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- •The Lumbar Spine
- •Contents
- •Contributing Authors
- •Preface
- •Acknowledgments
- •Epidemiology and the Economics of Low Back Pain
- •Pathophysiology of Nerve Root Pain in Disc Herniation and Spinal Stenosis
- •Biomechanical Considerations of Disc Degeneration
- •Clinical Spinal Instability Resulting from Injury and Degeneration
- •Morphologic Changes of End Plates in Degenerative Disc Disease
- •Spinal Instrumentation
- •Fracture and Repair of Lumbar Vertebrae
- •Genetic Transmission of Common Spinal Disorders
- •Genetic Applications to Lumbar Disc Disease
- •Clinical Neurophysiologic and Electrodiagnostic Testing in Disorders of the Lumbar Spine
- •Sensorimotor Control of the Lumbar Spine
- •Outcomes Assessment: Overview and Specific Tools
- •The Role of Outcomes and How to Integrate Them into Your Practice
- •Manual Therapy in Patients with Low Back Pain
- •Acupuncture and Reflexology
- •Returning Workers to Gainful Employment
- •Occupational Ergonomics
- •Preparation for Surgery
- •Surgical Approaches to the Thoracolumbar Spine
- •Surgical Approaches to the Lumbar Spine: Anterior and Posterior
- •Posterior and Anterior Surgical Approaches to the Lumbosacral Junction
- •Endoscopic Anterior Lumbar Procedures
- •Biology of Bone Grafting: Autograft and Allograft
- •Bone Graft Substitutes in Spinal Surgery
- •Spinal Instrumentation Overview in Lumbar Degenerative Disorders: Cages
- •Translaminar Screw Fixation
- •Lumbar Disc Disorders
- •Facet Joint Denervation: A Minimally Invasive Treatment for Low Back Pain in Selected Patients
- •Intradiscal Electrothermal Therapy
- •Operative Management of the Degenerative Disc: Posterior and Posterolateral Procedures
- •Posterior Lumbar Interbody Fusion
- •Operative Treatment of Anterior Procedures
- •Operative Treatment of Anterior and Posterior Fusion
- •Degenerative Disc Disease: Fusion Cages and Dowels
- •Minimally Invasive Procedures for Anterior Column Fusion and Reconstruction
- •Degenerative Disc Disease: Complications of Surgery
- •Dynamic Stabilization in the Treatment of Low Back Pain Due to Degenerative Disorders
- •Lumbar Artificial Disc Replacement: Rationale and Biomechanics
- •Lumbar Disc Replacement: Current Model, Results, and the Future
- •Disc Herniation: Definition and Types
- •Disc Herniation: Imaging
- •Disc Herniation: Nonoperative Treatment
- •Operative Treatment of Disc Herniation: Natural History and Indications for Surgery
- •Operative Treatment of Disc Herniation: Laminotomy
- •Chymopapain and Chemonucleolysis
- •Microscopic Lumbar Discectomy
- •Classification, Natural History, and Clinical Evaluation
- •Imaging of Spinal Stenosis and Degenerative Lumbar Spondylolisthesis with Stenosis

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.
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7. Abumi K, Panjabi MM, Kramer KM. Biomechanical evaluation of
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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).
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