Добавил:
kiopkiopkiop18@yandex.ru t.me/Prokururor I Вовсе не секретарь, но почту проверяю Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз: Предмет: Файл:
Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_6034_Библиотеки_им_академика_М_И_Перельмана.pdf
Скачиваний:
0
Добавлен:
02.09.2026
Размер:
20 Мб
Скачать
CHAPTER 41/DISC HERNIATION: DEFINITION AND TYPES / 403
Thus, the “about-average” natural history (described subsequently) is largel y based on clinical experience, and a mixture of literature information (28,37,43,45,46). The onset of dominating leg pain is usually the period with the most intense pain. Commonly, the pain fades out to some extent after a few w eeks and then tends to remain at about the same level for a total of approximately 1 to 3 months. Thereafter, the symptoms generally abate over another few months, and (almost) disappear in 50% to 70% of nonsurgical cases (28,37,46), and in about the same number of surgical cases in most reports (5,47,48), with as many as 80% to 90% in a few reports (28,49) (Fig 41-5). The remaining patients experience:
• long-lasting discogenic pain, which also tends to fade
off, but over a period of some years (50,51)
• peripheral neurogenic leg pain due to root damage (52)
• domination of a central nervous system component of
the pain (53).
Among these, psychosocial factors are associated with the majority of the pain (37).
Formation of a fibrous layer (54,55) is followed by a gradual reduction of the scar bulge (56) (Fig. 41-6). The rate of recurrent LDH is about 3% to 14% (54,57).
History and Physical
Several relevant issues of the clinical examination will be presented, but not all. For further details on clinical usefulness of history and physical signs, test repeatabil­ity, and so forth see Andersson and Deyo (58), Hunt et al. (59), or Vroomen et al. (60).
From the history taking, one of the most important questions is probably whether leg pain or paraesthesia dominates over back pain or vice versa. The distribution of the leg pain—radicular or diffuse—does not allow a clear distinction between disc herniation or other causes of sciatica to be made, as diffuse sciatica has often been reported where herniation has subsequently been verified at surgery.
As paresis in gradual progress is an indication for acute surgery, this should be explored during history tak­ing, as should possible cauda equina symptoms, where the sequence of symptoms most often is flatus inconti­nence, urinary retention, and groin hypoesthesia.
“Bowel strain” is also described to be reasonably in­dicative for herniation.
Whereas painful forward bending is highly correlated to herniation, there does not seem to be a consistent cor­relation with lying or sitting. Especially in the acute stage night pain is common, probably due to increased temper­ature and inflammation. Sitting has been thought to aggravate a herniation due to the increased intradiscal pressure (IDP), but is not often the most pain-free pos­ture. A possible explanation could be that the advantage of more space around the herniation due to reduced lor-
dosis—or even kyphosis—caused by sitting (61) exceeds the disadvantage from a small increase in herniation size (62) (Fig. 41-8). Moreover, the increase in IDP is proba­bly smaller than previously believed (63), and when sit­ting backwardly inclined with a backrest, the IDP is at least not higher than when standing (64).
Conversely, lumbar extension is generally omitted due
to the reduction in the foramen size (65).
Of the physical signs, the sagittal lumbar curve in standing is also influenced by the same principle: the lumbar curvature is flattened or even kyphotic, automati­cally arranged by a posterior rotation of the pelvis. This is done to enable the described mechanism of optimizing the space for the nerve root. Such a kyphotic curve might also be obtained by forward bending of the trunk. How­ever, in that case the addition of static back-muscle activ­ity compresses the herniated disc to an uncomfortable level. Thus, erect posture with flattened or kyphotic loin, or a supported (e.g., hands on the thighs) forward bended posture is characteristic.
A scoliotic list seems only moderately correlated to operative findings (66–68). In particular, the Finneson hypothesis that a certain side location of the herniation and the nerve root should cause a specif ic list direction does not seem valid (67).
A painful forward bending may distinguish disc herni­ation from recess stenosis, where leg pain also may dom­inate over back pain, but where forward bending usually relieves the sciatica (69). A lateral shift—usually away from the side of the LDH—during forward bending is often seen in LDH, but does not provide much help in distinguishing between herniation or recess stenosis.
Side bending toward the opposite side of the pain usu­ally relieves the pain (Fig. 41-8).
The straight leg-raising (SLR) test with radiating pain below knee le vel seems reasonab l y associated to disc her­niation (38), although the test reliability—like that for the ranges of motion mentioned earlier—seems lower than commonly believed (59). With the surgical finding as the
FIG. 41-8. With reduction of the lordotic curvature, and with lateral bending, the size of the herniation increases, but the enlargement of the intervertebral foramen is even more pro­nounced.
404 /SECTION V/SPECIFIC CLINICAL ENTITIES
“gold standard,” and without letting SLR influence the indication for surgery, the following was registered by Kosteljanetz et al. (48) (Fig. 41-9): Root compression, if present, was estimated to be caused by disc herniation in two-thirds of the patients in this study.This is the case for those patients with dominating leg pain of more than 6 weeks’ duration. It may be differently distributed in another group of patients, characterized otherwise.
The literature on SLR is confusing regarding the degree of leg angle and clinical symptoms. Some authors report that the smaller the SLR angle, the more intense the symptoms (70), whereas others do not find such cor­relation (71).
SLR is not very sensitizing to an extraforaminal herni­ation (41). The crossed SLR sign (lifting the symptom­free leg, increasing contralateral pain) seems highly cor­related to LDH, especially to complete and large herniations (5,67,72).
For a herniation affecting nerve root L4—or L2-L3, which are rare—the “femoral-nerve stretch test” may be valid if carried out correctly: the patient is in a prone position and the 90° flexed knee is lifted causing hip extension. To avoid co-movements of the lumbar spine, the pelvis is fixated by pressing on the lower third of the sacral bone.
The springing test is a “segmental lordosing” pressure placed successively on all lumbar segments with the patient lying prone. If it is painful, it may indicate which segment of the leg pain originates from, and may also help to differentiate pain arising in areas such as the sacroiliac joint.
Obviously neurologic signs—altered sensibility, re­flexes, muscle strength, and muscle atrophy—should be tested (refer to neurologic textbooks for more informa­tion).
Consideration of the piriformis muscle may be worthwhile. In many patients with disc herniation piri­formis myosis may contribute to some of the buttock
FIG. 41-9. One indication of sensitivity and specificity for straight leg raising.
and leg pain, especially for herniation at L5-S1, because the S1 root innervates this muscle. There has been some discussion whether leg pain is caused by “self-strangulation” in the major ischiadicus foramen where swelling of the muscle causes compression of the sciatic nerve, or whether it is simply referred pain. Pir­iformis involvement can be tested with (a) palpating the muscle for tenderness or (b) placing the ipsilateral foot on the other knee, fixating the pelvis with the “heel of the hand” on the anterior superior iliac spine (ASIS), and then pushing the knee tow ard the contralateral side, and asking for stretch pain.
Dynamic testing ad modem McKenzie should be per- formed. With extension, an increase in radicular pain indicates an active herniation (73). As the herniation increases, and the foramen decreases (65), possible cen­tralization of the pain with repeated extension indicates either that the healing has begun, or at least that the prog­nosis is good (74).
It seems likely that future tests ma y include b lood sam­ples elucidating whether or not an inflammatory process of the disc is present. Serum tested for glycosphingolipid is already optional, but its applicability in practice is still unclear (75).
REFERENCES
1. Boos N, Rieder R, Schade V, et al. The diagnostic accuracy of magnetic resonance imaging, work perception and psychosocial factors in iden­tifying symptomatic disc herniations. Spine 1995;20(24):2613–2625.
2. Fraser RD, Sandhu A, Gogan WJ. Magnetic resonance imaging find­ings 10 years after treatment for lumbar disc herniation. Spine 1995; 20:710–714.
3. Jensen R, Bliddal H, Hansen SE, et al. Severe low-back pain. II: Changes in CT scans in the acute phase and after long-term observa­tion. Scand J Rheumatol 1993;22:30–34.
4. Karppinen J, Malmivaara A, Kurunlahti M, et al. Periradicular infil­tration for sciatica: a randomized controlled trial. Spine 2001;26: 1059–1067.
5. Spangfort E. The lumbar disc herniation—a computer-aided analysis of 2,504 operations. Acta Orthop Scand Suppl 1972;142:1–95.
6. Wiesel SW, Tsourmas N, Feffer HL, et al. A study of computer-assisted tomography. I. The incidence of positive CAT scans in an asympto­matic group of patients. Spine 1984;9:549–551.
7. Jensen TT, Overgaard S, Thomsen NO, et al. Postoperative computed tomography three months after lumbar disc surgery. A prospective sin­gle-blind study. Spine 1991;16:620–622.
8. Brisby H, Olmarker K, Larsson K, et al. Proinflammatory cytokines in cerebrospinal fluid and serum in patients with disc herniation and sci­atica. Eur Spine J 2002;11:62–66.
9. Nishimura K, Mochida J. Percutaneous reinsertion of the nucleus pul­posus. An experimental study. Spine 1998;23:1531–1538.
10. Olmarker K, Blomquist J, Strömberg J, et al. Nucleus pulposus cells and indomethazin in nucleus pulposus-induced microvascular inflam­matory reactions in the hamster cheek-pouch. International Society of the Study of the Lumbar Spine, Burlington Vermont, June 25–29,
1996.
11. Olmarker K, Brisby H, Yabuki S, et al. The effects of normal, frozen, and hyaluronidase-digested nucleus pulposus on nerve root structure and function. Spine 1997;22:471–475.
12. Olmarker K, Nordborg C, Larsson K, et al. Ultrastructural changes in spinal nerve roots induced by autologous nucleus pulposus. Spine 1996;21:411–414.
13. Olmarker K, Rydevik B. Selective inhibition of tumor necrosis factor­alpha prevents nucleus pulposus-induced thrombus formation, intra-
CHAPTER 41/DISC HERNIATION: DEFINITION AND TYPES / 405
neural edema, and reduction of nerve conduction velocity: possible implications for future pharmacologic treatment strategies of sciatica. Spine 2001;26:863–869.
14. Olmarker K, Rydevik B, Nordborg C. Autologous nucleus pulposus induces neurophysiologic and histologic changes in porcine cauda equina nerve roots [see Comments]. Spine 1993;18:1425–1432.
15. Olmarker K, Storkson R, Berge OG. Pathogenesis of sciatic pain: a study of spontaneous behavior in rats exposed to experimental disc her­niation. Spine 2002;27:1312–1317.
16. Otani K, Arai I, Mao GP, et al. Experimental disc herniation: evalua­tion of the natural course. Spine 1997;22:2894–2899.
17. Park JB, Chang H, Kim KW. Expression of Fas ligand and apoptosis of disc cells in herniated lumbar disc tissue. Spine 2001;26:618–621.
18. Rannou F, Cor vol MT, Hudry C, et al. Sensitivity of anulus fibrosus cells to interleukin 1 beta. Comparison with articular chondrocytes. Spine 2000;25:17–23.
19. Satoh K, Konno S, Nishiyama K, et al. Presence and distribution of antigen-antibody complexes in the herniated nucleus pulposus. Spine 1999;24:1980–1984.
20. Specchia N, Pagnotta A, Toesca A, et al. Cytokines and growth factors in the protruded intervertebral disc of the lumbar spine. Eur Spine J 2002;11:145–151.
21. Yabuki S, Kikuchi S, Olmarker K, et al. Acute effects of nucleus pul­posus on blood flow and endoneurial fluid pressure in rat dorsal root ganglia. Spine 1998;23:2517–2523.
22. Ozawa K, Atsuta Y, Kato T. Chronic effects of the nucleus pulposus applied to nerve roots on ectopic firing and conduction velocity. Spine 2001;26:2661–2665.
23. Takebayashi T, Cavanaugh JM, Cuneyt OA, et al. Ef fect of nucleus pul­posus on the neural activity of dorsal root ganglion. Spine 2001;26: 940–945.
24. Frymoyer JW, Pope MH, Clements JH, et al. Risk factors in low-back pain. An epidemiological survey. J Bone Joint Surg Am 1983;65: 213–218.
25. Kelsey JL, White AA III. Epidemiology and impact of low-back pain. Spine 1980;5:133–142.
26. Frymoyer JW. Back pain and sciatica. New Engl J Med 1988;318: 291–300.
27. Kelsey JL, Githens PB, O’Conner T, et al. Acute prolapsed lumbar intervertebral disc. An epidemiologic study with special reference to driving automobiles and cigarette smoking. Spine 1984;9:608–613.
28. Weber H, Holme I, Amlie E. The natural course of acute sciatica with nerve root symptoms in a double-blind placebo-controlled trial evalu­ating the effect of piroxicam. Spine 1993;18:1433–1438.
29. Battié MC, Videman T, Gibbons L, et al. Determinants of lumbar disc degeneration—a study of lifetime exposures and magnetic resonance imaging findings in identical twins. Spine 1995;20:2601–2612.
30. Simunic DI, Broom ND, Robertson PA. Biomechanical factors influ­encing nuclear disruption of the intervertebral disc. Spine 2001;26: 1223–1230.
31. Aota Y, Onari K, An HS, et al. Dorsal root ganglia morphologic fea­tures in patients with herniation of the nucleus pulposus: assessment using magnetic resonance myelography and clinical correlation. Spine 2001;26:2125–2132.
32. Pedrini-Mille A, Weinstein JN, Found EM, et al. Stimulation of dorsal root ganglia and degradation of rabbit annulus fibrosus. Spine 1990; 15:1252–1256.
33. Sugawara O, Atsuta Y, Iwahara T, et al. The effect of mechanical com­pression and hypoxia on nerve root and dorsal root ganglia. Spine 1996;21(18):2089–2094.
34. Cornefjord M, Olmarker K, Rydevik R, et al. Mechanical and bio­chemical injury of spinal nerve roots: a morphological and neurophys­iological study. Eur Spine J 1996;5:187–192.
35. Olmarker K, Rydevik B, Holm S. Edema formation in spinal nerve roots induced by experimental, graded compression. An experimental study on the pig cauda equina with special reference to differences in effects between rapid and slow onset of compression. Spine 1989;14:569–573.
36. Rydevik BL, Myers RR, Powell HC. Pressure increase in the dorsal root ganglion following mechanical compression. Closed compartment syndrome in nerve roots. Spine 1989;14:574–576.
37. Hasenbring M, Marienfeld G, Kuhlendahl D, et al. Risk factors of chronicity in lumbar disc patients. A prospective investigation of bio­logic, psychologic, and social predictors of therapy outcome. Spine 1994;19:2759–2765.
38. Thelander U, Fagerlund M, Friberg S, et al. Straight le g raising test ver­sus radiologic size, shape, and position of lumbar disc hernias. Spine 1992;17:395–399.
39. Ohnmeiss D, Vanharanta H, Ekholm J. Degree of disc disruption and lower extremity pain. Spine 1997;22:1600–1605.
40. Ahn SH, Ahn MW, Byun WM. Effect of the transligamentous exten­sion of lumbar disc herniations on their regression and the clinical out­come of sciatica. Spine 2000;25:475–480.
41. Ohmori K, Kanamori M, Kawaguchi Y, et al. Clinical features of extraforaminal lumbar disc herniation based on the radiographic loca­tion of the dorsal root ganglion. Spine 2001;26:662–666.
42. Andersson GB, Brown MD, Dvorak J, et al. Consensus summary of the diagnosis and treatment of lumbar disc herniation. Spine 1996;21: 75S–78S.
43. Saal JA, Saal JS, Herzog R. The natural history of lumbar interverte­bral disc extrusions treated nonoperatively. Spine 1990;15:683–686.
44. Rasmussen C. Lumbar disc herniation: social and demographic factors determining duration of disease. Eur Spine J 1996;5:225–228.
45. Bush K, Cowan N, Katz DE, et al. The natural history of sciatica asso­ciated with disc pathology. A prospective study with clinical and inde­pendent radiologic follow-up. Spine 1992;17:1205–1212.
46. Weber H. The natural course of disc herniation. Acta Orthop Scand Suppl 1993;251:19–20.
47. Espersen JO, Kosteljanetz M, Halaburt H, et al. Predictive value of radiculography in patients with lumbago-sciatica. A prospective study (Part II). Acta Neurochir (Wien) 1984;73:213–221.
48. Kosteljanetz M, Espersen JO, Halaburt H, et al. Predictive value of clinical and surgical findings in patients with lumbago-sciatica. A prospective study (Part I). Acta Neurochir (Wien) 1984;73:67–76.
49. Pappas CT, Harrington T, Sonntag VK. Outcome analysis in 654 surgi­cally treated lumbar disc herniations. Neurosurgery 1992;30:862–866.
50. Krämer J. Presidential address: natural course and prognosis of inter­vertebral disc diseases. Spine 1995;20:635–639.
51. Weber H. Lumbar disc herniation. A controlled, prospective study with ten years of observation. Spine 1983;8:131–140.
52. Nakamura SI, Myers RR. Injury to dorsal root ganglia alters innerva­tion of spinal cord dorsal horn lamina involved in nociception. Spine 2000;25:537–542.
53. Hunt JL, Winkelstein BA, Rutkowski MD, et al. Repeated injury to the lumbar nerve roots produces enhanced mechanical allodynia and per­sistent spinal neuroinflammation. Spine 2001;26:2073–2079.
54. Ahlgren BD, Lui W, Herkowitz HN, et al. Effect of anular repair on the healing strength of the intervertebral disc: a sheep model. Spine 2000;25:2165–2170.
55. Carragee EJ. Point of view. Spine 2001;26:651–651.
56. Doita M, Kanatani T, Ozaki T, et al. Influence of macrophage infiltra­tion of herniated disc tissue on the production of matrix metallopro­teinases leading to disc resorption. Spine 2001;26:1522–1527.
57. Nykvist F, Hurme M, Alaranta H, et al. A prospective 5-year follow-up study of 276 patients hospitalized because of suspected lumbar disc herniation. Int Disabil Stud 1989;11:61–67.
58. Andersson GBJ, Deyo RA. History and physical examination in patients with herniated lumbar discs. Spine 1996;21:10S–18S.
59. Hunt DG, Zuberbier OA, Kozlowski AJ, et al. Reliability of the lumbar flexion, lumbar extension, and passive straight leg raise test in normal populations embedded within a complete physical examination. Spine 2001;26:2714–2718.
60. Vroomen PC, de Krom MC, Knottnerus JA. Consistency of history taking and physical examination in patients with suspected lumbar nerve root involvement. Spine 2000;25:91–96.
61. Bendix T. Adjustment of the seated workplace—with special reference to heights and inclinations of seat and table. Dan Med Bull 1987;34: 125–139.
62. Fujiwara A, An HS, Lim TH, et al. Morphologic changes in the lumbar intervertebral foramen due to flexion-extension, lateral bending, and axial rotation: an in vitro anatomic and biomechanical study. Spine 2001;26:876–882.
63. Wilke H, Neef P, Hinz B, et al. Intradiscal pressure together with anthropometric data—a data set for the validation of models. Clin Bio­mech (Bristol, Avon) 2001;16[Suppl 1]:S111–S126.
64. Andersson GBJ, Örteng ren R, Nachemson A, et al. Lumbar disc pres­sure and myoelectric activity during sitting. I: Studies on an experi­mental chair. Scand J Rehabil Med 1974;6:104–114.
65. Adams MA, May S, F reeman BJ, et al. Effects of backward bending on
406 /SECTION V/SPECIFIC CLINICAL ENTITIES
lumbar intervertebral discs. Relevance to physical therapy treatments for low back pain. Spine 2000;25:431–437.
66. Matsui H, Ohmori K, Kanamori M, et al. Significance of sciatic scoli­otic list in operated patients with lumbar disc herniation. Spine 1998;23:338–342.
67. Suk KS, Lee HM, Moon SH, et al. Lumbosacral scoliotic list by lum­bar disc herniation. Spine 2001;26:667–671.
68. Takahashi K, Shima I, Porter RW. Nerve root pressure in lumbar disc herniation. Spine 1999;24:2003–2006.
69. Jenis LG, An HS. Spine update. Lumbar foraminal stenosis. Spine 2000;25:389–394.
70. Jonsson B, Stromqvist B. The straight leg raising test and the severity of symptoms in lumbar disc herniation. A preoperative evaluation. Spine 1995;20:27–30.
71. Jensen R, Bliddahl H, Hansen SE, et al. Severe Low-back pain. II: Changes in CT-scans in the acute phase and after long-term observa­tion. Scand J Rheumatol 1993;22:30–34.
72. Kosteljanetz M, Bang F, Schmidt-Olsen S. The clinical significance of straight-leg raising (Lasegue’s sign) in the diagnosis of prolapsed lum­bar disc. Interobserver variation and correlation with surgical finding. Spine 1988;13:393–395.
73. Donelson R, Aprill CN, Medcalf R, et al. A prospective study of cen­tralization of lumbar and referred pain: a predictor of symptomatic discs and anular competency? Spine 1997;22:1115–1122.
74. Werneke M, Hart DL. Centralization phenomenon as a prognostic fac­tor for chronic low back pain and disability. Spine 2001;26:758–764.
75. Brisby H, Balague F, Schafer D, et al. Glycosphingolipid antibodies in serum in patients with sciatica. Spine 2002;27:380–386.
CHAPTER 42

Disc Herniation: Imaging

Josef Assheuer and Klaus-Peter Schulitz
PLAIN RADIOGRAPH
Following the Quebec Task Force on Spinal Disorders (1), a radiograph of the lumbar spine is of limited value in the first 7 weeks after onset of low back pain. Even with the pain radiating to the extremities with neurologic signs, radiography can delineate loss of disc height, vac­uum phenomena, and calcification, as well as sclerosis of the end plates, osteophytes, and focal end plate defects. Those signs are not specific for herniation; they are hardly found in acute disc herniation.
A radiographic examination is not recommended when disc herniation is suspected. It is the main purpose of radiographic evaluation to exclude low back pain (LBP), which was specifically caused by tumors, infections, inflammatory spondylarthropathies, and fractures (2).
Functional radiographs can delineate instability. Some biomechanical studies (3) showed increased hypermobil­ity after open discectomy at the level of operation. How-
ever, hypermobility can be found preoperatively at the same rate at the level of herniation as in adjacent levels (4–7). Postoperatively, no signif icant changes in hyper­mobility were found. Therefore, hypermobility does not seem to be a consequence of discectomy. Instability in the levels above or beneath the level of herniation is caused by increased stress in the moving segment caused by changes in motion pattern at these levels (4,5).
MYELOGRAPHY
Myelogram delineates the cerebrospinal fluid (CSF) space of the thecal sac including the subarachnoidal space of the nerve roots. An indentation or occlusion of this space can be regarded as an indirect sign of disc her­niation and must be differentiated from other space-occu­pying lesions (Fig. 42-1).Therefore, it is of minor impor­tance for the diagnosis of herniation.
compression of the dural poach of the nerve root L5
A
FIG. 42-1. A: The right dural poach of the nerve root L5 is not filled because of compression by a her­niation (myelography antero-posterior view). B: The mass compressing the dural sac and poach of the L5 nerve root can not be identified. It is probably a herniation according to the position of the mass (myelography, right oblique view).
dural poach of the nerve root L4
compression of the dural sac and of the dural poach of the nerve root L5
B
407
408 /SECTION V/SPECIFIC CLINICAL ENTITIES
radial fissure extending right side into the outer annulus
FIG. 42-2. Discography L4-5 antero-posterior view. The intradiscal injected contrast media extends in both le v els into the outer annulus according to grade 4.
Nerve root entrapment beyond the termination of the nerve root sheath caused by lateral or foraminal disc her­niation cannot be detected. High radiation exposure and invasive procedure as well as possible complications also have to be taken into account.
Myelography may be the only method to evaluate disc herniation and other stenosing diseases in patients having metal implants.
Functional myelography may be indicated to evaluate so-called dynamic entrapment in disc herniation in patients showing motion-dependent pain patterns. In future, functional myelography may be replaced by posi­tional magnetic resonance imaging (MRI) (8,9).
DISCOGRAPHY
Discography mainly demonstrates the internal state of the disc and it is very useful to classify types of internal derangement. The contrast medium injected into the center of the disc pushes the disc matrix aside and forms pools. The locations and patterns of these pools are the criteria for the staging of disc degenera-
tion (10–12). Five different types of discograms are distinguished based on consistently identifiable fea­tures in the shape and extension of the radiopaque shadow (13,14). There are different classifications. According to the pathoanatomic classification of Adams et al. (13), type 1 does not show any signs of degeneration (cotton ball), type 2 is a mature disc with the nucleus starting to coalesce into fibrous lumps (lob­ular or sandwich), type 3 demonstrates a degenerated disc with fissures and clefts in the nucleus and inner annulus (irregular), type 4 is a degenerated disc with radial fissures extending into the outer edge of the annulus (fissured) (Fig. 42-2), and type 5 has complete radial fissures that allow injected fluids to escape (rup­tured) (Fig. 42-3). Injection is done into at least two segments depending on the pain pattern. Herniation cannot be visualized directly but if type 4 and 5 are found, herniation is likely, especially if the contrast medium forms a pool beyond the intervertebral inter­space (Figs. 42-3, 42-4). The leakage of the contrast medium beneath the posterior longitudinal ligament (PLL) is not a relevant sign for herniation. Therefore,
Leakage of contrast media into the extradu­ral space
Complete fissure of the annulus
FIG. 42-3. Discography L4-5 reveals total degeneration of the disc with rupture of the annulus, allowing the intradiscal injected contrast media to escape into the epidural space according to grade 5.
Herniated disc material
FIG. 42-4. Discography L4-5.The rim of the herniated disc is marked by contrast media.
discography is not a relevant imaging modality to demonstrate herniation. Discography is widely used as a pain reproduction test to identify the segment causing the low back pain and sciatica. The reliability of this test is controversial because the referred pain depends to a high degree on the psychological profile of the patient (15–21).
CHAPTER 42/DISC HERNIATION: IMAGING / 409
COMPUTED TOMOGRAPHY
Computed tomography discriminates with high con­trast between bone structures and soft tissue. High reso­lution computed tomography (HRCT) visualizes the sub­arachnoidal sac, nerve root sleeves, and ligamentum flavum (Fig. 42-5) (22). Disc material can well be detected inside and outside the spinal canal. How e v er , CT does not differentiate between nuclear and annular tissue (Fig. 42-6). There is a high contrast between herniated disc material and epidural fat tissue (23,24). Contrast media after intravenous (i.v.) administration enhance vas­cular structures and delineate tissue with disturbances of the blood-tissue barrier. This is helpful in the diagnosis of vascular malformations and certain tumors such as meningiomas (25,26). Sometimes, after i.v. administra­tion of contrast medium, a rim of enhancement is observed at the margins of the herniated disc material. This may be related to epidural veins or edema of the neighboring tissue (27,28). Swelling and displacement of ganglia and nerve roots can be visualized as well as the indentation of the dural sac (Fig. 42-7). Howe ver, swollen nerve roots and ganglia with high content of water may have the same Hounsfield Units (HU) as disc material and it may be diff icult to distinguish one from the other.
disc L4/L5
ligamentum flavum
epidural fat
A
Disc
Endplate
Dural sac
ligamentum flavum
B
FIG. 42-5. A: Computed tomography of the disc level L4-5. B: Computed tomography of the level L4-5 4 mm below Figure 42-5A. C: Computed tomography of the level L4-5 8 mm below Figure 42-5A.
Cranial endplate of L5 vertebra
nerve root L5
Cranial facet L5
Caudal facet L4
Epidural fat
C
410 /SECTION V/SPECIFIC CLINICAL ENTITIES
focal extension of disc material
FIG. 42-6. By computed tomography herniation is delin­eated as focal extension of the disc. Differentiation between nucleus and annular tissue as well as between protrusion and extrusion is not possible.
Multiplanar reconstruction is helpful in these cases, espe­cially with foraminal disc herniations (23,29).
Conjoined nerve roots occurring on the L5-S1 level are likely to have the same attenuation as disc material and may be misinterpreted as a disc herniation (30,31). An accurate analysis of successive CT slices demonstrates this anatomic variant. It can be seen how two nerve roots outside the dura join the same dural sheath cranially. Both nerve roots occasionally leave the spinal canal by the same neuroforamina (32). The process is unilateral. A rounded lateral recess is always found with it. Intrathecal administration of contrast media verifies the diagnosis,
Herniation
displaced nerve root S 1
showing the common dural recess (33). This anomaly was found in 2% of the cases within a CT study, and in 14% within an autopsy series (32).
Most hematomas of the lumbar spine are located epidurally or subdurally. They may be confounded with disc herniations. The epidural mass has indistinct margins and extends over the surface of a vertebral body, being largest at the mid-vertebral level. The hematomas are iso­dense with the thecal sac and are indistinguishable from the nerve root and ganglia. They may arise from a tear of the fragile epidural veins because of disc disruption. Computed tomography follow-ups show a regression of
A
epidural fat
displaced nerve root S 1
thecal sac
B
FIG. 42-7. A: Computed tomography of the level L5-S1. A right side disc herniation displacing the right nerve root S1 dorsally. The nerve root is nearly indistinguish­able from the herniated disc material. B: Computed tomography of the le v el L5-S1 3 mm beneath the level of Figure 42-11A.The displaced nerve root is delineated by the surrounding epidural fat of low density.
CHAPTER 42/DISC HERNIATION: IMAGING / 411
soft tissue mass, obstructing the spinal canal
scar tissue
A
FIG. 42-8. A: Differentiation between scar tissue and possible reherniation is not possible (computed tomography native at the level L4-5). B: The enhancement of the intraspinal mass after intradiscal administration of contrast medium reveals reher niation and differentiation from scar tissue (computed tomography discography at the level of L4-5).
hematomas with the underlying disc herniation remain­ing (34–36). Epidural and subdural hematomas also may originate from hematologic disorders, hypertension, and atherosclerotic vascular diseases (36–38).
Because of their location, synovial cysts and synovial ganglia of degenerated facet joints may mimic disc frag­ments. They are broad-based to the zygapophyseal joint, mostly rounded, emerging into the central canal or subar­ticular recess. The mass may exhibit internal gas or a cal­cified rim (39–42). The thickened and protruding liga­mentum flavum and capsule are isodense with the disc and may cause diagnostic problems. Injection of contrast media into the relevant facet joint shows the communica­tion of the cyst with the joint space (43). Occasionally cysts can also emerge out of a degenerated disc and are difficult to differentiate from herniation. They may result from resorption or mucoid degeneration of an already existing herniation (44).
Perineural cysts (45), occurring beneath the per­ineurium at the level or beyond the dorsal root ganglion, and subarachnoidal cysts (cystic nerve root sleeve dilata­tion or meningeal diverticulum) (46) located proximally to the nerve root ganglion, should not be misinterpreted as herniation. They can be distinguished from herniation when the pressure erosion of the surrounding bone is regarded and contrast medium is filled in after intrathecal administration (47,48).
Nerve sheath tumors may be confounded with lateral herniations and because of their locations are only Schwannomas (49).
The main question with postoperative backaches (failed back surgery syndrome) is to find out whether the nerve root compression results from reherniation or scar tissue, especially epidural fibrosis. Native CT is not suit­able to answer this question (Fig. 42-8) (50). It shows
enhancing mass after intradiscal application of contrast medium
scar tissue
B
both scar tissue and reherniated disc material with identi­cal density. The location of both processes does not per­mit discrimination either, because scar tissue normally extends epidurally and laterally to the posterior aspect of the operated disc (51,52). Therefore, CT discography is necessary to clarify this condition (Fig. 42-8). If postop­erative spine hemorrhage and noninfectious inflamma­tory processes arise, they can be well visualized. Contrast enhancement of scar tissue depends on the time that passed between operation and CT examination with older scar enhancing less. Nevertheless, the diagnosis impro ves by 20% up to 3 years after operation (53,54).
PATHOMORPHOLOGIC DEFINITIONS AND NOMENCLATURE OF DISC HERNIATION
The grading of disc herniation mainly depends on the internal disarrangement of nucleus and annulus; the dis­placement of nuclear material is the most important fea­ture.
Resnick and Niwayama (55) and other authors (56) propose the following schema for disc herniation:
Annular bulge: Annular fibers are intact and the disc pro-
trudes beyond the intervertebral interspace around the
end plate (Fig. 42-9). Protrusion: Nuclear material protrudes through torn
fibers of the annulus, with the outermost fibers
remaining intact (Fig. 42-6). Extrusion: The nuclear material penetrates all of the
fibers of the annulus f ibrosus and lies under the PLL
(Fig. 42-10). Discal sequestration:The nucleus material penetrates the
posterior longitudinal ligament (PLL) and lies within
the epidural space or the nucleus material does not
412 /SECTION V/SPECIFIC CLINICAL ENTITIES
bony endplate of the vertebra L4
bulging disc
thecal sac
lig. flavum
FIG. 42-9. Computed tomography at the border of the disc L3-4 to the vertebra L4. The disc exceeds symmetrically and uniformly the contour of the margin of the vertebra.
bony fragment
Extruded disc material
FIG. 42-10. Computed tomography of the level L5-S1. The extruded disc material is clearly depicted. Possible rupture of the posterior longitudinal ligament cannot be visualized.
herniated disc
displaced nerve root
epidural fat
FIG. 42-11. Computed tomography of the level L4-5 (bony window). A bony fragment has extruded together with disc material into the subligamentous space of a 15-year-old trampoline jumper.
foraminal to extrafo­raminal extruded disc material with calcification
A
FIG. 42-13. A: Computed tomography of the level L3-4.An extruded mass of disc material extends from foraminal to extraforaminal with calcification. B: CT-discography ascertains extraforaminal herniation suspected by discography.
FIG. 42-12. Computed tomography of the level L5-S1. The herniation has displaced the left nerve root S1 dorsally.The epidural fat on the left side has nearly disappeared.
extraforaminal herni­ated disc
B