Schizophrenia: Biological Explanations

There are two explanations for schizophrenia that I am going to write about, psychological and biological. This Hub is going to focus on the biological explanation.

This explanation basically suggests that schizophrenia is a result of somatic (physical) factors in the brain or body and as such should have a somatic treatment e.g. drug therapy. Although there are many different biological explanations I am just going to focus on three:

• Genetic Inheritance
• Biochemical Imbalances
• Neuroanatomical Abnormalities

This explanation suggests that a predisposition to schizophrenia is passed through families on faulty genes. These faulty genes could lead to a person inheriting a biochemical imbalance or a brain structure abnormality which causes schizophrenia. Researchers believe that they will eventually find a single gene or a gene cluster with is responsible for the illness. Hong et al (2001) already found variations on the TPH gene in schizophrenia sufferers suggesting that this variation could be the cause of schizophrenia.

To investigate the link between twin and adoption studies are carried out with the hope of finding a link between genetic similarity and developing the disorder. Thus suggesting that the closer the genetic relationship the higher the chance of developing schizophrenia. The three studies that I am going to write about are:

1. Gottesman (1992)
2. Heston (1966)
3. Tienari et al (2000)

Gottesman (1992)

This study involved reviewing other family studies and seeing if there was a link between genetic similarity and the risk of developing schizophrenia. The results showed that an MZ (monozygotic/identical) twin who shares 100% genetic similarity has a 48% chance of developing the disorder if their twin has bee diagnosed. First degree relatives e.g. children of sufferers, share 50% genetic similarity and have a 6% chance of developing the disorder if their parent has been diagnosed. And finally second degree relatives e.g. grandchildren share 25% genetic similarity and have a 5% chance of developing schizophrenia if a grandparent has been diagnosed.

Heston (1966)

This was an adoption study that used a sample of 50 children of schizophrenic mothers that were adopted out to non-schizophrenic families at 1 month old. The results showed that 10% of these children went on to develop schizophrenia themselves whereas in a comparison group where 50 children from non-schizophrenic mothers were adopted, 0% developed schizophrenia. This supports the notion that schizophrenia has a genetic basis as the children that developed schizophrenia were the ones which had a biological mother who also suffered from the illness.

Tienari et al (2000)

This study took place in Finland and was an adoption study using over 155 adopted children whose biological mothers had all been diagnosed with schizophrenia. The study found that over 10% of the sample had been diagnosed with schizophrenia, therefore supporting both the Gottesman and Heston studies as it showed that children whose mothers had been diagnosed with schizophrenia were more likely to develop the disorder themselves compared to children whose biological parents were not schizophrenics.

This explanation argues that schizophrenia is caused by an imbalance of neurotransmitters (NT) specifically elevated levels of dopamine as key synaptic sites; hence this explanation is the dopamine hypothesis.

Neurotransmitters are chemicals that surround brain cells and allow cells to communicate with each other. Schizophrenia in particular has been linked to excessive levels of the neurotransmitter dopamine. Dopamine has many roles including regulating higher cognitive functions, behaviour and voluntary behaviour. When there is an excess of dopamine it is argued that a type of 'system overload' occurs where too many impulses are being transmitted, basically too much is happening at once. This can either occur as pre-synaptic neurons could be releasing too much dopamine or there are oversensitive receptor sites at the post-synaptic level. When this occurs, the symptoms of schizophrenia are produced.

Evidence:

There are three observations that have been made which link dopamine to schizophrenia.

• Antipsychotics relive some of the symptoms of schizophrenia by blocking dopamine, hence reducing its' activity. These drugs are effective for up to 85% of patients proving that dopamine must be linked to schizophrenia.
• Drugs that increase the production of dopamine e.g. cocaine are known to make schizophrenia symptoms worse. Therefore proving that high levels of dopamine is linked to schizophrenia.
• Autopsies performed on schizophrenics have shown higher than normal dopamine concentrations.
  

This explanations suggests that schizophrenia is caused by abnormalities in the structure of the brain; these abnormalities could very well be inherited.There are certain neuroanatomical abnormalities that have been linked to schizophrenia:

• Enlarged ventricles. These are fluid filled cavaties in the brain and are found in 67% of schizophrenics. These have been found in unmedicated patients which proves that they are not a result of medication.
  
• Less brain tissue, especially in the medial temporal lobe. This has been confirmed by MRI scans, hence is highly scientific evidence.
• Patients often have a smaller than usual hippocampus as confirmed by MRI scans and post mortems on patients. The hippocampus is the area of the brain that is involved in processing and memory.
• Patients may have a smaller than usual limbic system, this is the area of the brain involved in emotional expression.
• Reduced bloodflow in the pre-frontal cortex (hypofrontality.) The pre-frontal cortex is the area involved in higher levels of thinking and emotion so hypofrontality in this area suggests decreased neuronal activity,
  
• Post mortems of schizophrenics have also revealed that certain groups of neurons are organised in an abnormal way or are connected to each other differently compared to people who do not suffer from schizophrenia.