Low back pain resulting primarily from the paraspinal musculature is referred to as a myofascial pain syndrome. Spasm and overcontraction of injured muscles are the root cause for this syndrome, which was originally described by Simons, Travell, and Simons (1999) as a condition characterized by muscles that are shortened or contracted, with increased tone and stiffness, and that contain numerous trigger points (tender, firm nodules identified with muscular palpation). Usually there is an aggravating factor or history of direct or indirect trauma, but triggers can also include postural dysfunction and physical deconditioning (Panjabi, 2006).

The facet joints are paired diarthrodial synovial joints between the posterior elements of adjacent vertebrae, and have been implicated as a source of chronic low back pain since the early 1900s. The term facet syndrome was first coined by Ghormley (1933) when he described lumbosacral pain that often occurred after a twisting injury to the lumbar spine and that was accompanied by local paraspinal muscular tenderness, exacerbation of symptoms with hyperextension, and radiation of pain into the hips and buttocks without neurologic deficits. The innervation to the lumbar facet joints is derived from medial branches of the dorsal rami of the spinal nerves. With trauma to the joints, inflammation leading to pain, stiffness and secondary muscle spasm occurs. There is also an important correlation between degenerative changes and aging of the intervertebral disc and resultant increased transfer of stress to the facet joints, subsequently leading to accelerated degenerative changes there as well.

The outer annulus fibrosis of the intervertebral disc is innervated by the sinuvertebral nerves, first described by Luschka (1850). These nerves are derived primarily from the spinal nerves, with additional contributions from the sympathetic plexus. Only the outer third of the annulus is innervated; the inner two-thirds of the annulus and the nucleus pulposus are devoid of any nerve fibers. Thus, for the disc itself to be a pain generator, the presumption is that the outer third of the annulus must be exposed to a painful stimulus. Over time, as the disc succumbs to the physiology of aging, dehydration can result in annular tears or fissures (Vernon-Roberts & Pirie, 1977).

The disc can also play a role in back pain in the setting of an acute herniation. In this case, compression of an exiting nerve root or the collection of nerve roots contained within the dura from bulging disc material will result in lower extremity radicular pain—the classic sciatica. A large central disc herniation can present with predominantly low back pain in the setting of minimal or no lower extremity symptoms.

The vertebral body itself can be a source of low back pain in the setting of trauma, infection, or tumor. Compression fractures can be a source of significant acute and chronic back pain after trauma, especially in the elderly population where osteopenia (defined by WHO as a T-score on a bone density study of −1.0 to −2.5) or osteoporosis (defined by WHO as a T-score on bone density study below −2.5) is a predisposing factor for fracture even with minimal trauma (i.e., a fall from standing height). In the case of infection, osteomyelitis can cause bony destruction, leading to pain. Primary or metastatic spinal tumors can also lead to bony destruction and pain. A patient history of unintentional weight loss, fevers, chills or severe unremitting pain (i.e., the so-called red flags) should alert the physician to consider these possible differential diagnoses.

The SI joint is an often unrecognized source of pain in many patients. It can be injured with minimal trauma in the setting of a combined axial loading and abrupt rotational force, such as in falls, motor vehicle accidents and athletic injuries (Chou et al., 2004). Despite the existence of numerous physical examination tests to help evaluate for SI joint dysfunction, history and exam findings alone are not consistently reliable in making the diagnosis (Dreyfuss, Michaelsen, Pauza, McLarty, & Bogduk, 1996; Slipman, Sterenfeld, Chou, Herzog, & Vresilovic, 1998). If clinical suspicion is strongly in favor of SI joint pain, a diagnostic block with an appropriate response during the anesthetic phase of the injection can help in supporting the diagnosis.

Back pain and depression are intimately linked—several general population studies have shown their relationship. Currie and Wang (2004), for example, analyzed data from the Canadian Community Health Survey to explore the relationship of depression (as assessed by a structured diagnostic interview) to back pain in over 110,000 household residents. Overall, 9 % of those interviewed experienced back pain, but the incidence rate of depression in those with back pain was 19.8 %, whereas depression was experienced by only 5.9 % of those with no back pain (see also Gureje et al., 2008). Among patients with chronic low back pain, lifetime rates of depression are much higher, ranging from 45 to 65 % (Polatin, Kinney, Gatchel, Lillo, & Mayer, 1993). The direction of causation between depression and back pain is uncertain. Clearly, the onset of pain can lead to many adverse consequences—loss of income, decreased function, loss of enjoyment, etc.—all of which may lead to the onset of depression. In fact, a number of cross-sectional and prospective studies have shown that emotional distress worsens as back pain becomes more protracted. However, several studies have found that individuals who are depressed are more likely to develop chronic pain (see Fishbain, Cutler, Rosomoff, & Rosomoff, 1997, for a review). Many of the symptoms of major depression and chronic pain overlap, including sleep disturbance, loss of enjoyment, social withdrawal, memory and concentration difficulties. Thus, while depression may place individuals at risk for the development of chronic low back pain, it is certainly the case that pain can create or exacerbate depression, leading to a quite recalcitrant chronic pain syndrome.

The experience of back pain, especially if it is protracted, is one that almost inevitably produces anxiety. Worries about the basis of the pain, ability to work and function, dependence on narcotics, worsening of the pain, and concerns about the possibility of spine surgery, are common and intense. In fact, data from Gureje et al. (2008), who analyzed results from the World Mental Health Survey, found that community members in the United States who reported pain in multiple body areas were at greatly increased risk of having diagnosable anxiety disorders (generalized anxiety, panic disorder, social phobia or post-traumatic stress disorder), compared to respondents who did not report any pain. In a similar vein, McWilliams, Goodwin, and Cox (2004), analyzing data from the Midlife Development in the United States Survey (MIDUS), found that, compared to those without back pain, individuals with back pain were at risk for diagnosable panic attacks (odds ratio 2.69) and generalized anxiety disorder (odds ratio 2.54). Again, the question of whether the anxiety precedes or results from the back pain remains an open one. However, what is clear is that patients who experience significant anxiety do not respond as well to treatments for back pain as those who are less anxious.

Back pain cannot be measured directly. It can only be assessed through the patient’s self-report of the pain experienced, as well as changes in functional ability and usage of pain medication. Even when an underlying physiological cause of the pain can be identified, it is difficult to tell whether an individual’s experience of pain is appropriate. The concept of pain sensitivity revolves around whether the patient experiences pain of an intensity, and in a physical distribution, consistent with an identified cause. To the extent that inconsistency is found, the patient can be deemed as excessively pain sensitive.

Pain sensitivity can be assessed in several ways. The most widely researched of these utilizes the MMPI and MMPI-2, in which Scales 1 and 3, reflecting somatic preoccupation, are frequently found to be elevated in patients with chronic back pain (Keller & Butcher, 1991). Classic research by Bigos et al. (1991), who prospectively studied over 3,000 aircraft employees, demonstrated that elevations on MMPI Scale 3 were strongly associated (along with low levels of vocational satisfaction) with the development of back pain over a 4-year period. Recent research by Block, Ben-Porath, and Marek (2013), using a newer version of the MMPI, the MMPI-2-RF (Ben-Porath & Tellegen, 2008), found that patients who are candidates for spine surgery have elevations on Scale Rc1 (somatic complaints), relative to the general population, and that elevations on Rc1 are associated with reduced outcome of spine surgery (Block, Ben-Porath, Ohnmeiss, Guyer, & Marek, 2012).

Pain sensitivity that is more specific to back pain can be assessed by providing the patient with a body outline and having the patient shade in areas where pain is experienced. To the extent that such “pain drawings” are not consistent with the underlying physical pathology, the patient can be seen to be excessively pain sensitive. Such inconsistent pain drawings are associated with elevations on MMPI Scales 1 and 3 (Dennis, Rocchio, & Wiltse, 1981) and are associated with reduced effectiveness of conservative treatment for back pain (Takata & Hirotani, 1995) as well as spine surgery (Block, Ohnmeiss, Guyer, Rashbaum, & Hochschuler, 2001).

Of the panoply of negative emotions experienced by back pain patients, perhaps the most significant one is anger. Fernandez, Clark, and Ruddick-Davis (1999) asked chronic pain patients to rate the frequency with which they had experienced six emotions during the previous 30 days. Although guilt, shame, fear, sadness, shame, and envy were all commonly experienced, anger was the most frequently reported—about 70 % of the time. Several intriguing studies have shown that anger may actually increase pain awareness through physiological mechanisms. In one study, chronic back pain patients and non-pain control subjects were asked to recall experiences of both anger and sadness while activity of the lumbar paraspinal muscles was monitored (Burns, 2006). While both the pain patients and controls had elevations in paraspinal muscle tension in both emotional recall conditions, the pain patients (but not the controls) showed greater muscle tension elevations in the anger recall condition than in the sadness recall condition. The author concluded that excessive lumbar paraspinal reactivity may increase pain awareness in chronic low back pain patients. In a separate study, Bruehl, Chung, Burns, and Diedrich (2007) found that a particular type of anger, in which patients tend to directly express anger rather than suppress it (termed “anger out”), is associated with dysfunction in endogenous opioid release during painful conditions, leading individuals with “anger out” traits to experience heightened pain sensations.

The results reported above indicate that anger appears to be the most commonly experienced emotion associated with chronic back pain, and also may increase the pain experience through association with heightened physiological responses to pain. Fernandez and Turk (1995) suggested another way in which anger may adversely affect the course of chronic low back pain. They posit that anger may lead to maladaptive lifestyle changes, such as excessive use of drugs or alcohol, poor health habits, and lack of physical exercise, all of which may compound the adverse impact of back pain. Furthermore, if the patient is angry at a particular person or event, such anger may drive the patient to continue experiencing pain as a means of vindication. Such a notion receives support from recent research showing that those chronic back pain patients, who report an inability to forgive others, experience higher pain and psychological distress than do patients who are more forgiving, and that this appears to be mediated by relatively higher levels of state anger (Carlson et al., 2005).

Chronic back pain patients often have been the victims of abuse or abandonment as either adults or as children. In one study, more than half of the patients evaluated at a multidisciplinary pain clinic reported a history of at least one form of such abuse, with 90 % of the cases the abuse occurring during adulthood (Haber & Roos, 1985; see also Green, Flowe-Valencia, Rosenblum, & Tait, 1999). A number of other studies have shown that early experiences of abuse or abandonment may leave individuals particularly prone to the development of pain disorders, as well as general health problems. For example, Linton (1997) surveyed a sample of the general population in Sweden, as well as chronic pain patients, about their histories of physical and sexual abuse. All subjects, whether patients or not, were also questioned about any chronic pain symptoms they might have had. Analyses of the results revealed that the chances of women developing chronic pain were increased fivefold by physical abuse and fourfold by sexual abuse. In this study, there appeared to be little association of abuse with pain for the men. A different community-based study (Walsh, Jamieson, MacMillian, & Boyle, 2007) found that physical abuse, but not sexual abuse, predisposed woman toward chronic pain (see Davis, Luecken, & Zaruta, 2005, for a review). More generally, childhood physical abuse, parental instability and sexual abuse have been linked with poorer adult health outcomes (Irish, Kobayashi, & Delhanty, 2010) and with significantly increased likelihood of early disability retirement (Harkonmaki et al., 2008).

Opioid medication abuse is an increasingly problematic issue in the United States. The National Survey on Drug Use and Health (NSDUH, 2007) found that among individuals over the age of 12, 4.8 % had used a prescription pain reliever nonmedically in the previous 12 months. Despite such obvious indications that pain medications are frequently diverted for recreational purposes, they are still widely prescribed for individuals with low back pain. For example, Nyiendo, Haas, Goldberg, and Lloyd (2001) found that 31 % of patients with chronic non-malignant back pain who were referred to multispecialty clinics in Oregon were prescribed with opioid medications. Even more dramatically, Mahowald, Singh, and Majeski (2005) found a 61 % prescription rate among patients in a specialty spine clinic. These medications are frequently not used as prescribed, as exemplified by research conducted by Wunsch, Cropsey, Campbell, and Nicely (2008), who found that 61 % of chronic pain patients met the criteria for opioid abuse.

The use of narcotic medications in chronic back pain is controversial, with many expressing the view that chronic opioid therapy can be effective and cannot lead to abuse or addiction (c.f., Rosenblum, Marsch, Portenoy, & Jospeh, 2008). However, it appears that even when taken as prescribed, chronic opioid therapy is associated with poorer outcomes of both conservative treatment for spine pain (Dersh et al., 2008) and spine surgery. For example, Lawrence, London, Bohlman, and Chin (2008) found that 50 % of patients had been using narcotics on a daily basis for greater than 6 months prior to spine surgery, and such patients were much less likely to achieve excellent or good surgical results, compared to the patients who had not been on such a long-term opioid regimen. There is also evidence that opioid medications are not effective for relief of back pain nor are associated with improved functioning when prescribed for longer than 16 weeks (Martell et al., 2007). To the extent that back pain patients use opioids excessively, in a manner not prescribed, or for protracted periods, they are less likely to be responsive to any treatment.

In the setting of an occupational injury, it is critical to be aware of the large body of research demonstrating that back pain patients covered by workers’ compensation fare more poorly than do those who are covered by other insurance types. Workers’ compensation patients report more severe pain, greater disability, more emotional distress and greater life interference than non-compensation patients (Turk & Okifuji, 1996). A number of studies have shown that spine surgery outcome is reduced in patients receiving workers’ compensation payment (e.g., Atlas et al., 2009; Klekamp, McCarty, & Spengler, 1998). In fact, a meta-analysis by Harris, Mulford, Solomon, van Gelder, and Young (2005) found that workers’ compensation significantly increases the odds ratio for worse outcome of lumbar spinal fusion (odds = 4.33) and lumbar spinal discectomy (odds = 4.77).

Poor treatment results among workers’ compensation patients may not arise solely from economic considerations. Rather, workers’ compensation patients have a number of additional issues that may lead to reports of high pain levels and poor treatment outcome. First, these patients have frequently been unable to work for extended periods at the time of surgery. Research on chronic pain has clearly shown that the length of time a patient has been nonfunctional strongly influences treatment outcome. Dworkin, Handlin, Richlin, Brand, and Vannucci (1985) using multiple regression to examine the relationships among compensation, litigation, and employment status (time off work) in 454 patients undergoing treatment for chronic pain found that only time off work (and not workers’ compensation or litigation) predicted treatment outcome. In similar and even more dramatic fashion, Anderson, Schwaegler, Cizek, and Leverson (2006) found that patients who were working up to the time that they went in for anterior lumbar interbody fusion (ALIF) were 10.5 times more likely to have returned to work by 1-year post-op than were individuals who had not been working prior to surgery. Interestingly, this association was independent of workers’ compensation status and number of spinal levels treated.

Responses to treatment by patients receiving workers’ compensation may be influenced by a number of other work-related factors, including job dissatisfaction (Bigos et al., 1991) and high levels of anger or blame toward the employer (DeGood & Kiernan, 1996). Regardless of the cause, workers’ compensation is so widely recognized as a risk factor that Frymoyer and Cats-Baril (1987) have proposed that compensability is one of the strongest predictors of excessive disability among back injury patients.

The natural history for patients suffering from an episode of back pain is actually quite positive. In the majority of patients (approximately 90 %), symptoms will resolve with or without treatment in a period of 6–12 weeks (Andersson, 1999). Therefore, in the absence of a progressive neurological deficit, spinal instability, infection, or tumor, conservative efforts toward managing back pain are the preferred initial approach.