Back pain is a leading cause of disability. It occurs in similar proportions in all cultures. It can be due to specific causes but most are non-specific. Acute back pain occurring for less than three months is the most common presentation. It usually settles on its own, regardless of the treatment. Chronic back pain is complex, as it has a significant psychological component. 

The International Association for the Study of Pain (IASP) has defined chronic pain as persistent pain beyond the normal tissue healing time, assumed to be three months.¹ The National Institute of Health and Care Excellence (NICE) defines chronic low back pain as pain, stiffness or muscle tension in the low back region with or without leg pain for longer than six to 12 weeks.²

Types of pain and assessment

Nociceptive pain is due to persistent stimulation of nociceptor inflammatory mediators. Primary dysfunction in the nervous system can also lead to the persistent pain, known as neuropathic pain. This type of pain is either the result of direct injury to the nervous system or alteration in the processing of sensory input. Often both types of pain, nociceptive and neuropathic, exist together (see Table 1 and 2).

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In more than 80% of patients pain cannot be attributed to a specific cause. In a minority of patients, low back pain is caused by a specific serious disorder, such as spinal infection (0.01%), spinal compression fracture (4%) or cancer (0.7%). Spinal stenosis and cauda equina are present in 3% and 0.04% respectively.³

A practical approach is to take a focused clinical history and physical examination to find the underlying cause and extent of the neurological involvement. This approach will facilitate categorisation of the patient into one of the following categories:

• Non-specific low back pain
• Low back pain with local pathology
• Low back pain with radicular element
• Low back pain with underlying serious pathology

(‘red flags’).

The final category above includes the very minority of patients with serious underlying pathology that is associated with progressive neurological damage. This group of patients needs emergency referral and MRI scanning.

A clinician should enquire about location of pain, duration of symptoms, frequency of symptoms, intensity and nature of pain, relieving and exacerbating factors, as well as any previous related symptoms and response to treatment. The possibility of low back pain outside the spine should be considered such as aortic aneurysm (compression effect), systemic illness (infection of para spinal structures), and nephrolithiasis (referred pain). Patient should be assessed neurologically. The presence of any bladder or bowel dysfunction may indicate underlying neurological involvement. Urinary retention is the most frequent finding in cauda equina syndrome. In the absence of urinary retention, chances of cauda equina are 1 in 10,000.³

Clinicians should enquire about risk factors for malignancy and infection. Previous history of cancer, age > 50 years, unexplained weight loss, and failure to improve after four weeks are associated with higher likelihood for cancer.⁴ Risk factors predicting spinal infection have not been well studied but may include intravenous drug use, recent systemic infection, immunocompromised and endemic tuberculosis.⁵ Clinicians should be aware of risk factors for compression fractures, such as advanced age, osteoporosis and steroid use. The risk factors for ankylosing spondylitis include young age, morning stiffness and alternating pain in gluteal area.⁶

Nerve root involvement can be assessed by a straight leg raise test. A positive result on straight leg raise (production of pain at 30º-70º of leg elevation) has high sensitivity (91%) but modest specificity (26%) for diagnosing herniating disc.⁷ In contrast crossed straight leg raise test is more specific (88%) but less sensitive (29%).

Psychosocial factors should be assessed as they are stronger predictors of low back pain outcomes over physical examination findings or severity and duration of pain.⁸

Chronicity and effects on quality of life

Chronicity of low back can be due to end organ dysfunction or alteration in the processing of nervous system. The fundamental of the end organ dysfunction model is that the patient experiences pain because of a nociceptive focus in the spine.⁹ In the altered nervous system processing model, the patient with low back pain suffers from alterations in nervous system encoding or processing of sensory information, rather than from ongoing injury or dysfunction in the spine.¹⁰ The pain that most patients experience probably reflects both models.

Assessing the chronicity not only involves the duration of the pain but also includes the psychosocial impact of the pain. Psychosocial factors that may predict poorer low back pain outcomes include: presence of depression, passive coping strategies, job dissatisfaction, higher disability levels, disputed claims and somatisation.¹¹ The longer the duration of pain, the more likely the patient is to be depressed and out of work. Getting insight into these factors can be helpful. A biopychosocial model should be used to identify the following:

• Bio – identification of possible underlying pathology
• Psycho – distress, avoidance behaviour, current coping strategies
• Social – work related problems, family/friends circumstances.

Various tools can be used to assess the risk of chronicity of low back pain. One of them is Keele START back tool that is being successfully embedded in primary care.¹² It helps the physician to categorise patients into low, medium and high risk for chronicity of low back pain.

Chronic pain has a devastating effect on the quality of life of patients, who can often suffer from anxiety and depression.¹³ They have much poorer quality of life compared to the general population. Approximately 75% of patients report being less able or unable to sleep. Nearly one in five patients have trouble with relationships and one in six feel their pain is so bad they want to die.¹⁴

Realistic targets

Patients should be educated on the likelihood of favourable outcomes of low back pain and a significant  improvement in four weeks’ time.⁸ Clinicians should explain that early imaging usually cannot identify a precise cause, does not improve patient outcome and incurs additional cost.

General advice on self-management for non-specific low back pain is to remain active which is more effective than rest.¹⁵ Exercise programmes may be helpful. Where patients do need rest for severe symptoms, they should be encouraged to resume normal activities as soon as possible.

Barriers to effective pain management

There are numerous barriers to effective pain management. These vary depending on whether they are viewed from the standpoint of patient, the physician or the institution. Identification and acknowledging them is the first step in overcoming them.

Patient related barriers may include reluctance to report, reluctance to take medicines and lack of compliance. Healthcare professionals may exhibit barriers in the form of lack of knowledge, poor patient assessment and fears related to the prescription of analgesics, such as potential of addiction. Institutions have low priority for pain patients, non-availability of pain specialists and high cost of new medications.

Individualised treatment goals 

Generally the treatment of non-specific low back pain is the same. Setting individualised goals may improve outcome. As there will be patients who may have significant medical backgrounds, for them it may be more than six weeks before there is any sign of improvement. There may be patients who are tolerant to analgesics, which may alter the approach to treat their pain. At the same time, if an individual’s goal is not being achieved this may alert the physician. In such cases early referral to pain services may improve the outcome.

Medication options – a stepwise approach

For the management of acute or chronic low back pain, acetaminophen (paracetamol) is the first-line drug. Patients should be encouraged to take the full adult dose (1g x 4 per 24 hours). Acetaminophen is associated with asymptomatic elevation of aminotransferases at 4g/day in healthy individuals. The significance of this is not known.¹⁶ Non-selective NSAIDs are more effective than acetaminophen but are associated with well-known gastrointestinal and renovascular side-effects. Patients should be fully assessed for associated risk factors and NSAIDs should be prescribed for minimal effective dose and shortest duration necessary.

Opioids have a role when used judiciously. Because of substantial associated risks, the potential benefits and risks of opioids should be carefully considered before starting therapy. Evidence is insufficient to recommend one opioid over another. Failure to respond to time and dose-limited opioid therapy should lead towards re-evaluation and further referral. 

Skeletal muscle relaxants are a diverse group of drugs. They act on different sites. Commonly used are tizanidine (centrally acting, alpha agonist) and baclofen (centrally acting, GABA agonist). There is no compelling evidence that they differ in their efficacy or safety profile.¹⁷ They are indicated for acute and short term use only.

Antidepressant tricyclics such as amitriptyline are commonly prescribed for low back pain with a neuropathic element. Precautions should be taken in patients with ischaemic heart disease and arrhythmias. Serotonin and noradrenaline re-uptake inhibitors (duloxetine, venlafaxine) have not yet been studied for their role in back pain. 

Gabapentinoids (gabapentin/pregabalin) are commonly prescribed for back pain with radiculopathy. Benzodiazepines are as effective as skeletal muscle relaxants for acute or chronic low back pain with or without radiculopathy.¹⁷ Their use is associated with the potential for addiction and abuse. In the case of benzodiazepines, a time limited course of therapy is recommended. Corticosteroids are not recommended for the treatment of low back pain as they have not shown to be better than placebo.¹⁸

Most medication trials evaluated patients with non-specific low back pain. Evidence is limited about the benefits and risks associated with the long term use of medications for low back pain. Extended therapy should be limited to patients who clearly show functional benefits without major side effects.

Follow up and monitoring

Given that most patients will improve in four to six weeks, few require long term follow up. Reassessment of patients is necessary in those whose symptoms are not improving according to the severity of their pain. Review at six weeks if not substantially recovered.¹⁹ On reassessment if any serious pathology (red flag) is identified, consider appropriate help. Try to identify psychological risk factors and address appropriately.

Compliance with the prescribed treatment can be an indicator about patient behaviour towards pain. Early identification of those with underlying yellow flags (psychological issues) can improve the outcomes. Depending on the response to the initial pharmacotherapy, the patient might need escalation in the dose or addition of new medicines. Extra caution should be taken while prescribing opioids and drugs with sedative effects.

Interdisciplinary approach to pain 

As per IASP definition, pain has a psychological component. So along with physical and pharmacological therapy, psychological therapy has a role.²⁰ Moderately effective non-pharmacological therapies include:

• Acupuncture²¹
• Exercise therapy²²
• Cognitive behavioural therapy²⁰
• Spinal manipulation²³
• Intensive interdisciplinary rehabilitation.²⁴

There is insufficient evidence to recommend any specific treatment as first-line therapy. Patient expectation and engagement regarding benefit from specific therapy should be considered before choosing the intervention. Intensive interdisciplinary rehabilitation may not be available in all settings.

Treatment at pain clinic

Most patients who are referred to a pain clinic have already tried pharmacotherapy. Depending on the facilities in the pain clinic, additional options include:

• Rationalising pharmacotherapy
• Multidisciplinary rehabilitation (pain management programme)
• Interventions
• Neuromodulation.

Many chronic pain sufferers get benefit from slight changes in their medications. This change can be in the form of an increase in the dose of analgesics or adding more medicines with different mechanisms. NMDA receptor antagonist (ketamine) and cannabinoids can be potential options at this stage. However, scientific evidence is not compelling for this option.

Pain management programmes (multidisciplinary rehabilitation) involve a pain physician, psychologist, physiotherapist and occupational therapist. They are run over three to eight weeks, four to five hours per day, using cognitive behavioural therapy principles. There are individual and group based therapies, as well as scheduled team conferences to facilitate progress, troubleshoot patient problems, build consensus, aid communication regarding progress and adjust goals of therapy.²⁶ Long term follow up studies of multidisciplinary treatment programmes demonstrate improved return to work rates, pain reduction and improved quality of life.²⁷

Interventions range from trigger point injections (TPI) in the paraspinal area to invasive procedures such as transforaminal epidural and implantable devices. Development of new procedures and evolution of existing procedures continue as our understanding of pain pathophysiology improves. The evidence base regarding efficacy continues to strengthen. 

Depending on the diagnosis, different procedures can be performed. Facet joint arthritis is one of the common causes of chronic low back pain. Diagnosis of facet mediated pain can be confirmed by diagnostic block of the joints. Rhizotomy can then be performed for pain relief of eight to 12 months.²⁸ Chronic low back pain with radicular symptoms can be due to entrapped nerve roots. This entrapment can be either due to herniated disc (generally in patients < 50 years) or degenerative disc disease or foraminal stenosis (in patients > 50 years).

The possible interventions include interlaminar epidural or transforaminal epidural. In patients with radicular pain secondary to disc herniation, transforaminal epidural steroid nerve root injection is more effective than interlaminar epidural.²⁹ Other possible interventions for this group of patients include pulsed radiofrequency lesioning of the dorsal root ganglion.

Possible interventions for discogenic pain include intradiscal corticosteroid injection, intradiscal electrothermal therapy and ramus communicans nerve block. There are stringent guidelines from the International Association for Study of Pain (IASP) which state that two levels must always be tested as controls when performing provocative discography.³⁰ A disc is only considered to be provocative if concordant pain can be induced at the target level and if control levels were negative for provocation.

Reported prevalence of SIJ (sacroiliac joint) mediated pain in patients with chronic low axial pain varies from 15-30%.³¹ In addition to clinical examination, positive diagnostic injection is needed to confirm the diagnosis of SIJ mediated pain. Intervention related options include the injection of steroids in the joint. Pulsed radiofrequency lesioning of the lateral ramus (L5-S3) can provide pain relief for longer duration.³²

In older patients, chronic back pain is generally secondary to degenerative spine disease and/or spinal stenosis. Epidural corticosteroids can provide pain relief of variable duration.

Neuromodulation is indicated for patients who fail to respond to pharmacotherapy and interventions. It can be done electrically and chemically. Electrical neuromodulation, also known as spinal cord stimulation, is indicated for a number of conditions. Among patients with chronic back pain, failed back surgery syndrome patients are candidates for spinal cord stimulation.³³ The procedure involves insertion of leads in the epidural space, as a day case, with leads connected to a pulse generator. Stimulation of dorsal column by electrical impulses can impair the transmission of pain signals to the brain. Once implanted the stimulator can last up to 10 years.

Chemical neuromodulation involves the delivery of drugs into the intrathecal space via an intrathecal catheter in the subarachnoid space. Indications include patients who failed to respond to spinal cord stimulation or their pain is widespread.³⁴ Drugs are delivered directly to the subarachnoid space via implantable pump. Morphine, hydromorphone and ziconotide are commonly used. An intrathecal pump lasts for six to eight years and is replaced subsequently. This technique requires regular follow up and pump refill every six to eight weeks. It is associated with higher rates of complication as compared to spinal cord stimulation.

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