Biological explanation of Schizophrenia

Assumption: All mental disorders have a physical cause (micro-organisms, genetics, biochemistry or neuroanatomy).

Mental illnesses can be described  in terms of clusters of symptoms, symptoms can be identified, leading to the diagnosis of an illness, and diagnosis leads to appropriate physical treatments.

Prevalence of schizophrenia is the same all over the world (about 1%)

This supports a biological view as prevalence does not vary with environment

However, there are variations within broad geographical areas (e.g. Torrey 2002 –  found high rates of Sz in Ireland, 4% of the population, the incidence is also high in Croatia and Scandinavian countries but low in Spain and Italy and very low in some parts of Africa)

Gottesman and Shields reviewed the results of 5 twin studies looking for concordance rates for schizophrenia. These studies looked at 210 MZ twins and 319 DZ twins

It was found that in MZ twins there was a concordance rate of 35-58% compared with dizygotic twin rates that ranged from 9-26%. They also found a concordance rate in MZ twins of 75-91% when the sample was restricted to the most severe form of schizophrenia.

The milder forms of schizophrenia had concordance rates of 17-33% suggesting that there may be greater genetic loading with severe forms of schizophrenia. The twin studies have all assumed that the shared environmental effects for MZ and DZ twins are equal which may be incorrect

Twins are not representative of the wider population (gestational environment).

It is a very small sample. There are very few MZ twins in the population and only 1% are Sz.

Could the psychiatrist making the diagnosis in the child be influenced if he/she is aware that one of both of the parents are Sz?

In 2006, an Edinburgh University team found people carrying a variant of a gene called neuregulin had a higher chance of developing psychotic symptoms. However since then research has shown that Sz involves a huge number of genes with each of them making only a small contribution to the development of the disorder according to Robin Murray a leading schizophrenia researcher.

Risk rises with degree of genetic relatedness:

Spouse – 1% (same as general population)

Child – 13%

DZ twin – 17%

MZ twin – 48%

Effect of shared environment?

Neurons that use the transmitter ‘dopamine’ fire too often and transmit too many messages or too often.

Certain D2 receptors are known to play a key role in guiding attention.

Lowering DA activity helps remove the symptoms of schizophrenia

Which came first, schizophrenia or faulty chemicals?

Faulty chemicals cause schizophrenia but schizophrenia may cause faulty chemicals

There is a lack of correspondence between taking the drugs and signs of clinical effectiveness. It takes 4 weeks to see any sign that the drugs are working when they begin to block dopamine immediately. We cannot seem to explain this time difference.

It could be that the development of receptors in one part of the brain may inhibit the development in another.

Type 1 cases respond well to conventional anti-psychotic drugs.  Drugs such as Chlopromazine: Only effective at relieving the Positive Symptoms of the Illness.

Not effective for negative symptoms. Therefore suggested that Type 2 is related to a different kind of abnormality such as brain structure.

PET scans have suggested that drugs did not reduce symptoms of patients diagnosed with disorder for 10 yrs or more

There may be other neurotransmitters involved.

Possible that social and environmental factors trigger the condition.

Brain structure

Brain damage

Viral infection

Birth complications

People with schizophrenia have abnormally large ventricles in the brain.  Ventricles are fluid filled cavities. This means that the brains of schizophrenics are lighter than normal.

Swayze (1990) reviewed 50 studies of schizophrenics and found that many had abnormally large amounts of liquid in the cavities of the brain.

Suddath, who supports this found the same enlarged cavities when using MRI scans on schizophrenic twins.

Andreasen et 1990 – conducted a very well controlled CAT scan study and found significant enlargement of the ventricles in schizophrenics compared to controls.

However this was only the case for men and not for women. Therefore can’t generalise the findings to women.

• Unusually large corpus callosum
• High density of white matter in the right frontal and parietal lobe
• Small amount of grey matter in the temporal lobes
• A change in blood flow in the cerebral hemisphere
• MRI scan show unusually large ventricular enlargement but this is also seen in non-schizophrenics
• Hippocampus and the thalamus are all affected in the brains of schizophrenics

Beng-Choon Ho (2010) in a longitudinal correlational study of 211 schizophrenics found that antipsychotic drugs have measurable influence on brain tissue loss over time. This was supported by Lewis (2009) who administered antipsychotic drugs to primates and found a brain volume loss of 10%. 

However this was a correlational study so it does not show cause and effect. Lewis’s study was carried out on animals so we cannot extrapolate to humans without caution.

If the reduction in brain volume is the cause of the schizophrenic symptoms then it cannot explain why after 30 years of the initial onset, 35% of the schizophrenics are classified as  "much improved“ because the cortex does not grow back, if the structural differences were the cause then no improvement would be possible

• Decreased rate of blinking
• Staring
• Lack of the blink reflex in response to a tap on the forehead
• Poor visual pursuit movements
• Poor pupil reactions to light

In recent years, there has been a build-up of evidence supporting the role of viral infections in the development of schizophrenia, including the poliovirus, the flu virus and a virus called encephalitis lethargica ('inflammation of the brain that makes you tired').

Complications during pregnancy, abnormal foetal growth and complications during delivery are significant risk factors in the development of schizophrenia.

Those that play a significant role in the development of schizophrenia include: bleeding, diabetes and pre-eclampsia pregnancy complications, abnormal foetal growth and development problems including conditions such as low birth weight and reduced head circumference, complications of delivery including asphyxia (lack of oxygen) and emergency Caesarean section.

However, the effect of such complications is small in comparison with factors such as genetic pre-disposition to schizophrenia.