basics of lumbar pain · 2018. 11. 15. · otherwise, the diagnosis is made by computed tomography...

KPS 2018 Annual Meeting

2018 The Korean Pain Society Fall Training Conference

Chair

Basics of Lumbar Pain

HONG SOON KIM (Gachon Univ., Korea)

Chi-Bum In : Spinal Stenosis

2018 The Korean Pain Society Fall Training Conference | 43

1. Introduction

Lumbar spinal stenosis can refer to following anatomic states; narrowing of the intraspinal (central) canal, the lateral recess, the neural foramen. Stenosis of the intraspinal (central) lumbar canal is commonly caused by degenerative bone disease, and causes disability in the aging population. Lateral recess and neural foraminal stenosis causes lumbar radicu-lopathy, and related to degenerative bone disease and back pain.

2. Etiology

Spondylosis is the most common cause of Lumbar spinal stenosis. Disc degeneration can lead to disc protrusion and/or loss of disc height. The loss of disc height can cause loading of the posterior elements of the spine, and facet joint arthrop-athy, osteophyte formation and hypertrophy of the ligamentum flavum follow (Figure 1). Other causes include spondylo-listhesis, space-occupying lesions, traumatic and postoperative causes, Paget’s disease, ankylosing spondylitis, rheumatoid arthritis, diffuse idiopathic skeletal hyperostosis, Dwarfism, spinal dysraphism.

3. Pathophysiology

Mechanical compression and ischemia of spinal nerve roots have been proposed as the causes of neurologic symptoms in lumbar spinal stenosis. A role for inflammation of spinal nerve roots is less certain. Spinal nerve root compression may result from direct mechanical compression, increased intrathecal pressure can cause venous congestion, decreased arterial blood flow, and reduced impulse conduction along spinal nerve roots.

4. Symptom

The symptoms of lumbar spinal stenosis include discomfort, pain, sensory loss, and weakness in legs and low back pain. Neurogenic claudication is a typical symptom of lumbar spinal stenosis. This symptom is exacerbated with walking or standing, and relieved with sitting or lying. Many patients with lumbar spinal stenosis are symptomatic when active. Low back pain in lumbar spinal stenosis is not necessarily associated with the claudication symptoms.

5. Differential diagnosis

Peripheral vascular disease may be overlooked in diagnosing lumbar spinal stenosis. Both are associated with exertional

Spinal Stenosis

Chi-Bum InDepartment of Anesthesiology and Pain Medicine, Konyang University Hospital, Korea

KPS 2018 Annual Meeting2018 The Korean Pain Society Fall Training Conference

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KPS 2018 Annual Meeting | 44


exacerbation. However, the symptoms of neurogenic claudication can be distinguished from vascular claudication (Table 1). Neurogenic claudication often persists with when standing, and can be ameliorated by flexed posture. Bicycling is bet-ter tolerated by patients with lumbar spinal stenosis compared with patients with vascular claudication. Other diagnoses should also be considered; nonspecific back pain from spondylosis, polyneuropathy, osteoarthritis of the hip or knee, spinal cord vascular malformation, inflammatory conditions of lumbosacral nerve roots or cauda equine, congenital tethered

Fig. 1.

Table 1.

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Chi-Bum In : Spinal Stenosis


cord syndrome.

6. Diagnosis

Diagnosis of lumbar spinal stenosis requires the typical symptoms with a neuroimaging study that shows the narrowing of the intra spinal canal. Plain radiographs of the lumbar spine can support the diagnosis of lumbar spinal stenosis and magnetic resonance imaging (MRI) is the modality of choice for the diagnosis of lumbar spinal stenosis. Computed tomog-raphy (CT) may be preferable to MRI for bony anatomy.

References

1. Kerry L. Lumbar spinal stenosis: pathophysiology, clinical features, and diagnosis. Up to date. 2018; Available from URL: https://www.uptodate.com/contents/lumbar-spinal-stenosis-pathophysiology-clinical-features-and-diagno-sis?search=spinal%20stenosis&source=search_result&selectedTitle=2~65&usage_type=default&display_rank=2.

2. Katz JN, Harris MB. Clinical practice. Lumbar spinal stenosis. N Engl J Med 2008; 358:818.3. Ciol MA, Deyo RA, Howell E, Kreif S. An assessment of surgery for spinal stenosis: time trends, geographic varia-

tions, complications, and reoperations. J Am Geriatr Soc 1996; 44:2854. Atlas SJ, Delitto A. Spinal stenosis: surgical versus nonsurgical treatment. Clin Orthop Relat Res 2006;443:198.5. Jinkins JR. Gd-DTPA enhanced MR of the lumbar spinal canal in patients with claudication. J Comput Assit Omogr

1993;17:5556. Hall S, Bartleson JD, Onofrio BM, et al. Lumbar spinal stenosis, Clinical features, diagnostic procedures, and results

of surgical treatment in 68 patients. Ann Intern Med 1985; 103:271.

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Introduction

Low back pain (LBP) is a common clinical problem and has significant adverse socioeconomic implications. Various terms such as discogenic pain, internal disc disruption, and painful degenerative disc disease, has been identified as the pri-mary source of pain in lumbar region. In most cases of acute lower back pain, a definite pain generator cannot be defined. For chronic low back pain sufferers, an estimated 39% of cases can be attributed to the intervertebral disk. Disk degener-ation is a natural part of the aging process and normally begins about the third decade of life. Disk disruption is not to be confused with degenerative changes, which are a normal part of aging. In the right clinical setting, the disk can become a primary source of pain.

Anatomy

The human intervertebral disk consists of a firm, collagenous exterior annulus fibrosis and a gelatinous interior nucleus pulposus. The annulus is thicker anteriorly than superiorly, therefore herniations and tears are more common posteriorly. Two cartilage endplates cover the upper and lower surfaces of vertebral bodies. The cells that form the annulus fibrosus, particularly in the outer region, are fibroblast-like and arranged parallel to the collagen fibers, whereas those in the inner annulus fibrosus are chondrocyte-like. The nucleus pulposus contains collagen fibers that are randomly distributed and elastin fibers that are radially organized embedded in a highly hydrated aggrecan-containing gel.

The nerve supply to the human intervertebral disk consists of contributions from the sinuvertebral nerves and gray rami communicantes. These nerves are segmental and from the dorsal ramus, but recent studies have shown some contributions from the sympathetic chain in a nonsegmental distribution.

With the disc degeneration, there is a net loss of proteoglycans and water from the nucleus, leading to poor hydrody-namic transfer of axial stresses to the outer annulus fibrosus. The disc degeneration may result from an imbalance between the anabolic and catabolic processes or the loss of steady state metabolism that is maintained in the normal disc. Alterations in both anabolic and catabolic processes are thought to play key roles in the onset and progression of disc degeneration. The composition and structure of painful disc differed from those of non-painful degenerative disc. Specifically, normal fibroblasts in the annulus fibrosus were replaced by cartilage-like cells.

Pathophysiology

The development of radial fissures is believed to be related to repetitive shear, axial loads, and compression of the disk.

Discogenic Pain

Kibeom ParkDepartment of Anesthesiology and Pain Medicine, Keimyung University Donsgan Hospital,

Keimyung University, Korea


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Kibeom Park : Discogenic Pain


This process leads to vertebral endplate fractures, in which the fissures can develop by disk degradation over time. Intradis-cal disruption (IDD) results from lumbar disk degradation, its nuclear components, and development of radial fissures that extend from the nucleus into the annulus. IDD is believed to be the most common type of discogenic pain. Radial fissures may correlate with pain. A process of sensitization and neural ingrowth are proposed mechanisms of the development of IDD. Pain-associated proinflammatory mediators including calcitonin gene-related peptide, tumor necrosis factor, inter-leukin 1, interleukin 6, and substance P have been isolated from disks with this morphology. Modified Dallas Discogram Description method, the degrees of annular disruption could be classified into four grades. The definitions are Grade 0: the contrast medium is confined within the normal nucleus pulposus; Grade 1: the contrast medium flows into the inner third of the annulus through annular fissure; Grade 2: the contrast medium flows into the middle third of the annulus; Grade 3: the contrast medium flows into the outer third of the annulus, and extends circumferentially less than 30° arc at the disk center; Grade 4: the contrast medium flows into the outer third of the annulus, and extends circumferentially more than 30° arc at the disk center; and Grade 5: the contrast medium leakage into the outer space. Grades 0, 1 and 2 are normal, while Grades 3 and above are indicative of annular disruption.

Theoretically, any innervated vertebra and its peripheral structures might be the source of low back pain. An interver-tebral disc has such a structure and the endplate also has nerve supplies. Normally, one vertebral endplate has two nerve supplies: one enters the endplate along with perivertebral blood vessels, while the other that belongs to the sinuvertebral nerve branch that enters the endplate through the intervertebral foramen. The nerve density within the endplate is sim-ilar to that of the annulus, indicating that the endplate is also an important source of discogenic low back pain. Endplate damage-induced low back pain occurs quite often clinically. In clinical research, Endplate damage-induced low back pain accounted for 16.7% of chronic discogenic low back pain.

Diagnosis

It has been difficult to identify the cause of LBP. History for pain is important for impression. One study suggests that medical interview about LBP (i.e., LBP after sitting too long, LBP while standing after sitting too long, squirming in a chair after sitting too long, LBP while washing one’s face, and LBP in standing position with flexion) were useful for diagnosing discogenic LBP associated with DDD. Otherwise, the diagnosis is made by computed tomography after discography. The technique of injecting local anesthesia into a disc is analgesic discography (discoblock). However, it is invasive and harmful to the disc.

The high-intensity zone (HIZ) on a lumbar MRI T2-weighted image was associated with abnormal disc morphology in the discography. In addition, there was a significant relationship between the HIZ and pain reproduction. HIZ is a highly effective parameter in determining the intensity of discogenic LBP.

The various consensus statements of discographic criteria for the diagnosis of presumed discogenic pain are presented. The criteria proposed by International Association for the Study of Pain (IASP) is followed

1. Anesthetization of the target disc relieves patient’s accustomed pain for a period consonant with the expected dura-tion of action of the local anesthetic used

2. Any persisting pain can be ascribed to a coexisting source OR 1. Provocation of the target disc reproduces patient’s accustomed pain2. Provocation of at least two adjacent discs do not reproduce patient’s pain3. CT discography demonstrate a Grade 3 or greater annular disruption

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Added remark: Because of the propensity for false-positive responses, provocation discography alone is insufficient to establish the diagnosis of discogenic pain.

Later, the criteria for provocation discography set forth by International Spine Intervention Society (ISIS) were even more elaborate and, in addition to the criteria promulgated by IASP, made specific recommendations for the disc pressures and pain intensities

1. Provocation of the target disc reproduces concordant pain2. Degree of pain produced during the injection on a scale of 0–10 must be at least 7/103. Provocation of adjacent one to two discs does not reproduce pain-control level4. Affected disc exhibits Grade 3 or great fissure on CT discography5. Manometry is used to determine the type of the painful disc Unequivocal discogenic pain: pain at <15 psi above opening pressures and two control levelsDefinite discogenic pain: pain at<15 psi above opening pressure and one control level or <50 psi and two control levelsProbable discogenic pain: pain at<50 psi above opening pressure and one control levelIndeterminate disc: pain on disc injection, but none of the previous criteria met

Conclusion

Discogenic back pain is a common clinical symptom. Degenerated intervertebral disc cells and inflammatory cell infil-trates can stimulate reconstruction of nerve fibers of internal intervertebral discs and cause back pain at the same time. In the future, a full understanding of the specific mechanism of nerves throughout the course of discogenic back pain needs to be investigated. This will allow new methods and approaches for the treatment of discogenic back pain.

References

1. Hadjipavlou AG, Tzermiadianos MN, Bogduk N, Zindrick MR. The pathophysiology of disc degeneration: a critical review. J Bone Joint Surg Br 2008; 90: 1261-1270.

2. Peng BG, Pang XD, Li DM, Zhang XY, Kuang ZD, Du MK, Gao CH. Typing of discogenic low back pain. Zhonghua Guke Zazhi 2009; 31: 801-805.

3. Coppes MH, Marani E, Thomeer RT, et al. Innervation of annulus fibrosis in low back pain. Lancet 1990; 336: 189–90.4. Tonosu J, Inanami H, Oka H, Katsuhira J, Takano Y, Koga H, Yuzawa Y, Shiboi R, Oshima Y, Baba S, Tanaka S,

Matsudaira K. Diagnosing Discogenic Low Back Pain Associated with Degenerative Disc Disease Using a Medical Interview. PLoS One. 2016: 7; 11:e0166031.

5. Fang C, Zhang W, Chen L, Li H. The correlation between the high-intensity zone on a T2-weighted MRI and positive outcomes of discography: a meta-analysis. J Orthop Surg Res. 2017: 8; 12: 26.

6. Wagner AL, Murtagh FR, Arrington JA, Stallworth D. Relationship of Schmorl’s nodes to vertebral body endplate fractures and acute endplate disk extrusions. AJNR Am J Neuroradiol 2000; 21: 276-281.

7. Merskey H, Bogduk N. Lumbar discogenic pain. In: Merskey H, Bogduk N, eds. Classification of chronic pain. De-scriptions of chronic pain syndromes and definition of pain terms. 2nd ed. Seattle, WA: Task Force on Taxonomy of the International Association for the Study of Pain. IASP Press, 1994:180–1

8. Bogduk N. Lumbar disc stimulation (provocation discography). In: Bogduk N, ed. Practice guidelines for spinal diagnostic and treatment procedures. 1st ed. International Spine Intervention Society, 2004:20–46.

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이진영 : Basic interventions in lumbar lesion for beginners


Medial branch block

Zygapophysial or facet joints have been implicated as cause of back and referred pain. These joint can be blocked either by intraarticular injections or by medial branch injection that innervate the target joint. Medial branches of the lumbar dorsal rami as issuing from their respective intervertebral foramina cross the superior border of the transverse process, and then running along the junction of the transverse process and superior articular process before turning medially around the base of the zygapophysial joint and under the mamillo-accessory ligament (ex. L4 crosses the transverse process of L5). The L5 nerve differs that it is the dorsal ramus itself, rather than medial branch, runs along the junction of the superior articular process of the sacrum and ala of the sacrum.

Fig. 1. Schematic drawing of spinal cord and segmental spinal innervation

Basic interventions in lumbar lesion for beginners

이진영성균관대학교 의과대학 삼성서울병원 마취통증의학과


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Facet joint block

Facet joints are a well-recognized cause of pain in subjects with persistent spinal pain. Neuroanatomic, neurophysio-logic and biomechanical studies have demonstrated free and encapsulated nerve endings in facet joints, as well as nerves containing substance P and calcitonin gene-related peptide; facet joint capsules contain low-threshold mechanoreceptors, mechanically sensitive nociceptors, and silent nociceptors and lumbar and cervical facet joint capsules can undergo high strains during spine loading. Controlled local anesthetic blocks of facet joint or its nerve supply are routinely employed to diagnose facet joint pain.

Epidural block

Epidural injections are administered by accessing epidural space by multiple routes including interlaminar, transfo-raminal, and caudal. Interlaminar entry is considered to deliver the medication closely to the assumed site of pathology. Transforaminal approach is considered the target specific modality requiring the smallest volume to reach the primary site of pathology. The mechanism of action of epidurally administered steroids and local anesthetic injection is still not well understood. The achieved neural blockade alters or interrupts nociceptive input, the reflex mechanism of the afferent fibers, self-sustaining activity of neurons, and the pattern of central neuronal activities. Corticosteroids have been shown to reduce inflammation by inhibiting either synthesis or release of pro-inflammatory mediators. Local anesthetics provide short to long term symptomatic relief based on alteration of various mechanisms including excess nociceptive process, excess re-lease of neurotransmitters, nociceptive sensitization of nervous system and phenotype changes.

References

1. Dreyfuss P. Specificity of lumbar medial branch and L5 dorsal ramus blocks. Spine 1997; 22: 895-902.2. Manchikanti L. Medial branch neurotomy in management of chronic spinal pain. Pain Physician 2002; 5: 405-18.3. Manchikanti L. Effectiveness of therapeutic lumbar transforaminal epidural steroid injections in managing lumbar

spinal pain. Pain Physician 2012; 15: E199-245.4. Benyamin RM. The effectiveness of lumbar interlaminar epidural injections in managing chronic low back and lower

extremity pain. Pain Physician 2012; 15: E363-404.

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basics of lumbar pain · 2018. 11. 15. · otherwise, the diagnosis is made by computed tomography...

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