Reading and other language-based tasks are a large part of the curriculum in early education. After that, reading and language continue to be the foundations upon which most academic subjects are based. Every school subject, even science and math, has a large language component to instruction. It is therefore not surprising that difficulty with language-based tasks, most prominently reading, is a common complaint among children who are having problems in school.

In some children who present with a complaint of difficulty with reading, the problem can be attributed to an isolated reading disability (RD), more commonly referred to as dyslexia in the medical and psychological professions. Developmental dyslexia is defined as a chronic disorder characterized by difficulty with acquisition and use of written language that is unexpected on the basis of normal general development and overall cognitive aptitude. Theoretically, other exclusions include
emotional problems, educational deprivation, and sensory impairment. Although outside the scope of this discussion, it is important to mention that dyslexia is a lifelong disorder; residual effects, particularly slow reading, are observed in adults with the disorder.

Dyslexia is almost universally viewed as a specific disorder of the phonologic subdivision of the language system. However, pure dyslexia is more the exception than the rule; most children with dyslexia have deficits that are not limited to written language. The border between deficits in reading and deficits in broader aspects of language can be fuzzy, and most children with dyslexia have a broader language deficit that involves aspects of spoken as well as written language (e.g., problems with written composition).

Biomedical research has resulted in a consensus that the underlying deficit in dyslexia is in phonologic skills (or the ability to manipulate the sound structure of the language), which are essential for the development of the ability to decode, or “sound out,” words; the difficulty with decoding that children with dyslexia have thus places major constraints on their reading comprehension. However, despite these findings, current educational practice and psychiatry’s Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV) continue to disregard these findings when defining what constitutes a reading disability. The DSM-IV uses the term “reading disorder,” which is defined as reading achievement that is “substantially below that expected given the person’s chronological age, measured intelligence, and age-appropriate education,” but does not make any mention of problems with phonologic deficits. Interestingly, within the realm of “communication disorders,” the DSM-IV does have a diagnosis of “phonological disorder,” which is described as an articulation disorder in which there is a “failure to use developmentally expected speech sounds”; however, there is failure to establish the known connection between problems with certain phonologic skills (e.g., phonologic awareness) and difficulty reading.

Most public school systems define a reading disability on the basis of discrepancy criteria (a discrepancy between full-scale IQ and performance on tests of reading achievement) rather than by the appearance of a subtle neurocognitive deficit in phonologic awareness. Under public law 94-142, the Education for All Handicapped Children Act, passed in 1975, public school systems are required to provide services for children with handicapping conditions, including learning disabilities; however, children with dyslexia often have difficulty with broader aspects of language, which can adversely affect IQ scores (particularly the verbal subtests), making it difficult for children with dyslexia to meet the discrepancy criteria adopted by most public school systems. Their underlying language deficits lower both the aptitude and achievement, precluding a discrepancy. Furthermore, research has shown that the IQ-achievement discrepancy method of defining reading disabilities is not valid: studies have shown that children with IQ-achievement discrepancy and poor readers without a discrepancy both show impairments in phonologic skills.

Cognitive assessments of children with reading disability often reveal subtle deficits in inhibitory control and organization consistent with the diagnosis of ADHD. Comorbidity of dyslexia and ADHD is common. Studies from random samples have shown that approximately 36% of children with ADHD have RD and 15% of children with RD have ADHD; however, some researchers have reported comorbidity rates as high as 80%. Although some of these children present with both difficulty reading and difficulty staying on task, others present with reading as the only complaint, and subtle deficits in inhibitory control and organization become apparent only after cognitive testing. (The cognitive deficits associated with ADHD will be discussed in more detail in the section entitled, “The child who presents with difficulty staying on task.”)

The cause of developmental dyslexia is presumed to be congenital, with genetic and fetal developmental factors theorized as possible contributors to the development of brain differences that result in ineffective performance of reading and other language-based tasks. Investigations have elicited genetic contributions to dyslexia. Twin studies have pointed to heritability for single word reading and a variety of phonologic skills; recent twin studies have shown that approximately 58% of the deficit in dyslexia is attributable to heritable genetic influences. Linkage studies have implicated possible loci on chromosomes 1, 2, 3, 6, 15, and 18, with a locus on chromosome 6 (6p21.3) the best replicated finding so far.

Analyses of the neuroanatomic basis of acquired difficulty reading in adults (acquired alexia or dyslexia) are consistent with localization to the left angular gyrus. Neurobiologic studies of individuals with developmental dyslexia, including postmortem, electrophysiologic, and imaging studies, have implicated left perisylvian regions, and many theories have focused on postulates of temporal–parietal perisylvian dysfunction. Alternatively, Heilman and others have suggested that the development of phonologic skills may be linked to motor articulatory kinesthesis with localization in more anterior motor speech areas of the brain. More recently, functional magnetic resonance imaging (fMRI) studies have shown that when people with dyslexia are asked to sound out words or perform phonologic tasks, they show reduced activation in left posterior regions and overactivation in anterior and right posterior hemisphere regions. Interestingly, these patterns of activation normalize (i.e., become like normal readers) after people with dyslexia are provided appropriate intervention and are reading at normal levels.

Another very common school-related problem to which the pediatrician must respond is the child who has difficulty staying on task. This difficulty is often associated with symptoms of impulsivity and hyperactivity. Often, these symptoms will be due to ADHD; however, differential diagnoses, including language/learning disabilities and psychiatric disorders, need to be considered. Often the issue is “in addition to” rather than “instead of” ADHD, as is commonly true for language-based disabilities.

In recent years there has been increased public awareness of ADHD; however, the symptoms that comprise the disorder have been recognized under a variety of names (minimal brain dysfunction, hyperkinetic disorder, attention deficit disorder) for over 30 years. ADHD is common, affecting 3% to 5% of elementary school-age children, leaving little doubt about its impact on school functioning across a large population of children. Studies have revealed a higher incidence of ADHD in males than females, with a ratio of approximately 3:1; however gender-biased diagnostic criteria may account for the size, if not the direction, of the ratio.

ADHD is characterized by symptoms of hyperactivity, impulsivity, and a decreased ability to maintain on-task behavior, particularly during nonpreferred tasks. Currently, the DSM-IV uses the term “attention deficit/hyperactivity disorder” and includes three subtypes: “predominantly inattentive,” “predominantly hyperactive/impulsive,” and a combined type. By definition, signs must be observed prior to 7 years of age. The forms can change over the lifespan; one individual can have the hyperactive/impulsive type as a preschooler, the full syndrome until middle school, and the inattentive type thereafter.

It is children with the inattentive form that will often present with isolated complaints of school difficulty. In children with the hyperactive/impulsive or combined forms of the disorder, signs are typically recognizable at an early age and often include behavioral as well as academic difficulties. In the inattentive form signs may not be evident until the child enters school and begins engaging in nonpreferred activities that require a much greater ability to inhibit off-task behavior. With persistent, focused questioning, however, the clinician can often find a history of off-task behavior during the preschool years. (As is the case for dyslexia, it is important to mention that ADHD is no longer a diagnosis restricted to childhood. It has been reported that approximately 75% of those diagnosed in childhood continue to suffer from residual ADHD in young adulthood.)

The cause of ADHD appears to be heterogeneous. Various adverse environmental factors including infection, toxins such as lead, and prenatal exposure to tobacco or alcohol have been associated with symptoms of ADHD. Genetic factors have also been identified. Several genetic disorders have ADHD as part of the phenotype, and twin studies report heritability rates ranging from .6 to .9. Additionally, siblings of children with ADHD have a three- to fivefold increased risk of having the disorder. Although there is strong evidence for a genetic basis for ADHD, it is not yet clear which genes may be responsible. Most studies that have tried to link candidate genes to ADHD have concentrated on dopaminergic systems; however, there is also some indication that other systems may also be involved (serotonergic and catecholaminergic systems).

Like dyslexia, ADHD is often associated with comorbid conditions. What is more, these comorbid conditions are often differential diagnoses that must be considered in the evaluation of a child who presents with difficulty staying on task. As mentioned in the preceding section, ADHD is often associated with dyslexia and other language-based learning disabilities. These disorders also need to be considered as differential diagnoses, since problems staying on task can result from difficulty understanding verbal and written instructions. In addition, psychiatric disorders such as oppositional defiant disorder, conduct disorder, anxiety disorders, and mood disorders including depression are common comorbidities that must also be considered as possible causes/contributors to difficulty staying on task.

In considering the neurobiologic basis of ADHD, most researchers suggest that the disorder is the result of dysfunction within frontal intentional networks, which are critical for an organism’s “preparedness to act.” In this model, the core symptoms are thought to be secondary to abnormal selection of motor response to stimuli (difficulty in preparing the response to, rather than attending to, stimuli). The result is unresponsiveness to stimuli that should lead to action and defective inhibition of response to those that should not, with the latter resulting in impulsive and hyperactive behavior.

The neuropsychological profile of patients with ADHD is consistent with signs of insult to the frontal lobes and its interconnected subcortical regions, with most studies identifying deficits in the realm of “executive function,” including response inhibition and response preparation. Morphometric studies have consistently shown that children with ADHD have reduced total brain volumes (approximately 5% reduction compared to controls) and show abnormalities in frontal-subcortical regions. Reduction in prefrontal and premotor volumes and abnormalities in the volumes of the caudate and globus pallidus have been reported. In concordance with structural neuroimaging findings, functional neuroimaging studies have also revealed abnormalities in frontostriatal circuitry in individuals with ADHD.

A subgroup of individuals with the inattentive form of ADHD may have a deficit in overfocusing or shifting attention rather than in selection of motor response to stimuli. Two prominent models of attention suggest that parietal lobe dysfunction would be manifest as impairment of stimulus detection, as well as decreased performance on other sensory components of attentional processing including vigilance, selection, disengagement, and shifting. It follows that deficits in the overfocusing subtype are more likely due to pathology in parietal circuits.

Regardless of the chief complaint, the workup of school difficulties needs to take into consideration all possible causes. For instance, in a child who presents with a chief complaint of difficulty staying on task, it would not be appropriate to focus solely on ruling out the presence of ADHD. Several other possibilities that may be the real cause (differential diagnoses) of difficulty staying on task or that may be present in conjunction with ADHD (comorbid diagnoses) need to be considered and ruled out.