Mechanical or inflammatory low back pain.pdf

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Original Article

Mechanical or inflammatory low back pain. What are the

potential signs and symptoms?

Bruce F. Walker a,*, Owen D. Williamson b

a School of Chiropractic and Sports Science, Faculty of Health Sciences, Murdoch University, 6150 Murdoch, Western Australia, Australiab Department of Epidemiology and Preventive Medicine, Monash University, Alfred Hospital, Melbourne, Victoria, Australia

Received 7 November 2007; received in revised form 12 March 2008; accepted 10 April 2008

Abstract

Non-specific low back pain (NSLBP) is commonly conceptualised and managed as being inflammatory and/or mechanical in

nature. This study was designed to identify common symptoms or signs that may allow discrimination between inflammatory

low back pain (ILBP) and mechanical low back pain (MLBP). Experienced health professionals from five professions were surveyed

using a questionnaire listing 27 signs/symptoms.

Of 129 surveyed, 105 responded (81%). Morning pain on waking demonstrated high levels of agreement as an indicator of ILBP.

Pain when lifting demonstrated high levels of agreement as an indicator of MLBP. Constant pain, pain that wakes, and stiffness

after resting were generally considered as moderate indicators of ILBP, while intermittent pain during the day, pain that develops

later in the day, pain on standing for a while, with lifting, bending forward a little, on trunk flexion or extension, doing a sit up, when

driving long distances, getting out of a chair, and pain on repetitive bending, running, coughing or sneezing were all generally

considered as moderate indicators of MLBP.

This study identified two groups of factors that were generally considered as indicators of ILBP or MLBP. However, none of

these factors were thought to strongly discriminate between ILBP and MLBP. 2008 Elsevier Ltd. All rights reserved.

Keywords: Low back pain; Inflammatory; Mechanical; Signs; Symptoms

1. Introduction

Low back pain (LBP) is a common problem with point

prevalence ranging from 12% to 33%, 1-year prevalence

22e65% and lifetime prevalence 11e84% (Walker,

2000). While LBP is usually self-limiting, it can persistresulting in a substantial personal, social and economic

burden (Walker et al., 2003). In the majority of cases,

a specificdiagnosis for LBPcannot be defined on the basis

of anatomical or physiological abnormalities. Although

imaging strategies can be employed to exclude serious

causes of LBP (such as tumours and infections), anatom-

ical abnormalities, such as those associated with the aging

process, are commonly observed in otherwise asymptom-

atic, healthyindividuals (Deyo, 2002). While specific ther-

apies can be employed to correct identifiable anatomical

or physiological abnormalities, non-specific low backpain (NSLBP) can only be treated empirically.

Systematic reviews (Van Tulder et al., 2000; Assendelft

et al., 2004) have described the benefit of a broad range of

physical and pharmacological interventions over natural

history or placebotherapies, but have conceded that effect

sizes are small, with little difference in outcomes observed

when alternative therapies are compared. This apparent

lack of effect may, at least in part, be due to the tendency

to treat NSLBP as a homogenous condition, rather than

* Corresponding author. Tel.: 61 08 93601297; fax: 61 8 9360

1299.

E-mail address: [email protected](B.F. Walker).

1356-689X/$ - see front matter 2008 Elsevier Ltd. All rights reserved.

doi:10.1016/j.math.2008.04.003

Available online at www.sciencedirect.com

Manual Therapy 14 (2009) 314e320

www.elsevier.com/math
mailto:[email protected]://www.elsevier.com/mathhttp://www.elsevier.com/mathmailto:[email protected]


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a heterogeneous collection of as yet undefined but differ-

ing conditions, some of which might respond and others

that do not respond to a particular therapy.

There is therefore a need to identify subgroups within

the broad classification of NSLBP, and given the failure

of classification on the basis of anatomical and physio-

logical abnormalities, attempts have been made to iden-tify subgroups on the basis of symptoms and physical

signs (Kent et al., 2005). This syndromic approach has

been limited in the past because of the poor inter-rater

reliability of proposed classifications. More recently,

however, several subgroup classification systems have

been demonstrated to have moderate or good inter-rater

reliability (Fritz and George, 2000; Flynn et al., 2002;

Kilpikoski et al., 2002; Fritz et al., 2006). Subsequent

randomised controlled trials (Fritz et al., 2003; Childs

et al., 2004; Long et al., 2004; Brennan et al., 2006)

have indicated that patients with NSLBP who receive

treatment matched to subgroup classifications have bet-

ter outcomes than those who receive alternative thera-

pies. It therefore seems likely NSLBP does represent

a heterogeneous collection of conditions and that the

identification of subgroups can result in improved out-

comes through directed therapies.

NSLBP is commonly described as being mechanical

(Batt and Todd, 2000; Chaudhary et al., 2004; Valat,

2005) or inflammatory (Saal, 1995; Ross, 2006).

Although these labels have no universally accepted defini-

tions, there is evidence to support the involvement of both

mechanical and inflammatory factors in the generation of

LBP (Biyani and Andersson, 2004; Hurri and Karppinen,

2004; Igarashi et al., 2004; Abbott et al., 2006; Al-Eisaet al., 2006; Ross, 2006). Further, there are two distinct

types of treatment for LBP that seem to follow this noso-

logical separation. That is, mechanical treatments such

as mobilisation, manipulation, traction and exercise are

contrasted with notionally anti-inflammatory treat-

ments like non-steroidal anti-inflammatory medications

andcorticosteroid injections. There arestudies that exam-

ine signs and symptoms of specific inflammatory arthriti-

des of the spine such as ankylosing spondylitis (AS)

(Rudwaleit et al., 2006). But once conditions like AS

have been ruled out there are no studies that determine

whether or not inflammatory low back pain (ILBP) and

mechanical low back pain (MLBP) subgroups can be dif-

ferentiated within the NSLBP classification.

It would therefore seem useful to attempt to divide

LBP sufferers into groups that may respond more read-

ily to two types of treatment, mechanical or inflamma-

tory. If this were possible the number of inappropriate

therapy decisions could be decreased.

The aims of this study were to identify common

symptoms or signs that may allow discrimination

between ILBP and MLBP and determine whether the

different groups involved in the management of LBP

interpret these signs and symptoms in a similar manner.

2. Methods

Prior to the commencement of the study, the authors

designed a questionnaire listing 26 symptoms and signs

relating to LBP. The signs and symptoms were drawn

from thea prioriknowledge of the authors to be possibly

related to LBP. The questionnaire was then pre-testedon a group of four practitioners: a spine surgeon, rheu-

matologist, chiropractor and manipulative physiothera-

pist, resulting in the addition of a further question. The

final 27 signs and symptoms are found in Table 1. The

questionnaire also contained an additional row for

other signs and symptoms beyond the 27 nominated.

This row could be filled out at the discretion of the

respondent if they thought that there were other associ-

ated factors. Those surveyed were asked Please circle

the number (0e10) which in your opinion best matches

the sign or symptom as being from [mechanical]/[inflam-

matory] low back pain.

Responses were assessed on an 11-point semantic

differential scale (Streiner and Norman, 2003) requiring

the participants to indicate the degree, from strongly dis-

agree (0) to strongly agree (10), withwhich they associated

each symptom or sign with ILBP and/or MLBP. Partici-

pants were instructed to use the middle number (5) to

indicate neitherdisagree nor agree and to leave the answer

scale blank to indicate dont know. Respondents were

advised that it was important to assume that all serious

causes of LBP were excluded, including cancer, infection

and associated systemic disease.

In this study the low back was defined as the area

between the costal margins and inferior gluteal folds.A convenience sample of health professionals experi-

enced in the diagnosis and treatment of LBP were sur-

veyed. The sample included both orthopaedically and

neurosurgically trained spine surgeons, rheumatologists,

medical practitioners with a special interest in musculo-

skeletal medicine, chiropractors and manipulative

Table 1

Potential signs and symptoms of ILBP or MLBP.

Morning pain on waking Pain on trunk extension

Intermittent pain during day Pain on lateral bending

Pain l ater in th e da y Pa lpat ory pai n of mus cle s

Straight leg raising hurts Palpatory pain of spinous process

Pain wakes the person up Stiffness after resting

(includes sitting)

Pain on sitting for a while Morning and afternoon pain

Pain when standing

for a while

Doing a sit up is painful

Pain w hen lift ing Drivi ng lo ng dis tanc es is pain ful

Pain bending forward a little Pain on walking more than 50 m

Burning pain Pain on running

Aching pain Pain on repetitive bending

Stabbing pain Pain getting out of a chair

Constant pain Pain on cough or sneeze

Pain on trunk flexion

315B.F. Walker, O.D. Williamson / Manual Therapy 14 (2009) 314e320


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physiotherapists. Key informants identified from within

each group provided the names of Australian practi-

tioners who were highly regarded within their profes-

sions and likely to have an informed opinion about

the topic.

The Dillman method (Dillman, 1978) was used for

the dissemination of the questionnaire, explanatoryinformation, and follow up procedures. The sample

population initially received a herald postcard, then 2

weeks later the questionnaire followed by a reminder

which was sent to non-responders after 2, 4 and 6 weeks.

At 4-weeks a second questionnaire was also included

with the reminder. Each questionnaire was coded to

identify the profession of the respondent. The question-

naires had no other identifying information recorded on

them and were anonymous.

The study had ethics approval from James Cook

University and Monash University.

The same mode of data collection was used for the

entire sample. Data were analysed using SPSS/PC Ver-

sion 14 (SPSS Inc., Chicago).

The median score and 10th and 90th centiles were

calculated for each statement by ILBP and MLBP.

This method is often used when the data have a skewed

distribution (Altman and Bland, 1994).

The significance of median scores of agreement was

subjectively set and the scores are shown in Table 2.

For example a median score of 8 or more was regarded

as indicating high levels of agreement that the symptom

or sign was an indicator of ILBP or MLBP. While

a median score of 2 or less was regarded as indicating

high levels of disagreement that the symptom or signwas an indicator of ILBP or MLBP.

In addition, the difference between ILBP and MLBP

scores was calculated for each question, by respondent,

and a median difference in scores of 4 or more was

regarded as potentially indicating that the question

could be used to potentially differentiate between

ILBP and MLBP. Non-parametric statistics were used

to compare paired responses to statements (Wilcoxon

ranked sign test) and score differences by profession

(KruskaleWallis test).

A chi-squared analysis was used to compare response

rates by profession. Given the multiple comparisons

between profession groups, a Bonferroni correction

was applied, hence p < 0.005 was interpreted as indicat-

ing differences between profession groups.

3. Results

One hundred and thirty-four questionnaires were sent

out. Five were returned as undeliverable leaving 129

possible respondents. Of these, 105 respondents (81%)

completed the questionnaire, comprising 29 spine sur-

geons, 28 rheumatologists, 25 medical practitioners

with a special interest in musculoskeletal medicine, 26

chiropractors and 26 manipulative physiotherapists.

There was no difference in response rates between the

professional groups (c42 6.072; p 0.194).

Several respondents completed the other signs and

symptoms row which allowed the addition of a new sign

or symptom. When these were analysed there were no

new signs and symptoms but instead minor variations

or repetition of signs and symptoms from the existing list.

Morning pain on waking (median 8) demonstrated

high levels of agreement as an indicator of ILBP. Pain

when lifting (median 8) demonstrated high levels of

agreement as an indicator of MLBP.

Constant pain, pain that wakes, and stiffness after

resting (median 7) were generally considered as mod-

erate indicators of ILBP, while intermittent pain during

the day, pain that develops later in the day, pain on

standing for a while, pain bending forward a little,pain on trunk flexion or extension, pain doing a sit up,

pain when driving long distances, pain getting out of

a chair, and pain on repetitive bending, running, cough-

ing or sneezing (median 7) were all generally consid-

ered as moderate indicators of MLBP (Table 3). There

was, however, no consistency of agreement either

between or within professional groups. No statements

were associated with a median score of 3 or less indicat-

ing significant disagreement that any symptom or sign

was not an indicator of ILBP or MLBP to some extent.

Those signs and symptoms with a median score between

4 and 6 (weak or no agreement) are also seen inTable 3.

No statements were associated with a median score of

more than 7 for both ILPB and MLBP suggesting that

no statement indicated both types of pain, while no

statements were associated with a median score of 3 or

less for both ILBP and MLBP suggesting that no state-

ment excludes both types of pain. Although there was

a statistically significant difference (p < 0.05) in paired

responses to all statements apart from that relating to

aching pain, no statements were found to be associated

with a score of 7 or greater for one type of LBP and 3 or

less for the other indicating that none of the factors were

thought to strongly discriminate between ILBP and

Table 2

Median scores and their relative significance.

Median score Significance

10 Absolute agreement

9 Very high agreement

8 High agreement

7 Moderate agreement

6 Weak agreement

5 Neutral

4 Weak disagreement

3 Moderate disagreement

2 High disagreement

1 Very high disagreement

0 Absolute disagreement

316 B.F. Walker, O.D. Williamson / Manual Therapy 14 (2009) 314e320


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MLBP. The only statement that was associated with

a difference in response of 4 or greater was that relating

to morning pain on waking; suggesting that this was the

only statement that was thought to generally distinguish

ILBP from MLBP.

There were significant differences between professions

with respect to many of the statements being able to dis-

tinguish ILBP from MLBP (Table 3). For example, rheu-

matologists were more likely to regard constant pain and

pain that wakes a person as inflammatory and pain on

straight leg raising, lifting, running, repetitive bending,

coughing and sneezing as mechanical than the other

groups. Physiotherapists were more likely to regard pain

on lifting or repetitive bending as mechanical. Medical

practitioners with a special interest in musculoskeletal

medicine did not agree as strongly that pain wakes me

up or that constant pain is a sign of ILBP.

4. Discussion

Although NSLBP is commonly described as being

mechanical or inflammatory in nature and is treated

by mechanical and anti-inflammatory therapies, there

have been no previous attempts to distinguish these sub-

groups on the basis of symptoms or clinical signs. How-

ever, Rudwaleit et al. (2006) did study the clinical

history of 101 AS patients and 112 patients without

AS thereafter labeled as MLBP patients. In their

methods they used an external reference standard

known as the New York Criteria (Van der Linden

et al., 1984) to diagnose AS. They found four factors

that potentially separated the two groups, these were

morning stiffness greater than 30 min, improvement

with exercise but not with rest, awakening because of

back pain in the second half of the night and alternating

buttock pain. However, despite some similarity in their

results, their study differs from ours insofar as they com-

pared a specific inflammatory arthritide (AS) with all

other cases of back pain which they tagged MLBP.

In contrast we asked expert respondents to compare

non-specific ILBP with non-specific MLBP. In our ques-

tionnaire there were no pre-determined definitions or

external reference standards (other than exclusions) to

categorise non-specific ILBP or MLBP. Indeed this

was the reason for our study, to measure the opinion

Table 3

Twenty-seven signs and symptoms.

Sign or symptom ILBP (median,

10, 90 centiles)

MLBP (median,

10, 90 centiles)

Difference ILBPMLBP

(median, 10, 90 centiles)

Significance of difference

by profession (p value)

Morning pain on wakinga 8 (3, 10) 4 (1, 8) 4 (3, 8) 0.338

Intermittent pain during dayd 4 (1, 7) 7 (5, 9) 2.5 (7, 1) 0.001

Pain later in the dayd 5 (1.5, 7.5) 7 (4, 9) 2 (6, 2.5) 0.124

Straight leg raising hurts* 5 (1, 8) 6 (3, 9) 2 (7, 2) 0.002Pain wakes the person upc 7 (3, 9) 4 (1, 7) 3 (1, 7) 0.043

Pain on sitting for a whilee 5.5 (2, 8) 6 (4, 8) 0 (5, 2) 0.063

Pain when standing for a whiled 5 (2, 8) 7 (4, 8) 1 (5, 1) 0.096

Pain when liftingb 4 (1.2, 8) 8 (5, 9) 3 (7, 0) 0.024

Pain bending forward a littled 5 (2, 8) 7 (4, 9) 2 (6, 2) 0.012

Burning paine 5 (2, 8) 5 (2, 7) 0 (2, 5) 0.001

Aching paine 6 (3, 8) 6 (3, 8) 0 (4, 3) 0.130

Stabbing paine 5 (2, 8) 6 (3, 8) 1 (6, 3) 0.283

Constant painc 7 (3, 9) 5 (3, 7) 2 (2, 2) 0.000

Pain on trunk flexiond 5 (2, 8) 7 (5, 9) 1 (6, 1) 0.028

Pain on trunk extensiond 5 (1.5, 8) 7 (4.5, 9) 1 (6, 2) 0.008

Pain on lateral bendinge 5 (1.5, 7.5) 6 (5, 8.5) 1 (6, 2) 0.006

Palpatory pain of musclese 5 (1, 7.7) 5 (3, 8) 0 (5, 3) 0.000

Palpatory pain of spinous processe 5 (1, 8) 6 (3, 8) 0 (4, 2) 0.192

Stiffness after resting (includes sitting)c 7 (5, 10) 5 (2, 8) 2 (2, 7) 0.035

Morning and afternoonpaine 6 (3.5, 8.5) 5 (2, 8) 0 (2, 5) 0.443

Doing a sit up is painfuld 5 (2, 7) 7 (5, 9) 2 (6, 0) 0.098

Driving long distances is painfuld 5 (2, 8) 7 (5, 8) 1 (5, 1) 0.495

Pain on walking more than 50 me 5 (1, 8) 6 (3, 8) 1 (6, 2.8) 0.002

Pain on runningd 5 (1, 7) 7 (5, 9) 2 (6.5, 1) 0.000

Pain on repetitive bendingd 5 (1.5, 8) 7 (5, 9) 2 (6, 0) 0.011

Pain getting out of a chaird 5 (2, 8) 7 (5, 9) 1 (6, 1) 0.020

Pain on cough or sneezed 4 (1, 8) 7 (2.5, 9) 2 (7, 2.6) 0.001

Survey results.a High level of agreement as an indicator of ILBP.b High level of agreement as an indicator of MLBP.c Moderate indicators of ILBP.d Moderate indicators of MLBP.e

Variables not considered indicative of either inflammatory or mechanical.



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of experts about the extent to which MLBP and ILBP

can be distinguished by signs and symptoms.

Our study demonstrated some evidence that a number

of signs and symptoms are possible indicators of ILBP

or MLBP. However, there was no clear agreement either

within or between professions regarding whether state-

ments based on common signs and symptoms of LBPare either indicative of, or can distinguish between

inflammatory or mechanical causes of LBP.

An ideal statement for inclusion in an instrument that

distinguishes between ILBP and MLBP would have

a high score for one form of LBP, a low score for the

other form, a significant difference between the scores

for both forms and no significant difference between

professions with respect to interpretation. None of the

studied statements met each of these criteria.

Although morning pain on waking (median differ-

ence 4) and pain that wakes the person up (median dif-

ference 3) were thought to be broadly indicative of

ILBP and pain on lifting (median difference 3) was

thought to be broadly indicative of mechanical pain,

this was not universally recognised either within or be-

tween professional groups. Of these, morning pain on

waking is commonly used as a marker of pain due to in-

flammation (Garrett et al., 1994; Yazici et al., 2004).

The fact that morning pain is used as a marker of dis-

ease severity in inflammatory spondyloarthopathies

such as AS (Garrett et al., 1994) could explain why sev-

eral respondents suggested that this marker should have

been expanded in our survey to reflect the length of time

the pain lasted in the morning.

The relationship between inflammation and pain,however, is not clear. Although a recent study found

that the mean intensity of pain over 24 h was indepen-

dently associated with high levels of high sensitivity C

reactive protein in patients with acute sciatica (less

than 8 weeks), this association was not found in patients

with chronic LBP (Stu rmer et al., 2005).

Similarly, the relationship between pain that wakes

a patient up and inflammation is not clear. Sleep distur-

bance is commonly reported in people with non-specific

chronic pain, as well as those with inflammatory arthri-

tis (Menefee et al., 2000). The mechanisms by which

pain and inflammation cause sleep disturbance have

not, however, been well described and may differ.

Although the levels of inflammatory cytokines, such as

interleukin-6 may alter sleep behaviour (Mullington et al.,

2001), there did not appear to be an association between

improvements in pain and joint stiffness, and improve-

ments in sleep disturbance, in a smallgroup of patients be-

ing treated for rheumatoid arthritis with non-steroidal

anti-inflammatory drugs (Lavie et al., 1991).

Although pain on lifting is commonly thought to rep-

resent mechanical pain, the relationship between spinal

load and pain is not clear. Whilst there is strong evi-

dence that work activities such as lifting, bending,

twisting and vibration are a risk factor for the onset

and reporting of NSLBP, overall it appears that the

size of the effect is less than that of other individual fac-

tors (Waddell and Burton, 2000). It is postulated that

load, posture and creep may alter the mechanical prop-

erties of the spine, resulting in stress concentration in in-

nervated tissues such as the intervertebral discs, facetjoints and ligaments (Adams et al., 2002), but there is lit-

tle direct evidence that such factors are important in

NSLBP (Waddell, 2004). In overview the results could

be interpreted to suggest that movement or activity-re-

lated symptoms are more broadly indicative of MLBP

and that pain at rest is more indicative of ILBP.

Interestingly no variable was considered to represent

both ILBP and MLBP and using our analysis, 10 variables

were not considered indicative of either ILBP or MLBP.

While it is possible that varying educational para-

digms could explain variability between professional

groups, it does not obviously explain the variability we

found within groups. As the key participants (experts)

in this study were selected on their academic and profes-

sional standing, it is likely that these differences will be

transmitted down through the ranks of each profession

and sustains the inadequacy of the evidence.

The strength of this study is its good response rate and

its generalisability to a wide range of practitioners; how-

ever, the study does have some limitations. First, the

respondents were not randomly selected from within

their professional groups, therefore one cannot general-

ise the results to the entire population of professionals

in each group. However, our purposeful intention was

to get the opinion of approximately 20 experts fromeach group. In this way the answers to our primary ques-

tions are more likely to have content validity. Secondly,

the best method for defining subgroups within the broad

diagnosis of NSLBP has not been established.

The approach of this study was to suggest two possible

subgroups, ILBP and MLBP and investigate whether

experts within relevant professional groups could inde-

pendently agree on certain symptoms and signs. This

approach highlighted the variation within and between

participating groups. A similar approach would be to

use the Delphi technique (using an iterative/consensus

method) to define a set of symptoms and signs that could

be measured in trials of mechanical and anti-inflamma-

tory therapies. If symptoms and signs could be used to

define subgroups of patients with ILBP and MLBP, trials

could be conducted to determine if those who receive sub-

group specific treatment do better with the subgroup-spe-

cific treatment rather than non-specific treatment,

thereby confirming the validity of the subgroups. Despite

the limitations of this study, it is clear that considerable

diversity of opinion exists regarding symptoms or signs

that might be used to distinguish between MLBP and

ILBP, both within and between the professional groups

involved in the management of NSLBP.



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NSLBP is commonly labelled, conceptualised and

managed as being inflammatory and/or mechanical in

nature and this study identified two groups of factors

that were generally considered as indicators of ILBP

or MLBP. However, we identified few, if any, signs or

symptoms that members of professions involved in the

management of NSLBP could highly agree distinguishedbetween these aetiologies. While the general absence of

agreement regarding signs and symptoms of ILBP and

MLBP does not invalidate the pathophysiological para-

digms of mechanical and inflammatory pains, it does,

however, signal the need for further research.

This research should be aimed at testing the 17 indica-

tors identified for their ability to predict the outcome of

mechanical and anti-inflammatory treatments of LBP.

If further study establishes that they are able to predict

the outcome of the two treatment types, the number of in-

appropriate decisions to use either may be decreased.

Acknowledgments

The authors acknowledge that this paper was first

presented at the Spine Society of Australia Conference

2006 and that the abstract is published in the conference

proceedings, Journal of Bone and Joint Surgery, 88B,

Supp III: 448.

References

Abbott JH, Fritz JM, McCane B, Shultz B, Herbison P, Lyons B,

Stefanko G, Walsh RM. Lumbar segmental mobility disorders:comparison of two methods of defining abnormal displacement

kinetics in a cohort of patients with non-specific mechanical low

back pain. BMC Musculoskelet Disord 2006;7:45. doi:10.1186/

1471-2474-7-45.

Adams MA, Bogduk N, Burton K, Dolan P. The biomechanics of

back pain. Edinburgh: Churchill Livingstone; 2002.

Al-Eisa E, Egan D, Deluzio K, Wassersug R. Effects of pelvic skeletal

asymmetry on trunks movement. Three dimensional analysis in

healthy individuals versus patients with mechanical low back

pain. Spine 2006;31(3):E71e9.

Altman DG, Bland JM. Quartiles, quintiles, centiles and other

quantiles. BMJ 1994;309:996.

Assendelft WJJ, Morton SC, Yu Emily I, Suttorp MJ, Shekelle PG.

Spinal manipulative therapy for low-back pain. Cochrane Data-

base Syst Rev 2004;(1). doi:10.1002/14651858.CD000447.pub2.Art. No.: CD000447.

Batt ME, Todd C. Five facts and five concepts for rehabilitation of

mechanical low back pain. Br J Sports Med 2000;34(4):261.

Biyani A, Andersson GB. Low back pain: pathophysiology and

management. J Am Acad Orthop Surg 2004;12:106e15.

Brennan GP, Fritz JM, Hunter SJ, Thackeray A, Delitto A,

Erhard RE. Identifying subgroups of patients with acute/subacute

nonspecific low back pain results of a randomized clinical trial.

Spine 2006;31:623e31.

Chaudhary N, Longworth S, Sell PJ. Management of mechanical low

back pain e a survey of beliefs and attitudes in GPs from Leicester

and Nottingham. Eur J Gen Pract 2004;10(2):71e2.

Childs JD, Fritz JM, Flynn TW, Irrgang JJ, Johnson KK,

Majkowski GR, Delitto A. A clinical prediction rule to identify

patients with low back pain most likely to benefit from spinal

manipulation. Ann Intern Med 2004;141:920e8.

Deyo RA. Diagnostic evaluation of LBP; reaching a specific diagnosis

is often impossible. Arch Intern Med 2002;162:1444e7.

doi:10.1002/14651858.CD000447.pub2.

Dillman DA. Mail and telephone surveys. The total design method.

New York: John Wiley & Sons; 1978.

Flynn T, Fritz J, Whitman J, Wainner R, Magel J, Reindeiro D,

Butler B, Garber M, Allison S. A clinical prediction rule for classi-

fying patients with low back pain who demonstrate short-term

improvement with spinal manipulation. Spine 2002;27:2835e43.

Fritz JM, George S. The use of a classification approach to identify

subgroups of patients with acute low back pain. Spine 2000;25:

106e14.

Fritz JM, Delitto A, Erhard RE. Comparison of classification-based

physical therapy with therapy based on clinical practice guide-

lines for patients with acute low back pain. Spine 2003;28:

1363e72.

Fritz JM, Brennan GP, Clifford SN, Hunter SJ, Thackeray A. An

examination of the reliability of a classification algorithm for

subgrouping patients with low back pain. Spine 2006;31:77e82.

Garrett S, Jenkinson T, Kennedy LG, Whitelock H, Gaisford P,

Calin A. A new approach to defining disease status in ankylosing

spondylitis: the bath ankylosing spondylitis disease activity index.

J Rheumatol 1994;21:2286e91.

Hurri H, Karppinen J. Discogenic pain. Pain 2004;112:225e38.

Igarashi A, Kikuchi S, Konno S, Olmarker K. Inflammatory cytokines

released from the facet joint tissue in degenerative lumbar spinal

disorders. Spine 2004;19:2091e5.

Kent P, Marks D, Pearson W, Keating J. Does clinician treatment

choice improve the outcomes of manual therapy for non-specific

low back pain? A meta-analysis. J Manipulative Physiol Ther

2005;28:312e22.

Kilpikoski S, Airaksinen O, Kankaanpa a M, Leminen P, Videman T,

Alen M. Interexaminer reliability of low back pain assessment

using the McKenzie method. Spine 2002;27:E207e14.

Lavie P, Nahir M, Lorber M, Sharf Y. Nonsteroidal anti-

inflammatory drug therapy in rheumatoid arthritis patients: lackof association between clinical improvement and effects on sleep.

Arthritis Rheum 1991;34:655e9.

Long A, Donelson R, Fung T. Does it matter which exercise? A

randomized control trial of exercise for low back pain. Spine

2004;29:2593e602.

Menefee LA, Cohen MJ, Anderson WR, Dogrhamji K, Frank ED,

Lee H. Sleep disturbance and non-malignant chronic pain:

a comprehensive review of the literature. Pain Med 2000;1:156e72.

Mullington JM, Hinze-Selch D, Pollma cher T. Mediators of inflamma-

tion and their interaction with sleep: relevance for chronic fatigue

syndrome and related conditions. Ann N Y Acad Sci 2001;933:

201e10.

Ross JS. Non-mechanical inflammatory causes of back pain: current

concepts. Skeletal Radiol 2006.

Rudwaleit M, Metter A, Listing J, Sieper J, Braun J. Inflammatoryback pain in Ankylosing Spondylitis. A reassessment of the clinical

history for application as classification and diagnostic criteria.

Arthritis Rheum 2006;54(2):569e78.

Saal JS. The role of inflammation in lumbar pain. Spine 1995;20:

1821e7.

Streiner DL, Norman GR. Health measurement scales. A practical

guide to their development and use. 3rd ed. Oxford: Oxford

University Press; 2003.

Stu rmer T, Raum E, Buchner M, Gebhardt K, Schiltenwolf M,

Richter W, Brenner M. Pain and high sensitivity C reactive protein

in patients with chronic low back pain and acute sciatica. Ann

Rheum Dis 2005;64:921e5.

Valat JP. Factors involved in progression to chronicity of mechanical

low back pain. Joint Bone Spine 2005;72(3):193e5.



7/7

Van der Linden S, Valkenburg HA, Cats A. Evaluation of diagnostic

criteria for ankylosing spondylitis: a proposal for modification of

the New York criteria. Arthritis Rheum 1984;27:361e8.

Van Tulder MW, Sholten RJPM, Koes BW, Deyo RA. Nonsteroidal

anti-inflammatory drugs for low back pain: a systematic review

within the framework of the Cochrane collaboration back review

group. Spine 2000;25:2501e13.

Waddell G, Burton AK. Occupational health guidelines for the

management of low back pain at worke

evidence review. London:

Faculty of Occupational Medicine, Available from: ; 2000 [accessed 06.11.07].

Waddell G. The back pain revolution. 2nd ed. Edinburgh: Churchill

Livingstone; 2004.

Walker BF. The prevalence of low back pain. A systematic review of

the literature from 1966 to 1998. J Spinal Disord 2000;13:

205e17.

Walker BF, Muller R, Grant W. Low back in Australian adults: the

economic burden. Asia Pac J Public Health 2003;15:79e87.

Yazici Y, Pincus T, Kautiainen H, Sokka T. Morning stiffness in

patients with early rheumatoid arthritis is associated more strongly

with functional disability than with joint swelling and erythrocyte

sedimentation rate. J Rheumatol 2004;31:1723e6.

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