Lumbar Degenerative Disease

SECTION VI

Low Back

CHAPTER 45

Lumbar Degenerative Disease Saurabha Bhatnagar, MD Ogochukwu Azuh, MD Hans E. Knopp, DO

Synonyms Osteoarthritis of the spine Spondylosis Lumbar arthritis Degenerative joint disease of the spine Degenerative disc disease

ICD-10 Codes M47.817 M47.899 M51.36 M51.37 M54.5

Spondylosis without myelopathy or radiculopathy, lumbosacral region Other spondylosis, site unspecified Other intervertebral disc degeneration, lumbar region Other intervertebral disc degeneration, lumbosacral region Low back pain

Definition Low back pain (LBP), also known as lumbago, is a common condition that according to observational studies occurs in about 80% of people.1 In the United States, respondents of a survey of adults 18 and over by the National Center for Health Statistics revealed that LBP was the most common type of pain (28.1%) when compared to severe headache or migraine (16.6%) and neck pain (14.6%).2 Normal aging is a key component of the degenerative spine process and at times both are hard to differentiate. As such, literature has shown an increased prevalence in spine 244

degeneration with age in asymptomatic individuals. When comparing prevalence estimates of degenerative spine imaging findings in asymptomatic patients aged 30 and aged 80, disc degeneration (52% vs. 96%, respectively), disc bulge (40% vs. 84%), facet degeneration (9% vs. 83%), and spondylolisthesis (5% vs. 50%) increased with age.3 With age, all anatomic components of the spine are affected: bone, muscles, discs, ligaments, and joints. As a result of the alteration of the “spinal structural equilibrium,” this can lead to spinal instability, clinical syndromes, restricted range of motion (ROM), pain, and in worst cases, disability. The three-joint complex is the functional unit of the lumbar spine and comprises two consecutive vertebrae, the intervertebral disc, and the zygapophyseal (facet) joint (Fig. 45.1). The lumbar disc can be separated into three components: the nucleus pulposus, annulus fibrosus, and cartilaginous endplates. When axial forces are placed upon the nucleus, it distributes the tensile forces via the annulus and the endplates. The degeneration of the intervertebral discs has been thought to be the catalyst leading to secondary degeneration of the surrounding spinal elements. Degeneration of the discs has been shown to be nutrition-related. The main source of nutrition to the intervertebral discs is derived from the cartilaginous endplates and as one ages, permeability of the nutritional gradient from endplates decreases as well as blood supply. An imbalance between extracellular matrix synthesis and degradation occurs, which leads to loss of disc structure and function. There is histological evidence showing cracks and microfractures in the cartilaginous endplates, concentric tears (cleft formation) in the nucleus pulposus, and radial tears in the annulus fibrosus.4 The intervertebral discs receive innervation anteriorly and laterally from the gray ramus communicans and posteriorly from the sinuvertebral nerve, with a majority of free nerve endings found in the outer third of the annulus.5

CHAPTER 45  Lumbar Degenerative Disease

POSTERIOR JOINTS

THREE-JOINT COMPLEX

INTERVERTEBRAL DISC CIRCUMFERENTIAL TEARS

SYNOVIAL REACTION CARTILAGE DESTRUCTION

HERNIATION

RADIAL TEARS INTERNAL DISRUPTION

OSTEOPHYTE FORMATION CAPSULAR LAXITY

INSTABILITY

LOSS OF DISC HEIGHT

SUBLUXATION

LATERAL NERVE ENTRAPMENT

DISC RESORPTION

ENLARGMENT ARTICULAR

ONE-LEVEL CENTRAL STENOSIS

PROCESS (AND LAMINA)

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OSTEOPHYTES AT BACK OF VERTEBRAL BODIES

EFFECT OF RECURRENT STRAINS AT LEVELS ABOVE AND BELOW ORIGINAL LESION MULTILEVEL DEGENERATIVE LESIONS MULTILEVEL SPINAL STENOSIS FIG. 45.1  (Modified from Araghi A, Ohnmeiss DD. Natural history of the degenerative cascade. In: Yue JJ, ed. The Comprehensive Treatment of the Aging Spine: Minimally Invasive and Advanced Techniques. Philadelphia: Saunders/Elsevier; 2011:22.) The three-joint complex is the functional unit of the lumbar spine. The interdependence of each component is evident when they are subjected to biomechanical changes. Outlined is a sequence of degeneration.

With age, collagen content within the nucleus increases and the junction between the nucleus and the annulus becomes less demarcated. Thus tears in the annulus lead to degeneration, prolapse, extrusion, and then sequestration, which can all be sources of pain. As the mechanical load on the spine is altered, forces are distributed through the surrounding facet joints which, depending on one’s position, are responsible for 10% to 30% of lumbar weight bearing.5 These joints are diarthrodial synovial joints and, like all synovial joints, are subjected to degradation of cartilage, subchondral bone sclerosis, osteoporosis, osteophyte formation, and inflammation. This results in facet hypertrophy and, with increased repeated mechanical ­loading, can lead to joint laxity, subluxation, and narrowing of the lateral recess. In concert with disc height loss, it can then lead to central canal stenosis. Other bony elements of the spine (i.e., vertebral bodies, endplates, spinous and transverse processes) also undergo this degeneration process. The ligamentum flavum is a ligament that runs from C2 to S1, connecting lamina of adjacent vertebrae together. It is 80% elastin and 20% collagen and occupies the posterior lateral borders of the spinal canal. Aging causes ligament hypertrophy and in association with disc degeneration leads to bucking, seen as thickness on imaging. This results in spinal canal narrowing and can lead to compression of neural elements. The cause of ligamentum flavum hypertrophy is unknown, but has been postulated to be due to age-related fibrosis secondary to a decrease in elastin-to-collagen ratio.6 The spine is surrounded by a “core” group of muscles that aid in maintaining stability and equilibrium. These muscles are the abdominals (mostly transversus abdominis), diaphragm and pelvic floor muscles, erector spinae, and spinal multifidi.

As time passes, a degenerative myopathy occurs which contributes to the alteration of vector forces upon the spine, thereby shifting it out of equilibrium. An example of this is seen in primary camptocormia, also referred to as bent spine syndrome, relating to primary idiopathic axial myopathy.7,8 The most commonly involved lumbar levels are L4-L5 and L5-S1, as they undergo the most torsion and compressive forces during activity. Factors contributing to lumbar degeneration include environmental (diabetes mellitus, smoking, obesity), occupational (jobs with repetitive bending, stooping, prolonged sitting or vibratory stress), and psychosocial (stress, anxiety, depression), which can contribute to the perception of LBP).9,10 

Symptoms As previously described, lumbar degenerative disease is associated with the normal aging process. Findings on imaging such as intervertebral disc degeneration, facet joint osteoarthritis, spondylolysis, spondylolisthesis, spinal stenosis, and degenerative changes in paraspinal muscles are also seen in asymptomatic individuals. Approximately one third of individuals with substantial abnormalities on magnetic resonance imaging do not manifest any clinical symptoms.11,12 For those with symptoms, common complaints range from acute to chronic LBP. Onset can range from days to months. Positioning such as lumbar flexion, extension, rotation or lateral bending, or lumbar palpation can exacerbate symptoms. Pain with flexion, coughing, sneezing, or Valsalva can be associated with disc disease. Pain quality can be sharp, dull, achy, or shock-like. Severity can range from mild to severe. Pain can be localized at a specific region, as the patient will be

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able to point to exact location; or it can radiate locally or to a distant site. The presence of stiffness in the morning could be due to osteoarthritis. However, atypical symptoms of pain at night, fever, and recent weight loss could be due to malignancy or infection. Alleviating factors such as forward bending could signify compression of neural elements. Leakage of pain-related neuropeptides (e.g., substance P) from the disc secondary to annulus tears to surrounding free nerve endings or onto the nearby dorsal root ganglion can cause pain.5 Clinicians should also inquire about psychological symptoms such as anxiety, depression, or sleep disturbance as contributing factor symptoms. 

Physical Examination Many structures comprise the spinal element; therefore a physical examination should be geared toward discerning one of the five most common sources of LBP: discogenic, facet arthropathy or instability, radiculopathy or neural compression, myofascial or soft tissue, and psychogenic. Although usually found alone, they can also be found in combination. Hence, the goal of the physical examination is to narrow one’s differential diagnosis to lead to more cost effective testing and therapeutic strategies (Table 45.1). Paramount to any physical examination is inspection. In order to gain a sense of patient disability, one must observe the patient, paying close attention to posture, shape of spine (kyphosis, scoliosis, lordosis, back flattening), musculature (atrophy or spasms), skin (midline dimple or tuft of hair), ambulation, and facial expression. Lumbosacral spine movement should be assessed by flexion, extension, rotation, and lateral bending to each side. Hip and sacroiliac (SI) joints should also be tested, as pain from these areas can be referred (e.g., FABER, Gillet, Yeoman, and Gaenslen tests).13 A complete examination includes inspection of the lower extremities and a neurologic examination. Manual muscle strength testing, sensory (dermatomes), and proprioception testing should be performed. Functional muscle testing should also be performed. This can include gait analysis, body weighted squats, tandem walking, and walking/standing on tiptoes and heel. Deep tendon reflex testing (patellar tendon [L3, L4], hamstring tendon [L5], Achilles tendon [S1]) is of utmost importance, as subtle asymmetries could be the only finding on exams. Proprioception (dorsal columns), Babinski, and clonus (upper motor neuron findings) should also be checked. Of note, once the ankle reflex is lost, in half the cases, it does not return. Therefore in new cases of lower back pain, the absence of this reflex alone does not confirm recent root conduction impairment.13 Specialized specific tests for lower back syndromes can also be employed, including straight-leg raising, femoral stretch test, dural tension test, and Schober’s test. For patients in whom psychological factors are thought to contribute to their pain,14 Wadell et al. created a list of nonorganic signs of back pain. (Table 45.2). 

Functional Limitations Functional limitations are restrictions that prevent one from fully performing activities of daily living (ADL) from physical or mental causes and can lead to disability. This tends to affect one’s occupation, leisurely activities, hobbies, sports, and physical exercise. Although most patients complain of

back pain and stiffness, the functional limitations associated with lumbar degenerative disease depend on the structure that is affected. For example, if pathology is discogenic in origin, patients may have difficulty with forward bending, squatting, bending, and twisting. Those with pathology of the facet joint will have limitations with extension, side bending, standing, and walking down stairs. People with central spinal stenosis and stenosis of the lateral recess have difficulty with prolonged walking or standing, with relief coming from sitting and forward bending.13 Patients with ligamentous and myofascial pathology complain of pain that is associated with prolonged postural stress (e.g., standing or physical activity). Psychogenic pathology often involves complaints of pain out of proportion to physical examination, failure of multiple treatment remedies and associated complaints of anxiety or depression surrounding the inability to manage pain. 

Diagnostic Studies Radiography of the spine is usually the first imaging acquired due to its low cost and relative speed of acquisition. However, plain radiographs have a limited role, as difficulty in interpretation can lead to a high false-positive rate.15 The Eastern Association for the Surgery of Trauma, as an example, eliminates plain radiographs from their algorithm for the screening for thoracolumbar spinal injuries in blunt trauma.16 Anteroposterior (AP) and lateral radiographic views are the standard views performed. AP views can detect misalignment such as in scoliosis and spinal process misalignment indicative of rational injury from unilateral facet dislocation. Lateral views can evaluate disc height, spondylolisthesis, osteoarthritis, spondylosis, vertebral compression fractures, and facet arthropathy (Fig. 45.2). With oblique radiographic views, the patient (or x-ray tube) is angled between 30 and 45 degrees, allowing visualization of the facet joints, neural foramen, and pars interarticularis. It can show spondylolysis and facet pathology. Although flexion-extension radiographs are more common to the cervical region, they can still be performed in the lumbar region with the main goal of assessing ligament and spinal column instability in a dynamic spine. Magnetic resonance imaging (MRI) is the imaging modality of choice when examining the spinal cord, neural elements of the lumbar spine, ligaments, surrounding muscle, and soft tissue. MRI can detect canal and lateral recess stenosis, tumors, infection, hematomas, osteomyelitis, disc degeneration, and facet arthropathy.16,17 If one suspects pathology from a vascular etiology such as arteriovenous malformation or fistula, a magnetic resonance angiogram (MRA) can be performed. Computer tomography (CT) is the ideal imaging modality when assessing bony structures of the spine, as it demonstrates fractures of bony elements (transverse process, spinous process, pars interarticularis, vertebra), and dislocations (facet joints). Myelography is invasive and rarely used. This study involves injection of a contrast medium into the spinal canal to delineate the spinal cord and nerve root using real time radiography (fluoroscope) or CT and can detect location of neural impingement in the neural foramina and lateral recess, spinal cord injury, tumors, or cysts. Myelography may be the only method to evaluate patients who have a contraindication to MRI such as ferromagnetic implants. CT, when used in conjunction with myelography, is more

CHAPTER 45  Lumbar Degenerative Disease

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Table 45.1  Pseudospine Pain: Diagnostic Keys Condition

Diagnostic Keys

Vascular

Abdominal aortic aneurysm

Gynecologic

Endometriosis

Older than 50 years Abdominal and back pain Pulsatile abdominal mass Women of reproductive age Cyclic pelvic and back pain Young, sexually active women Systemically ill (fever, chills) Discharge, dysuria Missed period Abdominal or pelvic pain Positive pregnancy test result Men older than 30 years Dysuria Low back and perineal pain Flank and groin pain Hematuria Abdominal pain radiating to back Systemic signs (fever, nausea, vomiting) Elevated serum amylase Abdominal pain radiating to back Young to middle-aged women Widespread pain Multiple tender points Disrupted sleep, fatigue Normal radiographs and laboratory values Older than 50–60 years Hip or shoulder girdle pain and stiffness Elevated erythrocyte sedimentation rate Dramatic response to low-dose prednisone Younger men (ankylosing spondylitis, Reiter syndrome) Lower lumbosacral pain Morning stiffness (“gel”) Improvement with activity Radiographic sacroiliitis Older than 50–60 years Thoracolumbar stiffness or pain Flowing anterior vertebral calcification Buttock and leg pain Pain on resisted hip external rotation and abduction Transgluteal or transrectal tenderness Age 12–15 years Thoracic or thoracolumbar pain Increased fixed thoracic kyphosis 3 or more wedged vertebrae with endplate irregularities Pain or tenderness over greater trochanter Back pain Uneven shoulders, scapular prominence Paravertebral hump with forward flexion Women older than 60 years Severe acute thoracic pain (fracture) Severe weight-bearing pelvic pain (fracture) Aching, dull thoracic pain; relieved in supine position (mechanical) Loss of height, increased thoracic kyphosis Diffuse skeletal pain or tenderness Increased alkaline phosphatase Bone pain: low back, pelvic, tibia Increased alkaline phosphatase Characteristic radiographic appearance Older than 50 years Diffuse leg pain, worse at night Proximal muscle weakness Older than 50 years Back pain unrelieved by positional change—night pain Previous history of malignant disease Elevated erythrocyte sedimentation rate

Pelvic inflammatory disease Ectopic pregnancy Genitourinary

Prostatitis Nephrolithiasis

Gastrointestinal

Pancreatitis

Rheumatologic

Penetrating or perforated duodenal ulcer Fibromyalgia

Polymyalgia rheumatica

Seronegative spondyloarthropathies (ankylosing spondylitis, Reiter syndrome, psoriatic, enteropathic)

Diffuse idiopathic skeletal hyperostosis (Forestier disease) Piriformis syndrome Scheuermann kyphosis

Trochanteric bursitis, gluteal fasciitis Adult scoliosis Metabolic

Osteoporosis

Osteomalacia Paget disease Diabetic polyradiculopathy Malignant neoplasia

Modified from Mazanec D. Pseudospine pain: conditions that mimic spine pain. In: Cole AJ, Herring SA, eds. The Low Back Pain Handbook. Philadelphia: Hanley & Belfus; 1997.

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Table 45.2  Waddell Signs Five Nonorganic Physical Signs Are Described by Waddell Tenderness

Nonorganic tenderness may be either superficial or nonanatomic. Superficial tenderness can be elicited by lightly pinching over a wide area of lumbar skin. Nonanatomic pain is described as deep tenderness felt over a wide area rather than localized to one structure.

Simulation test

This is usually based on movement that produces pain. Two examples are axial loading, in which low back pain is reported on vertical loading over the standing patient’s skull by the clinician’s hands, and rotation, in which back pain is reported when the shoulder and pelvis are passively rotated in the same plane as the patient stands relaxed with feet together.

Distraction test

If a positive physical finding is demonstrated in a routine manner, this finding is checked while the patient’s attention is distracted. Straight-leg raising is the most useful distraction test. There are several variations to this test; most commonly, however, straight-leg raise is done in the supine position and then, while the patient is distracted, in the sitting position. This is commonly referred to as the flip test. However, one should keep in mind that biomechanically, the two positions are very different.

Regional disturbances

Regional disturbances involve a widespread area, such as an entire quarter or half of the body. The essential feature of this nonorganic physical sign is divergence of the pain beyond the accepted neuroanatomy. Examples include giveaway weakness in many muscle groups manually tested and sensory disturbances, such as diminished sensation to light touch, pinprick, or vibration, that do not follow a dermatomal pattern. Again, care must be taken not to mistake multiple root involvement for regional disturbance.

Overreaction

Waddell reported that overreaction during the examination may take the form of disproportionate verbalization, facial expression, muscle tension, tremor, collapsing, and even profuse sweating. Analysis of multiple nonorganic signs showed that overreaction was the single most important nonorganic physical sign. However, this sign is also the most influenced by the subjectivity of the observer.

Modified from Geraci MC Jr, Alleva JT. Physical examination of the spine and its functional kinetic chain. In: Cole AJ, Herring SA, eds. The Low Back Pain Handbook. Philadelphia: Hanley & Belfus; 1997.

A

B

FIG. 45.2  Chronic degenerative changes—plain film. (A) On a coned-down lateral film, the L4-L5 motion segment shows a vacuum phenomenon in the disc (large arrow), endplate remodeling with large anterior spurs (curved arrows), and grade I retrolisthesis (open arrow). (B) A standing lateral film shows multilevel degenerative disc disease with large posterior spurs, small anterior osteophytes, endplate remodeling, and moderately severe disc space narrowing at L2-L3, L3-L4, and L4-L5. (From Cole AJ, Herzog RJ. The lumbar spine: imaging options. In: Cole AJ, Herring SA, eds. The Low Back Pain Handbook. Philadelphia: Hanley & Belfus; 1997.)

useful than MRI in determining the degree of spinal stenosis at a given level and when specific lumbar segment localization is needed to perform decompressive surgery.17 Discography or discogram is a procedure in which contrast medium is injected into the nucleus pulposus to discern the

cause of discogenic pain. A normal disc can receive between 1 and 1.5 mL of contrast. If greater than 2 mL of contrast is injected, then degenerative disc disease is likely. During the provocative injection procedure, localization of pathologic disc degeneration (i.e., nucleus or annulus tears, fissures, or

CHAPTER 45  Lumbar Degenerative Disease

Table 45.3  Goals in Rehabilitation of Musculoskeletal Injury Acute Phase

Recovery Phase

Functional Phase

Treat clinical symptoms

Allow tissue healing

Correct abnormal biomechanics

Protect injured tissue

Restore normal strength and flexibility

Prevent recurrent injury

Modified from Micheo W, López-Acevedo CE. Medical rehabilitation— lumbar axial pain. In: Slipman CW, ed. Interventional Spine: An Algorithmic Approach. London: Elsevier Health Sciences; 2007:993.

disc protrusion) can be confirmed if pain is reproduced. The sinuvertebral nerve is thought to carry nociceptive sensation to the intervertebral disc. Hence, exploratory studies with blockade of the nerve as an alternative means of diagnosing pain of discogenic origin have been performed.18 Electrodiagnostic studies can be an adjunctive tool for patients in whom physical exam and imaging findings are equivocal and the diagnosis remains a conundrum. Electromyography is specific in diagnosing spinal stenosis and can detect neuromuscular disease that can mimic spinal stenosis.19 

Treatment Initial Studies have shown approximately 90% of people who develop acute LBP experience a resolution of the symptoms within 6 weeks.1,15 Hence, the physician’s main goal during the initial patient encounter should be one of reassurance and education regarding the pathophysiology and natural course of lower back pain. Anti-inflammatory medications should be the mainstay of pharmacological therapy and should be given on a time-contingent basis instead of a paincontingent basis.1 Muscle relaxants, heat and cold modalities, myofascial release, and a physical therapy regimen or exercise prescription should be trialed. Opioid dependency is an important consideration when prescribing these medications, and limiting their use for those with severe symptoms is recommended. There are numerous guidelines that suggest using safe prescribing habits (e.g., a maximum 7-day supply on prescriptions for opioids when issued to an adult for the first time). One should avoid restriction of activities (e.g., work or bed rest), as this leads to prolonged immobility. For those with psychological causes contributing to pain (e.g., sleep disturbances), medications such as melatonin, trazodone, or ramelteon could be employed. 

Rehabilitation The mainstay of rehabilitation, whether through physical or occupational therapy, should be patient education about their disease process, recognizing patterns of back pain and incorporation of exercise, and therapeutic modalities to achieve their goal. Spinal rehabilitation can be approached by delineating three separate phases: acute phase, recovery phase, and functional phase.20 Each phase has a specific goal, which must be met prior to progression to the next phase (Table 45.3).

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The acute phase of rehabilitation treatment should focus on gradual introduction to therapy by low-level activity and eliminating factors of non-compliance (i.e., symptom control). The goal of this phase is reduction of pain and inflammation, healing of injured tissue, and prevention of further tissue injury. Primarily, one starts by educating the patient about spine biomechanics and identifying one’s neutral spine position. From there, incorporate spine stabilization ­exercise via isometric and static exercises and gradual pain-free ROM exercise. Cryotherapy, transcutaneous nerve stimulation (TENS), massage, or electro-acupuncture can be incorporated at this stage. Acupuncture can be individualized to the cause of a patient’s biomechanical m ­ isalignment and can specifically target paraspinal or quadratus lumborum muscle spasms. After achieving pain-free range of motion, promotion to the recovery phase is warranted. Trying to restore the biomechanical relationships between normal and injured tissue highlights this stage. Emphasis is placed on physical activity during ADL tasks despite existence of pain, focusing on core strengthening, flexion-extension exercises, high exercise repetitions, dynamic flexibility in different planes, and progression of stabilization exercises from stable to unstable surfaces. Anti-inflammatory medications, analgesics, acupuncture, heat therapy, ultrasound, and TENS can be used at this stage. The goal of the functional phase is restoration of function for ADLs and biomechanical motion associated to workrelated activities. This is accomplished by eccentric loading of the spine through complete lumbar ROM exercises and the use of aggressive quota-based exercise programs. After one progresses successfully through the three phases, the focus of therapy is prevention of disability and building upon the foundation one has achieved from the rehabilitation process. This is achieved by promoting and managing healthy lifestyles through exercise and stressing independence from medical treatment. For those who fail therapy or have complaints of persistent pain and disability, it is best to refer them, if available and feasible, to a multidisciplinary care pain program. 

Procedures For those who fail conservative therapy and may benefit from a procedure, the general rule is to start from minimally invasive (e.g., local trigger point injections or “dry needling”) with progression to more invasive options. Local injections can be both diagnostic and therapeutic. Fluoroscopy with use of contrast medium has become the standard method of choice.21 Diagnostic techniques include epidural steroid injections, facet or sacroiliac joint blocks, and provocative discograms as mentioned previously. Therapeutic procedures include caudal, transforaminal, and interlaminar epidural injections; percutaneous and endoscopic spinal adhesiolysis; facet joint interarticular injections and medial branch neurotomy; sacroiliac joint blocks or radiofrequency neurotomy; intradiscal electrothermal therapy (IDET); intrathecal drug administration systems; and spinal cord stimulators.22 Epidural steroid injections are the most commonly performed procedure, with studies showing its benefit in temporary relief of radicular symptoms,23 the thought being that local infiltration of steroid will aid in reduction of

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inflammation. Recent case reports have questioned the uses of particulate steroid due to risk of paralysis with inadvertent intra-arterial injection.24 To show the efficacy of use of non-particulate steroid, Kennedy et al. showed that transforaminal epidural injection with dexamethasone does not have major differences when compared with triamcinolone. The facet (zygapophyseal joint) is a synovial joint and is innervated by the medial and articular branch of each lumbar dorsal ramus.25 When pathology is suspected, anesthesia can be obtained via intra-articular joint injection or local anesthetic blockade of medial branches (as articular branches are too small to be accurately targeted). This process can act as a diagnostic test to confirm the facet as the pain generator, paving the way for a more permanent medial branch neurotomy by radiofrequency ablation.26 Since the 1970s, minimally invasive intradiscal therapies such as chemonucleolysis, laser therapy, and percutaneous or endoscopic disc compression have been employed. The use of intradiscal steroid injection is debated, due to risk of discitis, and thermal application to the posterior annulus via intradiscal catheter (IDET) demonstrates favorable outcome, but only with stringent patient selection.27 Intradiscal oxygen-ozone (O2-O3) chemonucleolysis is an effective treatment procedure for neural compression secondary to bulging or herniated disc. The thought is that injection leads to dehydration of the disc, leading to decreased bulging or herniation of the disc tissue, enhanced tissue oxygenation, and anti-inflammatory effects.28,29 A new arena in therapeutic strategies for intervertebral disc and vertebral cartilage is the use of mesenchymal stem cells for repair and degeneration.30 Bone morphogenic protein, juvenile chondrocytes, and fibrin adhesives have also been trialed as other methods to decrease inflammation and slow the degenerative spine process. 

Technology For patients who progress to chronic intractable lumbar pain, new technology in the form of spinal cord stimulation is becoming frequently used. This technology works under the principle of neuromodulation via electrical stimulation of dorsal column, established in 1967.31 The electrical current alters pain processing by masking the sensation of pain, instead inducing a comfortable tingling or paresthesia.32 New technology is emerging for the stimulation of the dorsal root ganglion, which is a highly targeted form of neuromodulation. 

Surgery After failure of conservative and procedural management and after psychological and mental issues have been addressed, surgical treatment next becomes a viable alternative. A randomized controlled multicenter study with 2-year follow-up comparing lumbar fusion to nonsurgical treatment for chronic LBP found lumbar fusion to be significantly superior to nonsurgical treatment in improvement of pain and disability.33 Although the surgical management of lower back pain is constantly under debate, this study showed positive outcomes in a well-defined surgical group. Lumbar arthrodesis (fusion) has long been thought to be the “gold standard” of surgical management of lumbar

degenerative disc disease.34 The rationale of removing the nociceptive load by removal of the diseased disc material and then fusion of the selected segment to decrease motion of the already sensitized segment is the basis for treatment. The three main fusion techniques are posterolateral fusion, interbody fusion, and a 360-degree circumferential fusion, also known as a combination of interbody and posterolateral fusion. Posterolateral fusion targets only the posterior elements while interbody fusion can be performed via anterior or posterior approach. Minimally invasive spine surgery allows access to the spine with minimal disruption of skin and muscle, allowing for decreased intraoperative blood loss, postoperative pain, reoperation rates, hospital length of stay, and faster return to work.35 Lumbar disc arthroplasty (“artificial disc”) recently utilized in the United States after decades of use in Europe has proven a viable option for those looking to preserve lumbar motion instead of the restrictive nature of fusion. Even though there have been studies showing satisfaction of use, there still appears to be no conclusive evidence showing its long-term superiority in level I studies.34 

Potential Disease Complications As stated previously, lumbar degenerative disease is part of the normal aging process. This is evidenced by imaging studies of asymptomatic individuals showing some level of degeneration. However, for patients who are symptomatic, the process begins by advanced segmental degeneration via loss of disc height, osseous degeneration, neural compression (i.e., spinal stenosis, radiculopathy), and neurogenic claudication that leads to functional limitation. For those who suffer acute lower back pain, approximately 90% of pain resolves within 6 weeks. However, for those whose pain is unremitting, they can further go on to develop chronic pain. For individuals with persistent neurological deficits, emphasis is made on quick diagnosis and prompt treatment to prevent permanent neurologic loss. The incidence of mental disorders, whether it be anxiety, depression, or somatoform disorders, is high in patients with chronic pain. Therefore it is important to identify this cohort in order to target them for multidisciplinary care involving behavioral psychology or psychiatry. 

Potential Treatment Complications When considering treatment, whether it is medication, noninvasive, or surgical, no one has completely benign aftereffects. Upon initiating medication use, one always has to check the safety profile. Anti-inflammatory medications have been shown to have gastric, hepatic, and renal side effects. A common complaint for patients taking muscle relaxants is sedation. Heat and cold therapy can cause localized tissue injury if applied for too long or at extreme temperatures. Opioid therapy can cause overdose and dependence. Spinal injections can be complicated by dural puncture, spinal headache, cortisone flare, hypoglycemia, and rarely, hematoma, infection, intra-arterial cannulation, or neurological injury. For those undergoing surgery, appropriate patient selection is important. Surgical complications include vascular complications depending on approach,

CHAPTER 45  Lumbar Degenerative Disease

hematoma, dural tears, epidural fibrosis, postoperative ileus, implant loosening, infection, and spinal cord injury. Medical complications from surgery could be acute kidney injury, urinary retention, urinary tract infection, and pneumonia. It is vital to find the appropriate diagnosis and to educate the patient about the pathophysiology. Discussion of the risk versus benefit and potential complications before initiation of treatment is important.

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