions < Persecutory delusions < Grandiose delusions < Auditory hallucinations < Visual hallucinations.
[/quote]

Meehl warns clinicians against reflexively discounting as cognitive slippage those instances where someone distorts reality but the clinician can clearly see his motivations for doing so.

[quote author=Meehl]
We do not decide as to the presence or absence of cognitive slippage by inquiring whether the patient had motivations to distort, since everybody always has motivations to distort. The difference which is critical in evaluating this particular sign is the difference between those of us who are able to distort given our momentary motivational and affective condition, and those of us who are not. It is pretty clear that, most of the time, most of us are literally unable to distort reality into high accord with our desires. Furthermore, extreme degrees of motivational and affective pressure can often be brought to bear upon normal and neurotic individuals without producing more than a minimal amount of cognitive distortion.

My point is that when a person engages in a marked and refractory distortion of reality in the presence of only slightly ambiguous stimulus inputs and with opportunity for consensual validation (especially by the therapist), even though the drives are moderately strong or the affects moderately severe, his ability to achieve this distortion testifies not primarily to the strength of the motivational and affective variables but testifies primarily to his defect in cognitive control. The presence of such a defect, the individual’s talent—however he acquired it—for distorting, is an important aspect of the cognitive slippage sign.

Let me give an example of these distinctions from my own therapeutic practice. The patient, a semi-compensated schizotype, is a woman of high intelligence, having an advanced degree in one of the documentary social sciences, and a fairly wide acquaintance with abnormal psychology from her associates and her avocational reading. .. One day another patient of mine, with whom the first patient is not personally acquainted but whose name and appearance are familiar to her, is circumstantially forced to change her appointment time. I call the first patient on the telephone and find out whether it will be convenient for her to come one hour later than usual, which it is. As she is waiting for her interview, she sees the other woman emerge and recognizes her. She begins the session in a somewhat “sulky” manner, avoiding looking at me, and with her body slightly turned away as she speaks. To my tentative interpretation that she is angry with me but doesn’t wish to say why, she blurts out “Of course I am—and you know very well why! You changed the appointment because you like Mrs. X more than you like me, so you wanted to see her first.”

The rest of the hour is spent on ramifications of this bit of cognitive slippage, and neither interpretation, nor gentle (but authoritative) attempts at reality-definition by the therapist, seem to have the slightest effect. I want to emphasize that for this 50-minute period, the patient believes that I changed the hour because of my personal preference for the other patient, and that this is not merely a funny kind of obtrusive, obsessive thought which she is unable to get rid of. There is a critical difference between a neurotic’s saying, “I can’t get rid of the silly idea that you prefer the other patient, but I know that is nonsense,” and this schizotypic patient who says, “You’re just not telling me the truth, but I know that’s why you changed the hour.” In the first case, the intrusive thought is rejected by the rational ego and experienced as part of one’s symptomatology; in the second case, the rational ego fails to screen the thought for its absurdity and makes it its own, including a determined advocacy during the remainder of the hour.
………………………..

The essential features of “unreasonableness” (this is a better word rather than “illogicality,” since inductive inference and construction is involved rather than tight deductive syllogistic reasoning) seem to include the following:

1) Content of construction or hypotheses intrinsically improbable.

2) Systematic failure to consider alternative hypothesis of higher antecedent probability which would explain the same allegedly “corroborating” facts.

3) Confusion between “observation” and “immediate inference” in the verbal description of an allegedly corroborating fact (e.g., patient persistently fails to consider that his perceptions of other people’s thoughts, motives or affects are, strictly speaking, not observations but inferences).

4) Handling of discorroborative data by subsuming them under multiple alternative and ad hoc hypotheses, instead of re-examining the main one.

5) At the time, definite belief, as contrasted with admittedly unreasonable, obsessional concern or preoccupation.

If these features are present in the patient’s thinking, it should be considered evidence of cognitive slippage and the sign checked as present, regardless of whether you as therapist can understand or empathize with the motivation for the slippage. A failure to identify cognitive slippage often comes from overstressing the “dynamic understandability” of a patient’s cognitive slippage, whereby the clinician deceives himself into supposing that because the slippage is motivated in a way that the clinician can comprehend psychologically, therefore the slippage is somehow less extreme than it seems to be in terms of its content and evidence.
[/quote]

A striking bit of cognitive slippage found in schizotypes with paranoid defenses is “assumed mutual knowledge.” The patient refers to episodes or persons without explaining or narrating what would be essential for the listener to understand his discourse, as if somehow the listener must already know. This is an example of magical thinking and ideation.

Ambivalence
Intense, rapid shifts in feelings towards the same object or activity. It is not the same as liking some aspects of a person and not liking other aspects and thus being overall ambivalent. Schizotypic ambivalence is more unreasonable and uninfluencable, and it gives the impression as having come out of nowhere. The shifts in feelings occur without being perceptibly influenced by external events or experiences.
Example

[quote author=Meehl]

A patient has strong positive feelings toward his girl friend because of her affectional warmth, shared esthetic interests, and healthy sexuality. But from time to time he finds she is secretly stepping out on him, which makes him angry at her. This is not ambivalence, but merely the individual’s reaction to different facets of his reality, some of which are gratifying and others frustrating.

By contrast, consider the following example: During the course of treatment a patient recounts a series of episodes in her life and also brings in several current instances, in which a too-rapid, uncritical, and intense positive response was made to a new acquaintance. After a short “honeymoon” period, the patient begins to bring in rather minor or trivial incidents or remarks made by this new acquaintance, and manifests real hatred toward the person in recounting them. Nevertheless the patient is greatly concerned about the correct interpretation of these little episodes and continues to show a gross over-reaction to signs of affection or disinterest by the other party. The whole thing is greatly blown up out of proportion to the realities and has the earmarks of schizotypic ambivalence.
[/quote]

Body Image Aberrations

Body image aberrations involves experienced (perceived or quasi-believed) distortion of the body as to size, shape, connection, or causal relation to other bodies or objects. Examples: “It seemed I was expanded”; “Somehow I felt as if I was somehow connected to the chandelier”; “I am terrified by a feeling that I am sort of melting into you, that I am really getting mixed with you somehow—it’s hard to explain.”

Researchers have compared the schizophrenic body image aberrations with out of body experiences. The main differences are that for schizophrenic aberrations, there is difficulty in marking out the boundaries of the body, uncertainty in location of the body, blurred identity, confused thinking and a feeling of “going crazy” with loss of reality testing. For obe, identity remains intact, the location of the body is clear, and the experience may be integrated into the personality with no loss of reality testing.
 
All of this is definitely enlightening. In a way, it is kind of like the person who always sees the glass as half empty vs the one who sees it as half full.

I think all of us here on the forum can say that we have seen this sort of thing manifested right here in cyberspace. Though I'm sure there are individuals who manage to keep a tight facade on the forum but, in real life, in closer relationship with intensified social demands, reveal this sort of "cognitive slippage."

Lobaczewski was right: the important thing is the psychophysiological substratum on which all the rest of the personality is assembled. If that is faulty - slippery - then things are quite unstable though the degree of instability can vary from person to person.
 
It is somewhat enlightening for me as well. I'm almost certain I've experienced this sort of thing, but maybe someone can tell me if my experience doesn't match.

Some of the behaviors cross over into other afflictions like sentiments of narcissists. My father described the ultimate relationship as being like two people melding together and becoming one, although the outer manifestation would have been my mother becoming an extension of him. It sounds like he associated some kind of slipping with the feeling of love. It has always mortified me that I feel I know why he thinks this - and I've always tried to use him as an example of how I should NOT be.

I think me and others in my family are often victims of this slippage. When I started to observe my thoughts in the way I described in the "music as a narrative" thread, I became aware of these kind of cognitive slips. Food is a very powerful influence on this. It's also much more likely before or after sleep. The unique thing is that these slips can be addicting. If I've eaten something really insidious, I might wake up and I'll have a constant dialogue or rant running in my head making very little sense. A slip can be an intense dopamine hit, or it can be deeply disturbing, moreso than most of the thoughts one could have, except without any justification. If these thoughts aren't somehow taken care of or quarantined, I think it tends to polarize thoughts to extremes, to cause splitting even in mundane thoughts.

I suspect that some people with sufficient cognitive slippage use this slippage to justify their wishful thinking and to cancel out logic. When one slip is made, it produces an impression and that impression can be devoted to memory and used as a trigger to overcome that annoying rationality that's such a wet blanket (IE my father and his supremely blissful "meld"). If you were to track it down, it would be one of those things that you "just can't describe" - because it is a paradox by definition, and as far as your mentation is concerned it is nothing but a bridge to candyland.

I think the feeling that such a slip produces will be different for different people. For people who pay attention to rationality and understand scientific concepts, it might feel like an ache or be otherwise unpleasant. But the right slip at the right time may have an addictive effect, if it is not identified - and these moments are like the thoughts between thoughts, which are very subtle. I've become aware that for me, slippage is connected with a lack of presence of mind, a reduced attention span, or tunnel vision. Often it's a stark indicator of this state in me if I'm getting nothing done at all. If I sit down and try to self-remember, and be aware, it is like a momentary ache or throbbing in my head, and a mental feeling of a sort of waking up and priorities getting rearranged. Below that is an undercurrent of anxiety or fear, which seems to act as a kind of gravity that continually pulls me into this state.

Before I was able to observe all this, I had a tiny attention span and these moments would just have seemed like periods of blankness to me. Yet I could tell something odd happened in the transition. After going back over the memory over and over and trying to observe what I felt, and fostering a sort of real-time curiosity I guess, I started having more consciously detailed memories of those events.

I used to try and fit these slippages everywhere I could when I was young. Slipping for me was a way of life; I did my best to keep myself in a whirling bliss. So, I either was extremely bored or was doing the same things over and over again, indulging in very narrow pursuits. Any way I could press that button. At the same time concentration was extremely difficult, so I hated math, and without an attention span, I couldn't do well in English either. Still, I seemed to learn most of what I was taught easily without homework.

After I became able to observe it happening, my concentration improved. It's like a a huge button that you sit on and under your weight, the gears begin to turn. Most people can just sit on it and not have any other worry - that is sufficient for most things in life at least. But for me it seems sometimes the gears get running too fast and get out of alignment, so I have to watch the machine carefully and hold myself up a bit at the right moments, and sometimes reach in and set the gears back. It doesn't seem to take any extra time to do this, just effort, and I don't see that as any different than the kind of effort needed to apply the Work. I have some corroboration on this, because I was doing a psych evaluation and I found I was able to memorize and reorder long strings of numbers in my head (I don't remember how long). So while making me less error-prone, this practice also improves my attention span. I'm also not so weighed down by superfluous thoughts. I can often get straight from thought A to thought B pretty directly without lapses or confusion, and this efficiency allows me to think more things and ultimately pay more attention to what a conversation partner really means or is asking for. Again, before I became "watchful", this kind of concentration could occur, but I wouldn't be able to remember it because it is just so subtle. I would immediately forget what I was working on, or I would forget the conclusion I had come to, or the word I was trying to use.

I hope this is as useful as it is long-winded.
 
What a fertile ground for discussion Obyvatel is laying out! Thanks a bunch! :D

obyvatel said:
Schizotype Signs

Hypokrisia manifests as “associative loosening” and “aversive drift”.

Associative loosening results in a failure to bring different aspects of a problem together and leads to cognitive slippage in thought and speech.

Aversive drift is a steady progression of an individual towards a negative tone of affect leading to a gloomy pessimistic attitude towards life.

How does a schizotype appear? The answer to that question depends on how well he is compensated. It can be manifested through thought disorders, interpersonal fear or through laboratory tests measuring psychosomatic and neurological dysfunctions some examples of which would be eye tracking dysfunction, working memory impairment, motor dysfunctions etc. What is described is for people who were brought into treatment - which implies some level of decompensation.

{snip}
[quote author=Meehl]
As one learns more about the patient he is struck by the fact that with the passage of time everything tends to get some negative loading. You get the feeling that all activities and relationships are somehow subtly “poisoned” as soon as the patient tries to make them his own. No person remains a “good figure”; no idea remains clearly acceptable; no interest or hobby can retain its appeal. The patient’s psyche seems to have kind of a “reverse Midas touch”—everything he touches turns to garbage…
Even a voluntarily under-taken new hobby gradually becomes boring, then irksome, and then even anxietous or shameful (e.g., “I haven’t practiced my cello lately. I hate the sight of it.”).

How does this differ from a normal or even a neurotic outlook? Success in what is undertaken would maintain the behavior in a normal and neurotic people; for the schizotype, activities tend to take on a burdensome, negative emotional charge with time even if they are successful.[/quote]

This really fascinates me. I am reminded of the concept of how the human memory system works. Memories are always overwritten when recalled, and coloured by the context in which the recall occurs. It almost sounds like something similar is happening in schizophrenia, schizotype, schizoidia, and paranoia (the "class A personality disorders"). The main difference being that it's not really that there are errors in recalling and writing content per se, but rather that the metadata, associations and other cognitive/affective structures that combine concretes into coherent, meaningful content is infected with noise as time goes on.

There's also these quotes:
4) Handling of discorroborative data by subsuming them under multiple alternative and ad hoc hypotheses, instead of re-examining the main one.
[quote author=Meehl]
We do not decide as to the presence or absence of cognitive slippage by inquiring whether the patient had motivations to distort, since everybody always has motivations to distort. The difference which is critical in evaluating this particular sign is the difference between those of us who are able to distort given our momentary motivational and affective condition, and those of us who are not. It is pretty clear that, most of the time, most of us are literally unable to distort reality into high accord with our desires. Furthermore, extreme degrees of motivational and affective pressure can often be brought to bear upon normal and neurotic individuals without producing more than a minimal amount of cognitive distortion.

My point is that when a person engages in a marked and refractory distortion of reality in the presence of only slightly ambiguous stimulus inputs and with opportunity for consensual validation (especially by the therapist), even though the drives are moderately strong or the affects moderately severe, his ability to achieve this distortion testifies not primarily to the strength of the motivational and affective variables but testifies primarily to his defect in cognitive control.[/quote]

The bolded parts make me wonder whether these motivations to distort reality are simply post-hoc confabulations that come as a result of cognitive slipping, and aren't merely a convenient defence for the pathological ego structure? If so, this really drives the point home about how someone who engages in conversion and selection-and-substitution of data truly becomes enslaved to these unconscious schizoidal "leaks" in correct mental functioning.

[quote author=Meehl]Body image aberrations involves experienced (perceived or quasi-believed) distortion of the body as to size, shape, connection, or causal relation to other bodies or objects. Examples: “It seemed I was expanded”; “Somehow I felt as if I was somehow connected to the chandelier”; “I am terrified by a feeling that I am sort of melting into you, that I am really getting mixed with you somehow—it’s hard to explain.”

Researchers have compared the schizophrenic body image aberrations with out of body experiences. The main differences are that for schizophrenic aberrations, there is difficulty in marking out the boundaries of the body, uncertainty in location of the body, blurred identity, confused thinking and a feeling of “going crazy” with loss of reality testing. For obe, identity remains intact, the location of the body is clear, and the experience may be integrated into the personality with no loss of reality testing.
[/quote]

Sounds like the bottom fell out of the schizophrenic's theory of mind and proprioception. :O

Anyway, the subject raises shamanism-related questions:

1) Do all shamans have a schizotaxic CNS?
2) the C session speaks of schizophrenics having shamanic potential waylaid by epigenetics and environmental conditions. In what ways would associative loosening and cognitive slippage be utilized "properly" in a correctly-tuned spirit world-reading instrument?

[quote author=Wikipedia]Positive and negative symptoms
Schizophrenia is often described in terms of positive and negative (or deficit) symptoms.[18] Positive symptoms are those that most individuals do not normally experience but are present in people with schizophrenia. They can include delusions, disordered thoughts and speech, and tactile, auditory, visual, olfactory and gustatory hallucinations, typically regarded as manifestations of psychosis.[19] Hallucinations are also typically related to the content of the delusional theme.[20] Positive symptoms generally respond well to medication.[20]

Negative symptoms are deficits of normal emotional responses or of other thought processes, and respond less well to medication.[8] They commonly include flat or blunted affect and emotion, poverty of speech (alogia), inability to experience pleasure (anhedonia), lack of desire to form relationships (asociality), and lack of motivation (avolition). Research suggests that negative symptoms contribute more to poor quality of life, functional disability, and the burden on others than do positive symptoms.[21] People with prominent negative symptoms often have a history of poor adjustment before the onset of illness, and response to medication is often limited.[8][22][/quote]

Obviously a shaman would not have negative symptoms, since that would interfere with their normal human functions. So it would be more a matter of the brain being structured in such a way that the positive manifestations of schizophrenia can be controlled and channelled correctly to introduce certain concepts or perceptions to the shaman conducive to his or her aim as dictated by their magnetic center or positive emotions.

Since a higher emotional center is something you're born with, it makes sense that a healthy, robust instinctive substratum is set up to aid in the realization of its possibilities, and hence requires the participation of the conscious aspects of our emotions as well (System 1 and System 2 working in unison, in other words). In schizophrenics, I think this component of control seems to be lost, and thus these slips or intrusions of bizarre content or subtractions of essential content occur without rhyme or reason. An analogy to demonic possession could be drawn here.

A shaman I know is actually adamantly, militantly, anti-marijuana on the grounds that it erodes the possibilities of developing high spiritual connections. Several studies have linked marijuana use to the manifestation of schizophrenia and psychosis (which can be considered the manifestation of the positive symptoms of schizophrenia) in some genotypes. So there's that puzzle piece too, though I'm not sure how useful you'll find the anecdotal bit. :P
 
I do not know if there is correlation between real shamanic capacities and schizotypy. If we go with Meehl's formulation, schizotypy at its roots is characterized by a defect of integrating inputs at a neural level. The incoming sensory information may not be much different from the baseline or average case.

Anomalous experiences related to use of special substances is accompanied by heightened sensory experience. We know that there are usually a lot more available sensory inputs than what we are consciously aware of. There are filters which determine what signals we pay attention to and these cross the boundary from the unconscious and enter into the conscious domain. If the filters stopped working, and this boundary became loose and porous, we would be overwhelmed with more data input than we can process. The end result would be a failure to meaningfully integrate all the input but the cause is not an inherent defect but rather the system being overloaded beyond its capacity. In Meehl's computer analogy, this would be a case of data overload instead of faulty transistors though the end result would look similar - ie garbled output.

Real shamans are able to tune into signals which are not recognized by others. The shaman must also possess the ability to process this extra input and develop this ability further through discipline and knowledge to put it to good use. If this does not happen due to chemical imbalances caused by wrong diet and other environmental challenges and life experiences, the shaman is unable to integrate those extra signals which he receives and consequently shows symptoms of schizotypy. But at the root of it, the shaman is working with more data than normal. A schizotype could be working with the same input as another normal person but his failure to integrate this normal level of data is due to the inherent defect of the schizotaxic nervous system.

This is my current thinking which may or may not be correct. So fwiw.
 
A couple of recent articles on schizophrenia which may offer clues:

Schizophrenia tied to abnormal memory network in brain
http://www.sott.net/article/267645-Schizophrenia-tied-to-abnormal-memory-network-in-brain

...researchers at the RIKEN-MIT Center for Neural Circuit Genetics at the Picower Institute for Learning and Memory at MIT have uncovered what they term "a faulty brain mechanism" they believe is crucial in the eventual development of schizophrenia and other psychiatric disorders in humans. ...

The non-modified mouse brain goes into a resting state after running a maze, allowing the brain to process the information related to the maze experience. As an example, if you've ever played a puzzle game like Tetris or Sudoku, you might find after putting it down you are still playing the game in your mind. This style of information processing is indicative of normal brain function.

However, in the modified mouse brain, the team found the exact opposite occurs. Rather than going into a resting state, electrical activity in the hippocampus actually surged. ...

During its maze run, the non-modified mouse brain will fire off neurons in the hippocampus at key locations within the maze. These are known as place fields. Once out of the maze, the normal brain will replay these place fields in specific order during rest periods. This aids in building memory which allows the mouse to move through the maze faster the next time around.

This action, however, did not occur in the same way in the brains of genetically modified mice. The place cells, while collected during the maze run, were seemingly reactivated during the rest period in no discernible order. In fact, the place cells were reactivated at an abnormally high level and almost simultaneously.

"We think that in this mouse model, we may have some kind of indication that there's a disorganized thinking process going on," said Suh, a research scientist at the Picower Institute. "During ripple events in normal mice we know there is a sequential replay event. This mutant mouse doesn't seem to have that kind of replay of a previous experience."


and same study from a different angle:

Schizophrenia linked to abnormal brain waves
http://www.sott.net/article/267637-Schizophrenia-linked-to-abnormal-brain-waves

Schizophrenia patients usually suffer from a breakdown of organized thought, often accompanied by delusions or hallucinations. For the first time, MIT neuroscientists have observed the neural activity that appears to produce this disordered thinking.

The researchers found that mice lacking the brain protein calcineurin have hyperactive brain-wave oscillations in the hippocampus while resting, and are unable to mentally replay a route they have just run, as normal mice do.

Mutations in the gene for calcineurin have previously been found in some schizophrenia patients. Ten years ago, MIT researchers led by Susumu Tonegawa, the Picower Professor of Biology and Neuroscience, created mice lacking the gene for calcineurin in the forebrain; these mice displayed several behavioral symptoms of schizophrenia, including impaired short-term memory, attention deficits, and abnormal social behavior. ...

Previous studies have shown that in normal mice, "place cells" in the hippocampus, which are linked to specific locations along the track, fire in sequence when the mice take breaks from running the course. This mental replay also occurs when the mice are sleeping. These replays occur in association with very high frequency brain-wave oscillations known as ripple events.

In mice lacking calcineurin, the researchers found that brain activity was normal as the mice ran the course, but when they paused, their ripple events were much stronger and more frequent. Furthermore, the firing of the place cells was abnormally augmented and in no particular order, indicating that the mice were not replaying the route they had just run. ...

The researchers speculate that in normal mice, the role of calcineurin is to suppress the connections between neurons, known as synapses, in the hippocampus. In mice without calcineurin, a phenomenon known as long-term potentiation (LTP) becomes more prevalent, making synapses stronger. Also, the opposite effect, known as long-term depression (LTD), is suppressed. ...

The researchers believe the abnormal hyperactivity they found in the hippocampus may represent a disruption of the brain's "default mode network" - a communication network that connects the hippocampus, prefrontal cortex (where most thought and planning occurs), and other parts of the cortex.

This network is more active when a person (or mouse) is resting between goal-oriented tasks. When the brain is focusing on a specific goal or activity, the default mode network gets turned down. However, this network is hyperactive in schizophrenic patients before and during tasks that require the brain to focus, and patients do not perform well in these tasks.
 
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