CHAPTER 5 Mental Health Disorders

Attention Deficit-Hyperactivity Disorder

Pervasive Developmental Disorders

Autism

Asperger’s Syndrome

Rett Syndrome

Pervasive Developmental Disorder–Not Otherwise Specified

School Avoidance/Refusal and School Phobia

Tics and Tourette’s Disorder

Major Depressive Disorder

The most prevalent mental health problems encountered in school settings are discussed in this chapter. Along with Chapter 6, Substance Abuse, these chapters provide a broad overview of the psychiatric disorders of childhood and adolescence. Mental health disorders have an impact on cognition, behavior, emotions, and social functioning. This can occur directly through neurological mechanisms affecting domains such as attention, cognitive processing, and impulse control, and it can occur indirectly through psychosocial areas such as self-esteem, motivation, emotional regulation, and peer relationships. Disabilities in any of these areas can affect the school performance and school life of a child or adolescent. Current brain research provides data regarding the areas of the brain involved and the impact these disorders may have on learning.

The phenomenon of coexisting disorders is common in all of the conditions discussed in this chapter. An illness or impairment in one domain may be associated with—or may result in—a disturbance in others, such as affective disturbances in youth with attention deficit-hyperactivity disorder (ADHD), early onset of dysthymia in children with school phobia, or anxiety disorder in oppositional defiant disorder (ODD).

Child-centered nursing interventions involve an appreciation for both the neurobiological concerns and interventions with these disorders while also noting the important role of nurturing, socialization, education, and acculturation within the educational context that need to be addressed for optimum educational outcomes. The school nurse plays an important and vital role in the assessment, educational planning, treatment management, and remediation of learning problems caused by these disorders.

ATTENTION DEFICIT-HYPERACTIVITY DISORDER

I. Definition

A. Attentiondeficithyperactivity disorder (ADHD), a neurobehavioral condition, is one of the most common childhood disorders; it occurs in approximately 3% to 18% of children (CDC, 2005; Parker, 2005; Rowland, Lesesne, and Abramowitz, 2002).

1. Boys are approximately two to three times more likely to be diagnosed with ADHD than girls (CDC, 2005), and boys are more likely to have the hyperactive-impulsive type ADHD, and girls are more frequently diagnosed with the inattentive-type ADHD (Kliegman et al, 2006; Parker, 2005).

2. Symptoms of ADHD may persist into adolescence, and some continue into adulthood, where they may manifest as restlessness, disorganization, distractibility, job difficulties, substance abuse, accidents, or relationship problems (American Psychiatric Association [APA], 2000).

a. There is clinical support for a rule of thirds, which suggests that l in 3 children “outgrows” the disorder, meaning they develop adequate coping capacities for it, so they no longer exhibit symptomatic states. Another third outgrows the disorder in the transition between adolescence and adulthood, and the other third continues with symptoms into adulthood (Chenven, 2006).

B. Diagnostic and Statistical Manual of Mental Disorders (DSM-IV) diagnosis requires at least six symptoms of inattention and at least six symptoms of hyperactivity/impulsivity of more than 6 months’ duration in two settings, and symptoms must occur before 7 years of age. Symptoms must also substantially interfere with age appropriate development and academic or job skills (see Box 5-1).

II. Etiology

A. ADHD is associated with genetic factors and neuroanatomical abnormalities in the brain that are known to regulate motor and attention behaviors. Psychosocial, emotional, and environmental-exacerbating factors include coexisting mental disorders, coercive discipline, lack of consistency, exposure to media violence, parental unsociable behaviors or marital conflict, abuse, and neglect. Symptoms of hyperactivity or inattention can be secondary effects of medications (e.g., theophylline, albuterol, phenobarbital), hyperthyroidism, or lead poisoning (Kliegman et al, 2006). Prematurity and intrauterine exposure to alcohol, drugs, cigarettes, and unsafe carbon monoxide levels can contribute to ADHD.

B. The exact cause of ADHD is unknown, but it is believed to be genetic in at least 50% of the cases based on studies of twins (Anastopoulos and Shelton, 2001) and other family members affected by the disorder (Barkley, 1998). Dopamine transporter gene DAT1, dopamine receptor genes DRD4 and DRD5 (Rosenbaum et al, 2005), and Synaptosome-associated protein 25, SNAP-25, are genes thought to be associated with ADHD (Biederman, 2005; Thapar, O’Donovan, and Owen, 2005). Research continues in this area to try to identify other brain neurotransmitters and receptors that may be involved.

Box 5-1 DSM-IV Criteria: Attention-Deficit/Hyperactivity Disorder

A. Either 1 or 2:

1. Six or more of the following symptoms of inattention have persisted for at least 6 months to a degree that is maladaptive and inconsistent with developmental level:

Inattention

a. Often does not give close attention to details or makes careless mistakes in schoolwork, work, or other activities.

b. Often has difficulty sustaining attention in tasks or play activities.

c. Often does not seem to listen when spoken to directly.

d. Often does not follow through on instructions and fails to finish schoolwork, chores, or duties in the workplace (not due to oppositional behavior or failure to understand instructions).

e. Often has difficulty organizing tasks and activities.

f. Often avoids, dislikes, or is reluctant to engage in tasks that require sustained mental effort, such as schoolwork or homework.

g. Often loses things necessary for tasks or activities (e.g. toys, school assignments, pencils, books, or tools).

h. Is often easily distracted by extraneous stimuli.

i. Is often forgetful in daily activities.

2. Six or more of the following symptoms of hyperactivity-impulsivity have persisted for at least 6 months to a degree that is maladaptive and inconsistent with developmental level.

Impulsivity

a. Often blurts out answers before questions have been finished.

b. Often has trouble waiting one’s turn.

c. Often interrupts or intrudes on others (e.g. butts into conversations or games).

B. Some hyperactive-impulsive or inattentive symptoms that caused impairment were present before age 7 years.

C. Some impairment from the symptoms is present in two or more settings (e.g. at school or work and at home).

D. There must be clear evidence of significant impairment in social, academic, or occupational functioning.

E. The symptoms do not occur exclusively during the course of a pervasive developmental disorder, schizophrenia, or other psychotic disorder and are not better accounted for by another mental disorder (e.g. mood disorder, anxiety disorder, dissociative disorder, or a personality disorder).

Based on these criteria, three types of ADHD are identified:

1. ADHD, Combined Type: if both criteria A1 and A2 are met for the past 6 months.

2. ADHD, Predominantly Inattentive Type: if criterion A1 is met but criterion A2 is not met for the past six months.

3. ADHD, Predominantly Hyperactive-Impulsive Type: if criterion A2 is met but criterion A1 is not met for the past six months.

From American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders, ed 4 text revision, Washington, DC, 2000, American Psychiatric Association.

Brain Findings

ADHD is believed to have a neurological basis. Research has found evidence of a chemical imbalance or irregularity in certain neurotransmitters, especially dopamine and norepinephrine, consistent with the genetic results described in the previous section. PET studies have demonstrated hypometabolism of glucose (Pary et al, 2002) in particular areas of the brain thought to be involved in attention. When a student is challenged with academic problems, such as math, the typical brain fires up the frontal lobe and starts working; the brain of the student with ADHD does not. With correct stimulant medication, dopaminergic activity increases in the brain, and the student is able to work on the assigned task or class problem.

National Institute of Mental Health (NIMH) brain-scan studies indicate the volume of matter in several key parts of the brain is 3% to 4% smaller in children with ADHD who have never been on medication. The areas, compared in the sample and controls, include the cerebrum, cerebellum, gray and white matter for the four major lobes, and the caudate nucleus, a part of the basal ganglia. These key parts of the brain, except for the caudate, appear to stay on a parallel developmental path during childhood and adolescence in patients and controls. This suggests that genetic and early environmental effects on brain development are unchanging and not related to medication (Castellanos, 2002). Furthermore, the decreased brain volume may be a factor in some biological processes, which can manifest as hyperactivity or impulsiveness in the educational setting (Bower, 2002).

Researchers also found a smaller volume of white matter in children with ADHD who had never been on medication compared to the control group. Another study found an enlarged hippocampus in children and adolescents with ADHD compared to the control group. This study supports the hypothesis that the pathophysiology of ADHD involves the limbic system and limbic-prefrontal circuits (Plessen et al, 2006).

III. Characteristics

A. Inattention and distractibility: difficulty in organizing, tendency to lose things, makes careless mistakes, does not understand instructions, cannot follow instructions that require mental effort.

B. Selective attention: focuses on something he or she wants or enjoys.

C. Hyperactive: squirms and fidgets in seat, climbs and moves about when inappropriate, talks excessively.

D. Impulsive: interrupts conversation, has difficulty taking turns, blurts out answers, talks or acts without thinking.

E. Coexisting disorders include learning disorders, 20% to 60%; conduct disorder, 10% to 50%; oppositional defiant disorder, 30% to 60%; anxiety, 10% to 30%, tic disorders, 5% to 30%, and depression (Parker, 2005). Other disorders include obsessive-compulsive disorder (OCD), pervasive developmental disorder (PDD), and Tourette’s syndrome.

F. Associated symptoms may include motor coordination difficulties, disruptive sleep, susceptibility to accidents, and poisoning.

IV. Effects on Individual

A. Difficulty maintaining friendships, social immaturity.

B. Engages in socially unacceptable behaviors.

C. Poor academic performance may result in grade retention and potential school dropout.

D. Accident prone because of impulsivity.

E. The world is confusing because of multiple sensory distractions.

F. Poor self-esteem because of the lack of success and failure to earn rewards, which result from inappropriate behavior.

G. Frequent daydreaming and excessive boredom.

H. Difficulty achieving long-term goals.

I. Strained family and peer relationships.

J. Problems with driving (e.g., impulsivity combined with poor judgment, which lead to more frequent traffic citations, especially for speeding and accidents).

K. Susceptible to drug and alcohol abuse.

V. Health Concerns and Emergencies

A. Frequent visits to nurse’s office with psychosomatic complaints.

B. Poor weight gain with or without stimulant medications.

C. Higher risk for accidents.

VI. Management and Treatment

A. Rule out hearing loss or visual impairment.

B. Obtain family and social history. Address psychosocial stressors—such as parental relationship and psychopathology, chaotic living situation, and low social economic status—that may contribute to physical and behavioral symptoms, including headache, stomachache, agitation, and aggression.

C. Encourage increased caloric intake when weight gain is slow.

D. Monitor growth patterns every 6 months when medications that may suppress appetite and growth are given.

E. Various diets and nutritional supplements are advocated by family or practitioners, but research on effectiveness is inconclusive.

F. Pharmacological management is effective in 70% to 80% of children (Parker, 2005). Teens with ADHD who are treated are less likely to become involved in substance abuse than matched cohorts who did not receive treatment (Giedd, 2003; Stocker, 1999).

G. Liaison with teachers, parents, and physician regarding effectiveness and side effects of medications (See Table 5-1).

H. Count and securely lock-up prescribed medication; stimulants are subject to controlled substance rules. These medications are frequently abused by non-ADHD students.

I. Health intervention may include checking vital signs, observing for tics, and asking questions about medications.

J. Focus on positive behaviors, and find ways to increase child’s motivation and self-esteem. Behavioral approaches are helpful when providing stability, routine, and appropriate goals.

K. Provide listening, nonjudgmental ear to parents. Be aware that some parents may also have ADHD.

L. Ensure proper supervision on playground, at special events, and during field trips.

M. Become knowledgeable regarding individual, family, and peer group therapy and behavior management; encourage multiple modalities for the child, along with individual attention; manage medication; and offer consistent and encouraging nurse–student interactions.

N. Provide information and workshop for school staff.

VII. Additional Information

A. In 1991, ADHD was recognized as a qualifying disability for special education services by Part B of the Individuals with Disabilities Education Act (IDEA) and Section 504.

B. Progressive or static neurological disease (e.g., Tourette’s syndrome, absence seizures, fragile X syndrome) is ruled out before diagnosis. Treatment usually is multimodal and may include medication, behavioral modification using positive reinforcement, anger management and social skills training, and sensory integration therapy. Treatment is often complicated by coexisting disorders.

1. Less validated modalities include vision therapy, electroencephalographic (EEG) biofeedback, or neurofeedback (i.e., training the brain to increase the type of brain activity associated with sustained attention).

2. Restricted diets (e.g., Feingold) may be used. Most common diet restrictions are sugars, additives, and preservatives to eliminate possible allergens. Works best in children younger than 5 years and those with food or food additive allergies.

3. Nutritional supplements include liquid calcium and vitamin B complex to calm the nervous system or choline, which may improve memory and attention span.

4. Caution should always be used when combining nutritional and herbal supplements and pharmacotherapy. The effectiveness of over-the-counter (OTC) supplements has not been supported by research studies and may have unknown side effects in the treatment of children with ADHD.

C. ADHD can persist into adulthood. The prognosis is negatively affected by family history of ADHD; a disruptive family environment; and a comorbid condition (e.g., conduct disorders, anxiety, mood disorders). Adolescents and adults with ADHD who take stimulant medications cannot enlist in the armed services without a medical waiver, even if the medications have been discontinued; each branch has its own criteria. Career choices generally are not affected by ADHD, and many adults are successful in their chosen occupation.

Table 5-1 Medications for Attention Deficit-Hyperactivity Disorder

WEB SITES

Attention Deficit Disorder Association (ADDA) http://www.add.org

Children and Adults with Attention Deficit Disorder (CHADD) http://www.chadd.org

Developmental and Behavioral Pediatrics Online http://www.dbpeds.org

Family ADHD Resource http://www.ADDresources.org

National Resource Center on ADHD http://www.help4ADHD.org

OPPOSITIONAL DEFIANT DISORDER

I. Definition

A. Oppositional defiant disorder (ODD) is a negative, hostile, defiant, disobedient pattern of behavior lasting at least 6 months that includes at least four of the following symptoms: frequent loss of temper, arguments with adults, deliberate annoyance, active defiance or refusal of adult requests, a spiteful or vindictive manner, touchy and easily annoyed, angry, resentful, and blaming of others (APA, 2000). Significant impairment must also be displayed in academic, social, or occupational performance. Comorbid disorders include ADHD, anxiety disorders, mood disorders, learning disorders, language processing disorders, and substance abuse.

II. Etiology

A. Etiology is multicausal and includes biological, genetic, and environmental factors. ODD is common in families with mood disorders, serious marital discord, history of physical or sexual maltreatment of children, harsh or inconsistent discipline, or a succession of multiple caregivers. Often observed before age 8, but not later than early adolescence. More common among boys before puberty, but gender distribution is fairly equal thereafter. Prevalence rates range from 2% to 16% (APA, 2000).

B. Children with ODD may be anxious, which is often related to a learning or processing disorder that makes it difficult to function. An oppositional dynamic between the child and an adult emerges when the child with these subtle disabilities is anxious and feels the need to be in control.

C. There is evidence that genetics may be a factor, and ODD is affected by caregiver and child incompatibility.

1. Mothers with a depressive disorder are more likely to have a child with ODD. It is also more common in families where at least one parent has a history of ODD, mood disorder, antisocial personality disorder, substance-related disorder, conduct disorder (CD), or ADHD (APA, 2000).

Brain Findings

Studies suggest the neurotransmitters dopamine, serotonin, and noradrenaline play a role in ODD with the most significant impact caused by noradrenaline (Kariyawasam et al, 2002; Comings et al, 2000).

Cortisol levels have been found to be low in children with ODD. Children taking stimulant medication for ODD have increased levels of cortisol (Kariyawasam et al, 2002; Snoek, 2004). Conclusions of the research indicate that cortisol responsivity during stress is different in these children and may manifest in how aggressive children respond to stress (McBurnett, 2002).

III. Characteristics

A. Three classic characteristics are noncompliance, exaggerated emotional response, and tendency to blame others.

B. Difficulty being comforted or soothed and high motor reactivity during early childhood.

C. Defiant, annoying, spiteful, vindictive, resentful, argumentative behaviors.

D. Stubbornness, resistance to directions, unwillingness to compromise, testing of limits, and usually unable to accept blame.

E. Oppositional behaviors tend to increase with age.

F. Symptoms same in both genders, but boys have more persistent symptoms and more confrontational behaviors.

G. Aggression is generally verbal rather than physical.

H. Behaviors usually manifest in the home or with adults the child knows well; may not be observed in the school or community.

I. Affects social functioning with peers, siblings, and parents.

J. Often comorbidities include learning problems, depressed moods, hyperactivity, and addictive behaviors.

IV. Effects on Individual

A. Affects school achievement and social success.

B. Peer rejection leads to social isolation.

C. Negative appearance to parents and teachers stigmatizes student.

D. May be precursor to conduct disorder and later antisocial personality, delinquency, and potential future criminality.

E. Risk indicator of potential school dropout.

F. Strained family relationships.

V. Health Concerns and Emergencies

A. Dependent on severity of symptoms.

B. Monitor medication, observe for hyperactivity or other symptoms.

C. Child abuse potential for parents and staff includes both verbal and physical abuse. Child may react negatively at school in response to the abuse at home.

D. Child with lower cortisol levels may not react to or fear threatening situations or aggressive actions.

E. ODD may predict later depression and suicidal ideation and attempts.

VI. Management and Treatment

A. Early identification of disruptive behaviors for intervention and support.

B. Rule out hearing loss as cause for failure to follow directions.

C. Observe for depression or other comorbid conditions.

D. Do family, home, peer, and community assessment; include situational analysis (i.e.; who or what is present when an outburst occurs and what are the precedents).

E. Set limits and be consistent during any interactions. It is important that adults do not react emotionally to child’s oppositional behaviors.

F. Setting clear limits and consequences may be difficult, because these children are affected more by the emotion of the moment and do not seem to care about the consequences.

G. Daily privileges should be linked to the behavior that day. Over time the child begins to understand the consequences; this occurs over months not days.

H. Reinforce socially acceptable behaviors, and provide support that may not be found in the home.

I. Provide staff education regarding ODD and behavior management therapy.

J. Support limits on television viewing and any media that portrays violence (e.g., games, music, movies).

K. Encourage positive parenting, use of behavioral approach, and psychotherapy.

VII. Additional Information

A. Conduct Disorder (CD)

1. CD is more severe than ODD and includes persistent, repetitive behavior that ignores societal rules and can result in aggressive behaviors (bullying, threats, fighting, use of weapons, theft, arson). Behaviors may be against people, animals, and property.

2. CD includes significant antisocial behaviors: deceitfulness, lying, thievery, truancy, and rape. These behaviors must interfere significantly with academic, social, and occupational functioning. Three of the criteria described must be present during the previous 12 months, with at least one present in the last 6 months.

3. CD also has coexisting conditions: mood disorders, learning problems, thought disorders, anxiety, posttraumatic stress disorder, substance abuse, and ADHD. These may be diagnosed in preschool years and are not usually diagnosed after age 16 (American Psychiatric Association, 2000).

PERVASIVE DEVELOPMENTAL DISORDERS

AUTISM

I. Definition

A. Autism is a neurodevelopmental disorder involving impairments in language, social communication, and social interactions; repetitive and stereotyped behaviors manifest in one of these areas before age 3 as defined by DSM-IV (see Box 5-2). However, the median age of diagnosis is 52 to 56 months (CDC, 2007). Table 5-2 presents early risk indicators for autism.

B. The distinguishing behavior is a relative lack of interest in other people. Autism is the main disorder included in PDD, which are also referred to as autism spectrum disorders (ASD). This nomenclature highlights the wide range of symptomatic presentations, from severe to mild, that may occur.

II. Etiology

A. The etiology of this disorder is elusive; however, strong evidence exists for a genetic component, organic cause, or both. The prevalence rate of autism is reported as 1 per l50 (CDC, 2007).

1. More boys are affected than girls, generally reported to be a 4:1 ratio.

2. Autism is associated with fragile X syndrome, tuberous sclerosis, and a family history of similar disorders, depression, bipolar disorder, schizophrenia, or more subtle ASD and OCD.

3. Genes located on chromosomes 7 and 15 have been implicated as causative factors in some cases of autism. Research has also implicated gamma-aminobutyric acid (GABA) receptor genes found on chromosome 15 in some cases of autism (Rodier, 2000).

4. GABA is the major inhibitory transmitter in the brain and abnormalities of GABA transmission are associated with seizures and anxiety disorders. It is recognized that there are at least 10 or more genes involved, and that it is not the effects of a single gene but perhaps the interaction of particular genes or sets of genes that join together in certain combinations.

B. As research continues, a better understanding will emerge of how autism and related disorders occur.

Box 5-2 DSM-IV Criteria: Autistic Disorder

A. Total of six or more items from 1, 2, and 3, with at least two from 1 and one each from 2 and 3:

1. Qualitative impairment in social interaction, as manifested by at least two of the following:

a. Marked impairment in the use of multiple nonverbal behaviors—such as eye-to-eye gaze, facial expression, body postures, and gestures—to regulate social interaction.

b. Failure to develop peer relationships appropriate to developmental level.

c. A lack of spontaneous seeking to share enjoyment, interests, or achievements with other people (e.g., by a lack of showing, bringing, or pointing out objects of interest).

d. Lack of social emotional reciprocity.

2. Qualitative impairments in communication as manifested by at least one of the following:

a. Delay in, or total lack of, the development of spoken language (not accompanied by an attempt to compensate through alternative modes of communication, such as gestures or mime).

b. In individuals with adequate speech, marked impairment in the ability to initiate or sustain a conversation with others.

c. Stereotyped and repetitive use of language or idiosyncratic language.

d. Lack of varied, spontaneous, make-believe play or social imitative play appropriate to developmental level.

3. Restricted, repetitive, and stereotyped pattern of behavior, interests, and activities, as manifested by at least one of the following:

a. Encompassing preoccupation with one or more stereotyped patterns of interest that is abnormal either in intensity or focus.

b. Apparently inflexible adherence to specific, nonfunctional routines or rituals.

c. Stereotyped and repetitive motor mannerisms (e.g., hand or finger flapping or twisting or complex whole-body movements).

d. Persistent preoccupation with parts of objects.

B. Delays or abnormal functioning in at least one of the following areas with onset before age 3 years:

1. Social interaction

2. Language as used in social communication

3. Symbolic or imaginative play

C. The disturbance is not better accounted for by Rett syndrome or childhood disintegrative disorder.

1. Qualitative impairment in social interaction (e.g., impairment in nonverbal behaviors, failure to develop peer relationships, lack of social or emotional reciprocity).

2. Qualitative impairments in communication (e.g., delay or lack of spoken language, inability to initiate or sustain a conversation, stereotyped and repetitive use of language, lack of varied make-believe play).

3. Restricted, repetitive, and stereotyped patterns of behavior, interests, and activities, including motor stereotypes and mannerisms.

D. The disturbance is not better accounted for by another specific pervasive developmental disorder or by schizophrenia.

From American Psychiatric Association: Diagnostic and statistical manual of mental disorders, ed 4 text revision, Washington, DC, 2000, American Psychiatric Association.

Table 5-2 Early Risk Indicators for Autism

Age	Behavior
Under age 12 mos	Little eye contact Lack of response to name being called. Seldom pointing with finger to show interest. Does not show object by sharing it with person.
12 mos.	No babbling. No gesturing, pointing, waving bye-bye.
16 mos.	No single words.
23 mos.	No two-word spontaneous phrases.
Any age	Loss of language or social skills at any age.

Brain Findings

Results from postmortem and imaging studies have implicated many major structures of the brain in autistic disorders, including cerebellum, corpus callosum, basal ganglia, brainstem, and portions of the limbic system (see Figure 5-1). Unusually high levels of specific proteins associated with brain development have been reported in children with autism (Nelson et al, 2001), and parts of the frontal lobe are thicker than normal; this region controls decision making and planning. Other research suggests that the mirror neuronal system involved in understanding another person’s actions is impaired in those with autism (Schumann and Amaral, 2006). This may result in loss of empathy and language skills, as well as the ability to learn by imitative skills. Neurons in the limbic system where emotions are processed are plentiful but are one third fewer in number than normal.

FIGURE 5-1 Major brain structures implicated in autism.

Redrawn from Strock M: Autism spectrum disorders, pervasive developmental disorders (NIH Pub No NIH-04-5511), National Institute of Mental Health, National Institute of Health, US Dept of Health and Human Services, Bethesda, Md, 2004 (available online): www.nimh.nih.gov/publicat/autism.cfm.

Another biological theory is that autism may be caused by faulty wiring in the brain, or underconnectivity, that makes it inefficient (Grossberg and Seidman, 2006; National Institutes of Health, 2004). The cerebellum’s ability to assist in making predictions of ensuing thoughts, emotions, and motor movements appears to be affected. Several studies have documented abnormalities in the Purkinje cells essential to the wiring of the cerebellum, including a significant decrease in their size and number (Fatemi et al, 2002; Kern, 2003). These cells inhibit the action of other neurons. Furthermore, the male autistic brain has fewer neurons in the amygdala compared to males without the disorder. Whether this occurs at birth or later as a degenerative process is unknown (Schumann and Amaral, 2006).

Data reveal a reduction of the amino acid tryptophan, a precursor to serotonin, which may interfere with serotonin synthesis. Serotonin is produced in the brain, thyroid gland, and gastrointestinal (GI) tract; and it affects mood, aggressive behavior, anxiety, memory, neural development, pain, repetitive behaviors, and sleep.