Biology 202, Spring 2005
First Web Papers
On Serendip

In fairly recent years medical and social awareness of autism has grown to the level that more and more individuals are being diagnosed with the disorder and the diagnosis is coming at earlier stages in a child's development. Especially with the awareness brought by the movie "Rainman", autism has jumped to the forefront of medical issues as a disorder that affects approximately 425,000 Americans under the age of 18 (1) . This developmental disorder can provide an example to support the theory that the brain is responsible for all human behavior, rather than a soul or other element that could define personality and/or behavior.

Autism affects many important functions of human behavior, usually manifesting in early childhood, sometimes seemingly overnight. Most of the effects of this disorder impair an individual's social behaviors and can cause other behaviors such as repetitive actions and perseverations (2). Until recently the only diagnostic tests and defining characteristics that existed for autism involved behavioral studies. Researchers are now looking at the physical manifestations of autism in the brain structure of individuals with the disorder. More evidence is being uncovered to suggest that structural differences or abnormalities in the brain are what lead to the changes in behaviors observed in individuals upon the onset of autism (2). The cause for these structural and developmental changes in the brain cannot yet be determined, however a possibility exists that environmental factors contribute to the onset; even inflammation and vaccinations are being examined as possible causes.

Researchers have been able to map out areas of brain activity in autistic individuals and compare them to the active regions and amounts of activity in a control group of non-autistic individuals. It is estimated by some that autistic individual's brains are wired differently from birth which causes the different behaviors and effects of autism (1) . Whether the changes are present at birth or whether they occur gradually cannot be determined as of yet, but either way provides evidence to the fact that the changes in the brain bring about changes in behavior. Data to support the brain being responsible for behavior can be exemplified by Dr Fred Volkmar's statement. '"If you put 100 people with autism in a room, the first thing that would strike you is how different they are, the next thing that would strike you is the similarity'" (1) . In this respect different people's brains function in different ways accounting for the diverse variations of behaviors among a sample population which could be said to happen within a population of autistic individuals. However, the autistic individuals all possess similar changes in brain structure and development which cause them to behave in manners that are more similar to each other than to non-autistic individuals.

Two specific malfunctions are currently under research by scientists as the cause of the changes in behavior when a child first displays signs of autism: an abnormal pruning process (2), and abnormal changes in the limbic system; more specifically in the amygdala of the brain (4). In the first instance, pruning is a process that occurs several times during development to rid the brain of abnormally functioning neural connections. Pruning can help to maximize coordination of neural circuits (2). When pruning fails to function as may be the case in autism, brain size will increase and neural functioning and synapse will be decreased (2). This fits with studies conducted that found the brains of autistic children to be markedly larger in their early years as compared to a child without autism. This increased brain size is attributed to an increase in both grey and white matter that some feel causes a deluge of stimuli in the autistic brain; more than can be handled naturally. By adolescence the brain size of autistic children tends to have evened out in respect to those of non-autistic individuals, and in some cases they are even smaller than non-autistic children (1). However, by this point the damage has already occurred and the lack of pruning has left the brain with too many inefficient and damaged circuits.

A second difference or abnormality in the brain that could explain the change in behavior lies in the amygdala, which is part of the limbic system. The current definition of the limbic system includes parts of the hypothalamus, the septal area, the nucleus accumbens, the neocortical areas, and most importantly the amygdala. The amygdala is the part of this particular system that is most specifically involved in feelings and emotions. The amygdala is involved with the memory of specific cues that recognize fear and apprehension in human faces (3), which could explain the abnormal social behaviors of autistic individuals. This area also mediates emotional responses that humans possess from birth as well as learned emotional responses (3) and in the case of autism this could explain the lack of social responses and the flat manner of dealing with emotions and other people.

Although autism is not a newly discovered developmental disorder, many things are still unknown regarding the neurobiology of the disease and the exact definition of its effects on humans. The brain is such a complex organ and no two people possess the same brain which makes it difficult to measure and contrast brain differences among autistic individuals as compared to non-autistic individuals. However, with what little is known about brain structure and abnormalities in autism it is apparent that these changes can be considered responsible for the behavioral changes that often characterize autism.

References

1) New York Times, good overview of characteristics of autism

2) Hill, Elisabeth L. and Uta Frith. Understanding autism: insights from mind and brain. London: The Royal Society, 2003.

3) Kandel, Eric R. et al. Principles of Neural Science 4th edition. New York: McGraw Hill, 2000.

4) Salmond, C.H. et al. Investigating individual differences in brain abnormalities in autism. London: The Royal Society, 2003.


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