Pain of Spinal Origin:  Low Back Pain

CME California Physicians and Physician Assistants

CME Resource 2014, Volume 139, Number 4

Pages 68 - 74

Sacramento, CA


The editorial staff of this publication developed a comprehensive review of pain of spinal origin, of which we will specifically review the section on low back pain.  They define the low back pain syndrome caused by a variety of pathologies in the lumbar spine, in addition to adjacent structures. 

They note that in patients with chronic disabling low back pain the use of cognitive behavioral therapy, progressive relaxation, yoga, or meditation, combined with progressive activity or exercise therapy produce superior outcomes relative to lumbar spine targeted approaches, such as surgery.  They also report that therapies which address well-defined mechanical problems, including back strengthening exercises for muscle weakness or atrophy, have demonstrated improvement in patients, independent of the original specific pathologic or anatomic target pain generator. 

The authors describe the alteration that can occur in the central processing section of the brain receiving sensory input and note cortical somatosensory evoked potentials have been able to demonstrate an abnormal amplitude in this region of the brain.  They explain further that this sequence of events in the brain reflect changes in the neural interactions between pain perception and motor output seen in chronic low back pain patients. 

The authors report that there has been an increase in the prevalence of chronic low back pain over the past 23 years and there has been an increase in the rate of major depression as well with an association found between major depression and the development of chronic low back pain. 

Of all the various painful problems that are known to affect the low back, nonspecific low back pain remains the highest category and at approximately 85%. 

The authors provide a detailed list of risk factors, including obesity, smoking, low education, socioeconomic and job dissatisfaction levels, psychosocial distress, somatization, depression, and psychiatric or substance abuse history, in addition to genetic factors.  They also point out that the greatest challenge for the treating healthcare provider, particularly for persistent disabling low back pain, include maladaptive pain coping behaviors, nonorganic signs, functional impairment, and low general health status, in addition to psychiatric comorbidities. 

The editorial staff provide a detailed discussion of the pathophysiology associated with the transition from acute to chronic nonspecific low back pain.  They note that although most patients with degenerative spine changes, which would include disc herniations, spinal stenosis, and foraminal stenosis, do not have pain, the current thinking is that pain in patients with disc herniation and associated radiculopathy is primarily due to chemical inflammation and not only mechanical compression.  They find that inflammatory mediators play an important role in the pathogenesis of lumbar radicular pain and low back pain in lumbar degenerative diseases.  They report that epidural corticosteroid injections suppress the functional activity of inflammatory mediators, including cytokine interferon gamma and phospholipase A2, which are agents that are believed to decrease pain from inflammation in the epidural space and surrounding the nerve roots.  

In their discussion, the authors distinguish pain resulting from injury or lesions to a peripheral nerve, dorsal root ganglion, or dorsal root arising from trauma, compression, inflammation or ischemia representing peripheral neuropathic pain.  They state that in chronic low back pain with a peripheral neuropathic pain component, mechanisms that alter the structure and function of peripheral nerves in their central terminals include sensitization of neuroconnective tissue nociceptors, ectopic excitability, cross excitation, structural changes, and neural immune interactions.

The authors discuss nonspecific low back pain, lumbosacral radiculopathy, lumbar spinal stenosis, myofascial pain, epidural compression syndrome, lumbar facet joint syndrome, sacroiliac joint syndrome, spinal cord injury, and failed back surgery syndrome.

They do point out that although most patients with low back pain can show significant improvement within 2 to 3 weeks that we need to be alert for the possibility of serious disease, such as spinal metastatic cancer or vertebral and epidural space infection, herniated disc, radiculopathy, and spinal stenosis, and that standard red flags need to be ruled out when we treat a patient with low back pain.  They review the red flags, which would include patients with recent weight loss, prior history of cancer, nocturnal or pain at rest, age older than 50, recent trauma, fever, chills, history of injection drug use, chronic corticosteroid therapy, difficulty urinating, bowel or bladder incontinence, and neurologic deficits, such as saddle anesthesia, perianal or perineal sensory loss, or motor weakness in the extremities. 

As examples, they point out the red flags for spontaneous vertebral fracture include patients older than 70, female gender, recent trauma, or prolonged corticosteroid use, or for ages older than 50 with a history of prior cancer, unexplained weight loss, failure of conservative therapy, and identifying spinal malignancy. 

They describe well the list of yellow flag risk factors, which include maladaptive beliefs and attitudes and behaviors regarding the back pain and recovery, such as passivity or reluctance of self-image, dependence on the provider to cure, fear avoidance beliefs, beliefs that harm will come from activity and discomfort, depression, anxiety, maladaptive coping response to stress, social withdrawal or isolation, and lack of social support.  This list includes adversity, economic and work environment circumstances, job dissatisfaction, excessive and inflexible physical workplace demands, high levels of work-related stress, poor workplace social support, and adversarial or dysfunctional workplace relationships.  

They caution that early detection and intervention for problematic motivational, emotional, or social dysfunction are important because these factors influence the selection and effectiveness of therapeutic interventions. 

The authors discuss diagnostic testing and the current treatments available for chronic low back pain, including nonspecific, non-radicular pain, radiculopathy pain, spinal stenosis, vertebral compression fracture, facet joint pain, sacroiliac joint pain, degenerative disc disease, myofascial pain, failed lumbosacral spine surgery, spinal cord injury, cauda equina syndrome, and spondylolisthesis. 

The editorial staff of CME Resource does an excellent job in providing this comprehensive and timely review of the subject of low back pain. 

They do appropriately note that there is strong evidence in the current research that practicing yoga is associated with significant improvement in near term pain relief, back specific disability, general improvement, and long-term pain control.  They find that the evidence for improvement is moderate, however, with yoga for significant long-term improvement in back specific disability.  They do conclude by stating that yoga should be recommended for patients with chronic low back pain. 

Editorial Commentary:  Healthcare providers treating low back pain patients would do well to review this specific presentation in the CME Resource ( and should make a point to review this type of material, in which there is evidence-based research presented in the current updates in chronic low back pain diagnosis and treatment.  In particular, we should make note that the evidence is becoming increasingly strong at this time regarding the long-term benefit of therapies directed to improving mental and physical function, including counseling and conditioning/fitness activities. 

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