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Patients report widely diverging levels of disability and pain in response to neck problems, with some have almost no disability and little pain and others with severe interference with normal life and high pain report. There may be different neurological and pathological events which underlie this variety which reflect the neck syndrome present. Initially most work was on finding an anatomical site of injury or damage to explain the symptoms but this has led to limited success in explaining the clinical syndromes. The pain mechanisms which may be responsible for the reported symptoms are now increasingly investigated.
One way to allow more accurate whiplash treatment to be identified is to clarify which diagnosis and which pain syndrome in present in an individual patient’s neck pain problem. Neck injury can consist of long term postural abnormality, repeated small trauma in activity or an obvious event such as whiplash injury. Any inflammation which is present in these cases in known to significantly change the ways pain is processed both in the central nervous system of the brain and the spinal cord and in the locally damaged area. Even though most research has been performed on animals this can be taken seriously when considering pain in humans.
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.
Hyperalgesia in the neck occurs in all whiplash injuries to some degree, whatever the severity, but settles over two to three months in those who recover or only have mild symptoms. Hyperalgesia has been found to persist in those with ongoing and more severe pain symptoms. The nerves in the local areas of damage may be sensitised and patients with whiplash have been shown to have damaged structures in cases where pain and disability has continued. Another argument is that the nerves in the central nervous system become sensitised by the pain inputs and this is responsible for ongoing pain.
So there can still be damaged internal anatomical structures in neck pain syndromes which can be ongoing sources of pain, while central nervous system pain mechanisms are assumed to be mostly responsible. Cervical facet joint blocks have shown they are a potential pain source in a number of patients who have chronic whiplash. Referred pain, which is a pain which is felt in the body at a distance from the presumed pain source, is also common. Incoming stimuli from pain sites in discs, joints, ligaments or muscles may be interpreted as coming from regions which are neurologically linked to them.
Head pain can be referred from the upper neck segments of the third cervical vertebra and above, with arm pain potentially referred from those segments below this level and down to the first thoracic vertebra. Even in parts of the body where the patient is not complaining of any symptoms there may be evidence of a heightened pain response on testing. Both patients with general neck pain and whiplash may exhibit a hyperalgesic response to incoming stimuli. There may be a more involved upset in neurological functioning in the whiplash groups with overreaction to heat, cold and pressure.
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.
