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Low-back pain: aetiology and management options

Low back pain describes pain that occurs between the lower costal margins and the gluteal folds. Chronic back pain is back pain that persists for longer than three months. 

Back pain is one of the most common reasons for chronic disability and incapacity in the Western world. In the UK, up to 50 million working days are lost each year because of the condition. It costs the UK economy up to £5 billion (€5.8 billion) per annum and the NHS more than £480 million (€564 million). The lifetime prevalence of back pain is 60-85 per cent.

Aetiology

It is hypothesised that both nociceptive and neuropathic components contribute to a patient’s low back pain (LBP). The nociceptive component is due to stimulation of nociceptors in muscle, ligaments, tendons and small joints. 

This is also known as simple musculoskeletal back pain. It occurs predominantly in those aged 20-55 years. Pain occurs around the lumbosacral area and buttocks. It may radiate into the upper thigh, but rarely below the knees. 

Pain arising from intervertebral discs accounts for 40 per cent. This results from leakage of contents of the nucleus pulposus (central area) through disruptions of the annulus fibrosus (outer layer). Sacroiliac pain accounts for 20 per cent of musculoskeletal pain, with lower lumbar facet joint pain accounting for 10-15 per cent in young adults and up to 40 per cent of cases in the elderly. Sprains and tears of spinal ligaments may also be causative. 

Lumbar spine muscles may also be a source (myofascial pain). This is characterised by trigger points palpable in taut bands.

Neuropathic components are also involved. Neuropathic pain is defined as “pain resulting from a lesion or dysfunction of the peripheral or central nervous system” by the International Association for the Study of Pain. 

Neuropathic components of LBP can result from direct compression of nervous tissue or from irritation of nervous tissue by inflammatory mediators. Radicular nerves can be compressed at the intervertebral foramina, the lateral recess, or in the spinal canal. Posterior disc herniation can compress nerves directly. 

Discs become increasingly prone to herniation secondary to degeneration of the annulus fibrosus. Chemokines and cytokines released from degenerative discs can result in chemical stimulation and radicular nerve pain. 

The most common age for disc herniation is 30-55 years. Spinal stenosis occurs due to bone and ligament hypertrophy reducing the diameter of the spinal canal and intervertebral foramina.  This usually occurs after 55 years of age and causes compression and chronic inflammatory changes of the nerve roots. 

Epidural adhesions can also lead to neuropathic pain. They can occur secondary to surgery and chronic inflammation (as a result of leakage of nucleus pulposus from damaged discs or cytokines released from facet joints).

Since treatment differs for neuropathic and nociceptive components, it is important to distinguish the predominant component so that treatment may be tailored accordingly. To this end, a screening tool specific to LBP (painDETECT questionnaire; PD‑Q) has been developed by Freynhagen et al and validated to determine the predominant pain component.  

‘Red flags indicate the presence of tumours, infection, serious trauma, inflammatory diseases and Cauda Equina Syndrome. They include age <20 or >55, significant trauma, unexplained weight loss and widespread neurological changes’

In their large epidemiological study, they found the prevalence of a predominant neuropathic component of LBP to be 37 per cent — 35.3 per cent of LBP patients had a predominantly nociceptive type of pain. Patients with a predominant neuropathic component were shown to have higher average (6.6 vs 5.2), current (6.5 vs 4.6) and worst (8.1 vs 7.0) VAS pain intensity scores, longer duration of pain treatment (73 vs 56 months) and more physician visits for pain. 

They also were more likely to have depression (91.6 per cent vs 63.7 per cent), panic/anxiety disorders (15.4 per cent vs 3.9 per cent), sleep disorders (24.5 per cent optimal sleep vs 47.8 per cent) and reduced functionality (41.4 per cent remaining functionality vs 62.3 per cent). 

Thus, neuropathic predominant pain results in a decreased quality of life and separating neuropathic and nociceptive predominant pain should be made an early goal in the management of LBP.

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Chronicity: pathogenesis

Acute LBP can become chronic. A systematic review by Pengel et al shows that pain and disability scores decrease rapidly in the first month of LBP. Most of those off work also returned to work within one month. 

However, after three months, pain, disability and return to work remained almost constant. Approximately one-third of patients with LBP develop persistent pain that lasts for over one year. 

Breivek et al estimated the prevalence of moderate-to-severe chronic pain in Europe at 19 per cent. Chronic pain was defined as pain lasting more than six months, with an intensity of 5 or more on a Numeric Rating Scale: 0 (no pain) to 10 (worst pain imaginable). 

The prevalence of chronic pain in both Ireland and the UK was 13 per cent. The highest prevalence was 30 per cent in Norway and 42 per cent of these patients had pain located in the back, while 20 per cent reported the cause of their chronic pain as deteriorated or herniated discs, degeneration or fractures of the spine. Inadequately-managed acute LBP can increase the risk of chronicity.

Chronic pain results from changes in both the central nervous system (CNS) and peripheral nervous system (PNS). It is generally agreed that the risks of developing chronic pain include genetic predispositions and prior exposures to injury, as well as psychosocial factors that are less readily identified, such as catastrophising, social support, economic status, pain expectation and past experiences. 

Neuroimaging studies have identified the brain regions that are activated by noxious stimuli. The somatosensory cortices and the insula appear to process the sensory aspects of pain, including location, duration, intensity and character. 

The prefrontal cortex and limbic system are responsible for the emotional responses. The interaction between these sites allows emotional responses to alter the experience and perception of pain through interactions with the descending inhibitory modulatory system.

It has been suggested that an imbalance between facilitatory and inhibitory descending modulatory systems may underlie pathological pain states. Several human studies support the theory that chronic pain is related to dysfunction of descending inhibitory systems.

Targeting therapy at these mechanisms of nociception regulation provides opportunities for more successful acute pain management, as well as the prevention of chronic pain.

Management

The first step in the management of LBP is a diagnostic triage classifying patients as: (1) non-specific low back pain; (2) serious pathology; or (3) nerve root involvement. 

Diagnosis should focus on exclusion of serious pathology by assessing for red flags. 

Red flags indicate the presence of tumours, infection, serious trauma, inflammatory diseases and Cauda Equina Syndrome. They include age <20 or >55, significant trauma, unexplained weight loss and widespread neurological changes. 

Neurological examination should include power, reflexes, sensation and straight leg-raise. 

Routine use of imaging is not recommended. Imaging is only recommended at the initial visit for cases of suspected serious pathology. Imaging is sometimes recommended where sufficient progress is not being made after four-to-eight weeks. The imaging modality of choice is MRI. However, imaging reveals many false positives. 

MRIs of pain-free subjects have highlighted the presence of asymptomatic herniated discs, marked degenerative changes and nerve impingement. Thus, the findings from imaging need to be interpreted in the context of the clinical presentation. 

It is essential to assess associated disability. Specific questions should be asked about impairment of activities of daily living (personal care, mobility, work, social activities, sleep). Questionnaires can be used as more objective assessment tools (Oswestry Disability Index and the Roland Disability Questionnaire). Features of anxiety and depression should also be sought.

Management of non-specific LBP differs for acute and chronic presentations. For acute, non-specific LBP, the first step is advice and reassurance that the patient does not have a serious disease. Activity should be encouraged, with a gradual increase in activity levels, as tolerated (walking, cycling). Supervised back exercise programmes are not indicated for acute LBP. 

Early return to work and normal activities should also be stressed. Bed-rest is not recommended. Time-contingent medication can be prescribed, if necessary. Paracetamol is first-line, with NSAIDs second-line if tolerated where paracetamol is insufficient alone. Muscle relaxants, opioids, antidepressants and antiepileptic drugs can be considered as co-medication. 

For management of chronic, non-specific LBP, supervised back exercise programmes are recommended. 

There is no evidence that one form of exercise is superior to another. Expensive training programmes and equipment are not recommended. Similarly, modalities such as ultrasound and electrotherapy have no role in chronic, non-specific LBP. Recommendations regarding spinal manipulation vary. Addressing psychosocial issues is crucial with cognitive behavioural therapy (CBT) of proven benefit.

‘There is no evidence that one form of exercise is superior to another. Expensive training programmes and equipment are not recommended. Similarly, modalities such as ultrasound and electrotherapy have no role in chronic, non-specific LBP’

Targeting of the descending regulatory pathways provides a pharmacological avenue for prevention of chronification, and can improve pain intensity in chronic states. 

The diminished activity of serotonin and norepinephrine in the descending inhibitory pain pathway in the spinal cord is thought to contribute to persistent, chronic pain mechanisms. Unlike serotonergic pathways, the descending noradrenergic pathway has only been shown to have anti-nociceptive effects. 

Treatment of chronic pain includes monoamine reuptake inhibitors and opioids. Opioids are usually used for moderate-to-severe acute or chronic pain when pain control cannot be achieved with first- and second-line agents, paracetamol and NSAIDs for inflammatory pain and monoamine reuptake inhibitors and anticonvulsants for neuropathic pain. 

An expert panel, commissioned by the American Pain Society and the American Academy of Pain Medicine, reviewed the evidence on chronic opioid therapy for chronic non-cancer pain and concluded that it can be an effective therapy for chronic non-cancer pain in carefully-selected and monitored patients. 

The analgesic effects of opioids are mediated through the activation of mu-opioid receptors in the CNS that can inhibit afferent nociceptive impulses. Mu-opioid receptors in the mid-brain and brainstem activate descending inhibitory pain pathways or suppress descending facilitatory pain pathways.

Monoamine re-uptake inhibitors are drugs that block the reuptake of one or more of the three major monoamine neurotransmitters (serotonin, norepinephrine and dopamine). These include tricyclic antidepressants, SSRIs and SNRIs. They have been traditionally used for neuropathic pain but are also useful in chronic pain. They enhance the activity of descending inhibitory pathways by blocking serotonin or noradrenaline reuptake. 

The analgesic effect has been traditionally attributed to the blockade of noradrenaline reuptake over serotonin re-uptake. Serotonin can be pro- or anti-nociceptive, depending on which receptors it activates (5-HT1, 5-HT2 anti-nociceptive, 5-HT3 pro-nociceptive). Accordingly, the efficacy of SSRIs has been shown to be lower than that of SNRIs.

Tapentadol is a centrally-acting analgesic used for acute and chronic pain that combines mu-opioid receptor agonism with inhibition of reuptake of neuronal noradrenaline. It has been shown to potentiate descending pain inhibition in chronic pain patients.  

It is indicated for nociceptive, neuropathic and mixed types of chronic pain. It has been shown that there is a low risk of withdrawal after cessation, a favourable pharmacokinetic profile with low risk of interactions and low potential for abuse. It has also been shown to improve pain scores and quality of life scores (EuroQol 5D, SF-36) in patients with chronic LBP and osteoarthritis treated for one year. Furthermore, its long-term safety was also demonstrated in this study.

Tapentadol has also been shown to be effective for chronic LBP. It has been shown to reduce three-day average numeric rating scale (NRS-3) pain scores in chronic LBP patients with and without a neuropathic component who were being inadequately managed with WHO step I and II medications. 

Three-day average pain scores on an 11-point numeric rating scale were reduced by a mean of 2.4 in those without a neuropathic component and 3.0 in those with, from a starting mean of 5 after six weeks of titration. 

Tapentadol prolonged-release (PR) was administered twice daily and titrated up to a max of 250mg twice daily, with tapentadol immediate-release being used for acute pain episodes. 

Tapentadol was also associated with significant improvement in neuropathic pain symptoms, decrease in number of pain attacks and duration of spontaneous pain in the last 24 hours in patients with a neuropathic component. The most common treatment adverse effects (>10 per cent) reported were nausea, dizziness, dry mouth, fatigue, constipation, diarrhoea, nasopharyngitis and somnolence.

A recent randomised, controlled trial has shown tapentadol PR to be more effective in reduction of NRS-3 scores compared to oxycodone/naloxone PR in opioid-naïve chronic LBP patients with a neuropathic component after a three-week titration and nine-week continuation period. 

Improvements in painDETECT and Neuropathic Pain Symptom Inventory scores were significantly greater with tapentadol. This randomised, controlled trial also showed significantly lower incidences of constipation and nausea with tapentadol PR vs oxycodone/naloxone PR. 

Improvements in the Short Form-12 physical component summary and EuroQol-5 Dimension health status index and health state assessment were also significantly greater with tapentadol PR vs oxycodone/naloxone PR.

Conclusion

LBP has a lifetime prevalence of 60-to-85 per cent. Both nociceptive and neuropathic components contribute to the pain. 

It is important to establish the predominant aetiology so that treatment may be tailored accordingly. Screening tools can be used for this purpose. 

Patients with a predominant neuropathic component have been shown to have higher pain scores and suffer more comorbid conditions. 

An imbalance between facilitatory and inhibitory descending modulatory systems may underlie pathological pain states. 

Management begins with out-ruling of any red flags for serious pathology. Any comorbid psychosocial issues should be sought and addressed. Activity should be encouraged and time contingent analgesics prescribed. 

Tapentadol is a mu opioid receptor agonist that also inhibits re-uptake of noradrenaline and potentiates descending inhibitory pathways. It has been shown to be effective in reducing pain scores and improving quality of life scores in chronic LBP.

Disclosure

Dr Donal Harney and Dr Bill Walsh have written this article in consultation with Grünenthal Pharma Ltd. No payment has been made and the authors have retained full editorial control.

References on request

Date of Preparation: September 2016,  IRE/G16 0024

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