CBI – Literatuur college 2
Cognitive and Behavioral Interventions in Medically Unexplained Symptoms
and syndromes
Voorbereiding
The cognitive behavioral model of medically unexplained symptoms: A theoretical
and empirical review – Deary, Chalder & Sharpe (2007)
The cognitive behavioral model of medically unexplained symptoms: A
theoretical and empirical review – Deary, Chalder & Sharpe (2007)
This article discusses a theoretical, empirically based, cognitive behavioral model of
Medically Unexplained Symptoms (MUS) in general, and for chronic fatigue syndrome (CFS)
and irritable bowel syndrome (IBS) in particular.
Introduction: Defining terms
De term Medically Unexplained Symptoms (MUS) consists of three different aspects;
The occurrence of symptoms in the absence of obvious pathology.
Individual clinical syndromes such as chronic fatigue syndrome (CFS) and irritable
bowel syndrome (IBS).
A subset of the DSM-4 somatoform disorders category.
Recent reviews have validated the efficacy of CBT, but there has been less focus on the model
on which these treatments are based. This narrative review will focus primarily on the
theoretical base and empirical evidence for the CBT model of MUS in general, and for CFS
and IBS in particular.
The model
The CBT model of MUS retains to the three P’s – Predisposing, precipitating and
perpetuating factors. Treatment tends to initially focus on the perpetuating cycle, attempting
to dismantle the self-maintaining interlock of cognitive, behavioral and physiological
responses. The essence of any CBT model is a vicious circle, namely a perpetuating
interaction between different domains that maintain symptoms, distress and disability. The
CBT models of MUS, CFS and IBS propose a model of perpetuation that is autopoietic, also
known as ‘self-producing’. This means that the models propose a unique autopoietic
interaction of cognitive, behavioral and physiological factors, for the generation of physical
symptoms in the absence of physical pathology or psychopathology.
1
, Components of the CBT model for MUPS
Predisposing factors
Genetics and early experience – There is some evidence for a genetic influence in
the development of both unexplained fatigue and somatization, but this could simply
reflect the expression of an inheritable predisposition to general distress. There is also
some evidence that certain types of early childhood experiences increase the risk of
developing MUS. For example childhood experiences of parental illness could be a
risk factor and vicariously learned illness behavior could later serve to perpetuate
symptoms. Next to that, childhood adversities in the form of physical or sexual abuse
form a risk factor for MUS in general, IBS, CFS, fibromyalgia and somatizations
disorders. This is possibly linked through sensitization mechanisms.
Neuroticism and somatopsychic distress – Neuroticism (N) as a personality trait
refers to a stable life-long tendency to experience negative affect. It shouldn’t be seen
as just a psychological trait but more as a general predisposition to experience
“somatopsychic distress.”. N also seems to be an important predictor of generic
vulnerability to physical illness and psychological distress. It doesn’t come as a
surprise that high N is associated with MUS in general, and with both CFS and IBS. In
CFS, it is most likely the ‘negative’ self-critical aspect that is positively correlated
with neuroticism. An interesting possibility is that N could also explain the genetic
component of MUS, seeing as N is moderately inheritable itself. Next to that N is also
associated with several mechanisms the CBT model hypothesizes to be precipitating
and perpetuating of MUS. For example harm-avoidance or having a biased attention to
somatic danger signals such as pain or fear. Lastly, N seems to be higher in females,
which could explain why MUS seems to be slightly more prevalent among women.
Perpetuating factors
The CBT model proposes that cognitive and behavioral factors interact with physical factors
to produce symptoms.
Sensitization – Sensitization refers to the tendency to have a heightened response to
stimuli because of prior experience with them. Research has studied a specific
sensitization mechanism, known as long term potentiation (LTP). LTP can be
induced in pain pathways by prior experience of pain or harmful stimulation, which
lower the threshold for future stimulation. It is suggested that central mechanisms such
as vigilance and attention (or the effects of anxiety, depression or stress) may dampen
the inhibition of these pathways, lowering the threshold even further. This could lead
to normally harmless sensations being experienced as pain, leading in turn to further
sensitization and vigilance. Here we have the beginning of an autopoietic mechanism
maintaining the experience of pain. LTP also illuminates that previous physical trauma
leads to increased pain sensitivity.
o The HPA axis and sensitization – Physical and emotional stress in humans
causes a hormonal process, beginning in the hypothalamus, passing to the
pituitary glands and ending with the increased production of cortisol from the
adrenal cortex. Within this HPA axis system, both positive and negative
feedback loops exist to regulate the body's response to acute and chronic
2
Cognitive and Behavioral Interventions in Medically Unexplained Symptoms
and syndromes
Voorbereiding
The cognitive behavioral model of medically unexplained symptoms: A theoretical
and empirical review – Deary, Chalder & Sharpe (2007)
The cognitive behavioral model of medically unexplained symptoms: A
theoretical and empirical review – Deary, Chalder & Sharpe (2007)
This article discusses a theoretical, empirically based, cognitive behavioral model of
Medically Unexplained Symptoms (MUS) in general, and for chronic fatigue syndrome (CFS)
and irritable bowel syndrome (IBS) in particular.
Introduction: Defining terms
De term Medically Unexplained Symptoms (MUS) consists of three different aspects;
The occurrence of symptoms in the absence of obvious pathology.
Individual clinical syndromes such as chronic fatigue syndrome (CFS) and irritable
bowel syndrome (IBS).
A subset of the DSM-4 somatoform disorders category.
Recent reviews have validated the efficacy of CBT, but there has been less focus on the model
on which these treatments are based. This narrative review will focus primarily on the
theoretical base and empirical evidence for the CBT model of MUS in general, and for CFS
and IBS in particular.
The model
The CBT model of MUS retains to the three P’s – Predisposing, precipitating and
perpetuating factors. Treatment tends to initially focus on the perpetuating cycle, attempting
to dismantle the self-maintaining interlock of cognitive, behavioral and physiological
responses. The essence of any CBT model is a vicious circle, namely a perpetuating
interaction between different domains that maintain symptoms, distress and disability. The
CBT models of MUS, CFS and IBS propose a model of perpetuation that is autopoietic, also
known as ‘self-producing’. This means that the models propose a unique autopoietic
interaction of cognitive, behavioral and physiological factors, for the generation of physical
symptoms in the absence of physical pathology or psychopathology.
1
, Components of the CBT model for MUPS
Predisposing factors
Genetics and early experience – There is some evidence for a genetic influence in
the development of both unexplained fatigue and somatization, but this could simply
reflect the expression of an inheritable predisposition to general distress. There is also
some evidence that certain types of early childhood experiences increase the risk of
developing MUS. For example childhood experiences of parental illness could be a
risk factor and vicariously learned illness behavior could later serve to perpetuate
symptoms. Next to that, childhood adversities in the form of physical or sexual abuse
form a risk factor for MUS in general, IBS, CFS, fibromyalgia and somatizations
disorders. This is possibly linked through sensitization mechanisms.
Neuroticism and somatopsychic distress – Neuroticism (N) as a personality trait
refers to a stable life-long tendency to experience negative affect. It shouldn’t be seen
as just a psychological trait but more as a general predisposition to experience
“somatopsychic distress.”. N also seems to be an important predictor of generic
vulnerability to physical illness and psychological distress. It doesn’t come as a
surprise that high N is associated with MUS in general, and with both CFS and IBS. In
CFS, it is most likely the ‘negative’ self-critical aspect that is positively correlated
with neuroticism. An interesting possibility is that N could also explain the genetic
component of MUS, seeing as N is moderately inheritable itself. Next to that N is also
associated with several mechanisms the CBT model hypothesizes to be precipitating
and perpetuating of MUS. For example harm-avoidance or having a biased attention to
somatic danger signals such as pain or fear. Lastly, N seems to be higher in females,
which could explain why MUS seems to be slightly more prevalent among women.
Perpetuating factors
The CBT model proposes that cognitive and behavioral factors interact with physical factors
to produce symptoms.
Sensitization – Sensitization refers to the tendency to have a heightened response to
stimuli because of prior experience with them. Research has studied a specific
sensitization mechanism, known as long term potentiation (LTP). LTP can be
induced in pain pathways by prior experience of pain or harmful stimulation, which
lower the threshold for future stimulation. It is suggested that central mechanisms such
as vigilance and attention (or the effects of anxiety, depression or stress) may dampen
the inhibition of these pathways, lowering the threshold even further. This could lead
to normally harmless sensations being experienced as pain, leading in turn to further
sensitization and vigilance. Here we have the beginning of an autopoietic mechanism
maintaining the experience of pain. LTP also illuminates that previous physical trauma
leads to increased pain sensitivity.
o The HPA axis and sensitization – Physical and emotional stress in humans
causes a hormonal process, beginning in the hypothalamus, passing to the
pituitary glands and ending with the increased production of cortisol from the
adrenal cortex. Within this HPA axis system, both positive and negative
feedback loops exist to regulate the body's response to acute and chronic
2
