Friday, September 01, 2006

Causes and Effects

The OCR syllabus states that you need to know the causes and effects of one specific learning disability.

The example used here is that of Autism. The material is by Elizabeth Green as published in 'Psychology Review' (Vol 12, No2, November 2003)

The aim of research into autism is to progress towards a time when we can say "This is how it starts, this is what the biological implications are, and this is why autism is what it is'. At the moment we know a lot about different aspects of autism - the genetics, the biological abnormalities, the cognitive basis and the behaviour - but it is not possible to piece these together to form a coherent story of what causes the disorder. Years ago, people believed that autism might be caused by a lack of attention from parents or feelings of rejection in the early years of a child's life; this is not the case. Autism is now known to have a strong biological basis and the evidence suggests that there is often a genetic abnormality that makes a child more likely to develop autism. The best explanation of autism is that there are many factors which contribute to the disorder. New evidence also suggests that there may be a particular stage in development during which the major damage occurs.

Possible biological factors involved in causing autism -

Many anomalies in different areas of the brain have been implicated in autism and it seems clear that there is not one single abnormality that 'causes' autism.

General abnormalities: Many researchers have reported an overall enlargement of the brain (megalocephaly) in autistic people (e.g. Lainhart et al. 1997). They have found this by measuring the circumference of people's heads, by weighing the brain during autopsy and by ai using scanning techniques such as MRI and PET . Normally, the right side of the brain is bigger than the left side and it is thought -that the, enlargement seen in autopsies of autistic people is mainly of the left side, meaning that the brain is more of symmetrical than normal.

Abnormalities of the cortex: The most replicated cortical abnormalities are of the temporal and parietal lobes. Temporal lobe reduced blood flow has been reported, which indicates a decrease in normal activity. The temporal lobes have varied and complex roles, including a role in language and personality. This means that the effects of damage are also very variable. It is interesting to note that in some patients who have temporal lobe tumours, we see symptoms of autism, and further, there is the the reported case of a boy with a temporal lobe tumour whose symptoms decreased as the tumour regressed with treatment.

Abnormalities in the Limbic system: Probably the most solid findings of a biological basis of the disorder come from research into an area of the brain called the limbic system. The limbic system is located within and next to the temporal lobe and comprises several different structures that are important in emotion, learning and memory. Two important structures are the hippocampus and the amygdala, and abnormalities in both these structures have been found in the brains of people with autism. It is also known that humans with damage to the amygdala often show emotional problems that are similar to those seen in autism.

Similarly, solid findings of abnormality have been found in the cerebellum and brainstem of autistic patients. For example, some researchers have reported a decrease in the number of cells in the cerebellum and fewer connections with the limbic system. Other research has indicated an overall decrease in the size of both the cerebellum and brainstem.

Biochemical abnormalities: Messages are sent through the brain by neurotransmitters and therefore the balance of these chemicals in the brain is very important. Neurotransmitter dysfunction underlies many psychological disorders, such as depression and schizophrenia, and therefore it is important to look at the biochemistry of the autistic brain when searching for a cause. Most of the research has focused on the chemicals called serotonin and dopamine. Some studies have reported that there are high levels of serotonin. in .the brains of people with autism. however, high serotonin is found in several other disorders and may, perhaps, be a by-product of mental retardation rather than a causal factor. Other researchers have implicated dopamine abnormalities as a possible cause of the symptoms of autism, but there h is less evidence for this at the moment.

Genetic factors: The first piece of evidence for this is that, although it is extremely rare for autistic children to have a brother or sister who is also autistic, the rate of autism in siblings is much higher than in the general population. That is, the chance of your having autism is somewhere between 20 and 100 times higher than normal if you already have a sibling with autism. To look more at this familial link researchers use twin studies - a very important tool when examining the genetic influence on a disorder. Twin studies look at 'concordance rates', which means the percentage of twins where both twins have the disorder. To assess how much of the sibling effect is genetic and how much is because the twins develop and grow up in because the twins develop and grow up in the same environment, we compare the concordance rate of monozygotic (MZ) with dizygotic (DZ) twins. It is estimated that the percentage of both MZ twins having autism is between 60% and 90%, compared with less than 5% for DZ twins. This is very strong evidence for the role of genetics in the underlying cause of autism. However, it does not mean that autism is a completely genetic disorder. If autism were entrirely caused by genes, then MZ twins would have 100% concordance.

Conclusons: There is a range of evidence that there may be a specific period during foetal development when the biological abnormalities associated with autism originate. This period could be described as a 'window of vulnerability', because it may be that the brain is particularly vulnerable to damage during this time slot. Some brain abnormalities give us clues as to when they occur. For example, abnormal patterns of certain cerebellar neurones, when compared with normal patterns, indicate that damage must have occurred at or before the thirty-second week of pregnancy. Courchesne (1997) points out that many parts of the brain we know are abnormal in autism develop during the fifth week of gestation — maybe this is the window of vulnerability? Of course, there are abnormalities present in autism that could not have been caused during this window but it is very possible that these are either knock-on effects from the earlier damage, or they are caused by a different factor; we know that autism is not caused by one single factor.

The window of vulnerability hypothesis is probably one of the best theories we have to explain how autism occurs, as it pulls together the roles of biology, genetics and adverse events. It may be that an infection or trauma during this window could cause the damage, or it could be that a defective, gene acts at this point in foetal development. Thereafter, the damage that occurred during the window of vulnerability will have other .knock-on,effects and give rise to the multitude of abnormalities seen in the autistic brain.

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