Abstract
Introduction
Pain, comprising sensory and emotional elements, is influenced by pain catastrophizing, which magnifies pain and promotes helplessness and rumination. This study explores the relationship between pain catastrophizing and outcomes following selective nerve root blockade (SNRB) in patients with lumbar radicular pain (LRP).
Methods
A prospective cohort study of 103 LRP patients, confirmed by MRI, was conducted. All participants underwent SNRB at Umeå University Hospital. Outcomes were measured using PROMIS‐29 and the Pain Catastrophizing Scale (PCS) at baseline and several intervals up to 84 days post‐intervention. Patients were categorized into responder (≥30% pain reduction) and non‐responder groups and stratified into three groups based on baseline PCS scores. Changes in outcomes from baseline to 14 days post‐SNRB were analyzed in relation to PCS groups. PCS changes over time were evaluated between responders and non‐responders. Statistical analyses assessed PCS and outcome changes.
Results
Baseline pain catastrophizing was not a significant predictor of pain response to SNRB. However, responders demonstrated significant reductions in pain catastrophizing following the intervention, suggesting that SNRB may influence cognitive coping mechanisms related to pain.
Conclusion
SNRB reduces pain catastrophizing in LRP patients, although baseline catastrophizing does not predict pain outcomes. Addressing catastrophizing remains important but may serve better as an outcome measure rather than a predictor of treatment response.
Keywords: anesthesia, back pain with radiation, infiltration, nerve block
INTRODUCTION
The latest definition of pain, revised in 2020 by the International Association for the Study of Pain (IASP), describes pain as “an unpleasant sensory and emotional experience associated with, or resembling that associated with, actual or potential tissue damage.” This updated definition broadens the understanding of pain by including not just physical sensations but also emotional components. Hence, pain consists of two main components: a sensory component of painfulness, encoded by the lateral pain pathway, and a suffering component, encoded by the medial pain pathway. In addition to these ascending pathways, pain processing also involves a descending inhibitory pathway. Based on EEG findings and structural imaging, a model has been proposed in which pain is viewed as an imbalance between the two ascending pain pathways (medial and lateral) and the descending inhibitory pathway. 1 , 2 , 3
The sensation of pain can lead to suffering through associated feelings of unpleasantness and catastrophizing. 4 Pain catastrophizing is characterized by three main features: (a) a tendency to magnify the threat value of the pain stimulus, (b) feelings of helplessness in the face of pain, and (c) difficulty inhibiting pain‐related thoughts (rumination). 5 As such, catastrophizing acts as an amplifier, intensifying unpleasantness and pain through ineffective cognitive coping strategies. This combination of perceived unpleasantness and catastrophizing contributes to suffering, which can manifest in various behaviors, including anger, fear, frustration, anxiety, and depression, 4 , 6 , 7 as well as functional disability. 8 Moreover, catastrophizing as a cognitive coping mechanism may delay recovery. 9 , 10 Some evidence suggests that pain catastrophizing could be a useful predictor and an outcome measure of how the brain interprets and perceives noxious sensory inputs under various conditions, including during therapeutic interventions aimed at influencing this process 9 , 11 , 12 , 13 , 14
One way to assess whether pain catastrophizing predicts pain perception is to examine its ability to forecast the effects of analgesic interventions. Specifically, if catastrophizing influences pain mechanisms, it should be possible to use pain catastrophizing as a predictor of response to interventions like selective nerve root blockades (SNRB) in patients with radiculopathy. However, preliminary findings suggest that baseline pain catastrophizing may not significantly predict treatment outcomes. Recognizing this possibility, the current study not only evaluates the prognostic utility of baseline pain catastrophizing but also explores the dynamic changes in catastrophizing post‐intervention to understand its role as an outcome measure.
Disentangling the relationship between pain perception and catastrophizing is not only important for theoretical understanding but also has practical implications for clinicians treating pain. If catastrophizing reliably predicts pain response, this information could guide patient selection for specific interventions. Conversely, if the relationship primarily works the other way (i.e., pain predicts catastrophizing), then catastrophizing could serve as a valuable measure of treatment response, especially given its strong link to both physical and mental health. To clarify this relationship, the current study evaluates the prognostic utility of baseline pain catastrophizing in predicting response to SNRB and investigates how SNRB influences pain catastrophizing over time. This dual approach aims to determine whether pain catastrophizing serves better as a predictor of treatment outcomes or as an outcome measure reflecting changes post‐intervention.
MATERIALS AND METHODS
Study design and setting
This prospective cohort study included 103 patients diagnosed with persistent lumbar radicular pain (LRP) based on clinical symptoms and corresponding magnetic resonance imaging (MRI) findings of the lumbar spine. These patients underwent selective nerve root block (SNRB) at Umeå University Hospital between 2021 and 2023. This study utilizes the same cohort as previously reported in Karlsson et al. (2024) but explores distinct research questions by focusing specifically on the role of pain catastrophizing (PCS) in predicting and responding to SNRB. The PCS data were collected independently and were not included in the prior analysis, ensuring that this manuscript presents novel findings. 15
Inclusion criteria required patients aged 18 or older who were referred for spine surgery at the Spine Unit of Umeå University Hospital due to unilateral or bilateral intractable radicular leg pain, with or without accompanying low back pain. All patients had confirmed disc herniation or lumbar spinal stenosis at the corresponding level on MRI.
All patients were informed about the study both orally and in writing. Written consent was obtained from all patients participating in the study.
Outcome measurements
Outcomes were prospectively collected before and after the SNRB procedure. The Patient‐Reported Outcomes Measurement Information System (PROMIS‐29) questionnaire was used to assess pain intensity, pain interference, depression, anxiety, sleep disturbance, ability to participate in social roles, fatigue, and physical function. PROMIS‐29 is a widely recognized tool for evaluating pain‐related outcomes and has demonstrated strong validity and reliability for spine‐related disorders. 16 The Pain Catastrophizing Scale (PCS) was used to assess pain catastrophizing both before the SNRB and at 14, 21, 28, 35, 42, 56, 70, and 84 days after the procedure. The PCS is a well‐established tool, comprising four components: pain catastrophizing, helplessness, magnification, and rumination.
All patients underwent SNRB at the neurosurgical department of Umeå University Hospital, performed by a single designated neurosurgeon. The blockade targeted the potentially symptomatic nerve root, identified through clinical and radiological findings, and assessed by either a spine‐focused orthopedic surgeon or neurosurgeon at the hospital's Spine Unit. A mixture of 1 mL of Marcaine (2.5 mg/mL) and 1 mL of Depo‐Medrol (40 mg/mL) was prepared in a syringe. Using x‐ray image guidance to confirm the correct level and needle placement, the mixture was injected directly into the appropriate nerve root. After administering the anesthetic and steroid solution, the needle was withdrawn, and a bandage was applied to the injection site.
Statistics
Descriptive statistics for continuous variables are presented as means with a 95% confidence interval (CI), while categorical data are presented as numbers and percentages. Analysis of variance (ANOVA) was used to compare means between groups for variables with a normal distribution, which was assessed using histograms and QQ‐plots. Categorical data were expressed as numbers and percentages. The data were further stratified into two groups: responders, defined as patients who achieved at least a 30% reduction in the numeric rating scale (NRS), and non‐responders, defined as those with less than a 30% reduction. The Pain Catastrophizing Scale (PCS) was also grouped into three categories: PCS ≤15, PCS 16–24, and PCS >24. These cutoffs were based on previous categorizations, where PCS ≤15 indicated no sign of catastrophizing and PCS >24 indicated severe catastrophizing. 17
ANOVA was used to compare PCS scores across groups at baseline and at 14, 21, 28, 35, 42, 56, 70, and 84 days post‐SNRB. A paired t‐test was performed to compare baseline values with scores at each evaluation point. Additionally, a subgroup analysis was conducted for patients with severe catastrophizing (PCS >24), assessing their PCS reduction and the number of patients whose PCS scores dropped to ≤15 (no sign of catastrophizing) after the SNRB. A p‐value of <0.05 was considered statistically significant. All statistical analyses were performed using SPSS (IBM SPSS Statistics for Mac, Version 26.0, Armonk, NY: IBM Corp., USA).
Ethics
The study adhered to the ethical principles outlined in the Declaration of Helsinki and was approved by the Swedish Ethical Review Authority (Dnr 2023–01061‐01).
This study utilizes the same cohort as previously reported in Karlsson et al. (2024); however, we have adhered to ethical guidelines by ensuring that each publication addresses unique research questions and analyses, thereby contributing independently to the scientific literature without redundant dissemination of data.
RESULTS
Patient characteristics
This study included 103 patients (64 female, 39 male) with a mean age of 64 years (95% CI: 61–66). Baseline clinical characteristics are summarized in Table 1. Significant differences were observed between PCS groups at baseline, with higher levels of anxiety (p < 0.001), depression (p < 0.001), fatigue (p < 0.001), pain interference (p = 0.02), and reduced ability to participate in social roles (p = 0.01) and physical function (p = 0.018). However, there were no significant differences in sleep disturbance (p = 0.17) or pain intensity (p = 0.25).
TABLE 1.
Clinical characteristics of study population at baseline.
| PCS 0–15 | PCS 16–24 | PCS >25 | p‐value | |
|---|---|---|---|---|
| Age (Sd) | 62.1 (12.2) | 63.5 (14.2) | 64.6 (14.3) | 0.72 |
| Sex | 0.94 | |||
| Men | 14 | 8 | 17 | |
| Women | 22 | 15 | 27 | |
| Pain duration | 0.48 | |||
| <3 months | 3 | 1 | 2 | |
| 3–6 months | 1 | 3 | 2 | |
| >6 months | 32 | 19 | 40 | |
| Opioid consumption | 0.060 | |||
| Yes | 8 | 8 | 21 | |
| No | 28 | 15 | 23 | |
| Comorbidity | ||||
| Diabetes | 0.94 | |||
| Yes | 4 | 3 | 6 | |
| No | 32 | 20 | 38 | |
| Cardiovascular | 0.022 | |||
| Yes | 5 | 2 | 15 | |
| No | 31 | 21 | 29 | |
| Asthma | 0.51 | |||
| Yes | 9 | 3 | 8 | |
| No | 27 | 20 | 36 | |
| COPD | 0.54 | |||
| Yes | 2 | 0 | 2 | |
| No | 34 | 23 | 42 | |
| Cancer | 0.47 | |||
| Yes | 2 | 3 | 6 | |
| No | 34 | 20 | 38 | |
| Hypertension | 0.40 | |||
| Yes | 15 | 12 | 25 | |
| No | 21 | 11 | 19 | |
| Psychiatric disorder | 0.57 | |||
| Yes | 5 | 2 | 8 | |
| No | 31 | 21 | 36 | |
| Baseline PROMIS‐29 | ||||
| Physical function | 37.8 (8.0) | 38.8 (5.4) | 34.3 (5.1) | 0.018 |
| Anxiety | 49.3 (9.1) | 55.8 (7.4) | 62.4 (9.6) | <0.001 |
| Depression | 50.5 (8.5) | 53.3 (7.9) | 61.9 (8.9) | <0.001 |
| Fatigue | 51.6 (13.2) | 55.9 (11.2) | 61.6 (8.8) | <0.001 |
| Sleep | 54.6 (8.0) | 55.1 (6.5) | 57.6 (7.6) | 0.17 |
| Ability to participate | 42.8 (10.5) | 41.0 (5.9) | 40.2 (7.9) | 0.01 |
| Pain interference | 64.5 (8.8) | 65.4 (5.7) | 68.6 (5.3) | 0.02 |
| Pain intensity | 6.8 (1.9) | 7.0 (1.4) | 7.1 (1.7) | 0.25 |
The association between pain catastrophizing and outcomes after SNRB
Significant differences were observed between PCS groups and outcomes during the follow‐up period for fatigue, pain interference, anxiety, depression, and ability to participate, with poorer outcomes reported for patients with higher PCS scores. There were no significant associations between PCS groups and outcomes for sleep or pain intensity (Table 2). The differences in outcomes between PCS groups were generally most pronounced early in the evaluation period. To determine if PCS groups affected changes in outcomes differently, paired changes from baseline to 2 weeks post‐intervention were analyzed using ANOVA for the three PCS groups. No significant differences were found in individual changes between PCS groups for pain intensity (p = 0.83), anxiety (p = 0.90), depression (p = 0.55), fatigue (p = 0.20), sleep (p = 0.83), ability to participate (p = 0.82), or pain interference (p = 0.27).
TABLE 2.
Outcomes after SNRB in relation to groups of PCS at baseline.
| PCS 0–15 | PCS 16–24 | PCS >24 | p | PCS 0–15 | PCS 16–24 | PCS >24 | p | ||
|---|---|---|---|---|---|---|---|---|---|
| Physical function | Anxiety | ||||||||
| 14 | 40.3 (8.7) | 39.9 (5.7) | 37.8 (6.2) | 0.24 | 14 | 48.9 (9.2) | 54.5 (9.3) | 55.7 (10.4) | <0.001 |
| 21 | 40.6 (8.0) | 39.4 (5.4) | 38.3 (6.8) | 0.36 | 21 | 45.9 (8.5) | 53.7 (9.5) | 53.6 (11.4) | <0.001 |
| 28 | 40.1 (8.8) | 39.8 (5.0) | 37.7 (7.1) | 0.34 | 28 | 47.0 (9.3) | 52.9 (8.9) | 53.9 (11.1) | <0.001 |
| 35 | 40.7 (9.6) | 39.8 (5.7) | 37.8 (7.4) | 0.28 | 35 | 46.7 (9.0) | 53.7 (8.4) | 53.9 (11.2) | <0.001 |
| 42 | 40.2 (9.6) | 39.5 (5.8) | 37.0 (7.4) | 0.22 | 42 | 46.3 (9.4) | 51.4 (8.5) | 52.9 (11.5) | <0.001 |
| 56 | 40.5 (9.4) | 39.3 (6.2) | 36.8 (7.7) | 0.13 | 56 | 47.7 (8.6) | 52.3 (9.3) | 54.1 (11.2) | <0.001 |
| 70 | 40.6 (9.5) | 39.6 (6.3) | 36.2 (7.5) | 0.059 | 70 | 46.6 (9.1) | 53.5 (8.7) | 54.1 (11.4) | <0.001 |
| 84 | 40.5 (10.0) | 39.3 (6.0) | 36.4 (6.4) | 0.085 | 84 | 46.6 (9.0) | 54.5 (8.1) | 54.3 (11.3) | <0.001 |
| Fatigue | Depression | ||||||||
| 14 | 49.8 (11.7) | 54.8 (9.6) | 57.3 (9.4) | 0.006 | 14 | 49.4 (8.5) | 52.8 (7.9) | 59.5 (9.1) | <0.001 |
| 21 | 48.1 (11.0) | 55.6 (9.9) | 57.0 (10.7) | 0.001 | 21 | 47.6 (8.0) | 53.4 (7.3) | 58.4 (10.0) | <0.001 |
| 28 | 49.8 (12.9) | 53.8 (9.0) | 57.4 (11.1) | 0.018 | 28 | 50.1 (9.5) | 51.4 (7.6) | 59.4 (8.9) | <0.001 |
| 35 | 50.4 (12.3) | 55.1 (10.5) | 59.2 (11.1) | 0.005 | 35 | 49.1 (9.0) | 52.7 (7.4) | 59.3 (9.6) | <0.001 |
| 42 | 49 (12.2) | 53.4 (9.8) | 58.9 (10.5) | 0.001 | 42 | 49.3 (9.1) | 51.5 (7.1) | 59.5 (10.3) | <0.001 |
| 56 | 51.7 (12.9) | 54.5 (9.3) | 59.7 (10.9) | 0.011 | 56 | 49.8 (8.1) | 52.7 (8.0) | 59.7 (9.6) | <0.001 |
| 70 | 50.1 (14.1) | 56.9 (10.7) | 59.6 (9.5) | 0.003 | 70 | 48.3 (9.5) | 53.1 (7.2) | 60.2 (10.1) | <0.001 |
| 84 | 51.3 (13.8) | 56.1 (11.4) | 60.5 (9.4) | 0.007 | 84 | 48.6 (8.5) | 54.4 (8.4) | 60.1 (9.6) | <0.001 |
| Pain interference | Sleep | ||||||||
| 14 | 60.5 (8.9) | 62.4 (4.3) | 63.0 (7.6) | 0.33 | 14 | 51.9 (6.7) | 53.0 (7.6) | 54.5 (7.1) | 0.23 |
| 21 | 58.4 (9.4) | 62.6 (4.3) | 62.8 (7.0) | 0.03 | 21 | 51.4 (7.6) | 53.1 (7.3) | 53.2 (8.0) | 0.55 |
| 28 | 59.3 (9.6) | 62.8 (5.4) | 64.4 (7.4) | 0.022 | 28 | 52.8 (7.8) | 52.9 (7.0) | 54.2 (7.3) | 0.69 |
| 35 | 59.1 (10.1) | 62.5 (5.8) | 63.7 (8.9) | 0.07 | 35 | 52.0 (8.5) | 52.5 (8.1) | 55.4 (8.6) | 0.19 |
| 42 | 59.7 (9.7) | 61.9 (6.8) | 64.9 (8.2) | 0.036 | 42 | 51.7 (8.8) | 52.9 (7.0) | 55.5 (8.2) | 0.13 |
| 56 | 59.5 (9.9) | 63.7 (7.1) | 65.5 (8.2) | 0.014 | 56 | 52.5 (9.1) | 53.2 (5.8) | 56.2 (8.6) | 0.13 |
| 70 | 59.2 (10.8) | 63.7 (5.4) | 65.4 (8.1) | 0.012 | 70 | 52.2 (8.9) | 54.9 (6.8) | 56.4 (7.1) | 0.082 |
| 84 | 60.0 (11.2) | 63.6 (5.6) | 65.6 (7.4) | 0.033 | 84 | 52.0 (9.3) | 53.8 (7.9) | 56.8 (8.3) | 0.057 |
| Pain intensity | Ability to participate in social roles | ||||||||
| 14 | 4.8 (2.6) | 4.8 (2.2) | 5.1 (2.1) | 0.83 | 14 | 46.2 (10.0) | 43.5 (6.2) | 41.0 (7.4) | 0.02 |
| 21 | 4.7 (2.5) | 5.3 (2.2) | 5.0 (2.1) | 0.67 | 21 | 46.7 (11.3) | 43.3 (4.5) | 41.8 (8.2) | 0.051 |
| 28 | 5.1 (2.5) | 5.3 (1.9) | 5.5 (2.2) | 0.69 | 28 | 44.7 (10.0) | 43.5 (4.4) | 41.4 (8.0) | 0.21 |
| 35 | 4.7 (2.5) | 5.0 (2.1) | 5.5 (2.5) | 0.30 | 35 | 46.0 (11.7) | 45.0 (7.2) | 41.4 (8.4) | 0.088 |
| 42 | 4.9 (2.6) | 5.4 (2.1) | 5.9 (2.2) | 0.17 | 42 | 44.8 (11.6) | 43.4 (7.2) | 41.9 (8.7) | 0.41 |
| 56 | 5.1 (2.6) | 5.6 (2.0) | 6.4 (2.3) | 0.077 | 56 | 45.1 (10.6) | 43.5 (6.7) | 40.8 (8.1) | 0.11 |
| 70 | 5.2 (2.7) | 5.8 (2.0) | 6.3 (2.2) | 0.18 | 70 | 45.9 (11.8) | 43.1 (7.4) | 40.6 (8.1) | 0.063 |
| 84 | 5.2 (2.7) | 5.8 (2.0) | 6.3 (2.4) | 0.17 | 84 | 44.0 (12.1) | 42.1 (7.7) | 40.2 (7.7) | 0.28 |
The association between pain intensity and pain catastrophizing before and after the SNRB
Baseline PCS scores did not significantly predict the pain response to SNRB. Specifically, there was no significant association between baseline PCS scores and the likelihood of being categorized as responders (defined as those with at least a 30% reduction in pain post‐SNRB) (Table 3). Out of the total, 45 patients were classified as responders and 58 as non‐responders. The mean PCS score at baseline for responders was 22.6 (SD = 12.0), compared to 21.7 (SD = 12.3) for non‐responders, with no significant difference between the two groups (p = 0.71).
TABLE 3.
Mean PCS and subcategories of PCS (helplessness, magnification and rumination) at baseline in relation to patients categorized as responders with at least 30% pain reduction and non‐responders with less than 30% pain reduction after SNRB at the 14 days evaluation.
| Responders (n = 45) | Non‐responders (n = 58) | p‐value | |
|---|---|---|---|
| PCS (Mean) | 22.6 (19.0–26.2). | 21.7 (18.4–24.9) | 0.71 |
| Helplessness | 11.1 (9.3–12.8) | 10.3 (8.7–11.7) | 0.51 |
| Magnification | 4.0 (3.1–4.9) | 3.8 (3.1–4.6) | 0.79 |
| Rumination | 7.5 (6.2–8.8) | 7.6 (6.3–8. 8) | 0.96 |
| Responders (n = 45) | Non‐responders (n = 58) | Total | |
|---|---|---|---|
| PCS 0–15 | 14 | 22 | 36 |
| PCS 16–24 | 12 | 11 | 23 |
| PCS >24 | 19 | 25 | 44 |
| Total | 45 | 58 | 103 |
Note: Number of patients in each group of PCS at baseline in relation to responders and non‐responders 2 weeks after the SNRB, p = 0.62.
The PCS score significantly decreased after SNRB, with a mean change of 5.1 (95% CI: 2.8–7.5) at the final evaluation on day 84 (p < 0.001). Significant differences in mean PCS scores were observed between responders and non‐responders at days 14, 21, 28, 35, 70, and 84 after SNRB, with responders showing lower PCS scores (Figure 1). A paired t‐test comparing baseline scores to scores at these follow‐up times was conducted for both groups. Responders experienced a significant reduction in PCS throughout the study, with a mean change of 9.5 (95% CI: 5.9–13.0) between baseline and day 84 (p = 0.001). In contrast, non‐responders did not show significant improvement, with a mean change in PCS of 1.8 (95% CI: −1.1–4.6) from baseline to day 84 (p = 0.21).
FIGURE 1.
Mean PCS for responders and non‐responders before the blockade and at 14,21,28,35,42,56,70 and 84 days after SNRB. *Statistically significant (p < 0.05) difference between responders and non‐responders in PCS.
Significant differences between responders and non‐responders were observed in all subgroups of the PCS—namely, helplessness (p = 0.02), magnification (p = 0.025), and rumination (p = 0.027)—14 days after SNRB.
Analyze patients with severe catastrophizing, PCS >24 at baseline
Forty‐four patients had a PCS score greater than 24 at baseline. The mean PCS score in this group was 33.9 (95% CI: 32.0–35.7) at baseline and 23.4 (95% CI: 19.0–27.0) after SNRB (p < 0.001). Within this group, patients categorized as responders (defined as those with greater than 30% pain reduction) had a mean PCS of 18.7 (SD = 11.8) compared to 27.0 (SD = 11.8) for non‐responders at the 14 days evaluation after SNRB (p = 0.021). Of the 44 patients, 25 reported a PCS score of 24 or less 14 days after SNRB. Among these, 14 out of 25 were categorized as responders, while 5 out of 19 patients who still had a PCS greater than 24 were responders (p = 0.049) (Table 4). Only 11 of the 44 patients with PCS scores above 24 reported a PCS score of 15 or less at the 14 days evaluation after SNRB. Of these, 7 were responders and 4 were non‐responders, with no significant difference between the groups (p = 0.11).
TABLE 4.
Patients with severe catastrophizing at baseline (PCS >24), n = 44.
| Outcomes 14 days after SNRB for patients with PCS >24 at baseline | Responders, ≥30% pain reduction (n = 19) | Non‐responders <30% pain reduction (n = 25) | p‐value |
|---|---|---|---|
| Mean PCS | 18.6 | 27.0 | 0.021 |
| Number of patients | Total | ||
| PCS ≤24 | 14 | 11 | 25 |
| PCS >24 | 5 | 14 | 19 |
| Total | 19 | 25 | 44 |
Note: Mean PCS among responders ((≥30% pain reduction) and non‐responders (<30% pain) and the distribution among responders and non‐reduction) in relation to severe catastrophizing (PCS >24) 14 days after the SNRB. There was a significant reduction in number of patients with severe catastropizing (PCS >24) among responders 14 days after the SNRB p = 0.049.
DISCUSSION
In this study, we observed a significant increase in anxiety, depression, fatigue, pain interference, reduced ability to participate, and physical function with higher PCS scores in the groups at baseline. However, no significant differences were found for sleep disturbance or pain intensity. Not even when the patients were stratified into two groups, a responder group and a non‐responder group, at baseline were there any significant correlations between PCS score and pain intensity. The observed differences at baseline remained consistent throughout the entire follow‐up period, with poorer reported outcomes for patients with higher PCS scores. The differences in outcomes between the PCS groups were generally most pronounced at the beginning of the evaluation. However, individual paired comparisons between baseline and outcomes after 2 weeks did not show any significant differences in individual changes between the PCS groups across the various PROMIS‐29 outcome measures used for follow‐up.
While our study initially aimed to assess the prognostic utility of baseline pain catastrophizing in predicting pain response to SNRB, our univariate analyses revealed that baseline PCS scores did not significantly predict treatment outcomes. This finding challenges the prevailing assumption that baseline catastrophizing can serve as a reliable predictor for pain interventions. Instead, our significant findings regarding the reduction of PCS in responders highlight the potential of PCS as an outcome measure reflecting changes in cognitive coping mechanisms postintervention.
The association between high PCS scores and negative behaviors observed in our results aligns with previous research and theories, reinforcing the concept of catastrophizing as an amplifier of unpleasantness and pain intensity. This amplification leads to suffering, which manifests through behaviors such as anger, fear, anxiety, depression, and functional disability 4 , 6 , 7 , 8 Additionally, the lack of significant differences in pain intensity between PCS groups at baseline and throughout the entire follow‐up period supports the theory that the sensation of pain and the experience of suffering are distinct processes, transmitted via separate anatomical pathways and involving different neurophysiological mechanisms. Painfulness is encoded by the lateral pain pathway, while suffering, which involves cognitive, emotional, and autonomic components, is mediated by the medial pain pathway. The intensity of suffering is further shaped by the salience network, which processes the personal relevance of pain and contextualizes both the painful sensation and the associated suffering. 18 , 19 , 20 This neural processing includes the descending inhibitory pathway and the nucleus accumbens (part of the reward system) for pain perceived as pleasant, while the dACC and insula are involved in processing unpleasant pain, both being integral components of the medial pain pathway. 18 , 20
Physiological stress is defined as an unpleasant sensory, emotional, and subjective experience associated with potential tissue damage and bodily threat. 21 Stressors activate the fight‐or‐flight response, which has significant evolutionary importance. However, chronic stress provides no such benefits and is instead associated with various somatic conditions, including metabolic syndrome, obesity, cancer, and cardiovascular diseases. On a psychological level, prolonged exposure to stress is linked to mental health disorders such as depression, anxiety, and anger, which are behaviors connected to suffering 22 , 23 , 24 Since pain is considered a typical stressor, it can be argued that the removal of such a stressor would positively impact suffering and catastrophizing, a notion clearly supported by our results. PCS scores were significantly reduced following SNRB, with sustained improvements observed through the final evaluation at day 84. Significant differences in mean PCS scores were found between patients classified as responders and non‐responders at days 14, 21, 28, 35, 70, and 84 after the SNRB, with responders consistently showing lower PCS scores. Additionally, significant differences were observed between responders and non‐responders across all PCS subgroups. Responders demonstrated a sustained reduction in PCS throughout the study, with a notable mean change in PCS from baseline to day 84, while non‐responders showed no improvement in PCS during the follow‐up period. The significant effect of catastrophizing in relation to pain response warrants emphasis. Ho‐Jong et al. (2018) found that changes in pain catastrophizing were linked to improvements in pain intensity following spine surgery, suggesting that catastrophizing is not a stable construct but a dynamic one. 14 Similarly, the fluctuating outcomes of catastrophizing over time were associated with the pain‐reducing effects of SNRB. This supports the idea that catastrophizing may be more suitable for evaluating the effects of therapeutic interventions rather than for predicting outcomes.
Given that catastrophizing is an ineffective cognitive coping strategy that amplifies unpleasantness and pain, it becomes evident that for patients with high levels of catastrophizing, addressing these coping mechanisms and negative behaviors is essential alongside pain‐reducing interventions. To achieve significant overall improvement in their pain condition and its suffering dimension, both aspects must be targeted. Patient satisfaction is often closely tied to a reduction in suffering, so reducing the sensation of pain alone may be insufficient for those with high baseline catastrophizing. Our data show that the greatest improvement in PCS scores occurs in patients with baseline catastrophizing scores above 24, with a mean baseline score of 33.7 compared to 23.4 at 14 days post‐intervention. Similar improvements in other metrics, such as depression, anxiety, fatigue, and pain interference, were observed in this group. However, despite the magnitude of improvement, these patients still exhibit significantly higher levels of catastrophizing, depression, anxiety, fatigue, and pain interference compared to those with lower catastrophizing scores (0–15). Thus, while the intervention demonstrated a clear and significant effect, it was insufficient to fully normalize suffering in most patients with high catastrophizing. Nevertheless, a significant association was observed between the reduction in catastrophizing and pain reduction following the intervention.
There have been suggestions that catastrophizing could be used as a predictor for pain‐relieving interventions, with higher levels of catastrophizing indicating worse outcomes. Our results do, however, not support this. In fact, we observed larger improvements in some metrics for the highest catastrophizing group and comparable improvements between PCS groups in pain intensity and physical function. Historically, catastrophizing has been a construct primarily used to explain the impact of cognitive interventions on pain perception. Therefore, it is theoretically plausible that interventions aimed at the actual painfulness would show smaller or even undetectable effects related to catastrophizing. This pattern is consistent with previous studies that have shown relatively limited or even absent effects of catastrophizing on the nociception flexor reflex in experimental settings. 25 , 26
Catastrophic thinking has been shown to contribute to a higher level of pain and emotional stress and to be a potential risk factor for chronicity. 27 Picavet, who explored how catastrophic thinking affects pain and disability in neuropathic pain patients, found that higher levels of catastrophic thinking, particularly rumination and helplessness, were linked to increased pain and disability. 28 Furthermore, individuals who score high on PCS have been found to have more severe depression, anxiety, and consumption of analgesic medications. 29 Additionally, this group exhibited poorer scores on measures of depression, anxiety, fatigue, and ability to participate in social roles. In this context, the significant effect on PCS in the responders deserves to be emphasized. Since patients with lumbar back pain with radiculopathy have a severe risk for developing chronic pain, 28 provided that a reduction in pain catastrophizing has a positive effect on these associated variables, reducing catastrophizing might be as valid a primary goal for pain treatment as a reduction of pain scores per se.
By distinguishing between the sensory aspect of pain and the emotional suffering it causes, clinicians can develop more precise tools for patient assessment and management. This approach may lead to more effective and personalized pain management strategies that address both sensory and emotional components. Research suggests that pain catastrophizing may predict disability and emotional distress more effectively than pain intensity alone 18 , 30 , 31 , 32 , 33 Our study demonstrates the value of using pain catastrophizing, as measured by the PCS, to identify responders and monitor the therapeutic effects of SNRB. Consistent with previous findings, we propose that evaluating catastrophizing over time provides a more comprehensive assessment of pain‐related outcomes compared to relying solely on pain intensity. Our results highlight the importance of incorporating cognitive and emotional responses, such as catastrophizing, into the evaluation of treatment efficacy in pain management.
In summary, the results of the present study suggest that pain catastrophizing does not have any major effects on the outcome of a peripheral nerve blockade in patients with radicular leg pain, whereas the blockade influences catastrophizing. This finding suggests the possibility of using catastrophizing as an outcome variable for the treatment of peripheral neurogenic pain, but the construct might be less useful for patient selection.
Strengths and limitations
Our article contributes to the field of pain and pain catastrophizing by exploring the correlations between pain catastrophizing and peripheral neurogenic pain, showing that SNRB in patients with LRP will influence catastrophizing, but the effect of catastrophizing on SNRB could not be proven. The prospective design with rigorous monitoring of the PCS and NRS and other outcome variables, as well as the large sample size, ensures reliable and valid results. The thorough statistical data analysis provides rigorous results. Our findings may not have any clinical implications for patient selection for SNRB but may influence a change from the traditional outcome measure of pain intensity to also include the PCS.
Although this study has several strengths, the outcome measures were not adjusted to account for other variables that could influence the results after SNRB. The study is limited to a single institution and all the SNRB was performed by the same neurosurgeon, which limits the external validity. This constitutes a limitation of the study. Future research should further investigate some of these factors and aspects.
CONCLUSION
SNRB significantly reduces pain catastrophizing in patients with radicular pain.
However, baseline pain catastrophizing does not predict treatment response, suggesting that PCS may not be useful for patient selection in SNRB. Instead, reductions in PCS postintervention highlight its potential as a valuable outcome measure for assessing the efficacy of pain management strategies. Future research should explore the role of PCS in monitoring treatment outcomes and consider integrating cognitive coping mechanisms into comprehensive pain management protocols.
AUTHOR CONTRIBUTIONS
All listed authors have contributed to the manuscript substantially and have agreed to the final submitted version. This study was designed by J.W. and P.T.S. The statistical analysis was performed by J.W. and P.T. S. The data were analyzed by J.W. and P.T.S., and the results were critically examined by all authors. P.T.S. and J.W. had a primary role in preparing the manuscript, which was edited by J.Å., R.S., and A.A. All authors have approved the final version of the manuscript and agree to be accountable for all aspects of the work.
FUNDING INFORMATION
The study was financed by grants from the Swedish state under the agreement between the Swedish government and the county councils, the ALF agreement.
CONFLICT OF INTEREST STATEMENT
The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
PATIENT CONSENT STATEMENT
All patients were adults and were informed about the study both orally and in writing. Written consent was obtained from all patients participating in the study.
ACKNOWLEDGMENTS
We acknowledge all patients who contributed data to this study.
Tabatabaei Shafiei P, Åkerstedt J, Awad A, Sjöberg RL, Wänman J. A prospective study of the association between pain and catastrophizing after selective nerve root blockade. Pain Pract. 2025;25:e70017. 10.1111/papr.70017
DATA AVAILABILITY STATEMENT
Data is available on request due to privacy/ethical restrictions.
REFERENCES
- 1. Yearwood T, De Ridder D, Yoo HB, Falowski S, Venkatesan L, Ting To W, et al. Comparison of neural activity in chronic pain patients during tonic and burst spinal cord stimulation using fluorodeoxyglucose positron emission tomography. Neuromodulation. 2020;23(1):56–63. 10.1111/ner.12960 [DOI] [PubMed] [Google Scholar]
- 2. De Ridder D, Vanneste S. Burst and tonic spinal cord stimulation: different and common brain mechanisms. Neuromodulation. 2016;19(1):47–59. [DOI] [PubMed] [Google Scholar]
- 3. Vanneste S, Song JJ, De Ridder D. Thalamocortical dysrhythmia detected by machine learning. Nat Commun. 2018;9(1):1103. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 4. Wade JB, Riddle DL, Price DD, Dumenci L. Role of pain catastrophizing during pain processing in a cohort of patients with chronic and severe arthritic knee pain. Pain. 2011;152(2):314–319. [DOI] [PubMed] [Google Scholar]
- 5. Osman A, Barrios FX, Kopper BA, Hauptmann W, Jones J, O'Neill E. Factor structure, reliability, and validity of the pain catastrophizing scale. J Behav Med. 1997;20(6):589–605. [DOI] [PubMed] [Google Scholar]
- 6. Wade JB, Hart RP. Attention and the stages of pain processing. Pain Med. 2002;3(1):30–38. [DOI] [PubMed] [Google Scholar]
- 7. Bustan S, Gonzalez‐Roldan AM, Kamping S, Brunner M, Loffler M, Flor H, et al. Suffering as an independent component of the experience of pain. Eur J Pain. 2015;19(7):1035–1048. [DOI] [PubMed] [Google Scholar]
- 8. Severeijns R, Vlaeyen JW, van den Hout MA, Weber WE. Pain catastrophizing predicts pain intensity, disability, and psychological distress independent of the level of physical impairment. Clin J Pain. 2001;17(2):165–172. [DOI] [PubMed] [Google Scholar]
- 9. Wertli MM, Eugster R, Held U, Steurer J, Kofmehl R, Weiser S. Catastrophizing‐a prognostic factor for outcome in patients with low back pain: a systematic review. Spine J. 2014;14(11):2639–2657. [DOI] [PubMed] [Google Scholar]
- 10. Martinez‐Calderon J, Jensen MP, Morales‐Asencio JM, Luque‐Suarez A. Pain catastrophizing and function in individuals with chronic musculoskeletal pain: a systematic review and meta‐analysis. Clin J Pain. 2019;35(3):279–293. [DOI] [PubMed] [Google Scholar]
- 11. Scott W, Wideman TH, Sullivan MJ. Clinically meaningful scores on pain catastrophizing before and after multidisciplinary rehabilitation: a prospective study of individuals with subacute pain after whiplash injury. Clin J Pain. 2014;30(3):183–190. [DOI] [PubMed] [Google Scholar]
- 12. Forsythe ME, Dunbar MJ, Hennigar AW, Sullivan MJ, Gross M. Prospective relation between catastrophizing and residual pain following knee arthroplasty: two‐year follow‐up. Pain Res Manag. 2008;13(4):335–341. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 13. Veljkovic A, Gagne O, Abuhantash M, Younger ASE, Symes M, Penner MJ, et al. High pain catastrophizing scale predicts lower patient‐reported outcome measures in the foot and ankle patient. Foot Ankle Spec. 2022;17:19386400221093865. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 14. Kim HJ, Kwon OH, Chang BS, Lee CK, Chun HJ, Yeom JS. Change in pain catastrophizing in patients with lumbar spinal surgery. Spine J. 2018;18(1):115–121. [DOI] [PubMed] [Google Scholar]
- 15. Karlsson C, Carlsson E, Akerstedt J, Lilja P, von Essen C, Tabatabaei P, et al. Outcomes after selective nerve root blockade for lumbar radicular pain from lumbar disc hernia or lumbar spinal stenosis assessed by the PROMIS‐29‐a prospective observational cohort study. Acta Neurochir. 2024;166(1):306. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 16. Pennings JS, Devin CJ, Khan I, Bydon M, Asher AL, Archer KR. Prediction of Oswestry disability index (ODI) using PROMIS‐29 in a national sample of lumbar spine surgery patients. Qual Life Res. 2019;28(10):2839–2850. [DOI] [PubMed] [Google Scholar]
- 17. Sullivan MJL, Bishop SR, Pivik J. The pain catastrophizing scale: development and validation. Psychol Assess. 1995;7(4):524–532. [Google Scholar]
- 18. De Ridder D, Adhia D, Vanneste S. The anatomy of pain and suffering in the brain and its clinical implications. Neurosci Biobehav Rev. 2021;130:125–146. [DOI] [PubMed] [Google Scholar]
- 19. Beecher HK. Relationship of significance of wound to pain experienced. JAMA. 1956;161(17):1609–1613. [DOI] [PubMed] [Google Scholar]
- 20. Leknes S, Berna C, Lee MC, Snyder GD, Biele G, Tracey I. The importance of context: when relative relief renders pain pleasant. Pain. 2013;154(3):402–410. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 21. Kogler L, Muller VI, Chang A, Eickhoff SB, Fox PT, Gur RC, et al. Psychosocial versus physiological stress‐meta‐analyses on deactivations and activations of the neural correlates of stress reactions. Neuroimage. 2015;119:235–251. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 22. Russell G, Lightman S. The human stress response. Nat Rev Endocrinol. 2019;15(9):525–534. [DOI] [PubMed] [Google Scholar]
- 23. Staufenbiel SM, Penninx BW, Spijker AT, Elzinga BM, van Rossum EF. Hair cortisol, stress exposure, and mental health in humans: a systematic review. Psychoneuroendocrinology. 2013;38(8):1220–1235. [DOI] [PubMed] [Google Scholar]
- 24. Gilam G, Lin T, Fruchter E, Hendler T. Neural indicators of interpersonal anger as cause and consequence of combat training stress symptoms. Psychol Med. 2017;47(9):1561–1572. [DOI] [PubMed] [Google Scholar]
- 25. Toledo TA, Kuhn BL, Payne MF, Lannon EW, Palit S, Sturycz CA, et al. The effect of pain catastrophizing on endogenous inhibition of pain and spinal nociception in native Americans: results from the Oklahoma study of native American pain risk. Ann Behav Med. 2020;54(8):575–594. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 26. Rice DA, Parker RS, Lewis GN, Kluger MT, McNair PJ. Pain catastrophizing is not associated with spinal nociceptive processing in people with chronic widespread pain. Clin J Pain. 2017;33(9):804–810. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 27. Simic K, Savic B, Knezevic NN. Pain catastrophizing: how far have we come. Neurol Int. 2024;16(3):483–501. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 28. Picavet HS, Vlaeyen JW, Schouten JS. Pain catastrophizing and kinesiophobia: predictors of chronic low back pain. Am J Epidemiol. 2002;156(11):1028–1034. [DOI] [PubMed] [Google Scholar]
- 29. Martin MY, Bradley LA, Alexander RW, Alarcon GS, Triana‐Alexander M, Aaron LA, et al. Coping strategies predict disability in patients with primary fibromyalgia. Pain. 1996;68(1):45–53. [DOI] [PubMed] [Google Scholar]
- 30. Sullivan MJ, Thorn B, Haythornthwaite JA, Keefe F, Martin M, Bradley LA, et al. Theoretical perspectives on the relation between catastrophizing and pain. Clin J Pain. 2001;17(1):52–64. 10.1097/00002508-200103000-00008 [DOI] [PubMed] [Google Scholar]
- 31. Lumley MA, Cohen JL, Borszcz GS, Cano A, Radcliffe AM, Porter LS, et al. Pain and emotion: a biopsychosocial review of recent research. J Clin Psychol. 2011;67(9):942–968. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 32. Scott EL, Kroenke K, Wu J, Yu Z. Beneficial effects of improvement in depression, pain catastrophizing, and anxiety on pain outcomes: a 12‐month longitudinal analysis. J Pain. 2016;17(2):215–222. [DOI] [PubMed] [Google Scholar]
- 33. Semeru GM, Halim MS. Acceptance versus catastrophizing in predicting quality of life in patients with chronic low back pain. Korean J Pain. 2019;32(1):22–29. [DOI] [PMC free article] [PubMed] [Google Scholar]
Associated Data
This section collects any data citations, data availability statements, or supplementary materials included in this article.
Data Availability Statement
Data is available on request due to privacy/ethical restrictions.