Schizophrenia Theory

Not much is known about the early stages
of many medical conditions.

For Example: What is Schizophrenia?

The accepted definition (DSM IV TR is the gold standard) says a patient must have:

One of:

• Bizarre Delusions,
• Grandiose or Paranoid Delusions,
• Persecutory or Jealous delusions,
• Auditory Hallucinations,
• Incoherence or Loosening of Associations or Illogical Thinking,
• Blunt or inappropriate moods,
• Grossly Disorganized Behaviour.

 

Deterioration from a previous level of functioning in areas such as work or social relations or self-care. 

Continuous signs of the illness for at least six months.

Schizophrenia is a form of “madness”.

This is the common thought shared most people in thinking about this illness. I have always disliked the use of the word madness. Madness implies that there is no contact with reality. However, many schizophrenics are able to deal with reality quite effectively. It’s just that at times, they say things that are untrue from an outsider’s perspective.

Madness is a commonly used term for most people to describe a category of illnesses that doctor’s label as “psychoses".

This is distinct from illness categories that are labelled the “neuroses.” Patients suffering from the neuroses are supposedly not mad, but are only different from normal in the quantity of their symptoms, not the nature of their symptoms.

I will always remember one woman who had schizophrenia who was sharing a hospital room with a woman who had obsessive-compulsive disorder. (OCD). The OCD lady predominantly had a germ and cleanliness phobia. The schizophrenic woman said, “Doctor, that other woman, she’s mad.” In other words, the lady with madness or schizophrenia, felt that the woman with OCD had bizarre and unusual behaviour that was quite different from what it should have been.

 

The difference between these “neuroses” and “psychoses” would appear to be quite arbitrary, to many people. Sufferers from both conditions can appear “mad” to other people.
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It all makes a lot more sense when you look at the Paill Spectrum concept.

The Paill Spectrum model of disease would suggest that patients with schizophrenia have cross-links forming between neurones. These cross-links (perhaps also likened to a short circuit) cause voices and delusions (abnormal intense beliefs), to pop up into “thinking. This is not really a lot different to someone with OCD, where there are unusual intense beliefs, but not enough cross-linking to insert memories into “thinking.” Both diseases in the Paill Spectrum model really differ only in severity and extent of the cross-linking process.

 

Madness is a bad term. If a doctor really listens to people who have schizophrenia and has a think about what they are saying, it all makes a lot of sense, considering that "cross-links" are occurring.

There are thoughts from the wrong parts of the brain obviously being fed into the part of the brain that determines "reality". The isolated thoughts are correct in their "proper" context, but are incorrect when linked to the sense of "reality": reality being a brain interpretation of what we are "now" experiencing in the world. The rest of the brain is largely intact and other thought processes are quite normal.

Receptionist: Hearing Voices: Can be normal

In summary, schizophrenia is not a form of madness in the Paill Spectrum model. The Paill Spectrum model of disease would suggest that it is a cross-linked memory syndrome. Current thoughts from specific brain areas are "fed" by neural "short circuits" into parts of the brain where they should not be. This causes the affected person or schizophrenic to hear voices and to have intense inappropriate ideas or delusions.

The basic underlying abnormality in schizophrenia is the tendency to create memory and thought cross-links. This is no different to the cross-links formed in any other Paill Spectrum behavioural syndrome. The description of schizophrenia as a separate disease entity to other Paill Spectrum syndromes then becomes difficult to justify.

The other differences between Paill Spectrum Behavioural Syndromes lie in that different regions are more or less affected, at different ages. Different medicines may be needed to control a range of symptoms arising from differently affected regions as a result. Older patients do not seem to be susceptible to the same type of changes as are young patients. While their sense of reality was capable of being “overwhelmed,” they could bring themselves back to reality under their own voluntary thought control. When they concentrated on things and thought about them, they were able to see that what they were doing or saying, was not very sensible. They could control their psychosis. This did not occur in the younger patients with schizophrenia or schizophrenia like disorders. Back to Schizophrenia Top

 

 Mechanics of Neural Cross-Linking

Altered brain wiring entry allows signals from previously unconnected parts of the brain to enter the reality core. This gives the positive symptoms of schizophrenia: namely hallucinations.

 
Neurones have to connect to work together, much like this boat crew        

Voluntarily controlled input from undamaged parts of the brain can override the weird thoughts arising in the damaged reality core, in older patients.

The key concept is that the abnormal thoughts (abnormal in intensity and nature), are due to a quirky brain rewiring. This would cause symptoms to be a bit different in each individual. In short this illness can look quite different in many different people, and may not even be assessed as the same illness at all often at first presentation to a doctor. Common alternate diagnoses made by doctors include: Bipolar disorder, Psychotic depression or terms such as schizoaffective disorder.

The Paill Spectrum model does not support the current modern hypothesis that brain receptor abnormalities are responsible for the development of behavioural disorders such as schizophrenia.

The Paill Spectrum model also tells us that the drugs used to treat many psychiatric conditions are symptomatic relievers. They do not do anything to treat a cause, because there is no officially recognised cause. Many doctors believe that receptor abnormalities underlie the occurrence of the illness, even though no receptors abnormalities have even been found to be associated with the presence of the illness. Also the presence of no specific receptor has ever allowed doctors to predict the likelihood of the presence or progression or regression of the illness. There are many things about this illness that cannot be explained. While these drugs are useful, long-term use cannot be said to cure people. Disease progression will occur in the Paill Spectrum model.
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The old anti-schizophrenic medications suppressed a broad spectrum of brain activity. This caused visible slowing, flat affect (mood) and gives the characteristic appearance of the older schizophrenic patient on the traditional medications. The tendency of the older medications to bind to receptors more tightly, means there were fewer catch/ release cycles. This effectively mimics the effect of a slow CPU chip in a computer: Everything slows down. (Clock Block). Lots of brain chemistry stops working in lots of places.

 

The new drugs affect fewer types of chemicals in the brain, and are more specific in the types of dopamine receptors that are affected. They also bind less tightly to brain receptors, so there are more catch release cycles and the brain does not become as slowed. They have a faster “clock” speed as well as fewer effects, on "other" brain chemicals. This reduces the blunting and other symptoms associated with the clock blockers. (Traditional old anti-psychotic medications). The old drugs caused sedation, weight gain and poor volition. Volition is the sense of self-motivation and the ability to want to do things.

 

The model has implications. The exact areas of brain damage can be many and varied due to the nature of the damaging agent. There may be a role for different drugs in combination. This utilizes the affects of different drugs on different parts of the brain. Different medication effects on nerve transmitter speeds and different brain areas, could be important in getting the right mix of therapy. This is not a currently accepted practice, but perhaps will allow some patients to recover some extra symptomatic health in future.

  

Zyprexa is an anti-schizophrenic medication. Zyprexa (olanzapine) for many patients causes effects such as weight gain, better and more normal moods and better motivation or volition.

It appears to act by only mildly slowing the brain CPU speed (psychomotor clock), due to its looser catch / release cycle. This lets patients think fairly quickly and fairly normally, the patients do not become so sedated.

Also by affecting specific brain nerves in very specific brain areas very potently, it blocks signal inputs from "cross-links" next to the "reality core". Patients "experience" fewer bad signals. This translates into fewer hallucinations and fewer delusions.

Due to its more dopamine specific action, it allows existing brain inputs (non-dopaminergic) to enter the reality core with less competition. This means that patients can override abnormal brain activity in Paill Spectrum damaged areas, with "normal" signals from unaffected parts of the brain.
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Solian is another anti-schizophrenic medication. Solian seems to cause no weight gain, a fairly normal mood state and fairly normal motivation or volition. It would seem to accelerate the brain "CPU" speed or what doctors call the "psychomotor clock". (I.e. This medication would have very loose catch release cycles). This translates into patients feeling like they have a lot more energy and in patients wanting to do lot more things and to become more involved in relationships.

But is still a potent enough blocker to block inputs from cross-links next to the reality core. It would therefore either enhance existing "normal" brain signals entering the reality core or lessen competition from "bad" brain signals entering the reality core. (Again, due to its potent specific action on the dopamine receptors). Back to Schizophrenia Top

  

 

 

 

 

 

 

 

Schizophrenia as a disease,
fits the pattern you would expect of a Paill Spectrum disease.

• It is multifocal and varied in its presentation. There are a number of different symptom patterns even within the one patient over time.
• No one chemical treatment could be relied on to reverse "all" the symptoms in all the patients. This is due to the many slightly different areas and the slightly different types of damage occurring.
• The progress of the disease would be variable and relapsing. The infection would linger over many years with a generally progressively deteriorating clinical course.
• The infection often responds and relapses to changes in nutritional state. (Leaving home and setting up shop on your own as a young adult, results in poor nutrition with quite unexpected consequences, over a long period of time.)
• Very different symptoms in a number of patients. It should look like schizophrenia is a group of closely related diseases rather than just one disease with one symptom pattern.

 

On reviewing many patients with many illnesses including psychiatric illnesses such as schizophrenia, an impression of poor nutrition, difficult circumstances, bad habits such as vegetarianism (meat and B12 avoidance resulting), began to emerge. 

The general pattern suggests enhanced susceptibility to Paill Spectrum in many cases.

Thought Thread

The common thread between Paill Spectrum Behavioural Disorders is always abnormal intensity or abnormal types of thoughts, which may be associated with language or learning deficits. 
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Learning Deficits (Examples)

• Discrepancies between maths and English scores in older children.
• Poor learning in general in younger children.
• Dyslexia
• Dyspraxia
• Memory processing difficulties such as revisits, substitutions, flips, mirrors and drops are typical of Paill Spectrum infection in the symbolic speech processing area of the brain.

Normal

The control loop of the neurones forms a double negative system, so the result of excitation causes inhibition that causes excitation in turn.

Acutely or Post-acutely Ill: Scenario 1

Acutely or Post-acutely Ill: Scenario 2

Excitation of the presynaptic inhibitory dopaminergic neurone causes increased downstream (down-neuronal) excitation, resulting in restlessness, agitation, increased thoughts and
theoretically as a result auditory hallucinations

Catatonia

An “extreme” excitation scenario. Note pre-synaptic dopamine antagonists do not control or suppress the inhibition of the postsynaptic dopamine neurone. Local irritation is likely to bypass medication mediated postsynaptic dopamine antagonism. Back to Schizophrenia Top

 

Blanking

Local irritation may in some situations block the effect of dopamine inhibition of the postsynaptic neurone. An excited post-synaptic inhibitory neurone will cause inhibition of volition or activity.

Medicated

Reduces the effect of excess dopamine at the synapse, returning system activity to normal.

Chronic Illness

Less neurones results in less signals being processed, so a generally narrowed behavioural response spectrum with self down regulated but generally overexcited downstream neurones: may explain some persistent hallucinations

Two mechanisms exist for production of hallucinations and delusions: hard-wired cross-links probably related to neuronal synapse regrowth and distortion and neuronal activity regulation probably more responsible for some intensity effects. Back to Schizophrenia Top

For More Clinical Information: See :>>

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This page discusses brain and neuronal wiring and relationship to schizophrenia symptoms under the Paill Spectrum model, resulting from neural cross linking. The two stages of dopamine transmission are illustrated with their effects on symptoms of the disease.  The role of schizophrenic medications on dopamine receptors and brain signals is discussed. Neural cross linking causes delusions and auditory hallucinations due to neural cross-linking.

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