CHAPTER
60
The Natural History of
Spondylolisthesis
The natural history of spondylolisthesis is not completely
understood. This is largely because studies have not specifically
looked at the various subtypes of spondylolisthesis. Since devel-
opmental, acquired spondylolytic, and degenerative spon-
dylolisthesis have different etiologies, it is likely that their
natural histories would also be different. A review of the pres-
ent available literature does not allow the reader to clearly dif-
ferentiate between the natural history of developmental and
so-called isthmic spondylolisthesis.5
Most studies have a retrospective nature, lack differentiation
between different types of slips, and have limited follow-up. In
addition, most studies have focused on the isthmic spon-
dylolisthesis, not differentiating between true acquired stress
fractures through normal posterior elements or fractures
through dysplastic posterior elements, such as in spina bifida
occulta. As such, our understanding of this heterogeneous
group of processes that result in spondylolisthesis is limited.
For the purposes of this chapter, we will henceforth refer to
spondylolytic spondylolisthesis as acquired slips secondary to
true stress fractures through normal posterior elements.
Developmental spondylolisthesis will refer to slips with varying
degrees of dysplasia of the posterior elements and, in some
severe cases, dysplasia of the anterior column as well.
SPONDYLOLYTIC SPONDYLOLISTHESIS
There appears to be a genetic and familial association with
spondylolysis and spondylolisthesis (Fig. 60.1). Wiltse showed
that 26% of patients with isthmic spondylolisthesis had first-
degree relatives with a similar condition, indicating that there
may be a genetic familial effect.13 In a cadaveric study, White-
sides et al12 reported on two distinct populations with high
rates of spondylolytic spondylolisthesis, namely Aleut and
Arikara Plains Indians (27% incidence and 9% incidence of
spondylolisthesis, respectively). According to the authors, the
high familial incidence of spondylolisthesis in these reports
suggests an underlying developmental (rather than acquired)
etiology.
In a cohort of patients with spondylolytic spondylolisthesis
with a 45-year follow-up, Beutler et al1 showed that the risk of
progression was indeed very small.1 The clinical outcome of
patients with grade I or II slips was the same as the general
576
LWBK836_Ch60_p576-580.indd 576
Kim Hammerberg
Mustafa Khan
population, and patients with unilateral pars defects did not
progress to a frank slip. Also, they did not find any correlation
between the amount of slip progression and the presence of
back pain.
One of the most well-known studies about the natural his-
tory of spondylolytic spondylolisthesis is by Frederickson et al.4
The authors began by studying a cohort of 500 first-grade chil-
dren. Twenty-two (4.4%) subjects had unilateral or bilateral
defects of the pars interarticularis. These children were fol-
lowed up to age 18. Of note, only 34% of the original study
population was available for follow-up at age 18. At the latest
follow-up period, an additional eight children had radiographic
evidence of pars interarticularis defects. Thus, the incidence of
spondylolisthesis increased to 5.8%. Of the children with spon-
dylolisthesis, 70% had spina bifida occulta, which would be clas-
sified as developmental by Marchetti and Bartolozzi. There was
a genetic predisposition as well, since there was a higher inci-
dence of spondylolisthesis in the children of parents who had
spondylolisthesis themselves. Again this finding suggests a
developmental etiology. In this study, radiographic progression
was rare and minimal (seen only in four male patients) and was
never seen after age 16.
There have been conflicting reports in the literature about
risk factors for slip progression. Danielson et al3 reported on a
cohort of 311 patients with spondylolisthesis with respect to
radiographic progression. The mean age at diagnosis was
16 years, and the patients were followed for only 4 years. The
authors defined progression as a minimum slip increase of
20%. By this criterion, only 9/311 (3%) patients showed radio-
graphic progression. Although girls had a higher percentage
slip at diagnosis, they did not have a higher rate of slip progres-
sion. The authors concluded that they were unable to identify
any risk factors for progression, including gender, slip angle,
and lumbar index. Whitesides et al12 studied three radiographic
parameters (pelvic incidence, lumbar index, and sacral table
angle) in Aleut and Arikara Plains Indians cadavers to deter-
mine whether they had any etiologic or predictive value. They
concluded that only sacral table angle had etiological signifi-
cance in the development of spondylolytic spondylolisthesis,
whereas the changes in the shape of proximal sacrum and
lumbar index appeared to be secondary (Fig. 60.2). In particu-
lar, a low sacral table angle was associated with a higher incidence
of spondylolysis. Other authors have observed that factors
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 Chapter 60 The Natural History of Spondylolisthesis 577

A B

C D

Figure 60.1. Patient with L5 spondylolysis at the age of 2 years 5 months (A and B). Follow-up radiograph
at the age of 17 years 6 months shows progression to a grade I spondylolisthesis (C and D).

associated with the progression of isthmic spondylolisthesis

include females, 50% slip, and those children whose slip was
diagnosed before their adolescent growth spurt.2
Most patients with spondylolytic spondylolisthesis will expe-
rience some progression of their slips as adults, secondary to
disc degeneration. The slips rarely progress beyond grade II
(Fig. 60.3).

Figure 60.2. Methods of determining PI, STA, STI, and LI. STA is
that angle in the midline sagittal plane subtended by a line drawn from
the anterior aspect of the superior end plate of S1 to its posterior edge
and a line drawn from that point caudally to the posterior midline
point of the caudal end plate of S1. PI, pelvic incidence; STA, sacral
table angle; STI, sacral tilt index; LI, lumbar index. (Reprinted with
permission from Whitesides TE Jr, Horton WC, Hutton WC, Hodges L.
Spondylolytic spondylolisthesis: a study of pelvic and lumbosacral
parameters of possible etiologic effect in two genetically and geographi-
cally distinct groups with high occurrence. Spine 30(6S):S12--S21.)
DEVELOPMENTAL SPONDYLOLISTHESIS
Dysplasia of the bony hook at the lumbosacral junction (Wiltse
Newman type I; Marchetti--Bartollozi developmental type)
predisposes L5 to slip anteriorly on the sacrum (Fig. 60.4). The
predisposition to develop spondylolisthesis, especially high-grade
slips, also depends on the development of the anterior sacral
support. The slip can occur with intact or fractured posterior
elements. If the posterior elements remain intact, the canal

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 578 Section VI Spondylolisthesis

A B C

Figure 60.3. Grade II spondylolytic spondylolisthesis of L5 on S1 in an adult (A and B). The sagittal mag-
netic resonance image shows a dome-shaped sacrum with widening of the anteroposterior canal diameter at
the lumbosacral junction (C).

diameter will not increase as the slip progresses and may result
in compression of the neural elements. If the compression is
severe enough, L5 radiculopathy and even cauda equina syn-
drome from entrapment of the sacral nerve roots may result. A
study by McPhee et al showed that patients with dysplastic spon-
dylolisthesis are at higher risk of progression than spondylolytic
spondylolisthesis9 (Fig. 60.5).
In a long-term study of high-grade (Meyerding III or IV)
spondylolisthesis (treated with and without surgery) followed
out to an average 18 years, most had a good outcome.6 Forty-
five percent of the patients had minor neurological complaints,
but none had severe symptoms such as incontinence. Of the
patients who were treated nonsurgically, 36% were asymptom-
atic. This indicates that the prognosis for even high-grade
patients (with or without surgery) is varied and only rarely
involves severe symptoms or major neurological dysfunction. In
its most severe form, high-grade spondylolisthesis (grade V;
spondyloptosis), the entire vertebral body translates and angu-
lates anteriorly to the caudal vertebra, creating an acute lum-
bosacral kyphosis (Fig. 60.6). Takahashi et al10 described this
deformity as kyphospondylolisthesis. The angulatory change is
not observed in spondylolytic slips without dysplasia.
Yue et al studied 27 cases of spondyloptosis and found that
pars interarticularis defects were present in 89% of the cases.14

L4

S1 L5

A B C

Figure 60.4. Developmental spondylolisthesis that progressed from a grade III (A) to a grade IV (B). Note
the compression of the thecal sac at L5-S1 junction on magnetic resonance imaging (C).

LWBK836_Ch60_p576-580.indd 578 8/25/11 9:51:24 PM


A B
Figure 60.5. A 3-year-old patient with a grade I L5-S1 developmental spondylolisthesis (A), which progressed
to a grade II slip at age 7 (B). It progressed even further to a high-grade spondylolisthesis by age 14 (C).
In addition, spina bifida was also present in 89% of the cases. In
all (100%) of the cases, they noted that the proximal sacrum
had a rounded appearance, suggesting that epiphyseal injury to
the proximal sacrum during childhood/adolescence may be a
contributory factor. In a magnetic resonance imaging study of
patients with severe spondylolisthesis, Takahashi et al10 also
demonstrated a unique defect between the bony and cartilagi-
nous end plates of the sacrum.
DEGENERATIVE SPONDYLOLISTHESIS
In contrast to other types of spondylolisthesis, degenerative
spondylolisthesis is characterized by an intact neural arch with
Figure 60.6. Grade V spondylolisthesis (spondyloptosis) wherein
the L5 vertebral body has translated completely anteriorly over S1.
LWBK836_Ch60_p576-580.indd 579
Chapter 60 The Natural History of Spondylolisthesis 579
C
a progressive slip that leads to narrowing of the spinal canal.
Disc degeneration is thought to be the initiating event, which
is believed to result in microinstability of the spinal segment.
This is eventually followed by facet incompetence, ligamentous
laxity, and buckling of the ligamentum flavum.
Typically, the symptoms of degenerative spondylolisthesis are
neurogenic claudication and/or radiculopathy. It is most com-
monly seen in women older than 50 years and occurs most often
at L4-5 level. Matsunaga et al8 followed a cohort of patients with
degenerative spondylolisthesis and found that only 30% showed
a progression of the slip.8 Patients who presented with neuro-
genic claudication had a better outcome with surgical interven-
tion, whereas 76% of patients who presented without neurologi-
cal deficit did not deteriorate with time. In a randomized
prospective study, Herkowitz and Kurz7 demonstrated that
patients with degenerative spondylolisthesis treated by decom-
pression and fusion had a better outcome than those treated
with decompression alone. Surgical treatment was recently
shown to be superior to nonoperative treatment in the recent
SPORT (Spine Patient Outcomes Research Trial) study.11
CONCLUSION
On the basis of the literature, developmental spondylolisthesis
is more likely to progress than spondylolytic spondylolisthesis.
However, this risk of progression is surprisingly small. Surgical
intervention is advisable for patients with neurologic dysfunc-
tion who may or may not demonstrate slip progression. Neuro-
logic dysfunction is not commonly seen, most probably because
the neural arch is not contiguous (either due to the pars defect
or spina bifida). In case of degenerative spondylolisthesis, sur-
gical treatment for neurogenic claudication is indicated if non-
operative measures are unsuccessful.
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