- Email: [email protected]
Comparison of psychological and physical function in neuropathic pain and nociceptive pain: Implications for cognitive behavioral pain management programs
Available online at www.sciencedirect.com
European Journal of Pain 12 (2008) 731–741 www.EuropeanJournalPain.com
Comparison of psychological and physical function in neuropathic pain and nociceptive pain: Implications for cognitive behavioral pain management programs H. Clare Daniel a,b,*, Jane Narewska a, Michael Serpell c, Barbara Hoggart d, Robert Johnson e, Andrew S.C. Rice a b
a Pain Research Group, Department of Anaesthetics, Pain Medicine and Intensive Care, Faculty of Medicine, Imperial College London, UK Pain Management Centre, The National Hospital for Neurology and Neurosurgery, University College London Hospitals NHS Foundation Trust, Queen Square, London WC1N 3BG, UK c University Department of Anaesthesia, Glasgow University, Gartnavel General Hospital, UK d Birmingham Heartlands and Solihull NHS Trust, UK e United Bristol Hospitals and University of Bristol, UK
Received 11 June 2007; received in revised form 29 October 2007; accepted 9 November 2007 Available online 27 December 2007
Abstract Research has increased our understanding of the psychological and physical functioning associated with persistent pain and has facilitated the development of cognitive behavioral pain management programs to help improve people’s physical function and decrease their distress in the presence of persistent pain. The majority of this research has focused on nociceptive pain or pain of mixed etiology. There has been less focus on these aspects of neuropathic pain. It is possible that differences exist in the function and difficulties associated with nociceptive and neuropathic pain. These differences may be associated with our clinical observation that some people with neuropathic pain have difficulty applying some aspects of the theory and practice of cognitive behavioral pain management. The purpose of this study was to compare a single neuropathic pain condition (post-herpetic neuralgia) with a persistent pain of nociceptive origin (low back pain) and determine whether differences exist in: (1) physical and psychological function; (2) factors that increase difficulties; (3) responses to pain; (4) beliefs about pain and (5) problems experienced. The results suggest that the differences between the two groups were not on the major variables of pain, mood, cognition and physical function. The main differences were in factors that increase pain, people’s responses to pain, their beliefs about diagnosis and the cause of pain and the problems they reported as a result of experiencing pain. The implications of our findings for the development of cognitive behavioral pain management programs for people with neuropathic pain are discussed. Ó 2007 European Federation of Chapters of the International Association for the Study of Pain. Published by Elsevier Ltd. All rights reserved. Keywords: Neuropathic pain; Cognitive-behavioral pain management; Function; Impact
1. Introduction *
Corresponding author. Address: Pain Management Centre, The National Hospital for Neurology and Neurosurgery, University College London Hospitals NHS Foundation Trust, Queen Square, London WC1N 3BG, UK. Tel.: +44 845 155 5000x723487; fax: +44 20 7419 1714. E-mail address: [email protected] (H.C. Daniel).
Whilst it is possible to define both neuropathic and nociceptive pain and to identify distinctive features of each condition, this is generally done by reference to the etiology of the medical condition underlying the pain or features of the pain itself. There is a large literature
1090-3801/$34 Ó 2007 European Federation of Chapters of the International Association for the Study of Pain. Published by Elsevier Ltd. All rights reserved. doi:10.1016/j.ejpain.2007.11.006
732
H.C. Daniel et al. / European Journal of Pain 12 (2008) 731–741
regarding interference on psychological and physical functioning in respect of nociceptive pain. With a few exceptions (for example, Clark et al., 2000; Haythornthwaite and Benrud-Larson, 2000, 2001) less attention has been paid to these aspects of neuropathic pain. More specifically there is little evidence on whether differences in functioning and responses to pain exist between people with neuropathic and nociceptive pain. The differences in pain characteristics that exist between neuropathic and other persistent pain states, for example the spontaneous pain associated with neuropathic pain, are well recognized and included in questionnaires (Bennett, 2001; Backonja and Stacey, 2004; Bouhassira et al., 2005). There has been less focus on the contribution these differences make to functioning and responses to pain. It is recognized that the changes in physical and psychological functioning associated with persistent pain are influenced by psychosocial variables, for example, beliefs (Lame´ et al., 2005), psychological processes (Sullivan et al., 2001) and emotions (Vlaeyen et al., 2001). Research on psychosocial variables and pain has tended to focus on nociceptive pain or pain of mixed etiology although some evidence suggests that the findings apply to neuropathic pain (Jensen et al., 2002; Evans et al., 2003; Haythornthwaite et al., 2003). Cognitive behavioral pain management programs (PMPs) aim to improve psychological and physical function and reduce reliance on healthcare by changing responses to persistent pain (Morley et al., 1999). The majority of patients in a generic PMP have nociceptive pain or pain of mixed etiology. A few have only neuropathic pain. Clinical experience within this context suggests that some people with neuropathic pain distinguish their pain and problems from the mainstream and report differences in functioning and management of their pain. These same people report difficulties when applying some of the theories and principles of cognitive behavioral pain management, particularly activity pacing. It is possible that some components of generic PMPs do not match the difficulties experienced by some people with neuropathic pain. These interventions may require adaptation, however, this has been the focus of little research. We were unable to locate any published direct comparisons of physical and psychological functioning of people with neuropathic and nociceptive pain. In the context of a between group comparison we aimed to determine whether population differences exist when a single neuropathic pain condition (post-herpetic neuralgia) was compared with a persistent pain of nociceptive origin (biomechanical low back pain without radicular symptoms). Although we hypothesised that the two groups experience similar levels of psychological and physical functioning, we predicted that people with neuropathic pain would report: (1) a smaller association
between physical activity and pain increases; (2) different responses to their pain, notably less activity avoidance and less use of pacing; (3) different causal beliefs and (4) significant problems not addressed by generic PMPs.
2. Methods 2.1. Participants Participants aged 18 years or older were recruited from five pain management clinics (one in Scotland and four in England). They were experiencing either biomechanical low back pain (LBP) or post-herpetic neuralgia (PHN). It is recognized that difficulties can exist with the concept of LBP being solely due to nociceptive pain (Freynhagen et al., 2006). Inclusion and exclusion criteria were used to ensure as much as possible that the pain was not confounded by other types of pain, illnesses or conditions. To ensure the pain was persistent, those recruited with LBP had to have experienced pain for 6 months or longer and have a clinical diagnosis of persistent low back pain. They were excluded if they had experienced pain radiating down the leg below the knee within the last three months or had a systemic inflammatory disorder or other disorders that resulted in pain. Those with neuropathic pain had experienced PHN for more than 6 months after healing of the herpes zoster skin rash. Their diagnosis was confirmed by their physician. Those who had undergone neurolytic or neurosurgical therapy for PHN or experienced moderate to severe pain not attributable to their PHN were excluded. Following ethical committee approval (Glasgow West Local Research Ethics Committee, National Hospital for Neurology and Neurosurgery and Institute of Neurology Local Research Ethics Committee, Riverside Research Ethics Committee, Solihull Local Research Ethics Committee, and Central and South Bristol Research Ethics Committee) the personal details of 298 people who experienced either LBP (n = 190) or PHN (n = 108) were provided by consultants in pain management in the five pain clinics. These 298 people were mailed an information sheet and a letter inviting them to take part in the study. Seven days later this letter was followed by a telephone call to each person to answer any questions and ascertain if they wished to participate in the study. Those who gave verbal agreement were posted the questionnaires, a consent form and a stamped addressed envelope. A time was agreed for the researcher to telephone the participants to ensure all the questionnaires had been completed and any queries addressed. During this second telephone call the researcher attempted to answer the participants’ queries without influencing their choice of answers in the questionnaires. Participants were asked to return the questionnaires and consent form in the stamped addressed envelope.
H.C. Daniel et al. / European Journal of Pain 12 (2008) 731–741
2.2. Measures 2.2.1. The Sickness Impact Profile (SIP) (Bergner et al., 1981) The SIP is a subjective behavioral measure of health status that addresses physical and psychosocial behavior. It consists of 136 items, forming 12 subscales and has been validated on persistent pain populations (Jensen et al., 1992; Bacon et al., 1994). The higher the score, the greater the impact of the pain on physical and psychosocial behavior. 2.2.2. The Beck Depression Inventory (BDI) (Beck et al., 1961) The BDI assesses symptoms of depression. It is a 21 item, self-report questionnaire. Each item is rated on a 0–3 scale. A higher score indicates a greater number of symptoms of depression. The psychometric properties of the BDI are well established in psychiatric populations (Beck et al., 1988) but are disputed in the persistent pain population (Pincus and Williams, 1999; Morley et al., 2002; Pincus et al., 2004). Due to difficulties using this measure with persistent pain populations and to ensure that the confounding somatic items were not included in the analyses, the results of the BDI were analysed using the self-blame subscale identified by Morley et al. (2002) rather than the total score. 2.2.3. The Pain Anxiety Symptoms Scale (PASS) (McCracken et al., 1992) The PASS comprises of 40 self-report items of fear and anxiety behaviors related to pain. It contains four subscales; cognitive anxiety symptoms, escape and avoidance responses, fearful appraisals of pain and physiological anxiety symptoms related to pain. Participants make a frequency rating for each item on a scale from 0 (never) to 5 (always). The greater the score the more frequent the behaviors. The PASS has been validated for use on persistent pain populations. The alpha coefficients have been shown to be 0.94 for the total scale and range from 0.81 to 0.89 for the subscales (McCracken et al., 1992). Adequate test-retest reliability has been demonstrated (McCracken et al., 1993). 2.2.4. The Chronic Pain Acceptance Questionnaire (CPAQ) (Geisser, unpublished doctoral dissertation 1992; McCracken et al., 2004) The CPAQ quantifies the degree to which respondents are living a normal life despite pain. It comprises 20 self-report items forming two subscales; activity engagement (pursuit of life activities despite pain) and pain willingness (the degree to which people have experiences of pain without trying to avoid or control them and the recognition that avoidance and control can be unhelpful methods of responding to persistent pain). Items are rated on a 0 (never true) to 6 (always true)
733
scale. The higher the score the more participants are living a normal life despite pain. The internal consistency of the total score is Cronbach’s a = 0.78 and for the two subscales; 0.78 (pain willingness); 0.82 (activity engagement) (McCracken et al., 2004). 2.2.5. Personal and medical information A questionnaire was developed and piloted to address concepts discussed in the pain literature but for which there are no available standardised measures. In addition to personal demographics (Table 1) this questionnaire included the questions shown in Appendix 1. 2.3. Statistical analysis Data which were not normally distributed were identified by their skewness and kurtosis values, transformed into their square roots and treated as parametric data. Those that could not be transformed were treated as non-parametric data. Means and standard deviations are reported for parametric continuous data and medians and quartiles are reported for non-parametric continuous data. Outliers were determined by box plots and reduced to the next largest value in the data set for that variable (Tabachnick and Fidell, 2001). Between group comparisons of parametric continuous data were analysed using two tailed t-tests. Nonparametric continuous data were analysed using the Mann–Whitney U test. Chi-square tests were used for categorical data. Low back pain and post-herpetic neuralgia were entered as the dichotomous outcome variables in logistic regression to determine which variables were more likely to be associated with one of the two pain groups. A significance level of p < 0.05 was used throughout the study. Significant values are shown in bold. The statistical software used was SPSS for Windows (version 11.5). Content analysis was used to analyse responses to the qualitative questions. This involved categorizing and counting the presence of certain words or concepts to enable inferences to be made from the participants’ responses (Neuendorf, 2002). As we were interested in causal beliefs, responses to the question, ‘‘What diagnosis (if any) have you been given” were sorted into two categories; (i) diagnosis stated or (ii) no diagnosis stated/do not know diagnosis. Responses to the question ‘‘What do you think is happening in your body now to be causing your pain?” were analysed in two independent ways. First, they were categorized according to whether participants (i) gave a clear reason for their pain (e.g. ‘‘nerve damage due to shingles”), (ii) gave an ambiguous reason (e.g. ‘‘I’m not sure, maybe something’s not in the right place in my back”) or (iii) stated that they did not know. Second, the number of participants who used the word ‘damage’ were counted. Responses to the question
734
H.C. Daniel et al. / European Journal of Pain 12 (2008) 731–741
Table 1 Personal data for whole group and comparisons between LBP and PHN groups Whole group (n = 106)
LBP (n = 57)
PHN (n = 49)
t (df) or v2 (df)
Age (years) mean (s.d.)
61.55 (16.42)
53.32 (16.12)
71.12 (10.63)
t=
Gender n (%) Men Women
41 (38.7) 65 (61.3)
19 (33.3) 38 (66.7)
22 (44.9) 27 (55.1)
v2 = 1.49 (1)
0.24
Ethnicity n (%) White Other Missing
98 (92.5) 6 (5.7) 2(1.9)
52 (91.2) 3 (5.3) 2 (3.5)
46 (93.9) 3 (6.1) 0
v2 = 0.02 (1)
1.00
Relationship status n (%) Has a partner No partner Missing
65 (61.3) 39 (36.8) 2 (1.9)
36 (63.2) 20 (35.1) 1 (1.8)
29 (59.2) 19 (38.8) 1 (2.0)
v2 = 0.17 (1)
0.69
Living situation n (%) With someone Alone
77 (72.6) 29 (27.4)
43 (75.4) 14 (24.6)
34 (69.4) 15 (30.6)
v2 = 0.49 (1)
0.52
Employment status n(%) Working/studying Not working (due to pain) Not working (not due to pain) Other
34 (32.1) 13 (12.3) 52 (49.1) 7 (6.6)
30 (52.6) 7 (12.3) 17 (29.8) 3 (5.3)
4 (8.2) 6 (12.2) 35 (71.4) 4 (8.2)
v2 = 25.88 (3)
< 0.001a
Educational qualifications n (%) Up to secondary education Beyond secondary education Missing
59 (55.7) 43 (40.6) 4 (3.8)
29 (50.9) 26 (45.6) 2 (3.5)
30 (61.2) 17 (34.7) 2 (4.1)
v2 = 1.28 (1)
0.32
a
6.60 (104)
p-Value <0.001a
p 6 0.001.
‘‘People often say that pain causes many problems in their lives. These can either be physical or emotional. Please list what you believe are the three main problems that you experience because you have pain”, were also analysed in two independent ways. First, a count was made of the number of physical and emotional difficulties each participant stated. Second, a count was made of how many participants cited a problem that described allodynia (defined as pain experienced due to stimulus that does not normally provoke pain) as being one of the main problems experienced as this can be neglected in some generic PMPs. The first author and a qualified nurse manually coded the data. All categories were exhaustive and mutually exclusive. Kappa statistics were generated to assess inter-coder reliability.
3. Results The CONSORT diagram in Fig. 1 shows the numbers of people who were invited to participate, who responded, who were excluded or self-excluded and the final number of participants included in the study. A test of difference of proportions ( 0.154, 95% CI) revealed a difference in the response rates of the two groups. A significantly greater percentage of those with PHN (45%) returned usable data compared with those with LBP (30%). Data are not available to enable com-
parison between those who did and did not take part in the study. 3.1. Personal and pain data As expected, the PHN group were significantly older than those with LBP and those with LBP were more likely to be in paid employment. There were no significant between group differences in the other personal data (Table 1). The PHN group reported their main site of pain as being in the thorax (51%), head (26.5%), shoulder (12.2%), legs (8.2%) or upper limbs (2%). Table 2 summarises the pain data for the group as a whole and for the LBP and PHN groups. Those with LBP had experienced pain for a significantly longer period of time. There were no significant between group differences regarding pain intensity, pain distress, pain constancy and the number of reported good and bad days in a month. 3.2. Psychological and physical functioning Escape and avoidance responses were used significantly more frequently by the LBP group. The cognitive or mood variables did not distinguish the two groups (Table 3). Regarding interference due to pain, the only significant between group difference was that those with LBP
H.C. Daniel et al. / European Journal of Pain 12 (2008) 731–741
735
Invitation sent to 298 people
LBP (n=190)
PHN (n=108) PHN
LBP
26 could not be contacted
49 could not be contacted st
1 telephone call (7 days after letter posted)
39 did not wish to participate
20 did not wish to participate 3 met exclusion criteria
20 met exclusion criteria 59 with PHN agreed to participate
82 with LBP agreed to participate
Questionnaires sent
nd
2 telephone call (7 days after questionnaires posted)
PHN 1 participant withdrew
LBP 23 did not return questionnaires
59 with LBP returned questionnaires
52 with PHN returned questionnaires
PHN 6 did not return questionnaires
LBP 2 questionnaires were incomplete and excluded
57 with LBP (30% of those invited to take part) returned usable data
49 with PHN (45% of those invited to take part) returned usable data
PHN 3 questionnaires were incomplete and excluded
Fig. 1. CONSORT diagram outlining the recruitment process and numbers of people included and excluded. Table 2 Pain data for whole group and comparisons between LBP and PHN groups
Pain duration (months) Pain intensity (NRS 0–10) Pain distress (NRS 0–10) Pain constancy (NRS 0–10) Number of good days/month Number of bad days/month a
Whole group (n = 106) median [quartiles]
LBP (n = 57) median [quartiles]
PHN (n = 49) median [quartiles]
U (z)
69 [36; 144] 7 [4; 8] 5 [3; 8] 8 [5; 10] 5 [2; 10] 20 [10; 26.25]
97 [36; 180] 6 [4; 8] 5 [3; 7] 8 [5; 10] 5 [1; 12] 20 [10; 25]
58 [33.5; 98.5] 7 [5; 8] 6 [2.5; 8] 8 [4.5; 10] 5 [2; 10] 18 [10; 28]
1068.50 1190.50 1276.50 1375.50 1370.50 1355.50
p-Value ( ( ( ( ( (
2.08) 1.32) 0.76) 0.14) 0.17) 0.26)
0.04a 0.19 0.45 0.89 0.87 0.79
p 6 0.05.
reported significantly greater interference due to pain on a bad day (Table 4). The median time spent resting every day for the group as a whole was 2.5 h. There were no significant between group differences (LBP median 2.75 h; PHN median 2.0 h).
3.3. Factors that increase pain Pain type was entered as the outcome variable in a logistic regression analysis. Due to significant between group differences in age and duration of pain these were entered as predictor variables in addition to the factors
736
H.C. Daniel et al. / European Journal of Pain 12 (2008) 731–741
Table 3 Cognitive and mood data for whole group and comparisons between LBP and PHN groups
Frustration (NRS 0–10) median [quartiles] Anger (NRS 0–10) median [quartiles] Symptoms of depression (self-blame BDI) median [quartiles] Fearful appraisals of pain (PASS subscale) mean (s.d.) Physiological anxiety symptoms (PASS subscale) median [quartiles] Cognitive anxiety symptoms (PASS subscale) median [quartiles] Escape and avoidance responses (PASS subscale) mean (s.d.) Pain willingness (CPAQ subscale) mean (s.d.) Activity engagement (CPAQ subscale) mean (s.d.) Belief that future treatments will reduce pain (NRS 0–10) a
Whole group (n = 106)
LBP (n = 57)
PHN (n = 49)
U (z) or t (df)
p-Value
8 [5.75; 10] 5 [2; 8] 1 [0; 3]
8 [6.5; 10] 6 [2; 8] 1 [0; 4.50]
8 [4.5; 10] 5 [2.5;9] 1 [0; 3.00]
U = 1323.0 z = 0.48 U = 1384.50 z = 0.077 U = 1256.0 z = 0.915
0.63 0.94 0.36
14.33 (9.76)
15.26 (10.34)
13.24 (9.02)
t = 1.06 df 104
0.35
7.5 [2.75; 15.25]
9 [3; 16]
5 [2.0; 14.0]
U = 1222.0 z =
21 [12.75; 31.25]
22 [14; 34]
19 [10; 28.50]
U = 1121.50 z =
21.06 (10.14)
23.00 (9.35)
18.80 (10.64)
t = 2.17 df 104
0.03a
24.07 (10.97) 38.86 (12.65) 4 [1; 6]
23.74 (10.15) 38.40 (11.28) 5 [3; 6]
24.45 (11.94) 39.39 (14.17) 4 [0.5; 6.5]
t = 0.33 df 104 t = 0.40 df 104 U = 1103.00 z = 1.87
0.74 0.69 0.06
1.11 1.74
0.27 0.81
p 6 0.05.
Table 4 Interference due to pain: data for whole group and comparisons between LBP and PHN groups
Interference on a good day (NRS 0–10) Interference on a bad day (NRS 0–10) Psychosocial interference (SIP subscale) Physical interference (SIP subscale) a
Whole group median [quartiles]
LBP median [quartiles]
PHN median [quartiles]
U (z)
p-Value
4 [2; 8] 8 [5; 10] 11.99 [6.13; 28.25] 7.86 [1.82; 18.95]
4 [2; 8.50] 8 [6; 10] 15.70 [8.07; 30.71] 8.02 [2.34; 22.32]
5 [2; 7.5] 7 [4; 9] 10.31 [3.58; 21.51] 6.65 [0.84; 17.34]
1387.50 ( 0.06) 1002.0 ( 2.54) 1127.50 ( 1.71) 1234.0 ( 1.03)
0.95 0.01a 0.09 0.30
p 6 0.01.
reported to increase pain (Table 5). Pain being increased by touch or air movement and stress were predictive of PHN group membership. Pain being increased by activity and exercise or keeping still and resting were significantly less likely to be associated with PHN.
Table 5 Logistic regression model with pain type as the outcome variable and factors increasing pain as the predictor variables (n = 106) Variable
Odds ratio
p-Value
95% confidence interval Lower
Upper
3.4. Responses to pain
Age Duration
1.099 0.995
<0.001a 0.165
1.046 0.988
1.156 1.002
Table 6 summarises the participants’ responses to ‘‘What, if anything, helps to reduce your level of pain?”. Nobody with PHN reported finding pacing, osteopathy, TENs and medical interventions helpful. Nobody with LBP reported finding physiotherapy, removing anything that touches the painful area or applying pressure/touch or scratching the painful area helpful. Those with LBP had visited a significantly greater number of different types of health care providers (HCPs) since the pain started (LBP median 5 [quartiles 3.5; 6], PHN median 3 [quartiles 2; 4], U = 498.5, z = 5.78, p < 0.001) and attended a significantly greater number of appointments in the 3 months prior to participating in the study (LBP median 2 [quartiles 0.5; 4.5], PHN median 1 [quartiles 0.0; 3], U = 1076.5, z = 2.07, p = 0.038). The LBP group were significantly more likely to report that medical interventions helped
Factors increasing pain Exercise/activity Rest/keeping still Stress Touch/air movement Temperature
0.211 0.142 5.784 6.448 0.792
0.042c 0.022c 0.034c 0.003b 0.736
0.047 0.027 1.138 1.870 0.205
0.946 0.759 29.392 22.238 03.067
a b c
p 6 0.001. p 6 0.01. p 6 0.05.
to reduce their pain (v2(1, n = 106) = 6.44, p = 0.014). There were no significant between group differences regarding the number of participants having attended psychological or psychiatric appointments (v2(1, n = 106) = 1.17, p = 0.40) or appointments for complementary therapies (for example faith healing and Reiki) (v2(1, n = 106) = 0.03, p = 1.0).
H.C. Daniel et al. / European Journal of Pain 12 (2008) 731–741 Table 6 Numbers (%) of participants who reported finding treatments/behaviors helpful in reducing their pain v2
Factors that help to reduce pain
LBP n (%)
PHN n (%)
Medication Resting Stretch/yoga/pilates Medical interventions Warm Nothing Pacing/not doing things for too long Cool Osteopathy Breathing Distraction TENs Alcohol Pressure/touch/scratch Removing touch Physiotherapy
26 (45.6) 18 (31.6) 16 (28.1) 7 (12.3)
21 (42.9) 13 (26.5) 3 (6.1) 0
–a
6 (10.5) 6 (10.5) 6 (10.5)
7 (14.3) 4 (8.2) 0
0.346 –a –a
4 4 3 3 2 1 0 0 0
5 0 7 6 0 1 8 4 2
–a –a –a –a –a –a –a –a –a
(7) (7) (5.3) (5.3) (3.5) (1.8)
(10.2) (14.3) (12.2) (2) (16.3) (8.2) (4.1)
0.081 0.325
df
p-Value
1 1
0.78 0.57
1
0.56
a
a Chi-square not calculated because less than 10% of one or both groups endorsed the item.
Those with LBP were significantly more likely to be taking medication for their pain. Fifty one (89.5%) participants with LBP were taking medication for their pain compared with 37 (75.5%) with PHN (v2(1, n = 106) = 3.86, p = 0.049). There were no significant between group differences in the amount of reported pain relief afforded by medication. Fifteen (29.4%) of the LBP group and 14 (37.8%) of the PHN group who were taking medication reported a pain relief score of 3 or less out of 10 (where 10 = complete relief) (LBP median 5 [quartiles 3; 7], PHN median 5 [quartiles 2; 6.25], U = 856.50, z = 0.94, p = 0.35). Twenty seven (52.9%) participants with LBP reported experiencing medication side effects compared with 13 (35.1%) in the PHN group (v2(1, n = 88) = 2.26, p = 0.14). 3.5. Beliefs Participants’ responses to the question ‘‘What diagnosis (if any) have you been given?” were sorted into two categories; ‘diagnosis stated’ and ‘no diagnosis stated/don’t know diagnosis’. Two participants with LBP did not respond to this question and were categorized as ‘no diagnosis stated’. Ten (17.5%) of those with LBP did not give a diagnosis or stated that they did not know what diagnosis they have been given compared with 2 (4.1%) of those with PHN (v2(1, n = 106) = 4.76, p 6 0.05). Of the 47 (82.5%) of those with LBP who offered a diagnosis, 24 (42.2%) gave one diagnosis and 23 (40.35%) gave two or more diagnoses (j = 0.87). Of the 47 (95.9%) of those with PHN who gave a diagnosis, 45 (95.74%) gave one diagnosis and 2 (4.1%) gave two or more diagnoses (j = 1.00) (v2(1, n = 94) = 24.03, p < 0.0001).
737
Responses to the question ‘‘What do you think is happening in your body now to be causing your pain?” were sorted into three categories: (i) gave a clear reason for their pain (e.g. ‘‘nerve damage due to shingles”), (ii) gave an ambiguous reason (e.g. ‘‘I’m not sure, maybe something’s not in the right place in my back”) or (iii) stated that they did not know (Table 7). All participants responded to this question. There were significant between groups differences (v2(1, n = 106) = 22.93, p < 0.0001). A greater percentage of those in the PHN group provided a clear reason for their pain (j = 0.81) and a greater percentage of those with LBP provided an ambiguous answer or responded that they did not know (j = 0.83). The responses to the same question were also sorted depending or whether the word ‘‘damage” was used. Those with PHN were significantly more likely to use damage to describe the current cause of their pain. Four (7%) participants with LBP used the word damage compared with 17 (34.7%) of those with PHN (v2(1, n = 106) = 12.7, p < 0.001). All those with PHN who used the term damage did so in the context of nerve damage. 3.6. Difficulties experienced Participants were asked the question ‘‘People often say that pain causes many problems in their lives. These can either be physical or emotional. Please list what you believe are the three main problems that you experience because you have pain”. All participants responded to this question. Although the majority stated three problems, two participants with LBP reported 4 main problems, four reported 2, and one reported 1 main problem. Of the PHN group, two reported 2, and one reported 1 main problem. There were no significant between group differences regarding whether participants cited (LBP n = 32 [56.1%]; PHN n = 27 [58.7%]) or did not cite an emotional problem as one of the three main problems they experienced (v2(1, n = 106) = 0.068, p = 0.84). Those with LBP were significantly more likely to cite a physical problem as being one of their main problems (LBP n = 53 [93%]; PHN n = 34 [69.4%], (v2(1, n = 106) = 9.97, p = 0.002)). In the PHN group 32.65 % (n = 16) stated a problem that described allodynia (for Table 7 Categorized answers (n, %) to the question ‘‘What do you think is happening in your body now to be causing your pain?” Answers
LBP n (%)
PHN n (%)
v2
df
p-Value
Clear reason given Ambiguous answer Do not know
26 (45.6) 20 (35.1) 11 (19.3)
44 (89.8) 1 (2.0) 4 (8.2)
22.93
1
<0.0001a
a Data for the ‘ambiguous answer’ and ‘don’t know’ categories have been combined to increase the observed cell frequencies for the chisquare calculation.
738
H.C. Daniel et al. / European Journal of Pain 12 (2008) 731–741
example, ‘‘I no longer go out socially as the feeling of clothes against my skin is so uncomfortable that I don’t enjoy being out”), compared with 0% with LBP (v2(1, n = 106) = 21.92, p 6 0.001).
4. Discussion We compared the experience of people with neuropathic pain, specifically PHN who attend pain clinics with that of people with LBP who attend pain clinics. Differences emerged not in major variables of pain, mood, cognition and physical function but in: (1) factors that increase pain; (2) responses to pain; (3) beliefs about pain and (4) reported problems. These may have implications for cognitive behavioral PMPs for neuropathic pain. Our PHN population was comparable to those recruited in randomised controlled trials of medical therapy (Rice and Maton, 2001; Dworkin et al., 2003). Given that shingles is associated with an older population it is unsurprising that the PHN group were significantly older and less likely to be working (Dworkin and Portenoy, 1996). Despite different etiologies, mechanisms and pain sites, the two groups reported similar pain intensity, constancy, distress and number of good/bad days. The same was found for the majority of the cognitive and mood variables (self-blame, frustration, anger, acceptance, fear appraisals of pain and cognitive and physiological anxiety) and physical and psychosocial interference. These findings support growing evidence that people with neuropathic pain suffer to a similar extent as those with nociceptive pain (Haythornthwaite and Benrud-Larson, 2000) across many life domains (Benbow et al., 1998; Galer et al., 2000a,b; Meyer-Rosberg et al., 2001; Schmader, 2002) and may benefit from cognitive behavioral pain management. This latter point is supported by the finding that 38% of those with PHN who were taking medication gained only 30% or less pain relief and 35% reported side effects. This is despite recent successes in the analgesic pharmacotherapy of PHN (Hempenstall et al., 2005). The PHN group were more likely to associate increases in pain with touch, air movement and stress rather than activity and exercise as reported by those with LBP. These findings are unsurprising given that non-noxious stimuli can be associated with evoked neuropathic pain (Rasmussen et al., 2004). They may explain why those with PHN were less avoidant of activity and why no one in this group reported using pacing during increased pain. The paroxysmal nature of neuropathic pain may explain why some of this population struggle with pacing which aims to reduce pain contingent activity. Pain grabs attention and
interferes with cognitive processes and activity (Eccleston and Crombez, 1999). This grabbing of attention may be more urgent and unexpected in paroxysmal pain giving people no option but to stop activity and for pacing to be interrupted and become pain contingent. The finding that people with LBP were more likely to escape/avoid activity in response to pain fits with the fear-avoidance model (Vlaeyen et al., 2001) and may explain why those with LBP reported significantly greater interference during an increase in pain. This model is the framework for the component of cognitive behavioral pain management that aims to reduce fear of pain and avoidance of activity (de Jong et al., 2005a,b). The model proposes that negative appraisal of internal and external stimuli results in avoidance of activity and detrimental psychological and physical consequences. This study suggests that people with PHN are less likely to escape/avoid activity. We need to ascertain whether this is representative of other neuropathic pain conditions and how applicable the fear-avoidance model is to neuropathic pain. Visiting a greater number of HCPs since pain onset was not necessarily a manifestation of longer pain duration in the LBP group. They also reported significantly more visits in the 3 months preceding the study. It may be associated with their responses to ‘‘What diagnosis, if any, have you been given?” and ‘‘What do you think is happening in your body now to be causing your pain?”. A greater percentage of those with LBP did not state or did not know their diagnosis and were less likely to provide a clear reason for their pain. Not knowing the pain’s etiology is associated with an increased use of medical services in an attempt to have pain validated (Wells et al., 2003). Those with PHN were more likely to use the word ‘damage’, particularly in the context of nerve damage to describe their pain’s current etiology. This may reflect HCPs’ use of ‘damage’ to help people understand neuropathic pain but may conflict with the pain model used in generic PMPs discussed below. Those with PHN were more likely to describe allodynia as a significant problem. This is unsurprising given the characteristics of neuropathic pain. However, being one of the main problems experienced by this group, it has implications for PMPs. 4.1. Clinical implications The finding that people with PHN reported the same level of psychological and physical functioning as people with LBP suggests that cognitive behavioral PMPs may be appropriate for the PHN population. The more detailed findings suggest that some components of cognitive behavioral PMPs may require adaptation to meet their needs. Many of the findings for
H.C. Daniel et al. / European Journal of Pain 12 (2008) 731–741
the LBP group are compatible with the interventions of generic PMPs. Those with LBP were more likely to report that activity/exercise increased their pain and that they responded to pain by escaping/avoiding activity. This suggests that cognitive and pacing interventions aimed at reducing avoidance, increasing activity and reversing the detrimental effects of low activity levels are appropriate for the LBP population. However, people with PHN may experience these interventions as they are currently delivered as being less appropriate for them because they (i) associate increases in pain with touch or air movement rather than activity, (ii) are less likely to avoid activity and (iii) experience paroxysmal pain. We need to ascertain whether the models and interventions as they are currently applied in PMPs are useful and meet the needs of those with neuropathic pain or whether they require adaptation. As observed in this study allodynia can be a significant problem for people with neuropathic pain. Allodynia may not be addressed in PMPs unless identified as a significant problem by clinicians. We need to develop cognitive behavioral interventions that usefully address allodynia in a PMP setting. People with PHN were more likely to use ‘damage’ to describe the current cause of their pain. Some people with nociceptive pain (not due to an ongoing disease process) who attend PMPs believe that their pain continues due to ongoing muscle/tissue damage. They avoid movement for fear of worsening this damage and/or interrupting healing. To help relinquish this belief PMPs offer an alternative explanation of pain that removes the focus from ongoing tissue damage and instead describes central pain mechanisms. The word ‘damage’ is often avoided on generic PMPs. However, given our findings, damage may have a useful meaning for people with neuropathic pain in helping them to understand their pain. For example, a meaning such as permanent yet non-threatening changes in the nerve’s function may be helpful. We need to understand more about the meaning of damage for this population and may need to develop a model of neuropathic pain for use in PMPs that incorporates rather than excludes the concept of damage. There are some limitations with this study. Adopting a significance level of 0.05 may have increased the likelihood of Type 1 errors. A more conservative approach may have been appropriate. The current findings can only be applied to people who attend pain clinics and may not be representative of those who only attend primary care. The low response rate and the significant between group difference in the response rates may indicate selection bias. Recruitment rates may have been improved if researchers were present in the clinics to recruit participants rather than recruiting via letter. There were significant between group differences in
739
age and pain duration. However, age and pain duration correlated with very few other variables which suggests they did not strongly determine these variables or their association with one diagnostic group more than the other. We appreciated from the outset that there may be an age discrepancy. We avoided studying a mixed neuropathic population as its heterogeneity may have led to difficulties defining neuropathic pain. Recruiting a younger population by using neuropathic pain conditions such as HIV and diabetes related pain may have resulted in the co-morbidities of the underlying disease influencing the population. Manipulating either population to reduce the age discrepancy would have introduced selection bias. The results cannot be generalized to pain with a neuropathic basis other than PHN. However, to our knowledge this is the first study to address differences between neuropathic and nociceptive pain and the implications for cognitive behavioral PMPs. It is hoped that future research will elicit whether aspects of cognitive behavioral pain management require adaptation to meet the needs of people with other neuropathic pain conditions (Daniel and Van Der Merwe, 2006). In summary, a nociceptive (LBP) and a neuropathic (PHN) pain population were similar in their reports of pain, cognitions, mood and physical function. Differences existed in the factors that increased pain, responses to and beliefs about pain and the main problems experienced. These differences may indicate that some elements of cognitive behavioral PMPs require adaptation if they are to meet the needs of people with neuropathic pain.
Acknowledgement We would like to thank Amanda Williams, Christopher Eccleston and John Green for their input during the developmental stages of this study and Amanda Williams for her support and valuable comments on earlier versions of this manuscript. This study was funded by grants from The Dunhill Medical Trust and Pfizer Ltd.
Appendix 1. Questions used to elicit information not available in standardised measures. On average, how many hours a day do you spend resting (for example, lying down or sitting) because of your pain? People who have pain often say that the level of their pain changes from day to day. On average, how many days in a month would you say were ‘good’ days?
740
H.C. Daniel et al. / European Journal of Pain 12 (2008) 731–741
On average, how many days in a month would you say were ‘bad’ days? What increases your level of pain? (Please tick all that apply) Activity (e.g. walking, housework) Too much rest Stress Exercise Certain movements (e.g. bending, twisting) Temperature (e.g. heat, cold) Nothing, it just happens
Anger due to pain(0 = Not at all angry, 10 = The most angry I could be) Perceived pain interference on a good day(0 = The pain does not interfere with my life, 10 = The pain completely interferes with my life) Perceived pain interference on a bad day(0 = The pain does not interfere with my life, 10 = The pain completely interferes with my life) Pain relief provided by medication(0 = No relief, 10 = Complete relief) Beliefs that future treatments will be able to reduce pain(0 = I don’t think they will be able to reduce my pain at all, 10 = I think they will take away my pain completely)
Touching the painful area Other(s)_____________________________________
What, if anything, helps to reduce your level of pain? What diagnosis have you been given (if any)? What do you think is happening in your body now to be causing your pain? Since your pain started, who have you seen about your pain? Please tick the relevant boxes. General Practitioner Orthopaedic or Back Surgeon Physiotherapist Neurologist Chiropractor Osteopath Faith Healer Pain Consultant Psychologist / Psychiatrist Other(s)_____________________________________
People often say that their pain causes many problems in their lives. Please list the three main problems that you experience because you have pain. These may be either physical or emotional. In addition to the above, numerical rating scales (0–10) assessed: Pain intensity(0 = No pain, 10 = Pain as bad as I can imagine) Pain distress(0 = Not at all distressed, 10 = As distressed as I can imagine) Pain constancy(0 = Never in pain, 10 = In pain all of the time) Frustration due to pain(0 = Not at all frustrated, 10 = The most frustrated I could be)
References Backonja MM, Stacey B. Neuropathic pain symptoms relative to overall pain rating. J Pain 2004;5:491–7. Bacon NM, Bacon BA, Atkinson JH, Slater MA, Patterson TL, Grant I, et al. Somatization symptoms in chronic low back pain patients. Psychosom Med 1994;56:118–27. Beck AT, Ward CH, Mendelson M, Mock J, Erbaugh J. An inventory for measuring depression. Arch Gen Psychiatry 1961;4:561–71. Beck AT, Steer RA, Garbin M. Psychometric properties of the beck depression inventory: twenty-five years of evaluation. Clin Psychol Rev 1988;8:77–100. Benbow SJ, Wallymahmed ME, Macfairlane IA. Diabetic peripheral neuropathy and quality of life. Quart J Med 1998;91:733–7. Bennett M. The LANSS pain scale: the Leeds assessment of neuropathic symptoms and signs. Pain 2001;92:147–57. Bergner M, Bobbitt RA, Carter WB, Gilson BS. The sickness impact profile: development and final revision of a health status measure. Med Care 1981;19:787–805. Bouhassira D, Attal N, Alchaar H, Boureau F, Brochet B, Bruxelle J, et al. Comparison of pain syndromes associated with nervous or somatic lesions and development of a new neuropathic pain diagnostic questionnaire (DN4). Pain 2005;114: 29–36. Clark MR, Heinberg LJ, Haythornthwaite JA, Quatrano-Piacentini AL, Pappagallo M, Raja SN. Psychiatric symptoms and distress differ between patients with postherpetic neuralgia and peripheral vestibular disease. J Psychosom Res 2000;48:51–7. Daniel HC, Van Der Merwe J. Cognitive behavioural approaches and neuropathic pain. In: Cervero F, Jensen TS, editors. Handbook of clinical neurology. Pain, vol. 18. Edinburgh: Elsevier; 2006. p. 855–68. de Jong JR, Vlaeyen JWS, Onghena P, Cuypers C, den Hollander M, Ruijgrok J. Reduction of pain-related fear in complex regional pain syndrome type: I. The application of graded exposure in vivo. Pain 2005a;116:264–75. de Jong JR, Vlaeyen JWS, Onghena P, Goossens P, Marie¨lle EJB, Geilen M, et al. Fear of movement/(re)injury in chronic low back pain: education or exposure in vivo as mediator to fear reduction? Clin J Pain 2005b;21:9–17. Dworkin RH, Portenoy RK. Pain and its persistence in herpes zoster. Pain 1996;67:241–51. Dworkin RH, Corbin AE, Young Jr JP, Sharma U, La Moreaux L, et al. Pregabalin for the treatment of postherpetic neuralgia: a randomized, placebo-controlled trial. Neurology 2003;60:1274–83. Eccleston C, Crombez G. Pain demands attention: a cognitive-affective model of the interruptive function of pain. Psychol Bull 1999;125: 356–66.
H.C. Daniel et al. / European Journal of Pain 12 (2008) 731–741 Evans S, Weinberg BA, Spielman L, Fishman B. Assessing negative thoughts in response to pain among people with HIV. Pain 2003;105:239–45. Freynhagen R, Baron R, Gockel U, Tolle TR. painDETECT: a new screening questionnaire to identify neuropathic components in patients with back pain. Curr Med Res Opin 2006;22:1911–20. Galer BS, Gianas A, Jensen MP. Painful diabetic polyneuropathy: epidemiology, pain description and quality of life. Diabetes Res Clin Pract 2000a;47:123–8. Galer BS, Henderson J, Perander J, Jensen MP. Course of symptoms and quality of life measurement in complex regional pain syndrome: a pilot study. J Pain Symptom Manage 2000b;20: 286–92. Haythornthwaite JA, Benrud-Larson LM. Psychological aspects of neuropathic pain. Clin J Pain 2000;16:1–5. Haythornthwaite JA, Benrud-Larson LM. Psychological assessment and treatment of patients with neuropathic pain. Curr Pain Headache Rep 2001;5:124–9. Haythornthwaite JA, Clark MR, Pappagallo M, Raja SN. Pain coping strategies play a role in the persistence of pain in post-herpetic neuralgia. Pain 2003;106:453–60. Hempenstall K, Nurmikko TJ, Johnson RW, A’Hern R, Rice ASCR. Analgesic therapy in postherpetic neuralgia: a quantitative systematic review. PLoS medicine 2005;2:628–44. Jensen MP, Strom SE, Turner JA, Romano JM. Validity of the Sickness Impact Profile Roland Scale as a measure of dysfunction in chronic pain patients. Pain 1992;50:157–62. Jensen MP, Ehde DM, Hoffman A, Paterson DR. Cognitions, coping and social environment predict adjustment to phantom limb pain. Pain 2002;95:133–42. Lame´ IE, Peters ML, Vlaeyen JWS, Kleef MV, Patijn J. Quality of life in chronic pain is more associated with beliefs about pain, than with pain intensity. Eur J Pain 2005;9:15–24. McCracken LM, Zayfert C, Gross RT. The Pain Anxiety Symptoms Scale: development and validation of a scale to measure fear of pain. Pain 1992;50:67–73. McCracken LM, Gross RT, Hexum CL, Semenchuck EM. Factor structure and temporal stability of the pain anxiety symptom scale. Paper presented at the annual convention for the society of behavioral medicine, San Francisco, 1993.
741
McCracken LM, Vowles KE, Eccleston C. Acceptance of chronic pain: component analysis and a revised assessment method. Pain 2004;107:159–66. Meyer-Rosberg K, Burckhardt CS, Huizar K, Kvarnstroem A, Nordfors L, Kristofferson A. A comparison of the SF-36 and Nottingham health profile in patients with chronic neuropathic pain. Eur J Pain 2001;5:391–403. Morley S, Eccleston C, Williams A. Systematic review and metaanalysis of randomized controlled trials of cognitive behaviour therapy and behaviour therapy for chronic pain in adults, excluding headache. Pain 1999;80:1–13. Morley S, Williams AC, de C, Black S. A confirmatory factor analysis of the beck depression inventory in chronic pain. Pain 2002;99: 289–98. Neuendorf KA. The content analysis guidebook. London: SAGE Publications Ltd.; 2002. Pincus T, Williams A. Models and measurements of depression in chronic pain. J Psychosom Res 1999;47:211–9. Pincus T, Vogel S, Williams A, de C, Field A. The development and testing of the depression, anxiety, and positive outlook scale (DAPOS). Pain 2004;109:181–8. Rasmussen PV, Sindrup SH, Jensen TS, Bach FW. Symptoms and signs in patients with suspected neuropathic pain. Pain 2004;110:461–9. Rice ASC, Maton S. Gabapentin in postherpetic neuralgia; a randomised, double-blind, controlled study. Pain 2001;94:215–24. Schmader KE. Epidemiology and impact on quality of life of postherpetic neuralgia and painful diabetic neuropathy. Clin J Pain 2002;18:350–4. 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;17:52–64. Tabachnick BG, Fidell LS. Using multivariate statistics. 4th ed. Boston: Allyn and Bacon; 2001, p. 71. Vlaeyen JWS, de Jong J, Geilen M, Heuts PHTG, van Breukelen G. Graded exposure in vivo in the treatment of pain-related fear: a replicated single-case experimental design in four patients with chronic low back pain. Behav Res Ther 2001;39:151–66. Wells HJ, Pincus T, McWilliams E. Information processing biases among chronic pain patients and ankylosing spondylitis patients: the impact of diagnosis. Eur J Pain 2003;7:105–11.
European Journal of Pain 12 (2008) 731–741 www.EuropeanJournalPain.com
Comparison of psychological and physical function in neuropathic pain and nociceptive pain: Implications for cognitive behavioral pain management programs H. Clare Daniel a,b,*, Jane Narewska a, Michael Serpell c, Barbara Hoggart d, Robert Johnson e, Andrew S.C. Rice a b
a Pain Research Group, Department of Anaesthetics, Pain Medicine and Intensive Care, Faculty of Medicine, Imperial College London, UK Pain Management Centre, The National Hospital for Neurology and Neurosurgery, University College London Hospitals NHS Foundation Trust, Queen Square, London WC1N 3BG, UK c University Department of Anaesthesia, Glasgow University, Gartnavel General Hospital, UK d Birmingham Heartlands and Solihull NHS Trust, UK e United Bristol Hospitals and University of Bristol, UK
Received 11 June 2007; received in revised form 29 October 2007; accepted 9 November 2007 Available online 27 December 2007
Abstract Research has increased our understanding of the psychological and physical functioning associated with persistent pain and has facilitated the development of cognitive behavioral pain management programs to help improve people’s physical function and decrease their distress in the presence of persistent pain. The majority of this research has focused on nociceptive pain or pain of mixed etiology. There has been less focus on these aspects of neuropathic pain. It is possible that differences exist in the function and difficulties associated with nociceptive and neuropathic pain. These differences may be associated with our clinical observation that some people with neuropathic pain have difficulty applying some aspects of the theory and practice of cognitive behavioral pain management. The purpose of this study was to compare a single neuropathic pain condition (post-herpetic neuralgia) with a persistent pain of nociceptive origin (low back pain) and determine whether differences exist in: (1) physical and psychological function; (2) factors that increase difficulties; (3) responses to pain; (4) beliefs about pain and (5) problems experienced. The results suggest that the differences between the two groups were not on the major variables of pain, mood, cognition and physical function. The main differences were in factors that increase pain, people’s responses to pain, their beliefs about diagnosis and the cause of pain and the problems they reported as a result of experiencing pain. The implications of our findings for the development of cognitive behavioral pain management programs for people with neuropathic pain are discussed. Ó 2007 European Federation of Chapters of the International Association for the Study of Pain. Published by Elsevier Ltd. All rights reserved. Keywords: Neuropathic pain; Cognitive-behavioral pain management; Function; Impact
1. Introduction *
Corresponding author. Address: Pain Management Centre, The National Hospital for Neurology and Neurosurgery, University College London Hospitals NHS Foundation Trust, Queen Square, London WC1N 3BG, UK. Tel.: +44 845 155 5000x723487; fax: +44 20 7419 1714. E-mail address: [email protected] (H.C. Daniel).
Whilst it is possible to define both neuropathic and nociceptive pain and to identify distinctive features of each condition, this is generally done by reference to the etiology of the medical condition underlying the pain or features of the pain itself. There is a large literature
1090-3801/$34 Ó 2007 European Federation of Chapters of the International Association for the Study of Pain. Published by Elsevier Ltd. All rights reserved. doi:10.1016/j.ejpain.2007.11.006
732
H.C. Daniel et al. / European Journal of Pain 12 (2008) 731–741
regarding interference on psychological and physical functioning in respect of nociceptive pain. With a few exceptions (for example, Clark et al., 2000; Haythornthwaite and Benrud-Larson, 2000, 2001) less attention has been paid to these aspects of neuropathic pain. More specifically there is little evidence on whether differences in functioning and responses to pain exist between people with neuropathic and nociceptive pain. The differences in pain characteristics that exist between neuropathic and other persistent pain states, for example the spontaneous pain associated with neuropathic pain, are well recognized and included in questionnaires (Bennett, 2001; Backonja and Stacey, 2004; Bouhassira et al., 2005). There has been less focus on the contribution these differences make to functioning and responses to pain. It is recognized that the changes in physical and psychological functioning associated with persistent pain are influenced by psychosocial variables, for example, beliefs (Lame´ et al., 2005), psychological processes (Sullivan et al., 2001) and emotions (Vlaeyen et al., 2001). Research on psychosocial variables and pain has tended to focus on nociceptive pain or pain of mixed etiology although some evidence suggests that the findings apply to neuropathic pain (Jensen et al., 2002; Evans et al., 2003; Haythornthwaite et al., 2003). Cognitive behavioral pain management programs (PMPs) aim to improve psychological and physical function and reduce reliance on healthcare by changing responses to persistent pain (Morley et al., 1999). The majority of patients in a generic PMP have nociceptive pain or pain of mixed etiology. A few have only neuropathic pain. Clinical experience within this context suggests that some people with neuropathic pain distinguish their pain and problems from the mainstream and report differences in functioning and management of their pain. These same people report difficulties when applying some of the theories and principles of cognitive behavioral pain management, particularly activity pacing. It is possible that some components of generic PMPs do not match the difficulties experienced by some people with neuropathic pain. These interventions may require adaptation, however, this has been the focus of little research. We were unable to locate any published direct comparisons of physical and psychological functioning of people with neuropathic and nociceptive pain. In the context of a between group comparison we aimed to determine whether population differences exist when a single neuropathic pain condition (post-herpetic neuralgia) was compared with a persistent pain of nociceptive origin (biomechanical low back pain without radicular symptoms). Although we hypothesised that the two groups experience similar levels of psychological and physical functioning, we predicted that people with neuropathic pain would report: (1) a smaller association
between physical activity and pain increases; (2) different responses to their pain, notably less activity avoidance and less use of pacing; (3) different causal beliefs and (4) significant problems not addressed by generic PMPs.
2. Methods 2.1. Participants Participants aged 18 years or older were recruited from five pain management clinics (one in Scotland and four in England). They were experiencing either biomechanical low back pain (LBP) or post-herpetic neuralgia (PHN). It is recognized that difficulties can exist with the concept of LBP being solely due to nociceptive pain (Freynhagen et al., 2006). Inclusion and exclusion criteria were used to ensure as much as possible that the pain was not confounded by other types of pain, illnesses or conditions. To ensure the pain was persistent, those recruited with LBP had to have experienced pain for 6 months or longer and have a clinical diagnosis of persistent low back pain. They were excluded if they had experienced pain radiating down the leg below the knee within the last three months or had a systemic inflammatory disorder or other disorders that resulted in pain. Those with neuropathic pain had experienced PHN for more than 6 months after healing of the herpes zoster skin rash. Their diagnosis was confirmed by their physician. Those who had undergone neurolytic or neurosurgical therapy for PHN or experienced moderate to severe pain not attributable to their PHN were excluded. Following ethical committee approval (Glasgow West Local Research Ethics Committee, National Hospital for Neurology and Neurosurgery and Institute of Neurology Local Research Ethics Committee, Riverside Research Ethics Committee, Solihull Local Research Ethics Committee, and Central and South Bristol Research Ethics Committee) the personal details of 298 people who experienced either LBP (n = 190) or PHN (n = 108) were provided by consultants in pain management in the five pain clinics. These 298 people were mailed an information sheet and a letter inviting them to take part in the study. Seven days later this letter was followed by a telephone call to each person to answer any questions and ascertain if they wished to participate in the study. Those who gave verbal agreement were posted the questionnaires, a consent form and a stamped addressed envelope. A time was agreed for the researcher to telephone the participants to ensure all the questionnaires had been completed and any queries addressed. During this second telephone call the researcher attempted to answer the participants’ queries without influencing their choice of answers in the questionnaires. Participants were asked to return the questionnaires and consent form in the stamped addressed envelope.
H.C. Daniel et al. / European Journal of Pain 12 (2008) 731–741
2.2. Measures 2.2.1. The Sickness Impact Profile (SIP) (Bergner et al., 1981) The SIP is a subjective behavioral measure of health status that addresses physical and psychosocial behavior. It consists of 136 items, forming 12 subscales and has been validated on persistent pain populations (Jensen et al., 1992; Bacon et al., 1994). The higher the score, the greater the impact of the pain on physical and psychosocial behavior. 2.2.2. The Beck Depression Inventory (BDI) (Beck et al., 1961) The BDI assesses symptoms of depression. It is a 21 item, self-report questionnaire. Each item is rated on a 0–3 scale. A higher score indicates a greater number of symptoms of depression. The psychometric properties of the BDI are well established in psychiatric populations (Beck et al., 1988) but are disputed in the persistent pain population (Pincus and Williams, 1999; Morley et al., 2002; Pincus et al., 2004). Due to difficulties using this measure with persistent pain populations and to ensure that the confounding somatic items were not included in the analyses, the results of the BDI were analysed using the self-blame subscale identified by Morley et al. (2002) rather than the total score. 2.2.3. The Pain Anxiety Symptoms Scale (PASS) (McCracken et al., 1992) The PASS comprises of 40 self-report items of fear and anxiety behaviors related to pain. It contains four subscales; cognitive anxiety symptoms, escape and avoidance responses, fearful appraisals of pain and physiological anxiety symptoms related to pain. Participants make a frequency rating for each item on a scale from 0 (never) to 5 (always). The greater the score the more frequent the behaviors. The PASS has been validated for use on persistent pain populations. The alpha coefficients have been shown to be 0.94 for the total scale and range from 0.81 to 0.89 for the subscales (McCracken et al., 1992). Adequate test-retest reliability has been demonstrated (McCracken et al., 1993). 2.2.4. The Chronic Pain Acceptance Questionnaire (CPAQ) (Geisser, unpublished doctoral dissertation 1992; McCracken et al., 2004) The CPAQ quantifies the degree to which respondents are living a normal life despite pain. It comprises 20 self-report items forming two subscales; activity engagement (pursuit of life activities despite pain) and pain willingness (the degree to which people have experiences of pain without trying to avoid or control them and the recognition that avoidance and control can be unhelpful methods of responding to persistent pain). Items are rated on a 0 (never true) to 6 (always true)
733
scale. The higher the score the more participants are living a normal life despite pain. The internal consistency of the total score is Cronbach’s a = 0.78 and for the two subscales; 0.78 (pain willingness); 0.82 (activity engagement) (McCracken et al., 2004). 2.2.5. Personal and medical information A questionnaire was developed and piloted to address concepts discussed in the pain literature but for which there are no available standardised measures. In addition to personal demographics (Table 1) this questionnaire included the questions shown in Appendix 1. 2.3. Statistical analysis Data which were not normally distributed were identified by their skewness and kurtosis values, transformed into their square roots and treated as parametric data. Those that could not be transformed were treated as non-parametric data. Means and standard deviations are reported for parametric continuous data and medians and quartiles are reported for non-parametric continuous data. Outliers were determined by box plots and reduced to the next largest value in the data set for that variable (Tabachnick and Fidell, 2001). Between group comparisons of parametric continuous data were analysed using two tailed t-tests. Nonparametric continuous data were analysed using the Mann–Whitney U test. Chi-square tests were used for categorical data. Low back pain and post-herpetic neuralgia were entered as the dichotomous outcome variables in logistic regression to determine which variables were more likely to be associated with one of the two pain groups. A significance level of p < 0.05 was used throughout the study. Significant values are shown in bold. The statistical software used was SPSS for Windows (version 11.5). Content analysis was used to analyse responses to the qualitative questions. This involved categorizing and counting the presence of certain words or concepts to enable inferences to be made from the participants’ responses (Neuendorf, 2002). As we were interested in causal beliefs, responses to the question, ‘‘What diagnosis (if any) have you been given” were sorted into two categories; (i) diagnosis stated or (ii) no diagnosis stated/do not know diagnosis. Responses to the question ‘‘What do you think is happening in your body now to be causing your pain?” were analysed in two independent ways. First, they were categorized according to whether participants (i) gave a clear reason for their pain (e.g. ‘‘nerve damage due to shingles”), (ii) gave an ambiguous reason (e.g. ‘‘I’m not sure, maybe something’s not in the right place in my back”) or (iii) stated that they did not know. Second, the number of participants who used the word ‘damage’ were counted. Responses to the question
734
H.C. Daniel et al. / European Journal of Pain 12 (2008) 731–741
Table 1 Personal data for whole group and comparisons between LBP and PHN groups Whole group (n = 106)
LBP (n = 57)
PHN (n = 49)
t (df) or v2 (df)
Age (years) mean (s.d.)
61.55 (16.42)
53.32 (16.12)
71.12 (10.63)
t=
Gender n (%) Men Women
41 (38.7) 65 (61.3)
19 (33.3) 38 (66.7)
22 (44.9) 27 (55.1)
v2 = 1.49 (1)
0.24
Ethnicity n (%) White Other Missing
98 (92.5) 6 (5.7) 2(1.9)
52 (91.2) 3 (5.3) 2 (3.5)
46 (93.9) 3 (6.1) 0
v2 = 0.02 (1)
1.00
Relationship status n (%) Has a partner No partner Missing
65 (61.3) 39 (36.8) 2 (1.9)
36 (63.2) 20 (35.1) 1 (1.8)
29 (59.2) 19 (38.8) 1 (2.0)
v2 = 0.17 (1)
0.69
Living situation n (%) With someone Alone
77 (72.6) 29 (27.4)
43 (75.4) 14 (24.6)
34 (69.4) 15 (30.6)
v2 = 0.49 (1)
0.52
Employment status n(%) Working/studying Not working (due to pain) Not working (not due to pain) Other
34 (32.1) 13 (12.3) 52 (49.1) 7 (6.6)
30 (52.6) 7 (12.3) 17 (29.8) 3 (5.3)
4 (8.2) 6 (12.2) 35 (71.4) 4 (8.2)
v2 = 25.88 (3)
< 0.001a
Educational qualifications n (%) Up to secondary education Beyond secondary education Missing
59 (55.7) 43 (40.6) 4 (3.8)
29 (50.9) 26 (45.6) 2 (3.5)
30 (61.2) 17 (34.7) 2 (4.1)
v2 = 1.28 (1)
0.32
a
6.60 (104)
p-Value <0.001a
p 6 0.001.
‘‘People often say that pain causes many problems in their lives. These can either be physical or emotional. Please list what you believe are the three main problems that you experience because you have pain”, were also analysed in two independent ways. First, a count was made of the number of physical and emotional difficulties each participant stated. Second, a count was made of how many participants cited a problem that described allodynia (defined as pain experienced due to stimulus that does not normally provoke pain) as being one of the main problems experienced as this can be neglected in some generic PMPs. The first author and a qualified nurse manually coded the data. All categories were exhaustive and mutually exclusive. Kappa statistics were generated to assess inter-coder reliability.
3. Results The CONSORT diagram in Fig. 1 shows the numbers of people who were invited to participate, who responded, who were excluded or self-excluded and the final number of participants included in the study. A test of difference of proportions ( 0.154, 95% CI) revealed a difference in the response rates of the two groups. A significantly greater percentage of those with PHN (45%) returned usable data compared with those with LBP (30%). Data are not available to enable com-
parison between those who did and did not take part in the study. 3.1. Personal and pain data As expected, the PHN group were significantly older than those with LBP and those with LBP were more likely to be in paid employment. There were no significant between group differences in the other personal data (Table 1). The PHN group reported their main site of pain as being in the thorax (51%), head (26.5%), shoulder (12.2%), legs (8.2%) or upper limbs (2%). Table 2 summarises the pain data for the group as a whole and for the LBP and PHN groups. Those with LBP had experienced pain for a significantly longer period of time. There were no significant between group differences regarding pain intensity, pain distress, pain constancy and the number of reported good and bad days in a month. 3.2. Psychological and physical functioning Escape and avoidance responses were used significantly more frequently by the LBP group. The cognitive or mood variables did not distinguish the two groups (Table 3). Regarding interference due to pain, the only significant between group difference was that those with LBP
H.C. Daniel et al. / European Journal of Pain 12 (2008) 731–741
735
Invitation sent to 298 people
LBP (n=190)
PHN (n=108) PHN
LBP
26 could not be contacted
49 could not be contacted st
1 telephone call (7 days after letter posted)
39 did not wish to participate
20 did not wish to participate 3 met exclusion criteria
20 met exclusion criteria 59 with PHN agreed to participate
82 with LBP agreed to participate
Questionnaires sent
nd
2 telephone call (7 days after questionnaires posted)
PHN 1 participant withdrew
LBP 23 did not return questionnaires
59 with LBP returned questionnaires
52 with PHN returned questionnaires
PHN 6 did not return questionnaires
LBP 2 questionnaires were incomplete and excluded
57 with LBP (30% of those invited to take part) returned usable data
49 with PHN (45% of those invited to take part) returned usable data
PHN 3 questionnaires were incomplete and excluded
Fig. 1. CONSORT diagram outlining the recruitment process and numbers of people included and excluded. Table 2 Pain data for whole group and comparisons between LBP and PHN groups
Pain duration (months) Pain intensity (NRS 0–10) Pain distress (NRS 0–10) Pain constancy (NRS 0–10) Number of good days/month Number of bad days/month a
Whole group (n = 106) median [quartiles]
LBP (n = 57) median [quartiles]
PHN (n = 49) median [quartiles]
U (z)
69 [36; 144] 7 [4; 8] 5 [3; 8] 8 [5; 10] 5 [2; 10] 20 [10; 26.25]
97 [36; 180] 6 [4; 8] 5 [3; 7] 8 [5; 10] 5 [1; 12] 20 [10; 25]
58 [33.5; 98.5] 7 [5; 8] 6 [2.5; 8] 8 [4.5; 10] 5 [2; 10] 18 [10; 28]
1068.50 1190.50 1276.50 1375.50 1370.50 1355.50
p-Value ( ( ( ( ( (
2.08) 1.32) 0.76) 0.14) 0.17) 0.26)
0.04a 0.19 0.45 0.89 0.87 0.79
p 6 0.05.
reported significantly greater interference due to pain on a bad day (Table 4). The median time spent resting every day for the group as a whole was 2.5 h. There were no significant between group differences (LBP median 2.75 h; PHN median 2.0 h).
3.3. Factors that increase pain Pain type was entered as the outcome variable in a logistic regression analysis. Due to significant between group differences in age and duration of pain these were entered as predictor variables in addition to the factors
736
H.C. Daniel et al. / European Journal of Pain 12 (2008) 731–741
Table 3 Cognitive and mood data for whole group and comparisons between LBP and PHN groups
Frustration (NRS 0–10) median [quartiles] Anger (NRS 0–10) median [quartiles] Symptoms of depression (self-blame BDI) median [quartiles] Fearful appraisals of pain (PASS subscale) mean (s.d.) Physiological anxiety symptoms (PASS subscale) median [quartiles] Cognitive anxiety symptoms (PASS subscale) median [quartiles] Escape and avoidance responses (PASS subscale) mean (s.d.) Pain willingness (CPAQ subscale) mean (s.d.) Activity engagement (CPAQ subscale) mean (s.d.) Belief that future treatments will reduce pain (NRS 0–10) a
Whole group (n = 106)
LBP (n = 57)
PHN (n = 49)
U (z) or t (df)
p-Value
8 [5.75; 10] 5 [2; 8] 1 [0; 3]
8 [6.5; 10] 6 [2; 8] 1 [0; 4.50]
8 [4.5; 10] 5 [2.5;9] 1 [0; 3.00]
U = 1323.0 z = 0.48 U = 1384.50 z = 0.077 U = 1256.0 z = 0.915
0.63 0.94 0.36
14.33 (9.76)
15.26 (10.34)
13.24 (9.02)
t = 1.06 df 104
0.35
7.5 [2.75; 15.25]
9 [3; 16]
5 [2.0; 14.0]
U = 1222.0 z =
21 [12.75; 31.25]
22 [14; 34]
19 [10; 28.50]
U = 1121.50 z =
21.06 (10.14)
23.00 (9.35)
18.80 (10.64)
t = 2.17 df 104
0.03a
24.07 (10.97) 38.86 (12.65) 4 [1; 6]
23.74 (10.15) 38.40 (11.28) 5 [3; 6]
24.45 (11.94) 39.39 (14.17) 4 [0.5; 6.5]
t = 0.33 df 104 t = 0.40 df 104 U = 1103.00 z = 1.87
0.74 0.69 0.06
1.11 1.74
0.27 0.81
p 6 0.05.
Table 4 Interference due to pain: data for whole group and comparisons between LBP and PHN groups
Interference on a good day (NRS 0–10) Interference on a bad day (NRS 0–10) Psychosocial interference (SIP subscale) Physical interference (SIP subscale) a
Whole group median [quartiles]
LBP median [quartiles]
PHN median [quartiles]
U (z)
p-Value
4 [2; 8] 8 [5; 10] 11.99 [6.13; 28.25] 7.86 [1.82; 18.95]
4 [2; 8.50] 8 [6; 10] 15.70 [8.07; 30.71] 8.02 [2.34; 22.32]
5 [2; 7.5] 7 [4; 9] 10.31 [3.58; 21.51] 6.65 [0.84; 17.34]
1387.50 ( 0.06) 1002.0 ( 2.54) 1127.50 ( 1.71) 1234.0 ( 1.03)
0.95 0.01a 0.09 0.30
p 6 0.01.
reported to increase pain (Table 5). Pain being increased by touch or air movement and stress were predictive of PHN group membership. Pain being increased by activity and exercise or keeping still and resting were significantly less likely to be associated with PHN.
Table 5 Logistic regression model with pain type as the outcome variable and factors increasing pain as the predictor variables (n = 106) Variable
Odds ratio
p-Value
95% confidence interval Lower
Upper
3.4. Responses to pain
Age Duration
1.099 0.995
<0.001a 0.165
1.046 0.988
1.156 1.002
Table 6 summarises the participants’ responses to ‘‘What, if anything, helps to reduce your level of pain?”. Nobody with PHN reported finding pacing, osteopathy, TENs and medical interventions helpful. Nobody with LBP reported finding physiotherapy, removing anything that touches the painful area or applying pressure/touch or scratching the painful area helpful. Those with LBP had visited a significantly greater number of different types of health care providers (HCPs) since the pain started (LBP median 5 [quartiles 3.5; 6], PHN median 3 [quartiles 2; 4], U = 498.5, z = 5.78, p < 0.001) and attended a significantly greater number of appointments in the 3 months prior to participating in the study (LBP median 2 [quartiles 0.5; 4.5], PHN median 1 [quartiles 0.0; 3], U = 1076.5, z = 2.07, p = 0.038). The LBP group were significantly more likely to report that medical interventions helped
Factors increasing pain Exercise/activity Rest/keeping still Stress Touch/air movement Temperature
0.211 0.142 5.784 6.448 0.792
0.042c 0.022c 0.034c 0.003b 0.736
0.047 0.027 1.138 1.870 0.205
0.946 0.759 29.392 22.238 03.067
a b c
p 6 0.001. p 6 0.01. p 6 0.05.
to reduce their pain (v2(1, n = 106) = 6.44, p = 0.014). There were no significant between group differences regarding the number of participants having attended psychological or psychiatric appointments (v2(1, n = 106) = 1.17, p = 0.40) or appointments for complementary therapies (for example faith healing and Reiki) (v2(1, n = 106) = 0.03, p = 1.0).
H.C. Daniel et al. / European Journal of Pain 12 (2008) 731–741 Table 6 Numbers (%) of participants who reported finding treatments/behaviors helpful in reducing their pain v2
Factors that help to reduce pain
LBP n (%)
PHN n (%)
Medication Resting Stretch/yoga/pilates Medical interventions Warm Nothing Pacing/not doing things for too long Cool Osteopathy Breathing Distraction TENs Alcohol Pressure/touch/scratch Removing touch Physiotherapy
26 (45.6) 18 (31.6) 16 (28.1) 7 (12.3)
21 (42.9) 13 (26.5) 3 (6.1) 0
–a
6 (10.5) 6 (10.5) 6 (10.5)
7 (14.3) 4 (8.2) 0
0.346 –a –a
4 4 3 3 2 1 0 0 0
5 0 7 6 0 1 8 4 2
–a –a –a –a –a –a –a –a –a
(7) (7) (5.3) (5.3) (3.5) (1.8)
(10.2) (14.3) (12.2) (2) (16.3) (8.2) (4.1)
0.081 0.325
df
p-Value
1 1
0.78 0.57
1
0.56
a
a Chi-square not calculated because less than 10% of one or both groups endorsed the item.
Those with LBP were significantly more likely to be taking medication for their pain. Fifty one (89.5%) participants with LBP were taking medication for their pain compared with 37 (75.5%) with PHN (v2(1, n = 106) = 3.86, p = 0.049). There were no significant between group differences in the amount of reported pain relief afforded by medication. Fifteen (29.4%) of the LBP group and 14 (37.8%) of the PHN group who were taking medication reported a pain relief score of 3 or less out of 10 (where 10 = complete relief) (LBP median 5 [quartiles 3; 7], PHN median 5 [quartiles 2; 6.25], U = 856.50, z = 0.94, p = 0.35). Twenty seven (52.9%) participants with LBP reported experiencing medication side effects compared with 13 (35.1%) in the PHN group (v2(1, n = 88) = 2.26, p = 0.14). 3.5. Beliefs Participants’ responses to the question ‘‘What diagnosis (if any) have you been given?” were sorted into two categories; ‘diagnosis stated’ and ‘no diagnosis stated/don’t know diagnosis’. Two participants with LBP did not respond to this question and were categorized as ‘no diagnosis stated’. Ten (17.5%) of those with LBP did not give a diagnosis or stated that they did not know what diagnosis they have been given compared with 2 (4.1%) of those with PHN (v2(1, n = 106) = 4.76, p 6 0.05). Of the 47 (82.5%) of those with LBP who offered a diagnosis, 24 (42.2%) gave one diagnosis and 23 (40.35%) gave two or more diagnoses (j = 0.87). Of the 47 (95.9%) of those with PHN who gave a diagnosis, 45 (95.74%) gave one diagnosis and 2 (4.1%) gave two or more diagnoses (j = 1.00) (v2(1, n = 94) = 24.03, p < 0.0001).
737
Responses to the question ‘‘What do you think is happening in your body now to be causing your pain?” were sorted into three categories: (i) gave a clear reason for their pain (e.g. ‘‘nerve damage due to shingles”), (ii) gave an ambiguous reason (e.g. ‘‘I’m not sure, maybe something’s not in the right place in my back”) or (iii) stated that they did not know (Table 7). All participants responded to this question. There were significant between groups differences (v2(1, n = 106) = 22.93, p < 0.0001). A greater percentage of those in the PHN group provided a clear reason for their pain (j = 0.81) and a greater percentage of those with LBP provided an ambiguous answer or responded that they did not know (j = 0.83). The responses to the same question were also sorted depending or whether the word ‘‘damage” was used. Those with PHN were significantly more likely to use damage to describe the current cause of their pain. Four (7%) participants with LBP used the word damage compared with 17 (34.7%) of those with PHN (v2(1, n = 106) = 12.7, p < 0.001). All those with PHN who used the term damage did so in the context of nerve damage. 3.6. Difficulties experienced Participants were asked the question ‘‘People often say that pain causes many problems in their lives. These can either be physical or emotional. Please list what you believe are the three main problems that you experience because you have pain”. All participants responded to this question. Although the majority stated three problems, two participants with LBP reported 4 main problems, four reported 2, and one reported 1 main problem. Of the PHN group, two reported 2, and one reported 1 main problem. There were no significant between group differences regarding whether participants cited (LBP n = 32 [56.1%]; PHN n = 27 [58.7%]) or did not cite an emotional problem as one of the three main problems they experienced (v2(1, n = 106) = 0.068, p = 0.84). Those with LBP were significantly more likely to cite a physical problem as being one of their main problems (LBP n = 53 [93%]; PHN n = 34 [69.4%], (v2(1, n = 106) = 9.97, p = 0.002)). In the PHN group 32.65 % (n = 16) stated a problem that described allodynia (for Table 7 Categorized answers (n, %) to the question ‘‘What do you think is happening in your body now to be causing your pain?” Answers
LBP n (%)
PHN n (%)
v2
df
p-Value
Clear reason given Ambiguous answer Do not know
26 (45.6) 20 (35.1) 11 (19.3)
44 (89.8) 1 (2.0) 4 (8.2)
22.93
1
<0.0001a
a Data for the ‘ambiguous answer’ and ‘don’t know’ categories have been combined to increase the observed cell frequencies for the chisquare calculation.
738
H.C. Daniel et al. / European Journal of Pain 12 (2008) 731–741
example, ‘‘I no longer go out socially as the feeling of clothes against my skin is so uncomfortable that I don’t enjoy being out”), compared with 0% with LBP (v2(1, n = 106) = 21.92, p 6 0.001).
4. Discussion We compared the experience of people with neuropathic pain, specifically PHN who attend pain clinics with that of people with LBP who attend pain clinics. Differences emerged not in major variables of pain, mood, cognition and physical function but in: (1) factors that increase pain; (2) responses to pain; (3) beliefs about pain and (4) reported problems. These may have implications for cognitive behavioral PMPs for neuropathic pain. Our PHN population was comparable to those recruited in randomised controlled trials of medical therapy (Rice and Maton, 2001; Dworkin et al., 2003). Given that shingles is associated with an older population it is unsurprising that the PHN group were significantly older and less likely to be working (Dworkin and Portenoy, 1996). Despite different etiologies, mechanisms and pain sites, the two groups reported similar pain intensity, constancy, distress and number of good/bad days. The same was found for the majority of the cognitive and mood variables (self-blame, frustration, anger, acceptance, fear appraisals of pain and cognitive and physiological anxiety) and physical and psychosocial interference. These findings support growing evidence that people with neuropathic pain suffer to a similar extent as those with nociceptive pain (Haythornthwaite and Benrud-Larson, 2000) across many life domains (Benbow et al., 1998; Galer et al., 2000a,b; Meyer-Rosberg et al., 2001; Schmader, 2002) and may benefit from cognitive behavioral pain management. This latter point is supported by the finding that 38% of those with PHN who were taking medication gained only 30% or less pain relief and 35% reported side effects. This is despite recent successes in the analgesic pharmacotherapy of PHN (Hempenstall et al., 2005). The PHN group were more likely to associate increases in pain with touch, air movement and stress rather than activity and exercise as reported by those with LBP. These findings are unsurprising given that non-noxious stimuli can be associated with evoked neuropathic pain (Rasmussen et al., 2004). They may explain why those with PHN were less avoidant of activity and why no one in this group reported using pacing during increased pain. The paroxysmal nature of neuropathic pain may explain why some of this population struggle with pacing which aims to reduce pain contingent activity. Pain grabs attention and
interferes with cognitive processes and activity (Eccleston and Crombez, 1999). This grabbing of attention may be more urgent and unexpected in paroxysmal pain giving people no option but to stop activity and for pacing to be interrupted and become pain contingent. The finding that people with LBP were more likely to escape/avoid activity in response to pain fits with the fear-avoidance model (Vlaeyen et al., 2001) and may explain why those with LBP reported significantly greater interference during an increase in pain. This model is the framework for the component of cognitive behavioral pain management that aims to reduce fear of pain and avoidance of activity (de Jong et al., 2005a,b). The model proposes that negative appraisal of internal and external stimuli results in avoidance of activity and detrimental psychological and physical consequences. This study suggests that people with PHN are less likely to escape/avoid activity. We need to ascertain whether this is representative of other neuropathic pain conditions and how applicable the fear-avoidance model is to neuropathic pain. Visiting a greater number of HCPs since pain onset was not necessarily a manifestation of longer pain duration in the LBP group. They also reported significantly more visits in the 3 months preceding the study. It may be associated with their responses to ‘‘What diagnosis, if any, have you been given?” and ‘‘What do you think is happening in your body now to be causing your pain?”. A greater percentage of those with LBP did not state or did not know their diagnosis and were less likely to provide a clear reason for their pain. Not knowing the pain’s etiology is associated with an increased use of medical services in an attempt to have pain validated (Wells et al., 2003). Those with PHN were more likely to use the word ‘damage’, particularly in the context of nerve damage to describe their pain’s current etiology. This may reflect HCPs’ use of ‘damage’ to help people understand neuropathic pain but may conflict with the pain model used in generic PMPs discussed below. Those with PHN were more likely to describe allodynia as a significant problem. This is unsurprising given the characteristics of neuropathic pain. However, being one of the main problems experienced by this group, it has implications for PMPs. 4.1. Clinical implications The finding that people with PHN reported the same level of psychological and physical functioning as people with LBP suggests that cognitive behavioral PMPs may be appropriate for the PHN population. The more detailed findings suggest that some components of cognitive behavioral PMPs may require adaptation to meet their needs. Many of the findings for
H.C. Daniel et al. / European Journal of Pain 12 (2008) 731–741
the LBP group are compatible with the interventions of generic PMPs. Those with LBP were more likely to report that activity/exercise increased their pain and that they responded to pain by escaping/avoiding activity. This suggests that cognitive and pacing interventions aimed at reducing avoidance, increasing activity and reversing the detrimental effects of low activity levels are appropriate for the LBP population. However, people with PHN may experience these interventions as they are currently delivered as being less appropriate for them because they (i) associate increases in pain with touch or air movement rather than activity, (ii) are less likely to avoid activity and (iii) experience paroxysmal pain. We need to ascertain whether the models and interventions as they are currently applied in PMPs are useful and meet the needs of those with neuropathic pain or whether they require adaptation. As observed in this study allodynia can be a significant problem for people with neuropathic pain. Allodynia may not be addressed in PMPs unless identified as a significant problem by clinicians. We need to develop cognitive behavioral interventions that usefully address allodynia in a PMP setting. People with PHN were more likely to use ‘damage’ to describe the current cause of their pain. Some people with nociceptive pain (not due to an ongoing disease process) who attend PMPs believe that their pain continues due to ongoing muscle/tissue damage. They avoid movement for fear of worsening this damage and/or interrupting healing. To help relinquish this belief PMPs offer an alternative explanation of pain that removes the focus from ongoing tissue damage and instead describes central pain mechanisms. The word ‘damage’ is often avoided on generic PMPs. However, given our findings, damage may have a useful meaning for people with neuropathic pain in helping them to understand their pain. For example, a meaning such as permanent yet non-threatening changes in the nerve’s function may be helpful. We need to understand more about the meaning of damage for this population and may need to develop a model of neuropathic pain for use in PMPs that incorporates rather than excludes the concept of damage. There are some limitations with this study. Adopting a significance level of 0.05 may have increased the likelihood of Type 1 errors. A more conservative approach may have been appropriate. The current findings can only be applied to people who attend pain clinics and may not be representative of those who only attend primary care. The low response rate and the significant between group difference in the response rates may indicate selection bias. Recruitment rates may have been improved if researchers were present in the clinics to recruit participants rather than recruiting via letter. There were significant between group differences in
739
age and pain duration. However, age and pain duration correlated with very few other variables which suggests they did not strongly determine these variables or their association with one diagnostic group more than the other. We appreciated from the outset that there may be an age discrepancy. We avoided studying a mixed neuropathic population as its heterogeneity may have led to difficulties defining neuropathic pain. Recruiting a younger population by using neuropathic pain conditions such as HIV and diabetes related pain may have resulted in the co-morbidities of the underlying disease influencing the population. Manipulating either population to reduce the age discrepancy would have introduced selection bias. The results cannot be generalized to pain with a neuropathic basis other than PHN. However, to our knowledge this is the first study to address differences between neuropathic and nociceptive pain and the implications for cognitive behavioral PMPs. It is hoped that future research will elicit whether aspects of cognitive behavioral pain management require adaptation to meet the needs of people with other neuropathic pain conditions (Daniel and Van Der Merwe, 2006). In summary, a nociceptive (LBP) and a neuropathic (PHN) pain population were similar in their reports of pain, cognitions, mood and physical function. Differences existed in the factors that increased pain, responses to and beliefs about pain and the main problems experienced. These differences may indicate that some elements of cognitive behavioral PMPs require adaptation if they are to meet the needs of people with neuropathic pain.
Acknowledgement We would like to thank Amanda Williams, Christopher Eccleston and John Green for their input during the developmental stages of this study and Amanda Williams for her support and valuable comments on earlier versions of this manuscript. This study was funded by grants from The Dunhill Medical Trust and Pfizer Ltd.
Appendix 1. Questions used to elicit information not available in standardised measures. On average, how many hours a day do you spend resting (for example, lying down or sitting) because of your pain? People who have pain often say that the level of their pain changes from day to day. On average, how many days in a month would you say were ‘good’ days?
740
H.C. Daniel et al. / European Journal of Pain 12 (2008) 731–741
On average, how many days in a month would you say were ‘bad’ days? What increases your level of pain? (Please tick all that apply) Activity (e.g. walking, housework) Too much rest Stress Exercise Certain movements (e.g. bending, twisting) Temperature (e.g. heat, cold) Nothing, it just happens
Anger due to pain(0 = Not at all angry, 10 = The most angry I could be) Perceived pain interference on a good day(0 = The pain does not interfere with my life, 10 = The pain completely interferes with my life) Perceived pain interference on a bad day(0 = The pain does not interfere with my life, 10 = The pain completely interferes with my life) Pain relief provided by medication(0 = No relief, 10 = Complete relief) Beliefs that future treatments will be able to reduce pain(0 = I don’t think they will be able to reduce my pain at all, 10 = I think they will take away my pain completely)
Touching the painful area Other(s)_____________________________________
What, if anything, helps to reduce your level of pain? What diagnosis have you been given (if any)? What do you think is happening in your body now to be causing your pain? Since your pain started, who have you seen about your pain? Please tick the relevant boxes. General Practitioner Orthopaedic or Back Surgeon Physiotherapist Neurologist Chiropractor Osteopath Faith Healer Pain Consultant Psychologist / Psychiatrist Other(s)_____________________________________
People often say that their pain causes many problems in their lives. Please list the three main problems that you experience because you have pain. These may be either physical or emotional. In addition to the above, numerical rating scales (0–10) assessed: Pain intensity(0 = No pain, 10 = Pain as bad as I can imagine) Pain distress(0 = Not at all distressed, 10 = As distressed as I can imagine) Pain constancy(0 = Never in pain, 10 = In pain all of the time) Frustration due to pain(0 = Not at all frustrated, 10 = The most frustrated I could be)
References Backonja MM, Stacey B. Neuropathic pain symptoms relative to overall pain rating. J Pain 2004;5:491–7. Bacon NM, Bacon BA, Atkinson JH, Slater MA, Patterson TL, Grant I, et al. Somatization symptoms in chronic low back pain patients. Psychosom Med 1994;56:118–27. Beck AT, Ward CH, Mendelson M, Mock J, Erbaugh J. An inventory for measuring depression. Arch Gen Psychiatry 1961;4:561–71. Beck AT, Steer RA, Garbin M. Psychometric properties of the beck depression inventory: twenty-five years of evaluation. Clin Psychol Rev 1988;8:77–100. Benbow SJ, Wallymahmed ME, Macfairlane IA. Diabetic peripheral neuropathy and quality of life. Quart J Med 1998;91:733–7. Bennett M. The LANSS pain scale: the Leeds assessment of neuropathic symptoms and signs. Pain 2001;92:147–57. Bergner M, Bobbitt RA, Carter WB, Gilson BS. The sickness impact profile: development and final revision of a health status measure. Med Care 1981;19:787–805. Bouhassira D, Attal N, Alchaar H, Boureau F, Brochet B, Bruxelle J, et al. Comparison of pain syndromes associated with nervous or somatic lesions and development of a new neuropathic pain diagnostic questionnaire (DN4). Pain 2005;114: 29–36. Clark MR, Heinberg LJ, Haythornthwaite JA, Quatrano-Piacentini AL, Pappagallo M, Raja SN. Psychiatric symptoms and distress differ between patients with postherpetic neuralgia and peripheral vestibular disease. J Psychosom Res 2000;48:51–7. Daniel HC, Van Der Merwe J. Cognitive behavioural approaches and neuropathic pain. In: Cervero F, Jensen TS, editors. Handbook of clinical neurology. Pain, vol. 18. Edinburgh: Elsevier; 2006. p. 855–68. de Jong JR, Vlaeyen JWS, Onghena P, Cuypers C, den Hollander M, Ruijgrok J. Reduction of pain-related fear in complex regional pain syndrome type: I. The application of graded exposure in vivo. Pain 2005a;116:264–75. de Jong JR, Vlaeyen JWS, Onghena P, Goossens P, Marie¨lle EJB, Geilen M, et al. Fear of movement/(re)injury in chronic low back pain: education or exposure in vivo as mediator to fear reduction? Clin J Pain 2005b;21:9–17. Dworkin RH, Portenoy RK. Pain and its persistence in herpes zoster. Pain 1996;67:241–51. Dworkin RH, Corbin AE, Young Jr JP, Sharma U, La Moreaux L, et al. Pregabalin for the treatment of postherpetic neuralgia: a randomized, placebo-controlled trial. Neurology 2003;60:1274–83. Eccleston C, Crombez G. Pain demands attention: a cognitive-affective model of the interruptive function of pain. Psychol Bull 1999;125: 356–66.
H.C. Daniel et al. / European Journal of Pain 12 (2008) 731–741 Evans S, Weinberg BA, Spielman L, Fishman B. Assessing negative thoughts in response to pain among people with HIV. Pain 2003;105:239–45. Freynhagen R, Baron R, Gockel U, Tolle TR. painDETECT: a new screening questionnaire to identify neuropathic components in patients with back pain. Curr Med Res Opin 2006;22:1911–20. Galer BS, Gianas A, Jensen MP. Painful diabetic polyneuropathy: epidemiology, pain description and quality of life. Diabetes Res Clin Pract 2000a;47:123–8. Galer BS, Henderson J, Perander J, Jensen MP. Course of symptoms and quality of life measurement in complex regional pain syndrome: a pilot study. J Pain Symptom Manage 2000b;20: 286–92. Haythornthwaite JA, Benrud-Larson LM. Psychological aspects of neuropathic pain. Clin J Pain 2000;16:1–5. Haythornthwaite JA, Benrud-Larson LM. Psychological assessment and treatment of patients with neuropathic pain. Curr Pain Headache Rep 2001;5:124–9. Haythornthwaite JA, Clark MR, Pappagallo M, Raja SN. Pain coping strategies play a role in the persistence of pain in post-herpetic neuralgia. Pain 2003;106:453–60. Hempenstall K, Nurmikko TJ, Johnson RW, A’Hern R, Rice ASCR. Analgesic therapy in postherpetic neuralgia: a quantitative systematic review. PLoS medicine 2005;2:628–44. Jensen MP, Strom SE, Turner JA, Romano JM. Validity of the Sickness Impact Profile Roland Scale as a measure of dysfunction in chronic pain patients. Pain 1992;50:157–62. Jensen MP, Ehde DM, Hoffman A, Paterson DR. Cognitions, coping and social environment predict adjustment to phantom limb pain. Pain 2002;95:133–42. Lame´ IE, Peters ML, Vlaeyen JWS, Kleef MV, Patijn J. Quality of life in chronic pain is more associated with beliefs about pain, than with pain intensity. Eur J Pain 2005;9:15–24. McCracken LM, Zayfert C, Gross RT. The Pain Anxiety Symptoms Scale: development and validation of a scale to measure fear of pain. Pain 1992;50:67–73. McCracken LM, Gross RT, Hexum CL, Semenchuck EM. Factor structure and temporal stability of the pain anxiety symptom scale. Paper presented at the annual convention for the society of behavioral medicine, San Francisco, 1993.
741
McCracken LM, Vowles KE, Eccleston C. Acceptance of chronic pain: component analysis and a revised assessment method. Pain 2004;107:159–66. Meyer-Rosberg K, Burckhardt CS, Huizar K, Kvarnstroem A, Nordfors L, Kristofferson A. A comparison of the SF-36 and Nottingham health profile in patients with chronic neuropathic pain. Eur J Pain 2001;5:391–403. Morley S, Eccleston C, Williams A. Systematic review and metaanalysis of randomized controlled trials of cognitive behaviour therapy and behaviour therapy for chronic pain in adults, excluding headache. Pain 1999;80:1–13. Morley S, Williams AC, de C, Black S. A confirmatory factor analysis of the beck depression inventory in chronic pain. Pain 2002;99: 289–98. Neuendorf KA. The content analysis guidebook. London: SAGE Publications Ltd.; 2002. Pincus T, Williams A. Models and measurements of depression in chronic pain. J Psychosom Res 1999;47:211–9. Pincus T, Vogel S, Williams A, de C, Field A. The development and testing of the depression, anxiety, and positive outlook scale (DAPOS). Pain 2004;109:181–8. Rasmussen PV, Sindrup SH, Jensen TS, Bach FW. Symptoms and signs in patients with suspected neuropathic pain. Pain 2004;110:461–9. Rice ASC, Maton S. Gabapentin in postherpetic neuralgia; a randomised, double-blind, controlled study. Pain 2001;94:215–24. Schmader KE. Epidemiology and impact on quality of life of postherpetic neuralgia and painful diabetic neuropathy. Clin J Pain 2002;18:350–4. 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;17:52–64. Tabachnick BG, Fidell LS. Using multivariate statistics. 4th ed. Boston: Allyn and Bacon; 2001, p. 71. Vlaeyen JWS, de Jong J, Geilen M, Heuts PHTG, van Breukelen G. Graded exposure in vivo in the treatment of pain-related fear: a replicated single-case experimental design in four patients with chronic low back pain. Behav Res Ther 2001;39:151–66. Wells HJ, Pincus T, McWilliams E. Information processing biases among chronic pain patients and ankylosing spondylitis patients: the impact of diagnosis. Eur J Pain 2003;7:105–11.