The development of a novel questionnaire assessing alterations in central pain processing in people with and without chronic pain
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Philip D. Austin
,
Ali Asghari
Abstract
Background and aims
The purpose of this study was to (a) develop and (b) conduct exploratory factor analysis on a novel self-report instrument for symptoms associated with altered central pain processing.
Methods
We first developed a 25-item questionnaire based on previous literature identifying symptoms and behaviours that may reflect altered spinal and supraspinal pain processing. We then administered this questionnaire to 183 people with chronic pain (n = 99) and healthy individuals (n = 84). Exploratory factor analysis was conducted to identify the factor structure of the questionnaire.
Results
Our results support a two-factor solution for the 25-item questionnaire that accounted for 57.2% of the total variance of responses in people with and without chronic pain. Factor one (11 items) included items related to alterations in sensation of pain, while factor two (seven items) included items associated with emotional and fatigue symptoms. Seven items showed weak factor loadings and were eliminated. Reliability was excellent, while both factors showed strong correlations with previously-validated self-report Instruments: (pain catastrophising, mood, vigilance, pain self-efficacy) and conditioned pain modulation, providing evidence for their validity.
Conclusions
We have developed a questionnaire containing two factors that appear to be related to two different symptom clusters, one of which is specifically related to pain and one of which contains other health-related symptoms related to mood and fatigue. These factors show excellent internal consistency and validity. This questionnaire may be a quick, easy and reliable instrument to assess central pain processing in clinical settings.
1 Introduction
The most recent version of the International Classification of Diseases (ICD-11) has been developed with input from an international consensus group of clinicians and researchers in the field of pain [1]. It provides a classification that conforms to current neuroscientific and clinical understandings of pain with the intention of being more applicable in clinical settings. Within this taxonomy is a new and important classification of chronic pain – primary chronic pain [2]. This classification seeks to improve upon the categorisation of chronic pain conditions that appear to have a substantial and possibly primary contribution from additional physiological, psychological and social factors other than inputs from a site of damage or disease. This includes conditions that have previously and unhelpfully labelled as functional, somatoform or non-specific such as irritable bowel syndrome and fibromyalgia.
This novel term has been linked to the concept of “nociplastic” pain [1], suggested as pain present in people in whom nociceptive and neuropathic contributors cannot be identified [3]. Here, underlying mechanisms include alterations in central pain processing that play an important role in the development and maintenance of chronic pain [4], [5], [6]. Thus, it would be helpful to develop a simple self-report instrument that identifies the presence of nociplastic contributors to pain supporting a classification of primary chronic pain. The contributors to nociplastic pain are yet to be specifically identified but are distinguished by central nervous system hypersensitivity in the absence of demonstrable nociceptive or neuropathic inputs [3] Therefore, although the authors state that it is not a synonym for central sensitisation, those with nociplastic pain will exhibit features of altered central processing such as spread of pain and the presence of allodynia and hyperalgesia. Ideally, such an assessment tool would also have the ability to identify and even quantify physiological changes that are believed to contribute to nociplastic conditions such as alterations in pain modulation [7].
Psychometric instruments have been designed to assess the presence of CS in people with chronic pain. Of these studies, two evaluate symptoms in specific anatomical locations: the Clinical Classification of CS pain in patients with low back (±leg) pain [8] and the Allodynia Symptom Checklist that reports cutaneous allodynia in people with headache [9]. Alternatively, the Central Sensitivity Inventory evaluates somatic and other health-related symptoms thought to be common to conditions associated with CS [10]. Although these instruments show abilities to accurately assess specific CS-related features associated with regional anatomy or those common in conditions associated with CS, to date no self-report instrument has been designed to determine alterations in central nociceptive processing that may be associated with dysfunctional pain modulation.
The availability of an instrument evaluating symptoms reflecting altered central pain processing would be an invaluable aid in guiding more quickly the appropriate management of people presenting with chronic pain. In addition, it may help identify the likelihood of developing chronic pain in people without pain undergoing surgery or experiencing other types of trauma. Thus, the aim of this study was to develop and explore the factor structure of a novel self-report questionnaire measuring symptoms reported to be indicative of altered spinal and supraspinal pain processing in people with and without chronic pain.
2 Methods
2.1 Item development
The initial item pool was developed from a systematic search of the literature to identify and discriminate key symptoms and behaviours associated with altered spinal and supraspinal pain processes. Here, a search of Medline and EMBASE located 446 individual articles of which 347 were found in Medline and 103 were found in EMBASE. We identified seven potentially relevant studies which tested or validated a self-report instrument associated with peripheral or centrally mediated pain. Four of these instruments assessed only the severity of pain in patients with neuropathic and nociceptive pain conditions (Table 1). However, they do not assess or discriminate between peripheral, spinal or supraspinal pain process.
Pain symptom instruments excluded from the review with rational for exclusion.
| Acronym | Name of scale | Author | Rationale for exclusion |
|---|---|---|---|
| NPSI | Neuropathic Pain Symptom Inventory | Bouhassira et al. 2004 | Designed to discriminate between nociceptive and neuropathic pain |
| NTSS | Neuropathy Total Symptom Score-6 | Bastyr et al. 2005 | Designed to evaluate sensory symptoms in patients with diabetic peripheral neuropathy |
| LANSS | Leeds Assessment of Neuropathic Symptoms and Signs Pain Scale | Bennett 2001 | Designed to evaluate pain of neuropathic origin |
| PD-Q | PainDETECT Questionnaire | Freynhagen et al. 2008 | Designed to evaluate neuropathic pain in low back pain patients |
| StEP | Standardized Evaluation of Pain | Scholz et al. 2009 | Designed to differentiate between radicular and axial low back pain |
The three questionnaires chosen by the authors (PS, PA) for evaluation were the Central Sensitization Inventory (CSI) [10], the Clinical Criteria Checklist [11] and the Allodynia Symptom Checklist [9]. These instruments were selected as they contain items whose content are understood to verbally represent symptoms of spinal and supraspinal pain processes as defined by current literature [12], [13]. These instruments contain items intended to assess either pain symptoms specific to an anatomical region and somatic or other health-related symptoms common in people with pain conditions associated with CS and descending pain modulation [14]. Although these tools reliably and validly assess clusters of pain symptoms and emotional behaviours commonly associated with chronic pain conditions and central sensitisation, none are designed to detect alterations in endogenous pain modulatory pathways or validated against physiological tests that assess these pathways. First, we modified the stems of appropriate items from the reviewed instruments to increase the relevance to our study. For example, we modified item nine from the CSI from “I feel pain all over my body” to “my pain has spread to other parts of my body”, thus highlighting important temporal features of the spread of pain [14]. Second, we developed items based on human studies investigating symptoms associated with both spinal and supraspinal pain mechanisms (CS and descending pain modulation) [15], [16], [17], for example, “My pain is unpredictable and comes on for no apparent reason”. Third, we referred to current pain taxonomies [18]. Using these processes, we developed a list of 25 items for this questionnaire (Table 3).
2.2 Developmental process of questionnaire
The questionnaire developed from this review process included items relating to characteristics of pain, emotion, cognition, fatigue and sensitivities to external stimuli, all shown to be associated with altered spinal and supraspinal pain processing [19], [20], [21], [22]. Thus, we chose to adopt an exploratory approach to the analysis because the items were either newly-developed or modified and thus untested concerning factor structure. Each item was scored using a 4-point scale as follows: Never (0), Rarely (1), Sometimes (2) and Always (3) where the cumulative total score ranged from 0 to 75, with higher scores indicating a shift from antinociception towards pronociception.
2.3 Previously validated self-report instruments
For this exploratory study, we also wanted to assess the validity of our questionnaire. Given our aim to develop an instrument assessing symptoms associated with altered central nervous system pain processing, it was necessary to show the degree to which the content of items in our questionnaire compare against validated questionnaires (i.e. convergent validity) commonly used to assess theoretically-related cognitive and behavioural constructs in clinical and research chronic pain settings. For this study, both cases (people with pain) and controls (people without pain) completed the novel questionnaire and all other self-report instruments described below.
2.3.1 Pain vigilance and awareness questionnaire
The pain vigilance and awareness questionnaire (PVAQ) is a reliable and valid instrument assessing pain vigilance in patients with chronic pain conditions [23]. The PVAQ is a 16-item questionnaire where respondents make ratings of their vigilance and awareness of pain on a six-point Likert scale ranging from 0 (never) to 5 (always).
2.3.2 Pain anxiety symptom scale
The pain anxiety symptom scale (PASS) is a reliable and valid 20 item self-report instrument assessing pain-related anxiety [24], [25], where participants rate their anxiety in relation to their pain on a six-point Likert scale ranging from 0 (never) to 5 (always).
2.3.3 Pain self-efficacy questionnaire
The pain self-efficacy (PSEQ) is a valid and reliable 10-item questionnaire that assesses the confidence people have performing activities while in pain [26]. Participants rate their levels of confidence on a seven-point Likert scale ranging from 0 (not at all confident) to 6 (completely confident).
2.3.4 Pain catastrophising scale
The pain catastrophising scale (PCS) is a validated 13-item instrument used to assess catastrophic thinking describing different thoughts and feelings people may experience when in pain [27], [28]. Participants rate the degree to which they experience thoughts reflected in each item on a five-point Likert scale ranging 0 (not at all) to 4 (all the time).
2.3.5 Depression, anxiety and stress scale
The depression, anxiety and stress scale (DASS-21) is a valid and reliable set of three seven-item self-report scales designed to assess emotional states of depression, anxiety and stress [29], [30]. Participants rate their levels of emotional states on a four-point Likert scale ranging from 0 (Did not apply to me at all) to 3 (Applied to me very much or most of the time).
2.4 Previously validated physiological tests
2.4.1 Conditioned pain modulation (CPM)
We also wanted to test the criterion validity of our questionnaire against more objective physiological tests of pain modulation. Here in a sub-sample of 64 participants we used CPM. CPM describes the phenomenon through which a second (conditioning) noxious stimulus affects a primary (test) noxious stimulus in a different region of the body [31]. This technique is used to objectively measure the influence of top-down endogenous pain modulation in people with chronic pain by means of laboratory equipment. Under normal circumstances, a strong conditioning stimulus will activate endogenous pain inhibitory pathways where thresholds of the test stimulus increase either during or shortly after the conditioning stimulus is applied. For this study, both cases and controls participated in the CPM procedure. Participants were asked to rate their pain intensity during a pressure pain test stimulus prior to and immediately after a noxious cold-water immersion conditioning stimulus. Here, we used CPM protocols recommended by Yarnitsky and colleagues [32]. For this study, we used mechanical pressure device (Wagner Pain Test Algometer Force Ten FDX 50, CT, USA) for the test stimulus. Pressure pain thresholds (PPT) in Newtons were applied with ascending intensity to the dorsum of the foot contralateral to the dominant hand that was discontinued when the participant’s pain-rating reached 40/100 on a visual analogue scale indicating moderate pain. There then followed 1 min of cold-water immersion (Jeiotech Lab Companion RW-3025G) of the dominant hand to the lower-mid forearm given as the conditioning stimulus at a temperature of 10 degrees. We chose an intense conditioning stimulus as it has been shown to activate a greater degree of analgesia at the test site [33], [34] and thus a higher chance of observing not only CPM, but also differences in CPM scores between subgroups. The same mechanical pressure was then repeated to the dorsum of the contralateral foot immediately after the participants withdrew their upper limb from the cold-water bath. In order to gain more reliable pain rating scores, we accounted for reported differences in pain perception by handedness, a factor previously shown to add to individual variations in pain sensitivity [35]. To record percentage differences between baseline and post conditioning stimulus test pain scores, we used a baseline value of 100. All percentage increases in PPT scores (pain inhibition) were scored above 100 and percentage decreases in PPT scores (pain facilitation), scored below 100.
2.5 Participants
Cases were sampled consecutively from people with chronic non-cancer pain attending a hospital-based outpatient pain management program. All chronic pain diagnoses were verified using ICD-10 codes for chronic pain conditions [36]. Participants without pain were recruited using advertisements placed within the hospital as well as the hospital intranet and internet sites. Informed consent was given by all participants while the study gained ethical approval from the local institutional research Ethics Committee.
2.6 Statistical analysis
Based on previous descending pain modulation and CS studies, our a priori plan was to develop a questionnaire containing items relating to symptoms reflecting altered central pain processing that may contribute to nociplastic pain. Here, we wanted to determine the smallest number of latent variables explaining the covariation observed among items whose content reflect symptoms related to these central changes [37]. Thus, in order to understand and identify attributes captured by this novel questionnaire, we explored its factor structure using exploratory factor analysis (EFA) to determine the number and nature of factors describing the developed items (SPSS 23.0). Based on a sample size to item ratio of 5:1 [38], [39], we required a sample of at least 125 participants. We first examined the data for outliers, with a view to excluding any participants with z-scores on any item >3.29 or <3.29 [40].
In order to test the suitability of data for EFA we used the Kaiser-Meyer-Olkin (KMO) test and Bartlett’s test of sphericity [39] after which we extracted factors using principal axis factoring (PAF), a method noted for its ability to recover all relevant factors [41], and direct oblimin rotation, to allow factors to be correlated [38], [42]. Prior to EFA, we used parallel analysis (PA) to identify the number of factors to extract in subsequent EFA. Here, PA allows a higher degree of confidence of the number of factors to extract before using EFA and thus reduces the chance that a factor is due to chance. Additionally, we followed criteria suggesting items whose factor loadings were below 0.5 were considered for elimination [43].
We used Cronbach’s alpha to test the internal consistency of the factors observed using EFA and Pearson’s r correlation to determine associations between them and other validated psychological and physiological instruments used both in clinical and experimental chronic pain settings. Independent samples t-test was used to determine differences in mean scores for previously validated self-report instruments between chronic pain and control participants. The same statistical methods were used to determine differences in CPM scores between these groups for pre, post conditioning stimulus PPT scores and percentage differences between pre and post conditioning stimulus PPT scores.
3 Results
3.1 Participant demographics
No participants were excluded from analysis on the basis of outliers. Table 2 shows the characteristics of the 183 enrolled participants in relation to age, chronic pain status defined as pain that persists or recurs for more than 3 months [44] and gender. A considerable proportion of pain patients presented with back and neck pain (n=44, 44%) and widespread pain (n=20, 20%), while 11 (11%) participants presented with peripheral neuropathies (Table 2). Although there were significant differences in median age between the chronic pain and control groups, gender matching was identical.
Demographic distribution of chronic pain patients and healthy controls.
| Gender | n | % | |
|---|---|---|---|
| Control | Female | 70 | 83 |
| (Mean age – 40.5, SD – 15.23) | Male | 14 | 17 |
| Range – 21–85 years | |||
| Total (n=84) | |||
| Case | Female | 83 | 83 |
| (Mean age – 56.5, SD – 18.26) | Male | 17 | 17 |
| Range – 19–89 years | |||
| Total (n=98) | |||
| Pain diagnosis (cases) | |||
| – Osteoarthritis | 7 | 7.1 | |
| – Widespread pain | 20 | 20.4 | |
| – Neck and back pain | 44 | 44 | |
| – Tension headaches/migraine | 6 | 6.1 | |
| – Abdominal/pelvic pain | 5 | 5.1 | |
| – Peripheral neuropathies | 11 | 11.2 | |
| – Radiculopathy | 6 | 6.1 | |
| Pain duration (cases) | |||
| – mean – 8.5 years | |||
| – SD – 8.89 | |||
3.2 Exploratory factor analysis
3.2.1 Factor extraction
Initial PA prior to EFA supported extraction of two factors. The data was considered suitable for EFA following the KMO test for sampling adequacy (KMO=0.939), Bartlett’s test of sphericity (χ2=2853.50, p≤0.0001) and a sample size ratio to each item of 7.3:1. PAF revealed two factors. Here, the variance accounted for by these two factors was shown at 57.2% (Table 3). The first factor included items that described symptoms specifically related to pain (11 items). For example, this factor included items such as “my pain continues after the initial trigger stops” (0.91), “my pain is easily aggravated by minor triggers” (0.87), “I have more than one pain problem” (0.82), and “my pain has continued although I’ve been told everything is OK” (0.81). The second factor (7 items) included other health-related symptoms such as alterations in mood, fatigue symptoms and generalised hyper-reactivity. For example, this factor included items such as “I have trouble relaxing and switching off” (0.91), “I feel sad or depressed” (0.77), “I become easily annoyed” (0.74), “I feel nervous and on edge” (0.86) and “I feel sluggish and have little energy” (0.60). EFA using oblique rotation also showed a strong correlation between the two extracted factors (r=0.74).
Pattern matrix from exploratory factor analysis using principal axis factoring for extraction and Oblimin with Kaiser Normalisation for rotation.
| Items | Factor 1 | Factor 2 | Scale values- n (%) |
Missing | Median (IQR) | ||||
|---|---|---|---|---|---|---|---|---|---|
| 0 |
1 |
2 |
3 |
||||||
| Never | Rarely | Sometimes | Always | ||||||
| 1 | My pain is triggered by things that are not normally painful | 0.586 | 0.76 | 92 (50) | 45 (25) | 37 (20) | 7 (4) | 1 (0.5) | 0 (2) |
| 2 | I react to pain triggers more strongly than I used to | 0.719 | 0.042 | 43 (24) | 44 (24) | 63 (35) | 31 (17) | 1 (0.5) | 2 (3) |
| 3 | If I repeatedly touch or move a painful area the pain becomes more intense | 0.3058 | 0.316 | 43 (24) | 46 (25) | 58 (32) | 34(19) | 1 (0.5) | 1.5 (1) |
| 4 | My pain has continued even though have been told everything is ok | 0.811 | −0.083 | 84 (47) | 25 (14) | 27(15) | 42 (23) | 4 (2) | 1 (2) |
| 5 | My pain has spread to other parts of my body | 0.703 | 0.077 | 89 (49) | 33 (18) | 35 (19) | 23 (13) | 2 (1) | 0 (2) |
| 6 | My pain feels out of proportion to my diagnosis | 0.761 | 0.041 | 78 (43) | 42 (23) | 35 (19) | 26 (14) | 1 (0.5) | 1 (2) |
| 7 | My pain continues long after the initial trigger stops | 0.905 | −0.083 | 63 (35) | 31 (17) | 50 (28) | 36 (20) | 2 (1) | 1 (2) |
| 8 | My pain is easily aggravated by minor triggers | 0.874 | −0.035 | 59 (33) | 38 (21) | 50 (28) | 33 (18) | 2 (1) | 1 (2) |
| 9 | My pain is unpredictable and comes on for no apparent reasons | 0.786 | −0.068 | 68 (38) | 42 (23) | 35 (19) | 36 (20) | 1 (0.5) | 1 (2) |
| 10 | My pain does not ease when I take over the counter medicine (e.g. paracetamol, anti-inflammatory). | 0.670 | 0.112 | 60 (33) | 44 (24) | 49 (27) | 28 (16) | 1 (0.5) | 1 (2) |
| 11 | I have more than one pain problem | 0.815 | −0.062 | 70 (39) | 27 (15) | 30 (17) | 52 (29) | 3 (2) | 1 (3) |
| 12 | My sleep is often broken or disturbed | 0.452 | 0.288 | 41 (23) | 45 (25) | 51 (28) | 43 (24) | 2 (1) | 2 (1) |
| 13 | I feel sad or depressed | 0.002 | 0.765 | 57 (32) | 60 (33) | 54 (30) | 10 (6) | 1 (0.5) | 1 (2) |
| 14 | I feel nervous or on edge | −0.048 | 0.862 | 58 (32) | 53 (29) | 59 (33) | 11 (6) | 1 (0.5) | 1 (2) |
| 15 | I become easily annoyed | 0.059 | 0.742 | 42 (23) | 49 (27) | 75 (42) | 14 (8) | 2 (1) | 1 (1) |
| 16 | I have trouble relaxing and cannot switch off | −0.166 | 0.906 | 39 (21) | 54 (30) | 70 (39) | 17 (9) | 2 (1) | 1 (1) |
| 17 | I am sensitive to bright lights and/or loud noises | 0.288 | 0.375 | 56 (31) | 44 (24) | 50 (28) | 30 (17) | 2 (1) | 1 (2) |
| 18 | I jump with sudden noises, movement or touch | 0.257 | 0.415 | 47 (26) | 52 (29) | 58 (32) | 24 (13) | 1 (0.5) | 1 (2) |
| 19 | I get tired very easily | 0.386 | 0.442 | 34 (19) | 47 (26) | 52 (29) | 47 (26) | 2 (1) | 2 (2) |
| 20 | I often wake feeling unrefreshed | 0.218 | 0.555 | 31 (17) | 37 (20) | 77 (43) | 36 (20) | 1 (0.5) | 2 (1) |
| 21 | I feel sluggish and have little energy | 0.218 | 0.602 | 31 (17) | 54 (30) | 71 (39) | 24 (13) | 2 (1) | 2 (1) |
| 22 | I have to urinate often | 0.347 | 0.258 | 60 (33) | 48 (27) | 47 (26) | 25 (14) | 2 (1) | 1 (2) |
| 23 | My joints and muscles feel stiff | 0.590 | 0.187 | 36 (20) | 43 (24) | 54 (30) | 47 (26) | 2 (1) | 2 (2) |
| 24 | I get restless arms and legs | 0.197 | 0.435 | 67 (37) | 37 (20) | 53 (29) | 24 (13) | 1 (0.5) | 1 (2) |
| 25 | I feel discomfort and bloating in my abdomen | 0.014 | 0.605 | 50 (28) | 51 (28) | 62 (34) | 18 (10) | 1 (0.5) | 1 (2) |
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Seven items with factor loadings <0.5 were removed, and are shown in black. Item response frequencies (number and percentage of participants), median and interquartile range (IQR) for each item are shown for each item.
Factor loadings presented in the pattern matrix using PAF also revealed seven items showing factor loadings of 0.5 or less (items 3, 12, 17–19, 22, 24) (Table 3), showing that these items have lower correlations with other items in this questionnaire and also do not load sufficiently onto either of the extracted factors. Additionally, after reviewing the content of these weak-loading items and deciding they were unclear and or ambiguous regarding the latent variable they represent, we decided to eliminate them. Thus, EFA showed a two-factor solution with 18 items which appear to identify different symptom clusters: (a) pain symptoms (11 items), (b) other health-related symptoms (7 items).
3.3 Conditioned pain modulation
People with chronic pain showed significantly lower baseline PPTs than people with no pain (42.2 N±17.66 SD versus 55.67 N±17.24 SD, p=0.001). Immediately after the cold water immersion test, people with chronic pain showed reduced PPTs compared to baseline (40.65 N±16.74) whereas people with no pain showed increased PPTs compared to baseline (61.35 N±21.01 SD). Thus, in this study, people with chronic pain showed reduced CPM efficiency compared to people without chronic pain (94.6%±21.7 SD versus 110.4%±14.95, p=0.001).
3.4 Validity
Concerning the criterion validity of the two factors located within the questionnaire, factor one (pain symptoms) showed strongest correlations with the PASS-20 (r=0.72, p≤0.0001) and PSEQ (r=−0.71, p≤0.0001). Factor two (other health-related symptoms), also showed strong correlations with the DASS-21 (r=0.66, p≤0.0001), PASS-20 (r=0.65, p≤0.0001), the PCS (r=0.63, p≤0.0001) and PSEQ (r=−0.64, p<0.0001). Both factors further showed a moderate correlations with CPM testing (factor one r=0.41, p≤0.001; factor two r=0.46, p≤0.0001) (Table 4).
Pearson’s r correlations between factors 1 and 2 against factors of the novel questionnaire and previously validated psychological function questionnaires and physiological testing (CPM).
| Instrument | Pain symptoms total (factor 1) |
Health-related symptoms total (factor 2) |
|---|---|---|
| r-Value, (p value) | r-Value, (p-value) | |
| Pain symptoms total (factor 1) | 0.74 (<0.0001) | |
| Health-related symptoms total (factor 2) | 0.74 (<0.0001) | |
| PVAQ | 0.58 (<0.0001) | 0.54 (<0.0001) |
| PASS-20 | 0.72 (<0.0001) | 0.65 (<0.0001) |
| PSEQ | −0.71 (<0.0001) | −0.64 (<0.0001) |
| PCS | 0.66 (<0.0001) | 0.63 (<0.0001) |
| DASS-21 Total | 0.59 (<0.0001) | 0.66 (<0.0001) |
| DASS Stress | 0.52 (<0.0001) | 0.69 (<0.0001) |
| DASS Anxiety | 0.49 (<0.0001) | 0.52 (<0.0001) |
| DASS Depression | 0.56 (<0.0001) | 0.63 (<0.0001) |
| CPM | −0.41 (=0.001) | −0.46 (=0.0001) |
We found significant differences in mean scores for all self-report and physiological tests between cases and controls. Here, greatest difference were shown with previously validated self-report and both factors from our novel questionnaire showing p-values under 0.0001 (Table 5).
Means, standard deviations and percentage differences between cases and controls for factors derived from the novel questionnaire and previously validated questionnaires.
| Instrument | Mean (SD) of total scores |
Percentage difference between group mean total scores | p-Values | Possible range | Observed range | |
|---|---|---|---|---|---|---|
| Case | Control | |||||
| Pain symptoms total (factor 1) | 20.16 (6.65) | 5.68 (5.56) | 112% | <0.0001 | 0–33 | 0–32 |
| Health-related symptoms total (factor 2) | 11.72 (4.39) | 6.52 (4.54) | 57% | <0.0001 | 0–21 | 0–20 |
| PVAQ | 44.86 (12.89) | 31.3 (14.93) | 36% | <0.0001 | 0–80 | 0–65 |
| PASS-20 | 37.24 (18.45) | 15.70 (13.51) | 81% | <0.0001 | 0–100 | 0–74 |
| PSEQ | 32.74 (13.87) | 51.31 (9.66) | 44% | <0.0001 | 0–60 | 3–60 |
| PCS | 19.8 (12.2) | 6.44 (7.61) | 102% | <0.0001 | 0–52 | 0–48 |
| DASS-21 (double score)a | 35.5 (25.08) | 9.10 (12.28) | 118% | <0.0001 | 0–126 | 0–110 |
| – Stress (double score)a | 15.08 (10.48) | 5.92 (7.42) | 87% | <0.0001 | 0–42 | 0–42 |
| – Anxiety (double score)a | 8.36 (8.06) | 1.92 (3.84) | 129% | <0.0001 | 0–42 | 0–30 |
| – Depression (double score)a | 11.22 (9.78) | 1.26 (3.46) | 160% | <0.0001 | 0–42 | 0–42 |
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aAll DASS-21 item response scores are doubled to produce scores comparable with the original DASS-42.
3.5 Internal consistency
Using Cronbach’s α, we found excellent internal consistency for factor 1 (pain symptoms –0.94) and excellent internal consistency for factor 2 (other health-related symptoms –0.90).
4 Discussion
This study evaluated the psychometric properties of a novel questionnaire developed to assess symptoms and behaviours reflecting the state of spinal and supraspinal pain processing in people with and without chronic pain. This is part of a broader aim of seeking to develop an assessment tool that enables us to effectively identify people with a strong nociplastic component to their pain which may assist with classification and identification of appropriate treatment strategies.
As described, exploratory factor analysis using PAF showed a two-factor solution with 18 items which appear to identify different symptom clusters: (a) pain symptoms (11 items), (b) other health-related symptoms (7 items). Items within these two factors closely align with current knowledge where increased responsiveness of nociceptive neurons in the central nervous system to normal or sub-threshold afferent input is thought to be triggered by alterations in afferent, local spinal or descending neural signals [15], [18], [45]. Concerning factor one, included items may reflect increased responsiveness of spinal cord nociceptive neurons to external stimuli, e.g. “My pain is triggered by things that are not normally painful” (allodynia), “I react to pain triggers more strongly than I used to” (hyperalgesia) and “My pain has spread to other parts of my body” (increases in receptive field). These pain symptoms have been shown overwhelmingly to reflect adaptive changes in signal processing, in the absence of inflammation or nerve damage, due to prolonged increases in the excitability and synaptic efficacy in central pain pathways [14], [46]. However, although our understanding of nociplastic pain mechanisms has significantly improved, our ability to profile, diagnose and manage people with chronic pain conditions remains in question. Thus, items reflecting these symptoms may help to improve not only profiling, but additionally to expedite the diagnosis of chronic pain conditions in the absence of pathology.
Factor two items include other health-related symptoms that are not specifically pain-related but identify alterations in mood, cognitions and generalised reactivity. Here, included items reflect emotional and cognitive responses associated with chronic pain, e.g. “I feel nervous or on edge” (stress), “I have trouble relaxing and cannot switch off” (anxiety), “I feel sad and depressed” (depression) and “I often wake feeling unrefreshed” (fatigue). This factor correlates strongly with factor 1 and may also indicate changes in altered sensory processing. However, these symptoms are not specifically related to the sensation of pain and may indirectly measure changes that contribute to altered central processing such as changes in supraspinal and descending modulatory pain pathways. Concerning other health-related symptoms, there is now convincing evidence that brain regions serving emotion, cognition and sensation are functionally connected whereby emotional and behavioural cues can modify or enhance the experience and perception of pain through connections with descending pain pathways [47], [48], [49]. Additionally, the clinical association between fatigue and chronic pain is also common where 70% of patients report persistent fatigue [50], [51], [52]. Although underlying mechanisms linking fatigue to chronic pain are currently being explored [51], it has been shown that fatigue reduces the ability or inclination to participate both mentally and physically in both social and treatment settings [53], thus delaying positive responses to pain management.
Of the original 25 items, seven showed low factor loadings (<0.50) and were thus, eliminated (Table 3). Two of these items describe symptoms of sensitivity to external stimuli, while two further items describe the increased urge to urinate more often and restless arms and legs. One pain symptom-related item (If I repeatedly touch or move a painful area, the pain becomes more intense) also showed low factor loading (Table 2). Two further items also showed low factor loadings, where items referred to disturbance of sleep and becoming easily tired during the day.
Evidence for the validity of both factors was also shown against previously validated self-report instruments used to assess cognitive and emotional constructs commonly observed in people with chronic pain. This is not surprising given the strong association between emotional and cognitive factors and alterations in central nociceptive processing but additionally highlights the link between the two.
Although psychological factors that have previously shown no significant correlation with CPM [54], both factors of our questionnaire showed moderate and significant correlations with CPM. Our findings contrast with a meta-analysis of 37 studies by Nahman-Averbuch and colleagues examining CPM and psychological factors in both healthy people and chronic pain patients. Here they showed no significant correlations between CPM responses and factors such as stress (r=0.31) fear of pain (r=0.17), depression (r=0.24) and pain catastrophising (r=0.15) [54]. However, Marcuzzi and colleagues in a recent meta-analysis of 11 studies investigating CPM in people with irritable bowel syndrome showed significant correlations between reduced CPM responses and higher anxiety (r=0.17–0.64), stress (r=0.63) and pain catastrophising (r=0.38) [55]. Although the latter study showed some increased correlations compared to our CPM correlations, it should be noted that Nahman-Averbuch’s and our studies used samples from the general population that included healthy individuals and people with a range of chronic pain conditions. Marcuzzi and colleagues findings suggest evidence for strength of association between psychological factors and CPM in specific pain conditions and thus warrant further investigation. However, although our results showed strong correlations between CPM and several pain presentations, our sample sizes for each pain presentation were too small for meaningful sub-group analysis.
Overall, our results show that a short self-report instrument containing two factors could be used to evaluate symptoms shown to be indicative of altered spinal and supraspinal pain processing in people with and without chronic pain [14]. There is now also overwhelming evidence that central nervous system-mediated processes are an important component of the ongoing experience of pain, particularly where it is difficult to detect definitive evidence of inflammation or nerve damage [11], [56], [57]. Here, Woolf suggests that chronic pain perceived in the periphery is not due to a specific pathology, but instead reflects a state of excitability of central nociceptive and pain circuits [14]. To test the extent to which central pain processing may be contributing to a person’s experience of pain, there needs to be clear diagnostic criteria where currently no gold-standard exists. Although several self-report instruments exist, they either assess central pain characteristics of individual conditions or anatomical location [58], [59], or mood, fatigue and widespread pain-related symptoms in people with chronic pain [10]. Thus, the purpose of our study was not to develop a self-report questionnaire that assessed symptoms reflective of an individual disorder or general features observed in people with chronic pain, but as an instrument for identifying both local pain and other health-related symptoms that potentially reflect enhanced excitability in both spinal and supraspinal pain circuits.
5 Conclusion
In summary, this study has developed a questionnaire containing two factors that appear to identify two symptoms clusters, one of which is specifically related to pain and one of which contains other health-related symptoms related to mood, cognitions and behaviour. These factors also show excellent internal consistency and strong evidence for validity against psychological and physiological instruments, suggesting this questionnaire may be a quick, easy and reliable measure for central pain processing in clinical settings. Confirmatory analysis in larger sample is further required to establish whether a total score is appropriate for interpretation.
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Authors’ statements
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Research funding: This work was supported by the Australian and New Zealand College of Anaesthetists (16/003) with additional support from a private donation and the Profield Foundation.
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Conflict of interest: Authors state no conflict of interest.
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Informed consent: Informed consent has been obtained from all individuals included in this study.
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Ethical approval: The research related to human use complies with all the relevant national regulations, institutional policies and was performed in accordance with the tenets of the Helsinki Declaration, and has been approved by the authors institutional review board or equivalent committee.
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©2020 Scandinavian Association for the Study of Pain. Published by Walter de Gruyter GmbH, Berlin/Boston. All rights reserved.
Artikel in diesem Heft
- Frontmatter
- Systematic review
- Are there differences in lifting technique between those with and without low back pain? A systematic review
- Topical reviews
- Pain psychology in the 21st century: lessons learned and moving forward
- Chronic abdominal pain and persistent opioid use after bariatric surgery
- Clinical pain research
- Spinal cord stimulation for the treatment of complex regional pain syndrome leads to improvement of quality of life, reduction of pain and psychological distress: a retrospective case series with 24 months follow up
- The feasibility of gym-based exercise therapy for patients with persistent neck pain
- Intervention with an educational video after a whiplash trauma – a randomised controlled clinical trial
- Reliability of the conditioned pain modulation paradigm across three anatomical sites
- Is rotator cuff related shoulder pain a multidimensional disorder? An exploratory study
- Are degenerative spondylolisthesis and further slippage postoperatively really issues in spinal stenosis surgery?
- Multiprofessional assessment of patients with chronic pain in primary healthcare
- The impact of chronic orofacial pain on health-related quality of life
- Pressure pain thresholds in children before and after surgery: a prospective study
- Observational studies
- An observational study on risk factors for prolonged opioid prescription after severe trauma
- Dizziness and localized pain are often concurrent in patients with balance or psychological disorders
- Pre-consultation biopsychosocial data from patients admitted for management at pain centers in Norway
- Original experimentals
- Local hyperalgesia, normal endogenous modulation with pain report beyond its origin: a pilot study prompting further exploration into plantar fasciopathy
- Pressure pain sensitivity in patients with traumatic first-time and recurrent anterior shoulder dislocation: a cross-sectional analysis
- Cross-cultural adaptation of the Danish version of the Big Five Inventory – a dual-panel approach
- The development of a novel questionnaire assessing alterations in central pain processing in people with and without chronic pain
- Letters to the Editor
- The clinical utility of a multivariate genetic panel for identifying those at risk of developing Opioid Use Disorder while on prescription opioids
- Should we use linked chronic widespread pain and fibromyalgia diagnostic criteria?
- Book review
- Akut och cancerrelaterad smärta – Smärtmedicin Vol. 1
Artikel in diesem Heft
- Frontmatter
- Systematic review
- Are there differences in lifting technique between those with and without low back pain? A systematic review
- Topical reviews
- Pain psychology in the 21st century: lessons learned and moving forward
- Chronic abdominal pain and persistent opioid use after bariatric surgery
- Clinical pain research
- Spinal cord stimulation for the treatment of complex regional pain syndrome leads to improvement of quality of life, reduction of pain and psychological distress: a retrospective case series with 24 months follow up
- The feasibility of gym-based exercise therapy for patients with persistent neck pain
- Intervention with an educational video after a whiplash trauma – a randomised controlled clinical trial
- Reliability of the conditioned pain modulation paradigm across three anatomical sites
- Is rotator cuff related shoulder pain a multidimensional disorder? An exploratory study
- Are degenerative spondylolisthesis and further slippage postoperatively really issues in spinal stenosis surgery?
- Multiprofessional assessment of patients with chronic pain in primary healthcare
- The impact of chronic orofacial pain on health-related quality of life
- Pressure pain thresholds in children before and after surgery: a prospective study
- Observational studies
- An observational study on risk factors for prolonged opioid prescription after severe trauma
- Dizziness and localized pain are often concurrent in patients with balance or psychological disorders
- Pre-consultation biopsychosocial data from patients admitted for management at pain centers in Norway
- Original experimentals
- Local hyperalgesia, normal endogenous modulation with pain report beyond its origin: a pilot study prompting further exploration into plantar fasciopathy
- Pressure pain sensitivity in patients with traumatic first-time and recurrent anterior shoulder dislocation: a cross-sectional analysis
- Cross-cultural adaptation of the Danish version of the Big Five Inventory – a dual-panel approach
- The development of a novel questionnaire assessing alterations in central pain processing in people with and without chronic pain
- Letters to the Editor
- The clinical utility of a multivariate genetic panel for identifying those at risk of developing Opioid Use Disorder while on prescription opioids
- Should we use linked chronic widespread pain and fibromyalgia diagnostic criteria?
- Book review
- Akut och cancerrelaterad smärta – Smärtmedicin Vol. 1
