Having aspirations to become an educational psychologist, I've always held a solid interest in medical conditions such as Autistic Spectrum Disorders (ASD) and how they make a difference someone's behaviours. This interest has been further fuelled by my nephew having been identified as having high functioning ASD. Whilst I am acquainted with the behavioural areas 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 while others with ASD the perfect support.
The complexity of Autistic Spectrum Disorders is partially because of the fact that, until just lately, there were no clear natural functions which corresponded with the symptoms. Scientific developments in brain imaging in recent years, however, have enabled psychologists to commence to analyze ASD from a neurological perspective, and therefore the symptoms of ASD are beginning to be grasped more obviously as a manifestation of the neural disorder (Just et al, 2012).
Qualitative impairment in communal interaction
Qualitative impairment in communication
Restricted, repetitive, and stereotyped patterns of behaviour, hobbies and activities.
The above symptoms tend to be referred to as a triad of impairments. However, in the suggested DSM-V you have the possibility that the communal and communication impairments will be combined and that in the foreseeable future the definition will form a dyad of impairments instead (Pina-Camacho et al, 2011). During writing, however, a triad of impairments still prevails. This essay is concentrating not on the overall differences between your brains of typically expanding (TD) humans and humans with ASD, but on the neurological explanations for the most dominant behavioural symptoms of ASD. Appropriately the triad of impairments will be taken, one at a time, and possible neurological explanations will be explored.
Qualitative impairment in public interaction
Much of the neurological research on ASD focuses on this impairment following the structure of behavioural research on ASD. Indeed, one of the very most prominent ideas of ASD, the idea of Head (Baron-Cohen, 1985), focuses almost entirely on the social deficits, arguing that folks with ASD struggle with mentalising; they lack cultural insight and are unable to perceive the world from another person's viewpoint. From a neurological standing, however, it isn't enough to presume that individuals with ASD do not have a Theory of Head; instead, we must understand biologically why this can be so.
Superior temporal sulcus (STS) - plays an important role in cultural perception and it is implicated in the handling of several types of sensory information which are relevant to sociable connections, e. g. selective sensitivity to vocal and speech looks rather than to non-vocal noises and the handling of the motions of hands, face, sight, and body, especially if the motions relate to emotion in some way (Neuhaus et al, 2010).
Fusiform gyrus (FG) - region is thought to screen a selective reaction to human faces which is also known as the fusiform face area (FFA) (Neuhaus et al, 2010).
Prefrontal cortex (PFC) - a subdivision of the PFC is the ventromedial PFC, an area like the orbital frontal cortex and the ventral area of the anterior cingulate cortex - areas implicated in desire, reward, and feeling processing, and planning the near future. This region also offers extensive cable connections with the amygdala (Neuhaus et al, 2010).
Amygdala - involved in processing emotions, empathy, perspective taking and interpersonal judgements (Neuhaus et al, 2010).
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It seems highly possible that harm to an area in the "friendly brain" is likely to cause some noticeable communal deficit. Thus, ASD may be discussed, to a certain extent, through abnormalities in these regions when compared to TD humans. Various studies support this notion; the amygdala theory of autism, for example, proposes that there surely is an amygdala impairment in people who have autism, which can help describe the deficits in their interpersonal behavior (Baron-Cohen, 2000). Considering that the amygdala is firmly associated with feeling and also other public functions, irregularity in this region could well donate to the lack of social insight so often noted in people who have ASD. Within an earlier research, Baron-Cohen et al (1999) conducted an fMRI research comparing TD subjects with patients with high-functioning ASD or Asperger Syndrome (AS) on the mentalising task whereby individuals were asked to judge from an image of someone else's eyes what feelings that person was sensing. They found that when TD participants were attributing emotional says to the photos, there is increased activation in their STGs and amygdalas - areas associated with interpersonal perception and feeling. The ASD so that as group, however, did not show increased activation in the amygdala. Other research suggested that as well as decreased amygdala activity, people who have ASD tend to process encounters differently to TD people, using the right substandard temporal gyri (ITG) a location more commonly associated with processing objects, as opposed to the FFA (Schultz et al, 2000). Research by Pierce et al (2001) also found that there is either vulnerable or no activity in the FFA and the amygdala in response to the human face in autistic patients but found no evidence to claim that they used the ITG as a substitute. The variations in the results of Pierce and Schultz may be because of the samples, with Schultz using a sample including individuals with autism so when and Pierce using a sample only of members with autism. Caution is urged when positioning too much emphasis on the FG's connection with encounters as past research has advised that region may well not be face specific but may be activated when objects increase in familiarity (Gauthier et al, 1999).
Fletcher et al (1995) used Family pet scans to compare brain activity in normal volunteers when reading Theory of Brain stories, physical reviews and unlinked sentences. When activity through the Theory of Brain stories was compared with others, the authors discovered significant activation in the still left part of the medial frontal gyrus and in the posterior cingulate cortex - locations in the prefrontal cortex - recommending that these locations are specifically triggered when a person is mentalising. Furthermore, Castelli et al (2002) used Family pet scans on ten able parents with ASD or Asperger Symptoms (AS) whilst they watched a number of animated sequences, and were asked to attribute mental claims to the animations centered upon what that they had seen. The TD group revealed increased activation in their medial prefrontal cortex, superior temporal sulcus and temporal poles, areas associated with cultural cognition, as identified above. The autism group, however, revealed less activation than the standard group in all of these regions.
Qualitative impairments in communication
Symptoms in this impairment range between a total insufficient development of spoken dialect, to a person having satisfactory talk but being unable to put it to use in dialog with others, to stereotyped and repetitive use of language (DSM-IV) rendering it difficult to describe the impairment as a whole. There is also less literature generally on wanting to describe the communication deficit in ASD than there may be on seeking to explain the public deficit. This can be because aspects of the communication deficit are not applicable to people with AS or high-functioning ASD whereas the communal deficit is central to all or any ASDs.
Within the remaining hemisphere of the brain are two areas that govern the understanding and creation of conversation: Broca's area and Wernicke's area. Broca's area is in the frontal lobe which is primarily mixed up in production of talk; Wernicke's area is in the temporal lobe and is mainly involved with talk comprehension (Passer et al, 2009). Also in the kept hemisphere of the mind is the principal auditory cortex an area associated with hearing and so also largely involved with language creation and understanding (Passer et al, 2009).
One possible reason for too little vocabulary development is therefore more likely to involve harm or irregularities in the still left hemisphere of the mind plus more specifically in these areas. Boddaert et al (2004) used PET scans to compare the mind activity of eleven autistic children with six non-autistic mentally retarded children while they were listening to speech-like sounds. They found that there is less activation in speech-related areas, including Wernicke's area, in autistic children. In prior work with autistic adults (Boddaert et al, 2004) that they had found excessive right frontotemporal activity but this is not found with the kids. Research by Eyler et al (2012) measured the mind activity of forty small children with ASD and 40 TD toddlers during the demonstration of your bedtime history. Their results showed that a region of the remaining STG, a location which include both Broca's and Wernicke's area, was significantly less attentive to speech stimuli in the group with ASD than in the TD group. The TD small children exhibited dominance in the kept hemisphere of the brain, as one might expect, given the association between the kept hemisphere and terminology. Contrary to the Boddaert et al study, Eyler et al performed find that small children with ASD however shown stronger activation on the right anterior portion of the STG as opposed to the left. The distinctions in the results of the groups may be that the sample in the Boddaert et al review was significantly smaller than the test employed by Eyler et al, with only 11 autistic individuals compared to 40. Eyler et al propose that the right STG may be seeking to pay for the incompetent processing of the left STG but that by doing so the introduction of cultural communication and language abilities has been lost, thus providing a conclusion for not only language delay but also ineffective communication in people who have ASD.
Restricted, repetitive, and stereotyped patterns of behavior, interest and activities
There are incredibly few neurological studies focusing on this aspect of ASD. An fMRI study by Shafritz et al (2008) on repetitive behavior in ASD showed that the severity of restricted, repetitive behaviours was adversely correlated with activation in anterior cingulate cortex (ACC) and posterior parietal regions - areas associated with attention, determination and error detection (Neuhaus et al. 2010). Research by Thakkar et al (2008) helps this finding. Via an experiment on response monitoring they found efficient and structural abnormalities in the ACC in ASD individuals and suggested that this could cause rigid and repetitive, rather than responsive and flexible behaviour. As the cerebellum is concerned generally with muscular motion co-ordination but also plays a role in learning and memory space (Passer et al, 2009), Pierce and Courchesne (2001) evaluated the probability of a connection between cerebellar abnormality and exploration in autism. They placed an test where 14 autistic children and 14 TD children were in a sizable room with several exploration containers and inspired to play. The results revealed that children with autism spent significantly less time in dynamic exploration and were much more likely to activate in repetitive activities than TD children. They found that the more unnatural the cerebellar vermis, a location in the medial cerebellum (Passer et al, 2009) the less time put in in exploring a new environment.
Much more literature exists evaluating the neurological explanations of cultural impairments in ASD than in the other two impairments.
A vast amount of research prevails associating the interpersonal deficits in ASD with irregularities in a variety of parts of the social brain; the superior temporal sulcus, the fusiform gyrus, the prefrontal cortex and the amygdala.
A lack of activity in the still left hemisphere of the mind will probably contribute to the communication impairment noticeable in AS.
There is very little literature on the restricted behavior 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 - ultimately work could be conducted that may help to describe all three impairments somewhat than focusing on just a single one.
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