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CHAPTER 27/TRANSLAMINAR SCREW FIXATION / 293
FIG. 27-1. Ten years postoperative: In addition to the solid fusion posteriorly, spontaneous calcification of the immobilized disc occurred. Axial loads are shared equally in the anterior and posterior columns.
The mechanical stiffness of a segment instrumented with translaminar screws is 2.4 times that of an uninstru­mented segment; the stiffness was maintained for 5,000 cycles in static and cyclic loading tests (13,14).
The fact that the transfacet screw fixation in vivo might be less rigid than pedicle fixation may be an advantage rather than a disadvantage by promoting bone formation because rigid fixation results in stress shielding of the fusion and impedes bone remodeling (Fig. 27-1).
INDICATIONS
Translaminar screw fixation might be indicated in cases where segmental motion in the lumbar spine must be eliminated. It can be used as a primary fixation or as a supplemental procedure to protect and augment an exist­ing fixation.
Translaminar Screws as Primary Procedure
Segmental Dysfunction
Motion between two or more anatomic structures causes wear and tear and a gradual change in their microstructure and macrostructure that may or may not lead to altered func­tion and possibly pain (15). Given the complexity of the spine, diagnosis and localization of the pain source remains a challenging problem. In addition to clinical and radiologic examination (16), facet blocks and discography may be helpful to determine the painful segment. Temporar y fixa­tion with an external fixator also may be used as an invasive diagnostic method to identify a painful segment (17).
Once the diagnosis and localization of the painful seg­mental motion is established, posterior immobilization
with translaminar screw fixation provides a simple and effectiv e means of selectiv e fusion of the involved segment (18). Dysfunction of a segment before the development of significant macroscopic structural changes represents an ideal indication for translaminar screw fixation.
Lumbar Spinal Stenosis
Degenerative lumbar spinal stenosis can be effectively treated with surgical decompression. If the compressive structures are removed, reduced leg pain and increased walking distance may be e xpected (19). It is reasonab le to assume that the decompression may adversely affect the stability of the involved segment (7). Complete laminec­tomy with removal of a major portion of the facets, as may be required for lateral spinal stenosis, may jeopar­dize the segmental stability (8,20,21,22). Fusion also should be considered in these circumstances. Once the pos­terior elements have been removed, only transpedicular fix­ation systems are feasible. By using the more anatomic, atraumatic, and physiologic technique of “undercutting laminectomy,” an effective decompression of the spinal canal can be performed leaving the posterior elements essentially intact (23–28). If fusion is considered necessary under these circumstances, the translaminar screws can pro­vide fixation without considerable risk or lengthening of the operative time.
Revision Surgery
Persistent or recurrent pain after decompressive proce­dures might be associated with mechanical problems. Scar formation or persistent bony stenosis might irritate neurologic structures during motion. Therefore, immobi-
294 /SECTION IV/SURGERY
lization of a previously operated segment may be indi­cated. If there is foraminal narrowing as a result of disc space narrowing following prior discectomy, additional distraction will open the foramen (29). Resection of one facet joint or bilateral resection of more than 50% of both facets may produce segmental instability (30). Because translaminar screws rely on the integrity of the posterior elements, this technique is only possible where the lam­ina and facet joint are sufficiently intact to receive a 4.5­mm cortical screw. Because the posterior bone stock is reduced, careful posterolateral intertransverse dissection must be done.
Disc-Related Syndromes
Lumbar Disc Herniation
Excision of a protruding disc fragment through a lim­ited exposure is the accepted surgical treatment for herni­ated lumbar discs (31). A 5% to 10% incidence of recur­rent disc herniation and a 10% to 15% incidence of postoperative low back pain is to be expected with this technique (32). Routine concomitant fusion after disc excision is not justified. However, in the presence of long-standing back pain and degenerative changes in the involved segment, fusion may help to improve outcome.
FIG. 27-2. Tr ansarticular screw fixation as a supplement to increase stability at the lumbosacral junction.
achieved by supplementary transarticular screws fixation in the lumbosacral joint may help to overcome this anatomic disadvantage (Fig. 27-2).
Disc Resorption and Internal Disc Disruption
When the underlying pathology is the de generated disc itself (23,33), posterior fusion may help to reliev e pain b y immobilizing the segment. Posterior translaminar screw fixation is indicated if anterior surgery is not advised or indicated for other medical reasons or when posterior bony decompression is to be performed simultaneously.
Translaminar Screws as a Supplemental Procedure
Augmentation of Anterior Fusion
Translaminar screws eff iciently immobilize the poste­rior columns in the presence of an intact anterior column. If there is a structural deficiency anteriorly, anterior reconstruction with a compression-resistant device must be performed. Biomechanically, anterior struts are ideal in resisting compressive forces but inadequate in neutral­izing axial rotational forces. Therefore, supplemental translaminar screws are ideal in augmenting anterior pro­cedures by immobilizing the facets and thereby eliminat­ing axial rotation.
Augmentation of Pedicle Systems
The weak point in long lumbosacral pedicle constructs is sacral fixation. Different from the anatomy of the lum­bar pedicles, the sacral pedicles are wider and provide less solid bone for screw fixation. The additional stability
Repair of Anterior Pseudarthrosis
In cases of anterior pseudarthrosis, posterior supple­mental fusion is preferred to a repeat anterior procedure. Scar formation around the aorta, iliac vein, and vena cava may increase the operative risk of revision anterior surgery considerably. Translaminar screw fixation with additional posterior bone grafting offers a simple and effective method to stabilize the back.
CONTRAINDICA TIONS AND LIMITATIONS
Translaminar screws rely on bony purchase to the pos­terior elements of the vertebrae (lamina, facets, and trans­verse process). Therefore, the posterior elements must be substantial enough to hold a screw. Severe osteopenia might jeopardize the screw purchase. Screw loosening and pseudarthrosis are more likely to occur in these cases. Because transfixed facets eliminate rotation in the y and z axis, but are less effective in the x axis, an intact anterior column is mandatory for this technique. The translaminar screws provide segmental fixation at each level fused, but avoids intersegmental connections between each fused segment. In our series, there were no statistical differences in solid bony union between monosegmental and bisegmental fixations; the number of three segmental fixations was too few to allow valid statistical analysis. However, for mechanical reasons, we do not advocate translaminar fixation of more than two adjacent segments.
CHAPTER 27/TRANSLAMINAR SCREW FIXATION / 295
For the same reason, translaminar screws should not be used to extend an existing fusion.
OPERA TIVE TECHNIQ UE
The surgical exposure is performed through a standard midline incision. The spinous processes, lamina, facet joints, and transverse processes are visualized and decor­ticated to receive the bone graft. The facet joints are opened by excision of the capsule, and osteophytes are removed. The cartilage of the dorsal aspect of the joint is removed, taking care not to injure the underlying sub­chondral bone in order to avoid loss of screw f ixation.
The insertion of the screws by the Magerl technique is performed from the contralateral side of the spinous process of the segment to be fused, using a 50- to 54-mm long 4.5-mm screw. Fixation in slight flexion can be achieved if desired by applying interspinal distraction. Using a 3.2-mm drill bit, a hole is bored from the con­tralateral side of the spinous process into the opposite lamina. From there, the drill crosses the facet joint through its center and ends at the base of the transverse process (Fig. 27-3). This technique allows a nearly per­pendicular screw direction in relation to the plane of the joint to be fused. In obese patients, percutaneous inser­tion of the drill through a separate stab incision may be necessary to obtain the proper direction of the screw. A dissector may be introduced between the attachment of the ligamentum flavum and the lamina, to minimize the risk of penetrating the spinal canal during the drilling procedure. An iliac bone graft must be placed posteriorly along the bony structures previously decorticated.
The postoperative management is straightforward and simple. Mobilization is begun on the first or second post­operative da y. A soft corset brace is worn while out of bed for 3 months to restrict gross motions. Patients are en­couraged to walk, and no physical therapy is performed during the first 2 months.
PATIENTS AND RESUL TS
One hundred seventy-three consecuti v e patients under­went translaminar screw fixation of the lumbar spine, of which 145 (83%) were reassessed after an average fol­low-up of 58 months (34). Fifty-seven percent had a sin­gle-level fusion, 40% a two-level fusion, and 3% a three­level fusion. As a simultaneous procedure, 30% had a nucleotomy and 52% had a decompression of the spinal canal for clinically relevant symptoms of spinal stenosis.
A solid bony fusion, with a radiologically solid fusion mass and no apparent motion on the digitized flexion­extension radiographs in the fused segments, was docu­mented in 163 patients (94%) and 241 segments (96%). Radiolucency around the screws was detected in five patients (3%). Two screws were broken; however, no motion could be detected on the flexion-extension radi­ographs.
Preoperativel y the subjecti ve pain rating w as 7.6, w hich decreased to a pain rating of 2.9 at follow-up. Thirty-three patients (19%) were taking analgesics because of lumbar back pain. One hundred sixty (92%) of the patients stated that they would under go the same treatment again if in the same situation as prior to surgery.
FIG. 27-3. Correct position of the screws in axial computed tomography scan: through the lamina and the facet joint into the base of the transverse process. Permanent stability is achieved with a proper grafting technique.
REFERENCES
1. Hadra BE. Wiring of the spinous processes in Pott`s disease. Trans Am Orthop Assoc 1891;4:206–211.
2. Roy Camille R, Demeulenaere C. Osteosynthèse du rachis dorsal, lom­baire et lombo-sacré par plaque métallique vissée dans les pédicules vertébraux et les apophyses articulaires. Presse Méd 1970;78: 1447–1448.
3. King D. Internal f ixation of lumbosacral fusion. J Bone Joint Surg 1948;30A:560–565.
4. Boucher HH. A method of spinal fusion. J Bone Joint Surg (British) 1959;41:248–259.
5. Magerl F. Stabilization of the lower thoracic and lumbar spine with external skeletal fixation. Clin Orthop 1984;189:125–141.
6. Louis R. Fusion of the lumbar and sacral spine by internal fixation with screw plates. Clin Orthop 1986;203:18–33.
7. Abumi K, Panjabi MM, Kramer KM. Biomechanical evaluation of lumbar spinal stability after graded facetectomies. Spine 1990;15: 1142–1147.
8. Haher TR, O’Brien M, Dryer JW, et al. The role of the lumbar facet joints in spinal stability. Spine 1994;19:2667–2671.
9. Goel VK, Weinstein JN, Found EM. Biomechanics of lumbar and tho­racolumbar spine surgery. In: Goel VK, Weinstein JN, eds. Biome­chanics of the spine: clinical and surgical perspective. Boca Raton, FL: CRC Press, 1990:181–232.
10. Tencer A, Ahmed A, Burke D. Some static mechanical properties of the lumbar intervertebral joint, intact and injured. J Biomech Eng 1982; 104:193–201.
11. Heggeness MH, Esses SI. Translaminar facet joint screw fixation for lumbar and lumbosacral fusion. A clinical and biomechanical study. Spine 1991;16S:266–269.
296 /SECTION IV/SURGERY
12. Kornblatt M, Casey MP, Jacobs RR. Internal f ixation in lumbosacral spine fusion. A biomechanical and clinical study. Clin Orthop 1986; 203:141–150.
13. Deguchi M, Cheng, BC, Sato K, et al. Biomechanical evaluation of translaminar facet joint fixation. Spine 1998;23(12):1307–1313.
14. Vanden Berghe L, Mehdian H, Lee AJ, et al. Stability of the lumbar spine and method of instrumentation. Acta Orthop Belgica 1993;59: 175–180.
15. Eisenstein SM, Parry CR. The lumbar facet arthrosis syndrome. Clini­cal presentation and articular surface changes. J Bone Joint Surg 1987;69B:3–7.
16. Penning L, Blickman JR. Instability in lumbar spondylolisthesis: A radi­ologic study of several concepts. Am J Roentgenol 1980;134:293–301.
17. Olerud S, Sjöström L, Karlström G, et al. Spontaneous effect of increased stability of the lower lumbar spine in cases of severe chronic back pain. Clin Orthop 1986;203:67–74.
18. Stokes IA, Frymoyer JW. Segmental motion and instability. Spine 1987;12:688–691.
19. Grob D, Jeanneret B, Aebi M, et al. Atlantoaxial fusion with transar­ticular screw fixation. J Bone Joint Surg 1991;73B:972–976.
20. Hopp E, Tsou PM. Postdecompression lumbar instability. Clin Orthop 1988;227:143–151.
21. Katz J, Lipson S, Larson M, et al. The outcome of decompressive laminectomy for degenerative lumbar stenosis. J Bone Joint Surg 1991;73A:809–816.
22. Passuti N, Allioux JJ, Cistac C, et al. Sténoses lombaires dégénérativ es: interêt de l’instrumentation de Cotrel-Dubousset associé à la lamino­arthréctomie. Rev Chir Orthop 1990;76:23–29
23. Crock H. A short practice of spinal surgery. New York: Springer-Ver­lag, 1993.
24. De la Caffiniere JY. Evaluation du risque de glissement vertebral après traitement chirurgical d’une stenose lombaire. Rev Chir Orthop 1986; 72:73–80.
25. Getty CJ, Johnsson JR, Kirwan EO, et al. Partial undercutting facetec­tomy for bony entrapment of the lumbar nerve root. J Bone Joint Surg Br 1981;63-B(3) 330–335.
26. Grob D, Panjabi M, Dvorak J, et al. Die instabile Wirbelsäule-eine “In­vitro-” und “In-vivo-Studie” zum besseren Verständnis der klinischen Instabilität. Orthopäde 1994;23:291–298.
27. Nakai O, Okawa A, Yamaura I. Long term roentgenographic and func­tional changes in patients who were treated with wide fenestration for central lumbar stenosis. J Bone Joint Surg 1991;73A:1184–1191.
28. Senegas J, Etchevers JP, Vital JM, et al. Widening of the lumbar canal as an alternative to laminectomy in the treatment of lumbar stenosis. French J Orthop Surg 1988;2:93–99.
29. Humke T, Grob D, Dvorak J, et al. Foraminal changes with distraction and compression of the L4/5 and L5/S1 segments. Eur Spine J 1996;5: 183–186.
30. White AA, P anjabi MM, Posner I, et al. Spinal stability: evaluation and treatment. In: American Academy of Orthopedic Surgeons. Instruc­tional Course Lectures. St. Louis: CV Mosby, 1981:457–483.
31. Benini A, Magerl F. Selective decompression and translaminar facet screw fixation for lumbar canal stenosis and disc protrusion. Br J Neu­rosurg 1993;7:413–418.
32. Hanley EN, Shapiro DE. The development of low back pain after exci­sion of a lumbar disc. J Bone Joint Surg 1989;71A:719–721.
33. Weinstein J, Rydevik B. The pain of spondylolisthesis. Semin Sin Surg 1989;2:100–105
34. Grob D, Humke T. Translaminar screw f ixation in the lumbar spine: indications, technique, results. Eur Spine J 1998;7:178–186.
SECTION V
Specific Clinical Entities
CHAPTER 28

Lumbar Disc Disorders

Mats Grönblad
Medicine, to produce health, has to examine disease, and music, to create harmony, must investigate discord.
—Plutarch, c.e. 46–120
Low back pain, including that resulting from lumbar disc disorders, is multifactorial, as is the disability caused by it (1,2). Perhaps the most common causes of low back pain are musculoligamentous injuries and age-related degenerative processes of spinal structures (1). Degener­ative processes are partly age-related and partly geneti­cally determined (3–5). Spine problems and spinal degen­eration are not problems of modern society, they have been reported in ancient times as well (6).
SOFT TISSUE Definitions
Any muscle in the body may be strained or sprained, including low back muscles. Verifying such sprains as the cause of low back pain is, however, difficult. Often, how­ever, either the term low back strain (7,8) or sprain (9) is used for any acute low back pain symptoms that com­mence suddenly (e.g., at the workplace). Of note, how­ever, it has been suggested that sudden increases in phys­ical activity will mainly affect the intervertebral disc, which is the most vulnerable spinal structure, due to its avascular nature and low metabolic rate. Thus, adaptive remodeling changes in the disc could lag behind those in other spinal tissues (10).
History and Physical Examination
Whenever a patient visits for low back pain, the most important thing is to first exclude any serious underlying disease or disorder that may warrant specific treatment. The so-called red flags (Table 28-1) are of great help when trying to exclude serious underlying disorder. When one or more of the red flags has been determined to be present, there is up to a 10% probability that the
patient has a serious underlying disease causing the low back pain symptoms (13). A report of nighttime pain ma y also suggest underlying systemic disease (1) (e.g., malig­nant disease or inflammatory spondyloarthropathy). This is particularly the case if the pain shows progressive worsening with time. The combined history and erythro­cyte sedimentation rate have been reported to have rela­tively high diagnostic accuracy in vertebral cancer (14). Moderately accurate items for diagnosing ankylosing spondylitis are a need to get out of bed at night and to move around a bit as well as reduced lateral mobility of the spine (14).
Pain radiating below the level of the knee may be sug­gestive of sciatica, and should war rant a thorough neuro­logic examination. While in the waiting room the patient may complete a pain dra wing, depicting areas of pain and pain radiation, possibly with separate markings or colors for pain, numbness, and “pins and needles”. Viewing such a precompleted chart will give the examining ph ysi­cian a quick notion of the presence or absence of sciatic pain radiation. Pain drawings may be an important adjunct in the assessment of chronic low back pain (15–18) and have been shown to have acceptable repeata­bility (18).
One should be alert to signs of systemic disease (e.g., fever). F ollowing low back strain or sprains, possibl y sug­gesting a muscular source for the pain, palpating verte­bral muscles for tenderness can be done, but unfortu­nately, such palpation of tenderness is not reproducible between examiners (1). Interpreting limited spinal motion is also problematic, because the correlation with disability assessments or visual analog scale pain intensity is reportedly quite low (19). As well, in a normal busy clin­ical environment the reliability of such measurement of spinal motion is apparently quite low (20). With thor­oughly trained examiners, however, the inter-tester relia­bility for physical examination findings may be some­what better (21,22). Measures of spinal flexibility have been reported to be poor predictors of future back pain in an industrial setting (23). Borge et al. (24) recently con-
299
300 /SECTION V/SPECIFIC CLINICAL ENTITIES
TABLE 28-1. Red flags (somatic risk factors) for excluding
serious underlying disorder in patients presenting with low
back pain
Age: >50 years History of cancer Unexplained weight loss Pain: >1 month’s duration Absence of response to therapy Pain becomes worse at rest History of intravenous drug use Presence of an infection, particularly urinary tract infection
From Bigos S, Bowyer O, Braen G, et al. Acute low back problems in adults. Clinical practice guideline no. 14. Rockville, MD: Agency for Health Care Policy and Research, 1994:iii, 1–26 (AHCPR publication no. 95-0642) and Lurie JD, Gerber PD, Sox HC .A pain in the back. New Engl J Med 2000;343:723–726, with permission.
cluded, based on a systematic literature review, that there is presently no satisfactory answer whether or not physi­cal examination tests have any prognostic value in the nonoperative treatment of patients with low back pain. An exclusively medical approach for the measurement of physical disability following low back strain or sprains should probably be abandoned in favor of a multifactor­ial biopsychosocial approach to low back disability assessment (19,20).
Treatment
Following lumbar strain or sprains, the mainstay of any treatment should be to try to keep the patient active, not use bed rest as a treatment modality, and to support the patient in attempts to return to work as quickly as possib le (25–27). The choice of treatments should be based upon published guidelines for treating patients with low back pain (11,28–32). It may also be helpful, when attempting to predict further chronicity of the low back problem, to consider so-called yellow flags, which are suggested psy­chological risk factors for delayed recovery (Table 28-2).
TABLE 28-2. Yellow flags (psychological risk factors) that
may help predict prolonged recovery
Attitudes and beliefs: The experienced pain is harmful to
the spine Inadequate illness behavior (e.g., extended rest) Compensation Diagnosis and treatment: Causes confusion or fear about
outcome Emotions: fear, irritation, low mood Work issues: Belief that work is harmful; absence of
interest of employer; no possibilities for gradual return to
work; high biomechanical demands
From Kendall NAS, Linton SJ, Main CJ. Guide to assess­ing psychosocial yellow flags in acute low back pain:risk fac­tors for long-term disability and work loss. Wellington (NZ): Accident Rehabilitation & Compensation Insurance Corpora­tion of New Zealand and the National Health Committee, 1997, with permission.
DISC DEGENERATION Definition
A study by computed tomography (CT) discography on 300 patients with various prediscography diagnoses indicated a major role for intradiscal pathology in non­specific low back pain syndromes (33). Also by CT discography, Schwarzer et al. (34) determined internal disc disruption to be present in 39% of 92 subjects stud­ied. Such internal disc disruption was most commonly present at the L5-S1 and L4-L5 levels (34). Distinguish­ing pathologic disc degeneration from disc alterations due to normal aging is, however, problematic. In a clini­cal setting, it has only recently been possible to radiolog­ically evaluate the extent and distribution of disc degen­eration. Radiologic findings that have been interpreted as suggestive of disc degeneration are, however, also com­monly observed in asymptomatic subjects (35,36). In a large-scale magnetic resonance imaging (MRI) study on asymptomatic women betw een the ages of 16 to 80 y ears, Powell et al. (35) noted a linearly increased prevalence of one or more degenerate disc with age. Disc degeneration on MRI was, however, already present in more than one­third of the women between the ages of 21 to 40 years (35). A more recent study by Goupille et al. (37) com­pared spinal cadavers of subjects who had suffered from chronic low back pain, in the absence of radicular pain, with subjects who had been free of back complaints. No individual type of degenerati ve abnormality was found to relate specifically to low back pain, but the extent of pathologic change did sho w such a relationship with prior chronic low back pain (37).
Natural History
There is now moderate evidence indicating that physi­cal demands of work play only a minor role in the devel­opment of disc degeneration (3,38,39). In a recent large­scale longitudinal study on 1,165 nurses, low back pain at baseline was highly predictive of future low back pain, and the longer back pain was consistently reported (in a total of 8 follow-up questionnaires completed 3 months apart), the greater the likelihood that it would also be pres­ent at the next follow-up. Furthermore, the investigators show ed that disabling lo w back pain carried a w orse prog­nosis, as did back pain associated with sciatica (40). Thus, low back pain should not be regarded as an acute event that can be cured but as a persistent problem with intermittent exacerbations (1). As the observations by Smedley et al. (40) suggest, determining a presence or absence of disability, already at an early stage, is of para­mount importance.
Follow-up by MRI of asymptomatic individuals with lumbar disc abnormalities, for an average of 5 years, showed progression of disc degeneration findings in
41.5% of the subjects (41). Medical consultation at fol-
CHAPTER 28/LUMBAR DISC DISORDERS / 301
low-up was, however, not predicted by MRI findings at baseline, but by job-related variables (41). Another simi­lar 7-year follow-up study on asymptomatic subjects showed that MRI f indings were not predictive of either the development or the duration of low back pain (42). The individuals with the longest duration of low back pain did not have the greatest degree of abnormality on the baseline MRI scans (42). Interestingly, in school­children degenerative abnormalities on MRI have been shown to predict future recurrent bouts of low back pain (43). It was suggested that disc degeneration present soon after the phase of rapid physical growth predicted recur­rent pain up to early adulthood (43). At the other end of the age scale, a study by CT discography on 291 subjects with an age range of 17 to 79 years noted that the pro­portion of severely degenerated but painless discs increased with age, as did discs producing dissimilar pain (44). According to the investigators, such degenerated but asymptomatic discs, particularly in older subjects, may at least in part explain the well-recognized poor correlation between low back pain symptoms and radiographic images (44).
History and Physical Examination
In a study on male cadavers, examined radiographi­cally and osteologically, history of back injury showed a relationship with the presence of symmetric disc degen­eration, anular ruptures, and vertebral osteophytosis (45). In another study, lumbar disc degeneration, as observed by plain radiography, showed an age-independent associ­ation with both a history of lumbago and a history of sci­atica (46).
The same basic principles presented previously for muscular strain and sprain also apply to patients with disc degeneration. Thus, it is of paramount importance to first exclude serious underlying disorder (Table 28-1). Unfor­tunately, there are no clinical tests that are specific for internal disc disruption that can be diagnosed by CT discography (34). Recent studies suggest that for mea­surements of spinal range of motion, there is both poor intra- and inter-rater reliability (47). Furthermore, range of motion measurements show poor validity with respect to relationships with physical and functional impairment (19,48). There is currently also strong evidence that back function testing machines producing isometric, isokinetic, or isoinertial measurements have no predictive value for either future low back pain or disability (39). Waddell et al. (49) have presented a validated battery of measures of physical impairment that can be recommended. Whichever symptom characteristics or clinical signs are used, they should show acceptable intra- and interexam­iner repeatability and predictive validity with respect to major outcome measures of interest (50). Clinical obser­vation of overt pain behavior may also be helpful, even if there may be a problem of standardization (51).
Imaging
Plain Radiography
The main indication of imaging is to exclude serious
underlying disorder , when red flags are present (Table 28-
1) or otherwise. In older patients the possibility of osteo­porotic fracture should also be kept in mind (1). For the evaluation of disc degeneration, plain radiography pro­duces far too many nonspecific f indings, with doubtful clinical relevance (Figs. 28-1, 28-2). It is almost impossi­ble to reliably relate such f indings to clinical symptoms of low back pain. Overinterpretation is much too com­mon, and may have an adverse effect on the outcome by labeling the patient and increasing the sick role. This will have an effect opposite to the mainstay of the treatment protocol, namely to keep the patient active, functional, and to decrease perceived disability (52). Reliability of measurement may pose a problem (53).
CT and MRI
As is the case with plain radiography, these imaging modalities should be used mainly to exclude serious underlying disorder (Table 28-1) or when the patient has progressive or persistent neurolo gic deficit. Of note, there is now strong evidence that plain radiography and MRI findings have no predictive value for future lo w back pain or disability (39). They also do not correlate well with clinical symptoms in patients with nonspecific low back pain, or with work capacity (39).
FIG. 28-1. Plain radiograph anteroposterior and sagittal views of the lumbar spine of an asymptomatic 61-year-old woman. Note general disc narrowing and minor osteophytes both anteriorly and laterally. There is also slight scoliosis. (Courtesy of Dr. Kaj Tallroth, Or ton Hospital, Helsinki, Fin­land.)
302 /SECTION V/SPECIFIC CLINICAL ENTITIES
FIG. 28-2. Plain radiograph anteroposterior and sagittal views of a 46-year-old woman with low back pain. Disc nar­rowing, osteophytes, and end-plate changes appear only at the L4-L5 level. (Courtesy of Dr. Kaj Tallroth, Orton Hospital, Helsinki, Finland.)
CT should be combined with discography for imaging disc degeneration. With respect to MRI, it should be kept in mind that particularly disc bulges and protrusions are commonly observed in asymptomatic subjects, whereas disc extrusions are not (Table 28-3). But even when extrusions are observed, they should be interpreted within the entire clinical context to determine whether neural compromise is present or not. Bulges and protru­sions are particularly prevalent at the two lowest lumbar levels and the prevalence of disc bulges increases with age (36). There are now several studies that show MRI abnormalities in asymptomatic adults (1).
In a study on cadavers that used in parallel MRI, bio­chemical, and histologic analysis, decreased total proteo­glycan content and chondroitin-keratan sulfate ratio in subjects with low signal intensity on T2-weighted MRI could be observed, supporting the validity of MRI for diagnosing disc degeneration (54). Signal intensity on T2-weighted MRI has been considered the most sensi­tive available measure of disc degeneration (Fig. 28-3),
FIG. 28-3. T2-weighted sagittal magnetic resonance imag­ing scan (1.5 Tesla unit) of the lumbar spine of a 45-year-old man with low back pain. Note severe multiple level disc degeneration with end-plate abnormalities. The L4-L5 disc is almost totally obliterated, suggesting severe disc degenera­tion. (Cour tesy of Dr. Kaj Tallroth, Orton Hospital, Helsinki, Finland.)
whereas the assessment of disc height has less validity (55). In a large scale study, signif icant dehydration and degeneration on MRI was present in less than 5% at the two uppermost lumbar levels, whereas marked changes were observed at the two lowest lumbar levels in more than 20% of the patients (56).
Discography
TABLE 28-3. Presence of disc abnor malities on magnetic
resonance imaging in 98 asymptomatic subjects
%
Normal discs at all levels 36 Bulge (1 level) 52 Protrusion 27 Extrusion 1 Annular defects Abnormal finding in >1 disc 38
a
Disruption of the outer annulus fibrosus ring of the disc.
Modified from Jensen MC, Brant-Zawadzki MN, Obu­chowski N, et al. Magnetic resonance imaging of the lumbar spine in people without back pain. N Engl J Med 1994;331: 69–73, with permission.
a
14
When MRI and discography have been used in parallel for the assessment of disc degeneration, a high correla­tion has usually been observed (57–59). It is considered that MRI can be used for detecting early disc degenera­tion (58). Also quantitati ve disc manometry has been sug­gested to show good correlation with MRI for assessing disc degeneration (60). Disc manometry may be suitable for evaluating early stages of disc degeneration and may detect tears of annular fibers that go nondetected on MRI (60). Results are not entirely consistent, however (61).
Of all imaging modalities currently available, discog­raphy is the only one that can locate a degenerated and symptomatic disc and which visualizes internal disc dis­ruption (Figs. 28-4, 28-5) (33,34,62–65) (Table 28-4).