Disease-a-Month ] (2016) ]]]–]]]

Contents lists available at ScienceDirect

Disease-a-Month

journal homepage: www.elsevier.com/locate/disamonth

Chronic low back pain

Joseph Alleva, MD, MBA, Thomas Hudgins, MD,
Julia Belous, MD, Andrea Kristin Origenes

Epidemiology

Due to varied clinical diagnoses of chronic low back pain (CLBP) in previous literature,
findings about epidemiological features of CLBP are inconsistent. However, there is a wide range
of prevalence of CLBP recorded thus far. Rising prevalence of chronic low back pain is attributed
to the increased disability rates and healthcare costs.1 Individuals who are at risk for low back
pain (LBP) are those who are over the age of 30 years, obese or have a high body mass index
(BMI) (BMI 4 30 kg/m2), pregnant, do minimal exercise, and have other psychosocial factors
(i.e., stress, anxiety, and depression).2,3 About 2–7% of people with acute low back pain
experience chronic pain in later stages. “Some studies have shown that chronic low back pain
that lasts for more than 3 months affects an estimated 15–45% of the population. It is also
the most common cause of disability in individuals between the ages of 45 and 65 years.”4
Cross-sectional study conducted from 1992–2006 found that the prevalence of CLBP doubled
where the prevalence of CLBP was higher for women in both the years.1 Although the incidence
of LBP is low for children (1–6%), recent studies have shown a rise in the early occurrence of LBP
in adolescents.5

Pathophysiology

While nociception refers to physiological detection of noxious stimuli, pain is a psychological

term, involving unpleasant sensory and emotional experience. Understanding the pathophysi-
ology of pain perception is essential for effective treatment. The perception of pain starts with
peripheral sensory neurons or nociceptors that get activated by noxious stimuli via free nerve
endings in the skin and deeper tissues.6
These specialized nerve fibers transmit information using glutamate neurotransmitter about
the various types of pain, including sharp, dull, burning, or temperature-related.7 They enter the
spinal cord into the dorsolateral tract, ascend one to two segments, and synapse at the dorsal
horn onto the second-order neurons.7 After crossing over the anterior commissure, the signal
continues to ascend as part of spinothalamic tract of the anterolateral pathway into the
thalamus, where third-order neurons take the signal into somatosensory cortex for processing.
The perception of pain is further processed by projections to the insular cortex, amygdala,

http://dx.doi.org/10.1016/j.disamonth.2016.05.012
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hypothalamus, and anterior cingulate cortex. This combination of structures makes up what it
known as the “pain neuromatrix,” where pain perception is modulated with autonomic and
emotional responses.6
There are multiple triggers of pain in the lower back, including discs, ligaments, nerves, as
well as muscles surrounding the spinal cord. Lumbar muscle strain occurs when the muscle is
over-stretched, which causes damage to the muscle fibers, leading to a painful stimulus. Similar
mechanism of increased tension applies to ligaments, leading to back sprains and associated
pain. Nerve root compression is typically caused by lumbar disc herniation, leading to sharp
shooting painful sensation.
Intervertebral disc (IVD) pathology comprises a large portion of lower back pain (LBP)
generation, accounting for as much as 39–42% of cases.8 Discogenic pain is explained by
combination of nerve innervation, inflammation, and mechanical hypermobility.8 Normally, only
the outer one-third of the annulus fibrosus of the IVD is innervated by nerve fibers, but studies
of animal and human models have demonstrated that in degenerative IVDs the sensory nerve
innervation goes beyond the outer one-third into the inner layer of the disc. This process is
stimulated and perpetuated by the nerve growth factor (NGF), which is a prevalent factor of
inflammation.8 Research has also shown that degenerative IVDs produce increased number of
various pro-inflammatory molecules, including TNF-α, IL-1, IL-6, IL-8, prostaglandin E2, and NGF,
which all play a role in pathophysiology of LBP.8 Hypermobility of the degenerated IVD is also a
major factor in pain generation, since with age the number of cells in the annulus fibrosus
declines, making the disc more solid, mobile, and painful.8
Chronic LBP is defined as symptoms that last for more than 3 months.9 What makes LBP
progress from acute to chronic phase remains an area of debate and active research. According to
biopsychosocial model, psychological factors play a role in this process as well as variability in
pain thresholds and tolerance.6,8,9 It is likely that there is lack of peripheral pain stimulus in
chronic LBP and that the real issue lies in neuroplasticity associated with chronicity of pain.10
Studies have shown that patients with chronic LBP exhibit gray matter reduction in certain
regions of the brain, including prefrontal cortex (PFC), temporal lobes, insula, and somato-
sensory cortex.10 Also, the neuronal connectivity in patients with chronic LBP was found to be
disrupted with higher activation of PFC, cingulate cortex, amygdala, and insula.10 This indicates
that chronicity of LBP can be at least partially accounted for by neuroplasticity and up-regulation
of the pain matrix, leading to psychological and emotional propagation of pain.

Treatment strategies

The definition of chronic low back pain can vary depending on the resource. Generally it is
accepted to mean low back pain that has been present for 3–6 months despite medical
intervention. The standard medical intervention for the low back pain sufferer can also be
debated. For the purposes of this review, it would come to mean failed pharmacopeia,
rehabilitation, injection therapy, and perhaps even surgery. While it is beyond the scope of this
article to cover all these treatment measures, these authors will provide a brief summarization.
This will be followed by a description and analysis of multidisciplinary rehabilitation programs.
From a medication perspective, there exist a wide range of options to choose from. In a
systematic review of the literature, there are several prominent articles that lead to similar
conclusions. Opioids and NSAIDs are effective for treatment of CLBP when compared to placebo.
However, their side effects can offset their benefits in the long term, particularly the opioids.
There is no convincing improvement with regard to non-specific CLBP and the use of anti-
depressants when compared to placebo.11–13 A Cochrane review from the Spine journal would
point to insufficient evidence supporting injection therapy (facet, epidural, etc.) in the treatment
of CLBP. The article continues to point out that injection therapy could not be ruled out in
specific subgroups of patients.14 Similarly, lumbar spinal fusion has been shown to be effective in
patients with CLBP who failed non-surgical measure in lieu of degenerative disc disease. Both
the articles underscore the importance of proper patient selection.13
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Multidisciplinary approach

Multidisciplinary (also sometimes referred to as biopsychosocial model) rehabilitation is an

approach designed to address this population of patient with CLBP refractory to standard
measures. The team of healthcare providers involved in such a program typically includes
physical therapists, vocational therapists, social workers, and psychologists. There is a usually a
lead physician specializing in pain management orchestrating care. This person may be called
upon for injection therapy, for management of medication, or to asses any organic components
to the illness. Programs such as this tend to emphasize “well behaviors” (recreational, social, and
vocational activities) and avoidance of “sick behaviors” (complaining of pain and lack of activity).
Setting goals that are quantifiable by the patient and staff are also a critical component.
Following is an overview of such a program and what the literature supports.

Behavioral approach

The incidence of affective disorders (particularly depression), personality disorders, and

substance abuse is difficult to quantify in this population of patient. Fishbain study over 280
consecutive admissions in a comprehensive pain center and found that half of the men and
approximately two-thirds of the women suffered from affective disorders.15 With this in mind,
the psychosocial aspect of care is customized to the particular entity identified. It could entail
behavior modification, cognitive behavioral techniques, withdrawal assistance, as well as
pharmacotherapy. Bio-feedback and other relaxation techniques are often adjuncts utilized in
this part of the patient’s care.

Physical rehabilitation

The approach taken in a comprehensive pain program tends to differ from standard physical
therapy of low back pain. While it still may entail standard exercises such as core strengthening/
flexibility and reconditioning, the focus is on function. Modalities such as ultrasound and TENS
are not seen as curative but more as aids in modulating pain for a particular activity. The goal is
to assist the patient in discovering activities that do not increase the pain while at the same time
quelling fears that activity may do damage. Many times functions such as work tasks are re-
created and family/significant others are encouraged to be part of the rehabilitation.

Vocational rehabilitation

Even though this comes later in the program (as an individual increases function), it is
introduced as soon as possible. Studies have demonstrated that return-to-work outcomes
improve with early emphasis on this.16 This may take the form of altering a person’s job
description/work environment, career counseling, and/or education advancement.

Conclusions

Measuring success of such programs is a daunting task. Various studies use different metrics
such as decreased pain and/or disability. Also, not all programs are identical in their approach.
Finally you have the heterogeneity of that patient population. However, it is generally concluded
that programs such as these tend to be an effective means of lowering pain and disability when
compared to a fragmented approach.17,18 As with most complex medical conditions, more
attention to standardizing the approach and measured outcomes need be done to truly get a
sense of its value.
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