1. The amygdala
2. Frontal lobes
3. Temporal lobe
4. The cerebellum
5. Conclusion

Research on the cognitive deficits and neurology of individuals with autism suggests the presence of abnormalities in a number of areas. This may be because an early defect in the functioning of one or more areas of the brain alters the development of multiple other areas. The following sections describe evidence supporting dysfunctions in autism of four areas of the brain: The amygdala, the frontal lobe, the temporal lobe, and the cerebellum.

Do childhood vaccinations cause autism? Despite what appears to be compelling personal testimony, the experts generally agree that the research literature does not support a relationship. Four articles are linked to below. For the sake of fairness, one link (the last) argues that there is a relationship.

Misconceptions about Immunization by Stephen Barrett

Vaccines and Autism from WebMD

FAQs (frequently asked questions) about MMR Vaccine & Autism from the CDC

Autism And Vaccines by Tim O’Shea

The amygdala lies in the temporal lobe, and receives highly processed sensory input from other brain structures. It has reciprocal connections with many other areas, including the orbital and medial prefrontal cortex, which are also implicated in autism. The amygdala has been implicated in affective processing and emotion expression, social behavior, and vigilance/anxiety.

Autism and the Limbic System by Stephen M. Edelson

Amygdala from University of Idaho

Amygdala by David Givens

Affective processing and emotional expression
The amygdala is involved in emotional learning. Lesions in one area of the amygdala prevent the attachment of emotional meaning to sensory stimuli (Schultz, Romanski & Tsatsanis, 2000). For example, seeing the face of one’s mother might not bring up normal emotions of happiness and comfort in a young child with amygdala damage. One theory of the social deficits found in autism is that because the amygdala is damaged, impairing the linking of emotional meaning with stimuli, babies are unable to connect faces with comfort, food, and water, and so they do not form the early social bonds necessary for normal development (Schultz, Romanski & Tsatsanis, 2000).

Similarly, amygdala damage has been implicated in impaired recognition of emotional expressions in individuals with autism. In an emotion-recognition task where subjects judged emotions from pictures which showed only the eyes of the target person, individuals with Asperger’s Disorder did not show activation of the amygdala whereas normal subjects did (Baren-Cohen et al., 2000). The individuals with Asperger’s Disorder did much more poorly at this task than did the non-autistic subjects.

Social behavior
When newborn monkeys are given lesions to the amygdala and temporal lobe, they show increasing socioemotional disturbances, similar to those seen in autism, such as abnormal social interaction, absence of facial and body expression, and stereotypic behaviors (Bachevalier, 1994). Damage to the amygdala appears necessary for autistic-like disturbances: When only the hippocampus is lesioned, monkeys show only temporary disturbances in behavior. When only the amygdala is lesioned, they show continuing disturbances in behavior. This is even more severe when the temporal lobe is also lesioned. Finally, it is interesting to note that, similar to children with autism, the lesioned monkeys showed a great deal of variability in their socioemotional disturbances, suggesting that damage to identical areas of the brain can result in a wide variety of symptoms in different monkeys and children.

Anxiety and Vigilence
The amygdala has been implicated in fear and arousal. Neuroimaging studies in animals and humans have shown activation of the amygdala in response to fear-causing events. Amygdala activation in humans is also observed in response to photographs of facial expressions, and is stronger in response to fearful than happy faces (Whalen, 1998). On the basis of this, Whalen (1998) hypothesizes that the amygdala is part of a system which responds to ambiguous cues in the environment, such as fear on the face of another, or other ambiguous cues that potentially warn of danger, by increasing vigilance. It may do so by mediating naturally-occurring anti-anxiety chemicals (Schultz, Romanski & Tsatsanis, 2000). Damage to the amygdala could explain why individuals with autism often experience high levels of anxiety (Whalen, 1998).

Frontal Lobes from the Center for Neuro Skills

Cognitive and executive function
Damage to dorsolateral frontal cortex causes various general cognitive deficits, such as impaired working memory and planning (Stone, 2000). Individuals with autistic disorders have been found to have deficits in dorsolateral prefrontal cortex function, but the extent of the damage is not related to the severity of autistic symptoms (Dawson, Meltzoff, Osterling, & Rinaldi, 1998).

The executive dysfunction theory suggests that the symptoms seen in autism are due to impairment in executive functions such as the cognitive deficits described above (Robbins, 1997). Individuals with autism are impaired on neuropsychological tasks that are sensitive to frontal-lobe damage, such as the Wisconsin card sort task. This strongly suggests frontal-lobe involvement in autism. Tying those findings to a specific area in the frontal lobes, however, is a more difficult task. As mentioned, damage to the most likely area, dorsolateral frontal cortex, does not correlate with autistic symptoms. A more likely hypothesis is that executive dysfunction in autism is not due to damage to a specific area of the brain, but to multiple connected areas involved in executive function (Robbins, 1997).

Social Perception and the Theory of Mind
The orbitomedial and ventromedial prefrontal cortex have been implicated in difficulties with social behavior. Medial prefrontal cortex has been found to be activated in a task determining the intent of two shapes displaying anthromorphic behavior, suggesting that this area of the brain deals with inferring meaning from social activity (Schultz, Romanski, & Tsatsanis, 2000). In addition, patients with orbitofrontal or ventromedial cortical lesions have difficulty forming online theories about what others know and are thinking, as evidence by their tendency to make inappropriate comments and ramble and be insensitive to listeners, similar to high-functioning individuals with autism (Stone, 2000).

Theory of Mind suggests that autism is due to an inability to infer the mental states of others (Baren-Cohen, 2000). People with autism have difficulty performing tasks where they must infer another person’s mental state (Baren-Cohen, 2000). People with Asperger’s disorder are able to pass simple tasks about the beliefs of others, but appear to do so through using conscious, effortful strategies, rather than the automatic processing that normals use. In an emotion-recognition task mentioned in connection with the amygdala, where subjects judged emotion from pictures showing only the eyes of the target, individuals with Asperger’s disorder also showed less frontal activation than did normal subjects (Baren-Cohen et al., 1999).

A discussion about Theory of Mind: From an Autistic Perspective

Vigilance
In addition to inferring social behavior, the orbitomedial prefrontal cortex may be responsible for turning off the amygdala’s vigilance/anxiety response to fear stimuli, as discussed in the section on vigilance and the amygdala (Schultz, Romanski, & Tsatsanis, 2000). When the orbitomedial prefrontal cortex is lesion in rats, and the rats are then conditioned to have a fearful response to stimuli, the conditioning still takes place. Unlike in non-lesioned rats, however, the fear response doesn’t extinguish, suggesting the importance of the role of the orbitomedial prefrontal cortex in dampening fear responses (Schultz et al., 2000).

The temporal lobe, which is highly connected with the limbic system, has been implicated in both object and face perception as well as social behavior. It also plays a role in hearing and memory. It contains the amygdala, which is discussed above; this section discusses evidence for the involvement of other temporal lobe structures.

Object and face perception
Several temporal lobe areas have been shown to display different patterns of activation in normal versus autistic subjects in response to object and face perception. Normal subjects use the inferior temporal gyrus for object perception and the fusiform gyrus for face perception, but the opposite pattern is seen in autistic subjects (Schultz, Romanski, & Tsatsanis, 2000). In comparison with normals, individuals with autism show greater activation of the superior temporal gyrus on a task requiring inferring emotions from the eyes (mentioned above in regards to the amygdala and frontal lobes as well), at which they do more poorly than normals (Baren-Cohen et al., 2000), suggesting they may be attempting to use the superior temporal gyrus to compensate for damage to the amygdala. This evidence suggests that temporal lobe abnormalities may be due to an attempt to compensate for damage to other parts of the brain.

Social behavior
In a study by Bachevalier (1994), mentioned above in connection with the amygdala, the medial temporal lobe, including the amygdala and hippocampus, was removed from infant monkeys, who later developed autistic symptoms. When only the hippocampus was removed, behavioral disturbances were temporary. When only the amygdala was removed, autistic symptoms were still seen, but they were less severe than when the whole lobe was removed. This would suggest that while temporal lobe structures contribute to the severity of autistic symptoms, they are perhaps not the root cause.

The cerebellum lies in the hindbrain. It functions to keep motor movement smooth, accurate, and timely (Courchesne, Yeung-Courchesne, & Pierce, 1999). A few researchers have proposed that cerebellar dysfunction dysfunction is at the root of autism (e.g. Courchesne et al., 1999). Courchesne (et al., 1999) hypothesizes that the cerebellum also regulates timing and error-free performance not just in motor movement but also in the arousal system, sensory system, memory system, and numerous other systems. He argues that in individuals with autism, a part of the cerebellum called the vermis is damaged, preventing information from correctly leaving the cerebellar cortex . The cerebellum is then unable to regulate attention focus in other systems, which leads to the social impairments, stereotypies, and other symptoms seen in autism (Courchesne et al., 1999). Evidence supporting this theory is a study in which similar performance was found on an attention-shifting task between autistic subjects and patients with cerebellar lesions, as well as the presence of cerebellar abnormalities found in autistic patients (Courchesne et al., 1999). Various studies have found structural cerebellar abnormalities in autistic individuals (Williams, Hauser, Purpura, DeLong, & Swisher, 1980; Courchesne, Yeung-Courchesne, & Pierce, 1999; Hashimoto et al., 1995).

There are some problems with the cerebellar theory. It presents a new theory of cerebellar function based on largely one experiment; further supporting evidence is needed to support this theory. A second problem is that the studies of the cerebellar vermis haven’t matched autistic and control subjects for age and I.Q., both of which may impact results (Schultz, Romanski, & Tsatsanis, 2000).

The Cerebellum and Autism by Stephen M. Edelson

It is extremely difficult to point to one particular area of the brain and say that damage to that one structure causes autism. The evidence indicates multiple deficits in the structure and function of the brain in individuals with autism. However, some of these areas do seem to be more primary, more related to autistic symptoms, than do others, whose abnormalities seem to come about as an attempt to compensate for the damaged areas. In particular, there is strong evidence supporting one of the major theories of autism, known as the limbic system theory, which suggests that damage to the amygdala and the frontal cortex contributes highly to what appears to be the primary symptom of autism, social impairment. There is good evidence for temporal lobe involvement in the face perception and social behavior of individuals with autism, but in both cases this may be the result of damage to other areas of the brain. The differences seen in face perception in autistic subjects may be due to a lack of interest in faces; temporal lobe lesions contribute to impaired social behavior only when the amygdala is damaged as well. The cerebellar theory is an interesting and potentially promising theory, but needs more evidence to confirm the hypothesis that the cerebellum is, indeed, responsible for attention across a wide variety of systems. Research on the neurobiology of autism shows some promising leads, but it is a difficult subject to pin down, and more research in all areas is needed in order to develop a fuller understanding of autism.

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