Documentarul nu intra in prea multe amanunte despre autism. Cea mai frapanta caracteristica a autistilor e ca nu par capabili sa atribuie altora intentii (sa ghiceasca ce vor ceilalti), ceea ce ii impiedica sa dezvolte relatii sociale. Nu se stie exact din ce cauza au deficienta asta. Documentarul pare sa sugereze ca dezvoltarea creierului lui Derek in primele luni a fost afectata de o supra-oxigenare a creierului.
Din Encarta Encyclopedia 2008:
Many theories have been proposed to explain what goes wrong during brain development to cause autism. Research has centered on a number of factors that may be involved.Din Wikipedia:
Serotonin is a neurotransmitter that is produced in the brain. It has a range of functions in the body, including important roles in the central nervous system. It also affects mood, memory, and appetite control. In 1961 Daniel Freedman and colleagues found increased levels of serotonin in the blood of patients with autism. More recent research has found that increased serotonin, or hyperserotonemia, is present in about one-quarter of patients, is also present in some of their family members, and is caused by genetic factors.
Some children with autism show an increase in brain growth during the first year of life that later slows down so that most adults with autism do not have enlarged brains. This increased growth is thought to be due to increased connections between neurons. Most brain studies in autism have also found a decrease in the size of a particular brain region, the cerebellar vermis.
People with autism show less activity than normal in the mirror neuron system of the brain that some scientists believe allows the human brain to understand and learn from observing other people. A recent theory proposed that defects in the mirror neuron system may explain some aspects of autism. Additionally, people with autism often overreact emotionally to trivial events in their environments, suggesting a problem with the processing of what they perceive.
Many theories have been proposed to explain each of these findings, but more research is needed to understand what goes wrong during brain development.
Autism appears to result from developmental factors that affect many or all functional brain systems, and to disturb the course of brain development more than the final product. Neuroanatomical studies and the associations with teratogens strongly suggest that autism's mechanism includes alteration of brain development soon after conception. This localized anomaly appears to start a cascade of pathological events in the brain that are significantly influenced by environmental factors. Although many major structures of the human brain have been implicated, almost all postmortem studies have been of individuals who also had mental retardation, making it difficult to draw conclusions. Brain weight and volume and head circumference tend to be greater in autistic children. The cellular and molecular bases of pathological early overgrowth are not known, nor is it known whether the overgrown neural systems cause autism's characteristic signs. Current hypotheses include:
- An excess of neurons that causes local overconnectivity in key brain regions.
- Disturbed neuronal migration during early gestation.
- Unbalanced excitatory-inhibitory networks.
- Abnormal formation of synapses and dendritic spines.
Interactions between the immune system and the nervous system begin early during embryogenesis, and successful neurodevelopment depends on a balanced immune response. Several symptoms consistent with a poorly regulated immune response have been reported in autistic children. It is possible that aberrant immune activity during critical periods of neurodevelopment is part of the mechanism of some forms of ASD. As autoantibodies have not been associated with pathology, are found in diseases other than ASD, and are not always present in ASD, the relationship between immune disturbances and autism remains unclear and controversial.
Several neurotransmitter abnormalities have been detected in autism, notably increased blood levels of serotonin. Whether these lead to structural or behavioral abnormalities is unclear. Also, some inborn errors of metabolism are associated with autism but probably account for less than 5% of cases.
The mirror neuron system (MNS) theory of autism hypothesizes that distortion in the development of the MNS interferes with imitation and leads to autism's core features of social impairment and communication difficulties. The MNS operates when an animal performs an action or observes another animal of the same species perform the same action. The MNS may contribute to an individual's understanding of other people by enabling the modeling of their behavior via embodied simulation of their actions, intentions, and emotions. Several studies have tested this hypothesis by demonstrating structural abnormalities in MNS regions of individuals with ASD, delay in the activation in the core circuit for imitation in individuals with Asperger's, and a correlation between reduced MNS activity and severity of the syndrome in children with ASD. However, individuals with autism also have abnormal brain activation in many circuits outside the MNS and the MNS theory does not explain the normal performance of autistic children on imitation tasks that involve a goal or object.
A 2008 study of autistic adults found evidence for altered functional organization of the task-negative network, a large-scale brain network involved in social and emotional processing, with intact organization of the task-positive network, used in sustained attention and goal-directed thinking. A 2008 brain-imaging study found a specific pattern of signals in the cingulate cortex which differs in individuals with ASD.
Functional magnetic resonance imaging provides some evidence for the underconnectivity theory of autism. The underconnectivity theory of autism hypothesizes that autism is marked by underfunctioning high-level neural connections and synchronization, along with an excess of low-level processes. Evidence for this theory has been found in functional neuroimaging studies on autistic individuals and by a brain wave study that suggested that adults with ASD have local overconnectivity in the cortex and weak functional connections between the frontal lobe and the rest of the cortex. Other evidence suggests the underconnectivity is mainly within each hemisphere of the cortex and that autism is a disorder of the association cortex.