Psychology Essay

2017/8/2 PSY101 - Module 13.10

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M o d u le 1 3 .1 0 : D is o r d e r s in C h ild h o o d

M ost of the disorders w e have discussed so far are typically diagnosed in adulthood, although they can and som etim es do occur during

childhood. H ow ever, there are a group of conditions that, w hen present, are diagnosed early in childhood, often before the tim e a child enters

school. The D SM -5 separates the disorders of childhood and adolescence into three categories, as show n in Table 13.5.

Table 13.5 D isorders of Childhood and Adolescence

Internalizing D isorders Externalizing D isorders N eurodevelopm ental D isorders

Internalizing disorders involve

sym ptom s w here the em otions

are directed inw ard, or

internalized.

Exam ples of internalizing

disorders include:

School phobia

Separation anxiety disorder

Selective m utism

PTSD in childhood

D epressive disorders

N onsuicidal self-injury

Pediatric bipolar disorder

Attachm ent disorders:

Reactive attachm ent

disorder

D isinhibited social

engagem ent disorder

Externalizing disorders involve

sym ptom s that are distressing

and disturbing to others.

Exam ples of externalizing

disorders include:

D isruptive m ood

dysregulation disorder

O ppositional deﬁant

disorder

Conduct disorder

N eurodevelopm ental disorders

involve im paired developm ent of

the brain and nervous system .

Exam ples of neurodevelopm ental

disorders include:

Tic disorders:

Tourette's disorder

Attention

deﬁcit/hyperactivity

disorder (AD H D )

Autism spectrum disorders

Intellectual developm ent

disorder

Learning disorders

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Internalizing D isorders Externalizing D isorders N eurodevelopm ental D isorders

This section w ill focus on tw o conditions that are listed in the D SM -5 as neurodevelopm ental disorders, w hich involve developm ental problem s

in personal, social, academ ic, and intellectual functioning. These disorders are attention deﬁcit/ hyperactivity disorder and autism .

A tte n tio n D e fic it/ H y p e ra c tiv ity D is o rd e r

The sym ptom s of attention deﬁcit/hyperactivity disorder (AD H D ) w ere ﬁrst described by H ans H offm an in the 1920s. W hile taking care of his son

w hile his w ife w as in the hospital giving birth to a second child, H offm an noticed that the boy had trouble concentrating on his hom ew ork, had

a short attention span, and had to repeatedly go over easy hom ew ork to learn the m aterial. Later, it w as discovered that m any hyperactive

children— those w ho are ﬁdgety, restless, socially disruptive, and have trouble w ith im pulse control— also display short attention spans,

problem s w ith concentration, and distractibility. By the 1970s, it had becom e clear that m any children w ho display attention problem s often

also exhibit signs of hyperactivity. In recognition of such ﬁndings, the D SM -III (published in 1980) included a new disorder: attention deﬁcit

disorder w ith and w ithout hyperactivity, now know n as attention deﬁcit/hyperactivity disorder (AD H D ).

A child w ith AD H D show s a constant pattern of inattention and/or hyperactive and im pulsive behavior that interferes w ith norm al functioning.

Table 13.6 provides exam ples of inattention and hyperactivity.

Table 13.6 Sym ptom s of AD H D

Inattention M ay Be Characterized By... H yperactivity M ay Be Characterized By...

D iﬃ culty w ith and avoidance of tasks that

require sustained attention (such as

conversations or reading)

Failure to follow instructions (often resulting

in failure to com plete school w ork and other

duties)

D isorganization (diﬃ culty keeping things in

order, poor tim e m anagem ent, sloppy and

m essy w ork)

Lack of attention to detail

Becom ing easily distracted

Forgetfulness

Excessive m ovem ent, including:

Fidgeting or squirm ing

Leaving one's seat in situations w hen

rem aining seated is expected

H aving trouble sitting still (e.g., in a

restaurant)

Running about and clim bing on things

Blurting out responses before another

person's question or statem ent has been

com pleted

D iﬃ culty w aiting one's turn for som ething

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Frequently, the hyperactive child com es across as noisy and boisterous. The child's behavior is hasty, im pulsive, and seem s to occur w ithout

m uch forethought; these characteristics m ay explain w hy adolescents and young adults diagnosed w ith AD H D receive m ore traﬃ c tickets and

have m ore autom obile accidents than do others.

AD H D occurs in about 5% of children. O n the average, boys are 3 tim es m ore likely to have AD H D than are girls; how ever, such ﬁndings m ight

reﬂect the greater propensity of boys to engage in aggressive and antisocial behavior and thus incur a greater likelihood of being referred to

psychological clinics. Children w ith AD H D face severe academ ic and social challenges. Com pared to their non-AD H D counterparts, children w ith

AD H D have low er grades and standardized test scores and higher rates of expulsion, grade retention, and dropping out. They also are less w ell-

liked and m ore often rejected by their peers.

Previously, AD H D w as thought to fade aw ay by adolescence. H ow ever, longitudinal studies have suggested that AD H D is a chronic problem , one

that can persist into adolescence and adulthood. A recent study found that 29.3% of adults w ho had been diagnosed w ith AD H D decades earlier

still show ed sym ptom s. Som ew hat troubling, this study also reported that nearly 81% of those w hose AD H D persisted into adulthood had

experienced at least one other com orbid disorder, com pared to 47% of those w hose AD H D did not persist.

Life P ro b lem s fro m A D H D

Children diagnosed w ith AD H D face considerably w orse long-term outcom es than do those children w ho do not receive such a diagnosis. In one

investigation, 135 adults w ho had been identiﬁed as having AD H D sym ptom s in the 1970s w ere contacted decades later and interview ed.

Com pared to a control sam ple of 136 participants w ho had never been diagnosed w ith AD H D , those w ho w ere diagnosed as children:

had w orse educational attainm ent;

had low er socioeconom ic status;

held less prestigious occupational positions;

w ere m ore likely to be unem ployed;

m ade considerably less in salary;

scored w orse on a m easure of occupational functioning (indicating, for exam ple, low er job satisfaction, poorer w ork relationships, and

m ore ﬁrings);

scored w orse on a m easure of social functioning (indicating, for exam ple, few er friendships and less involvem ent in social activities);

w ere m ore likely to be divorced; and

w ere m ore likely to have non-alcohol-related substance abuse problem s.

Longitudinal studies also show that children diagnosed w ith AD H D are at higher risk for substance abuse problem s. O ne study reported that

childhood AD H D predicted later drinking problem s, daily sm oking, and use of illicit drugs. The risk of substance abuse problem s appears to be

even greater for those w ith AD H D w ho also exhibit antisocial tendencies.

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Fam ily and tw in studies indicate that genetics play a signiﬁcant role in the developm ent of AD H D . Burt (2009), in a review of 26 studies, reported

that the m edian rate of concordance for identical tw ins w as .66 (one study reported a rate of .90), w hereas the m edian concordance rate for

fraternal tw ins w as .20. This study also found that the m edian concordance rate for unrelated (adoptive) siblings w as .09; although this num ber

is sm all, it is greater than 0, thus suggesting that the environm ent m ay have at least som e inﬂuence. Another review of studies concluded that

the heritability of inattention and hyperactivity w ere 71% and 73% , respectively.

The speciﬁc genes involved in AD H D are thought to include at least tw o that are im portant in the regulation of the neurotransm itter dopam ine,

suggesting that dopam ine m ay be im portant in AD H D . Indeed, m edications used in the treatm ent of AD H D have stim ulant qualities and elevate

dopam ine activity. People w ith AD H D show less dopam ine activity in key regions of the brain, especially those associated w ith m otivation and

rew ard, w hich provides support to the theory that dopam ine deﬁcits m ay be a vital factor in the developm ent this disorder.

Brain im aging studies have show n that children w ith AD H D exhibit abnorm alities in their frontal lobes, an area in w hich dopam ine is in

abundance. Com pared to children w ithout AD H D , those w ith AD H D appear to have sm aller frontal lobe volum e, and they show less frontal lobe

activation w hen perform ing m ental tasks. Recall that one of the functions of the frontal lobes is to inhibit our behavior. Thus, abnorm alities in

this region m ay go a long w ay tow ard explaining the hyperactive, uncontrolled behavior of AD H D .

By the 1970s, m any had becom e aw are of the connection betw een nutritional factors and childhood behavior. At the tim e, m uch of the public

believed that hyperactivity w as caused by sugar and food additives, such as artiﬁcial coloring and ﬂavoring. U ndoubtedly, part of the appeal of

this hypothesis w as that it provided a sim ple explanation of (and treatm ent for) behavioral problem s in children. A statistical review of 16

studies, how ever, concluded that sugar consum ption has no effect at all on the behavioral and cognitive perform ance of children. Additionally,

although food additives have been show n to increase hyperactivity in non-AD H D children, the effect is rather sm all. N um erous studies,

how ever, have show n a signiﬁcant relationship betw een exposure to nicotine in cigarette sm oke during the prenatal period and AD H D . M aternal

sm oking during pregnancy is associated w ith the developm ent of m ore severe sym ptom s of the disorder.

Is AD H D caused by poor parenting? N ot likely. Rem em ber, the genetics studies discussed above suggested that the fam ily environm ent does not

seem to play m uch of a role in the developm ent of this disorder; if it did, w e w ould expect the concordance rates to be higher for fraternal

tw ins and adoptive siblings than has been dem onstrated. All things considered, the evidence seem s to point to the conclusion that AD H D is

triggered m ore by genetic and neurological factors and less by social or environm ental ones.

D ig D e e p e r

W hy Is the Prevalence Rate of AD H D Increasing?

M any people believe that the rates of AD H D have increased in recent years, and there is evidence to support this

contention. In a recent study, investigators found that the parent-reported prevalence of AD H D am ong children (4–17 years 2017/8/2 PSY101 - Module 13.10

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old) in the U nited States increased by 22% during a 4-year period, from 7.8% in 2003 to 9.5% in 2007. O ver tim e this increase

in parent-reported AD H D w as observed in all sociodem ographic groups and w as reﬂected by substantial increases in 12

states (Indiana, N orth Carolina, and Colorado w ere the top three). The increases w ere greatest for older teens (ages 15–17),

m ultiracial and H ispanic children, and children w ith a prim ary language other than English. Another investigation found that

from 1998–2000 through 2007–2009 the parent-reported prevalence of AD H D increased am ong U .S. children betw een the

ages of 5–17 years old, from 6.9% to 9.0% .

A m ajor w eakness of both studies w as that children w ere not actually given a form al diagnosis. Instead, parents w ere sim ply

asked w hether or not a doctor or other health-care provider had ever told them their child had AD H D ; the reported

prevalence rates thus m ay have been affected by the accuracy of parental m em ory. N evertheless, the ﬁndings from these

studies raise im portant questions concerning w hat appears to be a dem onstrable rise in the prevalence of AD H D . Although

the reasons underlying this apparent increase in the rates of AD H D over tim e are poorly understood and, at best,

speculative, several explanations are viable:

AD H D m ay be over-diagnosed by doctors w ho are too quick to m edicate children as a behavior treatm ent.

There is greater aw areness of AD H D now than in the past. N early everyone has heard of AD H D , and m ost parents and

teachers are aw are of its key sym ptom s. Thus, parents m ay be quick to take their children to a doctor if they believe

their child possesses these sym ptom s, or teachers m ay be m ore likely now than in the past to notice the sym ptom s

and refer the child for evaluation.

The use of com puters, video gam es, iPhones, and other electronic devices has becom e pervasive am ong children in

the early 21st century, and these devices could potentially shorten children's attentions spans. Thus, w hat m ight seem

like inattention to som e parents and teachers could sim ply reﬂect exposure to too m uch technology.

AD H D diagnostic criteria have changed over tim e.

A u tis m S p e c tru m D is o rd e r

A sem inal paper published in 1943 by psychiatrist Leo Kanner described an unusual neurodevelopm ental condition he observed in a group of

children. H e called this condition early infantile autism , and it w as characterized m ainly by an inability to form close em otional ties w ith others,

speech and language abnorm alities, repetitive behaviors, and an intolerance of m inor changes in the environm ent and in norm al routines. W hat

the D SM -5 refers to as autism spectrum disorder today, is a direct extension of Kanner's w ork.

Autism spectrum disorder is probably the m ost m isunderstood and puzzling of the neurodevelopm ental disorders. Children w ith this disorder

show signs of signiﬁcant disturbances in three m ain areas:

1. D eﬁcits in social interaction 2017/8/2 PSY101 - Module 13.10

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2. D eﬁcits in com m unication

3. Repetitive patterns of behavior or interests

These disturbances appear early in life and cause serious im pairm ents in functioning. The child w ith autism spectrum disorder m ight exhibit

deﬁcits in social interaction by not initiating conversations w ith other children or turning their head aw ay w hen spoken to. These children do

not m ake eye contact w ith others and seem to prefer playing alone rather than w ith others. In a certain sense, it is alm ost as though these

individuals live in a personal and isolated social w orld others are sim ply not privy to or able to penetrate.

Com m unication deﬁcits can range from a com plete lack of speech, to one w ord responses (e.g., saying "Yes" or "N o" w hen replying to questions

or statem ents that require additional elaboration), to echoed speech (e.g., parroting w hat another person says, either im m ediately or several

hours or even days later), to diﬃ culty m aintaining a conversation because of an inability to reciprocate others' com m ents. These deﬁcits can

also include problem s in using and understanding nonverbal cues (e.g., facial expressions, gestures, and postures) that facilitate norm al

com m unication.

Repetitive patterns of behavior or interests can be exhibited a num ber of w ays. The child m ight engage in stereotyped, repetitive m ovem ents

(rocking, head-banging, or repeatedly dropping an object and then picking it up), or she m ight show great distress at sm all changes in routine or

the environm ent. For exam ple, the child m ight throw a tem per tantrum if an object is not in its proper place or if a regularly-scheduled activity

is rescheduled. In som e cases, the person w ith autism spectrum disorder m ight show highly restricted and ﬁxated interests that appear to be

abnorm al in their intensity. For instance, the person m ight learn and m em orize every detail about som ething even though doing so serves no

apparent purpose.

Im portantly, autism spectrum disorder is not the sam e thing as intellectual disability, although these tw o conditions are often com orbid. The

D SM -5 speciﬁes that the sym ptom s of autism spectrum disorder are not caused or explained by intellectual disability.

Life P ro b lem s fro m A u tism S p ectru m D iso rd er

Autism spectrum disorder is referred to in everyday language as autism ; in fact, the disorder w as term ed "autistic disorder" in earlier editions

of the D SM , and its diagnostic criteria w ere m uch narrow er than those of autism spectrum disorder. The qualiﬁer "spectrum " in autism

spectrum disorder is used to indicate that individuals w ith the disorder can show a range, or spectrum , of sym ptom s that vary in their

m agnitude and severity: som e severe, others less severe.

The previous edition of the D SM included a diagnosis of Asperger's disorder, generally recognized as a less severe form of autistic disorder;

individuals diagnosed w ith Asperger's disorder w ere described as having average or high intelligence and a strong vocabulary, but exhibiting

im pairm ents in social interaction and social com m unication, such as talking only about their special interests. H ow ever, because research has

failed to dem onstrate that Asperger's disorder differs qualitatively from autistic disorder, the D SM -5 does not include it, w hich is prom pting

concerns am ong som e parents that their children m ay no longer be eligible for special services. 2017/8/2 PSY101 - Module 13.10

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Som e individuals w ith autism spectrum disorder, particularly those w ith better language and intellectual skills, can live and w ork independently

as adults. H ow ever, m ost do not because the sym ptom s rem ain suﬃ cient to cause serious im pairm ent in m any realm s of life.

Lin k to Le a rn in g vid e o

Select the follow ing link to open an instructive and poignant video highlighting severe autism .

Additionally, view the video below on Tem ple G randin: The w orld needs all kinds of m inds. D r. G randin w as diagnosed w ith

autism and is an autism activist. She earned a doctoral degree in anim al science.

The world needs all kinds of minds | T emple Gr andin

Currently, estim ates indicate that nearly 1 in 88 children in the U nited States has autism spectrum disorder; the disorder is 5 tim es m ore

com m on in boys (1 out of 54) than girls (1 out of 252). Rates of autism spectrum disorder have increased dram atically since the 1980s. For

exam ple, California saw an increase of 273% in reported cases from 1987 through 1998; betw een 2000 and 2008, the rate of autism diagnoses

in the U nited States increased 78% . Although it is diﬃ cult to interpret this increase, it is possible that the rise in prevalence is the result of the 2017/8/2 PSY101 - Module 13.10

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broadening of the diagnosis, increased efforts to identify cases in the com m unity, and greater aw areness and acceptance of the diagnosis. In

addition, m ental health professionals are now m ore know ledgeable about autism spectrum disorder and are better equipped to m ake the

diagnosis, even in subtle cases.

C au ses o f A u tism S p ectru m D iso rd er

Early theories of autism placed the blam e squarely on the shoulders of the child's parents, particularly the m other. H ow ever, no scientiﬁc

evidence exists supporting this claim . The exact causes of autism spectrum disorder rem ain unknow n despite m assive research efforts over the

last tw o decades.

Autism appears to be strongly inﬂuenced by genetics, as identical tw ins show concordance rates of 60% –90% , w hereas concordance rates for

fraternal tw ins and siblings are 5% –10% . M any different genes and gene m utations have been im plicated in autism . Am ong the genes involved

are those im portant in the form ation of synaptic circuits that facilitate com m unication betw een different areas of the brain. A num ber of

environm ental factors are also thought to be associated w ith increased risk for autism spectrum disorder, at least in part, because they

contribute to new m utations. These factors include exposure to pollutants, such as plant em issions and m ercury, urban versus rural residence,

and vitam in D deﬁciency.

C h ild V accin atio n s an d A u tism S p ectru m D iso rd er

In the late 1990s, a prestigious m edical journal published an article purportedly show ing that autism is triggered by the M M R (m easles, m um ps,

and rubella) vaccine. These ﬁndings w ere very controversial and drew a great deal of attention, sparking an international forum on w hether

children should be vaccinated. In a shocking turn of events, som e years later the article w as retracted by the journal that had published it after

accusations of fraud on the part of the lead researcher.

D espite the retraction, the reporting in popular m edia led to concerns about a possible link betw een vaccines and autism persisting. A recent

survey of parents, for exam ple, found that roughly a third of respondents expressed such a concern; and perhaps fearing that their children

w ould develop autism , m ore than 10% of parents of young children refuse or delay vaccinations. Som e parents of children w ith autism m ounted

a cam paign against scientists w ho refuted the vaccine-autism link. Even politicians and several w ell-know n celebrities w eighed in; for exam ple,

actress Jenny M cCarthy (w ho believed that a vaccination caused her son's autism ) co-authored a book on the m atter.

H ow ever, there is no scientiﬁc evidence that a link exists betw een autism and vaccinations. Indeed, a recent study com pared the vaccination

histories of 256 children w ith autism spectrum disorder w ith that of 752 control children across three tim e periods during their ﬁrst tw o years

of life (birth to 3 m onths, birth to 7 m onths, and birth to 2 years). At the tim e of the study, the children w ere betw een 6 and 13 years old, and

their prior vaccination records w ere obtained. Because vaccines contain im m unogens (substances that ﬁght infections), the investigators

exam ined m edical records to see how m any im m unogens children received to determ ine if those children w ho received m ore im m unogens

w ere at greater risk for developing autism spectrum disorder. The results of this study, a portion of w hich are show n in Figure 13.20, clearly 2017/8/2 PSY101 - Module 13.10

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dem onstrate that the quantity of im m unogens from vaccines received during the ﬁrst tw o years of life w ere not at all related to the

developm ent of autism spectrum disorder. There is not a relationship betw een vaccinations and autism spectrum disorders.

Figure 13.20 In term s of their exposure to im m unogens in vaccines, overall, there is not a signiﬁcant difference

between children with autism spectrum disorder and their age-m atched controls without the disorder

(DeStefano et al., 2013).

W hy does concern over vaccines and autism spectrum disorder persist? Since the proliferation of the Internet in the 1990s, parents have been

constantly bom barded w ith online inform ation that can becom e m agniﬁed and take on a life of its ow n. The enorm ous volum e of electronic

inform ation pertaining to autism spectrum disorder, com bined w ith how diﬃ cult it can be to grasp com plex scientiﬁc concepts, can m ake

separating good research from bad challenging. N otably, the study that fueled the controversy reported that 8 out of 12 children— according to

their parents— developed sym ptom s consistent w ith autism spectrum disorder shortly after receiving a vaccination. To conclude that vaccines

cause autism spectrum disorder on this basis, as m any did, is clearly incorrect for a num ber of reasons, not the least of w hich is because

correlation does not im ply causation, as you've learned. 2017/8/2 PSY101 - Module 13.10

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Additionally, as w as the case w ith diet and AD H D in the 1970s, the notion that autism spectrum disorder is caused by vaccinations is appealing

to som e because it provides a sim ple explanation for this condition. Like all disorders, how ever, there are no sim ple explanations for autism

spectrum disorder. Although the research discussed above has shed som e light on its causes, science is still a long w ay from a com plete

understanding of the disorder.

M odule 13.9