The Brain, The Body, The Behaviour – Schizophrenia (part 2)

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In my previous post I spoke about the symptoms of the psychotic mental illness that is schizophrenia, and also what schizophrenia risks doing to the physical body. In this post I’m going to (try, anyway) talk through what is going on in the mind of an individual with schizophrenia, what is happening in their brain, why is their brain acting the way it is, and how this links to the behavioural and surface symptoms of schizophrenia.

The Brain

There are too many theories of schizophrenia to factually pinpoint one as the truth. What makes this more complicated is that there are several different types of schizophrenia, with differing symptoms, and therefore different causes: (See my previous post if you need a recap on what the general symptoms of schizophrenia are)

  • Paranoid Schizophrenia – Hallucinations are the prominent symptom, whereas the speech and emotions are unaffected
  • Hebephrenic schizophrenia – The behaviour is disorganised and appears to be without purpose. Thoughts are also disorganised, and behaviour includes pranks, giggling, health complaints and iconic mannerisms.
  • Catatonic schizophrenia – This is the rarest diagnosis among schizophrenia. The individual has very unusual, minimal movements and may not even talk at all.
  • Simple schizophrenia – Weird name, because no sort of schizophrenia is simple for the patient. But the symptoms here are simple to remember. Positive symptoms are very rare, but negative symptoms are prominent early and get worse quickly.
  • Residual schizophrenia – The individual may have a history of psychosis and only experience negative symptoms as a residual factor of this.

As mentioned before, there is no simple, straightforward theory of schizophrenia – of how it comes about, or what happens when the individual is experiencing symptoms. This is similar to most mental health problems really, there is no simply pathway of how they came to have their mental health problem.

Within schizophrenia there are theories that their disorder is to do with their cranial (skull) development. There is evidence that individuals with schizophrenia had smaller than average cranial size. Cranial development is completed within the first few years of life, so it would be the individuals early development that may contribute to their risk of having schizophrenia later in life.

There is also evidence that the activity within the Basal Ganglia may contribute towards schizophrenic symptoms due to it’s involvement in the production and release of dopamine (this will be explained later). The Basal Ganglia is responsible for movement, emotions and sensory information integration. Therefore if it does not function ‘correctly’ it can lead to catatonic symptoms, emotional dysfunction, and issues with sensory information such as hallucinations and paranoia.

However the two most popular and descriptive theories of schizophrenia are the dopamine hypothesis and the glutamate hypothesis.

Dopamine hypothesis: 

  • Dopamine is a neurotransmitter that has several roles within the body. If you remember from my 3Bs post on depression dopamine is crucial in arousal, stimulation and mood regulation.
  • Dopamine works within what is called the mesolimbic pathway.
    • It is the reward pathway of the brain, so it makes individuals feel good when they do something well.
    • It is also linked to feeling good after sex, alcohol and drug use and is associated with addictions.
    • However when there is overactivity of this pathway it can lead to positive symptoms of schizophrenia.
  •  Dopamine also works in the mesocortical pathway. 
    • This is responsible for emotional response, motivation and cognitive functioning.
    • An overactivity in this pathway is linked to negative symptoms of schizophrenia.
  • Looking at where the mesolimbic pathway is within the brain can help us connect this hypothesis to the symptoms of schizophrenia
    • Broca’s area – This is the area of the brain that looks at language and speech. Therefore overactivity of dopamine here may result in illogical and disorganised language and speech.
    • Wernicke’s area – This is associated with auditory stimulus and sensory information. Overactivity of dopamine can result in auditory hallucinations.
    • Hippocampus – The hippocampus is quite a large area of the brain in relation to what it can do. However it is associated with the basal ganglia and hypothalamus  in the production and release of dopamine. Therefore dysfunction in this area can alter this.  Dysfunction of the hippocampus can also lead to disturbances in long term memory which is seen in a lot of schizophrenic patients, especially those with a history of trauma. The integration of information within the prefrontal cortex can also be affected because of dysfunction of the hippocampus. This can lead to symptoms relating to problem-solving, insight (especially insight into their own condition), reasoning, planning actions and disorganised thoughts.
  • The mesocortical pathway is slightly different:
    • The mesocortical pathway is also linked with the prefrontal cortex, so all symptoms associated with the mesolimbic pathway running through the prefrontal cortex can be duplicated here.
    • However in general there is a lack of explanation for negative symptoms compared to the positive symptoms in the research

 

Glutamate hypothesis 

  • Glutamate is also a neurotransmitter. The hypothesis has only recently been researched compared to the dopamine hypothesis, and is seen as an extension of that hypothesis rather than a separate one due to glutamate and dopamine working closely together in the body.
  • Glutamate uses things which are called NMDA receptors.
    • If there is low NMDA activity this can lead to a loss of drive in the mesortical dopamine neurons, which as seen above can lead to negative symptoms.
    • Also if there is low NMDA activity, dopamine in the mesolimbic pathway are not inhibited which can lead to positive symptoms.
  • Therefore in the glutamate hypothesis, as simply as I can put it, a shortage of glutamate affects the dopamine activity which can then produce symptoms.
  • However, as this research is fairly new there are inconsistent findings.

 

So those are the two main hypotheses for schizophrenia. Obviously this does not look at the environmental factors which may contribute to schizophrenia such as the diathesis-stress model, drug induced psychosis, and genetic factors. However it is interesting to see that there is a side to schizophrenia that people cannot control, and this is where anti-psychotic medication can come into use for many patients. It is also interesting to see that the symptoms do not include “stabbing people in the street” or “become a serial killer” because those simply are not symptoms of schizophrenia. Yes, they may be symptoms of hallucinations, or of simply feeling distressed due to their schizophrenia, however they are rare and quite easily managed!

Generally, those with schizophrenia are scared, confused, and stressed due to their symptoms. And by looking at the symptoms, I’m pretty sure you can understand why.

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