My Original Theory-2: Pathological Hypothesis of Schizophrenia: 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 hypotheses studied by Dr. Kon are introduced in
order to explain (1)the process from ARMS to onset of schizophrenia,
(2)disturbances of ego characteristic of schizophrenia,
(3)depressive moods seen with schizophrenia.
First, a pathological model of the process from ARMS to onset of
schizophrenia will be explained. What a person considers to be proper
interpersonal-distance is thought to be relative to the sensitivity of his dopamine receptors.
If a person is sensitive to dopamine, he may tend to take larger interpersonal-distances.
Some people are sensitive to dopamine from birth (for example,
those who possess excessive dopamine receptors), and they have sensitive traits
when coping with the world and others. Even if
they have the same experiences as others, they tend to release
excessive dopamine which makes them suffer. As a result, they tend to
select a lifestyle that involves fewer interpersonal relationships.
In a life in which they tend to be solitary, they may
become familiar with the arts, nature, and animals. In this way, they
grow up with sensitiveness to dopamine and they acquire a lifestyle that
helps them avoid the onset of schizophrenia. However, in adolescence, living
conditions change greatly. “They are given roles and
assignments that require interpersonal relationships,”
“they become sexually mature,” and “they are placed in situations that require more assertiveness and responsibility” etc..
Life and interpersonal relationships become increasingly complicated,
and they come to the point where their withdrawal strategy is no longer sufficient.
In the midst of this, strongly stressful situations related to “sexual affairs,
money, honor, and health” cause excessive dopamine to be emitted, and combined with high sensitivity to dopamine, they face the crisis of the onset of
schizophrenia. In addition, it is easy to predict these kinds of crises 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 disturbances of the ego, which is
specific to schizophrenia. The animal's nervous system, in general, forms the loop of (1)reception of stimulation at the sensory organ→(2)conditional reaction in the
brain→(3)reaction through motor system, autonomic nervous system, etc.
→(4)real outcomes→(5)reception of stimulation at the sensory organ.
Since there is no part to confirm the generation of self-consciousness in this loop,
the sense of active control of the ego , an obvious experience in humans,
cannot be explained.
“The first world model” and “the second world model” hypothesis is introduced
here, for further discussion. For humans, “the first world model” is the same process of “(1)reception of stimulation through
the sensory organ→(2)conditional reaction in the brain→(3)reaction through motor
system, autonomic nervous system, etc.,” as for other animals.
In addition, humans have “the second world model” in
the brain concurrently, and two kinds of signals from “the first world
model” and “the second world model” are compared. When there are
differences, “the second world model” will be modified to coincide with “the first world
model”. The function of “the second world model” to compare and transcribe the
“the first world model” resembles that of cerebellum transcribing kinetic
signals of cerebrum during exercise.
Further hypothesis is that a time lag exists between the two outputs from “the first
world model” and “the second world model,” and output from “the second
world model” is always begin adjusted so that it reaches the place where comparison is made slightly earlier (than the first world model). Sense of active
control and sense of self in 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 slightly earlier and the older one reaches the same
conclusion afterwards. This time-delay generates the sense of active
control and the sense of self that humans experience.
Basically, “the first world model” is good enough for humans to live (as
other animals), but the appearance of “the second world model” generated
self-consciousness, which is the fundamental feature of humans.
Because self-consciousness has been generated at the latest stage
of the evolution, it can be easily destroyed. When self-consciousness breaks down,
the following are seen according to the Jacksonism principle; “negative symptoms of schizophrenia triggered by the break down,” and “positive symptoms
caused by the loss of inhibition”.
Humans can confirm the existence of ego-consciousness because they
express their inner world through words, and other animals (to varying degrees by species) are assumed to have gained some similar mechanisms through the evolutionary process as well. Although animals cannot express themselves clearly, it is possible for them to have a sense of active control and a sense of self.
People also behave unconsciously, when they are out of mind (for
example, people pass through the train station ticket gate without being conscious
of it). This is a situation in which signals from “the second world
model” are weak and, so to say, the brain is nearly in the “automatic-drive” state.
In addition, when people are concentrating intensely and showing
their highly proficient skills, signals of “the second world model” perfectly
coincide with those of “the first world model,” and by contrast,
signals from “the second world model” sometimes feel as if they are being
blocked out. People describe this situation using words such as “I did it
without thinking about it,” “as if in a dream,” ”my body
reacted automatically,” etc. Based on the “time-delay hypothesis,” free
will is an illusion, and disturbance of ego is an experience (filled with
pain) that is generated when illusion is lost. There are many theses
on “rivet experiment,” a passive-consciousness hypothesis, which is
related to this discussion.
Come to think of it, signals transmitted from each sensory
organ do not reach the brain’s processing site simultaneously.
But the arrival time is supposed to be adjusted to be simultaneous, and thus
a subjective real world is composed. In that case, processing sites
that adjust the time-lag of signals arriving from each sensory organ
are considered t
o exist in the brain. Similarly, it should
o exist in the brain. Similarly, it should
be possible to assume there are sites in the brain, where the signals from
“the first world model” and “the second world model” are compared, and
the time adjusted. Also, it is assumed that trouble at these
sites will cause a disturbance of ego.
When the output from “the second world model” arrive after those of
“the first world model,” the disturbance of ego occurs. According to the
amount and sort of delay, they can be “passivity experiences
(experiences controlled by others), part of obsessive-compulsive
experiences, auditory hallucinations, autochthonous ideas,” and so on.
As for autochthonous ideas, arrival of both output are assumed to be
almost simultaneous. These situations are the first stages of
schizophrenia. For example, auditory hallucinations are explained as
follows; when the contents of what the person wants to say, which are
output of “the second world model,” arrive after those of “the
first world model,” they are perceived as “others are talking” or
“made to listen to.”
Next hypothesis is that “the dopamine antagonist delays the output
of ‘the first world model’ and ‘the second world model’ each to a
different extent because of its pharmacological traits”.
Antipsychotic drugs delay the output of “the first world model”,
but it is assumed to delay those of “the second world model” only
slightly or not at all. This hypothesis would be able
to explain the mechanism of how medicines cure the disturbance of ego.
As facts concerning time-delay hypothesis and medicines’ effects, it
is possible to state the different effects of medicine on the mesolimbic
system and the mesolimbic-cortical system, or to give examples of
different effects to the prefrontal area. For example, aripiprazole is
said to inhibit dopamine at the mesolimbic system and increase it at the
mesolimbic-cortical system; it is possible to explain the medicinal
effect using time-delay hypothesis. As seen in the above discussion,
if we suppose the dopamine system has some role at the site in the 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, that is, a hypothesis on symptom of depression, localization of
the pathology is not adopted, and a patient’s condition is considered in
terms of neurons’ temporal profile. There might be a localized symptom of
depression caused by a certain site in the brain, but true mechanism is not
clear. The symptoms of depression in the course 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 depression of far advanced stage
is related to the positive symptoms. Examined 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 their inner selves without defense; they become passive in
relationships with others in order to avoid being hurt. This extends
to the symptoms of depression at ARMS. You may say, excessive caution resembles
depression. 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
patients are forced to face completely uncommon experiences,
and they experience serious damage and loss of ego.
Neurological mechanism of the symptoms of depression that
occurs at this stage isn’t clear yet. When the acute phase of
schizophrenia is calmed down by an antipsychotic drug, symptoms of
depression also improve. Therefore, the dopamine system tends to be
considered as a contributing factor to depression. However, it is
better understood as a result of sharply blocking increased dopamine at the receptors’ level. So, the sharply increased dopamine is
assumed to trigger symptoms of depression. At the same time,
symptoms of apathy, which occurs along with Parkinson’s disease, are
well known as resembling the symptoms of depression. This is one example of
symptoms of depression accompanied by a decrease in dopamine. Once the
localization of pathology is clarified, it might be possible to propose a hypothesis
that explains these contradicting movements of the dopamine system.
This hypothesis best explains depressive symptoms in the early residual
phase. There, the mechanism that is common to the depressive symptoms
of bipolar disorders is assumed. “A group that responds to repeated
stimulation with increasing reactions” is assumed as a trait of brain neuron cells.
Because in the case of acute phase of schizophrenia and
bipolar disorders maximum stimulation is given to neurons,
the function of “a group which responds to repeated stimulation with
increasing reactions” is possible to break down.
The depressive symptom is supposed to start from here.
From this point of view, the depressive symptoms of schizophrenia
and bipolar disorders are classified into two categories; that is (1)results of
functional breakdown of “a group which responds to repeated
stimulation with increasing reactions,” and the breakdown is triggered
by excessive stimulation; (2)pathology of endogenous origin and positive
onset of depression. Dr. Kon’s hypothesis supposes the former symptoms．
In the case of medical treatment, medicine relevant to the dopamine
system are good for symptoms relating to time-delay, and medicine
relevant to the serotonin system are effective in aiding recovery of exhaustion
depression. When cognitive-behavioral therapy mainly works on
behavioral aspects, the target of therapy is “the first world
model” in the above hypothesis. Whereas, interventions that emphasize cognitive modification mostly target “the second world
model,” and through them attempts are made to alter “the first world model.”
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 may be clinical merits.
If patients understand the above hypothesis through psychoeducation,
the therapeutical effect of cognitive-behavioral therapy
the therapeutical effect of cognitive-behavioral therapy
for their schizophrenia may increase.
On the other hand, SST tries to change “the first world
model” through behavior, of which the effect modifies “the second
world model,” resulting in desirable change in cognition.