Fig. 15.1
Predicted probabilities and 95 % confidence intervals for internal disk disruption (IDD), facet joint pain (FJP), sacroiliac joint pain (SIJP), and other sources of low back pain (LBP) as a function of age (Adapted from DePalma et al. [27]; with permission)
Young adults (age 20–35 years) are reported to be more likely to have diskogenic pain as the source of chronic low back pain (70–98 %) regardless of gender or BMI. By age 50, diskogenic pain was still the most likely source of pain (40–65 %), except for women with low BMIs (average 18.5 kg/m2) in which sacroiliac pain was more likely (49 %). By age 65, men, regardless of BMI, were more likely to have a facet pain (30–54 %), while only women with BMI greater than 30 were more likely to have facet pain (46–64 %) [29].
15.2.1.4 Aggravating and Alleviating Factors
The literature suggests that that diskogenic LBP is worse with sitting, flexion, and rotational forces. Additionally, it has been reported that increasing intrathoracic pressure (coughing, sneezing, bearing down for a bowel movement, etc.) may ultimately transfer forces to a sensitized disk and aggravate diskogenic pain. Diskogenic pain may be alleviated with lying or standing, which correlates with Nachemson’s classical study looking at disk pressures in various positions (Fig. 15.2) [30–32].
Fig. 15.2
(a) Relative change in pressure (or load) in the third lumbar disk in various positions in living subjects. (b) Relative change in pressure (or load) in the third lumbar disk in various muscle-strengthening exercises in living subjects (Adapted from Nachemson [30])
By measuring intradiscal pressures, Nachemson’s landmark study has provided clinicians with a fundamental understanding of postural changes and its effect on intradiscal pressure. There is a linear relationship between the applied external load and the measured intradiscal pressure, with the highest strains occurring in the posterolateral region of the annulus fibrosus. Compared with pressures in the upright position, reclining reduces intradiscal pressure by 50–80 %, unsupported sitting increases the pressure by 40 %, forward flexion and weight lifting increases the pressure by 100 %, while forward flexion combined with rotation increases pressure by 400 % [30]. Figure 15.2 further shows the various positions and exercises and their corresponding disk pressures [33]. The greatest risk for annular strain is a combination of flexion, axial rotation, and compression forces, placing the most pressure in the posterolateral inner annular zone. These asymmetrical loads on the spine are believed to be the source of chronic mechanical overload and may explain why lumbar disk herniations tend to occur in the posterolateral region of the annulus fibrosis [31].
Additionally, it has been reported that aggravation of pain when rising from a seated position correlates with a probable positive diskogram and diskogenic pain. With zygapophyseal joint pain, there is no provocation of pain when rising from sitting position. SI joint pain on the other hand was associated with rising from sitting but is more unilateral and lacks a midline pain component [34]. Unfortunately, the side of a symptomatic annular tear on imaging does not correlate with the side of a patient’s back pain [35].
15.2.1.5 BMI
An elevated body mass index is associated with lumbar degenerative disk disease seen on lumbar MRI [36]. However, as noted previously, radiographic changes are not always associated with clinically painful disks [37, 38]. A recent study has indicated that a higher BMI does not correlate with diskogenic low back pain, but rather facet or sacroiliac joint pain [ [39]].
15.2.1.6 Gender
Gender differences also correlate with the source of LBP. Women, when adjusting for age and BMI, had increased odds of sacroiliac joint pain compared to diskogenic pain or facet joint pain. Younger men were more likely to have diskogenic pain as their source for chronic pain.
15.2.1.7 Surgical History
Unfortunately, a history of prior back surgeries can increase an individual’s likelihood for chronic LBP. Diskogenic pain is the most common reason for chronic LBP after a lumbar diskectomy (Table 15.1). Although radicular pain usually improves after a diskectomy, some have residual low back pain. It has been shown that the most common etiology in this situation is diskogenic pain (82 %) [40]. Conversely, if there has been a lumbar fusion especially when fused to the sacrum, sacroiliac joint pain is the most likely source of low back pain followed by diskogenic pain, facetogenic pain, and soft tissue irritation due to fusion hardware.
Table 15.1
Predictors of diskogenic pain
Midline pain |
Young age |
Male gender |
Smoker |
Pain aggravated with seated position or sit to stand |
Pain alleviated with supine or standing |
History of prior lumbar diskectomy |
15.2.1.8 Psychosocial Considerations
Since pain is a subjective experience, it is also important to explore the psychosocial issues. Evidence of psychosocial stressors can often amplify or prolong the pain response. Factors including emotional stress, anxiety, depression, occupational factors such as poor job satisfaction, involvement in litigation, number of failed previous treatments, poor sleep, avoidance behaviors, and catastrophic thinking all contribute to a better understanding of the patient’s condition, diagnosis, and therapy plan and also provide some prognostic value [41, 42]. These psychosocial factors are valuable tools in discriminating between symptomatic and asymptomatic disk herniation [43]. Additionally, it is important to inquire about health habits such as smoking and alcohol and drug use. Smoking has been associated with LBP and degenerative disk findings on imaging studies [44].
15.2.2 Physical Examination
The pertinent physical examination findings generally can be found on the focused exam of the lumbar spine. On general inspection, it is not uncommon to see some loss of lumbar lordosis, especially if there is secondary muscle guarding. Range-of-motion (ROM) testing can be utilized. As mentioned before, the presence of midline low back pain over the spinous process has been reported to be a good indicator for diskogenic pain. Thus, important information can be gathered by palpating over the spinous process. Conversely, if there is tenderness over the paramidline region, this may suggest facet or sacroiliac pain [26, 34]. In addition, paramidline pain can reflect myofascial pain.
With diskogenic low back pain that is axial in location, there generally should not be any associated neurological deficits. Still, it is always prudent on an initial evaluation to evaluate manual motor testing, sensory testing, and reflex exam. These are primarily used to rule out other more concerning issues.
Lastly, some patients may have secondary gain issues. They may present with symptom magnification or malingering. Waddell signs have been described as a way to screen for such patients (Table 15.2). However, some studies have suggested that Waddell signs are not a reliable method to discriminate from organic pain [45].
Table 15.2
Waddell signs
Signs | Description |
|---|---|
Distraction | Inconsistent findings of pain when patient is distracted. An example would be radicular pain with a positive straight leg raise, but when distracted there is no pain on seated straight leg raise |
Overreaction | Inappropriate, disproportionate reactions to a request. This may manifest with exaggerated verbalization, facial expression, tremors, or collapsing |
Regionalization | Motor or sensory abnormalities without anatomic basis. Diffuse give away weakness could go along with this |
Simulation | Lumbar pain with a light axial load on the head. Lumbar pain with simultaneous pelvis and shoulder rotation in unison |
Tenderness | Exaggerated sensitivity or dramatic reproduction of pain with light touch of the soft tissue or with skin rolling |
15.3 The Degenerated Disk: Imaging
The high prevalence of degenerative findings on MRI in asymptomatic individuals has led the clinical relevance of these findings to be questioned [46–48].
Still, imaging for chronic LBP is used and plain radiographs are typically the initial imaging choice. MRI is felt to be more helpful in the evaluation of diskogenic LBP [49]. Diskography has been considered by many to be the gold standard, not without controversy. Imaging findings are eloquently discussed elsewhere in this book; thus, they will only be briefly discussed here.
Some studies have shown a positive association between low back pain and reduced signal intensity and/or reduced disk height [50–52]. The relationship between degenerative findings on imaging and low back pain remains controversial, with conflicting conclusions in the literature. Many studies fail to show any association between structural abnormalities and symptoms [53–55]. In addition, abnormal structural findings are not predictive of the future development of low back pain [51].
In a patient with diskogenic pain, one would expect that there would be at least some disk desiccation on T2-weighted images (T2WI). The likelihood of diskogenic pain is unlikely if the disk appears well hydrated with normal architecture on MRI.
Annular fissures have been associated with diskogenic pain. These appear as high intensity zones (HIZs) on T2WI (Fig. 15.3). These were first described by April and Bogduk in 1992; the presence of an HIZ was found to be highly specific for a concordant reproduction of pain on diskography [56]. Other studies found the correlation between HIZ and reproduction of pain on diskography to be low [57–59]. The discrepancy in the literature has led the accuracy and reliability of HIZ as a sign of diskogenic pain to be questioned. A number of studies have described a high prevalence of HIZ in asymptomatic patients, ranging from 24 to 50 % in different studies [60, 61]. It is clear from the high prevalence of HIZs in the asymptomatic population that not all annular tears are painful. Aprill, who first described HIZs, has suggested that true symptomatic annular tears tend to be larger and not the commonly seen small HIZs.
Fig. 15.3
L5/S1 posterior disk high-intensity zone
Vertebral body endplate signal changes on MRI were first described by Modic et al. in 1988, when he correlated endplate changes on MRI with histopathological findings [62]. Modic et al. described three distinct subchondral bone marrow changes, or Modic changes. Type I changes appear edematous (dark on T1WI, bright on T2WI), type II have a fatty appearance (bright on both T1WI and T2WI), and type III changes appear sclerotic (dark on both T1WI and T2WI). Modic changes appear dynamic and are likely different stages of the same pathological process.
Modic changes have been associated with low back pain. Type I changes are more commonly associated with pain. There have been studies suggesting that type I Modic correlates with LBP 20–73 % of the time and has been associated with the reproduction of low back pain with diskography [53, 62–66]. More severe Modic changes, extending over 25 % of the vertebral height, had a 100 % concordance with pain on diskography in one study [58]. The presence of Modic changes in addition to other degenerative findings (loss of disk height and a reduction of disk signal) increased the specificity for positive diskography from 79 to 97 % [66]. Other studies have failed to demonstrate a statistically significant association between Modic changes and concordant pain on diskography [67–69].
Diskography is thought by many to be the gold standard for diagnosing diskogenic low back pain, although there is controversy. Diskography is considered positive when there is reproduction of concordant pain, outer annular tear (confirmed on post diskography CT scan), low pressure provocation, and normal control disk(s). Numerous studies have confirmed these criteria, suggesting this is a valid and reliable test [70]. However, intense debate continues. Recently, a published study suggested that diskography may cause accelerated progression of degenerative findings. Many clinicians have questioned these findings. Nevertheless, such findings do raise concerns [71].
15.4 The Degenerated Disk: Conservative Treatment
There are a variety of treatment options for diskogenic low back pain. Most treatments are focused on conservative options including physical activity, physical therapy, medications, lifestyle changes, complementary medicine, and injections. These treatments often have limitations in diskogenic low back pain. However, there are other interventions like biological injections that have shown promise for the future.
15.4.1 Physical Activity
Physical activity is a frequently used modality to address those with diskogenic low back pain. There is evidence to suggest that activity is better than inactivity in dealing with low back pain. Studies have shown that exercise improves pain, global well-being, and physical function [72]. It also produces multiple other health benefits compared to those who are sedentary and decreases risk of long-term disability [73]. Providers should encourage patients to start slow and advance to regular daily exercise. To remain engaged and continuously challenged, patients should be encouraged to vary the types of activity and set personal goals [73, 74]. Although bed rest had traditionally been the treatment for acute low back pain, this theory has been refuted. Patients with acute low back pain who were asked to avoid bed rest fared better than those who were asked to rest in bed for 48 h. By day 7, those who had remained active had more fully recovered compared to the bed rest group. Furthermore, there were no adverse outcomes in the non-bed rest group [75]. It should be emphasized to the patient that light activity can actually enhance the repair process and, conversely, fear avoidance behaviors can lead to a vicious cycle of chronic pain as an outcome [76].
15.4.2 Physical Therapy
Physical therapy has been shown to be helpful for those with nonspecific chronic low back pain, both in adult and pediatric populations [77, 78]. Active exercise is generally preferred to passive modalities. There are a number of exercise programs including activity as usual, aerobic activity (e.g., walking, cycling), aquatic activity (pool rehabilitation), directional preference (McKenzie method), flexibility training (e.g., yoga), proprioception/coordination (stability ball, wobble board), stabilization training (e.g., low load exercise targeting abdominal, pelvic, and spinal truck muscles), and strengthen training. There is some data that suggests lumbar strengthening and proper mechanics can increase stability and decrease stress and strain on the spine. In theory, this should help with pain [76].
15.4.3 Medications
Medications are commonly used for the management of low back pain. Acetaminophen (paracetamol), nonsteroidal antiinflammatory agents (NSAIDs), muscle relaxants, antidepressants, and pain medication are some of the more commonly prescribed medications for low back pain. A number of systematic reviews in the literature provide good evidence regarding the efficacy of these medications [79].
A number of studies have assessed the effectiveness of acetaminophen (paracetamol) for nonspecific low back pain. These studies suggest that it is helpful and that it is comparable or slightly inferior to NSAID use [79–84]. Acetaminophen has an excellent safety profile when administered in proper therapeutic doses (less than 4000 mg per day), but hepatotoxicity can occur with misuse and overdose. In the United States, acetaminophen toxicity has replaced viral hepatitis as the most common cause of acute hepatic failure and is the second most common cause of liver failure requiring transplantation. In response to this, the FDA in January 2014 issued a statement that combination prescription pain relievers that contain more than 325 mg of acetaminophen per tablet, capsule, or other dosage unit should no longer be prescribed because of a risk of liver damage.
NSAIDs are among the most commonly used medications for pain. They have been shown to be helpful for acute and chronic low back pain [79–81, 85]. There is currently insufficient evidence for aspirin (acetylsalicylic acid) use for low back pain. The mechanism of action of NSAIDs is the blockage of cyclooxygenase activity which converts arachidonic acid to prostaglandin H2, the precursor of prostanoids. COX exists as two isoforms: COX-1, which I is responsible for the hemostatic prostanoid synthesis, and COX-2, which is responsible for proinflammatory prostanoid production. COX-1 is constitutive within platelets and is associated with the production of thromboxane, which strongly promotes platelet aggregation.
NSAIDs have well-documented GI, renal, and cardiovascular side effects. COX-2 medications have less GI side effects, but both nonselective and COX-2 NSAIDs affect the kidney. Some COX-2 medications have been taken off the market because of increased atherothrombotic vascular events [86, 87]. More recent studies have suggested that all NSAIDs have a cardiovascular risk, with naproxen having the least risk [88]. Thus, it is recommended that NSAIDs be used with caution, especially in those with GI, renal, and cardiovascular risks. Additionally, as a person ages, NSAIDs become more risky. In general, NSAIDs should be used for the shortest time period possible.
The U.S. Food and Drug Administration requires that the summaries of product characteristics of all NSAIDs carry a boxed warning about the risks of cardiovascular disease, whereas the European Medicines Agency’s Committee for Medicinal Products for Human Use decided that coxibs (but not NSAIDs) should be contraindicated in patients with coronary heart disease or stroke and used with caution in patients with risk factors for coronary heart disease [89–91].
Muscle relaxants are occasionally used, as well. A Cochrane Review found that these medications are moderately superior to placebo for short-term relief in acute low back pain [92, 93]. There is a lack of evidence in chronic low back pain [82, 94, 95]. This whole class of medication is well known to cause sedation, although serious complications are quite rare.
Antidepressants are also frequently used for low back pain. Two high-quality systematic reviews found antidepressants to be more effective than placebo for pain relief. However, effects on pain were not consistent across antidepressants. Tricyclic antidepressants (TCAs) were slightly to moderately more effective than placebo [95, 96]. Selective serotonin reuptake inhibitors (SSRIs) have not been shown to be effective for pain relief. But serotonin and norepinephrine reuptake inhibitors (SNRIs) have been used for pain relief. In the United States, duloxetine is the only FDA-approved medication for chronic musculoskeletal pain and chronic low back pain.
Common side effects of TCAs include drowsiness, dry mouth, dizziness, and constipation. The common side effects of SSRIs and SNRIs are nausea, sexual side effects, and depression. There is a black box warning of suicidality with these medications. In addition, the SNRIs affect on norepinephrine can potentially elevate blood pressure.
Opioid medications are also used for low back pain. There is moderate evidence for short-term benefit. There is a lack of evidence for long-term use in chronic low back pain [79]. The most common side effects with these medications include dizziness, drowsiness, nausea, constipation, rash, and at high doses respiratory suppression. Yet other issues plague this class of medication. The risk for abuse and misuse poses a problem. The use of opioids has skyrocketed in many countries. For example, the most commonly prescribed medication in the United States is hydrocodone. Further concerns have been raised concerning opioid-induced hyperalgesia (increased sensitivity to pain) in chronic opioid use especially at higher doses [97, 98]. Additionally, opioids are known to affect the hormone system including testosterone, estrogen, thyroid hormones, growth hormones, ACTH/cortisol, and vasopressin [99–103]. Again, these have generally been documented at higher doses.
15.4.4 Lifestyle Modifications
Lifestyle modifications including smoking cessation, weight loss, and diet are considered an essential part of the comprehensive treatment for chronic low back pain. Multiple studies have demonstrated the association between smoking with low back pain and disk degeneration [104–107]. Smoking increases the risk of circulatory proinflammatory cytokines and affects healing. Smoking also compromises blood vessel integrity to spinal structures leading to degeneration of disks [105, 107]. Current and former smokers have a higher prevalence and incidence of low back pain compared to those who have never smoked. This association was stronger in adolescents compared to adults showing the importance of avoiding smoking early in life [105].
Obesity is an independent risk factor for development of low back pain [104, 108]. It is believed to have harmful effects on the lumbar spine by creating a biomechanics disadvantage leading to increased load bearing, excessive wear, and early degeneration. There is a positive relationship between body mass index (BMI) and low back pain. Those with BMIs >29 were 1.7 times more likely to have back pain compared to those with BMIs in the lowest 20 % of the population. Furthermore, a prospective cohort study found that patients with BMIs greater than 30 are at increased risk of developing chronic low back pain after an 11-year period compared to those who had BMIs less than 25 [108]. Having a healthy body weight is key for long-term treatment of chronic low back pain and is an addressable risk factor.
Diet is also a modifiable risk factor for the development of degenerative disk disease. Atherosclerotic disease from a typical western diet has been associated with degenerative disk disease in the spine. Postmortem studies have shown that DDD is seen more common when atherosclerotic disease is present in the arteries that supply the specific intervertebral disk. Specifically, aortic calcification and stenosis of the lumbar arteries were both associated with low back pain. Nutrition to the lumbar intervertebral disks is supplied by the lumbar arteries which originate from the abdominal aorta. Arterial occlusion is believed to decrease the vascular supply leading to the degeneration of disk [109, 110]. Other cardiac modifiable risk factors include hypertension, elevated LDL cholesterol, and hypertriglyceridemia [109]. A healthy diet has been shown to decrease the risk of atherosclerotic disease in a number of studies. Lifestyle modifications are an essential step in the treatment and management of chronic low back pain and must be addressed with all patients for optimal management.
15.4.5 Complementary Medicine
There is mixed evidence for the use of complementary and alternative therapies in the treatment of chronic low back pain. These therapies can include traction, osteopathic or chiropractic manipulation, acupuncture, herbs, vitamins, minerals, and homeopathic supplements.
Traction has been used historically to treat spine disorders. Multiple theories have been proposed to explain the benefits of traction including changing the disk nerve interface, decreasing nucleus pulposus pressure, and increasing foraminal area; however, the evidence is not clear. A systematic review on four randomized control trials shows that sustained lumbar traction with 30–50 % body weight is no better than low-dose sham traction, mineral baths, underwater massage, or traditional physical therapy for low back pain of greater than 4 weeks’ duration [111].
Spinal manipulation and mobilization also dates as far back as 2700 BC in China for the treatment of low back pain [112]. Spinal manipulation therapy is the use of high-velocity, low-amplitude manual thrusts to the spinal joints slightly beyond the passive range of joint motion, while spinal mobilization is the use of manual force to the spinal joints within the passive range of joint motion that does not involve a thrust [113]. There continues to be mixed evidence regarding efficacy. In a large meta-analysis of randomized clinical trials, there was no evidence to show that spinal manipulation was superior to standard treatment such as general practitioner care, analgesics, physical therapy, exercises, or back school [114]. Another study showed moderate evidence that spinal manipulation is similar in effect to a combination of NSAIDS and exercise in both the short and long term [112]. Given that they are at least as effective as other methods diskussed above, this may be another treatment option for patients.
Related posts:
Epidemiology of Lumbar Degenerative Disk Disease
To Fuse or Not to Fuse: That’s the Question
Lessons from a Life: The Journey of Spinal Neurosurgery in the United States
Minimally Invasive Operation for Lumbar Fusion, Canal Stenosis, Degenerative Scoliosis, and Spondylolisthesis. Is It Possible?
Degenerative Marrow Changes: Natural History Biomechanics in Relation to Symptoms
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