Atormac
Neurology India
menu-bar5 Open access journal indexed with Index Medicus
  Users online: 2065  
 Home | Login 
About Editorial board Articlesmenu-bullet NSI Publicationsmenu-bullet Search Instructions Online Submission Subscribe Videos Etcetera Contact
  Navigate Here 
 Search
 
  
 Resource Links
  »  Similar in PUBMED
 »  Search Pubmed for
 »  Search in Google Scholar for
 »Related articles
  »  Article in PDF (1,221 KB)
  »  Citation Manager
  »  Access Statistics
  »  Reader Comments
  »  Email Alert *
  »  Add to My List *
* Registration required (free)  

 
  In this Article
 »  Abstract
 » Epidemiology
 »  Etiopathogenesis...
 » Approach
 » Imaging
 » Treatment
 »  Treatment of Acu...
 »  Treatment of Chr...
 »  Treatment of Spe...
 »  Neurogenic Claud...
 » Conclusion
 »  References
 »  Article Figures
 »  Article Tables

 Article Access Statistics
    Viewed579    
    Printed9    
    Emailed0    
    PDF Downloaded91    
    Comments [Add]    

Recommend this journal

 


 
Table of Contents    
GUEST COMMENTARY
Year : 2019  |  Volume : 67  |  Issue : 3  |  Page : 671-678

Approach to non-compressive back pain


Department of Clinical Immunology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, Uttar Pradesh, India

Date of Web Publication23-Jul-2019

Correspondence Address:
Dr. Latika Gupta
Department of Clinical Immunology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow - 226 014, Uttar Pradesh
India
Login to access the Email id

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0028-3886.263183

Rights and Permissions

 » Abstract 


Back pain is the most common manifestation among rheumatologic conditions, with an 80% lifetime risk of development in each individual. Most patients have no specific identifiable etiology. Low back pain has always been an important public health problem, having a significant impact on the working class of the population. Hence, it is pertinent for the physician to be aware of the various causes of back pain and identify promptly the various red flags and poor prognostic markers. Lamentably, widespread access to technology and fear of litigation in this era of evidence based medicine has made us slaves of medical imagery in the context of back pain. It is crucial to recognize the teachings of ancient medicine, where keen observation, a detailed history-taking and a meticulous examination were the mainstay of good decision-making. Its precise management can help in obviating debility, preventing the work absenteeism, and consequently, decreasing health-care expenses.


Keywords: Back pain, management, nonspecific, non-compressive


How to cite this article:
Gupta L, Zanwar A, Misra DP, Agarwal V. Approach to non-compressive back pain. Neurol India 2019;67:671-8

How to cite this URL:
Gupta L, Zanwar A, Misra DP, Agarwal V. Approach to non-compressive back pain. Neurol India [serial online] 2019 [cited 2019 Dec 10];67:671-8. Available from: http://www.neurologyindia.com/text.asp?2019/67/3/671/263183

Key Messages: About 80% individuals experience back pain at least once in their lifetime, and more than a third progress to chronicity. Only a small proportion (15%) of patients with chronic low backpain have an identifiable etiology. Most patients with acute low back pain improve regardless of the specific management given. In its management, superficial heat is recommended and bedrest should be minimized. Pharmacotherapy is advocated when heat therapy fails; nonsteroidal anti-inflammatory drugs (NSAIDs) are the first choice medications. Acetaminophen is less effective and its use is limited to those with contraindications to NSAIDs. Non.benzodiazepine muscle relaxants can be used when the previous therapies fail. Opioids and tramadol should be reserved for refractory cases. Patients with risk factors for chronicity are best referred to a physical therapist at the earliest. A treatment failure at 4 weeks warrants a reassessment for chronicity, the red flag signs, and for a reevaluation of the etiology.




Back pain is a common rheumatologic condition known to humanity since the ancient times of the Papyrus.[1] Up to 80% individualsexperience back pain at least once in their lifetime.[2] The condition can often be frustrating for the physician and patient alike, often resulting in repeated visits to the hospital as well as work-absenteeism. The approach to treatment has evolved over the ages, from watchful waiting in the medieval times to diagnostic imagery at the dawn of the 21st century.

For classification purpose, low back ache (LBA) is defined as pain between the lower ribs and the gluteal folds, with or without non-neuropathic leg pain. Pain lasting for 24 h to 6 weeks is considered as acute, that lasting for 6–12 weeks is considered as subacute, and that lasting for more than 12 weeks is labeled as chronic LBA.[3] Up to 10% individuals experience back pain as a part of a neurologic syndrome, and 5% have other specific identifiable causes, while 85% have no specific identifiable etiology and come under the umbrella of nonspecific LBA [4] [Table 1].
Table 1: Causes of low back pain (LBP)

Click here to view


Like most other rheumatic disorders, chronicity is the hallmark of nonspecific back pain. Almost one-third of patients continue to suffer from back pain at 1 year. In those patients who improve, relapses are frequent.[5] A new episode is defined as a new onset back pain lasting for at least 24 h in a patient who has been pain free for 30 days; the pain should result in a significant and measurable decline in the functional status or in the scores assessed on a pain scale.


 » Epidemiology Top


LBA has always been an important public health problem, having a significant impact on the working class of the population. In this era of evidence-based medicine, global research is focused on defining the problem, as well as on determining new therapeutic modalities, both conservative and surgical. A PubMed search of “low back pain” returned 32,185 articles, of which one-third have emerged in the past 5 years.

The prevalence estimates of LBA from India paralleled those from rest of the world, with 750.2 annual years of healthy life lost per 100,000 individuals.[6] The effect is more marked in men. Around 42.4% young individuals are affected by the condition per year in India. Interestingly, one-fifth of them never consult a physician.[7] A recent data set from a World Health Organization (WHO) study which featured pooled analysis from six countries concluded that a poor socioeconomic and educational status are the key determinants of pain and the consequent disability. In the individuals assessed, 60% of Indians had no formal education, and 72% resided in rural areas, accounting for the highest percentage of patients in the high-intensity pain group, across all six nations.[8] This explains the rural–urban divide in rates of self-reported pain brought to light by a Community Oriented Program for Control of Rheumatic Diseases (COPCORD) study.[9] Myths concerning the condition as well as treatment are also prevalent in the Indian population, more so among the uneducated individuals.[10]


 » Etiopathogenesis of Nonspecific Back Pain Top


The discs, sacroiliac joints, and facets are the three potential pain generators in the spine. The latter two are most often implicated in the degenerative or inflammatory etiology, and present with chronic rather than acute low back pain (LBP). The widespread use of magnetic resonance imaging (MRI_ in the field of rheumatology has brought to light the common presence of lesions in the spine of healthy individuals. This has blurred the distinction between health and disease based on structural lesions, and explains the growing interest in understanding the role of pain pathways instead.

Often times called the 'non-injury model', this theory speculates that pain arises from a complex interaction between the nerve receptors within the connective tissues of the spine and the paraspinal muscles.[11] Hence, spinal lesions are no longer considered a necessary cause of back pain, and a benign muscle tension is considered as sufficient to explain the symptoms. It is well known that lumbo-pelvic kinematics are modified in patients with LBP. Disorganization of muscle function, documented by surface electromyography, while performing repetitive standing tasks, is a predictor of LBP development in previously pain-free individuals.[12] In addition, this muscle disorganization reduces with successful rehabilitation programs.

Researchers have also come to believe that genetics may have a greater role to play than previously thought, with the patients having LBP being predisposed to a naturally weaker capacity to withstand mechanical loading, which may be regarded as the second “hit” to the patient.[13]

Another evolving concept is that of spinal instability, wherein the neutral zone corresponds to the normal range of motion of each spinal segment. Displacement beyond this neutral zone triggers pain pathways.[14] However, the pain severity correlates poorly with spinal instability. This fact is well-demonstrable by dynamic imaging or with the success of surgical stabilization procedures.[15]

The concept of central pain sensitization syndrome has gained favor instead, with demonstration of augmented pain processing in the cingulate gyrus with functional MRI, as well as thinning of gray matter in areas responsible for inhibitory control.[16],[17] This central sensitization syndrome serves as a forerunner of pain amplification and its evolution to chronicity in predisposed individuals. Thus, chronic and nonspecific LBA finds its best fit in the spectrum of “fibromyalgianess,” explaining the natural history and the risk factors for persistence as well.


 » Approach Top


Most physicians experience a slight decline in enthusiasm when encountered with a patient complaining of pain back in a busy clinic. As a large majority of back pain syndromes are nonspecific, dismissal of the symptoms as unimportant may be a temptation one often times finds hard to resist. On the contrary, the widespread access to technology and the fear of litigation in this era of evidence-based medicine have made us slaves to medical imagery. In these times, it is common-place to find investigative medicine taking precedence over a good clinical examination, which is primarily dictated by the findings of an MRI at subsequent visits. An overview of the simplified approach to LBA is illustrated in [Figure 1]. Also, an approach to a suspected case having spondyloarthritis (SpA) is illustrated in [Figure 2].
Figure 1: Approach to low back pain

Click here to view
Figure 2: Approach to spondyloarthritis

Click here to view


It is crucial to recognize the teachings of ancient medicine, where a keen observation, a detailed history taking, and a meticulous clinical examination were the mainstay of good decision-making. Looking for red-flags signs [Table 2] comes handy, and should alert the physician to the presence of an underlying etiology that may need attention. It is in all such cases that one should not shy away from embarking on imaging. The diagnostic workup for specific etiologies has been summarized in [Table 3].
Table 2: Red-flag signs of low back pain

Click here to view
Table 3: Diagnostic workup in selected etiologies

Click here to view



 » Imaging Top


Plain radiography

The anteroposterior and lateral views demonstrate the general anatomy of the spine and lumbosacral alignment as well as the disc and vertebral body height. However, soft tissue structures are not properly evaluated by radiography. Oblique views are good for assessing the pars interarticularis and are best put to use for diagnosing spondylolysis. Findings of the “owl eye sign” (suggestive of anterior cord syndrome), the enlargement of the intervertebral foramen (indicating a pathology in the region such as a dumb-bell neurofibroma), and multiple lytic lesions or bony erosions (suggestive of an underlying spinal metastasis) should be looked for.[18] In patients with a past history of malignancy, MRI should be considered if radiological imaging is suspicious, or if the erythrocyte sedimentation rate is elevated, even when X-rays are normal.

Other special views include dynamic imaging of the lubar spine in flexion and extension to assess for instability, and an angled view of the sacrum to assess the sacroiliac joints for ankylosing spondylitis.

Computed tomography (CT)

The CT scan image can accurately depict the foraminal and extra-foraminal nerve root because the surrounding fat provides a natural contrast. The radiation exposure incurred to the pelvic areas limits its utility. Its use is limited to studies focused on the bone. Thus, it is often utilized in suspected fractures missed on plain radiographs.

Magnetic resonance imaging

The advent of MRI has enabled a comprehensive structural assessment of the spine, ranging from soft tissues to ligaments, and also of nerves. Recently, there has been a special interest in the lumbar vertebral body marrow and endplate lesions, termed “Modic changes.” These are seen as signal intensity changes in the end plate regions, particularly so in individuals with degenerative discs. They are classifiable as type 1, 2, and 3, representing histologic correlates of edema, fat, and sclerosis, respectively.[19] It has now become evident that Modic changes are fairly common in healthy individuals as well, and not always a forerunner of an inflammatory spinal disease. Intuitively, Modic lesions seem to be the imaging link between ongoing patho-mechanical processes in the degenerative spine. However, despite keen interest, researchers in the field have consistently failed to demonstrate a convincing correlation between these changes and the pain process.[20],[21]


 » Treatment Top


Of those patients who present with acute LBA, most of them do not have an identifiable cause, and lumbar sprain is most often implicated. Most such episodes subside by 2 months, only to recur later in the course of the disease.[5] Hence, management of acute back pain is focused on pain relief and improving function as soon as possible. The recurrence rates as well as severity, and duration of pain go on increasing with time. Eventual chronicity of LBP mandates consideration of balancing the benefit versus the risk of a treatment modality. As the etiology of chronic back pain is multifactorial, no single treatment modality is clearly superior to another. Treatment can be either nonpharmacologic or pharmacologic.


 » Treatment of Acute Nonspecific Lbp Top


Superficial heat is the standard of care. Heat reduces muscle spasm and facilitates improved mobility consequent to reduced pain. The effects are largely short-lived. The evidence base is moderate.[22] Massage, cold therapy, acupuncture, traction, lumbar supports, yoga, change of mattress, paraspinal injections, and spinal manipulation are not useful.[23]

Pharmacotherapy is reserved for those patients with inadequate relief to conservative measures. A nonsteroidal anti-inflammatory drug (NSAID) with or without a skeletal muscle relaxant is preferred over paracetamol. Recently, a Cochrane review concluded no benefit of paracetamol compared with a placebo.[24] A 2–4 week trial is usually sufficient. The choice of NSAID is governed by the patient choice and the associated comorbidities. Caution is advised as NSAIDs are associated with renal, gastrointestinal, and cardiovascular adverse effects, particularly so in the elderly. Only one-fourth of patients are able to stop NSAIDs, and the rest usually continue to suffer from chronic pain, necessitating a switch in the management approach, as underlined in the upcoming section.

Systematic reviews and meta-analyses support the efficacy of muscle relaxants in acute LBA.[25],[26] Among the muscle relaxants, cyclobenzaprine is a reasonable first-choice drug. Although used widely, it is not very clear whether muscle relaxants add any benefit to NSAIDs.[27],[28] For patients who cannot tolerate the sedating effects of muscle relaxants during the daytime, NSAIDs or acetaminophen during the day with muscle relaxants before bedtime may be helpful. The primary adverse effects (sedation, dizziness) of muscle relaxants relate to their central nervous system and anticholinergic activity; these are more likely to be problematic in older patients. Carisoprodol also has abuse potential, particularly in patients with a history of substance abuse and has been withdrawn from many European countries.[29]

Evidence to support the use of opioids and tramadol in acute LBP is limited.[30] These agents should be reserved for patients who do not have adequate relief from, or have contraindications to other agents. If opioids are used, it is advisable to limit their administration to a short-term use (<2 weeks). Limiting their use to the bedtime facilitates sleep, and reduces the chances of developing dependence or tolerance. The adverse effects include sedation, confusion, nausea, and constipation. Extended release formulations lead to tachyphylaxis and the consequent dose escalation to counter the developing inefficacy of the medication. Respiratory depression is an issue at higher doses than is used for acute LBP. Special attention should be paid to the elderly people. Misuse and abuse are a concern with opioids, though these are more common in patients using them for chronic back pain, where it is seen in up to 30–45% of patients.[31] Thus, the new Food and Drug Administration (FDA) guidelines mandate the signing of a pain contract and a three monthly urine testing as a screening test for the assessment of dependence.

There is no data on the use of antidepressants and immunosuppressants in acute LBA, and hence, they should not be used. Topical capsaicin has been shown to have a mild effect, while the data on lignocaine is limited.

It has been consistently observed that prolonged bed rest leads to a delayed recovery. Early return to work (RTW) reduces pain and disability. Patients are advised to engage in the maximum tolerated effort at a level which does not aggravate pain. Graded escalation of effort has the best outcome. RTW ought to be individualized. A sedentary worker with greater control of position, pace of work, and work hours can return to job early. For those engaged in manual labor at their work place, a transition period of lighter work is ideal for gradual improvement in the backache before the patients can resume their duties completely.[32]

The evidence for exercise is weak, and hence targeted spinal physiotherapy is reserved for individuals who fail the initial treatment and have risk factors for developing chronicity of pain. Patients with preexistent poor functional status and psychiatric comorbidities are particularly at risk.

Patient education is an important aspect of care. A systematic review found evidence that patient education reduces the acute LBP-related primary care visits.[33] Education should include information about the causes of back pain as well as the factors leading to a favorable prognosis, the generally minimal value of diagnostic testing, the activity and work related recommendations, and when to contact a clinician for follow-up.[33]

Thus, the salient features of management include patient education and at-length discussion of the harms and benefits of various drugs, keeping the dose as low as possible. One should consider intermittent prescriptions, begin with a short trial of a medication and discontinue it if the treatment goals are not met. A summary of the management of acute nonspecific LBP is illustrated in [Figure 3].
Figure 3: Management of acute nonspecific low back pain

Click here to view



 » Treatment of Chronic Nonspecific Back Pain Top


It should be remembered that while managing chronic back pain, drugs are a part of the management and are best used in combination with other nonpharmacologic measures. Evidence for different management modalities of chronic nonspecific back pain is summarized in [Table 4]. Given the adverse effect profile of pain medicines with long-term use, it is encouraged to use them intermittently, in an effort to reduce prescriptions to the minimum. Although the drugs available in the therapeutic armamentarium of pain management are many, only a handful have shown a measurable benefit. Some regulatory authorities and experts have opined against the WHO pain ladder for the management of chronic back pain.[34] The basis for this recommendation is the unproven efficacy of drugs other than the NSAIDs and opioids in the management of persistent back pain.
Table 4: Evidence for management of chronic nonspecific back pain[34]

Click here to view


Systematic reviews support the use of NSAIDs as first-line agents for chronic pain.[24] Although opioids form the second line medications for these patients, it is important to know that opioids have modest benefit and do not improve function.[35] Furthermore, more than half of the patients suffer from adverse effects. Abuse potential is another major concern with opioid usage, a problem reaching epidemic proportions in the United States. The Food and Drug Association (FDA) has rolled out a risk evaluation and mitigation strategy for training the clinicians to ensure a minimal opioid use, to combine opiods with other nonopioid medicines whenever possible, and limit the prolonged duration of use by using short-acting preparations.[36]

Spinal manipulation is another treatment modality with mixed reviews and questionable clinical benefits.[37] It involves the movement of a joint near the end of the clinical range of motion, and is believed to confer modest improvements in pain and function in chronic LBA. Minor transient adverse events such as increased pain, muscle stiffness, and headache occur in up to half of the patients. Most clinical trials have evaluated courses of twice-weekly manipulation for 2–3 weeks. Massages, acupuncture, radiofrequency neurotomy, and epidural steroid injections are considered ineffective, when evaluated with evidence-based systematic reviews.[38]

Chronic nonspecific LBA is now considered to be a continuum of chronic widespread pain syndrome, and hence, it is believed that directing the management to the psychosocial aspects would be more fruitful. Cognitive behavior therapy is advocated in those patients with refractory pain.[39] A 12–50 h per week of therapy is typically delivered over a period of 2–4 weeks. A multidisciplinary rehabilitation programme (MDRP) is particularly useful for those patients with anxiety, fear, and catastrophizing behavior. The MDRP has a moderate-sized effect with significant reduction of pain, disability, as well as a greater probability of return-to-work (RTW) at 1 year. In fact, a study found no difference in the outcome after surgical fusion compared with MDRP, and the latter modality is deemed to be more cost effective as well.[40] However, the evidence base on the group design of various activities, the best time of intervention, and the duration of treatment are still not clear. A summary of the steps in the management of chronic nonspecific LBP is given in [Figure 4].
Figure 4: Management of chronic nonspecific low back pain

Click here to view


The patient expectation forms the backbone of responsiveness to therapy, and this is not commensurate with adherence, highlighting the need to identify the strong undercurrent of psychosocial aspect of pain management, and also the need to shift focus from pharmacotherapy to multidisciplinary management.


 » Treatment of Specific Etiologies Top


Spondyloarthritis

SpA can manifest with chronic LBA, which is typically worse in the mornings and improves with physical activity. NSAIDs are the mainstay of therapy. Up to 90% patients report a remarkable improvement with NSAIDs.[41] Exercise plays an important role in maintaining spinal mobility and in reducing the debility from spinal ankylosis. Nonresponders to NSAIDs typically do very well on anti-tumor necrosis factor agents, although relapses are almost universal on discontinuation of medication. The advent of interleukin-17-directed therapies have brought forth secukinumab as the second line medication in the management of SpA.[41]

Spondylolysis/spondylolisthesis

This is yet another condition with a male predisposition. X-rays are often diagnostic of the condition in the young who present with back pain. While most patients can be managed conservatively with bracing and pain relief medications, those with grade II or IV spondylolisthesis often exhibit neurologic signs on clinical examination, and are potential candidates for surgery.[42]

Scheuermann's disease

This manifests as kyphosis in young males. Those with a potential for further skeletal growth benefit from bracing. Mild cases are manageable conservatively, with spinal corrective osteotomy reserved for those with higher grades of kyphosis.[43]

Diffuse idiopathic skeletal hyperostosis (DISH)

DISH is a systemic noninflammatory disease characterized by ossification of the enthesis. DISH often manifests with a plethora of metabolic complications such as obesity, hypertension, diabetes, hyperlipidemia, and hyperinsulinemia. Management is primarily targeted at the metabolic complications. The cardiovascular risk assessment is madatory. The back pain is intermittent and limited to stiffness in the vast majority. Thus, paracetamol usually suffices.[44] Occasionally, patients develop dysphagia or neurologic complications from fractures of the rigid spine, mandating immediate decompressive surgery with fixation.

Facet syndrome

Often seen in the elderly with degenerative spinal disease, this condition can closely mimic a slipped disc. Management is directed toward mobilization and physiotherapy, while radiofrequency ablation can be resorted to in cases with refractory pain.[45] Although some studies have shown benefit, there is no evidence to support the use of local glucocorticoid injections.[46]

Compression fracture

Treatment of spinal fractures is aimed at pain reduction and reduction of spinal mobility. Long-term assessment of bone health and anti-resorptive therapy are the mainstay of therapy. Only those with neurologic compromise need surgical intervention.

Spondylodiscitis

Antibiotic therapy is a pillar of treatment for spondylodiscitis and should be a part of the treatment in all cases. Neurologic deficits, sepsis, an intraspinal empyema, the failure of conservative treatment, and spinal instability are all indications for surgical treatment.[47]

Lumbar radiculopathy

Conservative treatment for sciatica is primarily aimed at reduction of pain and nerve irritation, either by analgesics, NSAIDs, or muscle relaxants. Bed rest is not advisable for prolonged periods. Those with neurologic compromise (cauda equina syndrome, progressive motor loss, with muscle strength <3 on a six-point scale) and hyperalgesia, despite maximum conservative treatment, need to undergo surgical therapy.[48]

Removal of disc herniation, and eventually part of the disc, or correction of foraminal stenosis are the main objectives of surgical procedures for sciatica. Treatment is aimed at decreasing the leg pain and corresponding symptoms, but not at reducing back pain.[48]


 » Neurogenic Claudication Top


The clinical course of neurogenic claudication is usually slow and most patients with mild or moderate pain have a favorable outcome with conservative treatment. Treatment of pain may include weak or strong opioid drugs against neurogenic pain (gabapentin, pregabalin) and physical therapy (muscle reinforcement, including body posture, as decreasing lordosis increases the spinal canal area and relieves pain).[49]

Decompressive surgery is the standard of care for severe manifestations. Less invasive interspinous devices that increase kyphosis locally are sometimes proposed in stenosis that affects only one disc level in people with serious comorbidities.

Prognosis

The prognosis for acute LBP is excellent; only one-third of patients seek medical care at all, and of those who do, 70–90% improve within 7 weeks. However, recurrences are common, and are seen in up to 50% of patients within 6 months and 70% within 12 months. The recurrences have a favorable prognosis, akin to the initial episode. 10–20% of these individuals go on to develop chronic LBP, more so among those with maladaptive pain-coping behaviors, poor general health status, and psychiatric comorbidities. Those with amplified pain and a tendency to avoid physical therapy are at a greater risk; hence, an early mobilization is the key to prevent long-term disability.[50]

The STarTBack screening tool is designed to be used by primary care physicians and has the best validation process. Thus, it may be used in randomized clinical trials and large, “real-life” cohort studies. It contains nine items: four deal with the patterns of pain and disability, four cover psychological aspects (kinesiophobia, anxiety, depression, and catastrophism) and one provides a score regarding the level of aggravation. Patients with at least four out of five positive items among the last five are at a high risk of chronicity.[51] Prescribing a treatment methodology adapted to the risk of chronicity produces a better result than standard care.[52],[53]

Prevention

Regular back muscle strengthening exercises have some value in preventing recurrences of LBP. Data on the usefulness of other modalities such as lumbar supports, or weight loss, for prevention of LBP are limited.


 » Conclusion Top


In the large number of cases with LBA, it is important to identify those with a recognizable etiology. Most cases are labeled nonspecific, with the possible etiology being lumbar muscle sprain. LBP is an evolving concept in the spectrum of fibromyalgianess. Early attention to risk factors of chronicity can go a long way in reducing debility.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
 » References Top

1.
Allan DB, Waddell G. An historical perspective on low back pain and disability. Acta Orthop Scand Suppl 1989;234:1-23.  Back to cited text no. 1
    
2.
Rubin DI. Epidemiology and risk factors for spine pain. Neurol Clin 2007;25:353-71.  Back to cited text no. 2
    
3.
Koes BW, van Tulder M, Lin C-WC, Macedo LG, McAuley J, Maher C. An updated overview of clinical guidelines for the management of non-specific low back pain in primary care. Eur Spine J 2010;19:2075-94.  Back to cited text no. 3
    
4.
Deyo RA, Weinstein JN. Low back pain. N Engl J Med 2001;344:363-70.  Back to cited text no. 4
    
5.
Carey TS, Garrett JM, Jackman A, Hadler N. Recurrence and care seeking after acute back pain: Results of a long-term follow-up study. North Carolina Back Pain Project. Med Care 1999;37:157-64.  Back to cited text no. 5
    
6.
Low back pain in India - Health statistics, demographics affected. Available from: http://global-disease-burden.healthgrove.com/l/76986/Low-Back-Pain-in-India. [Last accessed on 2019 Jun 22].  Back to cited text no. 6
    
7.
Chopra A, Saluja M, Patil J, Tandale HS. Pain and disability, perceptions and beliefs of a rural Indian population: A WHO-ILAR COPCORD study. WHO-International League of Associations for Rheumatology. Community Oriented Program for Control of Rheumatic Diseases. J Rheumatol 2002;29:614-21.  Back to cited text no. 7
    
8.
Stewart Williams J, Ng N, Peltzer K, Yawson A, Biritwum R, Maximova T, et al. Risk factors and disability associated with low back pain in older adults in low- and middle-income countries. Results from the WHO Study on Global AGEing and Adult Health (SAGE). PLoS ONE 2015;10:e0127880. doi: 10.1371/journal.pone. 0127880.  Back to cited text no. 8
    
9.
Joshi VL, Chopra A. Is there an urban-rural divide? Population surveys of rheumatic musculoskeletal disorders in the Pune region of India using the COPCORD Bhigwan model. J Rheumatol 2009;36:614-22.  Back to cited text no. 9
    
10.
Pagare VK, Dhanraj T, Thakkar D, Sareen A, Palekar TJ. Beliefs about low back pain: Status quo in Indian general population. J Back Musculoskelet Rehabil 2015;28:731-7.  Back to cited text no. 10
    
11.
Sorensen PH, Bendix T, Manniche C, Korsholm L, Lemvigh D, Indahl A. An educational approach based on a non-injury model compared with individual symptom-based physical training in chronic LBP. A pragmatic, randomised trial with a one-year follow-up. BMC Musculoskelet Disord 2010 17;11:212.  Back to cited text no. 11
    
12.
Bazrgari B, Xia T. Application of advanced biomechanical methods in studying low back pain - recent development in estimation of lower back loads and large-array surface electromyography and findings. J Pain Res 2017;10:1677-85.  Back to cited text no. 12
    
13.
A genetic basis for lower back pain? Bonekey Rep 2013;2:301. Published online 2013 Feb 20. doi: 10.1038/bonekey. 2013.35.  Back to cited text no. 13
    
14.
Panjabi MM. Clinical spinal instability and low back pain. J Electromyogr Kinesiol 2003;13:371-9.  Back to cited text no. 14
    
15.
Mulholland RC. The myth of lumbar instability: The importance of abnormal loading as a cause of low back pain. Eur Spine J 2008;17:619-25.  Back to cited text no. 15
    
16.
Roussel NA, Nijs J, Meeus M, Mylius V, Fayt C, Oostendorp R. Central sensitization and altered central pain processing in chronic low back pain: Fact or myth? Clin J Pain 2013;29:625-38.  Back to cited text no. 16
    
17.
Wasan AD, Loggia ML, Chen LQ, Napadow V, Kong J, Gollub RL. Neural correlates of chronic low back pain measured by arterial spin labeling. Anesthesiology 2011;115:364-74.  Back to cited text no. 17
    
18.
Marcy PY, Magné N, Bailet C, Pivot X, Dassonville O, Poissonnet G, et al. Liver metastases from head and neck squamous cell carcinomas: Radiological and biological features. Onkologie 2004;27:157-60.  Back to cited text no. 18
    
19.
Modic MT, Steinberg PM, Ross JS, Masaryk TJ, Carter JR. Degenerative disk disease: Assessment of changes in vertebral body marrow with MR imaging. Radiology 1988;166:193-9.  Back to cited text no. 19
    
20.
Kovacs FM, Arana E, Royuela A, Estremera A, Amengual G, Asenjo B, et al. Vertebral endplate changes are not associated with chronic low back pain among Southern European subjects: A case control study. AJNR Am J Neuroradiol 2012;33:1519-24.  Back to cited text no. 20
    
21.
Tonosu J, Oka H, Higashikawa A, Okazaki H, Tanaka S, Matsudaira K. The associations between magnetic resonance imaging findings and low back pain: A 10-year longitudinal analysis. PLoS One 2017;12:e0188057.  Back to cited text no. 21
    
22.
French SD, Cameron M, Walker BF, Reggars JW, Esterman AJ. A Cochrane review of superficial heat or cold for low back pain. Spine 2006;31:998-1006.  Back to cited text no. 22
    
23.
Stevens ML, Lin C-WC, de Carvalho FA, Phan K, Koes B, Maher CG. Advice for acute low back pain: A comparison of what research supports and what guidelines recommend. Spine J Off J North Am Spine Soc 2017;17:1537-46.  Back to cited text no. 23
    
24.
Enthoven WTM, Roelofs PDDM, Deyo RA, van Tulder MW, Koes BW. Non-steroidal anti-inflammatory drugs for chronic low back pain. Cochrane Database Syst Rev 2016;2:CD012087.  Back to cited text no. 24
    
25.
van Tulder MW, Touray T, Furlan AD, Solway S, Bouter LM, Cochrane Back Review Group. Muscle relaxants for nonspecific low back pain: A systematic review within the framework of the Cochrane collaboration. Spine 2003;28:1978-92.  Back to cited text no. 25
    
26.
Abdel Shaheed C, Maher CG, Williams KA, McLachlan AJ. Efficacy and tolerability of muscle relaxants for low back pain: Systematic review and meta-analysis. Eur J Pain Lond Engl 2017;21:228-37.  Back to cited text no. 26
    
27.
Childers MK, Borenstein D, Brown RL, Gershon S, Hale ME, Petri M, et al. Low-dose cyclobenzaprine versus combination therapy with ibuprofen for acute neck or back pain with muscle spasm: A randomized trial. Curr Med Res Opin 2005;21:1485-93.  Back to cited text no. 27
    
28.
Friedman BW, Dym AA, Davitt M, Holden L, Solorzano C, Esses D, et al. Naproxen with cyclobenzaprine, oxycodone/acetaminophen, or placebo for treating acute low back pain: A randomized clinical trial. JAMA 2015;314:1572-80.  Back to cited text no. 28
    
29.
Bramness JG, Furu K, Skurtveit S, Engeland A. Effect of the market withdrawal of carisoprodol on use of other prescribed drugs with abuse potential. Clin Pharmacol Ther 2012;91:438-41.  Back to cited text no. 29
    
30.
Chaparro LE, Furlan AD, Deshpande A, Mailis-Gagnon A, Atlas S, Turk DC. Opioids compared with placebo or other treatments for chronic low back pain: An update of the Cochrane review. Spine 2014;39:556-63.  Back to cited text no. 30
    
31.
Von Korff M, Merrill JO, Rutter CM, Sullivan M, Campbell CI, Weisner C. Time-scheduled versus pain-contingent opioid dosing in chronic opioid therapy. Pain 2011;152:1256-62.  Back to cited text no. 31
    
32.
Qaseem A, Wilt TJ, McLean RM, Forciea MA, Clinical Guidelines Committee of the American College of Physicians. Noninvasive treatments for acute, subacute, and chronic low back pain: A clinical practice guideline from the American College of Physicians. Ann Intern Med 2017;166:514-30.  Back to cited text no. 32
    
33.
Traeger AC, Hübscher M, Henschke N, Moseley GL, Lee H, McAuley JH. Effect of primary care-based education on reassurance in patients with acute low back pain: Systematic review and meta-analysis. JAMA Intern Med 2015;175:733-43.  Back to cited text no. 33
    
34.
Maher C, Underwood M, Buchbinder R. Non-specific low back pain. Lancet Lond Engl 2017;389:736-47.  Back to cited text no. 34
    
35.
Abdel Shaheed C, Maher CG, Williams KA, Day R, McLachlan AJ. Efficacy, tolerability, and dose-dependent effects of opioid analgesics for low back pain: A systematic review and meta-analysis. JAMA Intern Med 2016;176:958-68.  Back to cited text no. 35
    
36.
Gudin J. Risk Evaluation and Mitigation Strategies (REMS) for extended-release and long-acting opioid analgesics: Considerations for palliative care practice. J Pain Palliat Care Pharmacother 2012;26:136-43.  Back to cited text no. 36
    
37.
Rubinstein SM, van Middelkoop M, Assendelft WJ, de Boer MR, van Tulder MW. Spinal manipulative therapy for chronic low-back pain. Cochrane Database Syst Rev 2011;16:CD008112. doi: 10.1002/14651858.CD008112.pub2.  Back to cited text no. 37
    
38.
Chou R, Atlas SJ, Stanos SP, Rosenquist RW. Nonsurgical interventional therapies for low back pain: A review of the evidence for an American Pain Society clinical practice guideline. Spine 2009;34:1078-93.  Back to cited text no. 38
    
39.
Chou R, Loeser JD, Owens DK, Rosenquist RW, Atlas SJ, Baisden J, et al. Interventional therapies, surgery, and interdisciplinary rehabilitation for low back pain: An evidence-based clinical practice guideline from the American Pain Society. Spine 2009;34:1066-77.  Back to cited text no. 39
    
40.
Mannion AF, Brox JI, Fairbank JCT. Comparison of spinal fusion and nonoperative treatment in patients with chronic low back pain: Long-term follow-up of three randomized controlled trials. Spine J 2013;13:1438-48.  Back to cited text no. 40
    
41.
Van der Heijde D, Ramiro S, Landewé R, Baraliakos X, Van den Bosch F, Sepriano A, et al. 2016 update of the ASAS-EULAR management recommendations for axial spondyloarthritis. Ann Rheum Dis 2017;76:978-91.  Back to cited text no. 41
    
42.
Kalichman L, Hunter DJ. Diagnosis and conservative management of degenerative lumbar spondylolisthesis. Eur Spine J 2008;17:327-35.  Back to cited text no. 42
    
43.
Palazzo C, Sailhan F, Revel M. Scheuermann's disease: An update. Joint Bone Spine 2014;81:209-14.  Back to cited text no. 43
    
44.
Mader R. Current therapeutic options in the management of diffuse idiopathic skeletal hyperostosis. Expert Opin Pharmacother 2005;6:1313-8.  Back to cited text no. 44
    
45.
Goode AP, Carey TS, Jordan JM. Low back pain and lumbar spine osteoarthritis: How are they related? Curr Rheumatol Rep 2013;15:305.  Back to cited text no. 45
    
46.
Ramesh Chandra VV, Prasad BC, Mohan CK, Kalawat TC, Satyanarayana V, Lakshmi AY. An algorithmic approach for clinical management of low back pain. Neurol India 2016;64:950-7.  Back to cited text no. 46
    
47.
Ponciano A, Cruz G, Ventura C, Rabadão E, Saraiva da Cunha J. Infectious spondylodiscitis: 5-year analysis of a tertiary hospital in Portugal. Infect Dis (Lond) 2018;50:637-9.  Back to cited text no. 47
    
48.
Kreiner DS, Hwang SW, Easa JE, Resnick DK, Baisden JL, Bess S, et al. North American Spine Society. An evidence-based clinical guideline for the diagnosis and treatment of lumbar disc herniation with radiculopathy. Spine J 2014;14:180-91.  Back to cited text no. 48
    
49.
Ammendolia C, Stuber KJ, Rok E, Rampersaud R, Kennedy CA, Pennick V, et al. Nonoperative treatment for lumbar spinal stenosis with neurogenic claudication. Cochrane Database Syst Rev 2013:CD010712. doi: 10.1002/14651858.CD010712.  Back to cited text no. 49
    
50.
Menezes Costa L da C, Maher CG, Hancock MJ, McAuley JH, Herbert RD, Costa LOP. The prognosis of acute and persistent low-back pain: A meta-analysis. CMAJ Can Med Assoc J 2012;184:E613-24.  Back to cited text no. 50
    
51.
Beneciuk JM, Bishop MD, Fritz JM, Robinson ME, Asal NR, Nisenzon AN, et al. The STarT back screening tool and individual psychological measures: Evaluation of prognostic capabilities for low back pain clinical outcomes in outpatient physical therapy settings. Phys Ther 2013;93:321-33.  Back to cited text no. 51
    
52.
Hill JC, Whitehurst DG, Lewis M, Bryan S, Dunn KM, Foster NE, et al. Comparison of stratified primary care management for low back pain with current best practice (STarT Back): A randomised controlled trial. Lancet Lond Engl 2011;378:1560-71.  Back to cited text no. 52
    
53.
Maher C, Underwood M, Buchbinder R. Non-specific low back pain. Lancet Lond Engl 2017;389:736-47.  Back to cited text no. 53
    


    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4]
 
 
    Tables

  [Table 1], [Table 2], [Table 3], [Table 4]



 

Top
Print this article  Email this article
   
Online since 20th March '04
Published by Wolters Kluwer - Medknow