Musculoskeletal Imaging • Original Research
Lakadamyali et al.
STIR for Lower Back Pain
Musculoskeletal Imaging
Original Research
STIR Sequence for Depiction of
Degenerative Changes in Posterior
Stabilizing Elements in Patients
with Lower Back Pain
Hatice Lakadamyali1
Nefise Cagla Tarhan2
Tarkan Ergun1
Banu Cakır 2
Ahmet Muhtesem Agıldere2
Lakadamyali H, Tarhan NC, Ergun T, Cakır B,
Agıldere AM
OBJECTIVE. The aims of this study were to investigate whether degenerative posterior
paraspinal changes are a cause of lower back pain and to determine the age- and sex-related
distribution of these changes on MR images acquired with a STIR sequence.
Subjects AND METHODS. The lumbar MRI findings of 372 patients (141 men, 231
women; mean age, 51.2 years) with nonradicular lower back pain and of 249 healthy persons
acting as controls (126 men, 123 women; mean age, 49.3 years) were analyzed. The sagittal STIR
sequence was used for all MRI examinations. Presence of interspinous ligament edema, facet
joint effusion, neocysts, paraspinal muscle edema, subcutaneous edema, disk herniation, and
disk degeneration was evaluated, and the incidence of each finding was determined. All findings
were grouped according to age and sex. Chi-square, Fisher’s exact, and independent-samples
Student’s t tests and Spearman’s rank correlation analysis were used for statistical analysis.
RESULTS. The incidences of facet joint effusion, interspinous ligament edema, neocyst
formation, and paraspinal muscle edema were found to be statistically significantly higher in
patients with lower back pain than in controls. The incidences of intervertebral disk degeneration,
disk herniation, and subcutaneous edema in persons with and those without lower back pain
were similar. Intervertebral disk degeneration, disk herniation, subcutaneous edema, and muscle
edema were found to increase with age in both persons with and those without symptoms.
CONCLUSION. Degenerative changes in the posterior paraspinal structures were found
in a higher percentage of subjects with lower back pain than in controls. Use of a STIR
sequence with homogeneous fat suppression facilitates visualization of these changes.
D
Keywords: lower back pain, MRI, posterior paraspinal
soft tissue, STIR sequence
DOI:10.2214/AJR.07.2829
Received July 6, 2007; accepted after revision
April 23, 2008.
1
Department of Radiology, Baskent University, Alanya
Research Center, Antalya, Turkey.
2
Radiology Department, Baskent University
School of Medicine, Fevzi Cakmak cad. 10. Sok,
No 45 Bahcelievler 06490, Ankara, Turkey.
Address correspondence to N. C. Tarhan
([email protected]).
AJR 2008; 191:973–979
0361–803X/08/1914–973
© American Roentgen Ray Society
AJR:191, October 2008
iffuse degenerative changes in
the stabilizing elements of the
posterior aspect of the spinal col­
umn, which include facet joints,
interspinous ligaments, and paraspinal mus­
cles, occur in patients with lower back pain
(LBP). These degenerative changes also have
been encountered in persons without symp­
toms, and debate continues concerning wheth­
er these changes are the cause of LBP [1–3].
Although it can easily depict evidence of the
well-known causes of pain, such as in­fection,
fracture, and serious deformities, con­ventional
MRI does not show degenerative changes in
the posterior elements [4, 5]. These changes
can, however, be visualized if a fat-suppression
technique [4], such as the STIR sequence, is
used to acquire the images. Use of this
sequence enables diffuse homog­eneous fat
suppression, and degeneration can be tracked
as areas of high signal intensity within fat.
Conventional MRI is diagnostically insuf­
ficient in 85% of cases of LBP [5]. An expla­
nation for this diagnostic difficulty is that
pain can originate from any lumbar structure.
In most cases, LBP is assumed to be due to
muscular strain, injury to the ligaments, and
degenerative changes in the spine [6]. This
idea is debatable [1], however, because all of
these abnormalities are encountered in
persons without symptoms [2]. A small
number of reports in the medical literature
describe evaluation of the posterior elements
on fat-suppressed images [7, 8]. In those
studies, however, the investigators did not
visualize all of the posterior elements and
included only small numbers of patients.
The aim of this study was to investigate
the significance of the presence of degen­
erative changes in posterior spinal elements
in patients with LBP compared with the
findings in persons without such changes and
to see whether the changes are a cause of
LBP. Another aim was to determine among
persons with and those without LBP the ageand sex-related distribution of changes in the
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posterior elements on MR images obtained
with the STIR sequence.
Subjects and Methods
The study was conducted in two stages.
During the first stage, lumbar MR images of
patients with LBP without radiculopathy referred
to our department during the years 2000–2004
were interpreted. Patients with previous lumbar
spinal surgery, evidence of lumbar or sacral
tumors at MRI, diffuse bone metastasis, serious
congenital anomalies, severe scoliosis, diskitis,
osteomyelitis, serious lumbar vertebral fracture,
extruded or sequestered disks, spondylolysis, or
spondylolisthesis were excluded from the study.
The study group consisted of 372 patients. During
the second stage, a control group was formed that
included persons of the same ethnicity. This group
consisted of 249 volunteer patients referred to our
department for other MRI examinations who had
no history of LBP or sciatica, trauma, or lumbar
surgery within the last 6 months. Signed written
consent was obtained from all subjects. The group
with symptoms consisted of 231 women and 141
men (mean age, 51.2 ± 15.3 [SD] years; range,
15–85 years). The control group consisted of 123
women and 126 men (mean age, 49.3 ± 16.2 years;
range, 15–96 years). The study was approved by
the ethical committee of our institution.
The lumbar MR images of all subjects were
evaluated for pathologic changes in the posterior
elements of the spine. The MR images were
obtained with a 1.5-T unit (Symphony, Siemens
Medical Solutions) and a body coil. At conventional
MRI, the following sequences were used: sagittal
T1-weighted images (TR/TE, 600/10; number of
signals acquired, 2; matrix size, 230 × 384; slice
thickness, 4 mm; acquisition time, 2 minutes 32
seconds), sagittal T2-weighted images (3,250/ 92;
number of signals acquired, 1; matrix size, 230 ×
384; slice thickness, 4 mm; acquisition time, 1
minute 33 seconds), axial T2-weighted images
(3,400/90; number of signals acquired, 2; matrix
size, 230 × 384; slice thickness, 4 mm; acquisition
time, 2 minutes 0 seconds). In addition to the
conventional MRI sequences, a sagittal STIR
sequence (6,120–7,040/60–70; inversion time,
150 milliseconds; number of signals acquired, 2;
matrix size, 132 × 256; slice thickness, 4 mm;
acquisition time, 2 minutes 26 seconds) was used
for all MRI examinations.
Lumbar MR images were evaluated by two
radiologists experienced in musculoskeletal radiol­
ogy who made common decisions concerning
pathologic changes. Findings of intervertebral disk
degeneration, disk herniation (excluding extruded
disk and sequestered disk), interspinous ligament
degeneration or rupture, facet joint effusion,
neocyst formation (including synovial cysts next to
the facet joints and emanating from the inter­
spinous neo­arthrosis), intrinsic spinal muscular
degen­eration, and presence of subcutaneous edema
were recorded for all subjects. The frequencies of
the findings in each age group were calculated. The
presence of interspinous ligament degeneration or
rupture presenting as edema also was recorded for
each lumbar level in both groups.
Intervertebral disk degeneration was assumed
to be a loss of signal intensity of the disk or a
reduction in the height of the disk. Disk herniation
was defined as focal or diffuse extension of the
disk beyond its end plate. Degeneration or rupture
of the interspinous ligaments was seen as high
signal intensity between the spinous processes
of the lumbar vertebrae. Facet joint effusion was
visualized as high-signal-intensity fluid between
the superior and inferior facets at lumbar levels.
Cyst formation next to the facet joints and
emanating from the interspinous neoarthrosis
was seen as a round cystic lesion with high signal
intensity on STIR images. Intrinsic spinal muscle
degeneration manifested as edema of the posterior
paraspinal muscles with high signal intensity on
STIR images at the lumbar level. Subcutaneous
edema was visualized as a triangular area of
increased signal intensity of subcutaneous fat
behind the lumbar vertebrae and paraspinal
muscles, especially on midline images obtained
with the STIR sequence.
For data analysis, all subjects were divided
into six groups according to age: 15–30 years,
43 case and 42 control subjects; 31–40 years, 49
case and 47 control subjects; 41–50 years, 94 case
and 55 control subjects; 51–60 years, 87 case and
47 control subjects; 61–70 years, 50 case and 31
control subjects; and 71 years and older, 49 case
and 27 control subjects. Interspinous ligament
degeneration was evaluated according to the level
at which the edema occurred: T12–L1, L1–L2,
L2–L3, L3–L4, L4–L5, and L5–S1. The incidence
of all findings was calculated.
The study data were entered into a statistical
program (SPSS 11.0, SPSS) for data control.
Chi-square and Fisher’s exact tests were used to
compare nominal data variables, such as sex and
100
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Percentage
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40
30
70
60
50
40
30
20
20
Posterior Paraspinal Change
Fig. 1—Graph shows percentages of posterior paraspinal degenerative changes
according to sex in case group. White bars indicate men (141 of 372 subjects); gray
bars, women (231 of 372 subjects). ISL = interspinous ligament.
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Percentage
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Group 1 43/372
Group 2 49/372
Group 3 94/372
Group 4 87/372
Group 5 50/372
Group 6 49/372
Posterior Paraspinal Change
Fig. 2—Graph shows percentages of posterior paraspinal degenerative changes
according to age in case group. Group 1, 15–30 years; group 2, 31–40 years; group
3, 41–50 years; group 4, 51–60 years; group 5, 61–70 years; group 6, 71 years and
older. ISL = interspinous ligament.
AJR:191, October 2008
STIR for Lower Back Pain
Fig. 3—21-year-old man with lower back pain.
Sagittal STIR MR image shows high-signal-intensity
facet joint effusion (long arrows) at L3–L4, L4–L5, and
L5–S1 and small neocyst formation (short arrow) next
to L5–S1 facet joint.
Fig. 4—59-year-old man with lower back pain.
Sagittal STIR MR image shows facet joint effusion
(arrowhead) at L4–L5 with neocyst formation (long
arrow) next to it. Another neocyst (short arrow) is
present at higher level.
pathologic findings, in the two subject groups, the
sex groups, and the age groups. The independentsamples Student’s t test was used for finding the
concordance of ages between the case and control
groups. Correlation between grouped age-related
pathologic findings was tested with Spearman’s
rank correlation analysis. A value of r < 0.4
was accepted as weak correlation, 0.4 < r < 0.7
as moderate correlation, and r > 0.7 as strong
correlation. Values of p < 0.05 were accepted as
statistically significant.
symptoms is shown in Figures 1 and 2.
Posterior element abnormalities in order of
frequency were facet joint effusion (85.5%)
(Figs. 3–5), interspinous ligament degen­er­
ation or rupture with edema at L4–L5
(80.6%) and L5–S1 (79.8%) (Figs. 6 and 7),
neocyst formation and synovial cysts (62.4%)
(Figs. 3 and 4), subcutaneous edema (27.2%)
(Fig. 7), and intrinsic spinal muscle degen­er­
ation (24.7%) (Fig. 5). Intervertebral disk
herniation was encountered in 41.7% of all
cases and degeneration in 65.1%.
Degenerative changes in at least one
posterior element were found in only 76.3%
of the control group (190 subjects); 23.7%
(59 subjects) had no changes. The frequency
of pathologic changes in the posterior ele­
ments of the control group was as follows:
facet joint effusion, 45.8%; interspinous
ligament degeneration with edema at L4–L5,
32.5%; subcutaneous edema, 19.7%; neocyst
formation and synovial cysts, 15.3%; and
intrinsic spinal muscle degeneration, 4.8%.
Intervertebral disk herniation and disk
degeneration were encountered in 39.8% and
60.2% of this group, rates very close to the
frequencies in the group with symptoms.
The distribution of frequencies in the
control group according to sex and age is
summarized in Figures 8 and 9.
The most common imaging finding in
subjects with LBP was facet joint effusion,
which had a frequency of 85.5%. The frequen­
Results
Comparison of the case and control groups
revealed no statistical difference regarding age
but a significant difference (p = 0.02) re­garding
sex, women predominating. When pathologic
changes in posterior spinal ele­ments and
pathologic changes in the disks (herniation
or degeneration) were compared between sex
groups, statistical significance was found
only with regard to subcutaneous edema, the
frequency of which was higher in women
with and those without symptoms (control
group, p = 0.03; case group, p = 0.07).
All patients with LBP without radicu­
lopathy were given the diagnosis of patho­
logic change in at least one of the posterior
elements stabilizing the vertebral column.
The largest percentage of these patients
(25%) were 41–50 years old. The distribution
of the pathologic findings according to sex
and age as percentages in the group with
AJR:191, October 2008
Fig. 5—40-year-old man with lower back pain due
to multiple pathologic conditions. Sagittal STIR MR
image shows disk degeneration of lowest three
lumbar levels. Facet joint effusion (long arrows) is
present at multiple levels. Paraspinal muscle edema
(short arrows) is present at L4–S1.
Fig. 6—43-year-old man with lower back pain.
Sagittal STIR MR image shows interspinous
ligament degeneration and rupture at L2–L3, L3–L4,
and L4–L5 levels manifesting as increased signal
intensity (arrows) between spinous processes. Disk
degeneration is present at L4–L5 and L5–S1 levels.
cy in the control group was 45.8%. Case–
control group comparison of facet joint ef­
fusion by age group showed this finding to be
more frequent in the case group than in the
control group.
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Lakadamyali et al.
Most patients had interspinous ligament
degeneration or rupture at more than one level, mostly at the L4–L5 and L5–S1 levels and
in the 15- to 30-year and the 31- to 40-year
age groups. In the 15- to 30-year group with
symptoms, the incidence was 88.4% at the
L4–L5 and L5–S1 levels; in the 31- to
40-year group, the incidence was 89.8% at
the L4– L5 level and 73.5% at the L5–S1
level. Interspinous ligament edema was
encoun­tered mainly in the 41- to 50-year
Fig. 7—50-year-old woman with lower back pain.
Sagittal STIR MR image shows interspinous ligament
edema (short arrows) at L2–L3, L3–L4, L4–L5, and
L5–S1 levels. Subcutaneous edema (long arrow) also
is present.
(41.8% at L4–L5) and 61- to 70-year (41.9%
at L5–S1) age groups without symptoms.
Seventy-eight percent of the patients with
interspinous ligament edema had con­
comitant interver­tebral disk degenera­tive
changes at the same level. The case–control
group comparison of interspinous ligament
edema based on age group and spinal level
showed this finding to be more frequent in
the case than in the control group.
Neocyst formation and synovial cysts
were encountered mainly in the 15- to
30-year (69.8%) and 31- to 40-year (69.4%)
age groups with symptoms. In the subjects
without symptoms, these findings were made
mostly in the 71-year and older group
(22.2%). In the age-group comparison, these
findings were more frequent in the case than
in the control group. In most of the cases of
symptomatic facet joint cysts (95%), there
was concomitant effusion in the neighboring
facet joint; effusion was present in only 69%
of the subjects without symptoms.
Intrinsic spinal muscle injury was en­
countered most frequently in the 51- to 60year-old (32.2%) and 61- to 70-year-old (32%)
subjects in the case group. In the control
group, this finding was most frequent in the
71-year and older age group (14.8%). The
comparison of signal intensity increase in the
intrinsic spinal muscles according to age
group showed a higher frequency at all ages in
the case group than in the control group. All
intrinsic muscle injuries were accompanied
by interspinous ligament edema in subjects
with and those without symptoms.
The comparison of pathologic changes in
intervertebral disks (degeneration, herni­
ation) and structures other than disks (signal
intensity increase in the intrinsic spinal
muscles and subcutaneous edema) according
to age within the case and control groups
revealed a statistically significant relation. A
weak positive correlation between age and
pathologic condition was found for disk
herniation (control group, r = 0.348, p =
0.0001; case group, r = 0.299, p = 0.0001),
intrinsic spinal muscle injury (control group,
r = 0.208, p = 0.001; case group: r = 0.159,
p = 0.002), and subcutaneous edema (control
group, r = 0.325, p = 0.0001; case group, r =
0.327, p = 0.0001). A statistically moderate
positive correlation between age and
intervertebral disk degeneration was found
in both the case and control groups (case
group, r = 0.462, p = 0.0001; control group,
r = 0.508, p = 0.0001).
There was a statistically significant
difference in interspinous ligament degen­
eration or rupture at L3–L4 and L4–L5 only
between age groups of patients with symp­
toms (p < 0.05). No statistically sig­nificant
relation was found between age and inter­
spinous ligament edema at T12–L1, L1–L2,
L2–L3, or L5–S1, neocyst formation, or facet
joint effusion.
Case–control comparison showed a statis­
tically significant difference with regard to
the following pathologic conditions: facet
joint effusion (p = 0.0001), interspinous
ligament edema at all lumbar levels (p =
0.001 for T12–L1, p = 0.0001 for all other
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Fig. 8—Graph shows percentages of posterior paraspinal degenerative changes
according to sex in control group. White bars indicate men (126 of 249 subjects);
gray bars, women (123 of 249 subjects). ISL = interspinous ligament.
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Posterior Paraspinal Change
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Group 1 42/249
Group 2 47/249
Group 3 55/249
Group 4 47/249
Group 5 31/249
Group 6 27/249
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Posterior Paraspinal Change
Fig. 9—Graph shows percentages of posterior paraspinal degenerative changes
according to age in control group. Group 1, 15–30 years; group 2, 31–40 years;
group 3, 41–50 years; group 4, 51–60 years; group 5, 61–70 years; group 6, 71 years
and older. ISL = interspinous ligament.
AJR:191, October 2008
STIR for Lower Back Pain
levels), neocyst formation and synovial
cysts (p = 0.0001), and intrinsic muscle
degeneration (p = 0.0001). A similar relation
was found with regard to subcutaneous
edema (p = 0.03). Because, however, there
was a significant sex difference between
the case and control groups with regard to
subcutaneous edema, which was statistically
more frequent among women, a separate
evaluation was performed for men and
women. Thus within-sex comparison show­
ed subcutaneous edema more frequent in
patients with LBP than in those without
LBP, but the difference was not statistically
significant (men, p = 0.289; women, p =
0.180). Similarly, no statistically significant
difference was found in a comparison of
case and control groups with regard to both
intervertebral disk degeneration and disk
herniation (p > 0.05).
Discussion
This study, performed with subjects with
and subjects without symptoms who had
findings on MR images obtained with STIR
sequences, revealed that subjects reporting
LBP had a statistically significantly higher
ratio of facet joint effusion, interspinous
ligament injury, neocyst formation and
synovial cysts, and intrinsic spinal muscle
edema than did subjects with asymptomatic
changes. Intervertebral disk degeneration,
disk herniation, and subcutaneous edema,
however, were found to occur without a
statistically significant difference between
subjects with and those without symptoms. In
addition, the frequency of intervertebral disk
degeneration, disk herniation, subcutaneous
edema, and intrinsic spinal muscle edema
was found to increase with age whether or
not symptoms were present; intervertebral
disk degeneration was especially prominent.
The higher rates of facet joint edema,
interspinous ligament injury, neocyst for­
mation and synovial cysts, and intrinsic
spinal muscle edema among persons with
symptoms than among those without symp­
toms show that pathologic changes in the
posterior osteoarticular elements and soft
tissues of the spinal column may be the
cause of or a manifestation of the cause of
LBP. On the other hand, the similar rates of
intervertebral disk degeneration, disk herni­
ation, and subcutaneous edema in the case
and control groups indicate that these
findings may be found even if LBP is not
present. The age-related increase in inter­
vertebral disk degeneration, disk herniation,
AJR:191, October 2008
subcutaneous edema, and intrinsic spinal
muscle edema observed in both groups
indicates that those degenerative changes
may develop with age. Conventional MRI is
insufficient for visualizing these paraspinal
changes [5]. On STIR images, however, these
degenerative changes can be clearly visual­
ized owing to homogeneous fat suppression
and better depiction of edema than on
conventional MR images.
In a study by Jensen et al. [3], disk herniation
(diffuse or focal protrusion), being a frequent­
ly encountered asymptomatic finding, was as­
sumed to be an incidental finding on MR
images of patients with LBP. Savage et al. [9]
conducted a study with 149 patients with and
without LBP and found similar ratios and no
statistically significant difference between
the case and control groups regarding disk
herniation (excluding extruded or seques­
tered disks) and disk degeneration. Similar
findings were made in other studies [10, 11]
and in ours. As a result, we conclude there is
a poor correlation between LBP and disk
degeneration or herniation.
The posterior paravertebral elements
(facet joints, ligamentum flavum, interspin­
ous ligaments, supraspinous ligaments, and
para­spinous muscle structures) have a large
number of innervations. The interspinous
ligament, which is one of the most important
structures rendering stability to the spinal
column, is innervated by the medial branch
of the dorsal ramus [12, 13]. Acute trauma
sprains the interspinous ligament, and chron­
ic repetitive microtrauma usually results in
subtotal degenerative rupture of the ligament.
Degenerative changes in interspinous liga­
ments begin early in the second decade of life
in healthy persons. Rupture usually is present
in 20% of persons older than 20 years, especially at L4–L5 and L5–S1 [14]. In our study,
interspinous ligament rupture at L4–L5 was
found in 32% and at L5–S1 in 31% of healthy
subjects older than 20 years. Before this
study, only a limited number of studies
reported in the literature evaluated whether
an observed increase in interspinous ligament
signal intensity indicates the presence of
changes causing LBP. In a study conducted
with a small number of subjects with LBP
who had a mean age of 56 years, Jinkins [7]
found an increase in interspinous ligament
signal intensity on the fat-saturated T2weighted images of 71% of the subjects. The
control group was quite small, however, and
age distribution was not reported. Our study
revealed similar results with regard to presence
of interspinous ligament edema in the 51- to
60-year age group with symptoms; this find­
ing was most frequent at L4–L5 (75.9%) and
L5–S1 (82.8%). Our study was conducted
with a larger control group than Jinkins used,
and the results revealed a significantly higher
ratio of interspinous ligament edema in the
case group than in the control group, indicating
that the edema may be a cause of or a
manifestation of the cause of LBP.
In patients with interspinous ligament
injuries, the ligament becomes visible as an
area of high signal intensity on T2-weighted
images owing to inflammatory exudation and
inflammation of the fibrous bands. This high
signal intensity, however, resembles the fat
tissue surrounding the ligament on con­
ventional sequences, making it difficult to
differentiate. This problem necessitates use
of STIR [4] or fat-suppressed T2-weighted
sequences, both of which are effective at
showing inflammatory soft-tissue lesions, for
correct diagnosis [15, 16]. In their study
correlating imaging and surgical findings in
the cases of thoracolumbar trauma patients,
Lee et al. [17] found that fat-suppressed T2weighted imaging was highly specific and
sensitive for visualization of interspinous
ligament injury and correctly showed the
presence of the lesions. In our study, the
edematous and degenerative changes in the
posterior spinal elements not seen on
conventional T1- and T2-weighted images—
especially when the interspinous ligaments,
synovia, neocysts, and muscles were sur­
rounded by fat tissue—were easily visualized
on STIR images. Although it took approxim­
ately 20 seconds longer than the fat-sup­
pressed T2-weighted sequence, the STIR
sequence was especially preferred in our study
because it provided homogeneous fat sup­
pression with­out magnetic field inhomoge­
neity and with better depiction of edema.
It is thought [1] that degenerative changes
in the facet joint and an increased amount of
intraarticular fluid are among the important
overlooked causes of LBP. Study results [18,
19] support this idea in that LBP in some
patients was relieved after selective facet joint
block or facet denervation. Our study revealed
a higher frequency of facet joint effusion
among subjects with symptoms (85.5%) than
among subjects without symptoms (45.8%),
supporting the hypothesis that effusion
may be a possible cause or a manifestation
of the cause of LBP. Most degenerative
changes in the facet joint can be diagnosed
with conventional MRI [1]. However, joint
977
Lakadamyali et al.
effusion can be clearly visualized with the
STIR sequence, as found in our study. Our
study showed that 78% of cases of facet joint
effusion were accompanied by intervertebral
disk degeneration at the same level. The
explanation may be degenerative height
reduction of the intervertebral disk leading
to partial subluxation of the posterior facet
joint, which is usually accompanied by
intraarticular effusion [12].
Synovial cysts and neocysts of the pos­
terior spinal facets are rare lesions related
to degenerative lumbosacral changes [20].
These lesions may extend into the spinal canal
or be located in the posterior paraspinal soft
tissues. The number of studies in the literature
in which the frequency of synovial cysts and
neocysts was evaluated is small. In a study of
conventional sequences for MRI of patients
reporting back pain or sciatica, Doyle and
Merrilees [21] found a 7.3% frequency of
posterior synovial cysts. In our study group,
the rate of these cysts was 62.4%. We consider
the difference due to our use of the STIR
technique, which can clearly depict even
small cysts that are barely discernible from
the fat tissue in which they are embedded.
It is well known that synovial cysts
extending into the spinal canal can cause
neurologic symptoms. The clinical findings
of extraspinal cystic lesions, however, are
debated unless they cause a pressure effect
on the basic neurologic structures [1]. The
contribution to LBP of synovial cysts and
neocyst formation observed more frequently
in persons with symptoms (62.4%) than in
those without symptoms (15.3%) was prob­
ably due to degenerative and inflammatory
changes in the corresponding facet joints.
This supposition is supported by the results
of our study revealing that most of the
synovial cysts and neocyst formations in the
group with symptoms, unlike the subjects
without symptoms, were accompanied by
effusion in the neighboring facet joint.
Intrinsic spinal muscle changes can have a
direct (intrinsic spinal muscle strain or
rupture) or indirect (intrinsic spinal muscle
spasm) role in the pathogenesis of LBP [7].
Bennett and associates [8] used fat-sup­
pressed T2-weighted imaging to examine 20
gymnasts with a mean age of 16 years with
and without LBP and visualized muscle strain
only in those with LBP (19%). In our study,
increased intrinsic spinal muscle signal
intensity was observed in 12% of the subjects
in the 15–30 year age group with LBP. In the
other age groups, the rate of intrinsic spinal
978
muscle edema was higher in subjects with
symptoms (24.7%) than in those without
symptoms (4.8%). Thus we believe is it highly
probable that muscle strain is a cause of LBP.
Our study also revealed a statistically
significant age-related increase in intrinsic
spinal muscle edema. The age-related stati­
stically significant in­crease in inter­vertebral
disk degeneration and disk herniation and
of intrinsic spinal muscle edema shows that
degenerative changes in these structures may
appear with aging.
Acute or subacute degeneration of the
intrinsic spinal muscles, which originate
from and insert into the vertebrae (multifidus
and interspinales), usually develops owing to
intersegmental hypermobility, which leads
to degenerative rupture of the interspinous
ligament [22]. Jinkins [7] observed intrinsic
spinal muscle (interspinales and multifidus)
degeneration (abnormal signal intensity) in
only 7% of patients, but all patients with
increased muscle signal intensity had an
increase in interspinous ligament signal
intensity. In our study, the explanation for
the lesser degree of degenerative changes
observed in the intrinsic muscles than in
the interspinous ligaments is probably that
muscular tissue is stronger than ligamentous
tissue. Both muscular strain (which has high
signal intensity owing to muscle edema
or hemorrhage) and interspinous ligament
injury, can be overlooked, especially when
STIR sequences are not used.
The number of reports of evaluation of
edema of the subcutaneous soft tissues in the
posterior lumbar vertebral column is limited
[23, 24]. Furthermore, to our knowledge,
there are no reports of evaluation of the
presence of such edema in patients with LBP.
Increased signal intensity, which is assumed
to be subcutaneous tissue edema or fluid
collection, is believed to be an incidental
finding. The causes can be infectious,
inflammatory, traumatic, hydrostatic, and
even neoplastic. In their study involving
obese and nonobese persons without LBP,
Shi and associates [23] found that the rate
of the high signal intensity on fat-suppressed
T2-weighted images increased with age and
weight and among women. Similarly, in our
study, the incidence of subcutaneous edema
significantly increased with age and among
women. No statistically significant difference,
however, was encountered between persons
with and those without LBP with regard to
sex distribution of subcutaneous edema.
The higher ratio of subcutaneous edema
in persons with than those without LBP
might have been be due to poorer lymphatic
drainage in patients with LBP as the result of
pain-related restriction of physical activity.
Findings on MR images obtained with
conventional sequences in the evaluation of
patients with LBP who do not have evidence
of disk herniation usually do not contribute
to a definitive diagnosis, and patients receive
symptomatic treatment with no patho­
anatomic diagnosis [25]. An accurate diag­
nosis is important because it contributes to
the patient’s reassurance and trust in the
clinician [26]. If these changes are found,
patients can be treated and followed up
accordingly. Thus STIR sequences are im­
por­t ant for clear evaluation of the posterior
spinal structures as the possible cause of
LBP and for determination of the thera­
peutic approach.
Despite the large population, our study had
limitations. First, there was no correlation
between the lesions and the intensity of
symptoms (degree of pain). The lack of
control MRI examinations for evaluation
of the clinical and radiologic response to
therapy was another limitation.
The results of our study suggest that, with
high probability, degenerative changes in
the posterior paraspinal soft-tissue structures,
especially interspinous ligament edema, fac­
et joint effusion, neocyst formation, and
intrinsic spinal muscle edema, cause LBP in
some patients. Because of homogeneous fat
suppression and better depiction of softtissue edema, the STIR sequence is the best
imaging technique for visualizing the afore­
mentioned changes, and it adds only 2 min­
utes to the imaging examination. Therefore,
we suggest that for patients with LBP without
other obvious pathologic findings, the STIR
sequence be added to the MRI evaluation to
visualize degenerative changes in posterior
spinal structures as a possible cause of pain.
Acknowledgments
We thank Metin Karatas and Coşkun
Bakar for their help in performing the
statistical analysis.
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