Treatment of low back and neck pain: An evidence approach
Dr KS Dhillon FRCS, LLM
It is well known that musculoskeletal symptoms are common in adult communities and the prevalence of these symptoms increase with age. The most common site of pain from musculoskeletal disorders is the low back (23%) followed by the knee (19%) and the shoulder (16%) (1). The global point prevalence of low back pain (LBP) is the highest at 9.4% (2) and for neck pain it is 4.9% (3). LBP ranks highest in term of disability as measured by years lived with disability (YLD) and its prevalence and burden increases with age (2). Low back pain and neck pain constitutes a high proportion of a GP’s and an orthopaedic surgeon’s patient load. The treatment of musculoskeletal pain is financial burden and this burden can be expected to get worse with increasing lifespan of individuals and a larger aging population. Can this financial burden be reduced by providing evidence based care to patients with musculoskeletal pain? This review will be confined to the management of back and neck pain because of the similarities in the etiopathogenesis and the treatment of both these disorder as well as due to space constraints.
Treatment of low back pain
Definition and pathogenesis of back pain
Uniformity of definitions is essential to study prevalence and management outcome of low back pain. There is a lack of uniform definitions of low back pain in the literature. Acute back pain is defined as back pain that last for less than 6 weeks and subacute back pain is that which last between 6 to 12 weeks. Chronic low back pain is persistent low back pain that is present for at least 12 weeks. There will be patients with a history of back pain for many years who have repeated bouts of acute or subacute back pain but will not be classified as having chronic low back pain unless the episode of pain last at least 12 weeks. A recurrence of an episode of low back pain is defined as a return of low back pain lasting at least 24 hours and recurrent low back pain is defined as low back pain which has occurred at least two times over the past year with each episode lasting at least 24 hours (4).There are several classifications of low back pain; the most widely accepted is that proposed by Waddell. Waddell’s diagnostic triage divides low back pain into three categories;
• Specific spinal pathology such as tumour, infection, fractures, cauda equina syndrome ( ‘Red flags’) which occurs in about 1 to 2 % of the patients.
• Nerve root pain such as that caused by disc prolapse and spinal stenosis which occurs in about 5% of the patients.
• Non-specific low back pain which occurs in about 85 to 95% of the patients (5).
The first two categories fit into the classical disease model where the disease can be accurately diagnosed and appropriately treated. However, the third category does not fit into this model, where a proper clinical diagnosis can be made. Such a diagnosis of non-specific low back pain according to Waddell is ‘intellectually and scientifically inadequate and fails to provide any biological basis for real understanding’ which results in treatment remaining ‘empirical or based on unproven hypotheses’ (5). Claims of diagnoses such lumbar strain or degenerative spine disease as a cause of low back pain remain unfounded and leaves room for uncertainty about treatment, prognosis and clinical outcome (5).
The treatment of patients with specific spinal pathology such as tumour, infection, fractures and cauda equina syndrome (which occurs in about 1 to 2 % of the patients) and in patients with nerve root pain such as that caused by disc prolapse and spinal stenosis (which occurs in about 5% of the patients), is quite straight forward with good outcome. The major problem is the treatment of the 95% of the patients with non-specific back pain who make frequent visits to the medical practitioner and which poses a social and financial burden.
Treatment of non-specific back pain
A review of 15 national/international guidelines, which are based on publications of studies on management of low back pain, show that there is no role for routine imaging in the management of non-specific low back pain (6). The guidelines mention that psychosocial and occupational factors (‘yellow flags’) are associated with poor prognosis and these factors often produce chronicity of back pain.One of the most important therapeutic interventional factors in the management of the back pain is effective communication using simple non-medical terminology. The patient need to be reassured that there is nothing seriously wrong with his/her back. The patient should be advised to stay active and avoid bed rest. Activity should be gradually increased and the patient should be advised to return to work early even with the back pain (6).
All guidelines recommend that the first line of medicinal treatment for the pain should be the use of Paracetamol/acetaminophen. This should be followed with NSAIDS as the second line of treatment. However there is no irrefutable evidence that NSAIDS are more effective than placebo or no treatment at all for treatment of acute low back pain. It is the same with the use of muscle relaxants where there is conflicting evidence on the effectiveness as compared to placebo. NSAIDS can have gastrointestinal complications while muscle relaxation can cause dizziness, drowsiness and dependency among other complications (7).
The effect of opioids and compound analgesics is similar to that of NSAIDS but opioids and compound analgesic can have substantially higher risk of side effects as compared to paracetamol. The evidence for the use of, spinal manipulation, acupuncture, back exercises, bed rest, lumbar support, spinal injections, TENS, massage, topical applications and traction in the treatment of acute back pain, is at best conflicting in nature and is no better than the standard treatment of back pain with analgesics. However the use of cognitive behavioural therapy has been shown to reduce general disability in the long term (7).
Routine use of muscle relaxants is not recommended because any benefit can be outweighed by the adverse effects. Adjuvant agents such as anticonvulsants (Gabapentin, Pregablin) and anti-depressants (Amitriptyline) are not recommended for the treatment of acute low back pain (7).
Acute low back pain is generally self-limiting. However it is important to exclude specific spinal pathology such as tumour, infection, fractures, cauda equina syndrome (‘Red flags’) which occurs in about 1 to 2 % of the patients and needs immediate specific treatment. Usually rapid improvement in ‘pain (mean reduction 58% of initial scores), disability (58%), and return to work (82% of those initially off work)’ occurs within a month. Further improvement can occur up to about three months. After 3 months improvements of these parameters usually remain relatively constant. About 73% of patients will have at least one recurrence within 12 months (8).
Acute neck pain
Acute neck pain is defined as pain that is present in the back of the neck in the region from the superior nuchal line to a transverse line running through the tip of the spinous process of the first thoracic vertebra, which has been present for less than 3 months. Chronic neck pain is defined as that which is present for 3 months or more (7).As with the lumbar spine, serious causes of acute neck pain are rare but they should be promptly diagnosed and treated. The incidence of serious cause of acute neck pain is less than 1% and these include spinal tumours, spinal infections, epidural haematomas and aneurysms. Fractures are uncommon causes of acute neck pain and the incidence is less than 5%. In most of the patients the acute neck pain is idiopathic or is due to whiplash injury. There is level III evidence that degenerative cervical spondylosis is neither the cause nor a risk factor for idiopathic neck pain (7).
Various terminologies have been used to describe the degenerative changes in the cervical spine including cervical spondylosis; cervical osteoarthrosis, degenerative disc disease and degenerative joint disease, but all these changes constitute normal age changes of the cervical spine (9). There are studies that show that cervical spondylosis occurs slightly more frequently in symptomatic than asymptomatic individuals (10) (11). The prevalence of disc degeneration has been found be no different in symptomatic and asymptomatic individuals and the prevalence of uncovertebral osteophytes and osteoarthrosis of the synovial joints of the neck has been found to be less prevalent in symptomatic individuals (12). Hence finding of degenerative changes in the cervical spine on radiographs does not mean that these degenerative changes are the cause of neck pain.
Imaging of the cervical spine is not necessary in patients with acute neck pain in the absence of trauma and clinical evidence of serious underlying disorder. Level III evidence suggests that 40% of patients of patients recover fully from non-specific acute neck pain. About 30% will continue to have mild symptoms and 30% may continue to have moderate to severe symptoms (13,14).
Level III and level IV evidence shows that in patients with whiplash injury about 56% of them fully recover within three months and 80% recover fully within one or two years. However about 15–40% continue to have symptoms and 5% are severely affected (15, 16).
There is dearth of clinical studies on the treatment of acute neck pain. However, advice to remain active, resume normal activities and maintain neck movements has been found to be more effective than the use of rest or cervical collar in the treatment of acute neck pain (level I and II evidence). Gentle neck exercises are more effective than the use of collar and analgesic. There is insufficient evidence on the effectiveness of use of analgesic, opioids, muscle relaxants, acupuncture, cervical manipulation, traction and electrotherapy in the treatment of acute neck pain (7).
Chronic low back pain
Chronic low back pain (CLBP) is defined as pain in back, in the region from the lower costal margin to the inferior gluteal line, which last at least 12 weeks. According to Waddell’s diagnostic triage specific spinal pathology such as tumour, infection, fractures, cauda equina syndrome ( ‘Red flags’) occurs in about 1 to 2 % of the patients and nerve root pain such as that caused by disc prolapse and spinal stenosis occurs in about 5% of the patients. Majority of the patients with chronic low back pain fall into the category of non-specific low back pain which occurs in about 85 to 95% of the patients (5).There is level II (moderate) evidence that imaging of the spine is not recommended for patients with non-specific CLBP and there is moderate evidence that MRI of the spine is useful in patients with radicular pain and in patients suspected to have discitis or neoplasm of the spine (17). Level II evidence suggests that facet joint injections, MRI and discography are not reliable procedures for the diagnosis of facet joint pain and discogenic pain. There is level III evidence that radioactive bone scans are useful for the diagnosis of pseudoarthodesis after spinal fusion and for the diagnosis of stress fractures and malignancies. The use of electromyography as a diagnostic procedure in chronic nonspecific low back pain is not recommended (17).
Physical treatment for CLBP
There is insufficient evidence of the usefulness of physical treatment modalities, such as interferential therapy, laser therapy, lumbar support, short wave diathermy, ultrasound, thermotherapy, traction and TENS, in the treatment of CLBP and hence these modalities are not recommended for the treatment of CLBP (17).Exercise Therapy
There is level II evidence that exercise therapy helps to reduce pain and disability in the short term and there is strong evidence that exercise is more effective than ‘GP care’ in reducing pain, disability and return to work in the mid-term (3-6 months) in patients with CLBP. Reconditioning and back strengthening exercises are not recommended.Hence supervised exercise therapy is the first line of treatment of CLBP. Expensive training machines are not required. Cognitive-behavioural approach with graded exercise using exercise quotas is recommended. Group exercise programs are useful and they cost less than individual exercise programs (17).
Cognitive-behavioural treatment
There is strong level I evidence that behavioural treatment is more effective for pain, functional status and behavioural outcomes than placebo and or no treatment and there is also strong evidence that a graded activity programme using a behavioural approach is more effective than traditional care for returning patients to work (17). There is strong evidence that multidisciplinary biopsychosocial rehabilitation with functional restoration approach reduces pain and improves function in patients with chronic low back pain (17).Drug treatment
The complexity of the mechanisms causing chronic pain and the greater role of social, psychological, and economic factors makes the efficacy of drug treatment less clear in patients with CLBP (17).A survey of primary care patients shows that the most commonly prescribed drugs for back pain are non-steroidal medications (NSAIDS) (69%) followed by muscle relaxants (35%), narcotics (12%) and acetaminophen (4%) (18).
Antidepressants
Antidepressants block the reuptake of neurotransmitters (norepinephrine and serotonin) and modulate pain sensation. The most studied are the tricyclic antidepressants (such as Amitriptyline). There is strong evidence that such antidepressants are effective in relieving pain in patients with CLBP but they do not improve function or disability (moderate evidence). Antidepressants are usually used in combination with other drugs such as NSAIDS especially in patients with severe back pain. However antidepressants should not be used in patients with renal disease, glaucoma, chronic obstructive pulmonary disease, cardiac failure and in patients who are pregnant (17).Muscle relaxants
Muscle relaxants such as benzodiazepines are effective in the treatment of back pain (strong evidence) but there is insufficient evidence that they reduce muscle spasm. Their use can be associated with severe adverse events such as dizziness, drowsiness and addiction and hence used be only used for short durations (17).NSIADs
There is strong evidence that NSAIDs are effective for the relief of chronic low back pain (level A). The use of NSAIDs are recommended for the treatment of CLBP but these drugs should be used for the shortest duration possible and should not exceed 3 months because of possible side effects such as gastrointestinal complications (irritation, ulcers and bleeding) and cardiovascular complications (17).Opioids
There is strong evidence that weak opioids such as tramadol relieve pain and disability in the short term in patients with CLBP. Their use is recommended in patients with moderate and severe back pain who do not respond to analgesic/NSAIDs or are unable to take NSAIDS due to their side effects (17).Antiepileptic drugs (Gabapentin)
There is no evidence that antiepileptic drugs such as Gabapentin are effective in relieving pain in patients with CLBP and their use for treatment of CLBP is not recommended (17).
Epidural steroid injections
Review of literature shows that there is no evidence for the effectiveness of epidural/perineural steroid injections for non-radicular, non-specific low back pain and there is conflicting evidence of the effectiveness of such injections in the treatment of radicular pain.Epidural injections can be associated with complications though they are uncommon. These include Cushingnoid symptoms (with frequent use), post-dural puncture headaches, epidural abscess, chemical meningitis and Arachnoiditis.
The use of epidural injections is not recommended for the treatment of CLBP (17).
Facet block and Intradiscal Injections
There is no evidence for the effectiveness Facet block (joint and nerve) and for intradiscal corticosteroid injections in the treatment of chronic low back pain and the use of such injection for the treatment of CLBP is not recommended (17).Sacroiliac Joint Injections
There is only limited evidence (level C) that injection of the sacroiliac joint with corticosteroids relieves sacroiliac pain of unknown origin for a short duration of time (one month). The use of sacroiliac joint steroid injections is not recommended for treatment of CLBP (17).Surgery
Chronic back pain is a symptom and not a disease. Specific spinal pathology which fits into a classical disease model, where treatment can be effective, can be found in only about 6% to 7% of the patients. In about 85 to 95% of the patients with back pain no pathoanatomical diagnosis can be made and such pain gets labelled as non-specific back pain.Imaging findings such as degenerated disc, facet arthritis, spondylosis, spondylolysis and spondylolisthesis has no causal relationship to the pain in these patients. In the vast majority of patients the degenerated disc is implicated as the cause of chronic low back pain while in others the facet joints and sacroiliac joint is believed to be the cause of the pain. Although MRI scans can accurately depict the anatomical changes seen in the spine as degeneration of the spine sets in, the clinical significance of these changes remain elusive and the scans cannot help in elucidating the cause of the pain. Provocative discography which was in the past touted as a valid diagnostic test, has also failed to stand up to its usefulness. To date there is no imaging technique or diagnostic test which can localise the source of pain in patients with non-specific back pain.
Despite the inability to make a diagnosis in patients with non-specific low back pain, there has been a sharp increase in the number of patient undergoing spinal fusion for low back pain over the last two decades. Spinal fusion in patients with non-specific back pain is akin to treating a symptom (not a disease) with surgery. Logic dictates that such an approach cannot be very successful.
There is a dearth of level 1 studies in the medical literature comparing spinal fusion to non-surgical treatment of chronic low back pain. There are two relatively good level 1 studies (19, 20) with two to four years follow up comparing surgical to non-surgical treatment published so far, but they do not show superiority of surgical treatment over nonsurgical treatment. Furthermore spinal fusion is associated with significant and sometimes serious medical complications including mortality (21, 22, and 23).
Chronic neck pain
There is a dearth of evidence based publications in the medical literature on the treatment of chronic neck pain which is also the case for the treatment of acute neck pain. The general guidelines for treatment chronic neck pain remain the same as for acute neck pain with an emphasis on exercises of the neck as the mainstay of treatment.A randomised control trial in females with chronic neck pain by Ylinen et al showed that dynamic neck exercises and neck strengthening exercises, both, had beneficial effect in pain relief and disability as compared to a control group. The dynamic exercise group did neck lifts in the supine and prone position while the neck strengthening group did resistant exercises using an elastic band. The control group did aerobic and stretching exercises for half an hour, three times a week. All three groups were followed up after 12 months. The study found that both strength and endurance training for 12 months were effective in decreasing pain and disability in women with chronic, nonspecific neck pain and stretching and aerobic exercises were much less effective than strength training (24).
There is insufficient evidence to recommend the use of thermotherapy, therapeutic massage, EMG biofeedback, mechanical traction, therapeutic ultrasound, TENS and electrical stimulation in the treatment of chronic non-specific neck pain (25).
Conclusion
Non-specific neck and back pain is a symptom and not a disease entity and the findings on spinal imaging do not indicate that these findings are the source of pain since a large number of patients with no symptoms can have similar findings on imaging. There is no diagnostic test available to determine the source pain in patients with non-specific neck or back pain. Therefore logically surgery is not the answer to the treatment of such pain. Avoiding expensive surgery which can be associated with serious complications would be the best evidence based approach in the management of patients with non-specific neck or back pain.The best approach in the management of such patients would be effective communication and explanation to the patient that nothing is seriously wrong with them. They should be advised to remain active and avoid rest and immobilisation of the spine as far as possible. Exercises of the neck and back have been found to reduce pain. Cognitive-behavioural therapy has been found to be effective in the treatment of chronic pain. Acute pain usually settles with time in a significant number of patients.
The use of simple analgesics and NSAIDS for short duration of time does help to reduce the pain though there is not much evidence that they are better than no treatment at all. Mild narcotics can be added to NSAIDs if the pain does not settle with NSAIDs. Routine use of Anti-depressants and Muscle relaxants is not recommended but may be used briefly in patients with severe pain. There is no role for the use of anti-convulsants in the treatment of these patients.
Epidural and facet injections are not recommended because there is no evidence of their effectiveness in the treatment of patients with non-specific neck or back pain.
Almost all physical treatment modalities have not been found to be effective in the treatment of neck or back pain. The use of collars, lumbar supports, thermotherapy, ultrasound, traction, TENS, acupuncture, electrical stimulation and massage are not recommended in the treatment of neck and back pain because of lack of evidence of their effectiveness.
It is therefore quite obvious that an evidence based approach to the management of patients with non-specific neck and back pain will go a long way in reducing the financial burden of treating patients with these common conditions.
References
1. Urwin M, Symmons D, Allison T, et al. Estimating the burden of musculoskeletal disorders in the community: the comparative prevalence of symptoms at different anatomical sites, and the relation to social deprivation. Ann Rheum Dis 1998; 57:649–655.2. Hoy D, March L, Brooks P, et al. The global burden of low back pain: estimates from the Global Burden of Disease 2010 study. Ann Rheum Dis. 2014 Jun; 73(6):968-74. doi: 10.1136/annrheumdis-2013-204428. Epub 2014 Mar 24.
3. Hoy D, March L, Woolf A et al. The global burden of neck pain: estimates from the global burden of disease 2010 study. Ann Rheum Dis. 2014 Jul; 73(7):1309-15. doi: 10.1136/annrheumdis-2013-204431. Epub 2014 Jan 30.
4. Stanton TR, Latimer J, Maher CG, Hancock MJ. How do we define the condition ‘recurrent low back pain’? A systematic review. Eur Spine J. 2010; 19(4):533-9.
5. Waddell G. Subgroups within "nonspecific" low back pain. J Rheumatol 2005; 32; 395-396.
6. Bart W. Koes, Maurits van Tulder, Chung-Wei Christine Lin, Luciana G. Macedo, James McAuley, and Chris Maher. An updated overview of clinical guidelines for the management of non-specific low back pain in primary care. Eur Spine J. 2010 Dec; 19(12): 2075–2094.
7. Evidence-based management of acute musculoskeletal pain. Australian Acute Musculoskeletal Pain Guidelines Group. June 2003 at http://www.nhmrc.gov.au/_files_nhmrc/publications/attachments/cp94.pdf
8. Pengel LHM, Herbert RD, Maher CG and Refshauge KM. Acute low back pain: systematic review of its prognosis. BMJ. 2003 Aug 9; 327(7410): 323.
9. Gore DR, Sepic SB, Gardner GM (1986). Roentgenographic findings of the cervical spine in asymptomatic people. Spine, 1: 521–524.
10. Heller CA, Stanley P, Lewis-Jones B, Heller RF (1983). Value of x-ray examinations of the cervical spine. British Medical Journal, 287: 1276–1278.
11. van der Donk J, Schouten JSAG, Passchier J, van Romunde LKJ, Valkenburg HA (1991). The associations of neck pain with radiological abnormalities of the cervical spine and personality traits in a general population. Journal of Rheumatology, 18: 1884–1889.
12. Fridenberg ZB, Miller WT (1963). Degenerative disc disease of the cervical spine. A comparative study of asymptomatic and symptomatic patients. Journal of Bone and Joint Surgery 45A:1171–1178.
13. Gore DR, Sepic SB, Gardner GM, Murray MP (1987). Neck pain: a long-term follow-up of 205 patients. Spine, 12: 1–5.
14. Lees F, Turner JWA (1963). Natural history and prognosis of cervical spondylosis. British Medical Journal, 2: 1607–1610.
15. Radanov BP, Sturzenegger M, Di Stefano G (1995). Long-term outcome after whiplash injury: a 2-year follow-up considering features of injury mechanism and somatic, radiologic, and psychosocial findings. Medicine, 74: 281–297.
16. Kasch H, Bach FW, Jensen TS (2001). Handicap after acute whiplash injury: a 1-year prospective study of risk factors. Neurology, 56: 1637–1643.
17. Airaksinen O, Brox JI, Cedraschi C et al. European Guidelines for the Management of Chronic Non-specific Low Back Pain. Eur Spine J (2006) 15 (Suppl. 2): S192–S300. DOI 10.1007/s00586-006-1072-1.
18. Cherkin DC, Wheeler KJ, Barlow W, Deyo RA. Medication use for low back pain in primary care. Spine (Phila Pa 1976). 1998 Mar 1;23(5):607-14.
19. Fairbank J, Frost H, Wilson-MacDonald J, Yu l, Barker K, Collins R for the Spine Stabilisation Trial Group. Randomised controlled trial to compare stabilisation of the lumbar spine with an intensive rehabilitation programme for patients with chronic low back pain: MRC spine stabilisation trial. BMJ 2005;doi:10.1136/bmj.38441.620417.BF.
20. Brox JI, Nygaard OP, Holm I, Keller A, Ingebrigtsen T, Reikeras O. Four-year follow-up of surgical versus non-surgical therapy for chronic low back pain. Ann Rheum Dis 2010; 69:1643-1648.
21. Deyo RA, Mirza SK, Martin BJ, Kreuter W, Goodman DC, Jarvik JG. Trends, major medical complications, and charges associated with surgery for lumbar stenosis in older adults. JAMA 2010; 302(13):1259-1265.
22. Fritzell P, Ha¨gg O, Wessberg P, Nordwall A and the Swedish Lumbar Spine Study Group. Lumbar fusion versus nonsurgical treatment for chronic low back pain. A multicentre randomized controlled trial from the Swedish Lumbar Spine Study Group. SPINE 2001; 26(23): 2521–2534.
23. Brox JI, Sørensen R, Friis A, et al. Randomized clinical trial of lumbar instrumented fusion and cognitive intervention and exercises in patients with chronic low back pain and disc degeneration. SPINE 2003; 28 (17): 1913–1921.
24. Ylinen J, Takala E, Nykänen M, et al. Active neck muscle training in the treatment of chronic neck pain in women. JAMA. 2003; 289(19):2509-2516.
25. Abright J, Allman R, Bonfiglio et al. Philadelphia panel evidence-based clinical practice for neck pain guidelines on selected rehabilitation interventions. PHYS THER. 2001; 81:1701-1717.