According to the American Psychiatric Association (APA), Neurodevelopmental Disorders fit into six categories, they are: intellectual disability, communication disorders, autism spectrum disorder (ASD), attention deficit hyperactivity disorder (ADHD), specific learning disorder, and motor disorders. This new categorisation has been added as a new chapter to the Diagnostic and Statistical Manual of Mental Disorders, 5th Edition (DSM-5). For consistency and in order to follow the new American Psychiatric Association (2013) guidelines, autism will be referred to as ASD.
Number of changes has been introduced regarding diagnosis of attention deficit hyperactivity disorder (ADHD); sometimes referred to as ADD. Previously used 18 primary symptoms for ADHD continue to be divided into two major symptom domains: inattention and hyperactivity/impulsivity and at least six symptoms (in one domain) are required for the diagnosis (American Psychiatric Association, 2013). The changes to the diagnostic criteria were partly introduced in order to improve recognition of adult ADHD.
Different attentional networks were described by Posner and Petersen (1990) in their review of attention systems of the human brain. The review found three districts networks, which included: 1) alerting network – related to automatic processes, like sustained vigilance and focused on brain stem arousal systems along with right hemisphere systems; 2) orienting network – focused on parietal cortex; and 3) executive network – included midline frontal/anterior cingulate cortex. In 2011 review, Petersen and Posner updated their original framework with an addition of extra orienting networks and extra executive network They see a possibility in the future that additional control networks may be found, but we do not expect the number of control networks to be much larger than the number shown in their study. Nevertheless, attention clearly involves remarkably heterogeneous functions that are altered by a great number of psychological factors for example sensory and motivation processes.
ADHD is one of the most debilitating childhood disorders, defined by age inappropriate impulsiveness, inattention, and hyperactivity with many of the symptoms persisting into adulthood. Symptoms and developmental course indicate that ADHD diagnosis consists of two separate disorders probably with separate etiology (Sagvolden et al., 2005). Results from a twin study with learning difficulties by Willcutt et al. (2000) indicated that extreme ADHD scores were almost entirely attributable to genetic influences and extreme inattention scores were also highly heritable. Finding suggests that extreme hyperactivity and inattention may be attributable to different etiological influences in individuals with and without extreme inattention.
Children with the ADHD inattentive subtype are non-hyperactive, often daydreaming and appear indifferent and their attention issues are non-specific and likely related to deficient sensory processes, poor attention focus, and inaccurate information processing. Ordinarily such attention problems are associated with a family history of learning problems and extreme inattention scores were found to be highly heritable (Willcutt et al., 2000). Children with ADHD predominantly hyperactive/impulsive subtype do not have general attention problems and their attention issues are more specifically related to inability to sustain attention and decreased perseverance and are still present after controlling for general intelligence (Taylor et al., 1991).
It is well know that developmental disorders are typically comorbid. High comorbidity suggests that disorders have overlapping causes, or that the direct causes of one disorder affect the systems that cause some other disorder. Though, not enough research has been done yet to successfully explain the underlying causes of these comorbidities.
The multifaceted attention problems of children with ADHD may be related to dopamine dysfunction of at least two different neurobiological systems; some believe that both prefrontal loop and the limbic loop are involved. According to Posner and Petersen (1990) the prefrontal loop is mainly involved in directing attention and selecting the behaviour needed to achieve a given goal in a given situation. It is suggested that a dysfunctioning mesocortical dopamine branch will lead to attention deficiencies, for example inefficient orienting responses and abnormal control of eye saccades (Mostofsky et al., 2001). The limbic loop is verbally governed (by the rules) and involved in reinforcement and extinction processes. Problems in establishing verbally governed behaviour will result in difficulties with making and following plans.
Egner et al. (2008) demonstrate in their study that the neuroanatomical networks engaged to overcome distraction differ conclusively with the nature of the distracting stimulus information (Egner et al., 2007), thought they may have a process in common to detect distraction. It also highlights specialised cortico-limbic process for protecting goal-directed cognition from interference by emotional processing.
Oculomotor findings highlight that deficits in prefrontal functions, in particular response inhibition, contribute to behavioural abnormalities observed in ADHD. From a developmental perspective, such problems will cause difficulties in directing actions toward longer-term accomplishments and behaviour control. Olfactory processing depends on dopamine metabolism and orbitofrontal cortex functioning, both known to be affected in (ADHD). Findings from study by Schecklmann et al. (2011) suggest an association of cortical olfactory processing with hyperactivity and impulsivity in adult ADHD.
The ability to sustain attention to a routine task is an important aspect of executive control. A progressive decline in attention to a task and a fast phasic fluctuation in top-down attentional control are two of the many different processes involved in the behavioural demonstrations of deficient sustained attention (Johnson et al., 2007).
Failures to focus on will affect all parts of daily life (e.g. at school, in the work environment, driving etc.). At the clinical end, distractibility is the main diagnostic criterion of ADHD, but attention is also affected in other developmental disorders. Here we examine how attention is affected in ADHD and compare this to other developmental disorders.
Main Body
Friedman-Hill et al. (2009) found in their study that healthy children and adults can filter out high and low salience distractors equally well, whilst ADHD children were just as good filtering high salience distractors they were slower to respond on trials with low salience. ADHD children exhibited efficient attentional filtering when task demands were high, but showed deficient filtering under low task demands indicating that attention deficits in ADHD are unlikely to be an issue with implementing filtering, but rather failure to efficiently engage top-down control. These results imply that distractors which were so difficult to distinguish caused more behavioural interference for ADHD children than distractors which were very obvious.
We can examine this phenomena in the context of the biased competition model of attention. This model suggests limited neural and cognitive resources cause for some sensory inputs and responses to be processed at the expense of others. This leads to bottom-up perceptual interference from competing stimuli (Reynolds et al., 1999); distractors reduce efficiency neural and behavioural responses. It is however possible to override the stimulus-driven sensory by top-down, intentional feedback from a network of prefrontal and parietal regions (Kastner & Ungerleider, 2001).
Forster et al. (2014) found in a study of adults with ADHD that greater levels of distraction in ADHD can be reduced with an introduction of higher perceptual load in the task. Load Theory suggests high perceptual load can cut down distractor interference easily by filtering distractor stimuli from perception. These finding suggest that distraction in ADHD result from later attention mechanisms, such as the efficiency of executive cortical control, rather than the earlier selective attention mechanism. Competent cortical executive control is essential when early attentional selection fails. The load effects were also found to potentially account for the “hyperfocus” (HF) that has been observed in patients with ADHD (Schecklmann et al., 2008, Hupfeld et al., 2018). Patients with ADHD often experience periods of intensive concentration on certain tasks they find engaging or interesting (e.g. internet searching, playing video games) this is usually associated with perception of zoning out of the surrounding environment.
One way to address the neurodevelopment of covert attention is to study disorders of this process in groups of atypically developing children. ADHD is one of them and another condition that has been linked to deficits in attention and so is ASD. This is why we are going to focus on ASD in here to compare to ADHD to see how the attention differs between the disorders.
Two components of attention that have been commonly studied in both ASD and ADHD are: 1) orienting – prioritising sensory information and 2) sustained attention – linked to frontal areas for example anterior cingulate and dorsolateral prefrontal cortex (Petersen & Posner, 2012). Abnormalities in visual orienting have been well defined in ASD, with numerous studies showing that children with ASD show quite specific problems in disengaging and shifting attention under conflict conditions (Keehn et al., 2010). In contrast, children with ADHD generally achieve slowed reaction times when the stimulus is presented in the peripheral vision, but this is not the case when more complex conditions are introduced.
In their study of ADHD children and children with high functioning autism (HFA) Johnson et al. (2007) explored the differences in these groups on facets of sustained attention, response inhibition and response time variability (fast and slow). Using these measures, they found differences in sustained attention between the the two disorders. On the other hand, there is a possibility that response inhibition may be a shared feature of the two disorders. Regarding the pathology of ADHD children, there was an involvement of fronto-parietal attentional networks and sub-cortical arousal systems. Whereas, in HFA children they found prefrontal cortex dysfunction (Johnson et al., 2007).
In the study of f infant siblings of children with an autism spectrum disorder (Sibs-ASD) by (Holmboe et al., 2010) looked into process of inhibitory control (attention and inhibition are connected to the frontal cortex). The infants were reinforced to suppress attending to peripherally presented distractors, whilst concentrating their visual attention at a central animation (Freeze-Frame task). In order to vary the conditions the appeal of the central stimulus is changed within the task. Sibs-ASD infants had difficulty disengaging attention from a central stimulus.
Patients with ADHD present well researched deficiencies and consistently show deficits in attention, in particular selective, sustained, and flexible attention, with some intra-individual variation that accompanies the slow reaction times, which is generally believed to allow for the episodic attention lapses (Hart et al., 2013).
There is limited research on sustained attention in ASD, but Christakou et al., (2013) performed a direct comparison of sustained attention and ASD and ADHD in boys. The findings from the study show that during sustained attention both developmental disorders shared disorder-specific anomalies in brain function. Shared deficits were in showing in fronto–striato–parietal activation and default mode suppression. However, differences were found in disorder-specific fronto–striato–cerebellar dysregulation in ASD and more severe dysfunction in left dorsolateral prefrontal cortex (DLPFC) in ADHD.
similar impairment but with greater decrease in vigilance in ADHD over time (Swaab-Barneveld et al., 2000); similar deficits but more impulsive behaviour and autism (Riccio & Reynolds, 2001)
Conclusion
Inability to maintain attention focus varies in the overall population, but it is a the main deficit in ADHD. ADHD patients show consistent functional anomalies in two distinct domain-dissociated right hemispheric fronto-basal ganglia networks. The affected networks include the inferior frontal cortex, supplementary motor area, and anterior cingulate cortex for inhibition and dorsolateral prefrontal cortex, parietal, and cerebellar areas for attention (Hart et. al., 2013).
As Forster and colleagues (2014) argue, the phenomenon of hyperfocus in ADHD could be related to tasks with a high level of load, under which the distraction is weakened. Hupfeld et al. (2018) found hyperfocus tendencies are higher in those with more severe ADHD symptoms across multiple settings, dimensions, and real-world scenarios. People with high hyperfocus may indeed be less likely diagnosed with an attention deficit, due to their actual difficulty might being attention maldistribution, rather than attention deficit.
Thus, current literature indicates that sticky fixation (disengagement) is particularly problematic for children in autism, while general slowing of orienting, sustained attention and engagement are hallmarks of ADHD. Atypical attention in connection with atypical frontal cortex functioning is used as one of the markers of the broader ASD phenotype (Holmboe et al., 2010), whereas patients with ADHD have problems with sustained attention and engagement.
In conclusion to the first comparative fMRI study between patients with ADHD and ASD, Christakou et al., (2013) shown that the ordinarily compromised function of sustained attention is associated with both shared and disorder-specific dysfunctions. The findings suggest a more substantial frontal lobe activation impairment in ADHD typically associated with more severe performance deficits, but also emphasise joint striato–parietal and default mode network dysfunctions that could possibly shed a light on the underlying phenotypical overlap of poor attentive behaviours in both conditions.
It is well known that developmental disorders are typically comorbid. High comorbidity suggests that disorders have overlapping causes, or that the direct causes of one disorder affect the systems that cause some other disorder. Attention Deficit Hyperactivity Disorder (ADHD) and Autism Spectrum Disorder (ASD) are share behavioural-cognitive anomalies in sustained attention and are frequently comorbid. The question remains whether this shared cognitive phenotype is based on same or different fundamental pathophysiologies (Christakou et al., 2013). Rommelse et al. (2010) concluded in their study of family and twin studies, evidence of shared genetic foundation of ADHD and ASD, which suggests that both likely stem from similar familial/genetic factors. However, not enough research has been done to successfully explain the underlying causes of these comorbidities.
Finally, the research on attention was discussed in relation to ADHD and ASD as patients experience overlapping issues as well as having unique distinguishable issues related specifically to their disorder pathology. One of the questions remaining is whether the abnormal patterns of attention are symptoms of the disorder itself or whether original problems with attention actually cause any of the symptomatic issues of the condition. If this was indeed the case, future research could focus on answering whether anything could be done with earlier diagnosis of the conditions and any possibility of early intervention that could prevent the attentional issues developing into actual symptoms of the condition (e.g. problems with social cognition).
One way to address future research of attentional deficits/anomalies would be to study babies at risk of developing ASD or ADHD as both conditions are likely to run in families (Rommelse et al., 2010) children that have a member of family with one of these developmental disorders are already at risk of receiving diagnosis. Comparing the developmental path of the children that go on to develop the disorder to the neurotypical children could highlight early differences and inform what to focus on in future research.
2019-4-29-1556501869