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Pathophysiological dimension of spinal pain

Soft tissue trauma to a person’s spine stimulate the peripheral nerves located within the muscles and joints of the spine. These nerves are typically ‘A-Delta’ or ‘C’ fibres and they may respond to a stimulus such as tissue injury or direct pressure. At the peripheral level of the nervous system, tissue damage may result in the release of chemical mediators such as potassium, prostaglandin and bradykinin. These chemicals facilitate inflammation as part of the response to injury and they may induce swelling and engorgement. In addition to this, they stimulate peripheral nerve endings and can induce hypersensitivity. Thus areas of tissue that have not been damaged directly may become sensitised ( this is know as hyperalgesia and allodynia.)

Changes to the nerves (or neuroplasticity) may occur within the spinal cord after a peripheral injury. There may be an expansion in the size of the receptive field of the secondary neuron, which means that the nerve will now respond to a stimulus from adjacent areas. The threshold required to generate an nociceptive impulse (or pain signal) is reduced and in addition to this the impulse produced is of greater size and lasts longer than before. There is also a lowering of pain thresholds so that a previously painless stimulus can now trigger neural impulses (pain signals) thus leading to the sensation of pain.

Injury and pain itself can increase muscle tension around the spine and even trigger spasm of adjacent muscles. This is thought to be a primitive protective mechanism akin to the splinting of an injured body part. However, the tension may outlast the injury and actually exacerbate the symptoms. This may be associated with changes in posture and biomechanics that perpetuate the cycle of back pain.

The spine is a dynamic and sophisticated structure and physical activity is important to maintain optimal function even in the presence of back pain. If the patient rests too much following an injury this may worsen the condition by allowing loss of muscle strength. Specifically, stabilising muscles may be less effective in preventing joint wear and tear and may fatigue more easily and generate discomfort in their own right. Patients who remain active and strengthen the muscles of their back have a better outcome than those who rely on passive treatments.

The results of radiological investigations do not always correlate with reported symptoms and signs. Indeed, some people in severe pain will have no demonstrable pathology on imaging, while many others will have visible abnormalities on their scans and yet have minimal symptoms and signs. In addition, abnormalities such as intervertebral disc bulges may come and go. The role of surgical discectomy in patients complaining of low back pain with radiculopathy is controversial and in most people, symptoms will resolve with or without invasive surgical intervention.

The best approach for the management of spinal pain is one that incorporates assessments and interventions that consider the patient as a whole. A management strategy for back pain should be tailored to an individual’s requirements and aimed at helping the patient to cope with their symptoms.

The mainstay of a management plan should involve physical rehabilitation; the promotion of regular moderate exercises and resumption of normal activities where possible. Drug therapy may also give some relief. Taking analgesics regularly such as paracetamol and non-steroidal anti-inflammatories is associated with better symptom control than taking them erratically. It can be worth exploring alternative drugs in order to optimise analgesia to facilitate physical rehabilitation, such as tramadol. If chronic nerve pain is suspected, anti-neuropathic pain drugs should be tried such as pregabalin, gabapentin or nortriptyline. Procedures such as facet joint injections and specialised epidural steroid injections may give also selected patients significant relief in the hands of skilled operators