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Consciousness disease "schizophrenia"

Updated: May 29, 2022

Studying the "Study of Consciousness" (Stanislas Duanne) can further deepen your understanding of coaching theory.

I am studying to add a unique flavour to "unconscious rewriting".

This series of blog posts are my study notes. This time, the theme that follows the unconscious and conscious

I will write a "sign of consciousness".


The two consecutive evolutions of the human workspace must rely on biological mechanisms based on specific genes. Therefore, the following questions arise.

Can illness target the mechanism of human consciousness? For example, can genetic variation or brain damage reverse the direction of evolution and cause the global neuronal network to malfunction?

The long-distance neural connections in the cortex that underlie consciousness are generally fragile.

Neurons, whose axons are often tens of centimetres long, are more like monsters than any other cell type. Since it must support appendages that are more than a thousand times longer than normal cells, it creates unique problems with gene expression and molecular transport.

Transcription of DNA is always done in the cell nucleus, but they must send their final product to synapses located centimetres apart. A complex biological mechanism is required to solve this transport problem. It makes long-distance neural connections in evolved workspace systems more likely to be targeted for specific disorders.

I thought that the concept of "mental illness could explain the psychiatric symptom of schizophrenia."

Schizophrenia is a well-known illness that occurs in approximately 0.7% of adults, and adolescents and young adults lose contact with reality and develop delusions and hallucinations. (Positive symptom)

At the same time, it is a mental illness that experiences an overall decline in intelligence and emotional abilities (negative symptoms) such as speech disturbances and repetitive behaviours.

It has been challenging to identify the causes of these various symptoms until now.

However, these deficiencies are always fundamental to functions that appear to be related to the global workspace of human consciousness, specifically social beliefs, self-observation, metacognitive judgment, and even perceptual information. It seems that it is also adversely affecting access.

Clinically speaking, schizophrenic patients expose their overconfidence in their strange beliefs. Their metacognition and theory of mind are so severely impaired that their thoughts, knowledge, actions, and memories are indistinguishable from others'.

They transform the integration of knowledge by consciousness into a coherent network of beliefs, leading to delusions and confusion.

For example, the patient's conscious memory is sometimes terribly wrong.

After a few minutes of looking at a list of pictures and words, they often can't remember what they saw. Their metacognitive knowledge of when, where, and what they saw and learned was generally inferior. I am.

However, their implicit, unconscious knowledge is not compromised at all.

The research team of Stanislas Duanne and colleagues wondered, "Is there a fundamental flaw in the conscious perception of schizophrenic patients?"

Therefore, we decided to conduct a masking experiment for patients with schizophrenia.

Masking is a phenomenon in which the former disappears as a subjective experience when another image is displayed immediately after flashing a word or image.

The results of the experiment were precise. In patients with schizophrenia, the minimum display time required to see masked words was significantly different from healthy subjects. The threshold for conscious access has risen, and the image has remained in the sub-threshold area for much longer.

Moreover, they needed more sensory evidence data to report seeing the image.

Flushing the numbers under the threshold for only 29 milliseconds showed precisely the same priming effect as a healthy person, and there was no problem with unconscious processing.

The fact that these complex effects are maintained means that the feed-forward chain, which consists of unconscious processes from visual recognition to the addition of meaning, is largely unimpaired by the disease.

It has become clear that the main problem with schizophrenic patients seems to be in the process of integrating input information into a coherent whole.

The team of Duanne et al. Also found the separation seen between the intact conscious treatment and impaired conscious access in patients with multiple sclerosis. This disease damages white matter bonds. Patients with multiple sclerosis cannot consciously see the flashed words or numbers at the time of onset before the onset of other significant symptoms but unknowingly process them.

This discovery is essential for the following reasons:

white matter damage can selectively adversely affect conscious access.

Few patients with multiple sclerosis develop psychiatric disorders similar to schizophrenia, which indicates that loss of long-distance neural connections can play an essential role in developing psychiatric disorders.

Brain images show that schizophrenic patients have a significantly reduced ability to ignite consciousness.

Their brains are largely unimpaired in the early stages of visual and attentional processing. Still, they generate extensive, synchronized activities that generate P3 waves on the surface of the head, indicating the presence of conscious perceptual representations. I'm missing.

It also lacks another sign of conscious access, the emergence of a consistent brain web with large-scale interactions between distant cortical regions in the beta frequency band (13-30 Hz).

Do patients with schizophrenia have more direct evidence of anatomical changes in the Global Workspace Network? The answer is yes.

Diffusion tensor images show significant anomalies in long-distance axon bundles connecting cortical regions.

In addition to the nerve connections that connect the prefrontal cortex to the distant cortical areas, the hippocampus and thalamus, the nerve fibres in the corpus callosum that connect the two cerebral hemispheres are notably impaired.

The result is a severe disruption to resting connectivity.

In other words, in schizophrenic patients, the prefrontal cortex loses its position as the centre of interconnection at rest. As a result, the degree of integration of activity into the overall function is significantly lower than in healthy subjects.

This loss of connectivity may play a significant role in developing schizophrenia.

Many of the compromised genes in schizophrenic patients are among the molecular systems of two major neurotransmitters that contribute significantly to prefrontal synaptic transmission and their plasticity: dopamine D2 and glutamate NMDA receptors. It hurts either or both.

Even healthy adults may experience temporary schizophrenia-like mental illness when taking drugs such as phencyclidine (known as PCP or angel dust) or ketamine.

These drugs act by explicitly inhibiting neurotransmission at NMDA-type excitatory synapses. They play an essential role in top-down message transmission between distant cortical areas.

In a computer simulation of the Global Workspace Network built by Duanne, NMDA synapses are essential tissues for igniting consciousness, turning higher cortical areas into lower-order processors that activated those areas in the first place. It forms a long-distance loop that connects top-down.

Removing the NMDA receptors from the simulation loses widespread neural connections and eliminates ignition.

Other simulations have shown that NMDA receptors are equally crucial for the slow accumulation of evidence underlies well-thought-out decision making.

Extensive loss of nerve connections due to top-down explains to a large extent the negative symptoms of schizophrenia.

It does not affect the feed-forward transmission of sensory information but selectively interferes with wide-area integration through long-distance top-down loops.

Even patients with schizophrenia work perfectly well in feed-forward processing, including the complex effects that cause sub-threshold priming.

The flaw lies only in the subsequent firing and broadcast of information, which impairs conscious monitoring, top-down attention, working memory, and decision-making ability.

So what about the positive symptoms, their bizarre delusions and hallucinations? Cognitive neurologists Paul Fletcher and Chris Frith argue for a mechanism based on impediment to the transmission of information.

Like detective Sherlock Holmes, the brain works by drawing the best reasoning from perceptual and social input information.

Such statistical learning requires two-way information exchange.

The sensory domain sends messages to higher layers. At the same time, higher-order regions respond by top-down prediction as part of a learning algorithm that constantly attempts to explain information input from the sensory organs.

The learning process stops when the higher-order representations are accurate enough that the predictions match the input information passed bottom-up perfectly.

The error signals that the brain perceives (the difference between the predicted signal and the observed signal) are negligibly small, resulting in minimal surprise.

In healthy people, the predictive mechanism always cancels the effect of their actions on sensory input when they perform any action.

We aren't surprised to grab a coffee cup. The weight and heat of the cup felt by the hand can be easily predicted. And the motor cortex sends a top-down predictive message to the sensory cortex before the grasping motion announces that it will perform the grasping action.

This prediction works so smoothly that we usually don't notice it when we grab it. You will only notice that fact if you make a mistake, for example, when you unexpectedly grab a hot cup.

What if this top-down prediction wasn't working as a system? In that case, you will feel something is wrong, even when you grab a coffee cup. The moment you touch the cup, you'll wonder who or what is changing your senses, which is subtly different from what you expected. Especially the utterances feel strange.

You will hear your voice while speaking, which will sound humorous. However, the strangeness of the voice that comes into your ears always keeps your attention.

I start to wonder if someone is messing with my spoken language. As soon as it happens, you hear a mysterious voice inside your head and become convinced that your neighbour is trying to control your body and ruin your life.

Then, you will be searching for the hidden cause of the mysterious event that does not exist. Instead, it is a typical symptom of schizophrenia.

In short, schizophrenia is a disease that disrupts long-distance neural connections that broadcast signals throughout the brain and form the workspace system of consciousness.

In general, this type of illness does not cross the boundaries of the nervous system. Schizophrenia has a particularly significant impact on the biological mechanisms that maintain top-down long-distance neural connections in neurons.

In patients with schizophrenia, this dysfunction is not complete. Otherwise, the patient will lose consciousness.

In 2007, a neurologist discovered a surprising disease at the University of Pennsylvania.

On that day, young people with various symptoms were admitted to a university hospital. Most were women with ovarian cancer, but some only complained of headaches, fever, or flu-like symptoms.

However, their illness quickly changed unexpectedly, developing "significant symptoms of psychosis, such as anxiety, excitement, bizarre behaviour, delusions, paranoid thinking, and visual and auditory hallucinations." In addition, began to exhibit symptoms of acquired acute schizophrenia.

Over three weeks, the patient's consciousness declined, and EEG measurements detected the slow brain waves seen during sleep and coma. Eventually, they became immobile, unresponsive to stimuli, and in some cases, unable to breathe on their own. Some of the patients died within a few months.

Some later recovered and regained normal mental health and returned to their daily lives, but they did not remember anything when they lost consciousness.

Careful investigation revealed that all of these patients had caused a primary autoimmune disease.

Instead of monitoring external invaders such as viruses and bacteria, their immune system targets itself and selectively disrupts the NMDA receptors on the neurotransmitter glutamate, a molecule inside the body. It was.

This essential component of the brain plays a vital role in the top-down transmission of the information at cortical synapses.

When the cultured neurons were exposed to serous fluid taken from the patient, the NMDA receptors disappeared cleanly within a few hours.

But when they removed this deadly serous fluid, the receptors returned.

This case may be a medical condition that indicates that the disease selectively inhibits the long-distance neural connections that underlie all conscious experiences.

This focused attack immediately disrupts consciousness by first causing schizophrenia and then destroying the ability to stay awake.

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