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Review: Chronic Low Back Pain And Yellow Flags, What Treatments Are Effective?

Written by Kieran Macphail on . Posted in Corrective Holistic Exercise Kinesiology, For Health Professionals, For Movement Therapists, Low back pain, Orthopaedic Medicine

1. Introduction


Low back pain (LBP) is usually defined as pain localised below the costal margin (ribs) and above the inferior gluteal folds (buttock crease). It is the leading cause of disability worldwide and is becoming increasingly prevalent (Harkness et al. 2005, Hoy et al. 2012, Vos et al. 2012). Chronic low back pain (CLBP) is variously defined as lasting longer than 7-12 weeks, to 3 months (Anderrson 1999, Frymoyer 1988). LBP is typically classified as “specific” or “non-specific”. Specific LBP refers to symptoms caused by specific pathophysiologic causes, such as hernia nucleus, infection, inflammatory disease, osteoporosis, rheumatoid arthritis, fracture or tumour (Van Tulder and Koes 2010). There is no effective cure for non-specific low back pain (NSCLBP) (Van Middelkoop et al. 2011) and this represents the 90% of the LBP population that cannot be classified as specific LBP (Deyo et al. 1992). Most guidelines are based on the assumption that symptoms resolve spontaneously and that return to work equals recovery (Anderrson 1999, Van Tulder et al. 2006). However, when pain is assessed it appears patients may be returning to work despite their pain (Bowey-Morris 2011), and whilst spontaneous recovery occurs in approximately a third of patients after 3 months, 71% still have pain after 1 year (Itz et al. 2013).

CLBP patients with psychosocial, psychological and social, risk factors are known to have poorer outcomes and increased management costs (Grimmer-Somers 2006, Nicholas et al. 2011). The term “yellow flags” was originally used to describe psychosocial risk factors that predict disability in LBP patients (Kendall et al. 1999). These risk factors are predictors of return to work and disability in CLBP patients (Glattacker et al. 2013). The risk factors can be identified using a questionnaire or a clinical diagnosis (Watson and Kendall 2000). Questions cover beliefs that are associated with delayed return to work and disability. These include fears about pain, injury, recovery and being despondent or anxious. It is suggested that having a few strongly held negative beliefs or several weaker ones could be used to identify at risk patients (Nicholas et al. 2011). These beliefs increase a patient’s perception of threat and modern neuroscience suggests that pain is the conscious interpretation that tissue is in danger (Moseley 2007). These beliefs can be viewed as “thought viruses” (Butler and Moseley 2013). The term yellow flag has now been refined to encompass psychological factors that a physiotherapist could manage, whereas orange flags are now used for psychopathology, which requires specialist psychological management. Alternatively, when the yellow flag belief is positive, for example, an expectation that they will recover; it can be viewed as a positive “pink flag” (Gifford 2005). The more subjective components of the workplace such as perception are termed “blue flags”, and the more objective risk factors such as the nature of the work are termed “black flags” (Main et al. 2004).

2. Background

Yellow flags are now included in most LBP guidelines although there is wide variation in suggestions in how to assess and manage these patients (Koes et al. 2010). The New Zealand guidelines (National Health Committee 2004) suggest assessment with the acute low back screening tool and the Canadian guidelines are similarly specific (Rossignol et al. 2007), suggesting assessment at 4 weeks or straight away if chronic. However, the other guidelines are less specific in their assessment. The Australian, American, Dutch, French, German and United Kingdom guidelines suggest early assessment but are not specific about how to assess (Australian Acute Musculoskeletal Pain Guidelines Group 2003, Chou et al. 2007, The Dutch Institute for Healthcare Improvement (CBO) 2003, Agence Nationale d’Accreditation et d’Evaluation en Sante 2000, Drug Committee of the German Medical Society 2007, NHS 2008). Similarly, the Finnish and Norwegian guidelines list signs of “yellow flags” and are even more ambiguous on assessment (Malmivaara et al. 2008, Laerum et al. 2007). The European guidelines propose an initial assessment of “yellow flags” and then a review in detail if there is no progress in acute and sub acute low back pain (van Tulder et al. 2006) or assess initially in chronic patients (Airaksinen et al. 2006). In contrast the Italian guidelines recommend assessing psychosocial factors after 2 weeks (Negrini et a 2006) and after 2-6 weeks is suggested in the Spanish guidelines (Spain, the Spanish Back Pain Research Network 2005). The Austrian guidelines are less specific and they suggest patients who do not progress over time should be assessed (Friedrich and Likar 2007). In treatment patients with yellow flags are not specifically addressed but all guidelines at least briefly state the need for re-assurance and return to normal activities, which may aid yellow flag management. The European guidelines suggest the inclusion of a cognitive behavioural approach and the German guidelines suggest psychotherapy may be an education option for referral for multi-disciplinary treatment. Thus within the guidelines the importance of yellow flags is appreciated in assessment and for triage but there is ambiguity in the specifics of management.

The differences seen across the full range of physiotherapy approaches is far greater than within the guidelines. Within physiotherapy there are many different approaches to managing these patients as shown in table 2.1.

Table 2.1 Matrix of different Physiotherapy Approaches

Hands on   Hands off
More focused on the local tissue Maitland (2013), Society of Musculoskeletal Medicine (Atkins et al. 2010) McKenzie (McKenzie and May 2003) McGill (2007),Sahrmann (2002)
  Lee/ Vleeming (2001), O’Sullivan (Fersum et al. 2009)
More focused on central processes Dorko (2003) Neuro-developmental (Kolar et al. 2014) NOI/ Mind body group (Butler and Moseley 2013)



The Maitland and McKenzie approaches are the most utilised in the UK (Foster et al. 1999). These approaches and the traditional orthopaedic medicine approach (Atkins et al. 2010) are perhaps the most bio-medical focused, placing emphasis on finding and treating the tissues that is the cause. Other approaches such as that derived by O’Sullivan (Fersum et al. 2009) and, Lee and Vleeming (Lee 2001) attempt to classify patients that need more psychosocial input. With the new clinical model 4, the Society of Musculoskeletal Medicine is moving in the same direction (Atkins et al. In Press). The Neuro Orthopaedic Institute and Mind In Body groups place the most emphasis on a hands-off approach to psychosocial aspects (Butler and Moseley 2013). This approach is based on an understanding of the importance a patient’s perception has on their symptoms and thus the benefits of education and a graded return to normal activities. In contrast Dorko (2003) is a proponent of a hands-on approach to addressing the psychosocial aspects. Clinicians are aware of the importance of psychosocial factors in these patients (Scheermesser at al. 2012) but feel underprepared and may sometimes stigmatise these patients (Synnott et al. 2015). Thus whilst yellow flags are clearly important there remains a lack of clarity for clinicians looking at how to specifically manage these patients from guidelines and clinicians are using an incredibly varied set of approaches. This study aims to investigate how and why different physiotherapists choose to use the different approaches.

3. Literature Review

The literature review was undertaken with grounded theory in mind. The aim was to get an overview of the various different methods currently used in practice to provide context for the interviews. Issues around clinical reasoning and motivation to practice to were not reviewed so that the exploration of these areas would be more inductive.


3.1 Search strategy

Three approaches were used for retrieving literature. Searches were conducted initially using the terms yellow flags and low back pain, and treatment, or assessment, or management, using the databases PubMed, Embase, PEDro and CINHAL up to September 2015. This however did not identify any papers and it became clear that whilst the term yellow flags is used in the assessment literature it is not used in treatment papers. As such the searches were repeated using the term psychosocial and low back pain, and treatment, or assessment, or management. In addition content experts were consulted to ensure no additional papers were missed and citation tracking was implemented. No time limit was set for papers and foreign language papers that were identified using the English terms were included. Refworks was used to store and remove duplicates from the searches.


3.2 Selection of studies

The student researcher, KM, initially screened the title and abstract of the identified studies. The full text was then analysed. Studies were selected on the basis of the following selection criteria;

  1. Primary experimental design study of human participants with chronic (>12weeks) or recurrent (repeated episodes over 12 months) low back pain
  2. Participants must have yellow flags or measured psychosocial status commensurate with yellow flags
  3. Studies must cover the management of patients

Studies were excluded if;

1. The intervention group did not have yellow flags or measurable psychosocial factors

2. Looked at post surgical patients

3. Mixed groups of sub-acute and chronic patients

4. Mixed groups of neck and CLBP patients

5. The intervention was purely psychological (CBT) and outside the scope of traditional physiotherapy practice


3.3 Data management

Risk of bias was assessed as suggested by the Cochrane Back Review Group (Bendix et al. 1996) as shown in table 4.1. Studies with a score above 6 were considered low risk of bias. Studies with a score below 6 were considered high risk. Where any doubt remained an author of the study was contacted via email.

Table 3.1 Criteria for risk of bias analysis

1 Was the method of randomisation adequate?
2 Was the treatment allocation concealed?Was knowledge of the allocated interventions adequately prevented during the study?
3 Was the patient blinded to the intervention?
4 Was the care provider blinded to the intervention?
5 Was the outcome assessor blinded to the intervention?Were incomplete outcome data adequately addressed?
6 Was the drop-out rate described and acceptable?
7 Were all randomised participants analysed in the group to which they were allocated?
8 Are reports of the study free of suggestion of selective outcome reporting?Other sources of potential bias:
9 Were the groups similar at baseline regarding the most important prognostic indicators?
10 Were co-interventions avoided or similar?
11 Was the compliance acceptable in all groups?
12 Were the timing of the outcome assessment similar in all groups?


3.4 Search Results

In total 367 studies were identified, after screening titles and abstracts 11 remained. All 11 papers met the inclusion criteria. One foreign language paper met the inclusion criteria was included (Pfingsten and Hilderbrandt 2001), this paper was translated using google translate so that it could be included in the analysis. One paper (Bergstrom et al. 2012) was excluded as it included both neck and back patients in one homogenous group with no separate analysis of back pain patients. A clear limitation is that these studies look at groups of CLBP patients that show yellow flags on average, but within each cohort there will have likely been patients with very few yellow flags and possibly some with very significant yellow flags. Using table 4.1 of the Cochrane Back Review Group (Bendix et al. 1996) the studies were classified as high or low risk. One paper was high risk (Pfingsten and Hilderbrandt 2001) and nine were classified as low risk. The oldest trial that met the selection criteria was Alantra et al. (1994) as despite it’s age it met all quality criteria for selection. The 10 studies all looked at patients of 18 years or older with CLBP, using at least 6 months follow up. All but three were randomised controlled trials, with two being cohort studies (Pfingsten and Hilderbrandt 2001, O’Sullivan et al. 2015) and another with no randomisation (Vowles et al. 2007).


Figure 4.1 Flow diagram of literature review

3.5 Findings

The studies identified cover a broad spectrum of biopsychosocial interventions, with some focusing on more biomedical interventions, psychosocial interventions or a combination. Six studies looked at a predominantly biomedical approach.

3.5.1 Biomedical approaches: Passive approaches

Two studies with a low risk of bias from the same group have examined a passive biomedical intervention. Weiner et al. (2003, 2008) conducted randomised controlled trials of percutaneous electrical nerve stimulation (PENS). This involves delivering a low voltage electrical current through a specially designed needle to the adipose layer close to the nerves near the site of pain. In both studies patients were aged 65 or older, lived in the community and experienced moderate CLBP almost every day for more than 3-months. In their earlier study (Weiner et al. 2003) the authors measured psychosocial factors with the Geriatric Depression Scale and the mean score was 6.81, which equates to mild depression, indicative of yellow flags. In their later study (Weiner et al. 2008) psychosocial function measures showed mild to moderate levels of psychosocial stress across the Geriatric Depression Scale, the Chronic Pain Self-Efficacy Scale, the Catastrophizing Scale of the Cognitive Strategies Questionnaire and the Fear-Avoidance Beliefs Questionnaire. The combination of the scores across these measures shows these patients had yellow flags.

In their earlier study subjects were randomised to receive 6-weeks of twice weekly PENS and physical therapy or sham PENS stimulation and physical therapy (Weiner et al. 2003). The PENS and physical therapy group had significant reductions in pain intensity and pain related disability, the sham PENS and physical therapy group did not. These improvements remained at 3-month follow up. Furthermore, significant improvements in sit to stand, psychosocial function and lifting endurance were also seen in the PENS and physical therapy group. In their later study (Weiner et al. 2008) they had 200 participants, randomised to receive either PENS, brief PENS to control for treatment expectancy, PENS with general conditioning or brief PENS and general conditioning. All interventions were done twice a week for 6 weeks. The general conditioning consisted of up to 30-minutes walking and a further nine motor control exercises for 2-minutes each with 1-minute rest. This was accompanied by a home exercise programme of 12 stretches to be done for 3 repetitions, 3 times a day, and 30 minutes of additional walking above normal activity levels. After the 6-week intervention all four groups produced statistically significant improvements in present, average and greatest pain intensity measured on the short form McGill Pain Questionnaire. Interestingly the brief PENS of 5-minutes produced an equal improvement to that of the 30-minute PENS. Furthermore, the general conditioning protocol had no additional benefit on pain measures above that of the PENS interventions, however it did significantly improve fear avoidance in comparison to PENS. These studies suggest that whilst sham PENS is ineffective, 5-minutes is sufficient to have treatment effect, casting significant doubt over the authors proposed mechanism of effect and suggesting the effects may be more centrally driven. Furthermore they indicate the potential benefits of active interventions, in particular general conditioning, on fear avoidance beliefs.


3.5.2 Biomedical approaches: Exercise-based interventions

Four of the studies examined exercise-based interventions. Murtezani et al. (2011) found high intensity aerobic exercise outperformed a passive electrotherapy group not dissimilar to the approach of Weiner and colleagues. They randomised 101 patients to either a high intensity aerobic exercise group or a passive modalities group. They used the Hospital Anxiety and Depression Scale to measure psychosocial factors. The scores suggest the patient’s as a group were indicative of patients with yellow flags. The active group produced a 3.9 mean decrease in the visual analogue scale. Interestingly the control group produced no improvements in pain intensity, toe touch, anxiety and depression scores and disability. Suggesting the passive intervention was far less effective than that the results seen in Weiner and colleague’s studies (2003, 2008). Nonetheless the high intensity aerobic exercise intervention produced improvements across all these measures.

In contrast the other two low risk of bias studies looking low intensity aerobic interventions found no significant difference between their intervention and control groups. Hurley et al (2015) conducted a 3-arm assessor blind RCT of an individualised walking programme, an exercise group intervention and usual care physiotherapy, in 246 patients aged 18-62 with CLBP. Participants were recruited from those seeking help at the local hospital and this was used as a baseline as opposed to trials from the general population, which require a baseline pain score for inclusion. The psychosocial baseline assessment of these patients suggests as a group they were representative of patients with yellow flags. The walking programme was individualised and education on functional restoration and addressing fears around movement and the patient’s understanding of their problem were addressed. Patients were given a pedometer to measure their initial activity. From then on they had weekly contact with a physiotherapist, with the aim to progress them to 30-minutes total daily walking 5 times a week. This is in line with the recommendations of the American College of Sports Medicine and previous studies (Garber et al 2011, Tully et al. 2005, 2007). The exercise group attended a class based on the back to fitness programme (Moffett and Frost 2000) endorsed by the UK National Institute of Clinical Excellence guidelines, once per week for eight consecutive weeks. The physiotherapists providing the usual physiotherapy were free to prescribe education, advice, manipulation and exercise as usual but could not refer patients to an exercise group or a walking programme. Similarly, Mannion et al. (1999) compared modern active physiotherapy, muscle reconditioning on training devices, and low-impact aerobics, each done twice a week over 3-months. Modern active physiotherapy was considered to be 30 minutes of individual therapy focused on improving functional capacity and instructions on ergonomic principles. This involved isometric exercises, Theraband exercises and use of general-strength training devices. In addition patients were given home exercises and encouraged to perform them. As is quite typical in many studies the specifics of what was actually done in terms of exercises and all acute variables remains a mystery. Muscle reconditioning involved 12-weeks on the David Back Clinic programme in groups of two to three, which uses progressive isoinertial strengthening in all three planes of motion in a patient’s pain free range of motion. Sessions are proceed by a 5-10 minute cycling or stepping warm up, and relaxation and further undefined strengthening exercises were done between isoinertial exercises. The aerobics and stretching class consisted of a class with 12 people maximum, lasting 1-hour done to music. The initial 20 minutes was used for static stretching and low intensity whole body aerobic exercise. This was followed by 30 minutes of exercises targeted primarily at the legs and trunk. The last 15 minutes was used for cool down and relaxation. 148 participants met the inclusion criteria and 16, 10.8%, dropped out during the study. The three groups did not differ significantly in terms of compliance with 84.1% completing all 24 sessions. Interestingly in both studies all interventions were equally efficacious, despite all three interventions targeting different aspects of physical conditioning. Mannion et al. (1999) suggest this shows that the mechanism of benefit may be more central and possibly due to challenging beliefs around physical activity and chronic low back pain. This is further supported by the correlation between improvement in fear avoidance beliefs and self rated disability. Furthermore these correlations were also present in the devices and aerobics group where these effects were still seen at 6-months, but not in the active physiotherapy group where they were not seen. There were also improvements in spinal flexion and these improvements were correlated with improvements in pain and intensity and self-rated disability. Hurley et al. (2015) highlight that whilst there was no difference in outcomes, the walking programme had the greatest adherence and the lowest costs.

Vincent et al. (2014) compared total body resistance training with lumbar extensor training and a control group in obese individuals. Resistance training sessions were carried out three times a week for 4-months. The total body training group did one set of 12 exercises, for 15 repetitions at 60% of repetition maximum, with 60 seconds rest between sets. Load was increased approximately 2% every week to maintain a BORG perceived exertion from 16-18. The lumbar extension group did just the lumbar extension exercise from the total body resistance-training group. For the first week they did two sets once a week and after that they did one set once a week with same acute variables as the total body group. As is typical in these studies no information on the tempo of the exercises was provided. The control group received advice on healthy nutrition via leaflet from the American Heart Association, information about back pain and information on bodyweight back strengthening exercises. The total body training group had greater reductions in self-reported disability as measured on the Oswestry Disability Index and Roland Morris Disability Questionnaire. Pain Catastrophizing Scale scores decreased in the total body training group more than in the control group at age 4-months. Lumbar extensor training and total body training both decreased walking and chair rise pain severity significantly more than the control. From this it is tempting to imply that the lumbar extensor training was sufficient to improve physical function whilst the total body training provided additional benefits to perceived disability and psychosocial factors.


3.5.3 Psychosocial approaches: Pain education

Five studies looked at more directly addressing the psychosocial component of patient’s pain experiences, two of which looked specifically at the effects of pain education and were considered low risk of bias. Moseley and colleagues (2004) conducted a randomised controlled trial comparing pain neurophysiology education with traditional back school education. Each subject took part in a 3-hour 1:1 education session, which included a 20-minute break for a drink. Diagrams and hypothetical examples were used to convey ideas. The experimental neurophysiology education focused on the functional significance of the nervous system, nociception, synapses and how chemicals talk to each other, and the plasticity of the nervous system including peripheral and central sensitisation and movement control. The control group received more typical back education. This covered the anatomy of the spine including the vertebrae, intervertebral discs, trunk and back muscles, normal spinal curves, posture and movement. This included analysis of lifting technique in terms of joint forces and intradiscal pressures, lifting techniques loads and ergonomic advice, as well as advice on stretching, strengthening, endurance and fitness. No information on the nervous system was included. At the end of the session participants were given a 10 section workbook and asked to complete one section a day, each week day for 2-weeks, and then asked to answer the three questions at the end of each section. Subjects returned for assessment 15-week days after the initial assessment. This resulted in significant improvements in pain attitudes, pain catastrophizing scale, straight leg raise and forward bend. Roland Morris Disability Questionnaire was statistically significantly improved although the authors suggest this probably was not a clinically significant improvement. Thus suggesting significant benefits in nervous system based education

Vowles et al. (2007) looked at the effect of pain acceptance, pain control and continued practice instruction strategies on physical impairment, in 74 unemployed individuals on workers compensation with LBP for greater than 3 months. Participants were sent a Beck Depression Inventory, Fear of Pain Questionnaire Short-Form, Pain Anxiety Symptoms Scale-20, McGill Pain Short Form Questionnaire, Chronic Pain Acceptance Questionnaire and the Physical Impairment Index to complete before attending their appointment. The Physical Impairment Index involves seven standardised physical tests; spinal tenderness, a 10 seconds hold of both feet 6 inches off the floor in supine, a 10 seconds hold of both shoulders 6 inches off the floor in supine, total flexion, total extension, total side flexion and passive straight leg raise. After each task patients were asked to rate their pain on a scale of 0-10. These scores were added to create a composite pain score. The instructions for the first test were the same for all participants. For the second test participants were randomised in to three different groups, pain control, pain acceptance and continued practice. The pain control group instructions emphasised that it was possible to control pain through mental strategies or efforts and asked patients to prevent pain during tasks. The pain acceptance group instructions emphasised that pain did not need to influence activity and asked participants not to let pain influence their performance. The continued practice group were asked to continue as they had before, and were informed that improvements can occur with practice. At Baseline the acceptance group had significantly higher levels of physical impairment than the continued practice group. There was no significant difference with the pain control group. After the intervention the pain acceptance group reduced their scores by 16.3%, whilst there was a worsening of 8.3% in the pain control group and 2.5% reduction in the continued practice group. Interestingly there was no significant difference across groups in terms of pain during the tasks. This suggests that the pain acceptance strategy allowed the patients to improve their physical performance without any increase in pain. Conversely it suggests the pain control group had increased physical impairment with no improvement in pain. The authors note that 124 people in total were asked to start the trial and only 91 started. They state that authors experience suggested that the patients that refused to take part were afraid of exacerbating their symptoms. This skews the population of the study towards those who were more likely to do well with this intervention. Nonetheless it provides what appears to be an immediately useful approach for clinicians to use in explaining how to approach pain during exercise and activities of daily living. The combination of pain acceptance with pain neurophysiology education may prove even more advantageous but this remains to be seen.


3.5.4 Psychosocial approaches: Intensive cognitive behavioural therapy and functional restoration programmes

Three studies looked at what could be considered intensive rehabilitation programmes, with functional restoration and CBT components. Pfingsten and Hilderbrandt (2001) reported on the results of the functional restoration programme which they trialled over 10 years with 762 CLBP patients, from 1990 to 2000. This was lowest quality study of those identified, with no randomisation, blinding and no explanation of drop outs. Nonetheless, studies such as this provide inform us of methods utilised with this patient group. As expected patients who were off work had increased psychosocial and pain symptoms compared with working patients. Their programme consisted of a 3 week pre-programme of education, stretching and bodyweight exercises followed by an intensive 7 hours a day outpatient programme for 5 weeks. This involved aerobic, functional strength and endurance exercises, back school education, cognitive behavioural group therapy, relaxation training and vocational counselling. The programme reduced Numerical Rating Scale, Pain Disability Index, Allgemiene Depressionsskala (amount of depression), psychological distress (Fear Avoidance Beliefs Questionnaire) and healthcare utilisation. Furthermore work capability significantly improved. However, when they modified it to remove the work hardening component there were no such improvements. These results remained stable at 12-month follow up.

Two studies with a low risk of bias using intensive psychosocial based physiotherapy interventions were identified (Alaranta et al. 1994 and Lee et al. 2013). Alaranta et al. (1994) looked at a combined psychosocial activation and physical intervention in CLBP compared with an inpatient rehabilitation programme in 152 patients, with a control group of 141. All patients had been referred to receive inpatient rehabilitation in Finland. Subjects were stratified according to sex and age and randomised to either group. Both interventions started 3-weeks after assessment and lasted 3-weeks. The intervention group received 37-hours of guided self-controlled physical exercises, without passive physical therapy and 5 hours of discussion groups a week, and individual consultations for work problems. The programme included a range of cardiovascular activities and games, strength and endurance training based off the patients 1 repetition maximum, stretching, relaxation and cognitive-behavioural disability management groups. This group did not receive any passive physiotherapy. The inpatient therapy involved a large amount of passive therapy as well as back education, pool exercises, indoor and outdoor activities. The authors considered this programme to be 40-50% of the intensity of the intervention group. The other study (Lee et al. 2013) directly assessed psychosocial treatment in CLBP patients aged 18-55, with Orebro Musculoskeletal Pain Questionnaire scores of 106-145 indicating moderate psychosocial risk factors. Patients were randomised to either an integrated work rehabilitation group or the conventional treatment group. Physiotherapists in this study had postgraduate qualifications and had received training in the cognitive behavioural approach. Patients received individual treatment for up to 3 months. Conventional treatment typically involved a combination of electrophysical agents, lumbar traction, manual therapy, and exercise therapy. Dictated by the patients’ symptoms at presentation and on their response to treatment. The cognitive behavioural approach group received an individualised graded activity programme, pacing techniques, work conditioning, return-to-work goal setting, self-management strategies, job analysis, and ergonomic advice. The aim was to improve their physical and functional capabilities with thorough attention to return to work. The researchers took the step of calling patients who missed an appointment to remind of them of their next appointment. Patients were discharged when they were able to return to work, had a subjective improvement of 70% or greater or they reached a plateau.

In both studies the authors suggest the results for the primary intervention group are clinically significant. Alaranta et al. (1994) found that at 3-months lateral trunk flexion, trunk rotation and hamstring flexibility was 11-12% increased in the combined group compared with 2-9% in the inpatient group. Abdominal, back and squatting strength improved significantly more in the intervention group in comparison to the inpatient group. These trends remained at 1-year follow up. The intervention group had greater decreases in pain at 3-month (17.1 vs 9.1) and 12-month (15.9 vs 8.9) follow up as measured using the Million index. Usage of physiotherapy and medical services was significantly decreased in both groups with the intervention group performing best. Mean days of sick leave per year decreased by 14 days in the intervention group, although this was not statistically superior to the inpatient group. At baseline to 3-months and at 12-month follow-up there were significant improvements in depression, subjective symptoms, aspects of personality, beliefs in disease and control and psychosocial adjustment in both groups. Similarly Lee et al. (2013) found that at discharge, the patients in the cognitive behavioural approach group made significant improvements in work recovery expectation, pain self-efficacy, and were more satisfied than the conventional treatment group.


3.5.5 Classification based approaches

Two trials with low risk of bias using a classification-based approach were identified (O’Sullivan et al. 2015 and Vibe Fersum et al. 2013). Both approaches used the Cognitive Functional Therapy (CFT) approach developed by O’Sullivan (Dankaerts and O’Sullivan 2011).

O’Sullivan et al. (2015) recruited 47 patients with at least a 1 year history of NSCLBP to a waiting list. 26 met all the selection criteria and underwent an initial 3-months on waiting list where they repeated the baseline assessments at 6-weekly intervals. The study did not have a control group, but went to extensive lengths to establish that participants had a stable condition and establish a clear baseline for the group. Based on the STarT Back screening tool scores, 14 patients were high risk, eight were moderate, and four were considered low risk. These scores indicate that these patients had yellow flags. They were then put through a cognitive functional therapy programme, which, focused on improving functional movements and postures, and tackling pain behaviours. In addition they took patients through cognitive reconceptualisation of their NSCLBP experience. Questioning of beliefs around pain, their relationship to pain, pain coping, and the relationship of stress with their pain were assessed. The primary outcomes were the Oswestry Disability Index and the Brief Pain Inventory, the average of four pain scores, maximum, minimum, average and current pain in the last 24 hours. An average of 7.7 treatments was conducted over 12 weeks. Oswestery Disability Index scores were 22 points lower after treatment, 23 points lower after 3 and 6 months and 24 points lower after 12 months. The initial reduction equates to a 54% reduction from baseline. Pain scores were 1.6 points lower after treatment, 1.5 and 1.6 points lower after 3 and 6 months and 1.7 points lower 12 months. All these results represented statistically significant reductions.

Vibe Fersum et al. (2013) unusually specified that participant’s pain was provoked and relieved by specific activities, movements or postures. The numerical rating scale needed to average at least 2/10 over the proceeding 14 days and the Oswestry Disability Index needed to be greater than 14%. The authors state the selection criteria designed this way to select patients whose movement behaviour had a clear association with their pain disorder. Patients with greater than 4 months sick leave were excluded on the grounds that they would require a specific return to work programme. 121 participants met the inclusion criteria and were randomised to receive either a cognitive behavioural functional therapy or manual therapy and exercise. The three physiotherapists delivering the approach were experienced exponents of using a multidimensional classification system. Based on the classification system each patient received a tailored intervention targeted at improving the cognitive, movement or lifestyle component the classification system suggested was maladaptive or provocative. The Oreboro Musculoskeletal Pain Questionnaire was also used to target psychosocial interventions. The intervention had four main components. For each patient their vicious cycle of pain was explained in a personalised diagram based on their assessment findings. Specific movement exercises designed to normalise their maladaptive movement behaviours were given based on their movement classification diagnosis. Functional restoration based on the movements they reported avoiding or provocative, and a physical activity programme tailored to the movement classification. The initial session was 1 hour and follow-ups were 30-45 minutes. Patients were initially seen once a week for 2-3 weeks and then progressed to follow-ups every 2-3 weeks over the course of the 12-week intervention. The comparison group received joint mobilisation or manipulation techniques to the spine or pelvis as delivered by specialists in orthopaedic manual therapy with an average of 25.7 years experience. These physiotherapists had no prior experience of the classification system or cognitive behavioural functional therapy. 82.5% of the patients received exercises based on the physiotherapists’ findings. Initial appointments in this group were 1 hour and follow-ups lasted 30 minutes. Both sets of therapists underwent a half-day of training with a clinical psychologist on the concepts of a best practice cognitive approach to managing back pain. Both groups received 8 sessions on average. Their primary outcome measures were pain was measured using the pain intensity rating scale and the Oswestry Disability Index. A validated 15-item scale to self-evaluate back specific function. There is some confusion over the pain scale used as the test suggests it was average pain over the proceeding two weeks, whilst the table reporting the data suggests it was one week. There was no difference in medication usage between groups before or after treatment. A lack of compliance withdrawal was set at 50%, leading to 27.1% of the manual therapy and exercise group, and 17.7% from the cognitive functional therapy group failing to complete treatment, which precluded an intention to treat analysis. After the intervention average pain over the last week decreased from 5.3 to 3.8 and stayed 3.8 at 12-month follow up, in the manual therapy group. In cognitive functional therapy group it went from 4.9 to 1.7, and crept back to 2.3 at 12-month follow up. The Oswestry Disability Index decreased from 24.0 to 18.5 after intervention and was 19.7 at 12-month follow up in the manual therapy and exercise group. In the cognitive functional therapy group it decreased from 21.3 to 7.6 and was 9.9 at 12-month follow up. These results were all statistically significant in favour of cognitive functional therapy over manual therapy and exercise. It is clear which intervention they were hoping to prove effective and it is possible that increased effort consciously or unconsciously may have gone in to the treatment group. Further the clinicians treating the control may well have been less invested in the outcome of the subjects they treated. This may account for the treatment group receiving 30-45 minutes for follow-ups compared to 30 minutes in the control group. Nonetheless the results are in keeping with those of O’Sullivan et al. (2015) highlighting the benefit of a classification-based approach.

3.6 Discussion

Given the significant nature of the problem of chronic low back pain it is surprising only 10 studies met the inclusion criteria. These studies show a consistent pattern that a variety of interventions are able to decrease psychosocial symptoms, improve function and decrease perceived pain. Disappointingly none of the research on the popular Maitland and McKenzie approaches met the inclusion criteria. Of the studies included the reporting of how interventions were carried out is often not sufficient to allow reproducibility or use in practice.

Of all the studies those using the CFT approach had the most positive effects as measured by disability and pain. The other particularly effective approach was the walking programme of Hurley and colleagues (2015) which had the same effect as their exercise group and usual physiotherapy interventions for pain, disability and psychosocial measures but the walking programme had greater adherence and lower costs. This fits with some of the emerging research in whiplash pain which suggests a low cost telephone based intervention was equal to a more expensive and time intensive motor control intervention (Michaelef et al. 2014).

The admittedly very limited selection of two studies (Weiner et al. 2003, 2008) suggests that whilst passive interventions could positively affect pain, the addition of general conditioning was required to reduce fear avoidance. Similarly, Vincent et al. (2014) found that the lumbar extensor strengthening was sufficient to increase physical function but the total body programme was required to improve perceived disability and psychosocial measures. Improvements in fear avoidance beliefs are often associated with improved function (Crombez et al. 1999) nonetheless in these studies it appears that active treatment such as walking or whole body exercise is required to improve psychosocial measures. There were only two education-based studies but the positive results suggest pain acceptance and neurophysiology education in combination should be useful. The results from intensive functional restoration and CBT programmes suggests these kind of multidisciplinary programmes are effective across all measures, with Pfingsten and Hilderbrandt (2001) noting the importance of work hardening in promoting return to work.


3.7 Conclusion

Considering that CLBP is the leading cause of disability worldwide and those with yellow flags are known to suffer the worst and contribute most to societal cost it is surprising how few studies met the selection criteria. This review has shown that whilst the term yellow flags are used in the assessment literature and guidelines, the term psychosocial and the factors that make it up are used in the treatment literature. The studies selected highlight that passive, active; more comprehensive and simple education interventions can all positively impact the pain experience of this patient group. While passive interventions can improve pain, more whole body active approaches such whole body weight training or walking may be necessary to positively impact the psychosocial aspects. Comprehensive CBT and functional restorations are effective but the inclusion of work hardening may significantly aid in return to work. Pain education approaches involving pain neurophysiology education and pain acceptance were both effective compared with more traditional back school and pain avoidance approaches respectively. A combination of these may be useful clinically. The CFT approach was the most effective in terms of disability and self reported pain. Thus despite the lack of investigation in to several of the most prominent approaches this review shows the breadth of approaches available to clinicians.


Diet And Lifestyle As A Potential Cause Of Non-Specific Chronic Low Back Pain

Written by Kieran Macphail on . Posted in Back Pain and Diet, For Diet and Lifestyle Professionals, For Health Professionals, For Movement Therapists, Low back pain, Nutritional therapy

Low back pain (LBP) is usually defined as pain localised below the costal margin and above the inferior gluteal folds. It is the leading cause of disability worldwide and is becoming increasingly prevalent (Harkness et al. 2005, Hoy et al. 2012, Vos et al. 2012). Chronic low back pain (CLBP) is variously defined as lasting longer than 7-12 weeks, to 3 months (Anderrson 1999, Frymoyer 1988). LBP is typically classified as “specific” or “non-specific”. Specific LBP refers to symptoms caused by specific pathophysiologic causes, such as hernia nucleus pulposus, infection, inflammatory disease, osteoporosis, rheumatoid arthritis, fracture or tumour (Van Tulder and Koes 2010). There is no effective cure for non-specific low back pain (NSCLBP) (Van Middelkoop et al. 2011) and this represents 90% of the LBP population (Deyo et al. 1992). Most guidelines are based on the assumption that symptoms resolve spontaneously and that the prognosis is favourable. This assumption is founded on studies using return to work as an outcome (Anderrson 1999, Van Tulder et al. 2006). When pain is assessed it appears patients may be returning to work despite their pain (Bowey-Morris 2011). A recent systematic review found that whilst spontaneous recovery occurs in approximately a third of patients after 3 months, 71% still have pain after 1 year (Itz et al. 2013).
The etiologic factors remain to be ascertained for these patients. There have been many studies highlighting the lack of correlation between radiologic findings and LBP in asymptomatic (Baker 2014, Jensen et al. 1994) and symptomatic individuals (Chou et al. 2011, Endean et al. 2011). Even in patients with incidental findings tracked for 3 years there is not a strong association (Suri et al. 2014). The incidence of lbp is 2-4 times higher in Sweden, Germany and Belgium, compared with Nigeria, south China, and South East Asian farmers. Within lower income countries the incidence is lower in rural areas (Volinn 1997). A recent systematic review found a strong positive correlation between a country’s development and the prevalence of LBP (Hoy et al. 2012). These epidemiological features are similar to the prevalent conditions of western society such as diabetes, heart disease and cancer (Wild et al. 2004, Yusuf et al. 2001, Jemal 2011). Thus it may be that diet and lifestyle factors may play a role in the pathogenesis of CLBP.

Pain Physiology, Diet and Lifestyle

The neuromatrix theory of pain (Melzack 1990) outlines how pain is an output of the integration of nociceptive, cognitive and emotion-related input. Building on this Chapman, Tucket and Woo Song (Chapman et al. 2008) propose the nervous, endocrine and immune systems could be viewed as a “supersystem”. This “supersystem” is responsible for the output of chronic pain. Dysregulation of this “supersystem” could lead to chronic pain. They suggest dysregulation could occur due to genetic, epigenetic and environmental factors. Thus in both these models diet and lifestyle could play a role in causation and management of chronic pain through impacting the nervous, endocrine and immune systems, as well as others.

The Neuromatrix

Figure 1. Neuromatrix of Pain

Mechanical pain starts as nociceptive input from a nococipetor through group IV afferents, otherwise known as group C nerve fibers in the periphery. They synapse with second order neurons in the dorsal horn of the spinal cord, where they become part of the spinothalamic tract. From there, thalamocortical fibers, our third order neurons, transmit noxious stimuli to the limbic system where the brain “decides” to place a pain “neurotag” at the location of the original nociception (Moseley 2003).

Nociception transmission from the periphery

Figure 2. Nociception transmission from periphery to brain (Scholz and Woolf 2002)

In chronic pain the threshold for firing of the group IV afferents and other nociceptors is decreased. In this state it takes fewer inflammatory mediators such as prostaglandins, leukotrines, bradykinin, serotonin and cytokines to bind on their respective receptors on the nociceptors to stimulate nociceptive input.

Inflammation and nociception

Figure 3. Inflammation and Nociception (Seaman and Faye 2005)

An alternative situation is that the level of pro-inflammatory mediators could be increased due to diet and lifestyle as shown as biochemical injury in figure 3. Diet and lifestyle factors can increase the quantity of inflammatory mediators in specific tissues. This reduces the need for additional pro-inflammatory mediators to bind to the afferent to reach threshold (Seaman 2002). In reality the two situations may occur simultaneously to different levels contributing the CLBP experience.

Diet and Lifestyle and Chronic Low Back Pain

Diet and lifestyle has received limited research as a causative factor in CLBP. Pronk and colleagues (2010) examined the effects of an “optimal lifestyle” on chronic health problems over 2 years in 6848 healthy working subjects. They defined optimal lifestyle as, abstinence from smoking, adequate physical activity, eating 5 servings of fruits and vegetables each day, and consuming limited or no alcohol. Adherence to 3 of 4 principles was associated with lower near-term incidence of back pain, and adherence to all 4 increased the protective effect. When viewed in the context of Minich and Bland’s (2013) definition of lifestyle medicine it is evident there are many other factors that could be considered, as shown in table 1.

Table 1. Lifestyle Medicine Factors

Lifestyle Medicine

* Items in bold added to Minich and Bland’s (2013) definition

Lack of physical activity is associated with an increased risk of CLBP (Nilsen et al. 2011) but the key contributing environmental factors are work to rest ratio (Dijken et al. 2008), the physical demands (Hoogendoorn et al. 1999, Thorbjornsson et al. 2000). Breathing pattern disorders are common among symptomatic chronic pain patients (Perri and Holford 2004) and large-scale studies have found correlations with LBP frequency (Smith et al. 2006) and LBP development (Smith et al. 2009). This may be due to biomechanical (Rousell et al. 2009, Grimstone and Hodges 2003) and biochemical mechanisms (Chaitow 2004).

Table 2. Physical, Biochemical and Psychological Contributions of Breathing Patterns to Chronic Low Back Pain

Physical, Biochemical and Psychological Contributions of Breathing Patterns to Chronic Low Back Pain

Similar association have been found for sleep with a 13-year follow up study of LBP among 360 Finnish fire-fighters highlighting those with sleep disturbances were 2.4 times as likely to develop LBP (Lusa et al. 2014). Poorer sleep quality and efficiency in NSCLBP patients is well established via self-reported measures (Kelly et al. 2010) and sleep disturbance increases by 10% for every point increase on a 0-10 visual analogue scale (VAS) in LBP patients (Alsaadi et al. 2011), although there is no difference in sleep quality measured by actigraphy (van der Water et al. 2011).

Nutrition has been investigated as an etiologic factor in NSCLBP through cardiovascular risk factors. Obesity and being overweight are well-established risk factors for NSCLBP (Shiri et al. 2010b). This may be due to increased weight bearing but also due to the secretion of pro-inflammatory mediators such as CRP, interleuikin 6 and tumour necrosis factor by adipose tissue (de Heredia et al. 2012). More specifically atherosclerosis of the aorta and stenosis of the arteries supplying the lumbar spine are associated with disc degeneration and LBP (Kauppila 2009). Furthermore, in a study of over 18 000 Norwegian subjects with and without LBP over 11 years there was an association between low HDL lipids and elevated triglycerides after adjusting for confounding variables (Heuch et al. 2014). Similarly, low vitamin D status is associated LBP among Egyptian women (Lotfi et al. 2007). All these factors can be seen as markers of chronic systemic inflammation and this may be the common thread explaining the associations.
Epidemiological research has suggested meat and fruit consumption is associated with reduced LBP incidence whilst fish consumption is associated with an increased incidence of LBP. Lower omega 6 and polyunsaturated fatty acid intake appeared protective, as did high intakes of carotene and vitamin B6 (Perry et al. 2010). Of the minerals perhaps magnesium deficiency is the most likely to contribute to CLBP. It can enhance nociception and inflammation via neurogenic inflammation (Durlach et al. 2001). Animal models show magnesium deficiency leads to increased serum substance P, which stimulates immune cells and platelets to release pro-inflammatory mediators (Rang et al. 1994).
Of the other nutrition related factors there is a paucity of research investigating the influence of hydration and other beverages on LBP. Alcohol consumption does not appear to be associated with LBP (Ferreira et al. 2013). In addition, nutrition related conditions such as irritable bowel syndrome can impair motor control of the lumbar spine through inhibiting deep stabilizer muscles essential to lumbar spine stability (Tremolaterra et al. 2006, Wallden 2013).
Psychological stress can directly influence the musculoskeletal, endocrine, immune and nervous systems through the limbic system modifying chronic pain (Macphail 2014). Psychosocial risk factors for LBP chronicity are well known to lead to worse outcomes (Grimmer-Sommer 2008). Indeed the assessment of psychosocial factors is included in most guidelines for the management of LBP worldwide (Koes et al. 2010). Childhood abuse is associated with an increase in peripheralising of LBP later in life (Leisner et al. 2014) suggesting psychological processes can modify the pain experience even later in life.
Environmental factors have received little attention in the CLBP literature. A Meta-analysis of studies up to 2009 found that former smokers had a higher prevalence of LBP than non-smokers and lower incidence than current smokers (Shiri et al. 2010a). Similarly a systematic review of twin studies found smoking significantly associated with LBP (Ferreira et al. 2013). Sun exposure and secondary low vitamin D status is also associated LBP among Egyptian women (Lotfi et al. 2007).
Thus it may be that diet and lifestyle factors play a significant role in the pathogensis of chronic low back pain. This role should be considered as part of the potential contributors to the pain experience and the brains “decision” to place a “neurotag” in the low back area.


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C-Reactive Protein, Chronic Low Back Pain and, Diet and Lifestyle

Written by Kieran Macphail on . Posted in Back Pain and Diet, For Diet and Lifestyle Professionals, For Health Professionals, For Movement Therapists, Nutritional therapy


C-Reactive Protein (CRP) is best known as an acute phase protein and is typically assessed in most general blood work. High sensitivity CRP (hsCRP) may be a useful clinical marker of chronic inflammatory states in musculoskeletal conditions. It appears that it is raised in inflammatory chronic low back pain (CLBP) and associated with reduced pain thresholds, weakness and reduced function. It is also possible CRP could contribute towards the development and maintenance of CLBP by activating the complement system which increases peripheral nociception. Diet and lifestyle factors can promote raised CRP. A hsCRP level of < 1mg/l appears ideal and the higher the level the more emphasis should be placed on chronic inflammation as a contributor to symptoms. Diet and lifestyle can significantly reduce CRP levels and may be a useful adjunct in treating CLBP patients with elevated CRP. This might make CRP a useful clinical marker of inflammation in CLBP and a therapeutic target for diet and lifestyle interventions.


C-Reactive Protein (CRP) is best known as an acute phase protein and is typically assessed in most general blood work. More recently high sensitivity C-reactive protein (hsCRP) has been used in cardiovascular research as a marker of chronic inflammation. As chronic low back pain (CLBP) can have an inflammatory component it would be useful to have a clinical marker to assess in practice. Furthermore it may help us understand a component of how diet and lifestyle can influence CLBP.

C-Reactive Protein and Chronic Low Back Pain

In the 1940s CRP was considered as a possible marker of chronic low level inflammation but the standard assay lacks the sensitivity to determine normal ranges. Since the advent of the hsCRP test large-scale epidemiological studies have identified that CRP is a strong independent risk factor of future myocardial infarction, stroke, peripheral arterial disease, and vascular death among individuals without known cardiovascular disease [1]. In cardiovascular disease hsCRP is a sensitive and specific measure across many populations.  As these conditions are associated with inflammatory processes it is possible hsCRP may be a useful marker of chronic inflammation in musculoskeletal conditions such as chronic low back pain.

More recently CRP has received attention as a marker of chronic inflammation in musculoskeletal conditions. Chronic inflammation has been associated with arthritis [2], and chronic musculoskeletal injuries  [3-5]. Repetitive tissue injury has been theorised to contribute to lower level rises in chronic inflammation [3]. Inflammation and pain are intimately interrelated and pain perception may be higher in those with raised CRP. In a study of 99 pairs of twins, higher levels of CRP were associated with lower pain thresholds and increased pain sensation [6]. Similarly, in cancer patients CRP is significantly correlated with perceived pain [7]. Thus a hsCRP test could provide insight in to the inflammatory contribution chronic pain states.

CRP is also associated with poorer function in symptomatic individuals. Carp et al [4] found asymptomatic subjects averaged 0.8 mg/l, whereas those scoring 50-74 on the upper body musculoskeletal analysis (UMBA) averaged 1.8 mg/l, and those scoring over 75 on the UMBA averaged 5.4 mg/l. Interestingly, CRP was more strongly correlated with symptom levels than IL-1β, TNF-α and IL-6. Suggesting CRP may be the more clinically useful marker. These results are similar to that of Ravaglia et al [8] who found CRP levels were related to functional impairment. Cesari at al [9] found older adults with a CRP >6 mg/l had significant weakness and poorer physical function compared with those with a CRP <6 mg/l, conditions that may lead to chronic pain states. Carp et al explain their results by suggesting that worse disability is caused by worse injury and thus a greater acute phase response. However, injury and disability are not necessarily strongly associated. For example data from the LAIDBACK study has shown that at 3 years there is not a strong correlation between lumbar spine magnetic resonance imaging findings and symptoms [10]. It may be that in some patients it is the systemic inflammatory level that may be influencing the disability.

The association between raised CRP and CLBP is controversial. Studies looking at inflammatory pathologies such as herniated discs [11,12], nerve root inflammation [11], sciatica [13], and Modic changes [14] have shown positive correlations. Whereas those with smaller sample sizes and inclusion of acute and chronic patients in one heterogenous group have failed to show associations [15,16]. Briggs et al [17] conducted a population based study using 15 322 participants examining CRP levels, obesity and low back pain (LBP). They found that those with CRP levels of >30.0 mg/l had nearly twice the odds of reporting LBP. It should be noted they used standard CRP assessment and thus the figures are higher than for the hsCRP. Additionally, those with a body mass index >30 and elevated levels of CRP were 2 to 3 times as likely to report LBP. They found a significant association between LBP and elevated CRP, suggesting CRP could be a valuable marker of chronic inflammation in CLBP patients.

CRP is more than a useful marker and can contribute towards the development of chronic pain. Animal studies have suggested raised CRP plays a role in the chronic inflammation that leads to reduced tissue tolerance, and paves the way for chronic pain states [19]. Further, CRP may contribute to the initiation and continuation of joint pain [20]. In cancer patients elevated CRP can modulate pain [21] and contribute to the amplification and persistence of pain [22]. CRP can be viewed as both a marker for the underlying processes involved in increased pain sensation and a direct contributor to increased pain sensation. CRP activates the compliment system, which in turn sensitises peripheral nociceptors [23]. Effectors of the compliment cascade impact peripheral nociceptive sensitisation through the release of soluble factors and interacting directly with nociceptors. For example C5a and C3a injection can cause behavioural hyperalgesia in rats. In addition effectors of the complement cascade activate mast cells, which can sensitise nociceptors in multiple ways [23]. Thus CRP could feasibly contribute to the progression towards and maintenance of CLBP.

Diet and Lifestyle May Increase C-Reactive Protein Levels

As CRP may contribute to the underlying pathogenesis of CLBP it is prudent to consider some of the contributing factors in this process. Diet and lifestyle are powerful modulators of CRP levels and thus may contribute to the pathogenesis of CLBP through this mechanism. Smoking has been found to be associated with raised CRP [24]. Sleep disorders and poor sleep quality are associated with elevated CRP [25,26]. Psychological stress has been linked with raised CRP when perceived stress is increased [27], and during depression and loneliness [28]. Increased dietary saturated fat increases CRP whereas an equal increase in unsaturated fatty acids did not [29]. Higher carbohydrate intake was associated raised CRP levels in overweight and obese individuals [30]. Of the minerals magnesium has perhaps been most closely associated with CRP. Current recommendations for magnesium intake range from 310-420mg per day. King et al [31] found those who consumed less than the RDI of magnesium were greater than 1.45 times more likely to have a CRP level over 3.0 mg/l. 68% of US adults consumed less than the recommended daily intake (RDI), with 19% consuming less half the RDI. Of the vitamins deficiencies in vitamins B6 and D have received some interest. B6 appears to be utilised as part of the inflammatory process and thus those with elevated CRP level have significantly lower levels [32]. The interest in vitamin D and CRP has come from cardiovascular research. Low plasma vitamin D status is inversely associated with CRP levels [33]. Exercise can have both a positive and negative effect on CRP levels. However, overtraining such as that caused by playing professional soccer has been found to cause elevation in CRP during the season [34]. These results fit with the theme that deviations from a “healthy” lifestyle are associated with elevations in CRP levels.

Clinical Use

Given that there is an association between CLBP and CRP levels it is suggested a hsCRP test may be a useful clinical marker for managing these patients. This needs to be considered within a broader framework of the multitude of bio-psycho-social factors that influence CLBP. The question of what level is significant is unclear. In the literature there is no consensus for its use in musculoskeletal conditions. Levels as low as >1 mg/l have used, whilst the highest used is >6.0 mg/l. Thus in practice the measure can be used non-diagnostically with an appreciation of the cardiovascular research. It needs to be remembered that levels may be spiked during acute infection, trauma and post intense exercise. A level >1 mg/l is likely indicative of increased systemic inflammation, the higher this figure is the more significant a contributor it should be considered.

Pharmacological approaches have been considered for modifying CRP levels, with statins being potentially the most promising but diet and lifestyle changes can significantly improve CRP levels. An 8-week mindfulness programme reduced CRP levels from 2.98 to 2.09 [35]. Similarly, an 8-week programme of exercise decreased CRP levels by 38% and improved function in automotive workers with low back pain [36]. As visceral adipocytes produce CRP reducing body fat levels is another potential therapeutic target, and a carbohydrate restricted has been shown to reduce CRP levels [37]. More broadly going from 2 to 5 or 8 portions of fruit and vegetables per day significantly reduced CRP levels [38]. Furthermore, in a study of 1200 Puerto Rican adults aged 45-75 the variety of fruit and vegetable intake but not the quantity was inversely related with CRP levels [39]. Specifically, vitamin C intake from fruit and plasma vitamin C levels was inversely related to CRP levels in a cross-sectional study of 3258 British men aged 60-79 [40]. Other substances high in antioxidants have been found to favourably alter CRP levels including coffee [41], fruit juice [42,43] and dark chocolate [44]. Thus, diet and lifestyle modification of CRP levels may prove an effective component of CLBP treatment and may help reduce symptoms through other mechanisms as well.


CRP may be a useful clinical marker of chronic inflammation in chronic low back pain. It appears that it is elevated in inflammatory CLBP and associated with reduced tissue tolerance, reduced pain thresholds, weakness and reduced function. It may also contribute to peripheral sensitisation as part of the progression towards and maintenance of chronic pain. Diet and lifestyle factors can promote raised CRP. A hsCRP level of < 1mg/l appears ideal and the higher the level the more emphasis should be placed on chronic inflammation as a contributor to symptoms. Diet and lifestyle can significantly reduce CRP levels and may be a useful adjunct in treating CLBP patients with elevated CRP.



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The Tripod Position

Written by Kieran Macphail on . Posted in Corrective Holistic Exercise Kinesiology, Crossfit, For Everyone!, For Health Professionals, For Movement Therapists

Left foot and right arm support. The right leg and left arm can support or move in to a stepping forward pattern.

Left foot and right arm support. The right leg and left arm can support or move in to a stepping forward pattern.










This position is the tripod is a variation of a static lunge taught as part of the Dynamic Neuromuscular Stabilisation programme according to Pavel Kolar, and correlates to the 8-9 month developmental age. The right arm and left foot are supporting and the left arm and right leg are stepping forward. The clinician can support the left knee and foot centration, trunk centration and uprighting of the spine. The most common zones of contact are the support leg VMO/ medial epicondyle and mid thoracic spine, most commonly at or just below the apex of the kyphosis.

The clinician can advise the patient to breathe diaphragmatically, using the inhalation to facilitate spinal extension and the exhalation to facilitate relaxation of tight musculature. E.g. support leg posterior hip rotators and soleus, stepping forward leg iliacus and rectus femoris, even the pectoral muscles and the more tonic cervical musculature. Similarly, the eyes can be used to facilitate trunk extension by encouraging the patient to look up, even if the head is kept in neutral. Alternatively, the patient could be encouraged to look down to facilitate the deep cervical flexors. Tongue position can be emphasised, by encouraging the patient to place the tongue on the roof of the mouth behind the teeth.

At the support stance foot the patient can be encouraged to spread the toes and load evenly through the foot, using tibial external rotation to facilitate a neutral longitudinal and medial arch. The patient can be encouraged to load the support leg heel and drive the knee forward to encourage soleus mobility and functional centration of the ankle. As this is done the middle of the patella should remain in line with the second toe in most patients. At the hip, the patient can be encouraged to increase the depth of the hip crease or find the centrated position. Frequently trigger points can be active in the TFL, and various parts of the hip flexors in this position. Often the clinician can use myofascial trigger pointing in the position to alleviate these symptoms. The trigger pointing will need to be applied prior to the trigger point becoming active. E.g. Apply as the patient gets in to this position.

On the stepping forward leg the patient can encouraged to start by loading the hallux and this position can be used to mobilise a hallux towards full plantarflexion. At the stepping forward hip the patient can be encouraged to maintain a neutral rotation of the thigh, by activating the internal rotators. Further, by encouraging loading of the supporting knee, centration of the supporting hip can often be better felt.

At the trunk the patient can be encouraged to elongate the cranium away from the coccyx to create upright of the spine. At the thoracic spine the patient can be encouraged to broaden the shoulder blades and lift the trunk up through the shoulders to promote serratus activation. On the support hand the patient can be encouraged to spread the fingers with the middle finger facing straight ahead, in conjunction with this the elbow should face backwards, facilitating activation of the external rotators of the right shoulder. As this is done loading should remain even across both the ulnar and radial sides of the hand. At the head retraction and cervical elongation can be cued, in very aware individuals this can sometimes be facilitated by promoting conscious relaxation of the tongue and throat.

The difficulty is choosing the correct cue to give, and just correcting the key dysfunction, as suggested by Lewitt. In the picture above I would probably suggest the patient focus on conscious elongation of the spine and then progress to using the breath to facilitate uprighting of the spine and relaxation of the posterior hip rotators of the support leg.

If you have any questions please comment below or email me at kieran@kieranmacphail.com

Psychology, The Limbic System And Chronic Musculoskeletal Pain

Written by Kieran Macphail on . Posted in For Diet and Lifestyle Professionals, For Health Professionals, For Movement Therapists

The limbic system is a key component of an individual’s psychology. Mood, personality and risk reward behaviour are all intimately related to limbic function. The amygdala plays a particularly important role in this regard. The “thought viruses” discussed by Butler and Moseley [1] highlight how the amygdala and hippocampus, in particular, interact to produce behaviours that may then increase the likelihood of musculoskeletal symptoms. These behaviours may become learned further influencing symptoms.

Mood can directly alter the pain experience. In a study of 65 patients, pain tolerance but not ratings was significantly affected by reading depressive, neutral or positive statements. With positive statements increasing pain tolerance and the converse true for negative statements [2]. This highlights just how important attitude is in hardiness in dealing with musculoskeletal symptoms. This may be heavily influence by personality type.

Personality plays an important part in how someone handles a musculoskeletal dysfunction. McFadden and Woitalla [3] report on a patient with four different personalities who reported different function and pain on visual analogue scale and McGill pain questionnaire in each personality. Personality type is associated with coping ability and is strongly associated with the severity of symptoms. For example patients with facial pain and headaches score higher on the Minnesota Multiphasic Personality Inventory, compared to patients with intracapsular temporomandibular joint disorders [4]. Type D or the “distressed personality”, is especially sensitive to musculoskeletal symptoms. Mils et al [5] compared the symptoms of cancer survivors with Type D personality with the remainder of 3080 subjects. 19% had Type D personality and they reported more back pain and osteoarthritis during the study. Similarly, in 5012 students aged 15-18, the 10.4% of boys and 14.6% of girls with Type D personality were twice as likely to have musculoskeletal pain, and five times more likely to have psychosomatic symptoms [6]. Furthermore in borderline personality disorder the key differences compared with controls on neuroimaging are found in the limbic system [7]. Specifically areas that control and regulate emotions show hypometabolism and limbic regions show hypermetabolism when activated. The amygdala in particular shows hypermetabolism in response to emotive images compared with controls.

The amygdala helps mediate the reciprocal relationship between chronic pain and negative affective states such as fear and anxiety. The amygdala has a known role in emotions and affective disorders, and it is now implicated in pain modulation and emotional responses to pain [8]. The lateral capsular division of the central nucleus of the amygdala is know as the nocciceptive amygdala, and appears to integrate internal and external environmental information with nocciceptive input. The amygdala can facilitate and inhibit pain at different levels of the pain neuraxis.

The “thought viruses” outlined by Butler and Moseley [1] highlight how the interactions between the hippocampus and amygdala can influence behviours that are associated with worse outcomes among chronic pain patients. Thoughts around the severity of symptoms and reducing activity to protect an area are all likely mediated at least partially through the limbic system. With memories of past advice and past experience retrieved from the hippocampus and the risk reward weighed up in the amygdala. These thoughts are known to be associated with withdrawing from normal activities and protecting painful areas of the body. This can lead to a lack of stress on connective tissues leading to atrophy, architectural disorganisation, fibrosis, adhesions and contractures. If inflammatory mediators are predominating then the tissue is more prone to fibrosis as opposed to atrophy [9]. Fibrosed and atrophied tissues are likely to lead to myofascial pain through differing mechanisms.

Taken a stage further, in some the pain experience will lead to receiving treatment or finding ways of managing the symptoms through altering posture. Others receive encouragement to rest and possibly watch television in bed. Over time this behaviour is positively reinforced through operant conditioning and pain and behaviour may become learned [10]. This can lead to sickness behaviours and again is further associated with poorer outcomes.

An individual’s psychology is an important factor influencing how people respond to musculoskeletal symptoms. A poor mood increases pain sensation. A type D personality is a significant consideration in patients with chronic pain, and is evidently associated with poor outcomes. The amygdala and hippocampus are integral to the circuitry that leads to “thought viruses” producing the protective behaviours linked with illness behaviour and worse symptomatology.  These behaviours may become learned and reinforced leading to the downward spiral towards chronic pain.

If you would like to discuss any of the topics discussed in this post feel free to email me on kieran@kieranmacphail.com or comment below.


1. Butler, D. S., & Moseley, G. L. (2013). Explain Pain:(Revised and Updated. Noigroup Publications.

2. Zelman, D. C., Howland, E. W., Nichols, S. N., & Cleeland, C. S. (1991). The effects of induced mood on laboratory pain. Pain, 46(1), 105-111.

3. McFadden, I. J., & Woitalla, V. F. (1993). Differing reports of pain perception by different personalities in a patient with chronic pain and multiple personality disorder. Pain, 55(3), 379-382.

4. Mongini, F., Ciccone, G., & Ibertis, F. (2000). Personality characteristics and accompanying symptoms in temporomandibular joint dysfunction, headache, and facial pain. Journal of orofacial Pain, 14(1).

5. Mols, F., Oerlemans, S., Denollet, J., Roukema, J. A., & van de Poll-Franse, L. V. (2012). Type D personality is associated with increased comorbidity burden and health care utilization among 3080 cancer survivors. General hospital psychiatry, 34(4), 352-359.

6. Condén, E., Leppert, J., Ekselius, L., & Åslund, C. (2013). Type D personality is a risk factor for psychosomatic symptoms and musculoskeletal pain among adolescents: a cross-sectional study of a large population-based cohort of Swedish adolescents. BMC pediatrics, 13(1), 11.

7. Lis, E., Greenfield, B., Henry, M., Guilé, J. M., & Dougherty, G. (2007). Neuroimaging and genetics of borderline personality disorder: a review. Journal of psychiatry & neuroscience, 32(3), 162.

8. Neugebauer, V., Li, W., Bird, G. C., & Han, J. S. (2004). The amygdala and persistent pain. The Neuroscientist, 10(3), 221-234.

9. Langevin, H. M., & Sherman, K. J. (2007). Pathophysiological model for chronic low back pain integrating connective tissue and nervous system mechanisms. Medical hypotheses, 68(1), 74-80.

10. Tyrer, S. P. (1986). Learned pain behaviour. British medical journal (Clinical research ed.), 292(6512), 1.

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