Many pain patients are upset at being accused of catastrophizing. This theory claims that our concerns, worries, and fears about our pain are greatly increasing our pain, almost to the point of causing it.
The media picked up on the story and makes catastrophizing the actual cause of chronic pain, so this concept has been very damaging to pain patients seeking medical treatment for the physical causes of their pain.
My main point is this quote from a study:
“Catastrophizing is associated with the pain experience;
however, causation has not been established.”
An earlier post about this from 2009, Pain catastrophizing: a critical review, questions the validity of this concept since there is so much overlap with other negative affect constructs, like depression, which is usually a result of pain, not its cause.
Below are my annotations and comments on four full-text PMC articles about catastrophizing, proving that this concept is far from a proven mechanism of causation,
Manipulation of pain catastrophizing: An experimental study of healthy participants – PubMed – NCBI – J Pain Res. 2008 – free full-text PMC article
Pain catastrophizing is associated with the pain experience; however, causation has not been established
The present study enrolled 100 healthy individuals.
Participants were randomly assigned to repeat a positive, neutral, or one of three catastrophizing statements during a cold pressor task (CPT).
Outcome measures of pain tolerance and pain intensity were recorded
No change was noted in catastrophizing immediately following the CPT (F(1,84) = 0.10, p = 0.75, partial η2 < 0.01) independent of group assignment (F(4,84) = 0.78, p = 0.54, partial η2 = 0.04).
Pain tolerance (F(4) = 0.67, p = 0.62, partial η2 = 0.03) and pain intensity (F(4) = 0.73, p = 0.58, partial η2 = 0.03) did not differ by group.
This study suggests
- catastrophizing may be difficult to manipulate through experimental pain procedures and
- repetition of specific catastrophizing statements was not sufficient to change levels of catastrophizing.
Additionally, pain tolerance and pain intensity did not differ by group assignment.
This study has implications for future studies attempting to experimentally manipulate pain catastrophizing.
Studies which specifically manipulate catastrophizing prior to measuring pain are lacking from the literature and are necessary to establish causation.
The association between catastrophizing and pain has been found to vary depending on when catastrophizing is measured.
For example, catastrophizing measured immediately following experimental pain has been found to correlate more strongly to pain tolerance and severity than measures taken prior to the experimental pain experience (Dixon et al 2004; Edwards et al 2005)
Our findings were similar in that only post experimental pain measures of catastrophizing correlated significantly with pain tolerance.
We attempted to manipulate catastrophizing through the repetition of statements directly related to the specific constructs of rumination, magnification, and helplessness. Catastrophizing ratings following the CPT did not differ from ratings obtained prior to the CPT task.
Specifically, threat has been linked to pain catastrophizing in experimental pain (Jackson et al 2005), and Severeijns and colleagues (2005) manipulated catastrophizing specifically through the increase of threat level.
A person suffering from chronic pain will naturally feel a constant strong threat of not being able to do the things they must or want.
Our attempts to experimentally manipulate catastrophizing may have been ineffective due to an inadequate threat presented by the CPT to healthy participant
Similar to Severeijns and colleagues (2005), we did not observe group differences in pain tolerance or intensity.
Limitations of this study include a healthy sample which may not be generalizable to people experiencing pain
Future studies may wish to attempt to manipulate catastrophizing in individuals experiencing clinical pain or using a more ecologically valid pain stimulus such as delayed onset muscle soreness
Despite the limitations, the present study offers important methodological considerations for the design of future studies.
First, the repetition of phrases consistent with magnification, helplessness, and rumination did not significantly alter pain catastrophizing in comparison to neutral or positive phrases
Second, consistent with prior studies (Dixon et al 2004; Edwards et al 2005), measures of pain catastrophizing taken immediately following an experimental pain task better correlated to experimental pain outcomes
Finally, the present study failed to manipulate catastrophizing and the magnitude of change reported in a prior study which did successfully manipulate catastrophizing (Severeijn et al 2005) was small
Catastrophizing is associated with the pain experience;
With all the talk and enthusiasm for catastrophizing lately, most reports forget this most essential fact:
however, causation has not been established.
We attempted to experimentally manipulate catastrophizing in healthy individuals to observe the effect on pain tolerance and intensity.
We did not observe a change in pain catastrophizing following attempted manipulation.
Furthermore, group differences did not emerge for pain tolerance or intensity.
This study is one of the first to attempt to experimentally manipulate pain catastrophizing and offers important methodological considerations for future research.
Pain catastrophizing and pain-related emotions: influence of age and type of pain. – PubMed – NCBI – Clin J Pain. 2011 Sep; – free full-text PMC article
One of the most important determinants of the individual pain experience is pain catastrophizing [?], reflecting an excessively negative cognitive and emotional orientation toward pain.
This initial statement introduces a theory as fact,
The fact is that physical damage, like a broken bone, can be the “most important determinant of the individual pain experience”.
Its assessment by standard questionnaires, which ask participants to reflect on idiosyncratic past painful experiences, is important.
It is currently not known whether different types of pain differently shape pain catastrophizing.
Furthermore, as the regulation of emotions changes during the life span, age may affect pain catastrophizing, as well.
In this study, 134 healthy participants, differentiated into 2 age groups (20 to 40 y and 50 to 70 y), completed the Pain Catastrophizing Scale with reference to their past experiences with 3 common types of day-to-day pain (headache, back pain, dental pain).
On average, the different types of pain shared one-third of the variance in pain catastrophizing.
Pain-type-specific catastrophizing scores were more strongly related to ratings of sensory and emotional pain characteristics than standard catastrophizing scores.
In younger adults, pain catastrophizing was preferentially associated with emotional responses to pain whereas in older adults, it was preferentially associated with pain intensity ratings.
This study indicates that for day-to-day pain, catastrophizing significantly depends on pain type.
The results suggest the use of pain-type-specific instructions for catastrophizing questionnaires because it may lead to better prediction of clinically relevant pain characteristics, such as pain intensity.
Furthermore, pain catastrophizing seems to change during the life span, with a higher engagement of emotional versus sensory pain processing in younger compared with older adults.
From Catastrophizing to Recovery: a pilot study of a single-session treatment for pain catastrophizing – PubMed – NCBI – J Pain Res. 2014; – free full-text PMC article
Pain catastrophizing (PC) – a pattern of negative cognitive-emotional responses to real or anticipated pain –
- maintains chronic pain and
- undermines medical treatments.
Standard PC treatment involves multiple sessions of cognitive behavioral therapy.
To provide efficient treatment, we developed a single-session, 2-hour class that solely treats PC entitled “From Catastrophizing to Recovery” [FCR].
1) feasibility of FCR;
2) participant ratings for acceptability, understandability, satisfaction, and likelihood to use the information learned; and
3) preliminary efficacy of FCR for reducing PC.
So this study only proves that a session of XXX reduces pain catastrophizing and omits any mention or study of pain levels.
This study says nothing at all about pain because causation has not been established between catastrophizing and pain levels, though many researchers have lost sight of this fact.
Uncontrolled prospective pilot trial with a retrospective chart and database review component.
Seventy-six patients receiving care at an outpatient pain clinic (the Stanford Pain Management Center) attended the class as free treatment and 70 attendees completed and returned an anonymous survey immediately post-class.
The Pain Catastrophizing Scale (PCS) was administered at class check-in (baseline) and at 2, and 4 weeks post-treatment.
Within subjects repeated measures analysis of variance (ANOVA) with Student’s t-test contrasts were used to compare scores across time points.
- All attendees who completed a baseline PCS were included as study participants (N=57; F=82%; mean age =50.2 years);
- PCS was completed by 46 participants at week 2 and 35 participants at week 4.
- Participants had significantly reduced PC at both time points (P<0001) and large effect sizes were found (Cohen’s d=0.85 and d=1.15).
Preliminary data suggest that FCR is an acceptable and effective treatment for PC. Larger, controlled studies of longer duration are needed to determine durability of response, factors contributing to response, and the impact on pain, function and quality of life.
The highly positive results for the anonymous post-class survey suggest that FCR was well-received among participants, and that the majority of participants felt the class offered valuable information that they anticipated integrating into their lives.
This is truly a positive find because an early counseling intervention like this
- could help prepare someone to live with chronic pain and
- make the long-term course of it more psychologically bearable.
Most pain patients have had to learn on their own how to avoid despair and make a new life for themselves when pain is constant.
Results suggest that the positive treatment effect may strengthen over time, as indicated by the increasing effect sizes.
Additionally, the available data from participants who completed both follow-up assessments suggest that PCS continues to decrease throughout 4 weeks after treatment
Our finding that a single-session class may effectively reduce PC is particularly exciting because this novel form of specific and concentrated pain-CBT treatment may greatly expand access to low-cost, efficient care
Previous studies have shown that early reductions in PC are associated with subsequent improved response to other pain treatment modalities.27,28
Accordingly, there may be specific value in administering the FCR treatment as early as possible in the pain treatment process; future studies may examine whether the brief intervention optimizes response to multidisciplinary pain treatment or specific modalities, such as physical therapy.
Participants with baseline depression and anxiety diagnoses started and ended the study with higher PCS scores, but within-subjects’ treatment response remained similar to those without these diagnoses.
Several limitations merit consideration.
The main limitation of this pilot study is the uncontrolled design, which does not allow us to parse out any nonspecific treatment effects of the class environment or the process by which participants were referred to the class.
A second limitation is the fact that our study sample comprised the 57 participants who returned a baseline PCS during the class.
We were unable to track the 19 attendees who did not return a baseline PCS and therefore it is possible that these 19 attendees would evidence a reduced response to the class and their absence from the dataset would lead to an overestimation of treatment effects.
Of our 57 participants, 10.5% (N=6) did not complete a follow-up PCS. Our 89% follow-up response rate is quite high given that the class was offered as free treatment in the clinic and no compensation was offered for follow-up responses.
Nevertheless, it is plausible – perhaps likely – that only those who achieved best effects completed a follow-up PCS, thus introducing bias and again leading to an overestimation of FCR treatment effects.
The single-session FCR class appears to hold promise as an economical, high-impact, efficient, easily delivered, non-pharmacologic treatment for PC
Cut-Off Points for Mild, Moderate, and Severe Pain on the Numeric Rating Scale for Pain in Patients with Chronic Musculoskeletal Pain: Variability and Influence of Sex and Catastrophizing – Front Psychol. 2016; – free full-text PMC article
The 0–10 Numeric Rating Scale (NRS) is often used in pain management.
The aims of our study were
- to determine the cut-off points for mild, moderate, and severe pain in terms of pain-related interference with functioning in patients with chronic musculoskeletal pain,
- to measure the variability of the optimal cut-off points, and
- to determine the influence of patients’ catastrophizing and their sex on these cut-off points.
2854 patients were included.
- Pain was assessed by the NRS,
- functioning by the Pain Disability Index (PDI) and
- catastrophizing by the Pain Catastrophizing Scale (PCS).
Cut-off point schemes were tested using ANOVAs with and without using the PSC scores or sex as co-variates and with the interaction between CP scheme and PCS score and sex, respectively. The variability of the optimal cut-off point schemes was quantified using bootstrapping procedure.
The variability of the optimal CP scheme was low, as bootstrapping found the 5,7 CP scheme to be optimal in ~90% of the samples.
No clear association was found between the cut-off points and patients’ sex.
the level of catastrophizing influenced the optimal CP scheme:
the optimal scheme for patients with low catastrophizing tendency was 3,6, indicating that an NRS score ≤ 3 corresponds to mild interference of pain with functioning, 4–6 to moderate interference, and 7–10 to severe interference,
whereas the optimal scheme for patients with high catastrophizing tendency was the same as for the total patient sample, i.e., 5,7, indicating that an NRS score ≤ 5 corresponds to mild interference of pain with functioning, 6 and 7 to moderate interference and 8–10 to severe interference.
This clearly indicates that
- high catastrophizing has no correlation with pain scores, and
- only low catastrophizing correlates with lower pain scores.
In conclusion, we found that
- NRS scores ≤ 5 correspond to mild pain-related interference with functioning,
- scores of 6 and 7 to moderate interference and
- scores ≥8 to severe interference.
This interpretation of the NRS in terms of mild, moderate and severe interference with functioning is independent of the patient’s sex, but seems to be influenced by their catastrophizing tendency
This seems written to lead us to assume the catastrophizing causation theory is true, even though this was NOT shown in the study.
However, the difference in CP schemes we found for patients with lower and higher catastrophizing tendencies contradicts what is theoretically plausible.
Here, they don’t explicitly state what the theoretical possibility is so they can avoid saying “lower and higher catastrophizing tendencies do not correlate with pain levels”
The reason why we did not find the same optimal CP scheme in the subgroups of patients with lower and higher catastrophizing tendencies may be chance variability.
Yet, earlier in this article, they said:
The variability of the optimal CP scheme was low, as bootstrapping found the 5,7 CP scheme to be optimal in ~90% of the samples. This makes it unlikely that our findings were due to chance fluctuations.
But, when no evidence of the catastrophizing theory is present, they suddenly claim the results could be due to the exact “chance fluctuations” they stated as unlikely before.