Abstract
The Diagnostic and Statistical Manual of Mental Disorders and International Classification of Diseases classify mental health disorders on the basis of their putatively distinct symptom profiles. Although these nosologies are highly influential, they also have been derided as mere “field guides” because they focus solely on the superficial symptomatic expression of psychiatric syndromes rather than on the commonalities underlying psychiatric disorders. Recently, an alternative transdiagnostic perspective has emerged. This review addresses transdiagnostic processes that underlie a wide range of psychosocial problems commonly addressed by social work practitioners. First, we describe how the transdiagnostic perspective differs from categorical views of psychopathology and accords more closely with scientific evidence. Next, we review current experimental psychopathology and neuroscience research to detail the cognitive, affective, and neurobiological features of five transdiagnostic processes. Finally, we discuss how the transdiagnostic perspective may improve therapeutic outcomes and guide the implementation of targeted social work interventions.
Globally influential taxonomies, such as the Diagnostic and Statistical Manual of Mental Disorders (DSM) and International Classification of Diseases (ICD), have traditionally classified mental health problems on the basis of their putatively distinct symptom profiles. Yet, this classificatory system omits core commonalities across these conditions. Despite the historical dominance of the categorical taxonomic scheme, a growing consensus is emerging that the descriptive taxonomic approach to psychiatric classification may have reached the limits of its clinical and research utility. Alternative conceptualizations may afford more fine-grained etiologic and phenomenological descriptions and therefore may guide clinical practice efforts more effectively. In that regard, a transdiagnostic perspective is emerging from cognitive, behavioral, and neuroscientific research that reveals maladaptive processes underpinning a broad array of psychosocial maladies commonly addressed by social work practitioners. Rather than myopically fixating on distinctions between presumed psychiatric taxons, the transdiagnostic process perspective focuses more broadly on the commonalities bridging the varieties of human suffering. The aim of the present article is to explicate how a focus on transdiagnostic processes differs from the traditional taxonomic view and accords more closely with the current evidence from the fields of experimental psychopathology and neuroscience. To exemplify the transdiagnostic approach, we outline the clinical features of five key transdiagnostic processes at the root of human suffering and impaired psychosocial function: automaticity, attentional bias, memory bias, interpretation bias, and thought suppression. Then, we discuss the implications of the transdiagnostic approach for social work practice.
On the Origins and Limitations of the DSM
For more than 100 years, various taxonomic systems have organized the varieties of psychopathological experiences within distinct diagnostic categories (Kendler, 2009). Influenced by the traditions of the taxonomic biologists and Linnaean botanists of the 19th century, Emil Kraepelin, the most prominent of the early psychiatric nosologists, published his Compendium der Psychiatrie in 1883 (Compton & Guze, 1995). Although Kraepelin was convinced of the biological and genetic etiology of psychiatric disorders, Compendium der Psychiatrie was a purely descriptive text, classifying disorders on the basis of their characteristic patterns of symptomatic expression, prognosis, course, and clinical outcome (Gerard, 2007).
Kraepelin defended his descriptive approach by observing that
It has been impossible thus far to establish a classification upon an etiological basis. Although there are some agents that produce very definite symptoms, such as alcoholic intoxication, certain acute infectious diseases, head injury, and particularly the more profound forms of hereditary degeneracy, yet very many individual cases of insanity are wholly without any distinctive etiological features. And furthermore, one often has to admit that any single pathogenic factor may make itself known by a great variety of symptoms. Again, the causes of mental disease often work in conjunction with each other, rendering it extremely difficult to ascertain the relationship between the causes and the relationship between the causes and the symptoms (Kraepelin & Difendorf, 1915, p. 115). The grave defect here arises from the fact that there is apt to be an overvaluation of some symptoms resulting in the accumulation in one group of all cases having in common some one striking symptom. In this way, all sad and anxious emotional states came to be regarded as melancholia, all excited states as mania, and all delusional states accompanied by hallucinations as paranoia. The difficulty became apparent when a single case thus classified presents during its course the characteristics of several groups. It is, therefore, essential…to distinguish between transitory mental states and the disease form itself. The scientific conception of the disease demands knowledge not only of the present state, but also of the entire course of the disease (Kraepelin & Difendorf, 1915, pp. 115-116).
Interestingly, although a century had passed since Kraepelin rejected the possibility of an etiologically based nosology of psychiatric disorders, Frances (2009) echoed a similar sentiment vis-à-vis DSM-5:
First, let’s expose the absurdity of the DSM-5 claim that it will constitute a “paradigm shift” in psychiatric diagnosis and indicate the dangers inherent in pursuing this false goal. The simple truth is that descriptive psychiatric diagnosis does not need and cannot support a paradigm shift. There can be no dramatic improvements in psychiatric diagnosis until we make a fundamental leap in our understanding of what causes mental disorders. The incredible recent advances in neuroscience, molecular biology, and brain imaging that have taught us so much about normal brain functioning are still not relevant to the clinical practicalities of everyday psychiatric diagnosis. The clearest evidence supporting this disappointing fact is that not even one biological test is ready for inclusion in the criteria sets for DSM-5…Descriptive diagnosis is simply not equipped to carry us much further than it already has. The real paradigm shift will require an increase in our knowledge—not just a rearrangement of the furniture of the various descriptive possibilities (Frances, 2009, p. 2). The editors of the DSM-5 indicate that the new edition will provide new categories of disorders, alter some criterion sets, and emphasize matters of severity. But it will not divide psychiatric disorders into causally intelligible groups. Disregard for this issue—after 30 years’ experience with an appearance-driven policy—makes these proposed changes for the DSM-5 seem small. The big question—‘What are these disorders?-will remain unaddressed.…Much turns on causation. For practical psychiatrists, a cause is not some issue for philosophers to ponder but rather anything that makes a difference in the evoking or sustaining of a disorder. Causes may be single or multiple, necessary or sufficient, etiopathic or mechanistic; they are as diverse in human psychological life as the wide-ranging biopsychosocial model implies. But they must be specified to render the manifestations of psychiatric illness intelligible and their treatments rational. (p. 1854)
DSM also evidences a number of limitations typical of such descriptive “field guides.” It often proves difficult, for example, to distinguish conditions that manifest with similar symptoms. To wit: the current controversy regarding appropriate distinctions between grief, complicated grief, and major depressive disorder in DSM-5 remains unresolved. (Friedman, 2012). Use of polythetic criteria (i.e., when not all criteria need to be present to make a diagnosis) and arbitrary diagnostic thresholds have also been faulted, respectively, for contributing to excessive heterogeneity within diagnostic categories and to the current “epidemics” of attention-deficit hyperactivity disorder, childhood bipolar disorder, and autism spectrum disorders (Cooper, Balsis, & Zimmerman, 2010). In addition, although a maximally useful psychiatric taxonomy for practitioners and researchers alike would include only well-defined and mutually exclusive sets of disorders and constituent diagnostic criteria, many of the disorder taxons in DSM are overlapping with respect to diagnostic features and related clinical criteria. For example, impaired attentional and executive function is characteristic of major depression, schizophrenia, attention-deficit hyperactivity disorder, delirium, and various substance-related intoxication and withdrawal syndromes. Diagnostic overlap is also evidenced by the conspicuously high rates of psychiatric comorbidity observed in population studies (Kessler, Chiu, Demler, & Walters, 2005). Such comorbidity may be cross-sectional or longitudinal in nature. In the latter case, it is common for one disorder to emerge from the development of another disorder (e.g., onset of alcohol dependence following onset of generalized anxiety disorder, suggestive of an etiological link).
Other criticisms have been raised in relation to the DSM. Some observers have decried the burgeoning list of disorders (now in the hundreds) as yet another indication of the growing “medicalization” and stigmatization of human problems. Others have noted the excessive influence of pharmaceutical companies with regard to disorders selected for inclusion in the nosology. Still others have accused the APA of profiteering, given the monumental proceeds the organization takes in from sales of the DSM and related materials (Kirk & Kutchins, 1992) or for using psychiatric diagnosis as a means to exercise power (Greenberg, 2012). Many psychologists have called for functional analyses of maladaptive behavior and individually tailored treatments of mental health disorders, suggesting that DSM supports a more symptomatically oriented and prescriptive assessment and treatment approach (Andersson & Ghaderi, 2006).
To date, the DSM has evolved through seven editions. Although each edition has been lengthier and more inclusive vis-à-vis the number of psychiatric disorders described therein, the increasing complexity of this descriptive taxonomic approach to psychiatric classification has not enhanced its clinical and research utility.
A Shift From Traditional Views of Psychopathology to Transdiagnostic Processes
Over the past decade, an alternative conceptualization of mental health problems has emerged. Instead of categorizing putative psychiatric taxons by their distinguishing features, the transdiagnostic perspective attends to the common processes underlying the full panoply of psychological distress and manifold forms of suffering. This view is derived from a mature body of empirical research that has identified a common set of cognitive, affective, and psychophysiological processes across a wide array of diagnoses and conditions. Through the use of performance-based behavioral tasks, neuroimaging technologies, assessments of autonomic psychophysiology, and neuroendocrine measures, the biobehavioral correlates of transdiagnostic processes have been delineated and mapped onto phenomenological reports of persons experiencing psychological distress. In response to the dubious reliability and validity of the DSM, the National Institute on Mental Health has advanced a transdiagnostic system for research, the Research Domain Criteria (RDoC) that integrates information on a wide array of transdiagnostic processes into a matrix (see http://www.nimh.nih.gov/research-priorities/rdoc/nimh-research-domain-criteria-rdoc.shtml#toc_matrix) describing each process at multiple units of analysis, including genes, molecules, cells, circuits, physiology, behavior, and self-reports (Insel et al., 2010). Other transdiagnostic systems have been developed from the standpoint of clinical practice (e.g., Mansell, Harvey, Watkins, & Shafran, 2008).
The transdiagnostic perspective acknowledges that psychological states and traits, pathological or otherwise, exist on continua that may be normally distributed throughout the general population (Cannon & Keller, 2006; Insel et al., 2010). For instance, when individuals who do not meet criteria for a major depressive episode diagnosis are experiencing a sad mood state, they are likely to exhibit a negative memory bias (i.e., they recall more negative than positive pieces of information; Chepenik, Cornew, & Farah, 2007). Individuals diagnosed with major depressive disorder exhibit a more intense yet not qualitatively distinct form of negative memory bias which intensifies and prolongs their depressed mood (Mathews & MacLeod, 2005).
The transdiagnostic perspective emphasizes identification of the homeostatic functions of psychological symptoms over the apparent structural differences between types of psychological problems. From this point of view, the expression of a given symptom represents an attempt to adapt to a challenging environmental context. Lastly, this perspective suggests that clinical assessment and intervention should directly identify and target key transdiagnostic processes, rather than gathering information on diagnosis or allocating different services on the basis of separate disorders. In this way, a transdiagnostic approach to social work practice may be more efficient, parsimonious, and pragmatic, as practitioners can learn how to assess and intervene with a more circumscribed set of problems than the plethora of psychopathologies outlined in the DSM. Next, we discuss five key transdiagnostic processes that underlie a wide range of social, emotional, and behavioral problems encountered in many direct practice settings.
Automaticity
Although folk psychological notions often propose that all human behavior is under conscious control, a wide range of everyday actions and reactions are executed automatically without conscious intention (Bargh & Chartrand, 1999). Habitual behavior becomes automatized through hundreds of repetitions of consistent responses to a given stimulus, which result in rapid stimulus-response (S-R) processing by neural circuits involved in response execution (Schneider & Chein, 2003). Such automaticity depends upon consistent training of associations without variation in established S-R relationships (Shiffrin & Schneider, 1977). During habit formation, behaviors that were initially governed by explicit (i.e., conscious) associative networks in the brain involving regions of prefrontal cortex and the hippocampus come to be controlled by implicit (i.e., unconscious) sensorimotor corticostriatal circuits (Wood & Neal, 2007; Yin & Knowlton, 2006). Through this neurobiological shift, learned behaviors become reflexive sequences of action that can be evoked without volition or awareness by conditioned socioenvironmental cues. Furthermore, stress promotes automaticity and inhibits conscious decision making by modulating functional connectivity between prefrontal cortex and the striatum (Dias-Ferreira et al., 2009).
Although automaticity is an integral component of normal human learning that enhances efficiency, it may also subserve patterns of maladaptive cognition and behavior. For instance, persons with anxiety disorders report experiencing distressing thoughts that arise in an automatic and unbidden fashion even when they are identified as irrational and despite efforts to dispel them (McNally, 1995). In a similar vein, people diagnosed with depression tend to automatically hold negative self-evaluations and predict negative situational outcomes without conscious effort or intent (Andersen & Limpert, 2001). Automaticity of appetitive behavioral routines is evident in anecdotal reports of alcoholics who describe having the intent to have only one drink and “the next thing I knew, the bottle was empty,” previously abstinent crack addicts who describe being “lost” for days in a crack house after relapsing by taking a single “hit,” or the common occurrence of mindlessly bingeing on snack foods while watching television without awareness of sensations of satiety or the portion size consumed. Automaticity in addiction is also manifest in studies demonstrating that addictive behavior is rendered undeterred or insensitive to conditioned aversion (Dickinson, Wood, & Smith, 2002), conditioned cues associated with past drug use episodes can be processed without awareness (Yan, Jiang, Wang, Deng, He, & Weng, 2009), more severe substance use is associated with greater automatization of conditioned responses to substance-related stimuli (Gladwin & Wiers, 2012), and implicitly processed substance cues reliably predict substance use (Garland, Franken, & Howard, 2012; Rooke, Hine, & Thorsteinsson, 2008). Maladaptive forms of automaticity may subvert conscious intention and promote self-destructive behaviors (such as compulsive substance use, “cutting”, or trichotillomania) outside of volition and awareness.
Attentional Bias
Attention (whether deployed consciously or elicited unconsciously) allows information about motivationally salient objects or events to gain preeminence in the competition for information processing resources in the brain (Desimone & Duncan, 1995). In that regard, attended stimuli receive preferential information processing and thereby are more likely to govern behavior than unattended stimuli (Corbetta & Shuman, 2002). Attention gates perceptions of the stimulus to allow for evaluation of its motivational salience, which in turn facilitates execution of approach behaviors in response to appetitive objects or avoidance behaviors in response to aversive ones. Depending on their significance to the self, attended objects elicit approach or avoidance motivations, while the resultant emotional state further tunes and directs attention (Friedman & Förster, 2010; Lang & Bradley, 2011). Thus, attention and emotion are tightly coupled in a feedback loop that drives motivated behavior.
People exhibit an attentional bias toward emotionally significant stimuli, evidenced by the automatic capture and fixation of attention by objects and events that are congruent with their current mood state (Mathews & MacLeod, 2005). Thus, the attention of individuals experiencing dysphoric mood is biased away from neutral or positive stimuli and toward negative objects, persons, and events. This bias is associated with increased activity in regions of the brain that process emotional information, such as the amygdala and anterior insula (Costafreda, Brammer, David, & Fu, 2008; Frewen, Dozois, Joanisse, & Neufeld, 2008). In the laboratory, attentional bias can be observed with a dot probe task when participants exhibit faster reaction times to target probes replacing emotionally salient images compared with target probes replacing emotionally neutral images (Field & Cox, 2008). Disorder-specific forms of attentional bias have been identified among persons diagnosed with anxiety (Cisler & Koster, 2011), depression (Gotlib, Krasnoperova, Yue, & Joormann, 2004), eating disorders (Brooks, Prince, Stahl, Campbell, & Treasure, 2011), chronic pain (Schoth & Liossi, 2010), substance use disorders (Field & Cox, 2008), and prescription drug use disorders (Garland, Froeliger, Passik, & Howard, 2012), among others. For example, anxious persons involuntarily and rapidly orient their attention to threatening stimuli, which they may then consciously attempt to avoid (Cisler & Koster, 2011; MacLeod, Mathews, & Tata, 1986). Despite their deliberate attempts to avoid threatening objects and events, anxious individuals experience delayed disengagement of attention from threat (Fox, Russo, & Dutton, 2002). Similarly, individuals diagnosed with substance use disorders exhibit an automatic orienting of attention toward and delayed disengagement from substance-related cues like a bottle of beer or a crack pipe (Field & Cox, 2008). Such addiction attentional bias is associated with craving (Field, Munafo, & Franken, 2009), exacerbated by stress (Field & Quigley, 2009) and may increase substance use (Field & Eastwood, 2005). Thus, attentional biases cause preoccupation with emotionally significant objects or events, engendering an obsessive focus that may amplify and perpetuate fear, dysphoric moods, and addictive behaviors.
Memory Bias
All individuals, whether or not they are struggling with mental health problems, tend to exhibit mood-congruent memory, that is, we tend to recall information that is congruent with our current emotional state (Mayer, McCormick, & Strong, 1995). Memory tends to be biased toward information that conforms to the past learning history and current mental set of the individual. Memory bias may be an evolutionarily conserved adaptation, in that it may help alert individuals to potentially dangerous environmental contexts (Schacter, 1999). The presence of objects and events associated with past occurrences of threat or harm can rapidly and unconsciously elicit remembered responses; this process of fear conditioning is mediated in part by the amygdala (LeDoux, 2002). Moreover, by virtue of its functional and anatomic connections with the hippocampus (involved in processing conscious or “explicit” memories) and the striatum (involved in habit learning; LaBar & Cabeza, 2006), the amygdala subserves recall of emotional memories (Richardson, Strange, & Dolan, 2004). Memories of frightening events may be particularly accessible to recall, given that such events elicit heightened secretion of cortisol, a stress hormone that facilitates encoding of threat-related information into long-term memory by sensitizing neurons in the amygdala (Rodrigues, LeDoux, & Sapolsky, 2009). However, when sustained over time, elevated cortisol levels can result in excitotoxic neuron death (McEwen, 2003), which may partially account for altered hippocampal and amygdala volume among individuals with negative memory bias (Gerritsen et al., 2012).
Negative forms of memory bias have been observed among individuals meeting DSM criteria for mood and anxiety disorders, who remember a greater proportion of negative than neutral or positive memories (Mathews & MacLeod, 1994). Such memory biases are not artifacts of selective reporting and are evident on tests of implicit (i.e., unconscious) memory and semantic priming (Watkins, Vache, Verney, Muller, & Mathews, 1996). For example, when individuals are mired in a depressed mood, they are more likely to remember losses and regrets rather than former achievements. Similarly, persons diagnosed with major depressive disorder report greater frequency of overly general memories than specific memories (Williams, Teasdale, Segal, & Soulsby, 2000); in other words, they tend to recall generic synopses of past events rather than specific incidents. Such biased and overgeneralized forms of memory may preserve or exacerbate negative mood states by fueling a cycle of maladaptive cognitive processes, in which attentional biases form memory biases, which then foster negative interpretations of current life events based on the negative memories recalled (Garland et al., 2010). Negative interpretation of present events may bias attention to search for and encode future negative events, which are then more likely to be recalled than positive events, resulting in biased and partial accounts of past experience that emphasize narratives of misfortune and harm.
Interpretation Bias
Many situations and social encounters in everyday life involve ambiguity. As such, living demands adaptation to ambiguous contexts, where the outcomes of one’s actions are uncertain. Adapting to uncertainty induces stress (Monat, Averill, & Lazarus, 1972) and a sense of loss of control (Folkman, 1984). To reduce cognitive dissonance generated by ambiguity, individuals attempt to appraise the meaning of their experiences according to their life history and integrate this meaning into their ongoing autobiographical narratives. Because appraisal of ambiguous situations is conditioned on past experience, individuals may develop stereotypic ways of interpreting uncertain events. Thus, individuals may come to exhibit negative interpretation bias—a tendency to interpret ambiguous situations and events as having undesirable implications for the self (Holmes, Lang, & Shah, 2009).
Such negative interpretation bias may be evident when clients construe neutral comments as harshly critical and may be inferred when clients react to events and social encounters in a consistently negative manner. Moreover, interpretation bias may be detected with objective, performance-based measures such as the homophone task, in which individuals are required to spell an audibly presented word that has two possible spellings (one of which is neutral and one of which is emotional; e.g., tents-tense or pane-pain; Pincus & Morley, 2001); individuals diagnosed with anxiety and major depressive disorders tend to resolve these homophones negatively (Hayes & Hirsch, 2007; Mogg, Bradbury, & Bradley, 2006) and exhibit interpretation bias by interpreting ambiguous information negatively (Mathews & MacLeod, 2005). For instance, when a person who is experiencing anxiety or a dysphoric mood attempts to tell a joke in the middle of delivering a public talk or lecture, and a few individuals respond with laughter, they are more likely to interpret the people as people “laughing at them” than “laughing with them.” Individuals in anxious mood states tend to perceive neutral facial expressions as hostile or upset; such interpretation biases are associated with hyperactivity in the amygdala coupled with hypoactivity in the lateral prefrontal and anterior cingulate cortices, a pattern indicative of dysregulated emotional reactivity (Bishop, 2007). Interpretation bias may maintain psychological dysfunction by fueling maladaptive, self-confirmatory beliefs with misconstrued evidence that is then taken as veridical truth.
Thought Suppression
In response to unwanted mental experiences, people often attempt to suppress their thoughts and feelings as a means of coping; yet, the effort to not think about something can paradoxically increase its accessibility to consciousness. In that regard, thought suppression biases attention toward unwanted cognitions and affective reactions, resulting in the so-called rebound effects evident in studies in which attempted suppression results in enhanced accessibility of the very thoughts and emotions it is directed against (Wegner, Schneider, Carter, & White, 1987; Wenzlaff & Wegner, 2000). These rebound effects may be explained by Wegner’s (1994) ironic process theory, which states that suppression involves two processes (a) a conscious search for mental contents consistent with the desired psychological state and (b) an unconscious monitoring process that searches for mental contents that are inconsistent with the desired state. When the unconscious monitoring process deploys attention automatically to search for undesirable mental contents to be replaced, this search results in hyperaccessibility of unwanted cognitions (Wegner & Erber, 1992). Consequently, the recurrent and intrusive nature of the psychological targets of suppression is amplified by the very process employed to avoid them (Abramowitz, Tolin, & Street, 2001). Despite the fact that suppression is intended to decrease emotional responses, it increases sympathetic nervous system activity, resulting in heightened physiological stress reactivity evidenced by heightened galvanic skin response, finger pulse amplitude, and pulse transmission time (Gross & Levenson, 1993). Moreover, the self-regulatory effort required for thought suppression may be reflected in increased activation of the anterior cingulate and dorsolateral prefrontal cortices, brain regions involved in self-monitoring, and executive function (Mitchell et al., 2007); such increases in prefrontal cortex activity are coupled with decreased activation of the hippocampus and amygdala (Anderson et al., 2004; Depue, Curran, & Banich, 2007). Because suppression is so cognitively demanding, it depletes resources required for self-regulation; for instance, among alcohol-dependent individuals in treatment who attempt to suppress drinking-related thoughts under conditions of stress, suppression-related neurocognitive depletion is indexed by attenuated heart rate variability responses to stress and alcohol cues (Garland, Carter, Ropes, & Howard, 2012).
Suppression is common to many forms of psychological suffering and addictive urges. For example, when asked to suppress drinking urges following alcohol cue exposure, alcohol-dependent individuals evidenced speeded responses to alcohol-related statements relative to control phrases (Palfai, Monti, Colby, & Rohsenow, 1997). Such rebound effects have also been observed for appetitive behavioral habits. Experimental studies in which participants are induced to suppress thoughts of smoking (Erskine, Georgiou, & Kvavilashvili, 2010) and eating (Erskine & Georgiou, 2010) demonstrate that suppression leads to greater enactment of appetitive behavior. Suppression may also promote intrusive trauma-related thoughts that are integral to PTSD (Tull, Gratz, Salters, & Roemer, 2004) by disrupting emotional processing of traumatic memories and obstructing their integration into long-term memory (Elzinga & Bremner, 2002; Foa & Kozak, 1986). Presumably through such mechanisms, thought suppression significantly predicts the occurrence of PTSD as long as 3 years after a motor vehicle accident (Ehlers, Mayou, & Bryant, 1998; Mayou, Ehlers, & Bryant, 2002). In laboratory research, experimental induction of suppression of cognitions related to a traumatic incident resulted in a momentary reduction in thoughts about the trauma, followed by a resurgence of twice as many thoughts about the traumatic incident compared to the presuppression level (Beck, Gudmundsdottir, Palyo, Miller, & Grant, 2006). Suppression may also underlie the comorbidity between conditions; for example, research indicates that among persons diagnosed with comorbid substance dependence, psychiatric disorders, and extensive trauma histories, thought suppression promotes posttraumatic stress symptoms and drug craving (Garland & Roberts-Lewis, 2012). When sustained over time, suppression may exhaust resources for self-regulation, a limited capacity that is depleted through repeated acts of self-control (Baumeister, 2003; Muraven & Baumeister, 2000), resulting in impulsive, unintended, and counterproductive actions.
Discussion and Applications to Social Work
A clinical approach that attends to the aforementioned transdiagnostic processes confers advantages over the DSM/ICD system with regard to the case conceptualization and treatment planning process that is so essential to direct practice social work settings. The development of actionable treatment plans requires clear conceptualization of the pathogenic factors underpinning the presenting problem. Although the diagnosis of “major depressive disorder” suggests the presence of a number of relatively broad symptom clusters, it may not provide a clinician with the precision needed to guide the selection of effective interventions for a specific client. In contrast, if the clinician knows that this specific client fixates his or her attention on indicators of negative social feedback (i.e., an instance of attentional bias), exclusively remembers past failures (i.e., an instance of memory bias), interprets ambiguous situations as heralding disaster (i.e., an instance of interpretation bias), attempts to ignore unwanted thoughts (i.e., an instance of thought suppression), and compulsively binges on food when stressed (i.e., an instance of automaticity), identification of such transdiagnostic processes may help the clinician select a suite of targeted interventions.
For instance, the clinician could target attentional bias and automaticity through mindfulness training (De Raedt et al., 2011; Garland, Gaylord, Boettiger, & Howard, 2010; Garland & Howard, 2013), memory bias through a historical test of schema (Padesky, 1994), interpretation bias through cognitive restructuring (Beck, Rush, Shaw, & Emery, 1979), and thought suppression through cognitive defusion and acceptance techniques (Hayes, Luoma, Bond, Masuda, & Lillis, 2006). Thus, case conceptualization through a transdiagnostic approach points the way directly toward interventive strategies that are likely to positively influence these processes.
In essence, each transdiagnostic process can be targeted by a set of interventive techniques grounded in various theoretical orientations to social work practice. These techniques may include but are not limited to those which promote (a) exposure to distressing emotions, cognitions, body sensations, or conditioned socioenvironmental cues (Thyer, 1983); (b) mindful awareness and regulation of automatic affective and behavioral reactions (Garland, in press; Hölzel et al., 2011); (c) flexible cognitive reappraisal of stressful life circumstances as opportunities for learning, meaning, or growth (Garland, Gaylord, & Fredrickson, 2011); and (d) intentional cultivation of positive emotions and prosocial actions to foster interpersonal resources and a sense of connection (e.g., Garland, Fredrickson, et al., 2010). Although such techniques can be delivered from within standard, empirically supported therapeutic approaches (e.g., CBT), novel transdiagnostic intervention packages have been developed and tested (Garland, 2013; Mansell et al., 2008).
Conclusion
The taxonomies proffered in the current and past versions of DSM and ICD imply that clinical syndromes can be neatly delineated into orthogonal categories underpinned by distinct biological substrates. In contrast, empirical research over the past 30 years conducted in disciplines ranging from experimental psychopathology to the neurosciences suggest that a common set of cognitive, affective, behavioral, and neurophysiological processes underlie a wide range of psychosocial morbidities. Many of these processes are prevalent among persons with and without clinical symptomatology and may have evolved as conserved adaptations to the demands of survival in a harsh and dangerous world. Yet, in the context of modern society where such mortal threats are less commonplace, such processes have become maladaptive and undermine well-being. Recent findings from cognitive, affective, and neurobiological science indicate that the information-processing capacities of the human brain can be subverted by automatic habitual reactions, biased toward negative objects and events, and depleted through suppression.
Compared with categorical taxonomies, the transdiagnostic approach is more consistent with a dimensional model of psychological distress and more clearly identifies the processes whereby unwanted and maladaptive symptoms are produced. This approach parallels new insights into medicine. Among oncologists, there is recognition that cancer is extremely heterogeneous, and thus broad diagnostic categories cannot fully describe the multifarious pathways and mediators that undergird the disease (Chan & Ginsburg, 2011; Roukos, 2011). Thus, efforts in “personalized medicine” have been aimed at identifying the specific genetic and environmental mechanisms at play in a given instance of cancer (Gonzalez-Angulo, Hennessy, & Mills, 2010; Hamburg & Collins, 2010). This novel approach is founded on the notion that effective intervention is made possible through the identification of causal agents. At the same time, cancer involves a number cross-cutting processes (e.g., inflammation, metabolic dysregulation, oxidative stress) that underlie a broad spectrum of physical symptoms found in other diseases, like heart disease (Andreotti, Porto, Crea, & Maseri, 2002) and diabetes (Haffner, 2006). Unlike cancer, the various forms of psychological distress and their underlying transdiagnostic mechanisms detailed in this article cannot be reduced to a mere biological mechanism. Yet, like personalized medicine in cancer care, a transdiagnostic approach that accounts for variability stemming from individual differences and factors common to a wide range of psychosocial problems may hold considerable utility for social workers engaged in the alleviation of suffering.
The present discussion is limited in several respects. First, most of the literature pertaining to transdiagnostic processes is comprised of studies that compare differences in the magnitude, valence, and content of a given phenomenon (e.g., attentional bias) between individuals who do and do not meet the criteria for a given DSM diagnosis. To transcend the current nosology, research on transdiagnostic processes should examine the full range of their expression across the general population using analytic techniques that are sensitive to individual differences. Second, the majority of studies on transdiagnostic processes rely on a biobehavioral approach to understanding the phenomena in question. This is unsurprising, as nearly all such studies originate from the fields of psychology and neuroscience. Social work, with its unique emphasis and ethical commitment, would be well positioned to conduct a more holistic form of transdiagnostic research and practice that integrates biobehavioral knowledge with sociocultural, economic, and political perspectives in understanding and addressing human suffering.
The processes described in this article do not represent the sum total of transdiagnostic mechanisms, nor are they exclusively represented by the spectrum of diagnosable conditions listed herein. To wit, although these processes take various configurations according to the current concerns, emotional state, and learning history of the individual, there may be common biopsychosocial structures underlying the diverse clinical presentations of individuals served by social workers. Thus, to be of greatest benefit to vulnerable persons, we must advance the field of clinical social work by integrating findings from 21st century science into models of social work practice that eschew a single-minded fixation on taxonomy for the more broad-minded goal of addressing malleable mechanisms common to the varieties of human suffering.
Footnotes
Declaration of Conflicting Interests
The authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
Funding
The authors disclosed receipt of the following financial support for the research, authorship, and/or publication of this article: E.L.G. was supported in preparing this manuscript by grant R03DA032517 from the National Institute of Drug Abuse.