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The Nature, Diagnosis, and Treatment of Neuroticism: Back to the Future

October 2013
Clinical Psychological Science

DOI:10.1177/2167702613505532

Authors:

Barlow David

Boston University

Shannon Sauer

Boston University

Kristen K Ellard

Massachusetts General Hospital

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We highlight the role of neuroticism in the development and course of emotional disorders and make a case for shifting the focus of intervention to this higher-order dimension of personality. Recent decades have seen great emphasis placed on differentiating disorders into Diagnostic and Statistical Manual of Mental Disorders diagnoses; however, evidence has suggested that splitting disorders into such fine categories may be highlighting relatively trivial differences. Emerging research on the latent structure of anxiety and mood disorders has indicated that trait neuroticism, cultivated through genetic, neurobiological, and psychological factors, underscores the development of these disorders. We raise the possibility of a new approach for conceptualizing these disorders-as emotional disorders. From a service-delivery point of view, we explore the possibility that neuroticism may be more malleable than previously thought and may possibly be amenable to direct intervention. The public-health implications of directly treating and even preventing the development of neuroticism would be substantial.

Example profile of patient evaluated with a dimensional classification system. Higher scores on the y-axis indicate higher levels of the x-dimension; otherwise, the y-axis metric is arbitrary and used for illustrative purposes. A/N = anxiety/neuroticism; BA/P = behavioral activation/positive affect; DEP = unipolar depression; MAN = mania; SOM = somatic anxiety; PAS = panic and related autonomic surges; IC = intrusive cognitions; SOC = social evaluation; TRM = past trauma; AV-BI = behavioral and interoceptive avoidance; AV-CE = cognitive and emotional avoidance.

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Clinical Psychological Science

2014, Vol. 2(3) 344 –365

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DOI: 10.1177/2167702613505532

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Theoretical/Methodological/Review Article

Throughout history, philosophers and researchers have

attempted to understand the nature of anxiety and its

disorders. As early as 450 BC, the relationship between

an individual’s discrete emotions in response to stressors

and his or her enduring proclivity for such experiences

was of interest. For example, the Roman philosopher

Cicero proposed a theory of emotion that distinguished

between the temporary emotional state of anxiety (angor)

and the enduring tendency to experience anxiety (anxi-

etas; Lewis, 1970). Furthermore, in perhaps one of the

best-known historical conceptualizations of anxiety,

Freud (1924) distinguished between objective anxiety

signaling the presence of an immediate threat (e.g., a

loaded gun pressed to the temple) and neurotic anxiety

generated when an individual’s defense mechanisms are

no longer able to successfully repress an early traumatic

experience, which results in a persistent state of distress

(Reiss, 1997). In this article, we review a variety of

research areas with the purpose of shifting focus from

the study of discrete anxiety, mood, and related disorders

as defined in the Diagnostic and Statistical Manual of

Mental Disorders (5th ed.; DSM-5; American Psychiatric

Association, APA, 2013) to a broader understanding of

emotional or internalizing disorders. In particular, we

seek to call attention to higher-order temperamental fac-

tors that may be a more appropriate target for assessment

and intervention than may symptom-level manifestations

of these traits. Although relevant higher-order tempera-

mental dimensions associated with the experience of fre-

quent and intense negative emotions have acquired a

number of labels, we focus on the construct of “neuroti-

cism” as the first (Eysenck, 1947) and still most popular

(Lahey, 2009) conception of this trait.

Neuroticism is typically defined as the tendency to

experience frequent and intense negative emotions in

505532CPXXXX10.1177/2167702613505532Barlow et al.The Nature, Diagnosis, and Treatment of Neuroticism

research-article2013

Corresponding Author:

David H. Barlow, Department of Psychology, Boston University, 648

Beacon St., 6th Floor, Boston, MA 02215

E-mail: dhbarlow@bu.edu

The Nature, Diagnosis, and Treatment of

Neuroticism: Back to the Future

David H. Barlow1, Shannon Sauer-Zavala1, Jenna R. Carl1,

Jacqueline R. Bullis1, and Kristen K. Ellard2,3

1Department of Psychology, Boston University; 2Massachusetts General Hospital, Boston,

Massachusetts; and 3Harvard Medical School

Abstract

We highlight the role of neuroticism in the development and course of emotional disorders and make a case for shifting

the focus of intervention to this higher-order dimension of personality. Recent decades have seen great emphasis

placed on differentiating disorders into Diagnostic and Statistical Manual of Mental Disorders diagnoses; however,

evidence has suggested that splitting disorders into such fine categories may be highlighting relatively trivial differences.

Emerging research on the latent structure of anxiety and mood disorders has indicated that trait neuroticism, cultivated

through genetic, neurobiological, and psychological factors, underscores the development of these disorders. We raise

the possibility of a new approach for conceptualizing these disorders—as emotional disorders. From a service-delivery

point of view, we explore the possibility that neuroticism may be more malleable than previously thought and may

possibly be amenable to direct intervention. The public-health implications of directly treating and even preventing

the development of neuroticism would be substantial.

Keywords

anxiety disorders, temperament/personality and psychopathology, comorbidity

Received 7/8/13; Revision accepted 8/13/13

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The Nature, Diagnosis, and Treatment of Neuroticism 345

response to various sources of stress. These negative

emotions are usually broadly construed to include anxi-

ety, fear, irritability, anger, sadness, and so forth, but the

greatest focus has been on the experience of anxious or

depressive mood. Accompanying this exaggerated nega-

tive emotionality is the pervasive perception that the

world is a dangerous and threatening place, along with

beliefs about one’s inability to manage or cope with chal-

lenging events. These beliefs often are manifested in

terms of heightened focus on criticism, either self-gener-

ated or from others, as confirming a general sense of

inadequacy and perceptions of lack of control over

salient events (Barlow, 2002; L. A. Clark & Watson, 2008;

Eysenck, 1947; Goldberg, 1993).

The label neuroticism was first used by Eysenck

(1947) to describe this statistically derived personality

trait; Eysenck coined the term after the commonly used

clinical label at that time: neurosis—the early DSM cate-

gory comprising people with anxiety, depression, and

related disorders. Building on earlier work by Slater

(1943), who used the term neurotic constitution, Eysenck,

no fan of things Freudian even in the 1940s, regretted

employing this term and noted that “it would no doubt

be preferable in some ways to use a more neutral kind of

label” (p. 49). Nevertheless, he made it clear that indi-

viduals with the diagnosis of neurosis occupied the path-

ological extreme of the personality trait of neuroticism.

Eysenck also noted, in a prescient bit of writing, that

these two constructs could be relatively independent and

that “some so called ‘neurotic’ inmates (of a hospital)

show very little evidence of the ‘neurotic constitution’

and would likely be situated rather towards the normal

end of the distribution” (p. 48). He went on to theorize

that these individuals would have been subjected to

extreme life stress, whereas individuals high on the trait

of neuroticism would require relatively little life stress to

trigger neurosis, thereby clearly presaging the stress-dia-

thesis model of psychopathology.

Although the study of trait or temperament models of

anxiety and related negative emotions has continued for

decades, this literature has had decreasing influence on

nosological schemes. DSM-III (3rd ed.; APA, 1980) repre-

sented the advent of an objective, empirically based clas-

sification system for mental disorders; patients previously

receiving a diagnosis of neurosis were now classified

more narrowly into specific anxiety, depressive, and

related disorders. These new discrete diagnostic catego-

ries indeed had a meaningful impact on the development

of pharmacological and individual psychological treat-

ments, particularly for anxiety and mood disorders (e.g.,

Barlow et al., 1984). This approach allowed for the devel-

opment of interventions targeting specific forms of psy-

chopathology and the ability to evaluate treatment

response on the basis of discrete outcomes. Although this

“splitting” approach to nosology ensured high rates

of diagnostic reliability, there is evidence that it may

have come at the expense of validity; in other words,

the current diagnostic system may be overemphasizing

categories that are minor variations of a broader underly-

ing syndrome (T. A. Brown & Barlow, 2005, 2009).

Neuroticism, combined with other temperamental vari-

ables, likely represents this syndrome.

Despite the marked emphasis during the past 30 years

on discrete DSM-based categories of emotional disorders

and their treatment, a few investigators have continued to

focus attention on the existence and salience of broader

underlying syndromes. For example, Andrews (1990) and

Tyrer (1989) each argued for the existence of a “general

neurotic syndrome” as a more parsimonious and heuris-

tic account of emotional disorders. In addition, Lahey

(2009), summarizing the growing evidence for the pub-

lic-health significance of neuroticism, documented that

neuroticism is strongly associated with and predicts many

different mental and physical disorders, as well as treat-

ment seeking for not only mental disorders but also gen-

eral health services. Indeed, he underscored evidence

that neuroticism may act as a salient predictor of the

quality and longevity of our lives. Lahey called for a more

substantial focus on the nature and origins of neuroticism

and the mechanisms through which this trait is linked to

both mental and physical disorders. Moreover, Cuijpers et

al. (2010) examined the economic cost of the trait of neu-

roticism and found, in a large representative sample of

the Dutch population, that these economic costs were

enormous and exceeded costs of common mental disor-

ders. Cuijpers et al. noted that “we should start thinking

about interventions that focus not on each of the specific

negative outcomes of neuroticism but rather on the start-

ing point itself” (p. 1086).

The current review begins with a section highlighting

commonalities among the emotional disorders, including

high rates of comorbidity, broad rather than narrow treat-

ment responsiveness among comorbid disorders, and

shared neurobiological mechanisms. Next, we present

the emerging research on the latent structure of emo-

tional disorders that may underlie these observed com-

monalities followed by a brief description of theoretical

accounts of the origins of neuroticism or trait anxiety.

The following section describes common functional rela-

tionships in emotional disorders, particularly among

emotional expression, negative appraisals under stress,

and avoidance, as well as new approaches to conceptual-

izing these disorders and suggests the possibility of more

satisfying dimensional nosological and assessment

schemes. Finally, a review of diverse research on the mal-

leability of neuroticism in both normal and pathological

expressions sets the stage for a discussion of possible

new strategies for treatment and prevention that focus

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346 Barlow et al.

not on individual negative outcomes of neuroticism

in the form of the DSM-defined emotional disorders

but, rather, on neuroticism itself as well as related

temperaments.

Commonalities and Dimensions Among

Anxiety and Related Disorders

Empirical conceptions of the anxiety and major emo-

tional disorders are emerging that underscore their com-

monalities (Barlow, 2002; T. A. Brown, 2007; T. A. Brown

& Barlow, 2009). Major developments in at least three

areas—high rates of comorbidity, broad treatment

response across comorbid disorders, and shared neuro-

biological mechanisms—support this conception. First,

studies of phenomenology and nosology with a particu-

lar focus on comorbidity have suggested considerable

overlap among disorders. At the diagnostic level, this

overlap is most evident in high rates of current and life-

time comorbidity (e.g., Allen et al., 2010; T. A. Brown,

Campbell, Lehman, Grisham, & Mancill, 2001; Kessler,

Berglund, & Demler, 2003; Kessler et al., 1996; Kessler

et al., 1998; Kessler et al., 2008). In a study of 1,127

patients presenting at the Center for Anxiety and Related

Disorders (CARD) at Boston University, 55% of patients

with a principal anxiety disorder had at least one addi-

tional anxiety or depressive disorder at the time of assess-

ment, and this rate increased to 76% when lifetime

diagnoses were considered (T. A. Brown et al., 2001). To

take one example, of 324 patients diagnosed with DSM-

IV-TR (4th ed., text rev.; APA, 2000) panic disorder with

or without agoraphobia, 60% met criteria for an addi-

tional anxiety or mood disorder, breaking down to 47%

with an additional anxiety disorder and 33% with an

additional mood disorder. When lifetime diagnoses were

considered, the percentages rose to 77% of the patients

experiencing any comorbid anxiety or mood disorder,

breaking down to 56% for an additional anxiety disorder

and 60% for a mood disorder. The principal diagnostic

categories of posttraumatic stress disorder and general-

ized anxiety disorder were associated with the highest

comorbidity rates. Similarly, Merikangas, Zhang, and

Aveneoli (2003) followed approximately 500 individuals

for 15 years and found that relatively few people suffered

from anxiety or depression alone; when patients did

meet criteria for a single disorder at one point in time, an

additional anxiety or depressive episode disorder almost

certainly emerged at a later time.

These summaries are most likely conservative as a

result of artifactual constraints in DSM-IV-TR (which were

continued in DSM-5), such as the nature of inclusion-

exclusion criteria used. For instance, when adhering

strictly to DSM-IV-TR diagnostic rules, the comorbidity

between dysthymia and generalized anxiety disorder in

the T. A. Brown et al. (2001) study was 5%. However,

when the hierarchical rule that generalized anxiety disor-

der should not be assigned when occurring exclusively

during a course of a mood disorder was suspended, the

comorbidity estimate increased to 90%. These data also

ignore the presence of subthreshold symptoms that did

not meet diagnostic thresholds for one disorder or

another.

Second, psychological treatments for a given anxiety

disorder often produce improvement in additional

comorbid anxiety or mood disorders that are not specifi-

cally addressed in treatment (Allen et al., 2010; Borkovec,

Abel, & Newman, 1995; T. A. Brown, Antony, & Barlow,

1995; Tsao, Lewin, & Craske, 1998; Tsao, Mystkowski, &

Zucker, 2002). For example, we examined the course of

additional diagnoses in a sample of 126 patients who

were being treated at CARD for panic disorder with or

without agoraphobia (T. A. Brown et al., 1995). A signifi-

cant pre- to posttreatment decline in overall comorbidity

was noted (40% to 17%, respectively). This effect could

represent the generalization of elements of treatment to

independent facets of both disorders or the effective tar-

geting of “core” features of emotional disorders. The fact

that a wide range of emotional disorders (e.g., major

depressive disorder, obsessive-compulsive disorder,

panic disorder) respond approximately equivalently to

antidepressant medications has also been interpreted by

some researchers as indicating shared features among

these disorders (e.g., Hudson & Pope, 1990).

There are several possible explanations for high rates

of comorbidity and overlapping treatment response that

we have reviewed extensively elsewhere (T. A. Brown &

Barlow, 2002, 2009), including overlapping definitional

criteria, artifactual reasons (e.g., differential base rates of

occurrence in our setting), and the possibility that disor-

ders are sequentially related such that the features of one

disorder act as risk factors for another disorder. Another

more intriguing explanation, noted earlier, is that this pat-

tern of comorbidity argues for the existence of what has

been called a general neurotic syndrome (Andrews, 1990,

1996; Tyrer, 1989). Under this conceptualization, hetero-

geneity in the expression of emotional disorder symp-

toms (e.g., individual differences in the prominence of

social anxiety, panic attacks, anhedonia) is regarded as

trivial variation in the manifestation of a broader syn-

drome. We return to this argument later.

Third, recent research from affective neuroscience has

suggested the existence of a biological syndrome that is

common across emotional disorders. For example,

research among individuals with anxiety and related dis-

orders has suggested that hyperexcitability of limbic

structures, along with limited inhibitory control by corti-

cal structures, may be one explanation for the increased

negative emotionality among individuals with such

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The Nature, Diagnosis, and Treatment of Neuroticism 347

diagnoses (Etkin & Wager, 2007; Mayberg et al., 1999;

Porto et al., 2009; Shin & Liberzon, 2010). Specifically,

increased “bottom-up” processing through amygdala

overactivation, coupled with inefficient or deregulated

cortical inhibition of amygdala responses, has been

shown in studies of social anxiety disorder (Lorberbaum

et al., 2004; Phan, Fitzgerald, Nathan, & Tancer, 2006;

Tillfors, Furmark, Marteinsdottir, & Fredrikson, 2002),

posttraumatic stress disorder (Shin et al., 2005), general-

ized anxiety disorder (Etkin, Prater, Hoeft, Menon, &

Schatzberg, 2010; Hoehn-Saric, Schlund, & Wong, 2004;

Paulesu et al., 2010), specific phobia (Paquette et al.,

2003; Straube, Mentzel, & Miltner, 2006), and depression

(Holmes et al., 2012). This same amygdala overactivation

has also been found in individuals high in the personality

dimension of neuroticism (Keightley et al., 2003). Of

course, a few unique and idiosyncratic neurobiological

factors have also been associated with discrete DSM-IV-

TR diagnoses (Blair et al., 2008; Chorpita, Albano, &

Barlow, 1998), but it seems likely that the broader based

genetic and neurobiological commonalities reviewed

earlier may better account for the nature of emotional

disorders. Although these three commonalities among

emotional disorders have garnered attention, a recent

focus on the hierarchical structure of emotional disorders

may be more heuristic.

Latent Temperamental Structure of

Emotional Disorders

Emerging research on the latent dimensional features of

emotional disorders has revealed a hierarchical structure

that places emphasis on two genetically based core

dimensions of temperament: neuroticism and, to a lesser

degree, extraversion (Barlow, 2002). Extraversion, com-

monly associated with social qualities, broadly refers to

an energetic approach to the world, including activity

and positive emotionality in addition to sociability.

Although these traits have received various labels, includ-

ing negative affect, behavioral inhibition, trait anxiety,

and harm avoidance as alternate terms for neuroticism

and positive affect or behavioral activation as alternate

terms for extraversion, substantial existing literature has

underscored the roles of these constructs in accounting

for the onset, overlap, and maintenance of anxiety,

depressive, and related disorders (T. A. Brown, 2007;

T. A. Brown & Barlow, 2009; T. A. Brown, Chorpita, &

Barlow, 1998; Gershuny & Sher, 1998; Griffith et al., 2010;

Kasch, Rottenberg, Arnow, & Gotlib, 2002; Kessler et al.,

2011; Krueger, 1999; Watson, Clark, & Carey, 1988).

The study of trait or temperament models of anxiety

and related negative emotions has been ongoing for

decades in spite of the decreasing influence of this work

on nosological schemes. It is interesting that almost every

theory of personality structure references neuroticism-

and extraversionlike traits, which suggests the fundamen-

tal importance of these dimensions for functioning (John

& Srivastava, 1999). Current well-accepted personality

conceptualizations, such as the Big Three (Eysenck &

Eysenck, 1975; Tellegen, 1985; Watson & Clark, 1993) and

the Big Five (Digman, 1990; John, 1990; McCrae & Costa,

1987), prominently feature these dimensions of personal-

ity despite disagreement on additional traits (e.g., con-

straint in the Big Three and agreeableness, openness,

and conscientiousness in the Big Five) and different

methods of formulation.

In addition to understanding the structure of personal-

ity, researchers have been interested in the neurobiologi-

cal basis for such traits. Eysenck’s (1961, 1981) influential

theory led to the development of the Big Three, and he

was the first to implicate neuroticism and extraversion.

He based his trait theory on variations in levels of cortical

activation and autonomic nervous system reactivity and

suggested that extraversion/positive emotion is associ-

ated with moderate levels of arousal, whereas neuroti-

cism/negative emotion is associated with under- or

overarousal. A number of researchers have examined the

relationship of neuroticism (and extraversion) in the

development of anxiety and other negative emotions. For

example, Gershuny and Sher (1998) found, in a sample

composed of 466 young adults, that the combination of

high neuroticism and low extraversion at Time 1 seemed

to play an important and predisposing role in the emer-

gence of anxiety assessed 4 years later.

Further bolstering the importance of neuroticism and

extraversion in the experience of negative emotion, Gray

(1982; Gray & McNaughton, 1996) described a similar

trait theory and its neurobiological correlates that map

onto Eysenck’s (1961, 1981) traits, namely, the behavioral

inhibition system, behavioral approach system, and fight-

flight system. In Gray’s theory, the biological basis for

anxiety is the behavioral inhibition system’s (over)reac-

tion to novel signals or punishment with exaggerated

inhibition. High levels on Gray’s behavioral inhibition

system roughly relate to high levels of neuroticism and

low levels of extraversion in Eysenck’s model, and the

behavioral approach system roughly corresponds to high

extraversion and low neuroticism (Barlow, 2002). The

fight-flight system involves unconditioned escape behav-

ior (i.e., flight) and defensive aggression (i.e., fight) in

response to unconditioned punishment, such as pain,

and unconditioned frustrative nonrewards (Gray, 1991;

Gray & McNaughton, 1996). As such, the fight-flight sys-

tem may represent a biological vulnerability specifically

to the distinct emotion of fear/panic, as opposed to anxi-

ety more generally.

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348 Barlow et al.

In another trait theory, Kagan (1989, 1994) examined

children’s approach-and-withdrawal behavior and cre-

ated profiles characterizing their levels of behavioral inhi-

bition. Kagan’s (1989) definition of behavioral inhibition

is similar to Gray’s (1982) in that it involves a low thresh-

old for limbic arousal and uncertainty regarding unfamil-

iar events. Kagan considered these stable profiles as

representing temperaments; physiological (increased

salivary cortisol levels and muscle tension, greater pupil

dilation, and elevated urinary catecholamine levels) and

external (subsequent development of anxiety disorders)

correlates of behavioral inhibition have also been found

(Biederman et al., 1993; Hirshfeld-Becker et al., 1992).

Robinson, Kagan, Reznick, and Corley (1992) suggested

that temperament is clearly heritable; however, only 30%

of individuals who clearly met criteria for behavioral inhi-

bition as young children went on to develop anxiety dis-

orders (Biederman, Rosenbaum, Hirshfeld, & Faraone,

1990). Moreover, temperament (as described in Kagan

& Snidman, 1991) appears to be somewhat malleable,

which suggests that environmental factors are also impor-

tant determinants in temperament and anxiety vulnera-

bility. These findings support the notion of a “constraining”

biological vulnerability (in contrast to a “determining”

role of temperament) in the development of anxiety in

adolescence and adulthood, a theme to which we return

in our later discussion of treatment.

Finally, in one of the best known modern conceptual-

izations of temperaments related to anxiety and depres-

sion, L. A. Clark and Watson (1991) proposed two

genetically based core dimensions, neuroticism/negative

emotionality and extraversion/positive emotionality, as

part of their tripartite theory (L. A. Clark, 2005; L. A. Clark,

Watson, & Mineka, 1994; Watson, 2005). These concepts,

originally based on Eysenck’s (1961, 1981) model, are

also closely related to Gray’s (1982) constructs of behav-

ioral inhibition and behavioral activation both conceptu-

ally and empirically. Although the traits reviewed earlier

may turn out to be distinct in some way, current evidence

in this area from CARD and elsewhere (L. A. Clark, 2005;

Watson, 2005) lump these concepts together in a partially

heritable temperament that we have labeled neuroticism/

behavioral inhibition (or just neuroticism1) and behav-

ioral activation/positive affect (T. A. Brown, 2007; T. A.

Brown & Barlow, 2009; T. A. Brown et al., 1998; Campbell-

Sills, Liverant, & Brown, 2004).

We have been studying the latent structure of emo-

tional disorders for the past 20 years (e.g., T. A. Brown

et al., 1998; Zinbarg & Barlow, 1996) and have confirmed,

with some modifications, the tripartite model of emo-

tional disorders first proposed by L. A. Clark and Watson

(1991). For example, the findings from T. A. Brown et al.

(1998), which used a sample composed of 350 patients

with DSM-IV-TR anxiety and mood disorders, confirmed

a hierarchical structure. In this structure, neuroticism and

extraversion emerged as higher-order factors to the DSM-

IV-TR disorder factors, with significant paths from neu-

roticism to each of the five DSM-IV-TR factors. In accord

with a reformulated hierarchical model of anxiety and

depression (Mineka, Watson, & Clark, 1998), results

showed that extraversion was predictive of unipolar

depression and social anxiety disorder only (see also

T. A. Brown & McNiff, 2009). In addition, Rosellini,

Lawrence, Meyer, and Brown (2010) found recently that

agoraphobia (but not panic disorder) was associated

with low extraversion, which provided support for the

change in DSM-5 that separates agoraphobia from panic

disorder as a distinct, new, diagnosis. In this model, auto-

nomic arousal, which we consider to reflect largely the

phenomenon of panic, emerges as a lower-order factor

with significant paths from panic disorder and general-

ized anxiety disorder, which demonstrated a negative

relationship with autonomic surges.

These findings on latent structure have recently been

extended both by our research team (T. A. Brown, 2007;

T. A. Brown & Barlow, 2009) and by other researchers

(e.g., Griffith et al., 2010; Kessler et al., 2011). For exam-

ple, Griffith et al. (2010), studying a large sample of eth-

nically diverse adolescents and including both self-report

and peer-report measures of neuroticism, found that a

single internalizing factor was common to lifetime diag-

noses of mood and anxiety disorders and that this inter-

nalizing factor was all but isomorphic with neuroticism.

Noting the replication of earlier findings (e.g., T. A.

Brown et al., 1998), Griffith et al. suggested that these

results provided further evidence that neuroticism may

be the core of “internalizing” disorders. Using factor anal-

ysis, Krueger (1999) similarly found that the variance in

seven anxiety and mood disorders can be accounted for

by the higher-order dimension of internalizing/neuroti-

cism. Although the key features of the DSM anxiety and

mood disorders (i.e., the specific symptoms used to dis-

criminate between diagnoses) cannot be collapsed indis-

criminately into higher-order temperamental dimensions,

it seems safe to conclude, on the basis of these studies,

that what is common outweighs what is not. Thus, virtu-

ally all of the considerable covariance among latent vari-

ables corresponding to the DSM-IV-TR constructs of

depression, social anxiety disorder, generalized anxiety

disorder, obsessive-compulsive disorder, and panic disor-

der was explained by the higher-order dimension of neu-

roticism (and extraversion); bipolar disorder was not

included in these studies.

Our own framework for understanding the origins of

neuroticism as well as emotional disorders describes

three separate but interacting diatheses or vulnerabilities

(i.e., triple vulnerability theory; Barlow, 1988, 2000;

Barlow, Ellard, Sauer-Zavala, Bullis, & Carl, 2013). We

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The Nature, Diagnosis, and Treatment of Neuroticism 349

have explicated these vulnerabilities in some detail else-

where (Barlow et al., 2013) but included a general bio-

logical (heritable) vulnerability common across disorders,

a general psychological vulnerability consisting of a

heightened sense of unpredictability and uncontrollabil-

ity and associated changes in brain function resulting

from adverse early experiences, and a more specific psy-

chological vulnerability, also largely learned, accounting

for why one particular emotional disorder may emerge

instead of another. It seems increasingly evident that the

two generalized vulnerabilities identified in the triple vul-

nerability theory are implicated in the development and

expression of neuroticism itself (T. A. Brown, 2007; T. A.

Brown & Barlow, 2009). Indeed, we hypothesize that

these two generalized vulnerabilities function as direct

risk factors for the development of neuroticism, which in

turn mediates risk for the development of anxiety and

mood disorders. What is notable for our purposes is that

adverse experiences contribute strongly to changes in

brain function and that later experiences may alter result-

ing temperamental expression and associated brain cir-

cuits (Kagan & Snidman, 1991; Nemeroff, 2013).

The Nature of Emotional Disorders

Negative reactivity to emotional experience appears fun-

damentally connected to neuroticism and resulting emo-

tional disorder pathology. Emotional disorder is a term

that has been used to group anxiety, unipolar mood, and

related disorders, such as somatoform and dissociative

disorders (Barlow, 1991; Barlow et al., 2011; T. A. Brown

& Barlow, 2009). These disorders are characterized by a

number of shared emotional disturbances, which appear

to be closely linked to neuroticism. As described earlier,

individuals with emotional disorders, compared with

healthy individuals, have higher levels of negative affect

(e.g., T. A. Brown & Barlow, 2009) and report experienc-

ing more frequent and intense negative emotions

(Campbell-Sills, Barlow, Brown, & Hofman, 2006; Mennin,

Heimberg, Turk, & Fresco, 2005). In addition, individuals

with emotional disorders, compared with healthy indi-

viduals, report less emotional clarity (Baker, Holloway,

Thomas, Thomas, & Owens, 2004; McLaughlin, Mennin,

& Farach, 2007; Tull & Roemer, 2007; Weiss et al., 2012)

and acceptance of emotional experiences (McLaughlin et

al., 2007; Tull & Roemer, 2007; Weiss et al., 2012) and

find the experience of negative emotions more unpleas-

ant (Roemer, Salters, Raffa, & Orsillo, 2005).

In view of these reactions to negative emotions, it is

not surprising that individuals with emotional disorders

also display a range of cognitive and behavioral strate-

gies aimed at reducing encounters with or the impact

of negative emotions. Individuals with emotional disor-

ders exhibit early vigilant information-processing biases

toward negative information, but then they tend to

quickly turn their attention away from such negative

information (MacLeod & Mathews, 2012; Mathews &

MacLeod, 2005). These individuals also react strongly to

negative emotions when they occur with attempts to sup-

press or avoid the emotional experience (Aldao, Nolen-

Hoeksema, & Schweizer, 2010; Baker et al., 2004; Moore,

Zoellner, & Mollenholt, 2008; Tull & Roemer, 2007; Turk,

Heimberg, Luterek, Mennin, & Fresco, 2005). In addition,

individuals with emotional disorders, compared with

healthy individuals, display greater intolerance for uncer-

tainty, ambiguity, or situations that are perceived as uncon-

trollable, which leads to heightened negative affect. For

example, intolerance of uncertainty and distress have been

demonstrated across a range of disorders, including

depression, generalized anxiety disorder, and social anxi-

ety disorder (Boelen, Vrinssen, & van Tulder, 2010;

Boswell, Thompson-Hollands, Farchione, & Barlow, 2013;

Lee, Orsillo, Roemer, & Allen, 2010; Tolin, Abramowitz,

Brigidi, & Foa, 2003). Increased perceptions of emotions

as uncontrollable and intolerable as well as increased

attempts at emotional control are also evident across dis-

orders. A wide range of research has suggested that these

ways of interpreting and responding to negative emotions

paradoxically serve to increase and maintain negative

emotions and emotional disorder symptomatology. Thus,

we consider this pathological reaction to emotional expe-

rience as the phenotypic core of emotional disorders. The

following section discusses in detail the nature of these

response tendencies and their sequelae.

Evidence has suggested that how one interprets or

reacts to negative emotions when they occur can affect

the intensity and duration of the emotional experience

(Sauer & Baer, 2009; Sauer-Zavala et al., 2012). A clear

example of how this process unfolds can be seen in early

models of panic disorder (Barlow, 1988; D. M. Clark,

1986). In these models, physical symptoms associated

with initial panic attacks (e.g., increased heart rate) evoke

anxiety about impending consequences (e.g., heart

attack), which intensifies anxiety and its related physical

symptoms and possibly triggers additional panic attacks.

It is important to note that in individuals without panic

disorder, occasional panic attacks do not evoke strong

emotional reactions (nonclinical panic; Bouton, Mineka,

& Barlow, 2001). Thus, the central issue in panic disorder

is not the experience of panic attacks but the negative

emotional reaction to the intense fear (panic) itself.

Negative reactions or interpretations of emotions that

intensify the experience are also prominent in other anxi-

ety and depressive disorders. For example, in research on

obsessive-compulsive disorder, Rachman and de Silva

(1978) found that the content of ego-dystonic intrusive

thoughts under stress are similar in patients diagnosed

with obsessive-compulsive disorder and nonclinical

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350 Barlow et al.

control participants, which supports the notion that the

way these thoughts are interpreted and managed has

implications for the development of this emotional disor-

der. In addition, individuals with generalized anxiety dis-

order may find unexpected, uncontrolled emotional

reactions that result from unplanned or mildly threaten-

ing situations particularly aversive and may engage in

worry or checking behavior to regulate this emotional

experience (Newman & Llera, 2011). Once again, the

focus of an emotional disorder (panic attacks, intrusive

thoughts, and social evaluation) may be determined by

early learning experiences; however, the negative emo-

tional reaction itself and one’s attempts to cope with or

downregulate this emotional reaction are at the core of

the disorder.

Several constructs capturing the problematic reactions

to emotions that may be implicated in the transdiagnostic

development and maintenance of emotional disorders

have been identified; specifically, these constructs mea-

sure the tendency of individuals to find emotional experi-

ences aversive and, as such, engage in attempts to avoid

them. Anxiety sensitivity, defined as a propensity for

developing beliefs that anxiety-related symptoms will

have negative somatic, cognitive, and social conse-

quences (Reiss, 1991), is one such construct. Anxiety sen-

sitivity represents an individual’s characteristic way of

evaluating and responding to an emotional experience

(specifically anxiety) when it occurs, distinct from the

frequency or intensity of anxiety itself (Cox, Taylor, &

Enns, 1999; Lilienfeld, 1999). Although anxiety sensitivity

was originally introduced as a risk factor for panic disor-

der (Reiss, Peterson, Gursky, & McNally, 1986) and has

predominantly been studied in the context of this disor-

der (e.g., Maller & Reiss, 1992; Plehn & Peterson, 2002;

Rassovsky, Kushner, Schwarze, & Wangensteen, 2000), a

large literature also has implicated anxiety sensitivity in

the development of other anxiety disorders and depres-

sion (see Boswell, Farchione, et al., 2013; Naragon-

Gainey, 2010; Taylor, 1999).

For example, prospective studies have demonstrated

that anxiety sensitivity predicts the onset of anxiety and

depressive disorders (Maller & Reiss, 1992; Schmidt,

Keough, Timpano, & Richey, 2008) beyond the contribu-

tions of the tendency to experience anxiety (see McNally,

1996, for a review) and that reductions in anxiety sensi-

tivity during treatment predict symptom improvement

(Gallagher et al., 2013). In addition, anxiety sensitivity

has demonstrated incremental validity above trait neu-

roticism in the prediction of most mood and anxiety dis-

orders (Collimore, McCabe, Carelton, & Asmundson,

2008; Cox, Enns, Walker, Kjernisted, & Pidlubny, 2001;

Kotov, Watson, Robles, & Schmidt, 2007; Norton et al.,

1997; Reardon & Williams, 2007). These results support

the notion that how one relates to negative emotions is

just as important in the development of emotional

disorders as is the frequency and intensity of emotional

experience.

Another transdiagnostic construct that has been impli-

cated in the development and maintenance of emotional

disorders is experiential avoidance, defined as the unwill-

ingness to remain in contact with uncomfortable internal

experience (e.g., thoughts, emotions, sensations, memo-

ries, urges) through escape or avoidance (Hayes, Wilson,

Gifford, Follette, & Strosahl, 1996). Self-report studies

have demonstrated that individuals with anxiety disor-

ders (Begotka, Woods, & Wetterneck, 2004; Hayes,

Luoma, Bond, Masuda, & Lillis, 2006; Kashdan, Breen,

Afram, & Terhar, 2010) and depressive disorders (Berking,

Neacsiu, Comtois, & Linehan, 2009; Hayes et al., 2006;

Shahar & Herr, 2011; Tull, Gratz, Salters, & Roemer, 2004)

display high levels of self-reported experiential avoid-

ance. The existing literature also has suggested that expe-

riential avoidance both predicts generalized anxiety

disorder symptoms even when the variance associated

with frequency of negative affect is parceled out (Lee

et al., 2010) and mediates the relationship between neu-

roticism and posttraumatic stress disorder symptoms

(Maack, Tull, & Gratz, 2012; Pickett, Lodis, Parkhill, &

Orcutt, 2012). Furthermore, Cheavens and Heiy (2011)

recently found that avoidant coping partially mediates

the relationship between the experience of negative

emotions and major depressive symptoms among indi-

viduals high in experiential avoidance. Taken together,

these findings suggest that emotional disorder symptoms

are not simply a product of high levels of negative affect;

instead, the combination of strong negative emotions and

how one relates to them when they occur appears to be

important for the development of these disorders.

Individuals with emotional disorders also show defi-

cits in mindfulness (Cheavens et al., 2005; Hayes et al.,

1996), a related construct that refers to attention and

awareness toward the present moment in an accepting

manner regardless of how unpleasant the experience

(Kabat-Zinn, 1982). Studies have shown that deficits in

mindfulness are common across the emotional disorders

(Baer, Smith, Hopkins, Kritemeyer, & Toney, 2006;

K. Brown & Ryan, 2003; Cash & Whittingham, 2010;

Rasmussen & Pidgeon, 2011), which supports the case

for similar underlying constructs in these disorders.

Results of a recent study on the effects of dispositional

mindfulness on response to a laboratory stressor sug-

gested that individuals reporting higher levels of mindful-

ness display lower levels of self-reported anxiety and an

attenuated cortisol response than do individuals endors-

ing lower levels of this construct (K. Brown, Weinstein, &

Creswell, 2011). The impact of mindfulness on stress-

related cortisol secretion has been associated with atten-

uated amygdala activation in response to threat (Creswell,

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The Nature, Diagnosis, and Treatment of Neuroticism 351

Way, Eisenberger, & Leiberman, 2007). Consistent with

data on experiential avoidance, results from studies have

suggested that the degree to which one responds to neg-

ative emotions in a mindful manner predicts psychologi-

cal symptoms over and above the contributions of a

traitlike tendency to experience negative emotions (Sauer

& Baer, 2009; Segal, Williams, & Teasdale, 2002).

Evidence has suggested that many of the maladaptive

behaviors associated with emotional disorders serve a

function of facilitating escape or avoidance of intense

emotions. Such behaviors include overt situational avoid-

ance as well as more subtle forms of avoidance and safety

behaviors. For example, situational avoidance is a hall-

mark feature of social anxiety disorder, specific phobias,

posttraumatic stress disorder, depression, agoraphobia,

and panic disorder (APA, 2013). Subtle forms of avoid-

ance are also typical across most emotional disorders. In

generalized anxiety disorder and obsessive-compulsive

disorder, engaging in worry or compulsions (Newman &

Llera, 2011), respectively, are subtle ways of avoiding the

distress associated with experiencing anxiety. In social

anxiety, subtle avoidance can include behaviors such as

decreased eye contact or standing farther away from peo-

ple during conversations or safety behaviors, such as

engaging in social interactions only with a close friend

present. In panic disorder, subtle avoidance includes

avoiding activities that produce anxietylike sensations,

such as exercise or drinking coffee (i.e., interoceptive

avoidance). Safety behaviors across disorders include car-

rying around medications or even empty medication bot-

tles, making sure to always have a cell phone or water on

hand, or engaging in certain activities only with a “safe”

person.

Addressing such behavioral avoidance is an important

element of most cognitive-behavioral treatments for emo-

tional disorders, such as through use of fear and avoid-

ance hierarchies in anxiety disorder protocols or activity

scheduling in depression treatments. Some treatment

protocols posit behavioral avoidance as comprising the

core of the dysfunction, as in the example of behavioral

activation, a well-supported treatment for depression,

which is based on the notion that depressive symptoms

are maintained by chronic avoidance of engagement or

activity (Manos, Kanter, & Busch, 2010).

In addition to engaging in problematic avoidant

behaviors, individuals with emotional disorders engage

in cognitive coping motivated by avoidance. Such pro-

cesses include emotion suppression and rumination.

Emotion suppression is a strategy in which individuals

deliberately attempt to push unpleasant, emotion-induc-

ing cognitions out of awareness; paradoxically, this strat-

egy has been shown to produce rebound effects in which

the suppressed thoughts return with greater frequency

and intensity (Rassin, Muris, Schmidt, & Merkelbach,

2000; Wegner, Schneider, Carter, & White, 1987). High

levels of emotion suppression have been demonstrated

across emotional disorders, including depression, gener-

alized anxiety disorder, obsessive-compulsive disorder,

and posttraumatic stress disorder (Purdon, 1999), and

have also been shown to exacerbate symptoms

(Abramowitz, Tolin, & Street, 2001). In particular, emo-

tional suppression has been associated with increased

physiological arousal (Hofmann, Heering, Sawyer, &

Asnaani, 2009). It is hypothesized that emotion suppres-

sion, like other forms of avoidance, is a negatively rein-

forced behavior that produces short-term reductions in

negative affect, despite then spawning increased negative

emotions in the longer term.

Rumination refers to repetitively and passively focus-

ing on negative mood and its possible causes, meanings,

and consequences (Nolen-Hoeksema, 1991). Like sup-

pression, rumination can be conceptualized as an avoid-

ant strategy because passive focus on surface matters

may serve to protect individuals from more distressing

concerns (Lyubomirsky & Nolen-Hoeksema, 1995;

Lyubomirsky, Tucker, Caldwell, & Berg, 1999). Rumination

has been shown to intensify negative affect (Nolen-

Hoeksema, Wisco, & Lyubomirsky, 2008), which leads to

more rumination, in what Selby, Anestis, and Joiner

(2008) described as an emotional cascade; this process

continues until a maladaptive behavior (reassurance

seeking, substance use, binge eating, etc.) interrupts the

cycle. Rumination appears to be prominent across emo-

tional disorders (see Aldao et al., 2010) and prospectively

predicts increases in anxiety and depressive symptoms

(Butler & Nolen-Hoeksema, 1994; Calmes & Roberts,

2007; Hong, 2007; Nolen-Hoeksema, 2000; Nolen-

Hoeksema, Larson, & Grayson, 1999; O’Connor,

O’Connor, & Marshall, 2007; Sarin, Abela, & Auerbach,

2005; Segerstrom, Tsao, Alden, & Craske, 2000).

It seems clear that negative reactions to strong emo-

tions lead to similar forms of avoidant cognitive coping

(e.g., emotion suppression and rumination) common to

all emotional disorders. These strategies that intensify

already strong negative emotions appear to lead to

greater use of disorder-specific behavioral coping.

Overall, the literature has suggested that individuals with

emotional disorders experience strong negative emotions

with frequency and evaluate these experiences as aver-

sive. As a result of these negative reactions to their emo-

tions, such individuals are more likely to engage in

avoidant coping strategies to manage emotional experi-

ences, and these strategies, in turn, paradoxically increase

the frequency/intensity of negative emotions. Once

again, we suggest that this functional relationship, driven

by neuroticism, is at the core of disorders of emotion.

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352 Barlow et al.

Neuroticism/Trait Anxiety, Nosology,

and Dimensional Diagnosis of

Emotional Disorders

It was long thought that DSM-IV-TR represented the

zenith of a splitting approach to nosology we described

earlier and that began in the 1980s with the publication

of DSM-III, an approach basically unchanged in DSM-5.

The advent of an objective empirically based system of

classification of mental disorders was an enormous

advance over previous systems based on unsupported

etiological theories best exemplified by the term neuro-

sis. Beginning in the 1980s, with the splitting of neuroses

into anxiety, depressive, somatoform, and related disor-

ders, meaningful research on outcomes of pharmacologi-

cal and individual psychological treatments, particularly

cognitive-behavioral therapy, targeting these disorders

appeared (e.g., Barlow et al., 1984). It also became clear

at that time, on the basis of the pioneering work of Strupp

(1973), that clinical trials require the generation of

detailed individual therapeutic protocols to specify an

independent variable. As a result, these psychotherapeu-

tic treatments were increasingly characterized by well-

articulated individual protocols targeted to specific forms

of psychopathology as articulated in DSM-III and its suc-

cessors, particularly anxiety and depressive disorders.

These treatments were then evaluated empirically and

found efficacious in a variety of formats, uses, and set-

tings (Barlow, 1996, 2004, 2008; Barlow, Gorman, Shear,

& Woods, 2000; Heimberg, Liebowitz, & Hope, 1998;

Nathan & Gorman, 2007).

It is fair to say that these findings have had a substan-

tial impact in that public-health authorities have allocated

billions of dollars for training and dissemination of these

treatments (McHugh & Barlow, 2010). This approach to

nosology also has ensured high rates of diagnostic reli-

ability; however, as mentioned earlier, there was growing

suspicion both that advances in classification and treat-

ment development represented by this approach came at

the expense of diagnostic validity and that the current

system may be overemphasizing categories that are minor

variations of broader underlying syndromes. The careful

consideration of these broader underlying syndromes as

a conceptual approach to nosology would not imply a

return to a nonempirical system of classification based on

theories of etiology. Rather, this thinking points to a

quantitative approach using structural equation modeling

to examine the full range of anxiety and mood disorders

without the constraints of artificial categories, given their

strong relationship and potential overlap. Thus, our

evolving view is that DSM-5 emotional disorder catego-

ries do not qualify in any sense as real entities (Kendell,

1975) but do seem to be useful concepts or constructs

that emerge as “blips” on a general background of tem-

perament. The conceptualization of emotional disorders

in a more dimensional fashion should result in a more

satisfactory representation of salient aspects of these dis-

orders that would eliminate vexing issues of comorbidity.

But moving from this conceptualization to a dimensional

system of diagnostic assessment with implications for

treatment has proven an exceedingly difficult task even

in areas such as personality disorders in which there is

widespread agreement that this would be the preferred

approach (Widiger & Crego, 2013). The recent failure to

accomplish this goal in DSM-5 underscores these

difficulties.

In a preliminary attempt to conceptualize how this

effort might work for emotional disorders, we proposed

a dimensional classification scheme to reflect the research

described earlier (T. A. Brown & Barlow, 2009). The pur-

pose would be to create a profile that may provide a

more complete portrayal of a patient’s clinical presenta-

tion than would a more categorical approach that often

consists of several individual comorbid diagnoses. The

profile would highlight levels of constructs thought to be

important in forming a useful case conceptualization,

including neuroticism, extraversion (referred to as behav-

ioral activation/positive affectivity in this model), avoid-

ance, mood, and specific foci of anxiety (e.g., panic and

other autonomic surges, somatic symptoms, intrusive

cognitions, social evaluation, and trauma). Scores on the

dimension of trait neuroticism, arguably the most impor-

tant construct in this model, reflect the frequency, inten-

sity, and distress associated with negative emotions, as

well as perceptions of uncontrollability regarding future

challenges and low self-efficacy regarding one’s ability to

cope. The higher-order dimension of extraversion/posi-

tive affect is also represented because low levels of this

trait are specifically associated with major depressive dis-

order, social anxiety disorder, and agoraphobia, whereas

high levels are associated with euthymic states of bipolar

and cyclothymic disorders. As highlighted earlier, indi-

viduals with high levels of neuroticism are likely to dis-

play avoidance behaviors. In this dimensional system,

avoidance is broken into two types: behavioral/intero-

ceptive and cognitive/emotional.

Specific examples of disorder profiles highlight the

heuristic clinical value associated with dimensional clas-

sification of emotional disorders. For example, individu-

als with a principal diagnosis of panic disorder would

likely display profiles with high levels of neuroticism,

avoidance, and preoccupation with panic/autonomic

arousal and other somatic symptoms. In contrast, patients

presenting with posttraumatic stress disorder might dis-

play high neuroticism and preoccupation with panic/

autonomic arousal (flashbacks) and past trauma. Although

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The Nature, Diagnosis, and Treatment of Neuroticism 353

each diagnostic category is linked to a prototypic dimen-

sional profile, this classification system would allow clini-

cians to determine the extent to which other key features

are present that would potentially affect treatment plan-

ning. A new measure, the multidimensional emotional

disorder inventory (MEDI), recently was developed to

assess these important vulnerabilities and characteristics

of emotional disorders with a single assessment tool; the

ongoing MEDI validation study has suggested that this

measure may be a reliable and valid method for assessing

important emotional disorder dimensions (Rosellini,

2013). A representation of what a MEDI profile might look

like is shown in Figure 1. These data present clinical esti-

mates of constructs composing the dimensional scheme

from a patient seen at CARD with a principal diagnosis of

posttraumatic stress disorder (motor vehicle accident) and

additional diagnoses of generalized anxiety disorder and

subclinical depression. Under the current diagnostic sys-

tem, unless a patient meets full diagnostic criteria for a

comorbid disorder, information on the dimensions not

associated with the primary diagnosis are discarded.

Given that the rates of comorbidity among emotional dis-

orders are high, with even greater overlap at the subclini-

cal level (T. A. Brown & Barlow 2009), a dimensional

classification system would allow for the integration of

several important areas of functioning.

Malleability of Neuroticism

The evidence regarding the malleability of personality

traits over time or in response to therapeutic intervention

is mixed. As noted earlier, Kagan (1989, 1994) described

his conceptualization of behavioral inhibition as strongly

heritable and stable; however, empirical evidence, includ-

ing Kagan’s own work, has suggested that only 30% of

children who clearly met criteria for this trait as young

children went on to develop anxiety disorders, although

some of the participants may have remained shy. Several

additional studies have yielded similar results (e.g.,

Hayward, Killen, Kraemer, & Taylor, 1998; Hirshfeld-

Becker et al., 2007; Schwartz, Snidman, & Kagan, 1999).

These results led Kagan to view behavioral inhibition as

a constraining factor subject to environmental influences.

Such influences may include stress and having parents

diagnosed with anxiety disorders; behaviorally inhibited

third to sixth graders were more likely to experience

increased anxiety if they reported more daily hassles

(Brozina & Abela, 2006) and were more likely to be diag-

nosed with an anxiety disorder if their parents also expe-

rienced such disorders (Biederman et al., 2001).

L. A. Clark (2009) has reviewed research examining

stability and change in personality disorders in adults.

Contrary to the thinking of most personality theorists, as

well as a statement in the DSM-5, which holds that per-

sonality traits are stable, inflexible, and pervasive, is

Clark’s observation that the collection of traits and behav-

iors that make up the definition of most personality dis-

orders do change, albeit slowly over time, with the

greatest change occurring in the behavioral manifesta-

tions of these traits. Furthermore, researchers examining

longitudinal changes in negative traits, such as neuroti-

cism, in the normal population have observed gradual

100

A/N BA/P DEP MAN SOM PAS IC SOC TRM AV-BI AV-CE

Score

Fig. 1. Example profile of patient evaluated with a dimensional classification system. Higher scores on

the y-axis indicate higher levels of the x-dimension; otherwise, the y-axis metric is arbitrary and used for

illustrative purposes. A/N = anxiety/neuroticism; BA/P = behavioral activation/positive affect; DEP = uni-

polar depression; MAN = mania; SOM = somatic anxiety; PAS = panic and related autonomic surges; IC =

intrusive cognitions; SOC = social evaluation; TRM = past trauma; AV-BI = behavioral and interoceptive

avoidance; AV-CE = cognitive and emotional avoidance.

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354 Barlow et al.

age-related decreases that continue long into old age

(Roberts & Mroczeck, 2008; Roberts, Walton, & Viechtbauer,

2006). Similar age-related decreases in the related higher-

order construct of internalizing have also been found; spe-

cifically, internalizing means and indicator intercepts were

lower for older-aged cohorts (Eaton, Krueger, & Oltmanns,

2011; Oltmanns & Balsis, 2011). This pattern of results is

found at the mean level, which suggests that, summed

across individuals, neuroticism decreases across time. In

addition, change in neuroticism has been examined at the

individual level using growth modeling (Mroczek & Spiro,

2003); results suggested that there is great variability in

extent of change on temperamental variables, with some

people remaining at stable levels and other people chang-

ing a great deal (Helson, Jones, & Kwan, 2002; Small,

Hertzog, Hultsch, & Dixon, 2003).

At CARD, we have also investigated longitudinal

change in neuroticism, with particular focus on respon-

siveness to psychological intervention, and have encoun-

tered mixed findings. For example, in a study on the

treatment of panic disorder (T. A. Brown & Barlow, 1995),

comorbid anxiety and depressive diagnoses improved

immediately after successful treatment even though they

were not specifically targeted, which suggests, as

described earlier, the existence of an underlying temper-

amental vulnerability. But at a 2-year follow-up, comor-

bid diagnoses had returned to a level (30%) that was no

longer significantly different from pretreatment. This

result occurred despite the fact that, in the aggregate,

patients maintained or improved on gains for panic

disorder across the follow-up interval, which indicates

considerable independence between panic disorder

symptoms and related comorbidity. Although speculative,

and contrary to the more usual interpretations offered

earlier, these findings may suggest that current cognitive-

behavioral treatments are generally effective in address-

ing the specific symptoms and maintaining processes of

the targeted disorder (in this case, panic disorder) both

immediately and at follow-up but do not result in sub-

stantial reductions in general predispositional features

(e.g., neuroticism), which leaves patients vulnerable to

the emergence or persistence of other disorders. These

findings also raise the possibility that current psychologi-

cal treatments have become overly specialized because

they focus on disorder-specific features, such as panic

attacks in panic disorder or rituals connected to obses-

sional thought in obsessive-compulsive disorder, neglect-

ing broader dimensions that might produce more

favorable long-term outcomes across all disorders.

In a more direct evaluation of this issue, the temporal

stability (8 months) and predictive utility of self-reported

levels of neuroticism and extraversion in 41 individuals

diagnosed with major depressive disorder (most of whom

received some kind of treatment during this time) has

also been examined (Eaton et al., 2011; Oltmanns &

Balsis, 2011). Low levels of extraversion at Time 1 pre-

dicted poorer clinical outcome of major depressive disor-

der at the 8-month reassessment. Moreover, neuroticism

and extraversion were remarkably stable over time,

despite changes in clinical state. In fact, although more

than one third of depressed participants were classified

as no longer depressed at the 8-month follow-up, neu-

roticism and extraversion displayed the same high level

of temporal stability in this group as in a subgroup of

participants who were depressed at both assessment

points. Despite these overall findings, because there was

no information available regarding what types of treat-

ment patients received during this study, it is difficult to

determine how specific treatments may have affected the

temperamental constructs.

In contrast, other researchers have indeed found

changes in neuroticism as a function of time and treat-

ment. For example, we examined the temporal course

and temporal structural relationships of dimensions of

temperament (neuroticism, extraversion) within DSM-IV-

TR disorder constructs of depression, social anxiety dis-

order, and generalized anxiety disorder (T. A. Brown,

2007; T. A. Brown & Barlow, 2009). Outpatients with

these disorders (N = 606) were first examined at intake

and then reassessed at 1- and 2-year follow-ups. The

majority (76%) of patients received some kind of treat-

ment after intake, although not all at CARD, of varying

duration and quality. The overall rate of diagnosed anxi-

ety and mood disorders declined significantly during

follow-up from 100% at intake to 58% at the 2-year fol-

low-up. Despite the marked decline in DSM-IV-TR diag-

noses by the 2-year follow-up, test-retest correlations of

the factors and unconditional latent growth models indi-

cated that extraversion evidenced a very high degree of

temporal stability, consistent with its conceptualization as

a trait vulnerability construct that is relatively unaffected

by treatment. However, of the five constructs examined,

neuroticism evidenced the greatest amount of temporal

change and was the dimension associated with the larg-

est treatment effect. In addition to its inconsistency with

some prior research, such as that reviewed earlier (e.g.,

Kasch et al., 2002), this finding is clearly at odds with

conceptual assumptions that core dimensions of temper-

ament are stable, inflexible, and more resistant to psy-

chological treatment.

Levels of neuroticism and extraversion have also been

explored in a more specified context across a large ran-

domized controlled trial of cognitive therapy compared

with placebo for adults with major depressive disorder

(Tang et al., 2009). Results indicated that cognitive ther-

apy produced greater changes in both neuroticism and

extraversion than did placebo, but contrary to T. A.

Brown’s (2007) results, cognitive therapy maintained a

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The Nature, Diagnosis, and Treatment of Neuroticism 355

significant effect only for extraversion after controlling

for changes in depression symptoms during treatment.

Nevertheless, the Tang et al. (2009) study differs from

Brown’s study in the clinical features of the sample (pure

major depressive disorder vs. heterogeneous anxiety and

unipolar depressive disorders) and the degree of control

provided regarding the treatment condition (placebo

controlled and with stringent adherence/fidelity proce-

dures vs. naturalistic, heterogeneous treatment).

There is also evidence that neuroticism may operate

differently than the DSM-IV-TR disorder constructs in sev-

eral ways (T. A. Brown, 2007). For instance, uncondi-

tional latent growth models of each DSM-IV-TR disorder

construct revealed inverse relations between the inter-

cept and the slope; that is, higher initial disorder severity

was associated with greater change over time. However,

the intercept and the slope of neuroticism were positively

correlated (r = .47), which indicated that patients with

higher initial levels of neuroticism tended to show less

change in this dimension over time, and, conversely,

patients with lower initial levels of neuroticism tended to

evidence greater change. Thus, unlike the DSM-IV-TR dis-

orders, the stability of neuroticism increased as a function

of initial severity. In addition, parallel-process latent

growth models indicated that higher initial levels of neu-

roticism were associated with less change in the DSM-IV-

TR constructs of generalized anxiety disorder and social

anxiety disorder. Although neuroticism alone demon-

strated no temporal relation with depression, the pres-

ence of chronic stress moderated the relationship such

that high neuroticism resulted in less improvement in

depression as the level of chronic stress increased (T. A.

Brown & Rosellini, 2011). These results are consistent

with results from earlier work, as well as theory, that

showed that neuroticism has directional temporal effects

on Axis I psychopathology (cf. Gershuny & Sher, 1998;

Kasch et al., 2002; Meyer, Johnson, & Winters, 2001) but

that the converse does not seem to occur; that is, initial

levels of the DSM-IV-TR disorders did not predict increases

in temperament over time.

Finally, evidence has suggested that change in DSM

disorder constructs (e.g., depression, social anxiety disor-

der, and generalized anxiety disorder) is significantly

related to change in neuroticism (T. A. Brown, 2007). Of

particular interest is the finding that all the temporal

covariance of the DSM-IV-TR disorder constructs was

accounted for by change in neuroticism; that is, when

neuroticism was specified as a predictor, there was no

temporal overlap among disorder constructs. The corre-

lational nature of these findings precludes firm conclu-

sions about the direction of these effects. Nevertheless,

and counter to some earlier evidence and conceptualiza-

tions (T. A. Brown et al., 1995; Kasch et al., 2002), all of

these findings suggest that neuroticism may be therapeu-

tically malleable, and it is this malleability that mediates

the extent of change in the emotional disorders.

Some authors have suggested that decreases in neu-

roticism over time may partly reflect the fact that mea-

sures of temperament overlap to some degree with

symptomatic measures of anxiety and depression, which

results in distortions on estimates of temperament (mood-

state distortion; cf. L. A. Clark, Vittengl, Kraft, & Jarrett,

2003; Jylhä & Isometsä, 2006; Widiger, Verheul, & van

den Brink, 1999). That is, the measurement of neuroti-

cism consists of some combination of stable tempera-

mental variance (i.e., vulnerability) and variability

attributable to generalized distress that would be subject

to greater temporal fluctuation and would imply that

neuroticism is apt to covary with temporal fluctuations in

the severity of disorders. However, results from a recent

study have suggested that measures of neuroticism (and

extraversion) primarily capture true temperamental vari-

ance even in individuals with emotional disorders

(Naragon-Gainey, Gallagher, & Brown, 2013). In addi-

tion, a number of longitudinal studies have controlled for

the periodic occurrence of anxious or depressive symp-

toms and still found that neuroticism acted independently

in predicting anxiety and mood (Lahey, 2009; Spijker, de

Graf, Oldehinkel, Nolen, & Ormel, 2007).

In sum, the malleability of neuroticism and other tem-

peramental variables, particularly in response to treat-

ment, remains an unsettled question. The studies

described earlier, in which researchers have examined

changes in temperamental variables in the context of

naturalistic treatments or treatments targeting disorder-

specific symptoms, have yielded mixed findings. In some

studies, temperament dimensions appeared to change

during the course of treatment in the expected directions

(e.g., T. A. Brown, 2007; Kennedy, Rapee, & Edwards,

2009), whereas in other studies, no changes in tempera-

ment occurred (e.g., Kasch et al., 2002). Inconsistencies

also exist in the degree to which the different dimensions

of temperament respond to treatment across studies.

Indeed, the research reviewed raises questions about the

nature and mechanisms of change of temperament dur-

ing treatment of emotional disorders, how best to mea-

sure temperament, and whether directly targeting

temperament therapeutically would lead to more defini-

tive results.

Prevention and Treatment of

Neuroticism

In most of the studies in which researchers have exam-

ined changes in temperament in response to psychologi-

cal interventions, including the studies described in the

by Jacqueline Bullis on June 18, 2014cpx.sagepub.comDownloaded from

356 Barlow et al.

previous section, researchers have not provided a priori

hypotheses regarding how and why the study treatment

might affect temperament other than as a by-product of

symptom reduction. The interventions used were not

designed to target features of temperament but, rather, to

address symptoms. Within such studies, it is difficult to

interpret changes in temperament. One explanation for

the mixed findings across studies is that there may be

specific interactions between the intervention and

the dimensions of temperament that influence which

temperament variables respond and to what extent. Such

interactions have been largely unexplored in studies of

psychological-treatment outcomes. However, recent

research from pharmacological-treatment studies has sup-

ported this treatment-temperament interaction hypothe-

sis, and emerging research from our own laboratory has

suggested that dimensions of temperament can be more

directly targeted through specialized treatments. In this

section, we review recent evidence for treatments specifi-

cally designed to affect temperament and discuss briefly

our own efforts to develop a psychological treatment

focused on directly addressing neurotic temperament.

Most of the studies in which researchers examine

interventions specifically designed to target temperament

have come from the literature on psychopharmacology

(for a review, see Soskin, Carl, Alpert, & Fava, 2012).

Results from these studies have provided some evidence

for specific interactions between treatment agents and

temperament variables. To summarize, this research has

indicated that serotonergic drug agents (i.e., selective

serotonin reuptake inhibitors) produce dampening

effects on neuroticism (Fu et al., 2004; Harmer et al.,

2009; Harmer, Mackay, Reid, Cowen, & Goodwin, 2006;

Murphy, Yiend, Lester, Cowen, & Harmer, 2009; Quilty,

Meusel, & Bagby, 2008) and possibly to a lesser extent on

extraversion (McCabe, Mishor, Cowen, & Harmer, 2010),

whereas catecholaminergic (i.e., noradrenergic/dopami-

nergic) agents produce specific enhancement of extraver-

sion (McCabe et al., 2010; Tomarken, Dichter, Freid,

Addington, & Shelton, 2004). The specific neurobiologi-

cal properties of these agents have been hypothesized to

mediate such observed effects on temperament variables.

For example, serotonergic agents have been shown to

decrease hyperreactivity of the amygdala in response to

fear-inducing stimuli and to inhibit dopaminergic neuro-

transmission in areas of the prefrontal cortex. In contrast,

catecholaminergic agents upregulate noradrenergic and

dopaminergic neurotransmission, particularly within the

mesolimbic reward circuitry (Soskin et al., 2012). Despite

the obvious differences between pharmacological and

psychological treatments, the studies on preferential

effects of pharmacological agents on dimensions of tem-

perament have provided some support for the notion

that treatments can be designed to selectively target tem-

peramental variables. As a corollary, the pharmacologic

results also suggested that treatments, whether pharma-

cological or psychological, should not be expected to

produce equivalent changes in temperament. Some treat-

ments may produce no effects on temperament, whereas

other treatments may produce generalized or specific

effects on dimensions of temperament.

Behavioral interventions designed to specifically

address temperamental vulnerabilities are limited in num-

ber. Rapee, Kennedy, Ingram, Edwards, and Sweeney’s

(2005) intervention for children identified as behaviorally

inhibited was designed with the purpose of preventing

the later onset of anxiety and related disorders and serves

as one example. The program consists of a parent-focused

intervention that includes psychoeducation about the

nature of anxiety, traditional cognitive-behavioral strate-

gies (i.e., exposure and cognitive restructuring) directed

toward personal concerns, and training in behavior man-

agement techniques that prevent an overprotective par-

enting style. Results from randomized controlled trials

(Rapee et al., 2005; Rapee, Kennedy, Ingram, Edwards &

Sweeney, 2010) have indicated that this program is clearly

successful at preventing anxiety disorders, but for our

purposes, the most interesting findings are those on the

effects of the program on temperament.

Specifically, using a brief version of this program,

Rapee et al. (2010) found that levels of behavioral inhibi-

tion did not differ significantly on the basis of either par-

ent report or laboratory observation, despite the success

in preventing the later onset of anxiety disorders.

However, when the program was administered in a more

intensive format with higher risk children, compared

with a group that did not receive the treatment, reduc-

tions in measures of temperament did occur (Kennedy

et al., 2009). Rapee et al. also noted that differences

among groups seemed to increase with time, which sug-

gested to them that interventions directed at tempera-

ment (and related risk factors) might produce an

increasing trajectory of change in temperament over the

years, at least in children.

In addition, some work has been conducted in an

effort to identify intervention strategies specifically for

targeting positive affect (extraversion). For example, in

an experience-sampling study, Mata et al. (2012) found

that both participants diagnosed with major depressive

disorder and control participants reported increases in

positive affect directly following physical activity and

that depressed participants in particular demonstrated

a dose-response effect such that longer and more

intense instances of physical activity led to greater

increases in positive affect. Speisman, Kumar, Rani,

Foster, and Ormerod (2012) recently demonstrated in

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The Nature, Diagnosis, and Treatment of Neuroticism 357

animal laboratories that exercise increases neurogenesis,

which could possibly be one mechanism of action in suc-

cessful psychological treatments using exercise. Despite

strong preliminary evidence, this theory must now

undergo the slow process of scientific confirmation.

Given the clinical promise of therapeutically address-

ing temperamental vulnerabilities, we have devoted more

than a decade to developing a psychological treatment

that targets the putative, fundamental, underlying pro-

cesses of anxiety and mood disorders that may be more

closely related to temperament. This treatment, the uni-

fied protocol for transdiagnostic treatment of emotional

disorders (UP), which has been described in detail else-

where (Barlow et al., 2011), is a cognitive-behavioral

intervention designed to address core temperamental

processes in emotional disorders. The UP targets identifi-

cation and modification of the strong negative reactions

to emotions that lead to problematic, avoidant coping

across emotional disorders (Ellard, Fairholme, Boisseau,

Farchione, & Barlow, 2010). Amelioration of negative

reactions to emotions in turn changes the frequency and

intensity of future emotional experiences and thereby

affects temperamental constructs.

The UP has now been evaluated for its efficacy in

treating anxiety disorders in a series of preliminary trials

culminating with a small randomized controlled trial (N =

37) comparing a treatment group with a wait list control

group (Ellard et al., 2010; Farchione et al., 2012). Results

from these studies have indicated that the UP is an effica-

cious treatment for a range of anxiety disorders with sta-

ble improvements out to an 18-month follow-up (Bullis,

Fortune, Farchione, & Barlow, 2013). We have also

recently begun a large randomized controlled equiva-

lence trial (N = 250) comparing the UP with four well-

established single anxiety disorder treatment protocols

on the basis of patients’ principal diagnoses (generalized

anxiety disorder, obsessive-compulsive disorder, social

anxiety disorder, or panic disorder with or without

agoraphobia).

In following with the goal of assessing the extent to

which the UP addresses temperamental vulnerabilities in

addition to current symptoms, we have also conducted

an investigation of the effects of the UP on dimensions of

temperament (see Carl, Gallagher, Sauer-Zavala, Bentley,

& Barlow, 2013) in the context of the randomized con-

trolled trial mentioned in the previous paragraph (i.e.,

Farchione et al., 2012). In brief, our results indicated that

in the treatment group, compared with the wait list group,

the UP produced small to moderate effects on both neu-

roticism and extraversion from pre- to posttreatment, and

these changes in temperament are associated with

improvements in core symptomatology, functional

impairment, and quality of life (Carl et al., 2013). The

results of this investigation suggest the importance of

changes in temperament as they affect treatment out-

comes. Neuroticism and extraversion contributed to both

shared and distinct treatment outcomes. Decreased neu-

roticism at posttreatment and at 6-month follow-up pre-

dicted decreased anxiety and depressive symptoms.

Increased extraversion was associated with decreased

depressive symptoms at posttreatment and decreased

anxiety symptoms at 6-month follow-up, and changes in

both temperament variables predicted reductions in

functional impairment at 6-month follow-up. Finally,

extraversion alone was associated with higher quality of

life at posttreatment and at 6-month follow-up. Although

preliminary, these results suggest that there are both

common and differentiated outcomes associated with

changes in specific dimensions of temperament. Although

both neuroticism and extraversion can affect depression

and anxiety symptoms and functional impairment, only

extraversion appears to directly influence quality of life.

In future research, it will be important to investigate and

gain a better understanding of what accounts for the vari-

ability in the effects of these temperamental predictors

on treatment outcomes.

In summary, contrary to traditional conceptions, a

variety of research has suggested that dimensions of tem-

perament may be malleable over time or in response to

treatment, but such findings have been mixed, which

indicates that more research is required to identify spe-

cific conditions that affect temperament. Specifically,

recently developed interventions that target dimensions

of temperament more directly have provided preliminary

support for the notion that psychological interventions

can address temperamental vulnerabilities and that such

improvements are associated with a range of beneficial

treatment outcomes (Carl et al., 2013; Farchione et al.,

2012; Kennedy et al., 2009). If confirmed, these findings

may shift the focus of investigation into the nature, diag-

nosis, and treatment of emotional disorders.

Future Research Directions

The construct of neuroticism is almost as old as the study

of psychopathology itself, but recent developments

described herein suggest fresh, new directions for

research. Considered broadly, can we develop targeted

psychological interventions for neuroticism? If so, will

these interventions provide a more efficient and effective

way to affect the broad sweep of phenomena across the

spectrum of emotional disorders, including common pat-

terns of comorbidity and subthreshold symptomatic pre-

sentations? Will these conceptions move us further along

toward the goal of a more satisfactory dimensional sys-

tem for classifying the emotional disorders and facilitate

the development of diagnostic instruments that will

greatly simplify the process of assessment? And can we

by Jacqueline Bullis on June 18, 2014cpx.sagepub.comDownloaded from

358 Barlow et al.

usefully extend these research objectives to other rele-

vant temperaments, such as positive affect and perhaps

constraint? The accumulation of important basic research

covered briefly in this review suggests that it may now be

possible to translate these concepts into a fundamentally

new approach to the diagnosis, assessment, and treat-

ment of emotional disorders.

Author Contributions

D. H. Barlow developed the main thesis of the manuscript.

D. H. Barlow, S. Sauer-Zavala, J. R. Carl, J. R. Bullis, and K. K.

Ellard all contributed substantially to the literature review and

subsequent drafting of the manuscript in support of this thesis.

Acknowledgments

Portions of this article were presented by D. H. Barlow as the

James McKeen Cattell Address at the Annual Meeting of the

Association for Psychological Science, May 2012.

Declaration of Conflicting Interests

The authors declared that they had no conflicts of interest with

respect to their authorship or the publication of this article.

Note

1. We henceforth refer to this construct as neuroticism; how-

ever, it should be noted that the individual studies described

may have used alternate terms.

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Gender identity differences in age of first mental health diagnosis: A population-based study of childhood and adolescence

Article

Oct 2024

Introduction Gender minority (GM; i.e., trans, non-binary, and other gender diverse) individuals have an increased risk of mental health disorders, but few studies have explored disparities using population-based samples or the age of onset of this risk. Objectives The aim of the current study was to identify the age at which the gender identity disparity in physician-assessed psychiatric diagnosis and treatment for common mental health disorders can be first identified in a population-based sample linked to national health care registries. Methods All individuals aged 16 to 25 (n = 18,793) participating in the nationwide probability-based Swedish National Public Health Survey in 2018, 2020, or 2021 were included in the analyses. This sample could be linked to mental health care treatment history data in nationally comprehensive health care registries starting at age 8 years old. Results Individuals reporting a GM identity in adulthood were seven times more likely to having been diagnosed with depression and/or anxiety and about five times more likely to having been diagnosed with a neurodevelopmental disorder during childhood or adolescence compared to individuals with a cisgender identity. GM individuals’ increased likelihood of being diagnosed with depression and/or anxiety was significantly elevated from age 13, while their neurodevelopmental disorder diagnosis risk was significantly elevated from age 10, compared to cisgender individuals. Conclusions The results from this study are the first population-based evidence to show that GM individuals are more likely to be diagnosed and treated for mental health disorders early during childhood and adolescence compared to cisgender individuals. The early emergence of this increased risk requires further inquiry into causes of these early disparities. It also suggests a potential benefit of interventions that facilitate social belonging and inclusion and reduce stressors related to societal expectations of gender.

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The Impact of Individual Differences on Job Performance and Mental Health Among Accountants

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Research is limited on the relationship between accountants' personality traits and their work-related attitudes, behaviors, and self-perception. Therefore, this study examines the effects of accountants' personality traits on job performance and mental health. The study examined individual variations in general self-efficacy, self-esteem, and “the Big Five personality traits, including openness to experience, conscientiousness, extraversion, agreeableness, and neuroticism.” 192 accountants working in the Sakarya and Kocaeli regions participated in the study through online surveys. The findings indicate that positive personality traits, such as agreeableness and extraversion, have beneficial effects on both job performance and mental health. Additionally, self-esteem and self-efficacy were positively correlated with these variables. Conversely, neuroticism was identified as having a negative impact on both mental health and job performance. These results highlight the importance of assessing personality traits before hiring accountants. Neuroticism may increase the likelihood of experiencing difficulties in the accounting profession. Therefore, it is crucial to consider personality traits in the recruitment processes of accounting professionals.

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This paper examines the impact of AI anxiety and neuroticism on attitudes toward Artificial Intelligence (AI) through a quantitative approach. With the pervasive integration of AI technologies across diverse domains like social media platforms, smart devices, healthcare, and education, gaining insight into how individuals perceive and engage with AI becomes essential. A sample of 197 participants (32 males, and 165 females) completed surveys assessing their levels of AI anxiety, neuroticism, and attitudes toward AI. The data were collected via Google Forms using the following structured questionnaires: Artificial Intelligence Anxiety Scale (AIA), Artificial Intelligence Attitude Scale (AIAS-4), and Neuroticism Scale. The findings indicate significant negative correlations between AI anxiety (r=-.286, p<.01), neuroticism (r=-.196, p<.01), and attitudes toward AI, suggesting that individuals with higher levels of AI anxiety and neuroticism are inclined towards adopting more skeptical viewpoints regarding AI technologies. Moreover, the AI anxiety subscales (learning, r=-.152, p<.05; job replacement, r=-.257, p<.01; sociotechnical blindness, r=-.302, p<.01, and AI configuration, r=-.256, p<.01) also showed negative significant correlations with the attitudes toward AI. At the same time, neuroticism showed significant positive correlations with the composite score of AI anxiety (r=.301, p<.01) and all its subscales (learning, r=.219, p<.01; job replacement, r=.250, p<.01; sociotechnical blindness, r=.226, p<.01, and AI configuration, r=.277, p<.01). Understanding the role of AI anxiety and neuroticism in shaping attitudes toward AI can inform the development of strategies to mitigate negative perceptions and foster more positive attitudes toward AI technologies

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Milena Jeanann Kren

Maladjustment, or the inability to maintain relationships across different domains, has been long studied and taken into consideration regarding clinical diagnoses and employment performance (Lah, 1989). The first, but outdated, measurement was developed in the 1940s called the Rotter Incomplete Sentences Blank (RISB; Altus & Bell, 1945) and has been revised a single time in the 1970s to include a college and adolescent form; no content was updated regardless of the lack of contemporary scoring materials (Ames & Riggio, 1995; Torstrick et al., 2015; Weis, 2015). The goal of this study was to modify the outdated, qualitative maladjustment measurement into a close-ended, quantitative measurement that can be utilized across multiple domains. Both Confirmatory Factor Analysis (CFA) and Correlation Analysis were utilized to determine the dimensionality of the modified RISB and establish foundational validity of the modified RISB. Findings from this study will add to the research regarding measurement testing, as well as developing an objective measurement for maladjustment for use in the psychological community.

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This study aimed to determine accountants' personality profiles and test which personality traits make accountants happier at work and in social life. In this context, the relationships between the personality traits of professional accountants (within the scope of the Dark Triad and Big Five) and their job satisfaction, life satisfaction, and personality-profession fit were examined. In this direction, quantitative research was designed, and professional accountants participated (N = 202). According to the findings, it has been determined that the Dark Triad traits (narcissism, Machiavellianism, and psychopathy) of the accountants are at a low level. Levels of dark personality traits were negatively associated with life satisfaction, while job satisfaction and personality-occupation fit were not significantly associated. The highest score regarding Big Five personality traits (i.e., openness to experience, conscientiousness, extraversion, agreeableness, and neuroticism) was obtained in agreeableness among the accountants. A positive relationship was found between the openness to experience, conscientiousness, extraversion, and agreeableness characteristics of accountants and their job satisfaction, life satisfaction, and personality-profession fit, and a negative relationship with neuroticism. As a result, it has been concluded that accounting professionals with high levels of openness to experience, conscientiousness, extraversion, and agreeableness are happier in their work and lives.

Personality change through mindfulness-based interventions: A preregistered systematic review and meta-analysis

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Mindfulness-based interventions (MBIs) lead to improvements in mental health, and also increase trait mindfulness. Yet, trait mindfulness shows definitional and empirical overlaps with the personality dimension of neuroticism which is linked to mental health and is malleable through interventions as well. This meta-analysis examined whether previously reported associations between increases in self-reported trait mindfulness and mental health in MBIs, as well as in non-MBIs and treatment-as-usual (TAU) and waitlist controls, are mediated through concomitant changes in neuroticism on the between-study level. Data of 45 intervention studies (39 randomized controlled trials; total N = 2913) were investigated with three-level meta-analysis and the causal steps approach. Change in neuroticism mediated change in trait mindfulness and fully accounted for its mediational effects on mental health. Similar associative patterns were found for the active and TAU and waitlist control groups as well. Accounting for small-study effects did not alter this pattern of results. The findings highlight the relevance of neuroticism for intervention research and may explain previously observed apparent effects of trait mindfulness in non-MBIs and TAU and waitlist controls on mental health. The construct of trait mindfulness may need conceptual reconsideration and resharpening, and the investigation of personality change should be intensified in intervention research.

The Role of Rumination in Depressive Disorders and Mixed Anxiety/Depressive Symptoms

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Susan Nolen-Hoeksema

Several studies have shown that people who engage in ruminative responses to depressive symptoms have higher levels of depressive symptoms over time, after accounting for baseline levels of depressive symptoms. The analyses reported here showed that rumination also predicted depressive disorders, including new onsets of depressive episodes. Rumination predicted chronicity of depressive disorders before accounting for the effects of baseline depressive symptoms but not after accounting for the effects of baseline depressive symptoms. Rumination also predicted anxiety symptoms and may be particularly characteristic of people with mixed anxiety/depressive symptoms.

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Jun 1995

Comorbid diagnoses were examined in 55 principal generalized anxiety disorder (GAD) clients, and the effect of treatment for the principal disorder on those conditions was evaluated. High rates of comorbid diagnoses were present at pretherapy, with social and simple phobia being most common. The presence of additional diagnoses declined dramatically from pretherapy to follow-up and was significantly greater among clients for whom the GAD therapy had been successful than among clients for whom GAD outcome had been ambiguous. This was generally true regardless of whether clients reported at follow-up that they had received further therapy since the posttherapy assessment.

Effects of Self-Focused Rumination on Negative Thinking and Interpersonal Problem Solving

Article

Full-text available

Jul 1995

Hypotheses about the effects of self-focused rumination on interpretations of events and interpersonal problem solving were tested in 3 studies with dysphoric and nondysphoric participants. Study 1 supported the hypothesis that dysphoric participants induced to ruminatively self-focus on their feelings and personal characteristics would endorse more negative, biased interpretations of hypothetical situations than dysphoric participants induced to distract themselves from their mood, or nondysphoric participants. Study 2 showed that dysphoric participants who ruminated were more pessimistic about positive events in their future than the other 3 groups. Study 3 showed that dysphoric ruminating participants generated less effective solutions to interpersonal problems than the other 3 groups. In Studies 1 and 3, dysphoric ruminating participants also offered the most pessimistic explanations for interpersonal problems and hypothetical negative events. In all 3 studies, dysphoric participants who distracted were as optimistic and effective in solving problems as nondysphoric participants.

Responses to Depression and Their Effects on the Duration of Depressive Episodes

Article

Full-text available

Nov 1991

Susan Nolen-Hoeksema

I propose that the ways people respond to their own symptoms of depression influence the duration of these symptoms. People who engage in ruminative responses to depression, focusing on their symptoms and the possible causes and consequences of their symptoms, will show longer depressions than people who take action to distract themselves from their symptoms. Ruminative responses prolong depression because they allow the depressed mood to negatively bias thinking and interfere with instrumental behavior and problem-solving. Laboratory and field studies directly testing this theory have supported its predictions. I discuss how response styles can explain the greater likelihood of depression in women than men. Then I intergrate this response styles theory with studies of coping with discrete events. The response styles theory is compared to other theories of the duration of depression. Finally, I suggest what may help a depressed person to stop engaging in ruminative responses and how response styles for depression may develop.

A Guide to Treatments That Work

Article

Jul 2015

Like its three predecessors, the fourth edition of this book present current, informed reviews of research on treatments that work for a wide range of mental disorders. The 28 chapters cover pharmacological, psychosocial, and combined treatments for attention-deficit/hyperactivity disorder (ADHD), conduct disorder, disruptive behavior disorders, schizophrenic spectrum disorders, bipolar disorder in adults and children, major depressive disorder in adults and children, panic disorders, phobias, social and generalized anxiety disorders, obsessive-compulsive disorder, posttraumatic stress disorder (PTSD), eating disorders, sleep disorders, sexual dysfunctions, substance use disorders, gambling disorder, impulse control disorders, neurocognitive disorders, and personality disorders. Authors of most of the chapters were substantially involved in the development of the treatments reviewed in their chapters.

Mastery of Your Anxiety and Panic II and Agoraphobia Supplement: Therapist Guide

Article

Jan 1999
J Cognit Psychother

A Model for Personality

Book

Jan 1981

Hans J. Eysenck

H. J. Eysenck This book is not an introduction to personality research, it is not a textbook, and above all it is not a model of personality. The title, A Modelfor Personality, was chosen on purpose to indicate that we are here concerned with a discussion of how models in this field ought to be constructed, what their functions were, and whether such models or paradigms could with advantage be produced at this stage of development. One particular aspect of personality, extraversion introversion (E), has been chosen to exemplify the desiderata which emerge from such a discussion. It is not suggested that personality and E are synonymous - merely that this particular dimension is perhaps better known than any other, has had more experimental work done on it than any other and has acquired a better theoretical substructure, and more links with genetics and physiology, than any other. Hence it seems most likely to serve as an example of how a satisfactory model of personality might ultimately be constructed, i. e. by analogy with E. Other dimensions of personality, such as neuroticism-stability or psycho tic ism-superego functioning, are mentioned in the discussion, but only when they overlap or interrelate with E. The book uses E as an example to illustrate the way in which a model of personality can be constructed, but it is in no way a summary of all that is known about E.

A Guide to Treatments that Work

Book

Feb 2007

Much about this third edition of A Guide to Treatments That Work remains as it was in the first and second editions. Like its predecessors, this edition offers detailed evaluative reviews of current research on empirically supported treatments, written in most instances by clinical psychologists and psychiatrists who are major contributors to that literature. Similarly, the standards by which the authors were asked to evaluate the methodological rigor of the research on treatments have also remained the same. As before, they provide information on the quality of the research on treatment efficacy and effectiveness that is reviewed.

An outpatient program in behavioral medicine for chronic pain patients based on the practice of mindfulness meditation: Theoretical considerations and preliminary results

Article

Jan 1984

J. Kabat-Zinn

Anxiety Sensitivity: Theory, Research, and Treatment of the Fear of Anxiety

Book

Jan 1999

Steven Taylor

Anxiety sensitivity (AS) is the fear of anxiety sensations which arises from beliefs that these sensations have harmful somatic, social, or psychological consequences. Over the past decade, AS has attracted a great deal of attention from researchers and clinicians with more than 100 peer-reviewed journal articles published. In addition, AS has been the subject of numerous symposia, papers, and posters at professional conventions.© 1999 by Lawrence Erlbaum Associates, Inc. Why this growing interest? Theory and research suggest that AS plays an important role in the etiology and maintenance of many forms of psychopathology, including anxiety disorders, depression, chronic pain, and substance abuse. Bringing together experts from a variety of different areas, this volume offers the first comprehensive state-of-the-art review of AS--its conceptual foundations, assessment, causes, consequences, and treatment--and points new directions for future work. It will prove to be an invaluable resource for clinicians, researchers, students, and trainees in all mental health professions. © 1999 by Lawrence Erlbaum Associates, Inc. All rights reserved.

The Nature, Diagnosis, and Treatment of Neuroticism: Back to the Future

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