Monthly Archives: March 2013

Schizoaffective disorder: False memory as a logic error

Author: Genecks
Education: B.S. Neuroscience (2011)
Contact: Inbox at forums

The following are my opinions and not to be taken as a measure of my character. This is but a blog. Feel free to read this blog entry at your own risk. I do not claim to be a professional on any of these views. Many of the views discussed are speculations. I hope to present some original research that I have conducted.

As of late, I’ve been considering how schizoaffective disorder works.

Schizoaffective disorder is a psychiatric diagnosis that describes a mental disorder characterized by recurring abnormal mood and psychotic components. The mood component may be elevated or depressed (bipolar or depressive subtype), or simultaneously elevated and depressed (mixed episode), and these abnormal mood components alternate with, or occur together with, psychotic symptoms. For a diagnosis of schizoaffective disorder to be valid, according to current DSM criteria (but not ICD-10 criteria), there must be a period of at least two weeks of psychosis without mood disorder, and these symptoms cannot be due to medication(s), substance use or another medical condition.[1][2] In the ICD-10, schizoaffective disorder is seen as episodic, whereas in the DSM-IV it is treated as an uninterrupted illness. [3]


It would appear that schizoaffective disorder involves beliefs, psychosis, and mood variation. However, what I’m currently interested in is how schizoaffective disorder relates to false memories and forgetting.

False memory in schizophrenia patients with and without delusions.
Bhatt R, Laws KR, McKenna PJ.

School of Psychology, Cardiff University, Cardiff, UK.

Delusions are fixed ‘false beliefs’ and, although a hallmark feature of schizophrenia, no previous study has examined if delusions might be related to ‘false memories’. We used the classic Deese-Roediger-McDermott (DRM) paradigm to compare false memory production in schizophrenia patients who were currently experiencing delusions (ED), patients not experiencing delusions (ND) and healthy control participants. The ED group recalled twice as many false-positive memories (i.e., memory for words not previously seen) as both the controls and crucially, the ND group. Both patient groups also recognised fewer correct words than the healthy controls and both showed greater confidence in their false memories; however, on the recognition task, the ED group made more false-negative (i.e. rejecting previously seen words) high confidence responses than the ND group.

It would appear that in 2010, research has been conducted in relation to false memories and schizophrenia. It would appear that the results were in belief that people with a past psychiatric disorder, such as schizophrenia, did show a level of false memory development.

However, of current interest to me is how the false memory is generated.

From August to October of 2010, I researched semantics and episodic memory at the University of Illinois at Chicago. I often held talks with a professor after class, which was one he was teaching to me, and I became extremely fixated on studying semantics and episodic memory. The reason for this was because I had come to recognize that I held a false memory of a woman: Let’s call her Danny. However, in recognizing that I held a false memory of Danny, I noticed I held a false memory of Dani.

The women held similar characteristics: gothic, music interests, skin color, heritage, some personal habits, and so on. As such, a good blow to the head could possibly make a person mix up the two people. As such, with a blow to the head, an individual could misattribute and confabulate about who is who, thus mixing up the two people.

And there was a time when I did confabulate… but to myself without talking to either Dani or Danny.

The way I was able to recognize this, however, was that I had kept an online journal. I had also kept various journals throughout time. As such, I had been able to review my past: This review occurred sometime in August of 2010. Once I recognized that I held a false memory of Danny, I noticed I held a false memory of Dani. Perhaps it was my level of intelligence, cognitive speed, and level of critical thinking while in academia during my super-senior year that allowed me to quickly realize this issue and be amazed.

From having recognized these things, I considered that it all must be tied to semantics and episodic memory. It would be simply enough to say that an individual is schizophrenic, but in general, the issue delves into the cognitive neurobiology involved with semantics and episodic memory or, in other words, language and memory.

I dated Danny, but I did not date Dani.

So, I forgot Danny, and I forgot Dani. I had developed a false memory of both individuals.

But the real question here is why?

Well, I have a hypothesis about that, and my hypothesis is psychosis occurred. Once psychosis occurs, the memories and psychological contents belonging to particular individuals, identity, and how and where they are attributed can be re-arranged. The misattribution is then later catalyzed by dysphoric mania until a person has taken on false memories… and in taking on false memories, the person has become a new person with new memories (albeit false memories).

So, it would appear the process works like this:

1. Person encounters emotionally distressing stimuli that makes them paranoid
2. A paranoid belief is generated
3. Further stimuli may increase the paranoid belief, thus generating confidence in it validity
4. Enough stimuli causes an individual to have a psychotic break
5. The psychotic break then may or may not have further stimuli that leads to dysphoric mania
6. The dysphoric mania leads to transference and re-arrangements of mental contents, thus generating false memories
7. Once the dysphoric mania settles down, the individual has become a false person with false memories

Something that should be considered here, however, is motivated forgetting. In other words, what level of inhibition exists prior to the dysphoric mania for an individual to suppress the paranoid belief. For if an individual were not to suppress the paranoid belief, then some possible outcomes could occur: (1) the individual takes hold of the paranoid belief and freaks out on the emotionally distressing stimuli, then the stimuli is gone; (2) the individual takes hold of the paranoid beliefs, freaks out on the emotionally distressing stimuli, and then argumentation occurs to reduce the confidence of the paranoid belief (the stimuli is allowed to stick around but is now altered).

There is another possibility, and that would mean being a stoic, freeing whatever is bothering you, and giving little reason and explanation while not feeding into any emotional appeals.

It could be said that the person has dissociative identity disorder, but I think that would be an incorrect categorization. It would appear that a better categorization would be “false identity disorder,” whereby an individual is not him or herself, because he or she holds false memories in relation to events of his or her past.

For me, personally, I was in my late teens or so. I had underwent dysphoric mania, and I had an increased desire to learn the Japanese language by writing Kanji on my walls. Perhaps this was some outcome of the dysphoric mania. This happened after Danny and I broke up (it was a long-distance relationship). However, I later met a girl named Dani. I held a paranoid belief that Dani was Danny, because of similarities; but I dismissed the paranoid belief. Somehow, over time, I started to consider that Dani was Danny (they sure did have overlapping qualities): As such, the problem becomes over-lapping qualities or being able to find the similarities in things.

Next in question is how can a person determine if he or she has a false identity?

As such, this know goes into the realm that a false memory is a logic error. If an individual knows he or she holds at least one false memory, then it is true that the person also holds another false memory that he or she may not be aware of. However, with holding a false memory, a person must be made aware that a memory is false. As such, there is a level of debugging to occur.

For me, I was able to self-debug in 2010, because I was moving around stuff from one computer to another. I was moving around journals, pictures, and other things to a backup server. I was motivated to do this, because I wanted to have a linux server that could do grand-daddy backups. In doing that, I reviewed some of the stuff that was there. That was when I noticed that I held a false memory. In a lot of ways, it was serendipitous, because I held no intent to review the material with the goal of seeing if my memories were false or not.

So, I believe if an individual is found to have a false belief, then learning of the false belief will be a serendipitous event for the individual.

The next issue is dealing with law…

While I was dating Danny, I wrote about an experience that happened to her. However, there is a level of paranoia in writing about such experiences, because an individual does not want to be found out or caught because of illegal activity. However, in the situation with Danny, I was not the victim and I was not the attacker. I was a witness to the event, but I did nothing illegal: Although I could have reported it, this would have also meant that Danny would have gone to jail for doing illegal drugs. As such, I did not report it.

I did, however, write about it in a journal.

As such, for an individual who is prone to false memories, a journal would be the best way to prevent false memories from occurring. However, if an individual commits a crime, there becomes a problem with writing down why things happened. If an individual plans on committing a crime, there is also a problem with writing it down. If an individual witnesses a crime, there is a problem with writing it down, but not as much. However, if an individual does witness a crime (or believes he or she witnesses a crime or something that should be considered a crime), then the best thing a person can do is report it, especially if the individual was not involved with any criminal activity.

However, an individual may not be so interested in reporting the activity, especially if the individual does not have a large knowledge of criminal or civil law. As such, this can become a flaw in an individual’s thinking, thus preventing the individual from writing something down. However, if an individual is paranoid of being “caught” for something, then it would be reasonable to have a diary, have encryption on it, and hope that you don’t forget the password. However, if an individual does forget the password, that means there is a high level of severity in the memory repression and false memory. One could only hope that someday there is a security hacker who finds a way to crack past the password. However, that requires human resources. Depending on the severity of the crime will depend on the severity of resources thrown at cracking the password; and depending on the severity of the crime, there will be a level of repression.

All it would take, then, if for an individual to go through the seven-step process written above for false memories to be generated.

The reason I’ve listed schizoaffective disorder is because I consider it a kind of temporary insanity diagnosis. The individual has undergone a psychotic break, the individual has undergone dysphoric mania, and the individual has held a delusion (even though it may be unknown that it is a false memory) for more than two weeks (thus, the individual has been psychotic all along until the false memory has been noticed). The insanity ends when the individual recovers the false memory.

Until then, the individual is psychotic. However, is not to say that the individual holds a high level of psychosis, because psychosis often involves delusions and hallucinations. The reason I say this is not a high level of psychosis is because the individual is able to function. As such, the person is a high-functioning schizoaffective individual. If the individual is unable to hold a high-functioning life, then the individual would more than likely degenerate into a social monster.

As such, I have a view for what allows an individual to be high-functioning. This would be dependent on the individual’s training as a child in morality: right and wrong. Sure, determinism says that’s garbage and only consequentialism exists… But what I’m going to discuss here is Ribot’s law.

Ribot’s law states that memories that are strongly embedded into an individual, which would be memories developed at an early age, are less likely to be forgotten. As such, an individual who continues to recall such a memory developed at an early age is likely to strengthen the memory over time. As such, as a memory is strengthened, it is less likely to be lost.

Ribot’s Law of retrograde amnesia was hypothesized in 1881 by Théodule Ribot. It states that there is a time gradient in retrograde amnesia, so that recent memories are more likely to be lost than the more remote memories. Not all patients suffering from retrograde amnesia report the symptoms of Ribot’s Law.

source: Wikipedia

So, an individual who remembers being punished for a particular deed at a young age may wrap that memory around that deed, thus that memory and the punishment strengthens the individual’s personality and moral framework.

One may consider that an individual who is punished and abused for misdeeds as a child may become a righteous individual. However, that righteous individual may harass, intimidate, and smackdown people who appear to be doing wrong. I have a best friend who had a very Christian mother who would use a paddle on him and his sisters while they grew up. As such, he is a righteous guy, but he does not appear to take bullshit or crap from people; and he will bitch and complain about it.

I do the same, actually, as I come from a Catholic background. My punishments were different but many of them were physical to the point of abuse.

Reconsider of James Holmes

Author: Genecks
B.S. Neuroscience

These are but my opinions and speculations and to be of a measure of my character.

I’ve been considering James Holmes as of late. I believe I understand what happened to him. I’ve considered that he must have schizoaffective disorder. In that, I’m assuming he held some delusional, paranoid belief. Eventually, enough stimuli excited that delusional, paranoid belief and he had a psychotic break. Sometime after the psychotic break, he underwent dysphoric mania. From this point, he underwent a level of repression from the stimuli that were associated with and had excited his delusional, paranoid belief. After the repression occurred, he held a level of continued dysphoric mania whereby he had transference of mental contents from one part of his memory/personality to another part of his memory/personality. And then he became the Joker.

Of interest here, however, is Ribot’s law.

Behavioral epigenetics: Dissociation and repression

Something I have been wondering about as of late is the biological basis for dissociation and repression. I am an identity theorist when it comes to understanding psychological phenomena. Also, I do understand why psychology is around as a science. I, nonetheless, believe psychology is based on biological aspects of the central and peripheral nervous systems.

Of interest is dissociation and repression.

I’d like to start this with something I’ve read:

what is the difference between the two defense mechanisms Dissociation and Repression ?
Has it got to do with recent event (Dissociation) and past event (Repression) ?

A person’s reply:

This is a good question because it reminds me all the whimsical nature of USMLE tests.

Basically all about defense mechanisms is bullshit. If we had to say something useful about it, we could say they are just ways for the mind to cope with trouble. Beyond that, as far as I know, nobody has identified the Brodmann’s area in the brain where those defense mechanisms lie. Nobody, to my scant knowledge, has demonstrated any correlation with PET scans of the brain. Nobody, to my little reading, found any mutation in any gene that makes more people prone to use this or the other defense mechanism. There’s no animal model nor a drug that enhances any such mechanism.

However, these so called ‘defense mechanisms’ and their definitions do help psychiatrists make their language sophisticated. For example, blocking a painful memory (repression) or just taking the good side of it (dissociation) which in essence both are DENIAL, help psychiatrists keep their notes organized. Because they are always trying to find the neuron or the ion channel that controls either one, that’s how they can keep submitting grants, writing publications requesting more research on the topic, and we students try to memorize such capricious definitions of something that basically looks like denial. If we fail to get the right score, it’s not because such defense mechanisms are baloney, but it’s because we are repressing the fact we are poor students and don’t deserve to match.

source: (year: 2012)

Ok, first off, I have a couple of problems with the reply, regardless of the English used.

In the 2000s, behavioral epigenetics became more of a popular field of study. As such, I believe that more is to be conducted in the realm of behavioral epigenetics than before. However, the problem with behavioral epigenetics in the realm of human neurobiology is that you cannot easily grab a bunch of humans with dissociated or repressed memories and study them.

There are a few problems:

1) The individuals with repressed or dissociated memories more than likely do not know they have the amnesia
2) There are ethical problems with using humans as experimental subjects
3) If you could find individuals with repressed or dissociated memories, then I’m assuming the individual has been informed of this (they’ve been informed of a logic error).

The only way you could really get a great human subject is if you found individuals with repressed or dissociated, kept them blind to the fact that their memories are dissociated or repressed, and then experimented on them. However, that opens a whole new ethical problem: The individuals would want to know why you’re experimenting on them.

You could attempt to tell them that they have dissociated or repressed memories without telling them which or what memories, but once that occurs, the possibility for the individual to begin questioning the reality of the situation occurs. As such, the experimental data has the possibility for becoming biased.

Regardless, in a world where research scientists grab individuals with dissociated or repressed memories, they could attempt to look into the neurobiological causes of dissociated or repressed memories.

Sure, people could attempt to do MRI scans. They could lie to individuals with dissociated or repressed memories, thus hoping to get MRI scans before making the individuals aware of their memory problems.

Sure, blood work could be done. Some analysis of reflex motor control, REM cycle, and other topical studies could be done.

Beyond that, the molecular biological and electrophysiological work needed would fall into some serious ethical issues, as they would require surgery.

Regardless of having human animal studies, it would be difficult to determine whether or not a mouse or rat has dissociation or repression. I have considered that repression in mice may occur due to various condition training. I have read that when a certain experiment with stimuli is done to a mouse in a particular condition, it will give a particular response. However, when the mouse is put into a different condition (environmental setting) with the same stimuli, it will not give the response.

I believe the example was a toxin, for instance. I assume you could relay this also into drug addiction and overdoses.

With drug addicts, if they do drugs in a particular environment, they learn to develop a tolerance. However, you take the drug addict to a different condition, the tolerance will be decreased, because the condition has an influence on the tolerance, thus increasing the possibility for an overdose to occur.

As such, repression or dissociation in this situation could be analogous with the tolerance to the environment. In other words, developing a tolerance is learning to repress negative outcomes. However, in a different condition, the learned ability to repress a negative outcome is decreased, thus the ability for the negative outcome to surface is increased.

That’s a hypothesis at best, but there seems to be some similarity. And in terms of an animal model, that seems to be as close as things get.

As such, one might be able to develop a model for “love trauma” by giving a mouse drugs, which simulate love.

However, this is but speculation.

I believe there have been epigenetic studies conducted in relation to drug addiction in animal models. Loss of the drug could be considered traumatic. And if the trauma is enough, it could potentially dissociate and repress the animal. However, the thing would be finding a way to determine what the animal has dissociated from. As such, I assume an experiment where the drug is paired with a negative stimulus could eventually lead to the animal repressing/dissociating from the negative stimulus while having a desire for the drug. Dissociation or repression would be noticeable if the animal ignores or gains a tolerance to the negative stimulus. However, the methods whereby the negative stimulus occur would have to be considered. The negative stimulus could be a form of second-order conditioning. If the animal ignores the second-order negative stimulus while in the presence of it and continues to seek the drug, then the animal has dissociated, repressed, or forgotten about the second-order negative stimulus.

As such, it could be assumed that the animal has dissociated, repressed, or forgotten its memories. From this point, you could attempt to do neurobiological research on the animal for an animal model of dissociation or repression. From this point, a behavioral epigenetic relationship between dissociation and repression could be determined.

I think that might work, but it may not.

Either way, behavioral epigenetics in the realm of dissociation and repression are still starting out.

I’ve come across an article:
By: Robert Scaer, M.D.

Published in: Applied Psychophysiology and Biofeedback, (2001), 26(1), 73-91, based on a Keynote Address presented at the 31st annual meeting of the Association for Applied Psychophysiology and Biofeedback, March 29-April 2, 2000, Denver, CO.

He appears to go into some level of detail about dissociation as a neurobiological event. This is admirable. However, I do not like the animal model based on freeze events. I believe more can be done in developing animal models in relation to conditioning, trauma, stimuli, and dissociation.