Depression has a broad, adverse impact across numerous domains of functioning and reduces quality of life (Greer et al., 2010; McKnight and Kashdan, 2009). Approximately three out of five persons with a major depressive disorder report severe impairment associated with their syndrome (Kessler et al., 2003), and the economic burden in 2010 was estimated at $210.5 billion (Greenberg et al., 2015). Compared with patients with chronic medical conditions, people with depression report greater physical and mental impairment 2 years after treatment (Hays et al., 1995). However, despite the emotional and economic burdens related to functional impairment, clinical trials generally fail to focus on functional outcomes (McKnight and Kashdan, 2009), and relatively little theory or research focuses on the nature of that impairment and, in particular, the processes leading to it.
The criterion of clinically significant impairment was added to the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV; American Psychiatric Association, 1994) in 1994 in response to the lack of an objective somatic validator for the diagnosis and for the purpose of separating pathological disorders from nonpathological problems of living (Widiger, 2007), thereby ensuring that diagnosed disorders led to significant consequences (Spitzer and Wakefield, 1999). The relatively late inclusion of the impairment criterion was due partly to the assumption that impairment is inherent in some symptoms of depression (e.g., inability to concentrate, low energy), which would make the impairment criterion redundant (Spitzer and Wakefield, 1999). However, correlations between depression severity and degree of impairment are nowhere near perfect and, in fact, vary widely. In a review by McKnight and Kashdan (2009), the magnitude of this relationship ranged from 0.15 to 0.77 for social functioning and 0.08 to 0.77 for occupational functioning. Part of this variability is likely due to how depression severity was operationalized, with studies finding a stronger association between functional impairment and symptom severity in contrast to symptom count (Karsten et al., 2010). More recently, Fried and Nesse (2014) examined the impact of the severity of 14 individual depressive symptoms on impairment in five domains of functioning. The associations of impairment and the severities of symptoms varied widely by both individual symptom and domain of impairment.
In this same vein, the publication of the International Classification of Functioning, Disability and Health (ICF; World Health Organization, 2001) played an important role in emphasizing that functional impairment is a “dynamic interaction between a person's health condition, environmental factors and personal factors” (WHO, 2013, p. 5). Thus, environmental and personal factors moderate the impact of health conditions, enhancing or buffering their effects. The personal factors component of the ICF has been slower to develop and has tended to focus on identifying and classifying individual difference variables (e.g., demographics and personality) associated with impairment (Müller and Geyh, 2015). In contrast to moderating variables, much less attention has been focused on processes that mediate between health conditions and changes in functioning.
In addition to the simple severity of symptoms, previous research suggests that there may be other processes through which symptoms lead to negative outcomes. For example, Buist-Bouwman and colleagues (2008) found that embarrassment and concentration and attention problems mediated between depression and work functioning. Similarly, Hanson and Young (2012) found that the distress caused by individual depressive symptoms often was mediated by the meanings and implications attributed to the symptoms. For example, a symptom was distressing because it meant the person was “abnormal” or “no longer my real self.” Such cognitive content (in contrast to cognitive processes such as attention and memory) may similarly constitute processes leading from depressive symptoms to impairment. Although objectively establishing causal relationships between symptoms and impairment may be difficult, documenting clients' understanding of how impairment is caused by their depressive symptoms can be studied. These conceptualizations can provide insight into the processes by which impairment is generated in individual clients and potentially can be made use of in assessment and intervention.
The goal of the present study was to develop an understanding of the impairment experienced by depressed clients through eliciting their explanations of how their individual depressive symptoms cause impairment. Thus, the study extends previous work by focusing specifically on depression, on individual symptoms, and on mediating (as opposed to moderating) processes. Although it would be desirable to assume that patients' reports accurately represent the actual causal processes linking symptoms to functioning, we are cautious about making this inference and so we frame the issue in terms of clients' formulations. Because little previous research has addressed this specific issue, a thematic analysis methodology (Braun and Clarke, 2006) was used, which provided an inductive method for analyzing qualitative data without a priori hypotheses and which is free from extensive theory-building requirements (Charmaz, 2006; Corbin and Strauss, 2008). Similar qualitative methods have been applied recently to understanding self-management approaches taken by patients with long-term depression (Chambers et al., 2015).
This study was part of a larger project that assessed participants' understandings of how depressive symptoms cause distress and impairment (Hanson and Young, 2012).
Of the 18 participants, 16 were recruited from a suburban mental health clinic and 2 others were recruited from another university's research study (for details, see Hanson and Young, 2012). Participants needed to be at least 18 years of age, be free of current psychotic symptoms, and had experienced at least five DSM-IV symptoms of a depressive episode within the same 2 weeks at some point during the past 12 months (criteria for a major depressive episode have not changed in DSM-5). To enhance the generalizability of the results, no exclusions were made for comorbid psychiatric or medical disorders. In addition, because the study focused on depressive symptomatology as opposed to diagnosis, depression assessment was limited to depressive symptom severity. Severity of current depressive symptoms ranged from mild to severe, as measured by the Beck Depression Inventory-II (BDI-II; Beck et al., 1961, 1961–1996): range, 15–50; mean (SD); 29.4 (11.1).
Of the 33 individuals screened for eligibility, 18 participants completed the study, 13 did not attend their research appointment, and 2 did not meet eligibility criteria. Characteristics of the sample (which are reasonably representative of the suburban mental health center's catchment area; United States Census Bureau, 2000) are presented in Table 1.
The study was approved by the authors' university institutional review board. After providing informed consent, participants completed a semistructured interview regarding the reasons why their depressive symptoms were distressing and how their depressive symptoms caused impairment. First, the presence of a specific symptom was assessed using the relevant questions from the Structured Clinical Interview for DSM-IV (First et al., 1997). Symptoms consisted of feeling down or depressed, loss of interest or pleasure, changes in appetite, changes in sleep, low energy, feeling worthless or guilty, feeling discouraged, pessimistic or hopeless, trouble thinking or concentrating, suicidal ideation, and psychomotor agitation or retardation (the last of these was not coded due to its low frequency). Second, if a symptom was endorsed, questions were asked about how the symptom caused impairment (e.g., “How did [symptom] get in the way of your daily life?”; “How did [symptom] get in the way of doing other things?”). Follow-up questions were asked to clarify responses. The interview format followed the same steps for each depressive symptom. Although the same information was solicited about each symptom, the questions were not really identical because they were about different symptoms. The interviewer used his clinical skills to keep this point clear and to keep the interview from seeming repetitive. In addition, participants completed the BDI-II (Beck et al., 1961, 1961–1996) as a measure of overall depression symptom severity. Following this protocol, participants were debriefed and compensated with a gift card. The data collection protocol was administered by the first author. Interviews were audio recorded, transcribed, and entered into the MAXQDA2007 qualitative analysis program (VERBI Software. MAXQDA2007. [Computer Software]).
Coding the responses followed the procedures described by Braun and Clarke (2006) and the standards for reliability and validity for qualitative data described by Stiles (1993). After a thorough reading of the transcripts, the first author generated initial codes that provided a concise, descriptive label for each explanation of how a symptom caused impairment. Initial codes were then grouped together into themes based on common content. Next, in intensive discussions, the two authors together examined the definitions and boundaries of themes, which were then further developed and refined by rereading transcripts and comparing examples across participants and across symptoms. This procedure first was conducted for the first nine participants. After this, interviews were conducted with the remaining nine participants and the coding was repeated as just described, further developing the themes, as appropriate. The data collection and coding process was stopped at the point at which saturation was obtained, that is, when the “…data no longer spark new theoretical insights, nor reveals new properties of these core theoretical categories,” (Charmaz, 2006, p. 113).
Overall, the 18 participants endorsed 139 symptoms during the semistructured interview and provided responses about how each symptom impaired their daily life. Responses fell into three content areas: domains of impairment (what was impaired), experience of impairment (nature and severity of the impairment), and pathways to impairment (how symptoms led to impairment). Domains of impairment indicated the situations in which clients were impaired and closely mirrored the six domains delineated in the World Health Organizations Disability Assessment Schedule 2.0 (WHODAS 2.0; World Health Organization, 2010): cognition, mobility, self-care, interacting with others, participation in community activities, and completion of daily activities. These are not discussed further.
Experiences of Impairment
Participants described five types of impairment of increasing severity, representing how well the participant performed his or her usual activities. In eight instances, participants reported that, despite the presence of the symptom, they could do activities as easily and as well. Six of these instances concerned changes in appetite. In 16 other instances, activities still could be done as well as usual, but this required greater time, effort, or attention (“reduced efficiency”). The following exchange illustrates this type of impairment.
Researcher: “How is it that trouble thinking and concentrating gets in the way of daily activities?”
Participant: “It leads me to double, triple check things; it's slowed me down a good deal…and causes things to pile up.”
Alternatively, it was common for participants to report that their activities were completed, but less well than previously (“reduced performance”; 25 reports). The following example concerns psychomotor symptoms.
Participant: “…because I'm an instructor, so I have to be able to communicate with my students. And of course when my speech changes, and if it changes dramatically, then my communication isn't as effective.”
The other two types of impairment described not doing usual activities. In some cases, usual activities were actively avoided, by choice rather than due to an inability (“avoidance”; 26 reports). The following example demonstrates how, in response to “feeling hopeless,” the participant chose to disengage from her social network:
Participant: “I've got to be alone. Because it is hard being around other people because I guess they'll sense my unhappiness. And I just don't want to bother them with my problems. I've always been the strong one; I just don't want to get anyone else upset because I'm upset…”
Finally, sometimes participants reported that the symptom made an activity impossible to perform (“incapacitated”; 31 reports). As shown in the follow excerpt, impairment was experienced as complete instead of as a reduced ability or decision:
Researcher: “And how does [low energy] get in the way of daily life”
Participant: “I can't do anything…I have no interests when I have low energy. It's like ‘c'mon man, let's go somewhere’…no, [not] even stuff I used to enjoy.”
Experiences of impairment represents a continuum of impairment severity that ranges from no impairment to severe impairment but that was expressed in terms of efficiency, effectiveness, and capability. Participants routinely provided responses along different points of this continuum in reference to specific symptoms, suggesting that the burden of impairment is spread unequally across symptoms. More severe impairment ratings, characterized by “avoidance” and “incapacitated,” were most often associated with symptoms of depressed mood, feeling worthless or guilty, and suicidal ideation. In contrast, descriptions of less severe impairment (e.g., “reduced efficiency” and “reduced performance”) were most often associated with symptoms of sleep disturbance, low energy, and trouble thinking and concentrating. Appetite changes were described as “not impairing” by a majority of participants.
Pathways to Impairment
Participants described three processes by which a symptom of depression led to impairment in their daily lives. These distinctions were based on whether impairment was caused directly by a symptom, indirectly through other symptoms, or indirectly through mediating processes. This pattern of direct and indirect pathways is similar to what has been found for why depressive symptoms cause distress (Hanson and Young, 2012; Spitzer and Wakefield, 1999).
“Unmediated impairment” (55 reports; 48.2%) refers to impairment being either inherent in the definition of the symptom (e.g., psychomotor slowing) or a direct consequence of the symptom. For example,
Researcher: “How would having trouble thinking or concentrating impair your daily life?”
Participant: “I couldn't make decisions!”
In other situations, one symptom caused or exacerbated another symptom, and that second symptom directly caused the impairment. These “secondary symptom impairments” (26 reports; 22.8%) were mediated in the sense that that original symptom did not directly lead to impairment. However, they also might be conceptualized as “unmediated, one symptom removed” because the impairment came directly from symptoms and not from reactions to symptoms (as described below). The symptom most commonly identified as leading to a secondary symptom was “sleep problems” (reported five times) and is demonstrated in the following example.
Researcher: “How do sleep problems get in the way of your daily life?”
Participant: “They made me tired the following day, when I'd have a lack of concentration.”
In another example, eating less indirectly led to impairment.
Researcher: Eating less than usual—does that get in way of your daily life?
Participant: Yeah, I think it does…maybe sleeping more than usual....energy levels, as far as throughout the day, or even having energy for physical activities.
Researcher: And those are both related to how much you are eating?
Participant: Yeah, I think so…definitely.
In addition to responses indicating direct connections between symptoms and impairment, participants identified instances of symptoms causing impairment indirectly, mediated by cognitive, affective, and behavioral responses to depressive symptoms (“mediated”; 33 reports; 29.0%). For example,
Researcher: Okay, does your appetite being high, eating a lot, and gaining weight, does that interfere with your doing your everyday activities?
Participant: I'll say yes and I'll say it briefly. I'm ashamed because I'm so fat, so I don't want to be around people I used to be around.
Another excerpt illustrates how negative thoughts that accompanied depressed mood caused impairment:
Researcher: How does feeling sad and depressed get in the way of daily life?
Participant: I won't even make it out the door, because I might think, ‘what's the point,’ or ‘how is this going to help’…
Researcher: So it's related to bad thoughts and it's hard to get out of [that thinking]?
Participant: Right…even social activities, ‘what's the point of going to this.’ ‘You're not gonna blend in.’ ‘You have these problems.’ ‘They're going to think you're crazy or something's wrong with you.’ ‘They'll be able to tell.’
These three pathways of impairment capture the various ways in which participants reported that symptoms of depression caused impairment. Across all their symptoms, individual participants frequently reported all three pathways, and sometimes gave multiple pathways for individual symptoms. In addition, mediated pathways were commonly described in relation to affective symptoms (i.e., “feeling depressed,” “feeling worthless or guilty”) and suicidal ideation. These mediating pathways often consisted of negative cognitions that reduce motivation to engage in potentially rewarding activities (e.g., “Nobody's going to hire me”; “I'm not going to be able to finish school”; “What's the point of trying?”) or maladaptive coping behaviors that led to additional impairment (e.g., binge eating; substance abuse). These pathways were present across various domains of participants' lives, including occupational functioning, interpersonal effectiveness, parenting abilities, and numerous independent activities of daily living.
Thematic analysis of the symptom impairment data revealed three themes—domains of impairment, experiences of impairment, and pathways to impairment—which, respectively, represented participants' conceptualizations of what tasks are impaired, the type and severity of the impairment, and the processes by which symptoms caused impairment. Patterns of association between particular symptoms and particular experiences of, and pathways to, impairment emerged, which provides evidence that clients were able to conceptualize impairment at a symptom level. These associations were most apparent when contrasting cognitive/affective symptoms of depression (e.g., low mood, feeling worthless or guilty, suicidal ideation) and vegetative symptoms of depression (e.g., low energy, trouble thinking or concentrating, sleep problems). Impairment was often most severe (i.e., “avoidance,” “incapacitated”) in reference to cognitive/affective symptoms and less severe (i.e., “reduced performance,” “reduced efficiency”) in relation to vegetative symptoms. In addition, impairment caused by cognitive/affective symptoms tended to be described as “mediated,” whereas vegetative symptoms were more commonly described as causing impairment through “unmediated” or “secondary symptom” pathways. Thus, vegetative symptoms were more likely to be sources of impairments that are unmediated and less severe by reducing efficiency and reducing performance. In contrast, cognitive/affective symptoms were more likely to be sources of impairments that are cognitively mediated and more severe by precluding performance (avoidance and disability). It is worth noting that greater impairments were reported to come from psychological elaborations of symptoms than from basic vegetative changes. The idea that cognitive responses to symptoms lead to behavioral impairment is consistent with well-established, long-standing conceptualizations. For example, if we consider experiencing a symptom as a stressor, symptom-related impairment fits with the formulation that response to stress depends on the appraisal of that stressor (Lazarus and Folkman, 1984). Similarly, if we consider impairment as a response to symptoms, symptom-related impairment fits with the formulation that illness behaviors depend on the interpretation of the symptoms (Mechanic, 1986).
Participants' descriptions of experiences of impairment illustrate the language individuals use to convey the severity and nature of their impairment and which go beyond commonly used generic labels of “mild,” “moderate,” and “severe” (including the WHODAS 2.0; WHO, 2010). Comparison of our severity of impairment categories with those of the European Study of the Epidemiology of Mental Disorders (ESEMeD; see Buist-Bouwman et al., 2008, p. 453) is informative for both the similarities and differences. In addition to both sets of categories including being unable to carry out normal activities, the ESEMeD differentiates between decrements in quantity of work done and quality of work done. In contrast, although our findings did not differentiate these types of reduced performance, they did differentiate maintenance of performance that was more difficult to achieve (“efficiency”). In addition, our findings differentiated avoidance or delay of activities. This phenomenon is alluded to in the ESEMeD (“had to cut down/back”) but is not separated out and occurs in more than one category. Recognition of avoidance/delay as a separate phenomenon may be important because it may represent a coping mechanism whose use varies across individuals. Recent psychometric analysis of impairment category ratings of 741 participants indicates that avoid/delay represents a different dimension of impairment than does “as well, more difficult, less well, unable” (Fuller and Young, 2016). The point here is not that one approach is correct or incorrect, but that the full variety of patients' experience of impairment should be considered.
In addition to improving our clinical assessments, studying the nature of impairment may have the potential to improve clinical interventions and functional outcomes, which are of central concern to the client, other people in his or her life, and society in general (Greer et al., 2010). A formulation of pathways to impairment identifies opportunities to reduce impairments associated with depressive symptoms, but independent of symptom reduction itself. For example, impairments that are related to mediating cognitions could be reduced by cognitive therapy assessing the accuracy of those cognitions or through acceptance of the presence of the symptom without further elaboration or assignment of meaning. On the other hand, impairments that come directly from the symptom (unmediated) might be better addressed with acceptance of the presence of the symptom and the development of coping mechanisms (in addition to interventions targeted at symptom reduction). Understanding the types of impairment experience also may be useful. For example, therapeutic work might differ based on whether the client is struggling with a) the effort required to maintain his or her performance, b) coping with reduced performance, c) engaging in avoidance, or d) coping with incapacity. In addition, these issues related to different experiences of impairment may differ across domains of activity (e.g., social, work).
Furthermore, eliciting a client's conceptualization of the impairment caused by depressive symptoms invites a collaborative therapeutic alliance that uses a conceptualization based on the client's experience. Mutual agreement regarding treatment rationale and course constitutes a key component in building a therapeutic alliance (Horvath and Greenberg, 1989), which has robust relationships with symptom improvement across mental health conditions (Horvath et al., 2011; Martin et al., 2000) and depression, specifically (e.g., Arnow et al., 2013). Additionally, therapist credibility (Worthington and Atkinson, 1996) and a client's satisfaction with therapy (Tracey, 1988) and perception of the helpfulness of treatment (Iselin and Addis, 2003) are all positively influenced by the congruence between client's and clinician's views of etiology and treatment, and these benefits may extend to the etiology of impairment (i.e., pathways to impairment). Whether incorporating these kinds of focus on impairment into therapy does, in fact, affect outcomes is an empirical question that requires empirical research.
This study had three main limitations. First, the sample was small and obtained primarily at a suburban community mental health center in the Midwest; thus, the generalizability of the results to individuals in primary care or in rural or urban settings is unknown. Nevertheless, the sample was reasonably diverse in terms of education, ethnicity, sex, and depressive symptom severity. Second, the themes identified are limited by the insights of the participants and the abilities of the coders. Third, the sample was heterogeneous with respect to comorbid mental health or medical conditions, which allows for the possibility of misattributions for the sources or severity of impairment. On the other hand and as stated previously, the inclusion of individuals with comorbid conditions increases the generalizability of our results. All of these limitations are best addressed through replication and continued research.
This project succeeded in identifying clients' experiences of impairment and clients' beliefs about how depressive symptoms cause impairment, as well as in highlighting potential patterns between specific symptoms and these themes. The themes identified through this inductive process potentially can be applied to clinical interventions and can guide the development or refinement of impairment assessments. Clarifying clients' beliefs about the etiology of impairment has the potential to improve the therapeutic alliance as well as provide a basis for interventions that target the cognitive, behavioral, and affective processes that maintain or exacerbate symptoms of depression. Taken together, the findings demonstrate the heterogeneity of impairment experiences and take an initial step in bringing the clients' perspective of impairment into current clinical practice and research.
The authors declare no conflict of interest.
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