What Causes Chronic Pain From a Whiplash Injury?Despite many studies on whiplash patients, we still don't know why some people get better quickly while others suffer head and neck pain for months to years after the injury or accident. In this study from the Danish Pain Research Center, previous studies are continued looking for more clues to the problem.
In the past, risk factors for the development of disabling, chronic whiplash-associated disorder (WAD) were identified. These included female gender, number of non-painful symptoms, and total degrees of active neck range of motion. Using these risk factors, the researchers conducted this study. They put patients in one of two groups according to their risk (high vs.low) of developing a chronic whiplash-associated disorder (WAD).
Everyone was in a rear end or front-end car accident and had an acute whiplash injury. Symptoms of neck and jaw pain, headache, and/or decreased neck motion were reported within the first three days of the injury. It's during this time that scientists think cells called nociceptors become overly sensitive. Nociceptors are pain receptors, cells that recognize and process noxious or irritating, pain-inducing stimuli. When this happens, the patients don't recover, but go on to develop problems with chronic pain.
The high-risk group was further divided in two parts and labeled recovered high risk and nonrecovered high-risk whiplash patients. It was the high-risk group that was of interest to these researchers. Using tender points and mechano-sensitivity after injury, they tried to see if these two variables were different in the two groups. They asked the question: were the values different enough in the first few days after injury to use them as predictors of patients who would develop chronic WAD?
And they looked to see what happened to these early changes -- did they stay the same? Did they get better or worse over the next 12 months? Tender points were assessed by pressing on them and having the patient respond subjectively.
In other words, the patients labeled their pain from zero (no pain) up to four (unbearable pain). Besides the already established sensitive points, four paired (control) points were also pressed. Using points away from the neck helped show if the pain response to whiplash was specific (just the head and neck) or more generalized (all over the body).
A second measurement called stimulus-response between pressure and pain was taken. A special tool called an algometer was used. Pressure was applied using between 50 and 800 kPa. Three muscles were tested: the masseter (jaw muscle), the trapezius (on top of the shoulder), and tibialis (lower leg muscle). Different levels of pressure were applied randomly the first time. The same pattern or order of sequence was repeated each time the patient was re-tested. This is a test of mechano-sensitization (sensitivity of the mechanoreceptors that register pressure).
Non-recovery was defined as inability to return to work or failure to return to work at a level equal to the status before injury. This outcome measure was referred to as reduced work capacity. Decreased work hours, simplified tasks, loss of a job, undergoing retraining for a new job, and being on disability are all examples of reduced work capacity. Work capacity was chosen to define recovery because previous studies showed that high-risk patients were 10 times more likely than low-risk patients to experience reduced work capacity.
The researchers did compare jobs between those patients who did recover versus those who didn't. This could have been a deciding factor, but it turned out there were no real differences in this regard between the two groups. What they did find was that the non-recovered patients had more tenderness in all muscles tested (local and regional) compared to recovered patients.
They also had more sensitive mechanoreceptors, not at first, but later on at the end of the year. The non-recovered patients had limited neck motion during the acute phase as well as during the months leading up to the progression from acute to chronic pain. Even 12 months after the injury, all the muscles tested were still ultra tender to touch and pressure.
The fact that the nonrecovered patients had a hypersensitivity response early on after the injury (compared to the recovered group) suggests the possibility that something was going on even before the injury. The fact that there may be pre-injury factors that set off the sensitization process is new information. And the discovery that symptoms spread over time points to some kind of dynamic pain process after injury in these patients.
The authors weren't sure how to explain the spread and referral of muscle pain. There are many possible explanations but no real answers yet. Other research using the stimulus response function to measure pain responses after whiplash injury have proposed the possibility of changes in neurologic systems between the spinal cord and brain. Similar altered sensitization in patients with conditions like fibromyalgia support this idea.
All of these results take us back to the original question: are there other reasons for the chronic pain following whiplash injury than the injury itself? This study confirms what other studies have suggested: the pain sensitization is coming from a central pain control system.
Centralization of pain points the finger to the nervous system as the cause of the problem. Somehow these patients become overly sensitive to stimulus because nociceptive receptors respond to the slightest input of pressure. No more can be said beyond that without further study.
But these results do give us treatment ideas to help high-risk patients early on. Medications, psychologic treatment, or physical therapy may be able to take advantage of the plasticity of the nervous system and change the pain messages during the acute phase of recovery. Plasticity refers to the flexibility of the nervous system (brain and spinal cord) to change, recover, or return to normal function.
Helge Kasch, et.al. Deep Muscle Pain, Tender Points and Recovery in Acute Whiplash Patients: A 1-year Follow-Up Study. In Pain. November 15, 2008. Vol. 140. No. 1. Pp. 65-73.
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