The lumbosacral area contains a number of muscles arranged at different levels. These muscles stabilize the spine and allow movement of the low back in different directions (flexion, extension, rotation).

Erector spinae (ES) are the most superficial of the low back muscles. At lumbar region, the ES consists of a single muscle mass with three distinct groups: medially located spinalis, laterally located iliocostalis, and longissimus which is between these two (Fig. 5.1). The lower fibers of these muscles attach to the sacrum and iliac crest. Rostrally, the three muscles separate from each other approximately at L1–T12 vertebral level. The fibers of iliocostalis attach to T7–T12 ribs. The fibers of lumbar spinalis and longissimus attach rostrally to the transverse and spinal processes of lumbar and thoracic vertebrae. Unilaterally, ES provides lateral flexion and rotation to the opposite side. Bilaterally, these muscles extend the spine. The nerves for erector spinae originate from dorsal division of the spinal nerves.

Quadratus lumborum (QL) and multifidus muscles are located deeper than ES muscles (Fig. 5.1). QL is often implicated in low back pain. QL is rostrally attached to the lower level of the 12th rib and the transverse processes of the first four lumbar vertebrae. Its fibers end distally via aponeurosis to the lumboinguinal ligaments and attach to the medial part of iliac crest. Unilateral contraction of OL produces ipsilateral flexion of lumbar spine, whereas bilateral contraction helps with extension of the spinal column. Quadratus lumborum is innervated by the ventral rami of the 12th thoracic and upper three or four lumbar spinal nerves. Blood supply is derived from the lumbar arteries, lumbar branches of iliolumbar artery, and branches of subcostal artery.

Multifidus muscle fills up the groove in either side of the spinal processes of the vertebrae from the sacrum to the coccyx. The multifidus is composed of thin fasciculi which arise from the sacrum (as low as the fourth vertebrae), aponeurosis of the origin of sacrospinalis muscle, posterior medial surface of the ilium, and posterior sacroiliac ligament. In the lumbar region, its fibers attach to mamillary processes of all lumbar vertebrae. Deeper fibers connect to L2–L4 lumbar vertebrae and work to stabilize the joints at each segmental level. At the lower lumbosacral region, more superficial multifidus fibers are close to the skin due to the thinness of the overlying ES in this region. Multifidus muscles, like facet joints, are innervated by the medial branch of the dorsal ramus of the spinal nerves.

Muscle strain and disturbance play a major role in the pathophysiology of mechanical low back pain. Major low back muscles such as ES and QL are richly innervated. Irritation of nerve endings may lead to accumulation of pain mediators (glutamate, calcitonin gene-related peptide, and substance P) at the periphery causing peripheral sensitization. In patients with anatomically tight compartment for ES muscles, the compressed muscle can cause pain and discomfort especially during exercise, the lumbar compartment syndrome (Nathan et al. 2012).

Recently, the role of dorsal root ganglia (DRG) in chronic disc disease leading to low back pain has attracted much attention. It has been shown that DRG is very sensitive to pressure, and even light compression can cause long periods of repetitive firing (5–25 min) in DRG neurons (Howe et al. 1977). The ruptured disc material, due to proximity to DRG, can influence DRG neurons and upregulate expression of pain mediators and inflammatory agents to produce or enhance pain. In rats, experimental disc puncture at L5–L6 level causes persistent upregulation of calcitonin gene-related peptide (CGRP) in lumbar DRG neurons for the entire 8-week course of the study and a transient (2 weeks) increase in expression of inflammatory agents (interleukin-6, nerve growth and tumor necrotizing factors) in DRG (Miyagi et al. 2011). In a similar disc injury experiment in rats, after injury, there is upregulation of tetrodotoxin-sensitive sodium channel (NaV1.7), in L1–L5 DRG neurons. NaV 1.7 channels are associated with sensory transmission in sensory nerves (Sadamasu et al. 2014). Disc injury related to injection of Freund adjuvant into L5 disc results in increased expression of CGRP, substance P, and nerve growth factor both in DRG and the thalamus lasting for 8 weeks (Jung et al. 2011). A sizeable number of DRG neurons that innervate vertebral bodies are also CGRP positive (33 % of those innervating L5 vertebra) which suggests a role for this arrangement in bone-generated low back pain (Ohtori et al. 2007).

Facet joint disease is another condition often associated with chronic low back pain. Wakai et al. (2010) have shown that many DRG neurons have dichotomized axons which project both to facet joints and to low back muscles. These could be the source of referred pain. Approximately 17 % of all DRG neurons innervating the facet joints have other axons that extend to the lower back muscle.

The role of sympathetic nervous system in maintaining pain and its chronicity has long been suspected based on anatomical studies showing massive sprouting of sympathetic fibers into DRG after peripheral injury (McLachlan et al. 1993). Normally no sympathetic fibers are inside DRG, and noradrenergic innervation is present only in the adjacent blood vessels. Following peripheral injury, inflammation develops in DRG and sympathetic ganglia with influx of macrophages and T cell lymphocytes into DRG. This leads to the release of cytokines and increases discharge of DRG neurons. Sympathectomy or removal of sympathetic ganglia decreases the influx of macrophages and T cells into DRG and, consequently, decreases the magnitude of inflammation (McLachlan and Hu 2014). Sympathectomy attenuates the excitability of dorsal root ganglion neurons and pain behavior in a lumbar radiculopathy model (Iwase et al 2012). In chronic low back pain caused by root or DRG injury, sympathetic nervous system hyperexcitability may play a role in the maintenance of pain (sympathetically maintained pain).

In chronic pain states, peripheral sensitization (PS) due to accumulation of pain mediators and inflammatory agents leads to central sensitization (CS) that is believed to contribute to pain chronicity. This CS occurs at multiple levels of CNS starting with the spinal cord neurons and followed by the brain stem, thalamic, and cortical levels. There is evidence from molecular biology, electrophysiological investigations, and neuroimaging studies that pathological conditions associated with chronic low back pain are capable of inducing central sensitization. In conditions such as herniated disc or trauma, DRG and spinal nerve injuries lead to the generation of ectopic discharges in DRG neurons causing hyperexcitability of spinal cord sensory neurons. Light compression of DRG by experimentally induced nucleus pulposus increases evoked responses in the posterior thalamic neurons for a minimum of 40 min (Nilsson et al. 2013). Functional MRI of patients with chronic low back pain compared to asymptomatic age-matched volunteers has shown augmented activation in premotor, supplementary motor, insula, and anterior cingulate cortex in patients with cLBP (Kobayashi et al. 2009).

In clinical practice, a large number of analgesic agents are used for the treatment of chronic low back pain; these include non-anti-inflammatory analgesics (aspirin, acetaminophen), nonsteroidal anti-inflammatory agents (NSAID), tricyclic and tetracyclic antidepressants, muscle relaxants, cyclooxygenase-2 inhibitors, anti-spasticity agents (tizanidine), anticonvulsants (gabapentin, pregabalin), serotonin/norepinephrine inhibitors (duloxetine), opioid-like agents (tramadol), strong opioids (oxycodone, OxyContin), and topical anesthetic agents. Tricyclic antidepressants cause a 20–40 % reduction over placebo in short follow-up (4–8) weeks, but their long-term effect is not known (Staiger et al. 2003). The anticholinergic side effects are also of concern in older patients. Prospective and control studies with some other agents (non-NSAID analgesics, NSAID, muscle relaxants, and cyclooxygenase inhibitors) have shown either no or marginal improvement over placebo in chronic low back pain (Van Tulder et al. 2000, 2003; Nussmeier et al. 2005; Coats et al. 2004; Ostelo et al. 2005; Solomon et al. 2005). In a 12-week study (Vorsanger et al. 2008), both 200 mg and 300 mg of tramadol moderately improved low back pain compared to placebo (p = 0.052 and p = 0.009); the disability index, sleep quality, and patient assessment score also improved as secondary measures (p = 0.012). Topical NSAID diclofenac has shown some promise in reducing osteoarthritic pain, but systematic studies in chronic low back pain are lacking. In acute and subacute low back pain, one prospective, open-label study has suggested efficacy of lidocaine patch to improve pain and quality of life, and these positive effects were associated with high score in patient satisfaction (Gimbel et al. 2005). Controlled studies in chronic low back pain with lidocaine patch are not available. The most recent Cochrane review of literature on the effect of opioids on pain and function of patients with low back pain encompassed 15 blinded studies and 5,600 patients during the period of 2007–2012 (Chaparro et al. 2014). Both tramadol (weak opioid function) and strong opioids improved chronic low back pain and function over placebo (moderate for pain, mild for function). Two studies found a comparable effect in chronic low back pain for opioids with tricyclic antidepressants. No significant side effects were noted. None of the studies addressed long-term efficacy and safety. The long-term use of opioids is confounded by the development of addictive behavior.

In a recent review of chronic low back pain, Uhl et al. (2014) recommended tricyclic antidepressants (nortriptyline 25–150 mg daily), tramadol ER (100–300 mg daily), and lidocaine patch (5 %, one to three patches topically up to 12 h) as the first line of medical treatment. In view of limited supportive literature, the long-term efficacy of tramadol ER and lidocaine patch in treatment of cLBP is not well established. Despite medical therapy, most patients with chronic low back pain continue to experience pain and are not satisfied with their level of pain management.

Physical therapy (PT) is aimed to reduce pain, and therapists can educate patients to perform passive and active movements which potentially may prevent progression of low back pain and disability. While PT is commonly used in management of cLBP, well-designed studies are scant and methodological problems and paucity of high-quality investigations prevent drawing conclusions regarding the precise efficacy of physical therapy (Calvo-Muñoz et al. 2013).

Massage and heat and cold applications are temporarily effective for pain but show no long-term benefits. The few available high-quality studies advocate that spinal manipulative therapy (SMT) has no advantage in management of chronic low back pain (Rubinstein 2011). A recent review of yoga in chronic low back pain (ten randomized trials) suggested strong evidence for short-term and long-term effect on pain and moderate effect on pain-related disability (Cramer et al. 2013).

Transcutaneous electrical nerve stimulation (TENS) has been found to be ineffective based on two negative class I studies (level A evidence, AAN criteria—Appendices 3.​1 and 3.​2) (Dubinsky and Miyasaki 2010). Acupuncture data in low back pain are hard to interpret due to heterogeneity of participants and suboptimal quality of most studies. Improvements in pain and function are reported in some controlled studies, but the effects are transient (Rubinstien et al. 2010). Studies of ultrasound and shock therapy are limited, and available evidence suggests no appreciable effect on pain or functionality (Seco et al. 2011). Epidural injections with anesthetic agents (with or without steroids) improve pain flairs in cLBP, but the effects are generally transient. A recent review of the literature on this subject found 15 blinded, placebo-controlled studies with best results reported for radiculopathies due to disc herniation and spinal stenosis (Parr et al. 2012).

Surgical treatment of low back pain has produced mixed results. Spinal fusion alleviates pain and improves function in patients with degenerative spine disease, but the positive effects may not last long. Minimal spinal surgery without open surgery (with interbody fusion) in selected patients has produced good short-term results. Longer observations are needed, however (Spoor and Öner 2013).

A Cochrane review of six high-quality publications provided strong evidence that behavioral therapy had a moderate effect in decreasing pain, but no noticeable effect on patients’ functional status or behavioral health. The review concluded that both the type of patients that benefit from behavioral therapy and the type of behavioral therapy which is most effective still need to be determined (Van Tulder et al. 2001).

Two studies published from the Walter Reed Army Medical Center (WRAMC) first addressed the issue of BoNT efficacy, tolerability, safety, and quality of life in chronic LBP. The first study was double blind and placebo controlled (Foster et al. 2001). The second one was open label and prospectively assessed multiple treatment results (every 4 months) over a period of 14 months (Jabbari et al. 2006). Both studies used a similar protocol in respect to technique, dosing, and rating scales. The technique was based on the hypothesis that treatment results may not be optimal unless the whole length of erector spinae (ES) muscles in the lumbar region is exposed to and influenced by BoNT therapy. Hence, regardless of the location of pain or tender/trigger points (if present), injections were performed at five lumbar paraspinal levels (into lumbar ES) with a total dose of 200 units for unilateral LBP (blinded study) and 400–500 units for bilateral LBP (open study) (Fig. 5.2). Both studies used onabotulinumtoxinA (onaA). The third study performed by a different group reported on efficacy of aboA in a group of patients with chronic low back pain due to myofascial pain syndrome.