Investigating the role of the frontal cortex in autism

Little is known about the underlying neural developmental defects which result in the emergence of autistic behavior during the early years of life. The frontal lobe has been identified as the most likely region to be involved, and yet little is known about it. The frontal lobe plays a key role in higher order language, cognitive, emotional, and social faculties, each one affected by autism. This has provided support for the frontal lobe hypothesis of autism. Through the collection of data from MRI and postmortem anatomical, and also already existing neurofunctional, postmortem, and MRI results from more mature autistic patients, the authors find two suggestions:

1. In patients with autism, the frontal cortex is poor at interacting with other cortical regions

2. During early development, the frontal cortex appears to be irregularly over-connected with itself

Examining macroscopic evidence of early frontal maldevelopment

Brain growth of patients with autism is normal at birth, ranging from average to slightly smaller than average. However this is followed by a period of excessive growth which results in an enlarged brain volume at the toddler age. Investigations into which brain regions cause this growth indicate the frontal lobes to be at the site of peak growth. Grey and white matter in the frontal lobes are both disparately deviant in regards to other cortical regions. While several studies have shown that primary sensory cortices in autism function normally, the same cannot be said for the frontal lobes. The deficient functionality found in the frontal lobe is hypothesized as being a factor which disrupts the frontal lobes interaction with other areas of the brain. It is unknown whether autism is to be classified as disorder of overconnectivity, underconnectivity, or a combination of the two.

Examining microscopic evidence of frontal maldevelopment

There remains a lack of knowledge on the microstructural abnormalities that disrupt frontal neural circuit development, facilitate the macroscopic overgrowth of frontal white and grey matter, and facilitate abnormal frontal mediated behavior. Where the link exists between abnormal neuroinflammatory response and initial brain overgrowth in autism is a mystery. It has been suggested that activated glia could be a reflection of a fetal state or development. When it comes to cerebral cortical information processing, a cortical minicolumn is an essential component. Studies have shown that minicolumns and their surrounding neuropil space are unusually small in children with autism throughout the frontal cortex, but not the occipital cortex. One older study found an increased neuron density and reduced neuron size within the frontal cingulate cortex in a number of autistic cases. It is suggested that these glial and neuronal abnormalities are in some way connected.

Drawing a conclusion

This is the first time that studies have shown early developmental abnormalities at the microscopic level and the macroscopic level and the presence of the frontal lobes as the peak of cerebral pathology. The work of abnormal processes (neuroinflammation, migration defects, excess cerebral neurogenesis) cause deformity, which leads to the malfunction of frontal minicolumn micro-circuitry. This in turn leads to reduced connectivity effectiveness between brain regions.

The role of response inhibition and immediate arousal in children with high functioning autism

It has long been the goal of many researchers to investigate the number of impairments that underlie the symptoms which characterize Autism Spectrum Disorder (ASD). Through the use of the executive functioning criteria, studies on ASD have highlighted planning, cognitive flexibility, and working memory to be areas which are weak in individuals with the disorder. The area of response inhibition is what the authors chose to focus on. More specifically, the study aimed to use an immediate arousal task to examine inhibition of responses in children with high functioning autism (HFA), and to look for an association with impulsivity, hyperactivity, or inattention.

Procedure

Participants for the study consisted of 39 children with HFA and a control group of 29 average functioning children. Once written permission was obtained from the parents, questionnaires were sent to the children to ascertain their suitability and possible comorbid disorders. The task consisted of a computer based reaction test. Participants were instructed in condition A to press a response button as quickly as they could upon the appearance of a white cross onscreen. In condition B they were instructed to wait for an acoustic signal before reacting as fast as they could to a white cross onscreen. The speed of the presentation rate was varied. An A-B-B-A style of sequencing of conditions was used.

Results and discussion

The aim of the study was to examine whether or not there existed a response inhibition deficit in children with HFA. The presentation of an auditory signal and a visual stimulus produced an arousal effect which resulted in an increase in error rate and a decrease in reaction time. It was hypothesized that this effect would be strongest in children with HFA. Inhibition errors did increase with the addition of the auditory signal, however this was not unique to the HFA group. The results of this study suggest that children with HFA don’t have a deficit in the inhibition system. This result is in dispute of some studies.

The role of cognitive flexibility in adults with functioning autism

Researchers are agreed that both social inadequacy and a deficit in executive functioning are both large factors which encompass autism. The main aim of this study focuses on investigating cognitive flexibility, more specifically response inhibition, set shifting, and motor presetting in regards to autism. Additionally a priori analysis was conducted by investigating the effects of the stimulus probability on performance. The authors mention the failure of previous studies in this area. Earlier studies failed to mention the patient’s medication status and thus failed to control for it. Additionally, these earlier studies often used experiment groups with varying age ranges. The authors generate four questions:

1. Is HPA associated with problems presetting the motor system in favor of the most common response type

2. Is HPA associated with weak set shifting

3. Is HPA associated with weak response inhibition

4. Is HPA associated with sensitivity for the given stimulus probability

Procedure

The sample consisted of 23 adults with HFA, and a control group of 32 typically functional individuals. The task consisted of a computer based variant of the Sternberg reaction time paradigm. The task presented participants with a set of letters to be memorized and then another set was displayed. If the participant recognized an item from the memory set in the display set, they gave a ‘yes’ response, otherwise they gave a ‘no’ response. The baseline condition consisted of 50% of the trials requiring a ‘no’ response; the response bias condition consisted of 75% of trials requiring a ‘no’ response. Each condition consisted of 64 trials.

Results and discussion

The aim of this study was to examine elements of cognitive flexibility, mainly set shifting, response inhibition, presetting, and a priori planning in individuals with HFA. Results show that participants with HFA experienced no deficit in response inhibition and the ability to change the response set. Despite this, there was a slow speed of performance found in participants with HFA, in particular those on medication. This slowness in speed may have been a contributing factor to cognitive flexibility deficit found in earlier studies which did not control for it. The study identifies a possible ceiling effect caused by an overall slowness of responses.