Having aspirations to become an educational psychologist, I have always held a strong interest in clinical conditions such as Autistic Spectrum Disorders (ASD) and how they can affect a person’s behaviours. This interest has been further fuelled by my nephew having been recently diagnosed with high functioning ASD. Whilst I am familiar with the behavioural aspects of this disorder I lack knowledge on the neurological explanations. I wish to change this to increase my understanding of ASD in order to be better equipped to offer my nephew and others with ASD the best possible support.
The complexity of Autistic Spectrum Disorders is partially due to the fact that, until recently, there were no clear biological functions which corresponded with the syndrome. Scientific developments in brain imaging in recent years, however, have enabled psychologists to begin to research ASD from a neurological perspective, meaning that the symptoms of ASD are beginning to be understood more clearly as an expression of a neural disorder (Just et al, 2012).
According to the DSM-IV a person can be diagnosed with ASD when they exhibit symptoms under the following three primary criteria:
Qualitative impairment in social interaction
Qualitative impairment in communication
Restricted, repetitive, and stereotyped patterns of behaviour, interests and activities.
The above symptoms are often referred to as a triad of impairments. However, in the proposed DSM-V there is the possibility that the social and communication impairments will be combined and that in the future the definition will form a dyad of impairments instead (Pina-Camacho et al, 2011) . At the time of writing, however, a triad of impairments still exists. This essay is focusing not on the general differences between the brains of typically developing (TD) humans and humans with ASD, but on the neurological explanations for the most prominent behavioural symptoms of ASD. Accordingly the triad of impairments will be taken, one by one, and possible neurological explanations will be explored.
Qualitative impairment in social interaction
Much of the neurological research on ASD focuses on this impairment following the pattern of behavioural research on ASD. Indeed, one of the most prominent theories of ASD, the Theory of Mind (Baron-Cohen, 1985), focuses almost entirely on the social deficits, arguing that people with ASD struggle with mentalising; they lack social insight and are unable to perceive the world from another person’s viewpoint. From a neurological standing, however, it is not enough to assume that people with ASD do not have a Theory of Mind; instead, we must understand biologically why this may be so.
Brothers (1990) conducted a variety of studies, both with humans and other primates, and proposed that primates alone have social cognition – they are able to perceive psychological facts about others. Through the examination of evolutionary studies, as well as the study of clinical conditions which can affect social cognition, Brothers proposed a neural network of regions in the brain, which, combined create “the social brain”:
Superior temporal sulcus (STS) – plays an important role in social perception and is implicated in the processing of many types of sensory information which are relevant to social interaction, e.g. selective sensitivity to vocal and speech sounds rather than to non-vocal sounds and the processing of the motions of hands, face, eyes, and body, especially if the motions relate to emotion in some way (Neuhaus et al, 2010).
Fusiform gyrus (FG) – region is thought to display a selective response to human faces and is often referred to as the fusiform face area (FFA) (Neuhaus et al, 2010).
Prefrontal cortex (PFC) – a subdivision of the PFC is the ventromedial PFC, a region including the orbital frontal cortex and the ventral part of the anterior cingulate cortex – areas implicated in motivation, reward, and emotion processing, and planning for the future. This region also has extensive connections with the amygdala (Neuhaus et al, 2010).
Amygdala – involved in processing emotions, empathy, perspective taking and social judgements (Neuhaus et al, 2010).
A diagram of the regions of the brain thought to comprise the “social brain”. Data retrieved from:
It seems highly probable that damage to a region in the “social brain” is likely to cause some visible social deficit. Thus, ASD may be explained, to a certain extent, through abnormalities in these regions when compared to TD humans. Various studies support this idea; the amygdala theory of autism, for example, proposes that there is an amygdala impairment in people with autism, which can help to explain the deficits in their social behaviour (Baron-Cohen, 2000). Given that the amygdala is strongly associated with emotion along with other social functions, irregularity in this region could well contribute to the lack of social insight so often noted in people with ASD. In an earlier study, Baron-Cohen et al (1999) conducted an fMRI study comparing TD subjects with patients with high-functioning ASD or Asperger Syndrome (AS) on a mentalising task whereby participants were asked to judge from a photograph of another person’s eyes what emotion that person was feeling. They found that when TD participants were attributing emotional states to the photographs, there was increased activation in their STGs and amygdalas – areas associated with social perception and emotion. The ASD and AS group, however, did not show increased activation in the amygdala. Other research suggested that as well as decreased amygdala activity, people with ASD tend to process faces differently to TD people, using the right inferior temporal gyri (ITG) an area more commonly associated with processing objects, rather than the FFA (Schultz et al, 2000). Research by Pierce et al (2001) also found that there was either weak or no activity in the FFA and the amygdala in response to the human face in autistic patients but found no evidence to suggest that they used the ITG as an alternative. The differences in the results of Pierce and Schultz may be due to their samples, with Schultz using a sample including participants with autism and AS and Pierce using a sample only of participants with autism. Caution is urged when placing too much emphasis on the FG’s association with faces as previous research has suggested that this region may not be face specific but may be activated when objects increase in familiarity (Gauthier et al, 1999).
Fletcher et al (1995) used PET scans to compare brain activity in normal volunteers when reading Theory of Mind stories, physical stories and unlinked sentences. When activity during the Theory of Mind stories was compared with the others, the authors discovered significant activation in the left side of the medial frontal gyrus and in the posterior cingulate cortex – regions in the prefrontal cortex – suggesting that these regions are specifically activated when a person is mentalising. Furthermore, Castelli et al (2002) used PET scans on ten able adults with ASD or Asperger Syndrome (AS) whilst they watched a variety of animated sequences, and were asked to attribute mental states to the animations based upon what they had seen. The TD group showed increased activation in their medial prefrontal cortex, superior temporal sulcus and temporal poles, areas associated with social cognition, as described above. The autism group, however, showed less activation than the normal group in all of these regions.
Qualitative impairments in communication
Symptoms in this impairment range from a total lack of development of spoken language, to a person having adequate speech but being unable to use it in conversation with others, to stereotyped and repetitive use of language (DSM-IV) making it difficult to explain the impairment as a whole. There is also less literature in general on trying to explain the communication deficit in ASD than there is on trying to explain the social deficit. This may be because aspects of the communication deficit are not applicable to people with AS or high-functioning ASD whereas the social deficit is central to all ASDs.
Within the left hemisphere of the brain are two areas that govern the understanding and production of speech: Broca’s area and Wernicke’s area. Broca’s area is in the frontal lobe and is primarily involved in the production of speech; Wernicke’s area is in the temporal lobe and is mainly involved with speech comprehension (Passer et al, 2009). Also in the left hemisphere of the brain is the primary auditory cortex an area associated with hearing and thus also largely involved in language production and comprehension (Passer et al, 2009).
One possible explanation for a lack of language development is therefore likely to involve damage or irregularities in the left hemisphere of the brain and more specifically in the above areas. Boddaert et al (2004) used PET scans to compare the brain activity of eleven autistic children with six non-autistic mentally retarded children while they were listening to speech-like sounds. They found that there was less activation in speech-related areas, including Wernicke’s area, in autistic children. In previous work with autistic adults (Boddaert et al, 2004) they had found abnormal right frontotemporal activity but this was not found with the children. Research by Eyler et al (2012) measured the brain activity of forty toddlers with ASD and 40 TD toddlers during the presentation of a bedtime story. Their results showed that a region of the left STG, an area which includes both Broca’s and Wernicke’s area, was significantly less responsive to speech stimuli in the group with ASD than in the TD group. The TD toddlers showed dominance in the left hemisphere of the brain, as one might expect, given the association between the left hemisphere and language. Contrary to the Boddaert et al study, Eyler et al did find that toddlers with ASD however displayed stronger activation on the right anterior portion of the STG rather than the left. The differences in the results of the groups may be that the sample in the Boddaert et al study was significantly smaller than the sample used by Eyler et al, with only 11 autistic participants compared to 40. Eyler et al propose that the right STG may be trying to compensate for the incompetent processing of the left STG but that by doing so the development of social communication and language abilities is being lost, thus providing an explanation for not only language delay but also ineffective communication in people with ASD.
Restricted, repetitive, and stereotyped patterns of behaviour, interest and activities
There are very few neurological studies focusing on this aspect of ASD. An fMRI study by Shafritz et al (2008) on repetitive behaviour in ASD showed that the severity of restricted, repetitive behaviours was negatively correlated with activation in anterior cingulate cortex (ACC) and posterior parietal regions – areas associated with attention, motivation and error detection (Neuhaus et al. 2010). Research by Thakkar et al (2008) supports this finding. Through an experiment on response monitoring they found functional and structural abnormalities in the ACC in ASD participants and suggested that this may cause rigid and repetitive, rather than responsive and flexible behaviour. As the cerebellum is concerned primarily with muscular movement co-ordination but also plays a role in learning and memory (Passer et al, 2009), Pierce and Courchesne (2001) examined the possibility of a link between cerebellar abnormality and exploration in autism. They held an experiment where 14 autistic children and 14 TD children were in a large room with several exploration containers and encouraged to play. The results showed that children with autism spent significantly less time in active exploration and were more likely to engage in repetitive movements than TD children. They found that the more abnormal the cerebellar vermis, an area in the medial cerebellum (Passer et al, 2009) the less time spent in exploring a new environment.
Much more literature exists examining the neurological explanations of social impairments in ASD than in the other two impairments.
A vast amount of evidence exists associating the social deficits in ASD with irregularities in various regions of the social brain; the superior temporal sulcus, the fusiform gyrus, the prefrontal cortex and the amygdala.
A lack of activity in the left hemisphere of the brain is likely to contribute to the communication impairment visible in AS.
There is very little literature on the restricted behaviour impairment but recent work has proposed a possible association between cerebellar abnormality and exploration and between the ACC and repetitive behaviour.
Further work is needed in all three areas – ideally work could be conducted that could help to explain all three impairments rather than focusing on a single one.