Over the past 20 years or so, clinical psychology researchers have
developed cognitive models of psychopathology that have used constructs that
appear to capture the beliefs, attitudes and thought patterns associated with
psychiatric symptoms. These constructs have been used in many ways: to
understand and explain symptoms and to develop new interventions that intervene
by attempting to modify the psychological processes implied by the construct.
Clinical psychology researchers have never been terribly good at articulating
the exact theoretical nature of these constructs, but they are regularly
portrayed as inferred states or processes derived most often from
the clinical experiences of researchers or clinicians in their interactions
with patients (Davey, 2003).
The purpose of these constructs is to help understand psychopathology symptoms,
to provide a basis for developing interventions to treat the psychopathology,
and – in the case of those who advocate cognitive explanations of
psychopathology – to link thoughts, beliefs and cognitive processes to
subsequent symptoms.
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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