Critically discuss the association between ADHD and dyslexia


Critically discuss the association between ADHD and dyslexia

Fidgety Phil, he won't sit still; he wriggles, he giggles... The naughty restless child, growing more rude and wild.” Heinrich Hoffman (1846).

Comorbidity is, according to medical dictionaries, the simultaneous occurrence of two or more unrelated conditions or disorders. Whether comorbid disorders are always unrelated is questionable. Data from genetic research indicates that some cases of comorbidity may have a shared aetiology (Giler et al, 1992). What is indisputable however is that in cases of comorbidity a child's development may be hampered by two or more disorders, such as the coexistence of dyslexia and ADHD.

Attention deficit hyperactivity disorder (ADHD) is a major disorder in children (Giler et al, 1992). As early as 1846, the typical symptoms of ADHD were described by Heinrich Hoffmann, a physician who later founded the first psychiatric hospital in Frankfurt. His description of ADHD was depicted in the colourfully illustrated story of “Fidgety Philip” which was probably the first written mention of ADHD by a medical professional. This clearly shows that the diagnosis of ADHD is not an “invention” of modern times. The core symptoms of this disorder as defined by the DSM-IV (American Psychiatric Association, 1994) are inattention, impulsivity and hyperactivity. The level of attention of these children is inappropriate and they have difficulty concentrating, appear not to listen and are easily distracted. Their impulsivity is manifested by difficulty in self – restraint and the hyperactivity by fidgetiness or difficulty sitting in one place for any extended period of time. The prevalence of comorbid learning disabilities is high and overall ranges between 25% – 50%; most notable are dyslexia, dyscalculia and disorders of spelling and written expression (Barkley, 1997; Mayes et al., 2000).

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Dyslexia is among the most prevalent of the learning disabilities with estimates ranging from 5 - 12% (Shaywitz, 1998). It is characterised by difficulties in reading, writing and spelling, despite the ability to see and recognise the letters. The multi – symptomatic and heterogeneous nature of dyslexia has led to a number of competing theories attempting to explain the disorder is terms of its cognitive and neurobiological underpinnings.

The prevailing view of dyslexia involves the idea that learning an alphabetic writing system requires the brain to map letters to mental representations of the corresponding basic speech sounds (phonemes). The ‘phonological-deficit hypothesis' holds that people with dyslexia have specific problems in representing or recalling those sounds; hence the problems with mapping them onto letters. The theory is supported by observations that people with dyslexia have difficulty retaining speech in short-term memory and consciously segments it into phonemes. (Snowling, 2000).

The view that the cognitive basis of dyslexia is purely phonological has been challenged by the discovery that people with this disorder also have an array of subtle sensory defects. For example, they fare less well than control subjects in several auditory tasks that require the perception of brief or rapid speech and non-speech sounds (Tallal et al, 1993). They also seem to have difficulties with several visual tasks, such as those that involve the perception of motion (Stein and Walsh, 1997). Moreover, there is evidence that the brains of some dyslexics have subtle neurological abnormalities in certain areas of the visual and auditory systems, the so called magnocellular pathways (Galaburda and Livingstone, 1993). Researchers who support the magnocellular theory do not dispute the phonological-deficit hypothesis. Rather they contend that phonological problems are caused by a basic deficiency in hearing sounds and that a visual deficit might independently contribute to reading problems.

Jaskowski and Rusiak (2005) have argued that it is a deficit of attention, caused by dysfunction in the posterior parietal area of the brain that may be the cause of early sensory problems in dyslexia. Various studies have reported attention deficits in dyslexia, in both visual (Vidyasagar, 2004) and auditory (Petkov et al, 2005) modalities with or without accompanying ADHD. Facoetti et al (2005) reported focused attention problems in dyslexic children when visual and auditory stimuli were used in the same sample of participants. They suggested the poor ability to focus attention on one spatial location is the cause of the impaired reading skills displayed in dyslexic students.

The Continuous Performance Test (CPT) is a well – recognised and reliable measure of sustained attention that consistently discriminates ADHD from control groups by conventional performance indices such as reaction time, number of correct hits, misses and false alarms (Halperin et al, 1991). Interestingly, children with comorbid ADHD and dyslexia were reported to perform poorly on the CPT (Eliason and Richman, 1987). Up until the present decade, it remained unclear whether children with dyslexia show attentional deficits in the CPT in absence of ADHD. This question was addressed by Taroyan et al (2006) who used the CPT to test attentional performance on participants with only dyslexia. They wanted to see whether participants with ‘pure' dyslexia would also show abnormal CPT performance. Using a sample of 48 adolescents, their results showed no significant difference in mean reaction time, error rate or sustained attention between the ADHD and dyslexia groups. Their conclusion was dyslexic participants showed no behavioural signs of attentional difficulties; suggesting that abnormal attentional performance is not a ‘core' feature of dyslexia.

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There has been much speculation as to the causes of ADHD and it appears that no single cause applies to everyone with the disorder. Viruses, harmful chemicals in the environment, genetics, problems during pregnancy or anything that impairs brain development can play a role in causing the attention problem in ADHD (Barkley, 1998). However, there is strong evidence that suggests certain neurotransmitters play a large role in ADHD type behaviour (Keulers et al 2007). One prominent hypothesis is that ADHD symptoms arise from a deficit in inhibitory control implemented in the frontal - striatal brain networks (Barkley, 1998). Stimulant medication, such as Methylphenidate (MPH) is currently one of the primary treatment approaches for children with ADHD, the effectiveness of which has been shown empirically (Jensen et al, 2001). Research however, has not directly addressed the medications effect on the neural circuitry of attention. This is particularly important as inattention is a core feature of the disorder (Hales et al, 1999). Research carried out by Shafritz and colleagues (2004) addressed several neglected questions in ADHD research, primarily, unresolved questions regarding the neurobiological foundations of ADHD such as whether the effects of MPH are specific to ADHD or whether the effects can be seen in related developmental disorders such as dyslexia. Using functional magnetic resonance imaging to investigate the neural activity of selective and divided attention they had groups of adolescents with ADHD, a reading disorder (RD), ADHD combined with RD and a healthy control group. The tasks recruited a host of cortical areas, including the dorsolateral prefrontal cortex, the premotor cortex and regions of the basal ganglia; the area's most associated with motor control and learning. MPH led to an increase in activation in the basal ganglia for all experimental groups but had no effect on their performance. Subjects with ADHD also recruited the middle temporal gyrus significantly less than the comparison subjects; however MPH did not have a direct effect on activation in this region. The study also found MPH increased striatal activation for both the ADHD and RD participants. These results suggest that MPH may have similar modulatory effects in certain brain regions, whether or not the attention disorder is present. The findings also suggest those with ADHD and/or RD recruit comparable brain regions to complete certain tasks; indicating there are similar neurobiological underpinnings to the disorders.

A limitation of this study was that most of the ADHD and RD subjects were using MPH before the study was undertaken which could have cause fluctuations of neural functioning. It is therefore unclear whether additional neural effects of MPH would be seen in ADHD subjects with no prior use of MPH. This limitation was controlled for, in the study by Keuler et al (2007), by ensuring the participants were medication free for at least 72 hours prior to testing. This study evaluated the effect of MPH on the reading performance in children diagnosed with both ADHD and dyslexia. Their results showed only an improvement in reading scores in children with combined ADHD and dyslexia, not in the groups with just ADHD or dyslexia. These results are surprising as it would be hypothesised that if reading performance increases in the ADHD and dyslexia group, those with just dyslexia would also showed improved reading performance. This however was not the case. These results suggest those who have dyslexia with ADHD may have different neurobiological causations than dyslexia alone.

In addition to their primary difficulties, children with ADHD often display other difficulties such as cognitive deficits or social problems. It is important to consider these associated characteristics when discussing the comorbidity between ADHD and a learning disorder such as dyslexia. A key cognitive deficit evident in children with ADHD and dyslexia is executive function. These are the control processes in the brain that activate, integrate, and manage other brain functions (Welsh and Pennington, 1988). Executive functions are varied and include cognitive processes such as working memory and flexibility of thinking. There is general consensus that executive function is mediated by the prefrontal cortex. A number of behavioural studies report deficits in executive functioning in dyslexia (Brosnan et al, 2002; Reiter et al, 2005). Brosnan et al (2002) administered a variety of tasks assessing executive function in children with dyslexia. These tasks included the Digit Span task and the Tower of Hanoi task with results showing a consistent deficit in these executive function measures. The findings taken as a whole suggest that those with dyslexia show deficiencies in executive function relating to inhibition of distracters and to sequencing of events, a set of tasks associated with left prefrontal cortex functioning.

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It is not just in dyslexia that a dysfunction in executive function has been shown. Converging evidence from clinical, biological and neuropsychological studies suggests behaviour exhibited in ADHD also reflects an underlying problem in executive function. Douglas (1983) proposed that ADHD is characterised as a generalised deficit in self – regulation arising from deficiencies in the maintenance of attention, inhibition of impulsive responding and the need for immediate reinforcement. Neuropsychological studies have demonstrated that children with ADHD typically perform poorer than age matched controls on a range of executive function measures (Barkley, 1994). Although these findings generally corroborate the neuropsychological evidence of executive dysfunction, it is important to note that the findings are not always consistent and there may be important age and gender related differences.

Pennington et al (1993) compared RD, ADHD and RD with ADHD on a variety of phonological processes and executive functions. Their results found the two RD groups (RD only and RD with ADHD) were significantly impaired on the phonological processes but performed normally on the tests of executive function. The ADHD only group had the opposite profile. Thus, there was a double dissociation between the RD – only and ADHD – only groups. The comorbid group resembled the RD – only group which suggests their ADHD symptoms are secondary to the RD. The results also suggest that ADHD and dyslexia represent two distinct disorders. It would not be surprising if dyslexic children, not understanding or having serious difficulty with written material, became distracted and uninterested in school work. Teachers might view this behaviour as representing ADHD therefore these results have implications for the diagnosis of ADHD.

An important issue is whether the presence of early learning difficulties (LD) can lead to the development of ADHD or vice versa. When this topic was initially reviewed by McGee and Share (1988) the conclusion was that longitudinal research did not indicate that ADHD could lead to later LD's, but that early LD's might be associated with a rise in ADHD symptoms over development, even though this was not consistently shown across the studies reviewed. In their longitudinal study of children, Fergusson and Horwood (1992) reached the opposite conclusion, finding that early attention problems increased the risk for later reading difficulties, whereas reading difficulties did not increase the later risk for attention problems. Rabiner et al and Coie, (2000) evaluated 387 children followed from nursery through fifth grade (age 10 – 11) and found the same result; early attention problems may be associated with concurrent and later reading problems, but not vice versa. Velting and Whitehurst (1997) found that it was specifically inattention – hyperactivity in first grade (age 6 – 7) that was most closely associated with poorer reading skills. Chadwich et al (1999) followed four groups of children ages 7 – 8 over a 9 year period. These groups had ADHD, RD, both or neither. The results found no evidence that dyslexia led to hyperactivity at follow – up or vice versa. Thus, whereas early inattention at first grade may be predictive of lower reading ability later on, early hyperactivity is not likely to do so.

Children with ADHD and dyslexia frequently manifest impairments in writing (Adi-Japha et al, 2007). A novel approach to studying this association is taken by Adi-Japha and colleagues, who focused on the specific writing components of handwriting and spelling. They demonstrated that ADHD children manifested errors in handwriting and spelling which can largely be explained as impairments in the attentional processes necessary for motor planning. This is an intriguing finding, suggesting that the writing deficits in these children are mainly motor related, rather than being linguistic in nature as the children had normal reading skills. This finding has interesting links with the study already discussed by Shafwitz et al, (2004) who found the brain areas specifically related to motor control showing less activation in ADHD and RD groups when completing attentional tasks. Berninger et al (2008) found dyslexics to have poor handwriting and letter naming which they suggest is related to impaired verbal fluency. This claim challenges current approaches to treatment, pointing especially to the potential of remediation through education and the use of word processors, and not just stimulant medication.

In preparation for this essay, I watched a video on dyslexia and its outcomes. The video centred on a few individuals and looked at their lives retrospectively. The video focused on the emotional and social implications of dyslexia. In the 1980s relatively little was known about dyslexia, children with learning difficulties were termed as being “lazy” and “an underachiever”. This may have caused those with the difficulty to be stigmatised by friends and teachers. Given that most dyslexics fail to learn to read easily it is hardly surprising that early school experiences erode self esteem and set up subsequent triggers in later life around everyday scenarios requiring literacy skills. Caroll and Iles (2006) investigated whether children with learning disabilities including dyslexia have a higher vulnerability to emotional consequences such as anxiety. With a sample of 16 dyslexia sufferers and 16 controls they found dyslexic students had higher levels of academic and social anxiety. This supports other hypothesised associations between learning disabilities and vulnerability to emotional consequences such as anxiety (Cohen, 1986). This study has limitations however, namely that the sample was predominantly female. The gender differences in this study may reflect the fact that female dyslexic students in general felt more willing to talk about their experiences and worries. There is some evidence that female dyslexics are more prone to anxiety – related symptoms than male dyslexics (Hales, 1994). Therefore the study by Caroll and Iles may have overestimated the levels of anxiety present in the dyslexic students as a group.

Similar to dyslexia, ADHD also tends to be associated with comorbid psychiatric disorders (Biederman et al 2004). Disorders commonly associated to ADHD include conduct disorder, depression and anxiety disorder with a prevalence rate of over 16% (Alpert et al 1996). These results have been supported by Fischer et al (2007) who found their sample of ADHD adolescents had a 25% comorbidity rate with depression, generalised anxiety disorder and social phobia. These studies help answer the essay question as they provide further support for an association between ADHD and dyslexia by highlighting the peripheral commonalities between the two illnesses.

Foster et al (1999) investigated the role of the planum temporale asymmetry and its links with ear advantage in dichotic listening in children with dyslexia and ADHD. The planum temporale is considered to be a crucial structure in the language process for it serves as the auditory association cortex. Past research has consistently demonstrated that 60 - 70% of the population has a longer left planum temporale in the right hemisphere (Geschwind and Levitsky, 1968). However this pattern of asymmetry is not commonly found among individuals with dyslexia. Research has suggested that dyslexic sufferers tend to have either rightward asymmetry or symmetrical plana (plana of equal lengths in both hemispheres) (Morgan, 1996). There is evidence to suggest that atypical rightward asymmetry or symmetry of the planum temporale is associated with weaker verbal comprehension, poor phonological processing, and deficits in expressive language (Semrud-Clikeman et al., 1991) in dyslexic and non-dyslexic populations. Kibby et al (2007) also found rightward asymmetry in an ADHD population. This suggests ADHD and dyslexia have neurological similarities which could account for the high comorbidity rates. Further evidence for similarities between ADHD and dyslexia comes from studies investigating ear advantage in dichotic listening tasks. The right ear is directly connected to the left brain, the brain that processes language. If one has a left ear advantage, the sound first goes to the right brain; this information has to be rerouted to the left brain via the Corpus Callosum. Research has shown those with learning difficulties such as ADHD and dyslexia have a deficit in right ear advantage (REA). Combs (2002) investigated ear advantage in ADHD patients. Using otoacoustic emissions, Combs found there to be a lack of REA in most participants. In fact, results actually found there to be a left ear advantage. Research has found similar results in dyslexia sufferers. Using a dichotic listening task, Hugdahl et al (1995) found an absence of REA in left and right handed students with dyslexia. Bess (2001) found classroom acoustics to be of great importance in the learning potential of children with mild hearing problems. The finding that patients with ADHD lack a REA may put them at an auditory disadvantage in school, they may contribute to their inattention and subsequent difficulties in reading and writing. These results suggest there is a similar biological dysfunction in both ADHD and dyslexia adding to the literature of an association between the two disorders.

The research has discussed has pointed out similarities and differences between the two disorders. While both ADHD and its various comorbidities are likely to be the product of genetic, neurochemical and / or psychosocial interactions, if ADHD and dyslexia are relatively independent, different treatments may be needed to address the disorders separately. This hypothesis would suggest a role for multimodal treatment to effectively target the full complement of psychiatric features. In much of the research, it appears as though dyslexia could be a side effect of the inattention attributed in ADHD. Therefore, in cases where ADHD is exhibited with dyslexia, it may be best to treat the ADHD pharmacologically and then to address the reading disabilities by providing extra support in the classroom by means of computers and more one to one work with teachers. The remaining psychiatric symptoms such as the presence of a mood disorder may be treated using psychosocial interventions.

Adults with ADHD and / or dyslexia exhibit patterns of cognitive deficits including below average grades and increased rates of school dropout. As previously noted, it may be difficult to ascertain the degree to which academic underachievement is the result of behavioural disturbances; such as inattention, or whether the presence of a learning disorder such as dyslexia causes the child to exhibit symptoms such as inattention and irritability to deal with not being able to cope in the academic environment.

The research discussed suggests the comorbidity between ADHD and dyslexia is down to more than just chance. Biological and neurological systems have both been implicated in the presence of the disorders. What is still unknown is whether the changes in these areas cause the disorders, or whether the presence of the ADHD – dyslexia initiates a physical change in the body. This could be investigated by analysing brain activation in identical twins, where one twin suffers from the disorder and the other does not. This may establish whether or not the ADHD / dyslexia are the result of biological abnormalities. Other research has focused on the similarities of each group in relation to handwriting impairments and cognitive deficits (Adi-Japha et al, 2007; Brosnan et al, 2002) which may also reflect an underlying neurological similarity in relation to motor control. There are discrepancies in the literature as some research has not found these similarities (Pennington et al, 1993). This may be attributable to methodological inconsistencies and differences in assessment techniques. Nevertheless, it is clear that there are huge similarities between the two disorders on many dimensions.