Low Back Pain is one of the most common musculoskeletal conditions with a lifetime prevalence between 70-85%. Ninety percent of the population will improve, but the other 10% will go on to develop chronic low back pain (cLBP). Known as a "Western Epidemic," it is estimated that the total costs of LBP each year amount to 100 billion dollars in the United States alone (Tsoa 2008). Chronic pain is defined as pain lasting longer than 6 months that is not related to a malignancy. Our current belief of pain roots from the traditional medical model that pain is a "physical response to an organic dysfunction (Wolff 1991)." Throughout the medical community there has been a push to change that traditional thinking pattern. New pain models are being produced with reliable data to support their findings.
New Pain Models:
One such model is the kinesiopathologic model of pain. This model focuses on altered neural control and cortical feedback as the source of a patient's symptoms. It is no longer simply mechanical tissues that are involved. Since cortical regions are partially responsible for postural control, altered cortical activity could therefore be responsible for altered postural stability. Coincidentally, patients with cLBP often demonstrate postural instability and altered muscle timing. Researchers have speculated that patients with cLBP require a more direct influence of their executive motor systems to perform postural coordination tasks. In healthy subjects, these tasks are automatically controlled by sub-motor systems. Therefore, pain alters how the brain processes postural coordination. Several studies have shown decreased deep abdominal and back muscle activation along with increased superficial muscle activation in cLBP patients (Tsoa 2008). Repetitive posturing and abnormal movement patterns expose the lumbar spine to low load long duration forces, creating abnormal movement. Therefore, rehabilitation of cLBP should include retraining of postural coordination (Jacobs 2010).
Delving deeper in the altered muscle timing, Tsoa et al found decreased transversus abdominus (TrA) firing in patients with recurrent low back pain. The study demonstrated how cLBP patient's had poor anticipatory postural adjustments when performing rapid voluntary limb movements. Since anticipatory postural adjustments occur before movement, they must be controlled by the central nervous system. In healthy subjects, there was an appropriate feedforward mechanism, and subjects would involuntarily contract their TrA prior to arm movement. The same was not true for recurrent LBP patients. They demonstrated decreased TrA timing when asked to perform an arm movement.
Imaging of the brain in patients with cLBP has shown plastic changes that have occurred in the gray matter of the thalamus and prefrontal cortex. When confronted with a painful stimuli, these same individuals had increased cortical activation and decreased blood flow to the contralateral thalamus (Kobayashi 2009). Kobayashi found a disproportional exaggeration to painful stimuli, indicating there may be a behavioral characteristic to patients with cLBP. The authors outline a "pain matrix" that exists in patients with cLBP. The matrix includes the prefrontal cortex, insular cortex, posterior cingulate gyrus, supplementary motor area (SMA), and premotor areas (PMA) of the brain. The insular cortex and prefrontal cortex are both important in the affective and cognitive components of pain. Additionally, the SMA and PMA are involved in motor planning. It can be assumed that if these portions of the brain are altered in cLBP, their functions will be altered as well. Instead of promoting positive behaviors, cognition and motor planning focus on protective behavioral responses, trying to avoid pain.
Additionally, if we view pain from the neuromatrix approach, it must be understood as a multiple system output. As stated above, it is thought that pain reduces the cortical output capacity, which decreases cognitive functioning and increases error rate. As clinicians this is evident in our chronic pain patients, who are often easily distracted and forgetful. Moseley states that pain decreases the immune response, alters sympathetic nervous system activity, and decreased reproductive system activity. This same article found increased pain activation in the anterior cingulate cortex (ACC) (Moseley 2003). This region is responsible for emotional stability and strategizing motor planning. Consistently, patients had an exaggerated hypersensitivity to stimuli. Small inputs were enough to stimulate the brain and incur pain. With a heightened response and altered emotional control, we can see why these patients are timid to perform their typical ADLs.
How can we treat chronic pain?
In order to be successful when treating patients with chronic pain, you must understand their suffering as greater than simply a mechanical issue. You must search for the root of the patient's pain. The mechanism based classification of pain is a system that divides pain into categories based off the tissue/ structures that are involved. This classification divides pain into 5 categories: central sensitization, peripheral sensitization, peripheral nociceptive mechanism, sympathetically maintained, and cognitive-affective mechanism. Based off the particular mechanism that is being considered, the patient will present with specific symptoms. For central sensitization, the somatosensory system is at fault. Neurons and nociceptive pathways are receiving altered information. As clinicians, patients who suffer from this type of pain often report hypersensitivities to light, noise, mechanical pressure, and temperatures. Education, pain relieving modalities, and relaxation are KEY to a successful treatment. The peripheral mechanism is defined as pain "rooting from the peripheral nervous system" (Kumar 2011). These patients will often have positive neurodynamic tests. Treatment includes neural mobilization and nerve massage. The peripheral nociceptive mechanism is the traditional belief of pain that symptoms root from either a mechanical or visceral structure (anything but the peripheral nerves). Pain travels through small diameter afferents via the Gate Control Theory. Clinical presentation includes swelling, redness, pain with movement, and pain with palpation. Treatment includes exercise, manual therapy, stretching, and modalities. Sympathetically maintained pain is often defined as chronic pain that is "out of proportion to the injury." Clinical representation includes autonomic dysfunction (vasomotor changes and inflammatory responses) and deep achy pain that is unrelieved by positions. Treatments include Thermal therapy, TENS, and Sympathetic trunk mobilization. Finally, the cognitive affective mechanism includes the psychological component of pain. Graded exposure, relaxation, and distraction are all beneficial in treating this mechanism of pain. When seeing patient with chronic pain, often more than one of these mechanisms will be at play. Being able to differentiate which mechanisms are the root of the patient's symptoms will allow treatment to be most effective.
As we saw above, education is extremely important with these patients. But how do we educate? One systematic review we analyzed considered the effects of Neuroscience Education (NE) with your cLBP patients. NE is a cognitive-based education tool focused on decreasing pain and disability by increasing the patient's awareness of the nervous system. Our initial reactions were that patients would not have the capabilities to understand how the nervous system processes, but studies have reported that this method can have "immediate improvements in pain, cognition, and physical performance" (Louw 2011). The NE session could be administered in as little as 30-45 minutes and integrated with other physical interventions. Common resources used include teaching tools, hand-drawn images, pictures, workbooks, and neurophysiology pain questionnaire.
Additionally, the Moseley article suggests a 3 part intervention system that addresses identifying the painful stimulus, targeting components of the neuromatrix (while avoiding a flare up), and gradually introducing new stimuli to increase physical function. These concepts are very similar to what Louw identifies in his neuroscience education approach as explained above. Ultimately, respect the patient's suffering, make sure they understand his/her pain, and establish functional baselines.
While Neuroscience Education and other pain specific interventions are important, we cannot forget our core exercises when working with cLBP patients. Many of these patients exhibit altered muscle recruitment of the lumbar multifidi, which are responsible for intervertebral motion. Additionally, they demonstrate increased superficial back musculature activation with movement, which arguably increases spinal loading. One study we evaluated assessed 20 patients with unilateral LBP lasting >3 months. Ten of the subjects were placed in a "skilled intervention group" that involved using cognitive attention to activate the lumbar multifidi (LM). The other 10 subjects were put into an "extension exercise group" that focused on activating all paraspinal muscles together non-selectively. The study found that skilled training allowed for greater activation of the lumbar mulitifidi and reduced activity in the superficial paraspinals. This knowledge can potentially decrease abnormal spinal loading and the patient's symptoms.
In conclusion, respect your patients' symptoms. Many of these individuals have had pain for a long time. Their perception of pain is altered, which affects their ability to move properly. Repetitive abnormal movement creates more pain and more disability. Find the root of your patients' symptoms and begin to retrain how they think and move!
Here is a nice video that explains pain in patient friendly terms:
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