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.
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.
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.
The upper three main neck segments may refer pain into the head and the lower ones down to the first thoracic segment may refer pain into the arm. In some cases an increased response to stimulation may be present in areas of the body or limbs where the patients are reporting no symptoms. An increase in the responses to mechanical stimuli (hyperalgesia) is present in typical neck pain and in people who have whiplash, but the latter may have more complex disturbances of neurological functioning. They may react more strongly also to pressure, heat and cold, the reasons for this not being clear.
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.
