Hypothetical constructs have a long history in the study of psychology and human behaviour (MacCorquodale & Meehl, 1948; Cronbach & Meehl, 1955; Strauss & Smith, 2009), and their main purpose has been to help identify the theoretical mechanisms that underlie performance and behaviour (Whitely, 1983). In clinical psychology research, constructs have played an important part in the development of models of anxious psychopathology – especially in the years since cognitive approaches to understanding anxiety have become prevalent. Clinical constructs are often developed from the researchers own clinical experiences, and they represent hypothetical structures that usually attempt to summarize important aspects of the patient experience and integrate this with one or more theoretically important process that the researcher believes underlies the symptoms. In the past 20-30 years many theoretically influential clinical constructs have been developed during research on the aetiology and maintenance of anxiety disorders. Some of the more influential of these include inflated responsibility (Salkovskis, 1985), intolerance of uncertainty (Dugas, Gagnon, Ladouceur & Freeston, 1998), clinical perfectionism (Shafran, Cooper & Fairburn, 2002), and thought-action fusion (Shafran & Rachman, 2004), to name but a few. There is no doubt that clinical constructs have been influential in the development of theories of anxiety-based psychopathology, and these constructs have a prima facie clinical relevance and respectability by emerging from clinical experience, idiographic assessment, from illustrative case histories, exploratory qualitative methods, or content analysis of patient self-report statements (e.g. Frost, Steketee, Amir et al., 1997; Freeston, Rheaume, Letarte, Dugas & Ladouceur, 1994).
At this point it is important to understand the role that clinical psychology researchers see for the clinical constructs they develop. Without a doubt, in the majority of cases talk of a ‘causal’ or ‘explanatory’ role in the elicitation and maintenance of symptoms creeps into the discussion. For example, Koerner & Dugas (2006) note that intolerance of uncertainty “is thought to lead to worry directly” (2006, p201); Salkovskis, Wroe, Gledhill, Morrison et al. (2000) write that “the occurrence and/or content of intrusions (thoughts, images, impulses and/or doubts) are interpreted (appraised) as indicating that the person may be responsible for harm to themselves or others. This leads both to adverse mood (anxiety and depression) and the decision and motivation to engage in neutralising behaviours (which can include a range of behaviours such as compulsive checking, washing and covert ritualising)” (2000, p348; my italics); Shafran, Thordarson & Rachman (1996) write that “increased endorsement of dysfunctional beliefs, particularly TAF [thought-action fusion] is likely to exacerbate low self-esteem, depression, anxiety, and perceived responsibility for the event.” (1996, p379). The implication of causation of construct on symptoms is further alluded to in the box-and-arrow schematic models of emotion-based disorders that have become associated with research on some of these clinical constructs (Davey, 2003). There is no doubt that such constructs help us to conceptualize the psychological processes and states involved in a specific psychopathology, but is there any basis for assuming that their role is a causal one?
In order to elevate these hypothetical constructs to the level of empirically verifiable and usable entities the constructs have to become measurable and, in many cases, manipulable – especially if they are to prove useful in clinical interventions. This process usually proceeds with the researcher describing the defining features of the construct and developing an instrument to measure the construct. Once a set of the defining features of the construct has been established, subsequent measurement instruments are developed and validated. Having defined the construct’s main features and developed a measurement instrument, the construct is now experimentally manipulable and objectively measurable according to standard empirical and scientific tenets. Subsequent controlled manipulation of the construct may result in observable changes in symptoms, leading us to conclude that the construct plays a direct or indirect causal role in determining the appearance or strength of the symptoms. These manipulations may be in the form of potential therapeutic interventions or in the form of a controlled experimental manipulation (e.g. the effect of manipulation of inflated responsibility or intolerance of uncertainty on compulsive behaviour). At this point, the construct has become a recognizable explanatory feature of the psychopathology, supported by empirical evidence in the form of its measurable relationship with symptoms (through correlational and regression analyses) and demonstrable effects on symptoms (through experimental manipulation).
The process described above appears to be an admirable attempt by clinical researchers to objectify their clinical experiences and subject them to rigorous, scientific analysis. At the end of this process we have constructs that are measurable and manipulable and can be empirically tested in their relationship with psychopathology symptoms. However, we need to be aware that clinical constructs are not directly observable and need to be inferred from the behaviour and responses of our patients and experimental participants. Inferential techniques, by their very nature, rely on observable behaviour to tell us something about the existence and behaviour of the unobservable psychological mechanisms that underlie performance (Whitely, 1983; Strauss & Smith, 2009). What is important about these inferential processes is that we cannot use the same behavioural anchors to verify the construct and then use them as outcome measures in experiments/interventions to determine whether the construct has an explanatory role or causal effect.
This logical inconsistency appears to be what happens in the research history of many clinical constructs. The confounding factor is that the construct is verified on the basis of patient reports about their psychopathology experiences and their symptoms or on researchers’ assumptions about these experiences (e.g. Frost, Steketee, Amir et al., 1997; Shafran, Thordarson & Rachman, 1996; Chambless, Caputo, Bright & Gallagher, 1984; Dunmore, Clark & Ehlers, 1999). When unpacked, many validated measures of clinical constructs resemble a list of questions about symptoms. It should then come as no surprise that (1) measures of the construct are significantly correlated with measures of symptoms, and (2) manipulating the construct causes concomitant predictable changes in symptoms. This raises serious doubts about concluding that the construct or the psychological states defined by the construct cause the symptoms or are even an explanation of the symptoms. To be fair, there are good arguments for saying that clinical constructs have helped to develop effective interventions for anxiety disorders. But it’s impossible to say that they are effective because they address the ‘causes’ of symptoms rather than the symptoms themselves. If the same behaviours (symptoms) are used to both verify the construct and to explore the construct’s explanatory role in the psychopathology then construct and symptoms are essentially the same thing. Logically, many clinical constructs do not exist other than being extrapolated from the symptoms that they are developed to explain. This relationship between clinical constructs and the behaviours they are developed to explain is reminiscent of what Ryle (1949) called a category mistake. Ryle wrote that:
“..when we describe people as exercising qualities of mind, we are not referring to occult episodes of which their overt acts and utterances are effects; we are referring to those overt acts and utterances themselves” (1949, p26).
Given that very many clinical constructs are defined in ways that represent mental states of which symptoms are deemed to be their effects then we must seriously consider that the clinical construct approach to explaining psychopathology is also underpinned by a category mistake. In their discussion of constructs in clinical psychology research, Strauss & Smith (2009) distinguish between constructs developed as tools to measure and predict behaviour (constructs based on “nomothetic span”), and those constructs that go beyond the data used to support them and postulate entities, processes or events that are not directly observed but which may underlie behaviour - known as “construct representation” (e.g. Whiteley, 1983; Strauss & Smith, 2009; MacCorquodale & Meehl, 1948). It is arguable that the current approach to clinical constructs in clinical psychology research has generated a culture in which clinical constructs proliferate without being properly theoretically defined – especially in the sense that they might represent constructs based on nomothetic span or construct representation. It may well turn out that many of those clinical constructs that have been researched so avidly in the past 10-15 years are no more than basic redescriptions of the symptoms they are often thought to explain.
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 Clinical constructs as latent categorical variables can also be inferred statistically (e.g. Meehl, 1995; Ruscio, Ruscio & Carney, 2011), but these too will usually have their origins in clinical practice or clinical theory and are used to advance the development of causal theories (e.g. Haslam, 1997; Meehl, 1992). This discussion will be limited to those clinical constructs developed to explain (rather than categorize) anxiety disorders.
 “Nomothetic span” refers to the pattern of significant relationships among measures of the same or different constructs (i.e. convergent and discriminant validity) (Whitely, 1983; Strauss & Smith, 2009). Thus, the descriptive validity of a construct is established by observing that it is related to measures it should be theoretically related to and not related to measures that it should not be theoretically related to.