School Problems

Herschel R. Lessin MD

INTRODUCTION

It is an all too common scenario: The primary care provider is conducting an annual health maintenance examination on a school-age child. As the clinician is about to leave the examining room, the parent says, “Oh, by the way, my child is having trouble in school. The teacher thinks he might be hyper. I don’t know what to do.” School problem is a very broad term than can include almost any reason that a child does poorly in school. Whether in learning, behavior, or both, school problems are among the most common complaints that parents bring to the provider, who often is the first professional they contact for help. School problems can be broadly divided into three categories:

Cognitive (learning disability, central auditory processing defect, attention deficit hyperactivity disorder [ADHD])
Psychological (school avoidance, separation anxiety, shyness)
Physical

Considerable overlap exists within these categories and with other mental health disorders. This chapter provides a brief overview of school problems, with special emphasis on ADHD. Other problems, such as anxiety, depression, oppositional and conduct disorders, and major psychiatric problems (such as bipolar disorder and psychosis), are discussed as comorbidities under the diagnosis section of ADHD.

COGNITIVE PROBLEMS

Several cognitive problems manifest as school problems, the most dominant of which is ADHD. The following discussion provides a brief synopsis of learning disability and central auditory processing defect, with a more detailed examination of ADHD. More significant mental health diagnoses usually require a referral to an experienced mental health professional. These are discussed under the section on diagnosis of ADHD.

Learning Disability

Learning disability, a general term that encompasses many disorders of varying severity, is the most common cognitive disorder, occurring in 5% to 17.5% of children (Shaywitz, 1998). The Diagnostic and Statistical Manual-IV (DSM-IV) defines learning disability as individual achievement that is substantially below that expected for age, schooling, and level of intelligence. It represents a difference in how the brain processes information that it receives, not in the actual reception of the information (eg, visual or auditory impairment). It only is noted to be a problem when the disability causes functional impairment to the patient. Dyslexia, the most commonly used term, has no solid definition, although it usually refers to a problem with reading.

Learning disability should be suspected if a child of average or better intelligence has difficulty learning basic educational skills (eg, math or reading), and the skills in certain areas fall below performance in other areas. Learning disability is both familial and heritable (Shaywitz, 1998); thus, a thorough family history is extremely important for the child who presents with signs of learning disability. If the history suggests a learning disability, the provider must refer the patient to a child psychologist or other pediatric mental health professional who is able to perform psychoeducational testing. Learning disability is diagnosed when a discrepancy is found in performance or achievement and intelligence, as measured by standardized testing. Once diagnosed, specific educational remediation must be initiated based on the child’s individual needs.

Clinical Warning

Learning disability must be differentiated from true diminished mental capacity. True diminished mental capacity can be due to neurologic damage, genetic disorders and syndromes, trauma, central nervous system infection, and nonspecific causes of mental retardation. A child with true diminished mental capacity is limited in learning in any realm, as opposed to a child with learning disability, who has specific problem areas. Depending on the severity of the problem, the child with learning disability requires a specific educational program (mainstreaming or separate special education classes). A whole array of specific learning disabilities can be found in DSM-IV (1994).

Central Auditory Processing Defect

Although an exact figure is unavailable, a defect in central auditory processing is a cognitive problem seen fairly often in pediatric practice. The child with a disorder of central auditory processing has normal hearing but is unable to process the information heard and so does not understand it. Clinically, the youngster is suspected to have hearing loss, but repeated hearing tests are normal. A defect in central auditory processing thus sometimes is confused with ADHD.

Attention Deficit Hyperactivity Disorder

The DSM-IV (1994) defines ADHD as only one of a spectrum of attention deficit disorders. The syndrome has been known by many names over the years, including minimal brain damage, minimal brain dysfunction, hyperkinesis, attention deficit disorder, and ADHD. The various revisions of DSM have reflected these name changes by emphasizing different parts of the symptom complex in its classification and description, with DSM-IV (1994) dividing ADHD into various subtypes.

Clinicians often find themselves inundated with requests from schools and parents to evaluate large numbers of children for this problem. Depending on their level of interest and commitment, providers can effectively evaluate children with uncomplicated ADHD, but it takes substantial time and effort to do so properly. The use of pharmacologic therapy, particularly stimulant medications, has been the subject of longstanding and ongoing controversy in the media. The fact that medications used for ADHD are controlled substances in the amphetamine group also has troubled many providers and parents alike. There remains the undercurrent of whether any child who acts up in class should be medicated. Is this therapy prescribed for the patient’s benefit or for the teacher and parents? What has become clear over the past few years is that ADHD is a real disorder with a real physiologic defect and a real and effective treatment.

Pathology

Although the symptoms of ADHD have been recognized for more than 50 years, no theory has been universally accepted to explain the pathophysiology of the underlying defects. Rapid advances in neurobiology and noninvasive imaging, however, have lent support to the theory that ADHD is due to disregulation of neurotransmitters in the frontal lobes of the brain. Structural neuroimaging of the brain with magnetic resonance imaging (MRI) has shown abnormalities in the caudate nucleus and corpus callosum (Castellanos et al., 1996; Semrud-Clikeman et al., 1994). Functional brain imaging with MRI and positron emission tomography (PET) scanning has demonstrated diminished frontal lobe activity (Bush et al., 1998; Zametkin et al., 1990). All these studies, however, suffer from some methodologic flaws and other limitations.

While it is clear that ADHD is highly heritable, the actual genetic defect has yet to be determined. Molecular genetics studies suggest defects in the dopamine receptor and the dopamine transporter genes, giving support to the theory that defects in either gene result in diminished dopamine entry in frontal lobe synapses (LaHoste et al., 1996). This could explain why stimulants, which increase dopamine at the synapse, are helpful in children with ADHD. However, how do stimulants, such as amphetamines, paradoxically result in decreased motor activity? Barkley (1997) proposes that ADHD is a motor disinhibition syndrome. The frontal lobes are responsible for the regulation of motor activity. The neurons responsible for inhibiting such activity are underactive, due to a defect in dopamine transport. According to Barkley, by increasing available dopamine, stimulants allow the normal amount of inhibition to take place, thereby accounting for their paradoxical effects. The frontal lobes also are responsible for a wide range of high-level executive reasoning functions that are compromised in patients with ADHD. For a full discussion of this theory, the reader is referred to Barkley’s publications and books, several of which are annotated at the end of this chapter.

Other factors that may be implicated in the pathogenesis of ADHD include a history of the following:

Birth trauma
Head trauma
Prenatal teratogenic exposure, including maternal smoking (Millberger, Biederman, Faraone, Chen, & Jones, 1996) and drugs association with other syndromes, such as Gilles de la Tourette’s

Epidemiology

The prevalence of ADHD has been reported as between 2% and 9% of all school-age children, making it one of the most common disorders of childhood (Bauermeister, Canino, & Bird, 1994). The DSM-IV (1994) reports ADHD prevalence as being 3% to 5%. The male-to-female ratio is between 3:1 and 8:1. ADHD occurs across all socioeconomic strata. It clearly runs in families (Faraone & Biederman, 1994), with 80% of its variance explainable by family history (Barkley, 1998). Most children with ADHD have some other comorbidity, including one or more of the following:

Oppositional defiant disorder (ODD) (65%)
Learning disability (30%–40%)
Depression (30%)
Anxiety disorder (10%–20%)
Conduct disorder (20%)
Tic disorders (10%) (Biederman, Newcorn, & Sprich, 1991)

History and Physical Examination

A good history must include a general discussion of the following:

Behavior, including discerning whether there are problems at home or school, or discipline problems, including issues with aggression and anger
Performance in varied areas, including school work, homework, and household tasks, as well as organizational skills, staying with tasks, and overall learning difficulties
Social skills and behavior, including interaction with parents, teachers, and peers
Emotional responses to stressful situations, as well as frustration tolerance

The provider should ask a series of specific questions that are targeted to the diagnostic criteria discussed in the next section. In addition, the clinician must ask questions that can lead to diagnosis of the many comorbidities discussed previously, particularly ODD and depression. The age of onset of all symptoms and the realm in which they occur should be noted. The reader is referred to Chapter 19 and Chapter 28 for further discussion of relevant comorbid conditions. A workbook
with lists of questions based on DSM-IV (1994) criteria is annotated at the end of this chapter. This resource can serve as a template for the interview (Barkley & Murphy, 1998). The following suggestions also can be used to frame this interview:

The clinician should obtain a complete past medical history, with emphasis on possible central nervous system trauma.
The clinician also must obtain a thorough developmental history, with particular emphasis on birth history, temperament, and developmental milestones.
If any outside psychoeducational testing has been performed, the provider should review it.
Given the high incidence of heritability, the provider should elicit a careful family history, with emphasis on the parents’ own home and school histories.
The clinician also may explore symptoms of adult ADHD and, finally, discuss whether there is a family history of mental health problems, especially depression, bipolar disorder, anxiety disorder, and psychosis. This latter information is critical to making an informed determination.

In addition, the provider should ask whether there is a history of primary nocturnal enuresis (PNE). Special needs children have higher rates of PNE. This is especially true for youngsters diagnosed with ADHD. PNE in such children may be partly related to a “hyperactive” bladder or to behavioral problems encountered in toilet training. These problems may have emerged because of attentional impediments to efficient learning. Pervasive and chronic hyperactivity of the parasympathetic nervous system also may play a role in uninhibited bladder contractions (Yakinci, Mungen, Durmaz, Balbay, & Karabiber, 1997). Refer to Chapter 63 for more information about the diagnosis and management of PNE.

As with any patient contact, a thorough physical must be performed with special attention to the neurologic examination. The examination should focus on finding any signs of other neurologic disorder, metabolic problem (eg, hyperthyroidism), genetic disorder (eg, fragile X syndrome), hearing or visual impairment, or other developmental syndrome (eg, autism or pervasive developmental disorder). Refer to Chapter 19, Chapter 32, Chapter 46, Chapter 52, Chapter 53, and Chapter 60 for further information.

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