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Classifying patients with lumbar spinal stenosis using painDETECT: a cross-sectional study

  • Naoto Takahashi1, 2, 3, 4, 5Email author,
  • Osamu Shirado4,
  • Kazuki Kobayashi1, 5,
  • Ryosuke Mashiko1, 5 and
  • Shin-ichi Konno1
BMC Family PracticeBMC series – open, inclusive and trusted201617:90

https://doi.org/10.1186/s12875-016-0486-z

Received: 17 November 2015

Accepted: 13 July 2016

Published: 22 July 2016

Abstract

Background

The pathological mechanisms of lumbar spinal stenosis are unclear. Family doctors in the primary care setting may perform medical examinations of patients with lumbar spinal stenosis. Our aim was to use the painDETECT questionnaire to quantify the pathological mechanisms of low back pain and/or leg pain caused by lumbar spinal stenosis.

Methods

We enrolled 102 patients (37 men, 65 women) who had been newly diagnosed with lumbar spinal stenosis at 2 facilities. The patients’ conditions were evaluated using the painDETECT questionnaire, Numerical Rating Scale, Roland-Morris Disability Questionnaire, Japanese Orthopaedic Association Back Pain Evaluation Questionnaire, and 36-Item Short-Form Health Survey. The pathological mechanisms of low back pain and/or leg pain caused by lumbar spinal stenosis were classified based on results of the painDETECT questionnaire as nociceptive pain, neuropathic pain, or unclear type of pain (mixed pain). Statistical analyses were performed using the Kruskal–Wallis test. A value of p < 0.05 was considered to indicate statistical significance.

Results

The mean age of all patients in this study was 70.3 ± 2 years. The male:female distribution was 37:65 (36.3:63.7 %). In all, 72 (70.6 %) patients had chronic pain (duration of ≥3 months), and 30 (29.4 %) had subacute or acute pain (duration of <3 months). The pain was classified as nociceptive in 59 patients (57.9 %), neuropathic in 18 (17.6 %), and unclear in 25 (24.5 %). The neuropathic pain group had a significantly lower quality of life (p < 0.05) than did the other groups.

Conclusions

Patients with neuropathic back and/or leg pain caused by lumbar spinal stenosis may have lower physical and/or psychological quality of life than patients with such pain caused by other mechanisms.

Keywords

Lumbar spinal stenosis Nociceptive pain Neuropathic pain Cross-sectional study painDETECT questionnaire Numerical rating scale Roland–Morris Disability Questionnaire score Japanese Orthopaedic Association Back Pain Evaluation Questionnaire 36-Item Short-Form Health Survey Primary care

Background

Lumbar spinal stenosis (LSS) is the one of the most commonly encountered orthopedic disorders. Family doctors in the primary care setting may perform medical examinations of patients with LSS. Therefore, an understanding of the pathological mechanisms of LSS may be very helpful for these doctors.

LSS is defined as a reduction in the area of the spinal canal, lateral canal, and/or foramina. Symptoms of LSS may occur as a result of neurovascular mechanisms [13], such as reduced arterial flow in the cauda equina, venous congestion, increased epidural pressure, nerve root infiltration, and direct compression in the central canal and/or lateral recess [4]. Although the characteristic symptom of LSS is neurogenic intermittent claudication (NIC) [5, 6], other symptoms may appear as well, including low back pain (LBP), radicular pain and/or numbness down the leg, and motor weakness in the legs [710]. It is therefore important to analyze the pathological mechanisms of LBP and/or leg pain caused by LSS to alleviate the symptoms.

We considered the pain mechanisms according to a classification that included neuropathic pain, nociceptive pain, and mixed pain [11, 12]. Neuropathic pain is defined by the International Association for the Study of Pain as “pain initiated or caused by a primary lesion or dysfunction of the nervous system” [13]. It may be associated with abnormal sensations called dysesthesia or produced by normally nonpainful stimuli such as allodynia. Nociceptive pain may also be a result of the encoding and processing of harmful stimuli in the nervous system, reflecting the ability of the body to sense potential harm [14]. Because the developmental mechanisms responsible for neuropathic and nociceptive pain differ, treatment plans differ as well. Therefore, the pathological mechanisms of the pain should be precisely identified to arrive at an exact diagnosis of LSS-derived LBP and/or leg pain.

A recent study using the painDETECT questionnaire demonstrated that neuropathic pain was less common in patients with chronic LBP and that patients with neuropathic back and/or leg pain reported significantly more pain, disability, anxiety, depression, and reduced quality of life (QOL) than patients with nociceptive pain [15]. The pathological mechanisms of LSS, however, were unclear. Few studies have used the painDETECT questionnaire to quantify the pathological mechanisms of LSS [16, 17]. The purpose of this study was to quantify the pathological mechanisms of LBP and/or leg pain caused by LSS using the painDETECT questionnaire, and to report quality of life data in patients with LSS. This study may help to fully elucidate the epidemiology of LSS-derived LBP and/or leg pain in the primary care setting.

Methods

The ethics committees of the participating research institutions approved this study. Written informed consent was obtained from all patients prior to their participation.

This cross-sectional multicenter observational study was conducted nationwide at two hospitals with their attending spinal surgeons. The recruitment period was 1.5 years (1 April 2013 to 30 September 2014).

Patients

The study group included 102 consecutive patients (37 men, 65 women) who were newly diagnosed with LSS at two facilities: Aizu Medical Center Fukushima Medical University and the Fukushima Prefectural Minami-Aizu Hospital. Three spinal surgeons diagnosed the patients with LSS based on magnetic resonance imaging (MRI) findings of LSS, subjective symptoms, and neurological findings. All of the patients had subjective symptoms that included leg symptoms, LSS-related neurological findings, and MRI evidence of LSS. An independent radiologist assessed the MRI scans obtained for each patient at the time of diagnosis for evidence of LSS, including central, lateral recess, and foraminal stenosis. The MRI diagnosis of LSS was based on the following findings: (1) blockage of cerebrospinal fluid and/or the disappearance of fatty tissue surrounding the foramen on T1-weighted images in the sagittal view; (2) central stenosis, lateral recess stenosis, and/or foraminal stenosis caused by lumbar disc compression from the front, and/or increased size of the ligamentum flavum, and/or articular factors from the back in the axial view; and/or (3) compression of the nerve root surrounding the foramen in the coronal view. The ankle-brachial pressure index (ABI) was also checked in all patients to distinguish NIC from vascular intermittent claudication (ABI <0.9). The ABI is the systolic pressure at the ankle divided by the systolic pressure at the arm. It has been shown to be a specific and sensitive metric for the diagnosis of peripheral arterial disease [18].

The inclusion criteria for all patients were (1) a diagnosis of lumbar spondylosis, degenerative spondylolisthesis, or degenerative scoliosis with LSS; (2) pain and/or numbness in the lumbar dermatomal distribution; (3) motor or sensory neurological signs (hypoesthesia, hyperesthesia, allodynia, or dysesthesia) in the affected dermatomes; (4) cognitive capability to satisfy our inquiries; and (5) neurogenic NIC due to LSS. The exclusion criteria for all patients were (1) diagnosis of lumbar degenerative disease without LSS; (2) predominantly axial spinal pain; (3) rheumatoid arthritis; (4) known peripheral neuropathy; (5) history of workmen’s compensation or disability issues; (6) chronic depression and use of antidepressant medication; and (7) patients with an ABI of <0.9.

Methods

The painDETECT neuropathic pain screening questionnaire scores [17] were used to identify the three pain subgroups of patients with LBP and/or leg pain caused by LSS: (1) those with nociceptive pain, (2) those with neuropathic pain, and (3) those in whom the type of pain was unclear [15, 19]. We used the Japanese version of the painDETECT neuropathic pain screening questionnaire score [20]. The cut-off values for categorizing the type of pain based on the painDETECT neuropathic pain screening questionnaire scores were as follows: nociceptive pain, 0–12; unclear type of pain (mixed nociceptive and neuropathic pain), 13–18; and neuropathic pain, 19–38. The painDETECT neuropathic pain screening questionnaire is a reliable screening tool with high sensitivity, high specificity, and positive predictive accuracy. These parameters were each 84 % in a palm-top computerized version of the questionnaire and 85, 80, and 83 %, respectively, in a corresponding pencil-and-paper questionnaire [17]. Matsubayashi et al. [20] demonstrated that the Japanese version of the painDETECT neuropathic pain screening questionnaire has good validity and reliability, similar to that found with the original version.

Numerical rating scale (NRS) and Roland-Morris Disability Questionnaire (RDQ) scores [21] were used to compare the severity of subjective symptoms and the QOL associated with LBP at the patient’s first medical examination. The patients used the NRS for self-evaluation of their leg pain and/or numbness. Both the NRS and RDQ scores were evaluated at the time of the first medical examination. We used the Japanese version of the RDQ score [22].

The Japanese Orthopaedic Association Back Pain Evaluation Questionnaire (JOABPEQ) [23, 24] and the 36-Item Short-Form Health Survey (SF-36) [25] were used to compare the severity of subjective symptoms and the QOL associated with LBP and health at the patient’s first medical examination. The JOABPEQ has five subscales, and the SF-36 has eight. For both questionnaires, higher scores indicate better QOL. We used the Japanese version of the SF-36 [26, 27]. The SF-36 uses scores of 0 to 100, but the scores are not based on the norm.

The primary outcome was the type of pain—nociceptive, neuropathic, or unclear (mixed)—in patients with LBP and/or leg pain caused by LSS. At the first medical examination, we compared the patients’ demographic and clinical characteristics; NRS (LBP); NRS (leg pain, leg numbness); and RDQ, JOABPEQ, and SF-36 scores among the three pain groups using the Kruskal–Wallis test. We also compared these outcomes according to the duration of symptoms—i.e., <3 months (acute and/or subacute phase) or ≥3 months (chronic phase) after the onset of LBP and/or leg pain caused by LSS. A p value of <0.05 was considered to indicate statistical significance. The statistical analyses were performed using StatView 5.0 statistical software (SAS Institute, Cary, NC, USA). The statistical power analysis of this study was performed using G*Power 3.1 (Heinrich-Heine-Universität Düsseldorf, Düsseldorf, Germany) [28]. The power analysis utilized an effect size of 0.4, alpha level of 0.05, power (1 − beta error probability) of 0.95, and requirement of three groups. Finally, the total required sample size was calculated as 102.

Ethics

This study was approved by the ethics committees of the two participating research institutions: Aizu Medical Center Fukushima Medical University and Fukushima Prefectural Minami-Aizu Hospital. Informed consent was obtained from all patients.

Results

The mean age of all patients (n = 102) in this study was 70.3 ± 2 years. The male:female distribution was 37:65 (36.3:63.7 %). The NIC was radicular in 68.6 % (n = 70), caudal in 8.8 % (n = 9), and mixed in 22.6 % (n = 23). Spinal stenosis seen by MRI appeared at one level in 41.4 % (n = 42), two levels in 43.1 % (n = 44), and three levels in 11.7 % (n = 12). The causes of LSS were lumbar spondylitis in 55.0 % (n = 56), degenerative spondylolisthesis in 33.3 % (n = 34), and degenerative scoliosis in 11.7 % (n = 12).

The demographic and clinical characteristics of the patients with LBP and/or leg pain caused by LSS for each pain subgroup are shown in Table 1. The demographic and clinical characteristics of the patients with LBP and/or leg pain caused by LSS were similar among the three pain subgroups.
Table 1

Demographic and clinical characteristics at the first medical examination

Characteristic

Nociceptive pain

Type of pain unclear (mixed pain)

Neuropathic pain

p a

Age (years)

71.4 ± 1.36

69.0 ± 2.34

68.3 ± 2.91

0.720

Sex

   

0.572

 Male

18

11

8

 

 Female

41

14

10

 

Duration of pain

   

0.914

3 months

41

17

14

 

 <3 months

18

8

4

 

Affected spinal level

   

0.730

 L3–L4

18

9

3

 

 L4–L5

36

16

15

 

 L5–S1

5

0

0

 

NIC type

   

0.668

 Radicular

41

15

14

 

 Caudal

5

4

0

 

 Mixed

13

6

4

 

Spinal stenosis levels involvedb

   

0.373

 1

28

8

6

 

 2

25

11

8

 

 ≥3

6

6

4

 

Cause of LSS

   

0.672

 Lumbar spondylitis

30

15

11

 

  Degenerative spondylolisthesis

20

8

6

 

 Degenerative scoliosis

9

2

1

 

The demographic and clinical characteristics of the patients with LBP and/or leg pain caused by LSS were similar among the three pain subgroups

LBP low back pain, LSS lumbar spinal stenosis, NIC neurogenic intermittent claudication, LDH lumbar disc degeneration, MRI magnetic resonance imaging

aKruskal–Wallis test

bSeen on MRI

Among all patients with LBP and/or leg pain caused by LSS, 59 (57.9 %) had nociceptive pain, 18 (17.6 %) had neuropathic pain, and 25 (24.5 %) had an unclear type of pain (mixed pain) at their first medical examination (Table 2). In all, 72 (70.6 %) patients had chronic pain (duration of ≥3 months), and 30 (29.4 %) had subacute or acute pain (duration of <3 months). Among the patients whose LBP and/or leg pain caused by LSS had been present for ≥3 months, 41 (56.9 %) had nociceptive pain, 14 (19.5 %) had neuropathic pain, and 17 (23.6 %) had pain of unclear (mixed pain) at their first medical examination (Table 2). Among those whose LBP and/or leg pain caused by LSS had been present for <3 months, 18 (60.0 %) patients had nociceptive pain, 4 (13.3 %) had neuropathic pain, and 8 (26.7 %) had unclear pain (mixed pain) at their first medical examination (Table 2). The populations of the three pain subgroups [nociceptive, neuropathic, and unclear (mixed)] with LBP and/or leg symptoms caused by LSS (regardless of pain duration) were thus similar.
Table 2

painDETECT questionnaire scores at the first medical examination

Origin of pain

Patients, n (%)

Total patients

102 (100)

 Nociceptive pain

59 (57.9)

 Type of pain unclear (mixed pain)

25 (24.5)

 Neuropathic pain

18 (17.6)

Group with pain present ≥3 months

 

 Nociceptive pain

41 (56.9)

 Type of pain unclear (mixed pain)

17 (23.6)

 Neuropathic pain

14 (19.5)

Group with pain present <3 months

 

 Nociceptive pain

18 (60.0)

 Type of pain unclear (mixed pain)

8 (26.7)

 Neuropathic pain

4 (13.3)

LBP low back pain, LSS lumbar spinal stenosis

NRS scores for LBP, leg pain, and leg numbness in patients with LBP and/or leg pain caused by LSS were not significantly different among the three pain groups (Table 3). However, the RDQ score in patients with LBP and/or leg pain caused by LSS was significantly lower in the neuropathic pain group than in the other groups (p < 0.05) (Table 3). In contrast, there were no significant differences among the three pain groups regarding (1) the NRS scores for LBP, leg pain, or leg numbness or (2) the RDQ scores in patients with LBP and/or leg pain caused by LSS that had been present for ≥3 months or <3 months (Table 3).
Table 3

NRS and RDQ scores at the first medical examination

Parameter

Nociceptive pain

Type of pain unclear (mixed pain)

Neuropathic pain

p a

Total patients with pain at first examination

 NRS (low back pain)

4.75 ± 0.433

5.88 ± 0.561

6.39 ± 0.691

0.099

 NRS (leg pain)

5.59 ± 0.397

6.72 ± 0.618

6.39 ± 0.687

0.205

 NRS (leg numbness)

4.88 ± 0.422

5.56 ± 0.651

6.83 ± 0.556

0.101

 RDQ

9.00 ± 0.760

9.52 ± 1.16

6.68 ± 1.57

0.025a

Group with pain present ≥3 months

 NRS (low back pain)

5.27 ± 0.523

6.12 ± 0.587

6.43 ± 0.724

0.462

 NRS (leg pain)

5.61 ± 0.479

6.35 ± 0.722

6.57 ± 0.685

0.566

 NRS (leg numbness)

5.49 ± 0.513

5.82 ± 0.666

6.50 ± 0.618

0.713

 RDQ

9.66 ± 0.952

8.82 ± 1.41

13.7 ± 1.77

0.074

Group with pain present <3 months

 NRS (low back pain)

3.56 ± 0.715

5.38 ± 1.28

6.25 ± 2.06

0.275

 NRS (leg pain)

5.56 ± 0.729

7.50 ± 1.20

5.75 ± 2.18

0.275

 NRS (leg numbness)

3.50 ± 0.643

5.00 ± 1.52

8.00 ± 1.23

0.060

 RDQ

7.50 ± 1.19

11.0 ± 2.09

13.5 ± 3.97

0.125

Data are shown as mean ± standard error

The NRS scores of LBP, leg pain, and leg numbness in patients with LBP and/or leg pain caused by LSS were not significantly different among the three pain groups. However, the RDQ score in patients with LBP and/or leg pain caused by LSS was significantly lower in the neuropathic pain group than in the other groups (p < 0.05)

NRS numerical rating scale, RDQ Roland–Morris Disability Questionnaire

aKruskal–Wallis test

The five JOABPEQ subscales were LBP, lumbar function, walking ability, social life function, and mental health. The eight SF-36 subscales were physical functioning, physical role functioning, bodily pain, general health perceptions, vitality, emotional functioning, social role functioning, and mental health. The subscale scores of both questionnaires for each pain group are shown in Tables 4 and 5. There were statistically significant differences in three JOABPEQ subscales [lumbar function, social life function, and mental health (p < 0.05)] and in two SF-36 subscales [physical function and bodily pain (p < 0.05)] (Tables 4 and 5). In regard to pain duration, for patients whose pain had been present for ≥3 months after the onset of symptoms, there were statistically significant differences in two JOABPEQ subscales [lumbar function and mental health (p < 0.05)], but no statistically significant differences in any of the SF-36 subscales (Tables 4 and 5). For patients whose pain had been present for <3 months after the onset of symptoms, there were no statistically significant differences in any of the JOABPEQ subscales (p < 0.05), but there was a statistically significant difference in one SF-36 subscale [bodily pain (p < 0.05)] (Tables 4 and 5).
Table 4

JOABPEQ score for each pain type at the first medical examination

Parameter

Nociceptive pain

Type of pain unclear (mixed pain)

Neuropathic pain

p a

Total patients with pain at first examination

 Low back pain

50.8 ± 4.21

41.1 ± 7.30

30.9 ± 6.94

0.071

 Lumbar function

66.1 ± 3.66

64.9 ± 5.29

37.0 ± 7.80

0.005a

 Walking ability

44.8 ± 4.06

40.0 ± 4.37

35.3 ± 6.66

0.580

 Social life function

50.6 ± 2.99

36.8 ± 3.45

42.8 ± 5.79

0.015a

 Mental health

49.4 ± 2.47

40.6 ± 3.54

39.8 ± 5.17

0.048a

Group with pain present ≥3 months

 Low back pain

48.1 ± 5.07

41.1 ± 8.23

29.6 ± 8.13

0.188

 Lumbar function

63.6 ± 4.91

65.1 ± 6.87

38.1 ± 8.56

0.033a

 Walking ability

42.6 ± 5.04

39.5 ± 6.00

36.7 ± 7.06

0.881

 Social life function

49.5 ± 3.91

35.5 ± 4.30

44.1 ± 6.79

0.064

 Mental health

52.5 ± 2.81

41.1 ± 4.42

40.7 ± 5.60

0.032a

Group with pain present <3 months

 Low back pain

57.2 ± 7.55

41.0 ± 15.6

35.8 ± 14.8

0.373

 Lumbar function

71.8 ± 4.24

64.5 ± 8.42

33.3 ± 20.8

0.172

 Walking ability

49.7 ± 6.80

41.3 ± 5.41

30.5 ± 19.1

0.530

 Social life function

53.2 ± 4.17

39.5 ± 6.04

38.5 ± 12.2

0.204

 Mental health

42.2 ± 4.62

39.8 ± 6.26

36.5 ± 14.2

0.869

Data are shown as mean ± standard error

The JOABPEQ comprises five subscales. Higher scores indicate better quality of life

There were statistically significant differences in three JOABPEQ subscale scores [lumbar function, social life function, and mental health (p < 0.05)]. With respect to pain duration, for patients with chronic pain, there were statistically significant differences in two JOABPEQ subscale scores [lumbar function and mental health (p < 0.05)]. For patients with subacute or acute pain, there were no statistically significant differences in any of the JOABPEQ subscale scores (p < 0.05)

JOABPEQ Japanese Orthopaedic Association Back Pain Evaluation Questionnaire

aKruskal–Wallis test

Table 5

SF-36 score for each pain type at the first medical examination

Parameter

Nociceptive pain

Type of pain unclear (mixed pain)

Neuropathic pain

p a

Total patients with pain at first examination

Physical functioning

27.0 ± 2.14

30.2 ± 2.67

21.1 ± 4.73

0.040a

 Role physical

33.8 ± 2.15

34.5 ± 3.05

26.5 ± 4.13

0.326

 Bodily pain

35.8 ± 0.92

32.5 ± 1.64

29.6 ± 2.53

0.011a

 General health

42.4 ± 1.20

41.4 ± 1.99

39.5 ± 2.87

0.668

 Vitality

46.3 ± 1.43

41.6 ± 3.01

44.1 ± 2.73

0.396

 Social functioning

44.3 ± 1.66

40.5 ± 2.55

37.0 ± 4.53

0.179

 Role emotional

40.1 ± 2.16

36.5 ± 3.09

32.4 ± 4.04

0.160

 Mental health

46.3 ± 1.40

42.8 ± 2.61

42.1 ± 3.39

0.287

Group with pain present ≥3 months

Physical functioning

25.5 ± 2.58

28.4 ± 3.28

21.9 ± 5.29

0.201

 Role physical

32.2 ± 2.86

33.0 ± 4.15

28.2 ± 4.61

0.797

 Bodily pain

34.9 ± 1.11

30.9 ± 1.23

31.4 ± 2.96

0.103

 General health

42.2 ± 1.42

38.1 ± 1.85

39.8 ± 3.12

0.318

 Vitality

45.1 ± 1.72

38.9 ± 3.88

45.0 ± 3.18

0.471

 Social functioning

44.1 ± 2.00

39.7 ± 3.24

39.2 ± 5.09

0.473

 Role emotional

39.0 ± 2.88

35.1 ± 4.10

34.6 ± 4.49

0.522

 Mental health

46.6 ± 1.79

40.0 ± 3.20

44.0 ± 3.64

0.183

Group with pain present <3 months

Physical functioning

30.5 ± 3.80

34.0 ± 4.61

18.2 ± 11.9

0.197

 Role physical

37.3 ± 2.60

37.9 ± 3.69

20.4 ± 9.89

0.166

 Bodily pain

37.8 ± 1.58

35.9 ± 4.35

23.2 ± 3.55

0.021a

 General health

42.7 ± 2.29

48.5 ± 3.87

38.2 ± 7.90

0.335

 Vitality

49.2 ± 2.53

47.6 ± 4.12

41.0 ± 5.76

0.494

 Social functioning

44.7 ± 3.10

42.3 ± 4.26

29.2 ± 10.2

0.288

 Role emotional

42.7 ± 2.68

39.6 ± 4.33

24.7 ± 9.25

0.121

 Mental health

45.6 ± 2.19

48.8 ± 3.98

35.2 ± 8.49

0.292

Data are shown as mean ± standard error

The SF-36 comprises eight subscales (score of 0–100). Higher scores indicate better quality of life

There were statistically significant differences in two SF-36 subscale scores [physical function and bodily pain (p < 0.05)]. With respect to pain duration, for patients with chronic pain, there were no statistically significant differences in any of the SF-36 subscale scores. For patients with subacute or acute pain, there was a statistically significant difference in one SF-36 subscale score [bodily pain (p < 0.05)]

SF-36 36-Item Short-Form Health Survey

aKruskal–Wallis test

Discussion

The present study demonstrated four major points. (1) Overall, 58 % of the 102 patients with LBP and/or leg pain caused by LSS had nociceptive pain, 18 % had neuropathic pain, and 24 % had an unclear type of pain (mixed pain) at their first medical examination. (2) NRS scores for LBP, leg pain, and leg numbness in patients with LBP and/or leg pain caused by LSS were not significantly different among the three pain groups. The RDQ score in patients with LBP and/or leg pain caused by LSS, however, was significantly lower in the neuropathic pain group than in the other groups. (3) Three JOABPEQ subscales (lumbar function, social life function, and mental health) were significantly lower in the neuropathic pain group than in the other groups. (4) Two SF-36 subscales (physical function and bodily pain) were significantly lower in the neuropathic pain group than in the other groups.

The statistical power analysis performed in this study indicated a required total sample size of 102, and the power was 0.95. Therefore, we believe that the power of this study was adequate.

LSS may occur at different levels in the spinal canal. It may be caused by entrapment of nerve roots in the cauda equina due to hypertrophy of the osseus and soft tissue structures surrounding the lumbar spinal canal. Central canal stenosis may compress nerve roots in the cauda equina, whereas lateral recess stenosis and/or foraminal stenosis may compress nerve roots but spare the spine [29, 30]. Although the lower limb symptoms associated with LSS are mainly attributed to mechanoreceptive compression of nerve rootlets and/or the cauda equina, they are also associated with inflammation, ischemia, malnutrition, nerve degeneration, and nerve injury. They consequently have a complicated pathophysiology. The pathological mechanisms of lower limb symptoms caused by LSS involve nociceptive, inflammatory, and/or neuropathic pain components, which may result from postural changes or persistent compression of the nerve roots and/or cauda equina while walking.

The prevalence of neuropathic pain in the general population is unclear, although it has been reported at 3–9 % based on the results of various screening questionnaires in Europe and the United States [3134]. Few studies, however, have used the painDETECT to analyze the pathological mechanisms of LBP and/or leg pain caused by LSS in primary care-referred patients. Beith et al. [15] studied patients from southeastern England who had LBP with or without leg pain and had been referred for physiotherapy. The authors reported that 59 % of the patients reported what was identified to be nociceptive pain, 16 % had neuropathic pain, and 25 % had an unclear type (mixed pain). This result is very similar to that obtained in the present study of the pathological mechanisms of LSS-derived LBP and/or leg pain (nociceptive pain, 58 %; neuropathic pain, 18 %; unclear pain (mixed pain), 24 %). Therefore, our findings may accurately elucidate the pathological mechanisms of LSS-derived LBP and/or leg pain in the primary care setting.

The NRS scores for LBP, leg pain, and leg numbness in our patients with LBP and/or leg pain caused by LSS were not significantly different among the three pain groups. However, the RDQ score, three JOABPEQ subscale scores (lumbar function, social life function, and mental health), and two SF-36 subscale scores (physical function and bodily pain) were significantly lower in the neuropathic pain group than in the other groups. These data suggest that the neuropathic pain component produced significantly lower scores than its non-neuropathic pain components and reduced the patients’ physical and/or psychological QOL. Therefore, patients with neuropathic back and/or leg pain caused by LSS should be diagnosed as soon as possible after referral. A previous study [35] compared JOABPEQ scores between patients with LBP who experienced either neuropathic pain or nociceptive pain as assessed by the Japanese version of the painDETECT. Their findings suggest that neuropathic pain affects the social and psychological well-being of patients with LBP and demonstrate that patients with neuropathic back and/or leg pain caused by LSS might have particularly low physical and/or psychological QOL.

Finally it is considered that the impact of this study on education, health services and research regarding primary care would suggest that it may be very important to elucidate the pathological mechanisms and the epidemiology of LSS-derived LBP and/or leg pain by classifying the patients with LSS using painDETECT in order to analyze either neuropathic pain or non-neuropathic pain, and this may be helpful to examine how to treatment for LSS-derived LBP and/or leg pain in primary care setting.

The present study has some limitations that require attention. First, we studied only a small population, although we believe that the power was adequate in this study. Future studies must plan to evaluate a larger population. Second, this study had a cross-sectional design—it was not a longitudinal study. We did not evaluate therapeutic efficacy for LSS in this study. Hence, future studies should evaluate the therapeutic efficacy for each pain group caused by LSS, including conservative versus surgical therapy. Third, it was considered the lack thorough clinical and laboratory investigation in this study, since our study utilizes only questionnaires to classify the pain introduced by LSS. A clinical study with post-licensure surveillance should be implemented, ideally by setting up a database that includes all patients seeking treatment for LBP and/or leg pain caused by LSS, minimizing losses to follow-up, and using validated methods to gather clinically relevant data including demographic information, clinical features, common co-morbidities, conservative and/or surgical treatments applied to each patient, experience and training standards of the care providers applying each treatment, and each patient’s clinical evolution [36].

Conclusions

It may be important to analyze the pathological mechanisms of neuropathic pain and non-neuropathic pain in patients with LBP and/or leg pain caused by LSS. Patients with neuropathic back and/or leg pain caused by LSS may experience particularly low physical and/or psychological QOL.

Abbreviations

ABI, ankle-brachial pressure index; JOABPEQ, Japanese Orthopaedic Association Back Pain Evaluation Questionnaire; LBP, low back pain; LSS, lumbar spinal stenosis; MRI, magnetic resonance imaging; NIC, neurogenic intermittent claudication; NRS, numerical rating scale; QOL, quality of life; RDQ, Roland–Morris Disability Questionnaire; SF-36, 36-Item Short-Form Health Survey

Declarations

Acknowledgments

No funds were received in support of this work. No benefits in any form have been or will be received from a commercial party related directly or indirectly to the subject of this manuscript. The submitted manuscript does not contain information about specific medical devices or drugs.

Availability of data and materials

Results from the dataset are presented in the paper. The raw data for this study is available from the first author upon request.

Authors’ contributions

NT, OS, KK, RM, and SK made substantial contributions to the conception and design of the work. NT, KK, and RM acquired the data. NT, OS, and SK analyzed the data and contributed to its interpretation. NT and SK drafted the manuscript. All authors critically appraised the content of the manuscript and read and approved the final manuscript.

Competing interests

The authors declare that they have no competing interests.

Consent for publication

Not applicable.

Ethics approval and consent to participate

This study was approved by the ethics committees of the participating research of institutions of Aizu Medical Center, Fukushima Medical University (Reference number: 1842) and Fukushima Prefectural Minami-Aizu Hospital (Reference number: H26-001). All patients gave informed consent.

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

Authors’ Affiliations

(1)
Department of Orthopaedic Surgery, Fukushima Medical University School of Medicine
(2)
Department of Pain Medicine, Fukushima Medical University School of Medicine
(3)
Department of Orthopaedic Surgery, Hoshi General Hospital
(4)
Department of Orthopaedic and Spinal Surgery, Aizu Medical Center Fukushima Medical University
(5)
Department of Orthopaedic Surgery, Fukushima Prefectural Minami-Aizu Hospital

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Copyright

© The Author(s). 2016