Cervical Pain and Disability - Part One

By Jonathan Blood Smyth

The amount of neck pain and disability suffered by patients varies greatly from very low pain levels and virtually no disability to high pain levels which interfere significantly with activities of daily living. The underlying reasons for this are likely to be related to the pathological and neurological mechanisms at work in the differing neck pain syndromes. Initial focus was on identifying pathology in the cervical spine which could be responsible but this approach has not led to a complete understanding. Attention has moved towards the underlying pain mechanisms potentially responsible.

The first step towards targeting more specific and accurate e.g. whiplash treatment at someone with neck pain is to understand which neck pain syndrome is dominant in the patient's presentation. Repetitive minor events, sustained postural stresses or a defined incident such as a whiplash injury may all contribute to trauma suffered by the neck. If inflammatory changes are present due to these factors then this is understood to have profound effects on the way pain is processed in the local area of tissue damage and in the spinal cord and brain, the central nervous system. Animal research work provides most evidence but can be interpreted to understand human pain.

A whole series of chemical and neurological processes are set off by an injury and its following inflammation, all of which makes the central nervous system develop an increased response to all feelings coming in. Patients with whiplash and those with standard neck pain where the diagnosis is not clear have both been shown to have reduced tolerances to pain and a reduced threshold to pain. This reaction is termed hyperalgesia which is used to describe an increased pain response to a stimulus which is normally painful.

All whiplash injuries, whatever their severity, show some degree of hyperalgesia, but those who have mild symptoms or recover completely show a decrease over 2 or 3 months. In patients with chronic and with more severe pain presentation this hyperalgesia persists. As whiplash patients are known to exhibit damaged neck and head structures after their injury, this could cause localised areas of sensitisation. A second explanation is that there has been sensitisation of the central nervous system which then overreacts to incoming stimuli, interpreting them as pain and being responsible for pain maintenance.

While neurological mechanisms in the central nervous system may be responsible for some of the pain problems it is important not to forget that damaged neck structures may exist and be sources of pain. The neck facet joints have been shown to be ongoing pain sources in a percentage of patients with chronic whiplash. Referred pain may also occur and this is pain felt in an area away from the presumed region of damage or difficulty. The nervous system may interpret incoming pain from internal structures such as discs and facets as being in areas who share close neurological links with them.

The neck segments from cervical vertebra three upwards can refer head pain whilst those from there down to the first thoracic can give arm pain. There can be an increased pain response on testing in parts of the body where there are no reports of pain symptoms from the patients. Hyperalgesia, an increased response to mechanical inputs, is common to both whiplash patients and those with general neck pain. Whiplash patients however, may exhibit more complicated neurological disturbance with increased reactions to cold, heat and pressure but these results are not well explained.

A more widely occurring sensitivity response to incoming signals is present in patients with higher pain reports and who have more widespread symptoms. These findings are typical of syndromes such as whiplash and cervical nerve root disorder (radiculopathy, where the nerve root which is on its way out of the spinal canal towards the body is compressed or otherwise compromised along its route), both perhaps triggering a complicated change in the excitatory responses of the central nervous system to arriving pain inputs. However, this central mechanism might be kept going and sensitised by pain coming in continually from altered tissues in the neck. - 32188

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