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Mental Health An Issue of Primary Care Clinics in Office
Practice The Clinics Internal Medicine 1st Edition S.
Manning Digital Instant Download
Author(s): S. Manning, R. Gillies
ISBN(s): 9781416051152, 1416051155
Edition: 1
File Details: PDF, 1.57 MB
Year: 2007
Language: english
 Prim Care Clin Office Pract
34 (2007) xi–xii

Preface

Ralph A. Gillies, PhD J. Sloan Manning, MD

Guest Editors

Primary care clinicians often provide continuity of care, emphasize pre-

vention, and address chronic illness with their patients. All these endeavors
require the active involvement of the patient in treatment planning and
adherence. An active and healthy therapeutic alliance that recognizes that
patients are the chief consumers of health care is essential in this regard.
This critical role in directing one’s health care can be either facilitated or
complicated by a patient’s emotional, cognitive, and behavioral strengths
or weaknesses (ie, mental health). It is widely recognized that patients
who have mental health concerns often present first to their primary care
physician, and most continue to receive treatment of their mental concerns
(eg, depression, anxiety) in primary care. This reality is compounded
because many health conditions that affect a patient’s level of functioning
(eg, chronic pain, diabetes, headaches) often have mental health comorbid-
ities that influence the course of illness and treatment.
Primary care clinicians are well positioned to identify and assist patients
who have mental health concerns. This central or de facto role in mental
health care, however, is complicated by factors that hinder the delivery of
evidenced-based care that is optimally integrated into the clinical process
as a whole. Among the obstacles to such a rational approach to health care
are an undue focus on acute rather than chronic health issues; lack of spe-
cific training in the recognition, assessment, and management of mental dis-
tress or illness; and financial obstacles (mental health carve-outs and other
obstacles) that prevent the effective collaboration among diverse health pro-
fessionals necessary to implement and manage effective treatment.
0095-4543/07/$ - see front matter Ó 2007 Elsevier Inc. All rights reserved.
doi:10.1016/j.pop.2007.06.002 primarycare.theclinics.com
xii PREFACE

The articles in this issue present the latest information on mental health
problems commonly seen in primary care. Each article offers practical sug-
gestions on how clinicians can address these problems to improve overall
care. We hope that the information contained here will be embraced by
readers and enrich insight into mental distress and dysfunction as a biopsy-
chosocial phenomenon. It is hoped that someday the fragmentation
currently evidenced in health care delivery that hinders integrated and
comprehensive approaches will give way to systems that honor mental
health as fundamental to health.

Ralph A. Gillies, PhD

HB-3041 1120 15th St.
Department of Family Medicine
Medical College of Georgia
Augusta, GA 30912-3500, USA
E-mail address: [email protected]

J. Sloan Manning, MD
PrimeCare of Hickory Branch
501 Hickory Branch Road
Greensboro, NC 27409, USA
Mood Disorders Clinic
Moses Cone Family Practice Residency
1125 N. Church Street
Greensboro, NC 27401, USA
E-mail address: [email protected]
 Prim Care Clin Office Pract
34 (2007) 445–473

Attention Deficit/Hyperactivity
Disorder in Adults
Shannon B. Moss, PhD*, Rajasree Nair, MD,
Anthony Vallarino, DO, Scott Wang, MD
Baylor Family Medicine Residency at Garland, 601 Clara Barton Boulevard,
Suite 340, Garland, TX 75042, USA

Attention deficit/hyperactivity disorder (ADHD), once considered to be

a disorder only of childhood, has gained recognition as a legitimate disorder
among adults. As professionals’ awareness of this disorder and its concom-
itant media attention have increased, more adults have begun to identify
themselves as having symptoms of adult ADHD, leading them to present
to their primary care providers. Many of these providers, however, may
be ill-equipped to identify, diagnose, and treat the symptoms of adult
ADHD. Reasons for primary care physicians’ lack of comfort in managing
ADHD symptoms in adults may be multifactorial, and include high rates of
self-diagnosis, lack of guidelines for evaluation and management, higher
rates of comorbid psychiatric and substance use disorders, and the need
for treatment with drugs of potential abuse [1,2].
The purpose of this article is to present information on the prevalence,
clinical presentation and associated features, diagnosis, and treatment of
adults who have ADHD, in order to provide primary care physicians with
the necessary tools for managing these patients.

Prevalence
Prevalence estimates of ADHD in children range between 2% and 18%
in community studies. A recent Centers for Disease Control report from the
National Survey of Children’s Health (NSCH-2003) indicated that, in 2003,
approximately 4.4 million children aged 4 to 17 years had a history of
ADHD [3]. Data regarding the persistence of ADHD into adulthood

* Corresponding author.
E-mail address: [email protected] (S.B. Moss).

0095-4543/07/$ - see front matter Ó 2007 Elsevier Inc. All rights reserved.
doi:10.1016/j.pop.2007.05.005 primarycare.theclinics.com
446 MOSS et al

(ie, ADHD symptoms among adults previously diagnosed with childhood

ADHD) vary somewhat by study, with reports ranging from 1% to 36%
[4–7]. This variation is likely caused by variation in methodology (eg, pro-
spective reports versus meta-analysis) and diagnostic criteria used; however,
there is some agreement amongst studies that the number of adults who con-
tinue to be functionally impaired because of ADHD symptoms is greater
than the number of adults meeting full ADHD diagnostic criteria. For
example, though one study found 8% of adults who had been diagnosed
with childhood ADHD continued to meet Diagnostic and Statistical Man-
ual of Mental Disorders, Third Edition, Revised (DSM-III-R) criteria for
ADHD in adulthood, an additional 3% reported continued impairment
due to sub-threshold ADHD symptoms [7]. Similar results were reported
in a later study using Diagnostic and Statistical Manual of Mental Disor-
ders, Fourth Edition (DSM-IV) criteria. In a study of ADHD symptom per-
sistence into adulthood, Faraone and colleagues [8] found a persistence rate
of 15% at age 25 when full DSM-IV criteria were applied; however, persis-
tence was estimated to be between 40% and 60% when including ADHD in
partial remission. Extrapolating from this data and a childhood prevalence
of 8%, the study authors estimate adult ADHD prevalence at age 25 to be
1% for the full criteria and an additional 2% for cases in partial remission
[8]. This finding is somewhat lower than more recent research suggesting
prevalence rates of 4.4% [9]. Further, it appears that those who have
more severe childhood ADHD, defined as having both attentional and
hyperactive symptoms, are at greater risk for persistence than those who
have attentional or hyperactive symptoms alone [6]. As in children, adult
ADHD appears to be more commonly identified in males, with reported
male-to-female ratios ranging from 1.7:1 to 2.2:1 [10,11].

Pathophysiology
The pathophysiology of adult ADHD is not well- understood, but is con-
sidered to be multifactorial, consisting of genetic, environmental, and neuro-
biologic influences. Medications used to treat ADHD influence the
dopaminergic and noradrenergic systems of the nervous system, which
may give some insight into abnormalities in neurologic pathways and the
potential for genetic locus identification. With the emerging trends in genetic
evidence, it is increasingly likely that the pathophysiology of ADHD is com-
plex, involving the action of multiple genes and environmental factors.

Family studies
ADHD is considered a heritable disorder, with approximately 70% her-
itability, one of the highest among psychiatric disorders [12,13]. In recent
years, many family, twin, and molecular genetic studies have shown a strong
probability that genetic factors influence the development of ADHD.
 ATTENTION DEFICIT HYPERACTIVITY DISORDER IN ADULTS 447

Children of parents who have ADHD have up to a sevenfold increase in

their likelihood of developing ADHD when compared with children of
non-ADHD parents. Although it is important to understand that to date
no single gene has been implicated as the sole cause of ADHD, there is re-
search to support multiple chromosomal sites that may influence the suscep-
tibility of developing ADHD. Specifically, the dopamine receptor gene
(DRD4) and the dopamine transporter gene (DAT) have been associated
with ADHD [13]. A recent adoption study reinforced the genetic link, find-
ing that adoptive relatives of ADHD-affected children had lower rates of
ADHD and other associated conditions than biological relatives of ADHD
patients [14]. In a study of monozygotic twins, behavioral discordance
was evident at age 2, and low birth weight and delayed motor development
were significant markers for development of ADHD [15]. Neuro-imaging of
high-risk concordant twins has yielded significant differences in the affected
areas of prefrontal lobes compared with discordant twins, further confirm-
ing a genetic etiology for the development of ADHD [16].

Environmental factors
Although all environmental factors required for emergence of ADHD are
not known, several have been implicated, including physical or toxic as-
saults on the brain and psychological stressors [17]. Prenatal exposure to
nicotine has been identified as a significant risk factor for the development
of ADHD [15,18–20]. Consumption of alcohol and caffeine and maternal
stress during pregnancy have also been implicated in a multitude of studies;
however, a recent meta-analysis failed to identify the significance of these
factors, mainly because of contradictory and inconsistent findings among
studies [20]. Further, exposure to lead, low birth weight, single parenthood,
and low parental education levels and socioeconomic status have all been
implicated in the etiology of this complex disorder [15,19,21].

Neurobiologic factors
Several structural abnormalities in the brain have been documented in
patients who have ADHD. In 2003, Sowell and colleagues [22] found
a statistically significant correlation between reduced brain volume and
ADHD when compared with non-ADHD peers. Specifically, the prefrontal
lobe, frontal cortex, cerebellum, and subcortical structures were found to be
affected. Further, different areas of the brain were found to be affected in
monozygotic discordant and concordant twins, accounting for genetic and
environmental factors as etiology for these different structural changes
[16]. The concordant high-risk twins showed reduction in brain volume in
orbitofrontal subdivision and posterior corpus callosum, whereas the discor-
dant pairs had volume reduction in the right inferior dorsolateral prefrontal
cortex.
448 MOSS et al

Diagnostic criteria
Diagnostic and Statistical Manual of Mental Disorders criteria
The Diagnostic and Statistical Manual of Mental Disorders, Fourth
Edition, Text Revision (DSM-IV-TR) criteria for ADHD diagnosis were
originally developed for the diagnosis of childhood ADHD. These criteria
require either six symptoms of inattention (ie, failure to attend to detail, dif-
ficulty sustaining attention, not listening when spoken to, failure to follow
through on tasks, organizational deficits, difficulty concentrating, losing
items, distractibility, forgetfulness) or hyperactivity/impulsivity (ie, fidget-
ing, difficulty staying seated, excessive running/climbing, difficulty playing
quietly, acts as though ‘‘driven by a motor,’’ excessive talking, difficulty
awaiting one’s turn, interrupting frequently, prematurely responding to
questions) be present for a diagnosis of ADHD. In addition, the symptoms
must result in significant impairment observable in at least two settings, and
must be present before age 7. Individuals may be diagnosed with one of the
three subtypes: predominantly hyperactive-impulsive type, predominantly
inattentive type, and combined type [23].
The use of the DSM diagnostic criteria has been problematic in adults.
One of the most significant concerns is the lack of adults in the field trials
used to establish the diagnostic criteria for ADHD. In fact, before DSM-
IV, there was no indication in the diagnostic criteria that ADHD could per-
sist into adulthood; as a result, many of the criteria are not age-appropriate
for adults (eg, ‘‘runs or climbs excessively’’) [24]. Though some effort has
been made to adjust the criteria to include behaviors more appropriate
for adults through the addition of words such as ‘‘work’’ and ‘‘workplace,’’
further studies are still needed to determine if the symptoms of ADHD in
childhood are representative of those in adulthood [25,26]. For instance,
one study found that several of the DSM criteria did not adequately discrim-
inate between ADHD and non-ADHD adults; criteria found to discriminate
between the groups included fidgeting, difficulty remaining seated, difficulty
awaiting one’s turn, and engaging in potentially physically harmful behav-
iors [11].
It is also unclear if the minimum of six criteria for children would result
in under-diagnosis when applied to adults, because many ADHD adults
learn to compensate for their deficiencies by modifying their environments,
relying on others, or choosing careers and lifestyles that more easily accom-
modate their symptoms [25,27]. Research regarding the validity of minimum
criteria for diagnosis is inconsistent to date [28]. One of the most recent stud-
ies indicated significant symptom decline with age, particularly with regard
to hyperactivity and impulsivity [29]. The study authors caution that,
though ADHD adults may not meet full diagnostic criteria, they may con-
tinue to experience significant functional impairment because of their resid-
ual symptoms and thus warrant treatment.
 ATTENTION DEFICIT HYPERACTIVITY DISORDER IN ADULTS 449

Another concern regarding DSM criteria is the age of onset requirement.

Adults presenting with ADHD symptoms may have difficulty with the ret-
rospective recall required to meet this criterion and rarely present with ele-
mentary school documentation or a family member who can report on their
behaviors before age 7 [25,30,31]. The validity of the age of onset criterion
has been questioned in prior research, which indicated that a large number
of ADHD children did not experience symptoms until after age 7. This was
particularly true for those who have ADHD predominantly inattentive type,
of whom 75% did not have symptoms until after 9 years of age [32]. This
and other research have led some to suggest that the age of onset criterion
be modified or eliminated [25,33].

Utah criteria
A second set of criteria often used for adult ADHD diagnosis is the Utah
Criteria [34,35]. The Utah Criteria require that childhood and adult criteria
be met for a diagnosis of ADHD in adults. Childhood criteria include
a childhood diagnosis per the DSM-IV, hyperactivity, attention deficits,
and one of the following: school behavior problems, impulsivity, over-excit-
ability, and temper outbursts. Adult criteria include motor hyperactivity and
attention deficits, and two of the following: labile affect, temper outbursts,
excessive emotional reactivity, disorganization, impulsivity, and associated
features of ADHD. Per the Utah Criteria, adult ADHD may only be diag-
nosed in the absence of other psychiatric disorders.
One of the most frequent criticisms of the Utah Criteria is its exclusion of
inattentive symptoms. This is of particular concern given previous research
indicating slower decline of inattentive symptoms as compared with hyper-
activity and impulsiveness as ADHD patients age [29]. The inclusion of af-
fective symptoms is also of concern given the many mood disorders that
may be characterized by labile mood [25]. Further, requiring that other psy-
chiatric disorders must be absent for ADHD diagnosis would likely result in
the under-diagnosis of many symptomatic adults given the high rates of co-
morbidity of ADHD with other psychiatric diagnoses [36,37].

Clinical presentation
With increased public awareness of adult ADHD comes increased self-re-
ferral and self-diagnosis in the general population [2]. Many adults begin to
suspect they suffer from ADHD during the process of having their children
evaluated and treated for ADHD. Whereas children are more likely to be
referred for evaluation because of the negative impact their behavior has
on others, adults are more likely to seek treatment because of the negative
ramifications of their behavior on their own lives, though not all may iden-
tify their symptoms as indicative of ADHD [38]. Faraone and colleagues
identified the primary presenting complaints of adults diagnosed with
450 MOSS et al

ADHD, comparing those who suspected themselves of having ADHD and

those who did not. Interestingly, both groups presented with similar symp-
toms, the most common being difficulty concentrating, disorganization, fail-
ure to complete projects, inattentiveness, and poor school performance.
Affective complaints included anxiety, increased temper, and depression [2].
Other affective complaints, such as hostility and emotional lability, may
also prompt adults who have ADHD to seek treatment [11,39,40]. Cognitive
complaints, including poor concentration and impaired memory, are com-
mon in these patients as well [1,34,37,39,41–43]. Poor academic and work
performance may result in part from poor organizational, prioritization
and time management skills, and lack of attention to details or over-focus
on unimportant details [1,34,37,39–43]. Not surprisingly, these patients also
report making a high rate of careless errors and experiencing impatience,
low frustration tolerance, and impulsivity [37–39,41–43]. Low self-esteem
often accompanies these complaints [40] (Box 1).

Associated features and impact

In trying to understand adult ADHD more fully, it is worthwhile to ex-
amine some of the areas affected by this condition, because functional and

Box 1. Clinical presentations of adult ADHD

Poor concentration
Fidgeting
Difficulty remaining seated
Impulsivity (eg, difficulty awaiting one’s turn)
General disorganization
Failure to complete projects
Inattention
Poor school and work performance
Poor time management
Poor anger management
Cognitive impairment
Anxiety/depression
Hyperfocused
Substance abuse
Hostility
Emotional lability
Low self-esteem
Problems in family and relationships (divorce, separation)
Increased rate of motor vehicle accidents

Adapted from Refs. [1,2,11,37–43].

 ATTENTION DEFICIT HYPERACTIVITY DISORDER IN ADULTS 451

psychosocial deficits present substantial difficulties in various aspects of the

lives of ADHD adults.

Academic and work performance

The aforementioned deficits may lead ADHD adults to complain of poor
work performance or academic underachievement, which in school may be
accompanied by more grade retention, higher drop-out rates, lower grade
point averages, increase probation rates, and poor college adjustment
[12,44–47]. Additionally, 20% of ADHD patients may have auditory
processing deficits [12]. At work, symptoms may result in higher rates of
unemployment, frequent job changes, lower occupational status, and more
work absences, which in turn results in lower socioeconomic status
[7,11,34,37,39,42,45,48–51].

Social interactions
Strained relationships with spouses, other family members, friends, and
coworkers may result from a lack of understanding of the disorder and frus-
tration with the symptoms [11,35,37,39]. In the workplace, inattention, pro-
crastination, and attention to insignificant detail can lead to frequent
frustration and strained relationships. For example, the inability of adults
who have ADHD to manage time appropriately and needing to enlist co-
workers to assist in task completion can cause workplace conflict, as can dif-
ficulty monitoring and inhibiting their own behavior (eg, interrupting,
excessive talking) and engaging in socially inappropriate behavior (eg, ex-
plosive outbursts, making rude comments, engaging in phone conversations
during meetings) [1,2,12,38]. Their interpersonal difficulties may contribute
to conflicts in social acceptance, with ADHD patients exhibiting poorer so-
cial skills and self-esteem than their non-ADHD peers [47,52–54].
Family and romantic relationships can be strained as well, as demon-
strated by higher rates of separation and divorce among ADHD patients
and lower rates of marital, family, and social life satisfaction [11,45,54].
Common complaints include not listening to or interrupting others, inatten-
tiveness to others’ emotional needs, disorganization in managing household
responsibilities (eg, finances), and poor communication and problem-solv-
ing [55]. The presence of an ADHD child can compound the family strain.
The chance of an adult ADHD patient having children who share their di-
agnosis is approximately 50%, which may result in a chaotic household
when symptoms are not well-controlled [2].

Driving
Adults who have ADHD exhibit a significantly higher rate of traffic acci-
dents and greater rates of damage in such accidents as compared with non-
ADHD adults. Barkley and colleagues found that adolescents who had
452 MOSS et al

ADHD were four times more likely to have had a motor vehicle accident than
their non-ADHD peers [56]. Their data also found that ADHD adolescents
were more likely to have driven an automobile before being of legal driving
age, less likely to employ sound driving habits, more likely to have had their
licenses suspended or revoked, and more likely to have received repeated traf-
fic citations (mostly for speeding). These driving problems are reportedly
apparent to others as well as the patients themselves [11,57].

Substance abuse
ADHD patients are more likely to develop substance abuse, and at an
earlier age, than those who did not have ADHD [58,59]. The risks of sub-
stance abuse are further increased by the presence of comorbid bipolar or
conduct disorders [7]. Several reasons for the elevated substance abuse rates
have been proposed, including self-medication of ADHD symptoms and
gaining social acceptance [60]. Unfortunately, ADHD adults have lower re-
mission rates and longer periods of substance abuse than their non-ADHD
peers [26,61].

Health care costs

It is interesting to note that people who have ADHD have higher health
care costs than non-ADHD individuals. A comparison of 9-year median
medical costs between the two groups indicated ADHD medical costs as
$4306 versus non-ADHD medical costs of $1944 [62]. Similar findings
were reported by Secnik and colleagues [49], who found significantly greater
outpatient, inpatient, prescription, and total health care costs among
ADHD individuals as compared with non-ADHD individuals. Higher rates
of substance abuse treatments and increased treatment frequency because of
noncompliance with medical recommendations may contribute to these
health care costs [52]. Further, health care costs of ADHD patients’ family
members are also higher, which may be caused by elevated stress, depres-
sion, and substance abuse found in these families [52,63].

Assessment
Whereas primary care physicians often recognize and treat ADHD in
children, they may experience difficulties in identifying and diagnosing the
disorder in adults. As of this writing, there are no tests diagnostic for
ADHD; however, a thorough history accompanied by questionnaire and
checklist data can be beneficial in clarifying the diagnosis. Neuropsycholog-
ical assessment may also help elucidate patients’ deficits and provide target
areas for treatment. It should also be noted that, in addition to the ap-
proaches below, patients should be screened for other psychiatric disorders,
given their high rates of comorbidity with ADHD.
 ATTENTION DEFICIT HYPERACTIVITY DISORDER IN ADULTS 453

Interviews
The first step in conducting an ADHD assessment is a thorough inter-
view. Patients should be queried about ADHD symptoms, both past and
present. Murphy and Schachar [64] recommend asking specific questions
rather than open-ended questions to improve the accuracy of retrospectively
reported symptoms. Patients should be asked to provide an educational and
occupational history, including conduct and disciplinary actions, to deter-
mine if symptoms (eg, losing homework, difficulty staying in one’s seat,
excessive talking, difficulty playing quietly) of ADHD were present in child-
hood, and to discern the functional impact of the symptoms on performance
[1,65]. When possible, collateral information should be obtained; this may
be done by way of reviewing school records or seeking input from patients’
family members [1,65]. Input from each of these sources can provide infor-
mation on the presence of ADHD symptoms during childhood as discussed
above; further, family members may be able to provide information on cur-
rent symptoms and functioning. Questioning patients about their perfor-
mance in a variety of situations during the prior week, the level of effort
required to function, and coping strategies used may also provide valuable
information regarding functional impairment [40,65,66]. Given the heritabil-
ity of ADHD, assessing family history of ADHD may provide insight into
the patient’s presenting symptoms [42]. Although not necessary for obtain-
ing a history of ADHD symptoms, diagnostic interviews are available to
assist with the interview process, including the Brown Attention Deficit
Disorder (ADD) Scale, Conners’ Adult ADHD Diagnostic Interview for
DSM-IV, and the Diagnostic Interview Schedule [40].

Rating scales
Several rating scales are available to assist with adult ADHD diagnosis.
Research indicates significant positive correlations between ratings of adults
who have suspected ADHD and their significant others [11,41,67]; however,
they should not be used alone as diagnostic tools because of unacceptable
rates of false positives [26,68].
Many of the available rating scales use Likert-type scales to assess symp-
toms, have acceptable psychometric properties, can be administered in
5 minutes or less, and require no additional training of the administrator
(eg, Brown ADD Scale for Adults, Conner’s Adult ADHD Rating Scale,
Adult ADHD Self Report Scale, ADHD Rating Scale-IV) [26,69,70]. Scales
such as Connor’s Adult ADHD Rating Scales can be administered to
a spouse or parent, and thus can assist in gathering collaterals’ views of pa-
tients’ symptoms. The Wender Utah Rating Scale, based on the aforemen-
tioned Utah Criteria, takes 10 minutes to administer and is also commonly
used [35]; however, criticism of this scale is similar to that of the Utah cri-
teria on which it is based, with research indicating that it measures affective
and conduct disorders not specific to ADHD and lacks field testing [71,72].
454 MOSS et al

Neuropsychological assessment
Compared with non-ADHD adults, ADHD adults exhibit significant def-
icits in a variety of functional domains and on specific neuropsychological
tests. For example, meta-analyses of neuropsychological performance differ-
ences between ADHD and non-ADHD adults have revealed deficits in
verbal memory, focused and sustained attention, behavioral inhibition, and
abstract problem solving among ADHD adults [73,74]. Reviews of the liter-
ature suggest that specific neuropsychological assessments found to discrim-
inate between the two groups include continuous performance tasks, the
Stroop task, Trail Making Tasks, the Controlled Word Association Test,
and Weschler intelligence measures, with most effect sizes being moderate
[75,76]. The Digit Symbol subtest of the Weschler intelligence scale appears
to be the most effective subtest for identifying ADHD adults, particularly
when used in combination with the Arithmetic subtest [75–77]. Both the
Digit Symbol and Arithmetic subtests are measures of working memory,
which suggests that other assessments of working memory may also be sen-
sitive to ADHD in adults.
As with rating scales, there are no neuropsychological assessments to
date that are diagnostic of adult ADHD. Despite this, neuropsychological
assessment can assist patients with legal services, such as seeking accommo-
dations through the Americans with Disabilities Act, and targeting deficient
areas for treatment and vocational counseling [66,78].

Laboratory and radiological tests

Routine laboratory and radiological tests are useful for differentiating
ADHD from common medical conditions that can mimic symptoms of
ADHD. Common laboratory tests include complete blood count, metabolic
profile, including liver function tests, and thyroid function studies. Serum
lead level and heavy metal screening should be undertaken if history warrants.
Serum vitamin B12 level should be obtained in patients who have anemia, nu-
tritional deficiencies, and cognitive impairment. Electroencephalogram and
computed tomography of the head should be performed in patients who
have a recent history of trauma to the head or history suggestive of seizure dis-
orders. In patients who have concurrent sleep disorder symptoms, polysom-
nography should be undertaken to rule out obstructive sleep apnea (OSA)
as the etiology for ADHD symptoms [1,79].

Comorbidity
Psychiatric comorbidity is significantly higher in ADHD adults as com-
pared with non-ADHD controls, and may often be the primary concern
with which patients present to their primary care providers [36,37]. Bieder-
man and colleagues [53] found that 44% of a sample of ADHD adults had
 ATTENTION DEFICIT HYPERACTIVITY DISORDER IN ADULTS 455

at least one comorbid psychiatric diagnosis. Mood disorders are among the
most commonly reported comorbidities in the literature, and occur at signif-
icantly higher rates in ADHD adults as compared with controls [11,49,80,81].
Rates of major depressive disorder among adult ADHD samples range from
11.5% to 53.5%, and dysthymia rates range from 11.5% to 25% [9,41,82–
84]. Rates of bipolar disorder and cyclothymia are reported to be 19.4% and
25%, respectively [9,82]. The high rate of mood disorders in this population
may be caused in part by the difficulties of living with the symptoms of
ADHD; however, it is not possible to attribute causality, because the cause
for each disorder is likely multifactorial [39]. It is important that comorbid
psychopathology be identified, given that failure to identify bipolar illness
or misattributing mood symptoms solely to ADHD may lead to iatrogenic
worsening of a bipolar disorder treated with antidepressants or
psychostimulants.
Anxiety disorders are also commonly reported at a greater rate among
ADHD adults than controls [49,53,80,81]. For example, rates of generalized
anxiety disorder range from 8% to 53% among ADHD adults [9,82,83].
Similarly, agoraphobia, panic disorder, post-traumatic stress disorder, so-
cial phobia, and specific phobia have been noted to occur at higher rates
among ADHD adults than non-ADHD peers [9,54].
Antisocial disorder, conduct disorder, and oppositional defiant disorder
among ADHD adults have also been frequently investigated. The majority
of research to date indicates a higher rate of each of these disorders among
ADHD adults [7,11,41,49,53,81]. One study suggests that the prevalence of
comorbid antisocial personality disorder in ADHD adults is tenfold com-
pared with non-ADHD peers [7]. Both conduct disorder and antisocial per-
sonality disorder have been found to be more common in adult ADHD
males than females [54].
Rates of substance use have also been found to occur at significantly
higher rates among ADHD adults versus non-ADHD adults, with one study
reporting a five times greater risk [7,9,11,41,49,53,81]. Identified substances
of abuse have included alcohol, cannabis, and amphetamines [84]. Some
gender differences have been identified, with males exhibiting significantly
greater rates of alcohol abuse than females [54]. One potential explanation
for the elevated rates of substance use is self-medication of untreated
ADHD symptoms [43]. It is also possible that impulsivity characteristic of
ADHD contributes to higher rates of abuse in this population.
Other disorders identified more frequently among ADHD adults include
enuresis, stuttering, speech and language disorders, and tics [53,54].

Differential diagnosis
ADHD should be considered in the differential of any condition present-
ing with complaints of inattention, fatigue, and hyperactivity, as well as in
456 MOSS et al

patients presenting with depression, anxiety, substance abuse or bipolar

disorder [2,53] (Table 1).

Medical diagnoses
A complete history and physical examination should be conducted in pa-
tients presenting with symptoms of ADHD. A medical diagnosis should be
suspected particularly in patients with recent onset of symptoms. The most
common disorders that may present with symptoms similar to those of
ADHD include thyroid disorders (hypo- and hyperthyroidism), seizure dis-
orders (petit mal or partial complex), drug interactions, hepatic diseases,
lead toxicity, post-head injury and hearing deficits [1]. Sleep-disordered
breathing, OSA, has been found to present with sleep disturbances, inatten-
tion, and cognitive impairment, which resolve with treatment for OSA.
Hence, OSA should be considered in the differential of patients who have
ADHD and who have symptoms of snoring, excessive daytime somnolence,
inattention, and memory difficulties [79].

Psychiatric diagnoses
Given the frequency of comorbid psychiatric diagnoses with ADHD and
its symptoms overlapping with other psychiatric diagnoses (eg, poor concen-
tration, restlessness, talkativeness), conducting a thorough history and
symptom evaluation is paramount. Mood disorders share many symptoms
with ADHD. For example, both major depressive disorder and ADHD
share symptoms of decreased concentration, attention, and memory; how-
ever, unlike ADHD, major depressive disorder is marked by neuro-vegeta-
tive symptoms (eg, anhedonia and appetite disturbance) [1,48]. Questioning
the patient about the course of symptoms to determine if cognitive symp-
toms occur in the absence of mood symptoms can also clarify the diagnosis
[66]. Bipolar disorder and ADHD also share common symptoms, including

Table 1
Differential diagnosis of adult ADHD
Medical Psychiatric
Thyroid disorders (hypo/hyperthyroidism) Major depression
Head trauma Bipolar disorders
Obstructive sleep apnea Generalized anxiety disorder
Seizure disorders Substance abuse and dependence
(petit mal or partial complex)
Vitamin B12 deficiency Personality disorders (antisocial and borderline)
Drug interactions
Heavy metal poisoning
Hearing deficits
Liver disease
Lead toxicity
Adapted from Refs. [2,79,85].
 ATTENTION DEFICIT HYPERACTIVITY DISORDER IN ADULTS 457

hyperactivity, decreased attention, and mood lability [1]. Excessive spend-

ing, delusions or other psychotic symptoms, grandiosity, racing thoughts,
and decreased need for sleep help differentiate ADHD from mania or hypo-
mania. Anxiety disorders (eg, generalized anxiety disorder) share attention
and concentration deficits with ADHD, but excessive worry and somatic
symptoms seen in these disorders are not characteristic of ADHD [1,66].
Personality disorders must also be differentiated from ADHD. Borderline
personality disorder, like ADHD, is characterized by impulsivity, mood
lability, and hostility [48]; however, these symptoms in ADHD patients
are typically intermittent, shorter in duration, and less severe. Further,
ADHD is not characterized by the dichotomous thinking, abandonment
fears, or self-injurious behavior seen in borderline personality disorder [48].
Antisocial personality disorder shares impulsivity and affective lability with
ADHD; however, an arrest history and lack of insight into and remorse
regarding the behaviors seen in antisocial personality disorder can assist in
differentiating the two disorders [1,85] (Table 2).

Treatment
The mainstay of adult ADHD treatment includes pharmacological inter-
ventions, behavioral interventions, or a combination of both, with the goals
of symptom remission and return to full social functioning. Studies in chil-
dren indicate that combined treatment results in greater symptom improve-
ment and is superior to pharmacotherapy alone, especially in improving
non-ADHD symptoms and functional impairment [86]. Multiple other stud-
ies comparing cognitive-behavioral therapy to pharmacological manage-
ment indicate that cognitive-behavioral therapy alone may be insufficient,
and that combined treatment is more effective than either treatment alone
in control of symptoms and improving functional status [80,83,87].

Table 2
Differentiating ADHD from other psychiatric diagnoses
Psychiatric diagnosis Distinguishing characteristics
Major depressive disorder Neuro-vegetative symptoms
(eg, anhedonia, appetite disturbance)
Bipolar disorder Excessive spending
Delusions
Insomnia
Anxiety disorders Excessive worry
Somatic complaints
Borderline personality disorder Dichotomous thinking
Abandonment fears
Self-injurious behavior
Antisocial personality disorder Arrest history
Lack of insight into and remorse for behaviors
Adapted from Refs. [1,48,66,85].
458 MOSS et al

Pharmacological
As in childhood ADHD, medications, especially central nervous system
stimulants, have shown to significantly improve adult ADHD symptoms
[88–91]. Much of the evidence for adult ADHD treatment is based on treat-
ment efficacy in children and adolescents; long-term data are lacking in the
treatment of adult ADHD. The presence of psychiatric and medical comor-
bidities and substance abuse in adults who have ADHD makes drug choices
difficult. Patients should be counseled that medications provide only symp-
tomatic relief, and that concurrent psychotherapy and counseling are
recommended to acquire necessary organizational and social skills for
independent adult functioning.
Although stimulants are effective in ADHD treatment, physicians’ con-
cerns about the use of controlled substances with abuse potential play a sig-
nificant role in the choice of medications. In a recent survey, 38% of
physicians responded that they prefer prescribing a nonstimulant medica-
tion, and 58% preferred prescribing a noncontrolled medication without ev-
idence of abuse potential [92]. In 2003, atomoxetine, a nonstimulant, was the
first drug to receive United States Food and Drug Administration (USFDA)
approval for the treatment of adult ADHD.

Stimulants
Stimulants are typically the first-line agents used in the treatment of adult
ADHD [89–91]. Patients who have moderate to severe impairment in two
different settings (occupational, social, academic, and family) should be con-
sidered for treatment with stimulants [89]. Methylphenidate (MPH), dextro-
amphetamines (DEX), mixed amphetamine salts (levoamphetamine and
dextroamphetamine) (AMP) and pemoline are the stimulants commonly
used in the treatment of adult ADHD [89]. They act by blocking the
reuptake of dopamine and norepinephrine, resulting in their accumulation
in the presynaptic cleft. Amphetamines also increase these neurotrans-
mitter levels in the presynaptic cleft by direct release of dopamine and
norepinephrine.
MPH and amphetamines are the most commonly used agents in the treat-
ment of adult ADHD, with no significant differences in efficacy, side-effect
profiles, and response rates [87,89]. Pemoline, a weak stimulant, has been
withdrawn from the market amid concerns of increased risk of hepatotoxic-
ity [93]. Earlier studies in adults showed a lesser stimulant response rate in
adults compared with children, with rates ranging from 25% to 78% [88,94,95].
This difference in clinical response could be caused by the diagnostic criteria
used, insufficient doses of medication, and the presence of comorbid psychi-
atric disorders. Recent studies with higher doses of stimulants (1.1 mg/kg/
day of MPH) have shown more than 75% therapeutic response in ADHD
symptoms [96–98]. Similar results were described by Weisler and colleagues
[98] using mixed amphetamine salts.
 ATTENTION DEFICIT HYPERACTIVITY DISORDER IN ADULTS 459

Stimulants have an immediate onset of action, and extended-release formu-

lations should be used whenever possible to increase compliance, provide lon-
ger duration of symptom relief, and decrease the potential for abuse. Some of
these are Concerta (McNeil Pediatrics, Fort Washington, Pennsylvania),
Adderrall XR (Shire, Wayne, Pennsylvania), and Ritalin LA (Novartis, East
Hanover, New Jersey). Patients should be initiated on the lowest dose avail-
able and titrated up until symptom relief is obtained with least side effects.
Patients who fail to have a response to one group should be tried on the other
before initiating second line treatments [89]. Most patients on stimulant
therapy take ‘‘drug holidays’’ on weekends and on vacation, mainly from con-
cerns of adverse effects; however, there are no significant data on the efficacy of
this practice, and it should not be advocated to patients [2,89].
In addition to relief of ADHD symptoms, stimulants have been shown to
improve self-esteem, cognition, and social and family functioning [89]. They
also have shown improvement on comorbid anxiety, conduct, and tic disor-
ders [89]. Further, stimulants have a protective effect against substance
abuse and improve driving skills [99,100]. A recent meta-analysis of six stud-
ies (two with follow-up in adolescence and four in young adulthood) showed
a 1.9-fold reduction in risk for substance use disorders and later drug and
alcohol use disorders in youths who were treated with stimulants compared
with youths who did not receive pharmacotherapy for ADHD [99].

Nonstimulants
Nonstimulants are typically used to treat patients who do not tolerate
stimulants, or who have comorbid psychiatric or medical conditions in
which stimulants are contraindicated [89]. These agents can be used in com-
bination with stimulants to treat comorbid psychiatric disorders and may
help in decreasing the stimulant dose required. Commonly used medications
include atomoxetine, tricyclic antidepressants (TCAs), and buproprion.
Atomoxetine, a norepinephrine reuptake inhibitor, is the first drug to re-
ceive USFDA approval for the treatment of adult ADHD. Earlier studies of
atomoxetine in children have shown similar efficacy and tolerability com-
pared with stimulants [87,90]. Two large, multicenter, randomized control
trials of 10 weeks duration using atomoxetine indicated reduction of inatten-
tive and hyperactive and impulsive symptoms, with less than 10% discontin-
uation rate caused by adverse effects [101]. It has been increasingly used in
patients who have comorbid anxiety disorders, substance use disorders, and
tics. A use study for treatment initiation with atomoxetine indicated that
patients were more likely to receive atomoxetine than a stimulant if they
had a psychiatric diagnosis or alcohol dependence [102]. Atomoxetine has
the added benefit of not being a controlled substance and having no abuse
potential.
Most of the evidence on TCA efficacy for ADHD is based on child and
adolescent studies. For example, in one study, desipramine at a target dose
of 200 mg yielded a 68% response rate over placebo in a 6-week period
460 MOSS et al

[103]. Most common adverse effects include cardiac side effects, increased
seizure risk, dry mouth, and constipation.
Buproprion is an antidepressant with dopamine and noradrenergic ago-
nist effects. It has been shown to be efficacious as a second-line agent in
the treatment of ADHD, especially in patients who have comorbid bipolar
disorder, depression, or substance abuse [104]. In a 6-week trial comparing
patients receiving sustained-release bupropion (up to 200 mg twice a day) to
patients receiving placebo, bupropion treatment was associated with a 42%
improvement in ADHD symptoms, compared with 24% reduction in pla-
cebo [105].
Other rarely used nonstimulant medications include mono amino oxidase
inhibitors, clonidine, and cholinergic agents with structural similarities to
nicotine (ABT-418) [106]. Clondine may also be used as an adjunct to stim-
ulants in the treatment of comorbid aggression and insomnia [89].

Adverse effects
Most common side effects of stimulants are mild and include distur-
bances of sleep, appetite and mood, weight loss, nervousness, irritability, ag-
itation, and confusion [87,89,96]. Most of these side effects can be effectively
managed by giving medications with meals, lowering the dose, changing the
timing of administration to earlier in the day, or using long-acting prepara-
tions [89]. Stimulants are contraindicated mainly in patients who have pre-
vious history of sensitivity, glaucoma, hyperthyroidism, hypertension, and
acute psychosis. Further, they should be used with caution in patients
who have a prior history of abuse of stimulants [89]. MPH and bupropion
may cause seizures in adults who have seizure disorders; hence, these pa-
tients should be stabilized with anti-seizure medications before using higher
doses of medications [89].
Stimulant and nonstimulant medications may also be associated with in-
creased rates of cardiovascular side effects, such as palpitation, tachycardia,
and hypertension, because of their pressor and chronotropic effects; hence,
close monitoring of vitals should be done before the initiation of treatment
and at periodic intervals [96,107–109]. In 2006, the USFDA issued a warning
on all stimulants, prompted by sudden unexpected deaths in children and
adolescents using stimulants between 1999 and 2003 [110]. They recommend
against the use of stimulants in children or adolescents who have known
serious structural cardiac abnormalities, cardiomyopathy, heart rhythm
abnormalities, or other serious cardiac disorders. Further, the American
Heart Association suggests careful evaluation for cardiac disease before ini-
tiation of stimulant therapy in adults. They recommend careful evaluation
of patients’ family histories for sudden death at less than 40 years of age,
long QT Syndrome, cardiac arrhythmias, hypertrophic cardiomyopathy
and personal history of heart disease, symptoms of palpitation, dizziness,
or syncope [111]. A basal electrocardiogram before the initiation of medica-
tions (especially TCAs) may be useful in monitoring of these patients.
 ATTENTION DEFICIT HYPERACTIVITY DISORDER IN ADULTS 461

In 2006, the USFDA also issued a warning on all stimulants and atom-
oxetine because of the potential for psychotic or manic symptom develop-
ment, especially in children and adolescents. Atomoxetine may also
increase suicidal thoughts and thus carries an additional USFDA warning
[112]. Hence, patients should be closely monitored for behavior change, psy-
chosis, and suicidal ideation while on treatment with these medications.

Nonpharmacological
Numerous strategies for assisting ADHD adults in managing their symp-
toms have been suggested anecdotally; however, there is a paucity of re-
search investigating the benefits of nonpharmacologic interventions [113].
The most frequently researched interventions are cognitive-behavioral, of-
fered both in individual and group formats, and with and without pharma-
cological treatment. Cognitive-behavioral therapy includes identification
and modification of patients’ maladaptive thought patterns and instruction
in behavioral modifications to minimize functional impairment [114]. Data
indicate that cognitive-behavioral therapy results in statistically significant
improvements in ADHD symptoms, functional impairment, depression,
anxiety, hopelessness, health status, and self-esteem [80,83,115,116].
Skills typically taught during cognitive-behavioral therapy include
psychoeducation about ADHD symptoms and medications, strategies for
improving motivation, concentration (eg, minimizing distractions, self-mon-
itoring), listening, impulsivity, organization and time management (eg, using
a calendar, making lists; working during personally optimal times of day),
emotional regulation, self-esteem, problem-solving skills, and mindfulness
[1,37,80,115,116]. Additional specific recommendations are listed in Box 2.
Other strategies recommended to assist ADHD adults include couples/fam-
ily therapy and support groups, such as the Attention Deficit Disorder
Association (www.add.org) and Children and Adults with Attention Deficit
Disorder (www.chadd.org) [34,117,118].

Special considerations
Primary care/psychiatry
Adult ADHD is often under-diagnosed. In one study, only 25% of adults
who had ADHD were diagnosed in childhood, even though retrospective as-
sessments supported the presence of childhood ADHD. One potential expla-
nation for under-diagnosis of adult ADHD is primary care physicians’ lack
of knowledge of ADHD presentation in adults. Rates of adult ADHD iden-
tification are significantly higher among psychiatric settings as compared
with primary care settings (52% versus 27%), and ADHD is recognized
at younger ages in primary care settings [2]. Education and training may
be necessary to overcome this discrepancy [2].
462 MOSS et al

Box 2. Strategies for management of ADHD symptoms

Behavioral strategies
 Minimize distractions (eg, no clutter on desk, no working near
windows)
 Develop a daily routine
 Use a calendar to schedule activities
 Make ‘‘to do’’ lists, and keep them in sight
 Keep note pads available to write down things to remember
 Use a filing system
 Take time each evening to prepare for the next day
 Work at personally optimal times of day
 Break large tasks down into smaller tasks and create respective
deadlines
 Prioritize tasks
 Consider and determine pros and cons of multiple options
before acting
 Delegate tasks when necessary
 Ask friends or family to remind of dates and deadlines
 Take a ‘‘time out’’ when becoming upset or frustrated
 Make multiple sets of keys
Other beneficial strategies
 Educate patient about ADHD symptoms and medications
 Anger management
 Mindfulness training (eg, meditation)
 Encourage patient to reward self for positive changes and
symptom management

Adapted from Refs. [2,37,38,80,114,115,117–119].

Substance abuse
ADHD symptoms, such as poor impulse control, may present unique
challenges to treatment, especially in patients with concurrent substance
abuse [60,120,121]. Early treatment of ADHD, with concomitant manage-
ment of substance abuse, may result in increased rates of compliance and
abstinence [60,120,121]. Stimulants should be used with caution in patients
who have history of stimulant abuse or dependence [89]. Recent studies of
long-acting stimulants in patients who had ADHD and history of substance
abuse yield positive effects, with no significant increase in substance abuse
[120,121]. In patients who have concurrent substance abuse, atomexitine,
desipramine, and bupropion may be preferable to methylphenidate because
they are associated with a decreased risk of abuse [26]. When treating
 ATTENTION DEFICIT HYPERACTIVITY DISORDER IN ADULTS 463

patients who have concurrent substance abuse, increased vigilance is advised

to include compliance evaluation, random drug screens, and coordination
with addiction counselors [122].

Pregnancy and lactation

There is little known about the effect of ADHD treatment on pregnancy
and lactation. Patients who have ADHD have 38% more unplanned preg-
nancies, and more and more young adults who have ADHD present to pri-
mary care physicians for preconception counseling [12]. All stimulants and
nonstimulants except bupropion are pregnancy category C (ie, inability to
rule out risk); however, there is no indication for therapeutic termination
of pregnancy for patients who become pregnant on ADHD medication.
Further, abrupt withdrawal of psychotropic medications upon diagnosis
of pregnancy may result in unfavorable physiological effects and possible re-
emergence of symptoms [123]. Therefore, each patient should be properly
counseled regarding risks and benefits of treatment, and patients wishing
to discontinue or change medications should be closely monitored.
A recent evaluation by the National Toxicology Program Center for the
Evaluation of Risks to Human Reproduction concluded that there are insuf-
ficient data associating methylphenidate therapy in pregnant women and
pregnancy loss and reproductive effects in humans [124]; however, a similar
study of amphetamines and methamphetamine [125] revealed potential neu-
robehavioral alterations, low birth weight, and shortened gestation. A con-
founding effect of other potential drug use could not be ruled out in these
patients. The effects of stimulant and nonstimulant medications on lactation
are still unknown, and amphetamines and methylphenidate are contraindi-
cated by American Academy of Pediatrics during lactation [126] (Table 3).

Pearls
Adult patients who present with cognitive complaints (including inatten-
tion), mood complaints, and functional impairment in school, work,
and interpersonal relationships may be exhibiting ADHD symptoms.
Assessment of adult ADHD should include educational and occupational
history, collateral information (both from significant others and school
records when available), and assessment of prior and current func-
tional impairment. Diagnostic interviews and rating scales may facili-
tate this process.
Neuropsychological testing may be helpful for treatment planning, voca-
tional counseling, and assisting patients with legal services.
Assessment for adult ADHD should include assessment of mood, anxi-
ety, and personality disorders, and substance abuse caused by high
rates of comorbidity and symptom overlap.
 464
Table 3
Treatment of adult ADHD
Duration
Medication of action Dose Side effects Comments
Methylphenidate (MPH)
Short-acting: (Ritalin, Methylin) 3–5 h 10–80 mg/day Insomnia Titrate dose weekly by 5–10 mg.
Loss of appetite Monitor pulse rate and Blood pressure.
Weight loss Pregnancy risk: category Ca
Headache Contraindicated in lactation.
Nervousness

MOSS
Intermediate-acting: (Ritalin 3–8 h 20–80 mg/day Increase in
SR, Methylin ER, Metadate ER) pulse rate and

et al
blood pressure
Long-acting: (Metadate CD, 8–12 h 10–80 mg/day
Ritalin LA)
Concerta 10–12 h 18–72 mg/day
Daytrana (patch) 10–12 h 10–60 mg/day patch Patch on for 9 hours and off for 15 h.
Dextroamphetamine (DEX)
Short-acting (Dexedrine) 4–6 h 5–45 mg/day Insomnia Titrate by 5 mg per week.
Loss of Pregnancy category C
appetite Monitor blood pressure and
Weight loss pulse.
Headache
Nervousness
Increase in
pulse rate and
blood pressure
Long-acting (Dexedrine spansules) 6–8 h 5–45 mg/day
Mixed amphetamine salts (AMP)
Adderall 4–6 h 5–40 mg/day Insomnia Pregnancy category C
Loss of Monitor blood pressure and
appetite pulse.
Weight loss Dosing in the morning to
Headache reduce sleep disturbances.
Adderall XR 8–10 h 5–60 mg/day Nervousness Titrate by 2.5–5 mg per week.
Palpitation,

ATTENTION DEFICIT HYPERACTIVITY DISORDER IN ADULTS

tachycardia,
elevation of
blood
pressure
Bupropion 12 h 37.5–450 mg/day Insomnia Pregnancy category B
(Wellbutrin) Increased risk Effect on lactation unknown.
of seizures Contraindicated in patients
Headache with seizures and bulimia.
Response after 4–5 weeks
Atomoxetine 24 h 40–80 mg/day Sleep Pregnancy category C
(Strattera) disturbance Effect on lactation unknown.
Nausea Should be discontinued in
Vomiting patients who develop jaundice
Dyspepsia or have elevated liver function tests.
Abdominal
pain
Headache
Changes in
blood
pressure and
pulse rate
Jaundice and
hepatotoxicity

465
(continued on next page)
 466
Table 3 (continued )
Duration
Medication of action Dose Side effects Comments
Tricyclic antidepressants (TCA)
Desipramine or imipramine 24 h 10–150 mg/day Dry mouth Monitor therapeutic levels.
Constipation Response after 4 weeks
Changes in Monitor ECG before and after
pulse rate, stabilization on treatment.
blood pressure

MOSS
Conduction
abnormalities

et al
Nortriptyline (Pamelor) 10–150 mg/day
Pemoline 37.5–75 mg/day Insomnia Pregnancy Category B
(Cyclert) Weight loss Effect on lactation unknown.
Decreased Withdrawn from the market because of
appetite hepatotoxicity.
Headaches Monitor liver function tests.
Nervousness
Hepatotoxicity
a
FDA use in pregnancy ratings: category A, no risk indicated in controlled studies; B, no evidence of risk in humans; C, inability to rule out risk;
D, positive evidence of risk; X, contraindicated in pregnancy.
Data from Refs. [2,88,89].
 ATTENTION DEFICIT HYPERACTIVITY DISORDER IN ADULTS 467

A retrospective diagnosis of childhood ADHD should be investigated

in all adult patients diagnosed with adult ADHD, and may be facili-
tated by open-ended questions and structured interviews.
Prenatal tobacco exposure has been documented to be a significant risk
factor in the development of ADHD.
Stimulants (methylphenidate and amphetamine) are the first-line agents
in the treatment of adult ADHD.
Stimulants and nonstimulant medications used in the treatment of
ADHD may cause changes in pulse rate and blood pressure. Hence,
vitals should be monitored before the starting of medications and at
periodic intervals.
Stimulants should not be used in patients who have underlying cardiac
disorders, or in patients who have positive family history of sudden
cardiac death, other severe cardiac arrhythmias, and structural
abnormalities.
Atomoxetine and stimulants can induce mania, psychosis, and suicidal
ideations; thus, ADHD patients should be closely monitored for
behavioral changes.

Summary
The diagnosis and treatment of adult ADHD can be daunting for primary
care providers. One factor contributing to this is the lack of criteria based on
field studies with adults, rather than extrapolated from childhood symptom
data; however, recent research has provided indications that, though the
symptom presentation may change somewhat over time, many of the charac-
teristics of adult ADHD are similar to those manifested in childhood. Pro-
viders’ awareness of these changes in presentation and familiarity with
strategies that can be easily implemented in the primary care setting are nec-
essary to insure that symptomatic adults are identified. Further, providers
must be aware that symptoms commonly attributed to mood, anxiety, and
personality disorders may be indicative of adult ADHD, and therefore war-
rant careful evaluation. By obtaining a childhood history, collateral informa-
tion on childhood and current functioning (when possible), and assessing
current symptoms, providers will be able to identify these patients and provide
treatment, including facilitating interventions to minimize patients’ func-
tional impairment (eg, psychological intervention, vocational counseling).

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 Prim Care Clin Office Pract
34 (2007) 475–504

Recent Advances in the Understanding

and Treatment of Anxiety Disorders
Steven L. Shearer, PhDa,b,*
a
Residency Training Program in Family Medicine,
Department of Family Medicine, Franklin Square Hospital Center,
9101 Franklin Square Drive, Suite 205, Baltimore, MD 21237, USA
b
Anxiety and Stress Disorders Institute of Maryland,
6525 North Charles Street, Towson, MD 21204, USA

Anxiety is ubiquitous. Everyone experiences episodic or situational anxi-

ety symptoms. Diagnosable anxiety disorders are the most common mental
health disorders, more prevalent than both affective and substance abuse
disorders. In the general population, 1-year prevalence for any criterion-
based anxiety disorder is 16% [1], and lifetime prevalence is 28.8% [2]. Com-
pared with median age of onset among mood disorders (age 30), median age
of onset among anxiety disorders is much younger (age 11) [2].
Anxiety disorders can adversely affect quality of life, mobility, education,
employment, social functioning, health care, and physical well being.
Although the directional sequence of comorbidity varies, a primary anxiety
disorder often contributes to secondary depression or substance abuse. The
presence of an anxiety disorder is significantly associated with thyroid disease,
respiratory disease, gastrointestinal disease, arthritis, migraine headaches,
and allergic conditions, and, this comorbidity with physical conditions is
significantly associated with poor quality of life and disability [3].
Anxiety disorders impose a societal economic burden comparable with the
cost of depression, with 54% of the cost expended for nonpsychiatric medical
care of physical complaints [4]. Individuals with anxiety disorders incur two-
fold the primary care costs and overall health care costs compared with those
without anxiety disorders, even when adjusted for medical comorbidities [5].
Among patients presenting to their primary care physician with a new
complaint, point prevalence of anxiety disorders was 16.4% [6] Lifetime
prevalence rates for anxiety disorders in primary care settings range from

* Department of Family Medicine, Franklin Square Hospital Center, 9101 Franklin

Square Drive, Suite 205, Baltimore, MD 21237.
E-mail address: [email protected]

0095-4543/07/$ - see front matter Ó 2007 Elsevier Inc. All rights reserved.
doi:10.1016/j.pop.2007.05.002 primarycare.theclinics.com
476 SHEARER

14% to 30% [7]. Most people suffering from anxiety disorders seek treatment
in primary care settings, and, most present with generalized anxiety disorder
(GAD), panic disorder, and posttraumatic stress disorder (PTSD) [7].
Although anxiety disorders are prevalent, costly, and disruptive to
patients’ lives, rates of detection and of evidence-based treatment remain
low in primary care settings [7]. Surveyed family physicians report that
they are much more knowledgeable about effective treatments for depres-
sion (88%) compared with panic disorder (17%) and generalized anxiety
disorder (13%) [8]. Nearly half of primary care patients with anxiety disor-
ders remain untreated; however, when treated, the care received from
primary care physicians and psychiatrists is similar [9].
This review summarizes the phenomenology, diagnosis, and evidence-
based treatment of panic disorder, specific phobia, social anxiety disorder,
generalized anxiety disorder, and obsessive–compulsive disorder (OCD).
(Posttraumatic stress disorder [PTSD] is reviewed in the article by Nakell in
this issue.) Given the brevity of this review, preference is given to literature
from the last 4 years that has contributed to better understanding and treatment
of the anxiety disorders.

Panic disorder and agoraphobia

Prevalence
Lifetime prevalence is 22.7% for isolated panic attacks, 3.7% for panic
disorder, and 1.1% for panic disorder with agoraphobia (ie, anxiety or
avoidance related to situations in which escape may be difficult or in which
help may not be available) [10]. Although agoraphobia especially is associ-
ated with substantial severity, impairment, and comorbidity, even isolated
panic attacks are associated with meaningful role impairment [10]. Other re-
cent data suggest higher lifetime prevalence for panic disorder (5.1%) and
lower lifetime prevalence for agoraphobia (0.17%) but confirm that the
presence of agoraphobia reflects a more severe variant of panic disorder
[11]. Individuals with panic disorder coupled with agoraphobia were more
likely to seek treatment and had earlier ages at onset and first treatment,
longer episodes, and more severe disability, impairment, panic symptom-
atology, and Axis I and II comorbidity than those having panic disorder
without agoraphobia [11].

Etiology and perpetuation

Despite the obvious burst of sympathetic arousal, no specific biological
dysfunction seems to underlie most panic attacks. Isolated panic attacks
are common; panic disorder is much less common. Susceptibility to panic
disorder is moderately heritable, but etiology is multifactorial [1], including
adverse early experiences that may sensitize an individual to feelings of
being overwhelmed or loss of control.
 TREATMENT OF ANXIETY DISORDERS 477

Components of the fear-conditioning process and temperamental ‘‘anx-

iety sensitivity’’ (ie, fearful response to anxiety symptoms) both seem to
aggregate in families. Panicky arousal and compelling symptoms that
occur in the context of such preexisting vulnerabilities may initiate a vi-
cious cycle. In short, fearful self-monitoring and efforts to control or
avoid panicky arousal that is deemed dangerous only escalate panic
proneness.

Clinical presentation and impact

In the fourth edition of the Diagnostic and Statistical Manual of Mental
Disorders (DSM-IV-TR), panic disorder is defined by discreet episodes of
marked autonomic arousal (eg, tachycardia, palpitations, sweating, trem-
bling, shortness of breath, chest pain, dizziness) that are accompanied by
catastrophic thinking (eg, fear of fainting, going crazy, losing control, dying)
and are not directly caused by a substance or medical condition. Episodic,
acute panic is the defining feature, but the ongoing impact of panic disorder
is more a function of worry about and avoidance of anxious arousal and/or
physical symptoms between panic attacks. Panic attacks can occur in any of
the anxiety disorders; however, fear of panicky arousal that feels dangerous,
unprovoked, and unexplained, plus the consequences of that fear, are what
define panic disorder.
When, in about half of cases, panic disorder includes attribution of pos-
sible panic to particular places or situations (eg, driving, crowds, flying, en-
closed places), often with significant avoidance, it is designated as panic
disorder with agoraphobia. The DSM-IV-TR portrays agoraphobia as
a complication of panic disorder; however, recent data suggest that such
a one-way causal relationship between spontaneous panic attacks and ago-
raphobia is incorrect [12].
Panic attacks, unlike ordinary anxiety, can feel truly life threatening.
Therefore, sufferers usually first seek care in emergency or primary care set-
tings and may be quite persistent in seeking medical consultations despite
reassurance. They often are consumed by daily ‘‘what if?’’ worries related
to the perceived dangerousness of panic attacks (eg, ‘‘What if I pass out
while driving? What if my doctor is wrong and this is cardiac? What if I
can’t sleep at all? What if this happens while I’m sitting in church?’’). If there
is prominent depersonalization or derealization during panic, fear usually
focuses on ‘‘going crazy’’ or ‘‘losing control.’’
A person may also experience being awakened from sound sleep by ter-
rifying panic. Nocturnal panic attacks are non–rapid eye movement events
that are distinguished from sleep terrors, sleep apnea, nightmares, or dream-
induced arousals and are not linked with differences in sleep architecture.
Nocturnal panic attacks are common among patients with panic disorder,
with 44% to 71% reporting at least 1 experience [13]. In a randomized, con-
trolled trial, cognitive–behavioral treatment effectively reduced panic
478 SHEARER

disorder severity, frequency of daytime and nocturnal panic attacks, and

worry about nocturnal panic [14].
In primary care, patients typically present with unexplained symptoms or
pain rather than direct complaints about panic attacks. It often is difficult to
distinguish whether the presenting symptoms are a contributor to panic, a cor-
relate of panic, or a compounding factor in the experience of panic. Various
reports have suggested that panic disorder frequently contributes to noncar-
diac chest pain (40%), palpitations (45%), unexplained faintness (20%), irri-
table bowel syndrome (40%), and unexplained vertigo and dizziness (20%) [1].
Untreated panic disorder often is a chronically recurring, stress-sensitive
disorder with a waxing and waning course marked by residual symptoms
such as agoraphobia and somatization even during periods when panic at-
tacks have ceased [15]. It is linked with higher medical utilization, medical co-
morbidity (eg, asthma, irritable bowel syndrome), poorer subjective physical
and emotional health, depression, substance abuse, higher likelihood of sui-
cide attempts, lower educational achievement, higher likelihood of unemploy-
ment and low work productivity, impaired social and marital functioning, and
financial dependency that cannot be attributed to comorbid disorders [16].

Assessment
Screening with the five-question Anxiety and Depression Detector’s two
panic disorder questions (ie, In the past 3 months: ‘‘Did you ever have a spell
or an attack when all of a sudden you felt frightened, anxious or very uneasy?’’
‘‘Would you say that you have been bothered by ‘nerves’ or feeling anxious or
on edge?’’) yields high sensitivity (.92) and modest specificity (.74) [17].
A positive screening result should prompt further questioning informed
by the DSM-IV-TR criteria, a review of recent stressors, screening for affec-
tive disorders and substance abuse, and inquiry about the perceived danger
in panic. There are many other instruments for assessing panic disorder and
agoraphobia [18], but most are too time consuming or redundant for routine
use in primary care.
Assessment must include consideration of medical conditions commonly
associated with anxiety or panic (eg, paroxysmal atrial tachycardia, supra-
ventricular tachycardia, asthma, hyperthyroidism, Meniere’s). Most pa-
tients with panic disorder will not have positive findings that explain their
panic attacks. However, panic disorder has been linked with a twofold in-
crease in risk for coronary heart disease even when relevant confounding
factors are controlled [19].

Treatment
Both pharmacologic and nonpharmacologic treatments have an evidence
base of established effectiveness for panic disorder. Limitations of these ev-
idence bases and evidence regarding alternative treatments will be summa-
rized in another section below.
 TREATMENT OF ANXIETY DISORDERS 479

Selective serotonin reuptake inhibitors (SSRIs) are the drug of choice for
treatment of panic disorder with no indication of differential efficacy within
this class. Many placebo-controlled, randomized trials, meta-analyses and
systematic reviews have reported medium to large effect sizes for SSRIs rel-
ative to placebo for periods up to 1 year [20].
Data also support comparable efficacy of the extended-release form of
the serotonin/norepinephrine reuptake inhibitor (SNRI), venlafaxine, in
panic disorder [21]. Although other second-generation antidepressants
may also be helpful, supporting evidence is modest. Use of bupropion in
panic disorder usually is discouraged because evidence supporting its use
is lacking, and many patients report that it is uncomfortably activating or
worsens panic attacks. Both the tricyclic antidepressants and monoamine
oxidase inhibitors have shown effectiveness in panic disorder but have
been relegated to second-line use.
One report suggests that benzodiazepines prevail as the most common
treatment for panic disorder in primary care despite treatment guidelines
to the contrary [22]. However, a more recent report suggests that SSRIs/
SNRIs are most commonly used for anxiety disorders by both primary
care physicians and psychiatrists and that primary care physicians are less
likely than psychiatrists to prescribe benzodiazepines [9]. Benzodiazepines
are considered second-line or adjunctive treatment because of failure to ad-
dress frequent comorbid depression, tolerance or abuse potential, effects on
driving, and possible deleterious effects on cognitive–behavioral treatment
(CBT), especially with as-needed use [22]. Benzodiazepines, usually in ex-
tended-release or longer-acting forms, are sometimes administered concom-
itant to the first few weeks of an SSRI trial. Neither buspirone nor beta
blockers have shown effectiveness for panic disorder in controlled trials [20].
Both initiating and discontinuing drug treatment of panic disorder often
are complicated by side effects that can mimic or augment symptoms of
panic attacks. Beginning antidepressants at half (or less) of the usual start-
ing dose, gradual increases, and repeated reassurance usually are recommen-
ded. Because of its short half-life, paroxetine is especially prone to causing
both common (eg, dizziness, nausea, lethargy, headache) and uncommon
(eg, anxiety, tremor, confusion, paresthesias) discontinuation symptoms.
Among SSRI-treated patients with panic disorder, 45% experienced a dis-
continuation syndrome, which subsided within a month in all but three pa-
tients who had been taking paroxetine for a long time. Discontinuation
syndromes appeared to be fairly common even when performed with slow
tapering and during clinical remission [23].
Approximately 40% of patients with panic disorder cannot tolerate or do
not respond to SSRI or venlafaxine trials of adequate dose and duration.
Many patients who do not respond to medication trials will respond to
CBT; and, many patients who do not respond to CBT will respond to medica-
tion trials. The addition of CBT to imipramine treatment of panic disorder was
associated with less severe side effects and fewer dropouts as a result of
480 SHEARER

perceived side effects than treatment with imipramine alone [24]. It should be
noted also that physician experience (ie, years since residency training) has
been linked with medication response in panic disorder even in drug trials [25].
Many patients seem to benefit from the combination of medication and
CBT in the short term, but combined treatment actually may be associated
with worse outcome in panic disorder compared with CBT alone [26]. A re-
cent Cochrane Database Review suggests that either combined therapy or
psychotherapy alone may be chosen as first-line treatment for panic disorder
with or without agoraphobia, depending on patient preference [27].
In more than 24 controlled trials, CBT has shown effectiveness for panic
disorder that is at least comparable to pharmacologic treatment and may
have effects of greater duration when treatment ends. True remission of
panic disorder with high end-state functioning occurs in 50% to 70% of pa-
tients who receive CBT [28].
The cognitive component of CBT usually begins with patient education
(eg, symptoms, autonomic nervous system, fear conditioning, generaliza-
tion) and gentle challenging of the distorted assumptions and catastrophic
thinking that perpetuate the vicious cycle of panic disorder. The belief
that panic is dangerous must be addressed repeatedly, often with encourage-
ment of relevant self-talk (eg, ‘‘This feels dangerous but it’s not’’). Patients
need very specific reassurance, (eg, ‘‘No, you will not faint, have a heart at-
tack, go crazy, or lose control because of panic’’).
Avoidance of bodily arousal or places associated with past panic attacks
is gradually reframed not as a solution but as the primary perpetuator of
panic disorder. Every effort is made to encourage patients’ willingness to ac-
cept panic and, eventually, to seek panic to defuse its power over them. This
process usually requires time, patience, and repetition, often over a period of
months.
The behavioral component of CBT emphasizes exposure to panicky
arousal with the goal of gradual habituation to such cues. If there is no ag-
oraphobia, interoceptive (ie, focused on stimuli within the body) exposure
may focus on voluntary provocation of bodily symptoms associated with
panic, (eg, running stairs to recreate tachycardia, hyperventilating to recre-
ate shortness of breath, spinning to recreate dizziness, staring in the mirror
to recreate depersonalization). With agoraphobia, in vivo exposure may fo-
cus on graduated exposure to places or situations associated with panic, (eg,
driving, riding the subway, shopping, elevators).
Many patients do not have access to specialist-delivered CBT because of
financial means, insurance barriers, or geographic location. Books based on
CBT principles are available for physician-assisted, self-directed treatment
[29]. Web-based, self-directed CBT for panic disorder is evolving, but there
are data suggesting that it may be an effective alternative [30]. Many physi-
cians recommend aerobic exercise, relaxation exercises, diaphragmatic
breathing exercises, or yoga for patients with panic disorder. Although there
is a limited evidence base for judging the effectiveness of such techniques,
 TREATMENT OF ANXIETY DISORDERS 481

their likely amelioration of bodily sensitization (ie, lowered threshold for

panic and hyperreactivity to bodily sensations) suggests that they may
have indirect benefits for patients with panic disorder.

Panic disorder: pearls

 Do not underestimate the importance of patient education, (eg, ‘‘The
tachycardia and hypertension you have during panic are not dangerous
and will keep you from passing out’’, ‘‘Your chest pain and shortness of
breath are caused by hyperventilation but are not dangerous’’). Educate
about how symptoms reflect false alarms from the autonomic nervous
system, that panic feels dangerous but it’s not, and that panic is usually
short circuited by the very willingness to have it rather than trying to
control or avoid it.
 Encourage reading and CBT, (eg, self-directed CBT [29] or referral for
specialist-delivered CBT [31–34]). Emphasize that the best route to re-
covery is through willing acceptance and, eventually, even seeking panic.
 When initiating an SSRI or SNRI for panic disorder, start low, go slow,
reassure often, and, when discontinuing, taper slowly. Use benzodiaze-
pines judiciously.

Specific phobias
Prevalence
Lifetime prevalence of specific phobias is 12.5% [2]. Developmentally
normal, transient fears (eg, darkness, separation, intruders, water) are com-
mon among children; however, prevalence of specific phobias among chil-
dren has been reported as high as 17.6% [35].

Etiology and perpetuation

The etiology of specific phobias is likely multifactorial with variation
across phobia types and individuals. Conditioning and genetic models
have both garnered support and criticism. The fear-conditioning model de-
picts a specific phobia as the product of pairing an alarm of anxious arousal
with a situation that has high likelihood of acquiring phobic properties.
However, twin studies support a nonassociative model that postulates
largely innate vulnerability to phobias based on exaggerated fear response
to evolutionary, survival-relevant cues or a largely innate deficiency in adap-
tation to such cues [36].

Clinical presentation and impact

In DSM-IV-TR, specific phobias are defined by excessive and persistent
fear that is cued by presence or anticipation of a specific stimulus. Although
482 SHEARER

the person usually recognizes that the fear is excessive or unreasonable, ex-
posure to the stimulus almost invariably provokes immediate anxiety that
may take the form of a panic attack. Contact with the phobic stimulus is en-
dured with intense distress or it is avoided entirely. The avoidance, anxious
anticipation, or distress must interfere significantly with the person’s normal
routine, occupational or academic functioning, or social activities and
relationships.
Most people who have specific phobias do not present for treatment.
Conversely, most anxiety disorders that present in primary care settings
are not specific phobias. The DSM-IV-TR requires that the distress and
avoidance associated with the phobic stimulus are not better accounted
for by another disorder that may have different treatment implications.
For example, if panic attacks occur primarily in response to catastrophic
thinking about anxious arousal, panic disorder is the likely diagnosis, and
a selective serotonin reuptake inhibitor or interoceptive exposure to bodily
arousal is indicated. Apparent phobias may focus primarily on contamina-
tion and illness concerns or fear related to intrusive thoughts about losing
control that would suggest OCD. A trauma history could be relevant to
onset or perpetuation of some apparent phobias that actually reflect post-
traumatic stress disorder.
Typical phobic stimuli include small animals (eg, dogs, cats, snakes,
spiders, bees, rats, mice); natural environment (eg, heights, water, dark,
thunderstorms); situational (eg, closed spaces/confinement, flying, bridges);
other (eg, choking, vomiting); and, blood-injury-injection phobia. Rather
than a specific phobia, so-called ‘‘school phobia’’ in children may reflect sep-
aration anxiety, social anxiety, panic attacks, depression, attention/learning
problems, bullying, or willful refusal without anxiety.
Specific phobias cued by commonly encountered stimuli (eg, pets, insects)
or accompanied by panic attacks may significantly affect mobility, social or
employment possibilities, and quality of life. In contrast, someone with a se-
vere snake phobia could easily arrange a lifestyle that precludes potential
contact with the phobic stimulus.
Dental phobia or blood-injury-injection phobia may lead to avoidance of
needed health care with potentially serious consequences. Similarly, poor di-
abetic control has been reported among diabetics with blood-injury-injection
phobia [37].

Assessment
Although screening instruments and phobia-specific questionnaires are
available [18], they are unlikely to be helpful in the primary care setting.
If a specific phobia is suspected, the primary care physician should clarify
first whether the presentation is best explained by another anxiety disorder
with different treatment implications. If specific phobia seems the likely di-
agnosis, the physician should clarify the impact on functioning and decide
 TREATMENT OF ANXIETY DISORDERS 483

whether graduated exposure is indicated, either by encouraging patient

education and self-conducted exposure or by making a specialty referral.

Treatment
Medication generally is not indicated in the treatment of specific phobias
and may dilute the effectiveness of behavioral treatment. Graduated expo-
sure to the feared stimulus is first-line treatment for specific phobias. Prelim-
inary reports suggest that the effects of such exposure treatment for specific
phobias may be augmented by acute administration of d-cycloserine just be-
fore exposure [38]. However, in one report, d-cycloserine did not enhance
the reduction of spider fears or the generalization of treatment of a single
session of exposure-based therapy [39].
Confronting a hierarchy from less to more fear-arousing situations and,
most importantly, staying in the situation until anxiety diminishes, usually
leads to gradual habituation of the fear response. Recent reviews have docu-
mented the effectiveness of CBT for specific phobias in both children [40]
and adults [41]. For example, 14 controlled studies of in vivo (ie, in real-
life situations) exposure for specific phobias have consistently shown benefit
[41]. Although in vivo exposure is the standard, exposure may be helpful
whether it is based on imaginal, in vivo, or virtual reality cues and whether
it is self-conducted or specialist-conducted [41–43]. Self-help approaches
yield greater benefit for specific phobias than for other anxiety disorders
[44,45].
Preparatory cognitive therapy may set the stage for exposure treatment by
addressing distorted risk assessments, anxiety-arousing self-talk, feelings of
being overwhelmed, and the demoralization that accompanies chronic avoid-
ance. Anxiety management skills may be taught to encourage acceptance of
distress, without escape or distraction, to best facilitate extinction. Recent em-
phasis in CBT has moved toward encouraging willingness to seek and accept
anxiety rather than to control it through conscious effort or techniques.
Results of both functional magnetic resonance and positron-emission to-
mography imaging studies suggest that exposure-based CBT modifies the
dysfunctional neural circuitry that underpins specific phobias [46–49]. How-
ever, relapse after successful treatment is likely if intermittent, self-con-
ducted exposure is abandoned.
Blood-injury-injection phobia is a special case of specific phobia with
different treatment implications. Contact with most phobic stimuli prompts
increased arousal typified by tachycardia; however, exposure to blood-
injury-injection cues provokes the opposite. Initial hyperarousal is followed
moments later by abrupt bradycardia and hypotension thought to reflect
remnants of evolutionary adaptation to predator attack, (ie, no movement
and staunched blood flow promote survival). If this vasovagal response is
marked, syncope can result and may contribute to subsequent phobic con-
ditioning to such cues. Exposure treatment is indicated, often beginning
484 SHEARER

with verbal descriptions or pictures, but progressing to direct exposure to

the relevant cues (eg, donating blood). The vasovagal response requires spe-
cial adaptation. Patients are instructed to increase muscle tension or to stim-
ulate memories of angry feelings to counter bradycardia and hypotension
during exposure [50].

Specific phobias: pearls

 Most individuals with specific phobias do not present for treatment.
Most individuals who present with ‘‘phobias’’ do not have specific pho-
bias. Consider whether the presented fears are best explained by a diag-
nosis of panic disorder with agoraphobia, OCD, or PTSD.
 Graduated exposure, whether self/parent conducted [51] or specialist
conducted, is likely to be helpful if it is repetitive and sustained long
enough for anxiety to diminish before the exposure is terminated.
 Blood-injury-injection phobia is uniquely characterized by bradycardia
and hypotension that can cause syncope. Although exposure treatment
is still indicated, deliberate muscle tension or angry imagery may be nec-
essary to prevent vasovagal syncope.

Social anxiety disorder (Social phobia)

Prevalence
Conservative estimates suggest that lifetime prevalence of social anxiety
disorder is 5% [52]. Primary care data suggest similar lifetime prevalence
(5.7%) [53]. Compared with patients with other psychiatric disorders in pri-
mary care, social anxiety disorder was characterized by greater functional
impairment, fewer visits, and tenfold the number of concomitant substance
abuse disorders [53].

Etiology and perpetuation

As with panic disorder, the vulnerability for anxious apprehension,
caused by hypersensitive fear circuits in the brain or adverse developmental
experiences, seems to be fundamental to the etiology of social anxiety disor-
der. Both shyness and behavioral inhibition (ie, wariness in response to nov-
elty) are moderately heritable and associated with subsequent development
of social anxiety disorder [1]. Understanding of the neurobiology of social
anxiety disorder is evolving [54].
Most of us experience memorable embarrassment without becoming
consumed by the possibility of recurrence. If embarrassment is accompanied
by panic, shame, repetitive replays in memory, and preexisting propensities
for performance anxiety and worry-proneness, social anxiety disorder is
the likely result. More than one third of social anxiety disorder sufferers
report posttraumaticlike reexperiencing of socially stressful events with
 TREATMENT OF ANXIETY DISORDERS 485

accompanying hyperarousal and avoidance [55]. Social anxiety becomes

self-perpetuating, because self-absorption and self-monitoring impede social
performance, creating a vicious cycle, and subsequent avoidance preempts
exposure that would facilitate habituation and disprove distorted
assumptions.

Clinical presentation and impact

Social anxiety disorder has evolved as the preferred term in the literature,
but the DSM-IV-TR still uses the term social phobia. The diagnosis is de-
fined by persistent fear of social or performance situations that involve pos-
sible scrutiny and disapproval by others. Exposure to a feared situation
provokes marked distress, panic attacks, or preemptive avoidance. Worry-
ing about possible bungled performance and subsequent embarrassment
may be very specific (eg, public speaking, musical performance, or athletics)
or may be generalized across many social situations (eg, dating, introduc-
tions, parties, speaking to authority figures, using the telephone, writing/eat-
ing in public, public restrooms).
Hyperhidrosis, body dysmorphic disorder, or paruresis may complicate
social anxiety disorder. Comorbidity between social anxiety disorder and
other anxiety disorders, substance abuse disorders, and affective disorders
is common. The high prevalence of alcohol abuse, especially in socially anx-
ious men, has been explained by the self-medication hypothesis [1], but the
interrelationship is complex [56]. Social phobics experience similar anxiety
with and without alcohol, but they remember this experienced anxiety less
precisely, perhaps serving as a reinforcer for the use of alcohol for the pur-
pose of self-medication in future situations [57].
Popular press critics have disparaged social anxiety disorder as merely the
medicalization of shyness and normal performance anxiety. Shyness corre-
lates with but does not effectively predict social anxiety disorder, (ie, true so-
cial anxiety disorder does not develop in most shy individuals) [1]. True
generalized social anxiety disorder is usually marked by significant avoid-
ance, with deleterious impact on social relationships, lower academic and
occupational achievement, lower quality-of-life ratings, and a rate of at-
tempted suicide as high as 22% [58].
Social anxiety disorder is characterized by early-onset (mean, 15 years)
and a disruptive, unremitting course if untreated; yet, more than 80% re-
main untreated [53]. A long-term, prospective, longitudinal, naturalistic
treatment study found that social anxiety disorder has a chronic course
and a greater adverse impact on social functioning than depressive symp-
toms or chronic medical illnesses [59]. Only 35% of patients with social anx-
iety disorder recovered after 10 years of prospective follow-up, and the
postrecovery relapse rate was 34% during the 10-year follow-up [59]. In
short, the evidence confirms that generalized social anxiety disorder is triv-
ialized by popular conflation with shyness.
486 SHEARER

Assessment
Two well-studied tools appropriate for assessment or for tracking
treatment of social anxiety disorder in the primary care setting are the
self-administered Social Phobia and Anxiety Inventory and the physician-
administered Leibowitz Social Anxiety Scale [18]. However, for brief screen-
ing, use of only three questions identifies social anxiety disorder with 89%
sensitivity and 90% specificity, (ie, ‘‘Is being embarrassed or looking stupid
among your worst fears?’’ ‘‘Does fear of embarrassment cause you to avoid
doing things or speaking to people?’’ ‘‘Do you avoid activities in which you
are the center of attention?’’) [60].

Treatment
The SSRIs and the SNRI venlafaxine are established as effective
treatments for social anxiety disorder with the added advantage of treating
common comorbidities [61]. A recent meta-analysis of 15 randomized,
double-blind, placebo-controlled trials reported effectiveness of the SSRIs
for social anxiety disorder with benefits in both social and occupational
functioning [62].
Second-line treatments may include clonazepam, mirtazapine, and gaba-
pentin [63]. The benefits of beta blockers are limited to very specific perfor-
mance situations (eg, public speaking, musical/dance/athletic performance)
rather than generalized social anxiety disorder [61].
As in specific phobias, preliminary evidence shows that d-cycloserine may
augment exposure therapy in social anxiety disorder. In a randomized,
double-blind, placebo-controlled trial, 50 mg of d-cycloserine administered
1 hour before exposure therapy sessions (ie, public speaking) resulted
in greater effectiveness compared with a placebo before exposure sessions
[64].
Five meta-analyses support the efficacy of cognitive behavioral therapy
for social anxiety disorder, suggesting that in vivo exposure to social cues
and cognitive interventions are most efficacious [65]. A subsequent, random-
ized, double-blind, placebo-controlled trial found that both fluoxetine and
CBT were effective for social anxiety disorder, but combined treatment
had no further advantage, and many patients remained symptomatic after
14 weeks of treatment [66]. In a Norwegian primary care setting, exposure
therapy combined with sertraline showed deterioration at 1-year follow-up
compared with exposure alone [67]. In a randomized, controlled trial, indi-
vidual CBT for social anxiety disorder was superior both to intensive group
CBT and to SSRIs [68].
Active ingredients in CBT for social anxiety disorder are being identified.
For example, in a randomized, controlled trial, cognitive therapy showed
superiority to social anxiety exposure therapy coupled with applied relaxa-
tion techniques [69]. Similarly, in a randomized, controlled trial comparing
group therapy based on CBT versus exposure without explicit cognitive
 TREATMENT OF ANXIETY DISORDERS 487

intervention, only participants who received the cognitive component con-

tinued to improve after treatment ended with data suggesting that this
was mediated by changes in the estimated ‘‘social cost’’ in anxious situations
[70]. Given frequent comorbidity with depression, it is noteworthy that
CBT’s effect on social anxiety mediated 91% of the improvement in depres-
sion, but decreases in depression only accounted for 6% of the improvement
in social anxiety [71].
Patients’ accessibility to CBT is a continuing concern. Initial data suggest
that internet-delivered CBT supplemented with telephone support or expo-
sure is effective for social anxiety disorder [72,73].

Social anxiety disorder: pearls

 When patients present shyness, apparent isolation, or interpersonal
discomfort, screen for social anxiety disorder by asking about fears of
embarrassment and related avoidance of social activities.
 Among patients with social anxiety disorder, watch for comorbid sub-
stance abuse (especially alcohol in men), depression, and other anxiety
disorders.
 SSRIs and venlafaxine may be useful for social anxiety disorder; how-
ever, a more conservative approach would begin with self-help CBT
readings [74] and/or referral for specialist-delivered CBT [31].

Generalized anxiety disorder

Prevalence
Reported 1-year and lifetime prevalence of GAD is 2.1% and 4.1% [75].
In an earlier study, 1-year prevalence for GAD was 1.5%; however, 3.6%
presented with at least subthreshold syndromes of GAD [76]. Such
subthreshold presentations are as seriously impairing as full GAD [77]
and are significantly related to elevated risk of subsequent psychopathology
[78]. There is an 8% point prevalence of GAD in primary care settings,
suggesting that this is the anxiety disorder most often seen by primary
care physicians [79].

Etiology and perpetuation

Generalized anxiety disorder seems to be the product of biological and
psychological vulnerabilities similar to those described for panic disorder
and social anxiety disorder. Although GAD is moderately heritable, findings
suggest that it is a nonspecific tendency to develop emotional disorders that
is heritable rather than GAD specifically [1].
For vulnerable individuals, worry becomes a self-perpetuating, self-rein-
forcing habit. Worry reduces subjective uncertainty, contributes to subjec-
tive vigilance and preparedness, usually dampens autonomic arousal, and
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 RIVERSIDE ESSAYS
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 Riverside Essays
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The Riverside Literature Series
 PROMOTING
GOOD CITIZENSHIP
BY

JAMES BRYCE

BOSTON NEW YORK CHICAGO

HOUGHTON MIFFLIN COMPANY
The Riverside Press Cambridge
COPYRIGHT, 1909, BY YALE UNIVERSITY PRESS
COPYRIGHT, 1913, BY ADA L. F. SNELL

ALL RIGHTS RESERVED

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 CONTENTS
Introduction vii

Indolence 1

How to overcome the Obstacles to Good

Citizenship 26

The two essays by Mr. James Bryce included in this volume

are reprinted by permission of Yale University from Mr. Bryce’s
lectures on the Dodge Foundation, published in book form by the
Yale University Press under the title of The Hindrances to Good
Citizenship.
 INTRODUCTION
Mr. Bryce has for a long time been a man of international
prominence. His wide influence is undoubtedly due to many causes,
but it may, in general, be traced to two characteristics: Mr. Bryce is a
humanist who sympathetically watches the progress of nations and
the guiding of governments; he is also a historian. In his biographical
study of John Richard Green he has skillfully analyzed the aptitudes
of the historian, and in so doing has pointedly, if unwittingly,
described himself. Accuracy, he says,—a desire for the exact truth,
—keen observation, sound judgment, imagination, and, following
inevitably from these, command of literary exposition, are the powers
which a historian needs. Each of these qualities Mr. Bryce himself
possesses in large measure. It is his historical power, enabling him
to observe and record the significant phases and events of human
life, plus his sympathetic interest in its present-day manifestations
which explain, in some degree, his singularly eminent position as an
authority on matters pertaining to human institutions in various
countries.
Mr. Bryce was born in northern Ireland in 1838, of Scotch-Irish
parents; and he combines in his nature the stalwart intellectual
propensities of the Scot and the artistic attributes of the Celt. He was
educated at the University of Glasgow, and later went to Oxford
where he won many honors. After finishing his collegiate work he
was admitted to the bar and practiced law in London until 1882. At
the age of thirty-two he was appointed Regius Professor of Civil Law
at Oxford. Up to this point his life had been almost exclusively that of
a student and a scholar; and already at this time he was recognized
as a man of remarkable historical ability. The year 1880 marked a
change in his life. He presented himself to the workingmen of Tower
Hamlets, London, as a candidate for a seat in the House of
Commons. Mr. Stead tells us that Mr. Bryce, in this first campaign,
addressed his open-air audiences somewhat after the manner of a
professor lecturing in a classroom; he succeeded, nevertheless, in
getting himself elected, and for over twenty-five years thereafter was
a member of Parliament. During these years he held various
responsible offices having to do with home and foreign
administrative work. The practical results of his political influence
were advancement in public education, the securing of more
extensive parks and open country spaces for the pleasure of the
poorer classes, and the furtherance of international peace. In 1907,
Mr. Bryce was appointed ambassador to the United States, which
office he resigned in 1913 to carry on literary work.
Mr. Bryce’s knowledge is the result not only of university training
and experience in public life, but also of varied reading. He has read
art, science, history, and has always been an interested student of
poetry. In speaking once to Americans of Swinburne, he suddenly
paused and asked, “Who are writing your songs and stirring your
heart,—or isn’t your heart being stirred? Nothing is more important
than that each generation and each land should have its poets. Each
oncoming tide of life, each age, requires and needs men of lofty
thought who shall dream and sing for it, who shall gather up its
tendencies and formulate its ideals and voice its spirit, proclaiming
its duties and awakening its enthusiasm, through the high authority
of the poet and the art of his verse.” How extensively Mr. Bryce has
read the poets, both ancient and modern, one perceives from the
references and allusions in his Studies in Contemporary Biography.
The most important source of Mr. Bryce’s knowledge, the one
which has furnished the material for nearly all his books, has been
his first-hand observation and study of many countries. When still a
young man he wandered alone over Mount Ararat, since the native
guides refused to follow him to the unknown wilds of that lonely
peak. He visited the Ottoman Empire in 1876, and, as a result of his
investigations there, became an advocate of the Bulgarian cause; in
fact it was his speeches on the Eastern Question which first made
him prominent politically. Mr. Bryce has traveled also in Iceland; he
was in Africa just previous to the Boer War; he has been all over
South America; and he knows the United States as few Americans
know it. He has studied these countries with great faithfulness,
observing keenly every phase of the political and social life. An
interesting sample of his method of gathering information is found in
the chapter on “The Position of Women” in The American
Commonwealth. When traveling in the West he noticed that all of the
women seemed so very well dressed that apparently none could be
the wife or daughter of a workingman; but close observation
dispelled this illusion. Idling in a bookstore one day in Oregon, he
noticed a woman who was asking for a certain magazine. After her
departure he asked the salesman who she was, and found that she
was the wife of a workman, and the magazine a Paris fashion
journal. “This,” says Mr. Bryce, “set me to observing female dress
more closely, and it turned out to be perfectly true that the women in
these little towns were following the Parisian fashions very closely,
and were, in fact, ahead of the majority of English ladies belonging to
the professional and mercantile classes.” Thus no detail, however
trivial, escapes him; the pleasant and unpleasant phases of our
American life, our manners, clothes, scenery have all been noted
and reckoned with in the statement of tendencies and conclusions.
As a parliamentarian Mr. Bryce is said to have been direct,
honest, and always illuminating. His ability to command attention
was due not to any great oratorical gift, but rather to his scholarly
view of any matter under debate. Mr. Justin McCarthy reports that
the members of the House who might be dining, smoking, or reading
in the rooms assigned for these purposes, would, when the news
was passed around that Mr. Bryce was speaking, leave these
pleasant diversions, and betake themselves with great speed to the
debating chamber. “I have many a time,” he says, “heard
Conservative members murmur, in tones not altogether expressing
absolute satisfaction at the disturbing information, ‘Bryce is up—I
must go in and hear what he has to say.’ ... Everybody knows that
when he speaks it is because he has something to say which ought
to be spoken and therefore ought to be heard.” Mr. Bryce was able to
command attention also because of his reputation as a courageous
nonpartisan. He never advocated a measure or policy for mere party
reasons or for personal aggrandizement. Not infrequently he has
fought bravely with the minority of his own party, and has at times
suffered bitter attacks, as when he remained resolutely pro-Boer
during the rampant jingoism of the South African War. But however
widely political enemies might differ from him, they respected his
sincerity and his luminous view of governmental problems. It is
further characteristic of Mr. Bryce’s public life that he never, in his
desire for the welfare of his own country, lost sight of what is due
other nations. In practice as well as in precept he upheld the doctrine
that “patriotism consists not in waving a flag, but in striving that our
country shall be righteous as well as strong.”
Mr. Bryce’s books deal, for the most part, with historical subjects
and present-day governments. The Holy Roman Empire, written
when he was only twenty-four years old, is still regarded by able
historians as an accurate and authoritative work; and, in the
judgment of literary critics, it is written with so much charm of style
that it is destined to become an English classic. All of the books
which have to do with foreign nations are characterized by a tactful,
faithful, and above all a truthful, handling. It was The American
Commonwealth which made the citizens of the United States regard
Mr. Bryce as a friend of the Republic; but he is not so regarded
because he has always stroked the gleaming pinions of the
American eagle. Although he does seem to share the hope
universally cherished by Americans that we shall, in spite of grave
national defects, “win out” in the end, he has nevertheless, in direct
and unadorned statements, pointed out our faults. As an example of
his characteristic straightforwardness of speech, take the following
sentence: “America has little occasion to think of foreign affairs, but
some of her domestic difficulties are such as to demand that careful
observation and unbroken reflection which neither her executive
magistrates, nor her legislatures, nor any leading class among her
people now give.” Mr. Bryce has never ceased to insist that America
suffers from lack of honest, courageous leadership in dealing with
such problems as municipal evils and the insidious influence of
“vested interests.” Our heedlessness and indifference to public
matters is our national sin, but Mr. Bryce foresees a cure for our
defects in the increasing zeal with which the younger generation is
assuming the public burden; but how great must be its zeal and how
steady its purpose if anything is to be accomplished, one is made
poignantly aware by reading the account of the Tammany Ring in
The American Commonwealth.
When a man of Mr. Bryce’s ability and experience points out
definitely the chief obstacles to good citizenship and furthermore
indicates the means by which these may be overcome, one may be
as sure that he will say something which should be heeded as were
the members of the House when he was a parliamentarian. In 1909,
Mr. Bryce gave at Yale University a series of lectures which were
later published by the Yale University Press under the title
Hindrances to Good Citizenship. The main obstacles to good
citizenship are defined as indolence, private self-interest, and party
spirit.
The first lecture, “Indolence,” brings to mind the chapter in The
American Commonwealth on “The War Against Bossdom,” with its
vigorous concluding words, “In America, as everywhere else in the
world, the commonwealth suffers more often from apathy or
shortsightedness in the upper classes, who ought to lead, than from
ignorance or recklessness in the humbler classes, who generally are
ready to follow when wisely led.”
In the second lecture, “Private Self-Interest,” Mr. Bryce states the
causes which produce a body of citizens who care more about their
own advancement than about the welfare of the country. The most
important of these causes are tariff issues, appropriations of public
money for local interests, governmental contracts, public
officeholding,—all representing “the insidious power of money which
knows how to play upon the self-interest of voters and legislators,
polluting at its source the spring of Civic Duty.”
The third lecture considers party spirit as a hindrance to
citizenship. Mr. Bryce acknowledges the practical necessity for
parties in the management of popular governments, and also the
perplexing difficulties of a party leader who must decide between
conscience and party. There is nevertheless but one course open to
him: he must follow his conscience; only he must carefully
distinguish between conscience and angular independence which is
lacking in common sense and in willingness to defer to others in
unimportant matters. For the average man the question is a simple
one; relieved of the burdens of party leadership, he should follow his
intelligence rather than his party. A large number of independent
voters secures most effectively the right administration of public
business.
The last lecture in the series, “How to Overcome the Obstacles
to Good Citizenship,” suggests various means by which a more
satisfactory body of citizens may be secured. In method and style
this lecture is illustrative of the author’s peculiar strength in
exposition.
Mr. Bryce’s writings are remarkable for the lucid organization of a
wealth of detail into significant principles and sound conclusions; for
vividness in the presentation of whatever pertains to humanity, and
for gracious, winning English. One finds always in his work simplicity
in the unfolding of material which has been carefully gathered and
calmly judged. There is perfect clarity in the handling of a mass of
detail, and such skillful subordination of it and masterly emphasis of
important principles that the reader easily catches the bearing on the
central thought of every illustration or description. There is also in the
writing a solidity and firmness, a bracing stalwartness—qualities
which are the result of the writer’s own sturdy nature. But this is not
all. The author’s almost novelistic power of seeing persons and
things makes his writing as vivid as a story; even his most abstract
propositions are tangible and real. And the material is, moreover, so
sympathetically and earnestly treated that it is at times lifted above
mere pedestrian exposition and becomes warm with the feeling of
the writer. The everyday words and unadorned sentences, infused
with the spirit of the one who writes, become potent to stir
slumbering ideals. Suddenly over the level way of mere intellectual
matters falls a dreamy light, a Celtic graciousness of manner; and
the reader no longer journeys along a mere brown path, but sees the
familiar scenes of the way idealized by the touch of poetry. The value
of skillful exposition as an asset for leadership, or for the
accomplishment of any other purpose, Mr. Bryce fully appreciates. A
command of language is a power possessed by nearly every one of
the men, eminent in the nineteenth century, whom Mr. Bryce
describes in his Studies in Contemporary Biography. By means of it
Mr. John Richard Green wrote the most brilliant history of modern
times; through the stirring editorials of the Nation, Mr. Godkin was
able to arouse an indifferent American public to a more earnest
consideration of the national welfare; and it was Mr. Gladstone’s gift
of “noble utterance” which more than any other talent enabled him
for many years to hold an authoritative political position. Mr. Bryce’s
own rare power as a writer of vigorous, persuasive English is one of
the qualities which has made him in a certain sense a citizen of the
world with an almost world-wide influence.
However helpful Mr. Bryce’s method may be for the student who
is attempting to understand and master the technique of successful
English, it is the subject-matter which is primarily of importance. It is
valuable for the student since it may serve to stimulate the
investigation and expression of certain questions connected with the
administration of public matters in his own town or city; and it may
also suggest the explanation and judgment of measures proposed to
secure better government, such as the Referendum. But the
essential worth of the material lies in the fact that it is a tonic for
relaxed vigilance in public affairs. It would be well to require every
citizen of the United States to read in school days The American
Commonwealth; one ventures to say that there would be, as a result,
a steady advancement in the right understanding and fulfillment of
civic duties; but even a limited acquaintance with Mr. Bryce should
serve to define in clearer terms the elements of a sane and effective
patriotism. And Mr. Bryce’s own life, unfalteringly and resolutely
devoted to a just administration of governments, together with its
unfailing graciousness in the most trying situations, furnishes an
invigorating example of the truly successful statesman.
Ada L. F. Snell.
 Promoting Good Citizenship

INDOLENCE
Dr. Samuel Johnson, being once asked how he came to have
made a blunder in his famous English Dictionary, is reported to have
answered, “Ignorance, Sir, sheer ignorance.” Whoever has grown old
enough to look back over the wasted opportunities of life—and we all
of us waste more opportunities than we use—will be apt to ascribe
most of his blunders to sheer indolence. Sometimes one has omitted
to learn what it was needful to learn in order to proceed to action;
sometimes one has shrunk from the painful effort required to reflect
and decide on one’s course, leaving it to Fortune to settle what Will
ought to have settled; sometimes one has, from mere self-indulgent
sluggishness, let the happy moment slip.
The difference between men who succeed and men who fail is
not so much as we commonly suppose due to differences in
intellectual capacity. The difference which counts for most is that
between activity and slackness; between the man who, observing
alertly and reflecting incessantly, anticipates contingencies before
they occur, and the lazy, easy-going, slowly-moving man who is
roused with difficulty, will not trouble himself to look ahead, and so
being taken unprepared loses or misuses the opportunities that lead
to fortune. If it be true that everywhere, though perhaps less here
than in European countries, energy is the exception rather than the
rule, we need not wonder that men show in the discharge of civic
duty the defects which they show in their own affairs. No doubt
public affairs demand only a small part of their time. But the spring of
self-interest is not strong where public affairs are concerned. The
need for activity is not continuously present. A duty shared with
many others seems less of a personal duty. If a hundred, a
thousand, ten thousand other citizens are as much bound to speak,
vote, or act as each one of us is, the sense of obligation becomes to
each of us weak. Still weaker does it become when one perceives
the neglect of others to do their duty. The need for the good citizen’s
action, no doubt, becomes then all the greater. But it is only the best
sort of citizen that feels it to be greater. The Average Man judges
himself by the average standard and does not see why he should
take more trouble than his neighbours. Thus we arrive at a result
summed up in the terrible dictum, which reveals the basic fault of
democracy, “What is Everybody’s business is Nobody’s business.”
Of indolence, indifference, apathy, in general, no more need be
said. It is a sin that easily besets us all. We might suppose that
where public affairs are concerned it would decrease under the
influence of education and the press. But several general causes
have tended to increase it in our own generation, despite the
increasing strength of the appeal which civic duty makes to men who
are, or if they cared might be, better informed about public affairs
than were their fathers.
The first of these causes is that manners have grown gentler and
passions less angry. A chief duty of the good citizen is to be angry
when anger is called for, and to express his anger by deeds, to
attack the bad citizen in office, or otherwise in power, to expose his
dishonesty, to eject him from office, to brand him with an ignominy
which will prevent his returning to any post of trust. In former days
indignation flamed higher, and there was little tenderness for
offenders. Jehu smote the prophets of Baal. Bad ministers—and no
doubt sometimes good ministers also—were in England beheaded
on Tower Hill. Everywhere punishment came quicker and was more
severe, though to be sure it was often too harsh. Nowadays the arm
of justice is often arrested by an indulgence which forgets that the
true aim of punishment is the protection of the community. The very
safeguards with which our slower and more careful procedure has
surrounded trials and investigations, proper as such safeguards are
for the security of the innocent, have often so delayed the march of
justice that when a conviction has at last been obtained, the offence
has begun to be forgotten and the offender escapes with a trifling
penalty, or with none. This is an illustration of the principle that as
righteous indignation is a valuable motive power in politics, the
decline in it means a decline either in the standard of virtue or in the
standard of zeal, possibly in both.
Another cause may be found in the fact that the enormous
growth of modern states has made the share in government of the
individual citizen seem infinitesimally small. In an average Greek
republic, he was one of from two to ten thousand voters. In England
or France to-day he is one of many millions. The chance that his
vote will make any difference to the result is so slender that it
appears to him negligible. We are proud, and justly proud, of having
adapted free government to areas far vaster than were formerly
thought capable of receiving free institutions. It was hoped that the
patriotism of the citizen would expand with the magnitude of the
State. But this did not happen in Rome, the greatest of ancient
republics. Can we say that it has happened in the modern world?
Few of us realize that though our own share may be smaller our
responsibility increases with the power our State exerts. The late
Professor Henry Sidgwick once travelled from Davos in the
easternmost corner of Switzerland to the town of Cambridge in
England and back again to deliver his vote against Home Rule at the
general election of 1886, though he knew that his own side would
have a majority in the constituency. Those who knew applauded, his
opponents included, but I fear that few of us followed this shining
example of civic virtue.
Thirdly, the highest, because the most difficult, duty of a citizen is
to fight valiantly for his convictions when he is in a minority. The
smaller the minority, and the more unpopular it is, and the more
violent are the attacks upon it, so much the louder is the call of duty
to defend one’s opinions. To withstand the “ardor civium prava
iubentium”—to face “the multitude hasting to do evil”—this is the
note and the test of genuine virtue and courage. Now this is, or
seems to be, a more formidable task the vaster the community
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