My Original Theory-2: Pathological Hypothesis: First/Second World Model, Time-delay Hypothesis, Temporal profiles of Neurons Tadashi Kon(Shinagawa Psychosomatic medicine Clinic)
〒108-0075 2-14-10-10F Kounan,Minato-Ku,Tokyo,Japan see also http://shinbashi-ssn.blog.so-net.ne.jp/2008-05-04 In this section, the pathological hypothesisis introduced in the order to explain (1)the process from ARMS to onset of schizophrenia, (2)ego-disturbances which are characteristic to schizophrenia, (3)depressive moods which are seen with schizophrenia. First, pathological model of the process from ARMS to onset of schizophrenia is explained. Man’s proper interpersonal-distance is considered to reflect【比例するとか、関係すると言う意味なので何か別の動詞 rerate A to B】 the sensitivity of dopamine receptors. If he is sensitive, he may tend to take longer interpersonal-distance. Some people are sensitive to dopamine from birth (for example, with excessive dopamine receptors), and they have sensitive traits【世界と他人に対しての過敏】. Even if when【トル】 they have the same experiences as others, they tend to emit excessive dopamine which makes them suffer. As a result, they tend to select a life style that deals with fewer interpersonal relationships. In a life 【主語】tends to decline to isolation【be lonely】, they may become familiar with arts, nature, and animals. In this way, they grow up with sensitiveness to dopamine and they somehow acquire the way to live without the onset of schizophrenia. However, after【at】 the age of adolescence, living conditions change greatly. “Rolls and assignments which require interpersonal relationships are given【→変】,” “they meet opposite sex【sexually matured とか言えるように思う】,” “chances in which activeness and self-duty are required increase【SV離れ過ぎじゃないか】,”etc., life and interpersonal relationships get much more complicated. The phase in which they can’t solve problems any more only by familiar withdrawal strategy emerges【SV離れすぎ】. In midst of this, dopamine is emitted excessively under strongly stressed situations【さて strongly stressed なのかな】 concerning “sexual affairs, money, honor,and health”, and combined with sensitiveness towards【あやしい】 dopamine, they face crisis of the onset of schizophrenia. In addition, it is easy to imagine【イマジンではないでしょう、もっと現実的な想定です】 these kinds of crises do exist prior to the obvious onset. Psychotic like experiences (PLEs, later ARMS : at risk mental state), which are attracting attention recently, possibly correspond to these situations.
Next is the pathological hypothesis of ego-disturbances, which are specific to schizophrenia. The animal’s nervous system (except for human【いやヒトも含めてでしょう】), in general, forms a loop as (1)reception of stimulations at the sensory organ→(2)conditional reaction in the brain→(3)reaction through kinetic【→motor】 system, autonomic nervous system, etc.→④real outcomes→⑤reception of stimulations at the sensory organ. Since there isn’t a part to guarantee【これかな？】 the formation of self-consciousness in this loop, sense of active control of ego ,which is obvious experience to human, can’t be explained.
“First world model” and “second world model”hypothesis is introduced here, for further discussions. As to human, “first world model” is involved in the process of “①reception of stimulations at the sensory organ→②conditional reaction in the brain→③reaction through kinetic system, autonomic nervous system, etc.,” assumed to be the same as other animals. In addition, as to human, “second world model” is in the brain concurrently, and two kinds of signals from “first world model” and “second world model” are compared. When there are differences, “second world model” will be modified to coincide. The function of the “second world model” to compare and transcribe the “first world model” resembles that of cerebellum transcribing kinetic signals of cerebrum at exercise.
Further hypothesis is that timelag exists between outputs from “first world model” and “second world model,”and always outputs of “second world model” is adjusted so that they reach the comparatively matching part slightly earlier (than the first world model). Sense of active control and sense of appropriation of me on behavior, that is to say, formation of ego-consciousness can be explained by this time-delay hypothesis. For example, although the two compulsive computers give almost the same conclusions, the second evolutionary newer computer gives the answer swiftly earlier, and the older one reaches the same conclusion afterwards. This time-delay generates the sense of active control and the sense of appropriation of me that people experience.
Basically, “first world model” is good enoughto live on for human (as other animals), the appearance of “second world model”generated self-consciousness. Although self-consciousness is the fundamental trait of human, as it generated at the latest stage of the evolution, it can be easily destroyed. When self-consciousness breaks down, according to the Jacksonism principle, “negative symptoms (of schizophrenia) triggered by the break down,” and “positive symptoms caused by the loss of restraint” are seen.
Human can confirm the existence of ego-consciousness because he expresses the inner world by words, the other animals (perhaps in different extent by species) are assumed to have some similar mechanisms through the evolutional process as well. Although animals cannot express clearly by themselves, it is possible for them to have the sense of active control andsense of appropriation of me.
People also behave unconsciously, when they are out of mind (for example, people pass through the ticket booth without being conscious about it). This is the situation which signals from the “second world model” weakened and, so to say, it is nearly in the “automatic drive” state. In addition, when people are highly concentrated and showing their proficient skills, signals of the “second world model” strictly coincide with these of the “first world model,” on the contrary, the signals from the “second world model” are some times felt like being blocked. This may be a situation those words are told that“I did it without thinking about it,” “as if in a dream (worked hard??),” ”body reacted automatically,” etc. Based on the “time-delay theory,” free will is an illusion, and ego-disturbance is an experience (filled with pain) that is generated when illusion is lost. There are many theses on “rivet experiment,” a passive-consciousness hypothesis, whichis relating to this discussion.
Come to think of it, signals that are transmitted from each sensory organ don’t reach the processing site in the brain simultaneously. But the arrival time is supposed to be adjusted as simultaneous, and the subjective real world is composed. In that case, the existence of processin gsites in brain that are adjusting time-lag in the arrival of signals from eac hsensory organ is supported. Similarly,it should be possible to assume there is a site in brain, where the signals from “the first world model” and “the second world model” are compared and the time is adjusted. Also, it is assumed that troubles occure at this site will cause the ego-disturbance.
When the outputs from “the second world model”arrive after those of “the first world model,” ego-disturbance occurs. According to the amount and sorts of the delay, it can be “made experiences (experiences controlled by others), part of obsessive-compulsive experiences, auditory hallucinations, autochthonous ideas,”and so on. As to autochthonous ideas, arrivals of both outputs are assumed to be almost simultaneous. These are the situations of acute stage of schizophrenia. For example, auditory hallucinations are explained as follows; when the contents of what the person wants to say, which are the outputs of “the second world model,” arrive after those of “the first world model,” they are perceived as what “others are talking” or “are made tolisten to.”
Next hypothesis is that “the dopamine antagonist delays the outputs of ‘the first world model’ and ‘the second world model’ each by different extent because of its pharmacological traits”. Major (Antipsychotic drug) delays the outputs of “the first world model”, but it is assumed to delay those of “the second world model” only slightly or it is assumed not to delay. This hypothesis will be able to explain the mechanism of how medicines cure the ego-disturbance. As facts concerning time-delay hypothesis and medicines’ effects, it is possible to state the different effects of medicines tomesolimbic system and mesolimbic-cortical system, or to give examples of differenteffects to prefrontal area. For example, aripiprazole is said to restrict dopamine at mesolimbic system and increase it at mesolimbic-cortical system; it is possible to explain the medicinal effect using time-delay hypothesis. As seen in the above discussion, if we suppose dopamine system acts some role at the site in brain where two signals from the first and second world model are compared, time-delay hypothesis combines with dopamine hypothesis.
As to the last theme, symptom of depression, the localization of pathology is not adopted, and patient’s condition is considered in terms of neurons’ traits. There might be a localized symptom of depression caused by a certain site in brain, but reality is not cleared. The symptoms of depression of schizophrenia can be seen through all the stages from ARMS to far advanced stage to residual phase. Usually, depression of ARMS and residual phase is related to the negative symptoms of schizophrenia and that of far advanced stage is related to the positive symptoms. If you see this more precisely, it is possible to understand as follows; at ARMS, people recognize their sensitiveness and understand the differences between the world and themselves at least to some extent, so they think it is dangerous to express inside ofthem without defense; they become pessimistic in relationship with others inorder to avoid being hurt. This extends to the symptoms of depression at ARMS. Excessive caution resembles depression, you may say. The symptom of depression, at the latter stage of residual phase, also assumes the same mechanism.
On the other hand, at the far advanced stage of schizophrenia, the parties are forced to face with completely heterogeneous experiences apart from common ones, they experience serious damages and loss of ego. Neurological mechanism of the symptoms of depression which occurs at this stage isn’t clear yet. When acute phase of schizophrenia is calmed down by antipsychotic drug, symptoms of depression also get better. Therefore, dopamine system is easy to be considered as a contributing factor to depression. However, it is better understood as the effect caused by blocking sharply increased dopamine at receptors’ level. So, sharply increased dopamine is assumed to trigger symptoms of depression. But at the same time, symptoms of apathy, which occurs along with Parkinson’s disease, are well known as resembling that of depression. This is one example of symptoms of depression accompanied the decrease in dopamine. Once the localization of pathology is clarified, hypothesis that explains these contradicting movements of dopamine system might be presented.
This hypothesis best explains depressive symptoms in early residual phase. There, a mechanism that is common with the depressive symptoms of bipolar disorders isassumed. “A group which responds to repeated stimulations with increasing reactions” is assumed as a trait of cells of brain neurons. In the case of acute phase of schizophrenia and bipolar disorders, because maximum stimulations are given to neurons, the function of “a group which responds to repeated stimulations with increasing reactions” is easy to break down. From here, the depressive symptom is supposed to start.
From this point of view, the depressive symptoms of schizophrenia and bipolar disorders are classified into two; that is ①the result of functional break down of “a group which responds to repeated stimulations with increasing reactions.” The break down is triggered by excessive stimulations; ②the pathology of essential and positive onset of depression. This (Kon’s) hypothesis is based on the first condition (①)．
In the case of medical treatment, medicines relevant to dopamine system are good for symptoms relating to time-delay, and medicines relevant to serotonin system are effective to recovery of exhaustion depression. When cognitive-behavioral therapy mainly works on behavioral aspects, the target of the therapy is “the first world model” of the above hypothesis. Whereas, interventions that put emphasis on cognitive modification mostly target on “the second world model,” and through them “the first world model” are tried to change. If therapists become very aware of whether to approach “the first world model” through behavior or to get closer to “the second world model” through cognition, there might be clinical merits. Therapeutic effect of cognitive-behavioral therapy to schizophrenia may increase, if parties understand the above hypothesis through psychological education. On the other hand, SST tries to change “the first world model” through behavior, and then, the effect modifies “the second world model,” resulting in desirable change in cognition.
2011-11-24 19:55