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Focus On
Understanding and treating
spinal stenosis
Introduction
Classification
Lumbar spinal stenosis is narrowing of the central spinal canal,
lateral recess or the neural foramen. After initial recognition of
spinal stenosis in 1802, a gradual understanding evolved over
the next 150 years.1-4 Harris and Macnab described the importance of disc degeneration in the pathogenesis of stenosis.5
Macnab highlighted the lateral recess beneath the posterior
facet joint.6 Verbiest identified neurogenic claudication as a
result of spinal canal stenosis. 7
Lumbar spinal stenosis is classified according to its aetiology
(Table I).11 Postacchini divided the stenosis into primary (congenital), secondary (acquired) or combined forms.12
The congenital type is rare. There are anatomical abnormalities such as short pedicles in achondroplasia. Other causes
include hypochondroplasia, diastrophic dwarfism, Morquio's
syndrome, hereditary exostosis and cheirolumbar dysostosis.
The majority of patients present with acquired stenosis because
of degeneration in the fifth to seventh decades.
Anatomically, spinal stenosis can be central, within the lateral
recess, or in the foramen. Central canal stenosis occurs at the
level of the intervertebral disc with midline sagittal narrowing.
Lateral recess stenosis occurs when the traversing nerve root is
compressed beneath the superior articular process of the inferior vertebra, i.e. beneath the thickened facet joint.
Hansraj et al divided spinal stenosis into typical and complex
lumbar spinal stenosis (Table II).13,14 Typical cases were treated
with decompressive surgery, while complex stenosis required
decompression and fusion.
Anatomical considerations
The shape of the lumbar spinal canal varies and may be an oval,
rounded triangular or trefoil configuration.8 The trefoil configuration usually occurs at the fifth lumbar level, making L4-L5 the
narrowest level 9 (Fig. 1), and occurs in 25% of the population,
only appearing in adulthood.10 The anteroposterior diameter of
the lumbar spinal canal is critical in the pathogenesis and is
affected by the length of the pedicles.11
Pathogenesis
Kirkaldy-Willis et al described the sequence of degenerative
changes which result in central or lateral recess stenosis.15
Central canal stenosis (Fig. 2) is mainly created by hypertrophy of the ligamentum flavum, facet joint osteophyte formation and degenerative spondylolisthesis (Fig. 3).
Table I.
Aetiological classification of lumbar spinal stenosis
Congenital
Idiopathic
Achondroplastic
Fig. 1
View of the L5 vertebra showing the trefoil configuration of the spinal canal.
(Reprinted with permission from JBJS - Eisenstein S.M, The trefoil configuration of
the lumbar vertebral canal; A study of South African skeletal material. J Bone Joint
Surg [Br];62-B(1):73-7).
Acquired
Degenerative
Iatrogenic – post-surgical
Metabolic – Paget’s disease, fluorosis
Post-traumatic
Stenosis due to spondylolisthesis
Combined
Congenital with secondary degenerative changes
©2010 British Editorial Society of Bone and Joint Surgery
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T. S. RAJAGOPAL, R. W. MARSHALL
Table II.13,14
Typical lumbar spinal stenosis
•No previous lumbar spine operation
•No radiographic evidence of instability
•Degenerative spondylolisthesis < grade I, with no instability
•Degenerative scoliosis with < 20° curve
Complex Lumbar Spinal Stenosis
•Previous lumbar spine operation
•Radiographic evidence of instability
•Radiographic evidence of post operative junctional stenosis
•Degenerative spondylolisthesis > grade I, with instability
•Degenerative scoliosis with > 20° curve
Fig. 2
Fig. 3
Sagittal and axial T2-weighted MRI scans showing central canal stenosis.
Sagittal, axial and coronal T2-weighted MRI scans in an 80-year-old patient showing a degenerative spondylolisthesis at L4-L5. There is lateral recess stenosis but
there is no compression of the exiting nerve root on the coronal images (arrowed).
Lateral recess stenosis results from compression between
the medial aspect of a hypertrophic superior articular facet and
posterior aspect of the vertebral body and disc (Fig. 4). Hypertrophy of the ligamentum flavum and/or facet joint capsule, vertebral body osteophyte and disc protrusion exacerbate the
stenosis. The traversing nerve root is compressed in the lateral
recess (i.e. the L5 nerve root in the L4-L5 lateral recess).
Foraminal stenosis is rare and mainly occurs in isthmic
spondylolisthesis, where the exiting nerve root (i.e. the L5 nerve
root in L5-S1 isthmic spondylolisthesis) is compressed in the distorted foramen. It also occurs in far lateral disc herniation where
the exiting nerve root is compressed in the foramen, or extraforaminal zone (Fig. 5).
Lateral recess and foraminal stenosis are distinct entities
with different clinical implications.16
Natural history
The course of spinal stenosis is chronic and benign. Johnsson,
Rosen and Uden reported on 32 patients followed up for a mean
of 49 months (10 to 103) without any treatment.17 Of the
32 patients, 15% improved, 70% stayed the same and only 15%
became worse. The majority of patients followed up for four
years thus remained unchanged.
Despite a benign natural history, the long term is characterised by slow deterioration. A randomised study by Amundsen et
al compared surgical and conservative treatment with a ten-year
follow-up.18 The outcome was more favourable for surgical treat-
Fig. 4
Sagittal and axial T2-weighted MRI scans in a 74-year-old patient showing lateral
recess stenosis at L4-L5
ment, but an initial conservative approach was recommended
as late treatment still achieved a good result.
Clinical features
History. The symptoms are insidious, presenting in the sixth or
seventh decade. There may be a long history of low back pain
but the leg symptoms lead to presentation.
The patient with central canal stenosis has bilateral leg symptoms which are vague and often described as heaviness, soreness or weakness. The cardinal symptom is neurogenic
claudication which presents as numbness, weakness or discomfort in the legs; this may come on with walking or prolonged
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UNDERSTANDING AND TREATING SPINAL STENOSIS
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Differential diagnosis
Peripheral Vascular Disease. Table III shows the differences
between neurogenic and vascular claudication
Hip Osteoarthritis. Anterior thigh pain can be present in hip
arthritis as well as in spinal stenosis with involvement of the L3
or L4 nerve roots. However, pain on passive rotation of the hip
should alert the clinician to the possibility of hip disease. The two
conditions can coexist, so nerve root blocks and/or hip joint
injections with local anaesthetic and steroid may be necessary
to differentiate between them.
Peripheral Neuropathy. This diagnosis is determined more by
neurological symptoms than pain, and produces a stocking pattern of numbness. Electrophysiological testing confirms the
diagnosis.
Trochanteric Bursitis. Sometimes spinal stenosis patients are
diagnosed as having trochanteric bursitis. Some have suggested
a predisposition to this condition because of an “altered pelvic
balance”.22
Investigation
Fig. 5
Sagittal, coronal and axial T2-weighted MRI scans in a 62-yearold patient showing foraminal stenosis (arrow) caused by a far
lateral disc prolapse at L4-L5
standing and is relieved by sitting or rest. The patients are able
to walk further when leaning on a shopping trolley or walking
uphill because spinal flexion increases the space available for
the cauda equina and unfolds the ligamentum flavum. The painfree walking distance may vary.
Patients with lateral recess stenosis present with unilateral
radicular symptoms of leg pain along with numbness, paraesthesiae or burning in a dermatomal distribution. Pain radiates from
the buttock to the posterior thigh and lateral calf because most
compression occurs at L4-L5. If there is a higher lumbar lesion
then anterior thigh pain will be present. The symptoms may also
be provoked by walking.
Cauda equina syndrome or major neurological deficits are
very rare in the presence of canal stenosis.
Examination. Physical findings are limited. The diagnosis is
made from the history and confirmed with imaging. There may
be limitation of lumbar spinal extension, sensory deficit, muscle
weakness, limited straight leg raise, absent knee reflexes and
absent ankle reflexes.19 Neurological abnormalities are uncommon at rest. The “Shuttle walking test” has been suggested as a
reliable objective assessment of walking distance.20 Loss of
distal vibration sense may be present but is common in older
patients anyway. Signs of cervical myelopathy may be detected,
as lumbar spinal stenosis is associated with cervical canal narrowing in 5% of the patients (Tandem stenosis).21
Radiographs. Plain radiographs of the lumbosacral spine may
show narrowing of the disc space, facet joint osteoarthritis,
degenerative spondylolisthesis or degenerative scoliosis. Radiographs are also useful to exclude conditions such as tumour or
infection. Dynamic instability can be demonstrated by lateral
radiographs taken in the standing position with spinal flexion
and extension.
Computed Tomography (CT) Myelography. CT or CT myelography is useful in patients who have a contraindication to magnetic resonance imaging (MRI) scan (pacemaker, metallic
implants, etc.). On CT, midsagittal lumbar canal diameters of
less than 10 mm are regarded as an absolute stenosis while less
than 13 mm represents relative stenosis.23
MRI. MRI is the investigation of choice in confirming the diagnosis of spinal canal stenosis. Standard MRI examination includes
T1- and T2-weighted sagittal and axial sequences. The typical
findings in central or lateral recess stenosis include thickening
of the ligamentum flavum, facet joint hypertrophy and synovial
cysts, a trefoil appearance of the thecal sac, vertebral endplate
osteophytes and obliteration of perineural fat in the neural
foramina.
Parasagittal images can overdiagnose the incidence of foraminal stenosis. We recommend additional T2-weighted coronal
and Short T1 Inverted Recovery (STIR) sequences which demonstrate the nerve roots very well and confirm that the incidence of
foraminal stenosis is low in degenerative spondylolisthesis or
spinal stenosis, but exists mainly in isthmic spondylolisthesis or
extraforaminal disc protrusion.24
Neurophysiology. Peripheral neuropathy is a frequent concomitant finding or differential diagnosis in elderly patients with
spinal stenosis. Neurophysiological assessments including electromyography and nerve conduction studies are useful in identifying peripheral neuropathy and in differentiating between
radiculopathy and mononeuropathy (e.g. femoral neuropathy in
diabetics).
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T. S. RAJAGOPAL, R. W. MARSHALL
Table III.22,32 Differences between neurogenic and vascular claudication
Symptom/sign
Neurogenic Claudication
Vascular Claudication
Pain
Relief of symptoms
Walking up hill
Walking down hill
Cycling
Walking distance
Neurological symptoms
Neurological signs
Pulse
Skin
Proximal to distal
Relieved by sitting/forward bending
Better
Worse
No symptoms
Variable
Commonly present
May be positive especially after walking
Present
No changes
Distal to proximal
Relieved by standing
Worse
Better
Symptoms present
Fixed
Not present
Negative
Absent
Atrophic changes
Management
Conservative treatment. Analgesics,
non-steroidal
antiinflammatory drugs (NSAIDs), weight loss and physiotherapy are
used in the management of patients with spinal stenosis. Porter
and Hibbert25 reported that nasal calcitonin improved the symptoms of neurogenic claudication but a further randomised controlled study in 2004 showed no benefit.26
There is conflicting evidence in the literature about the use of
epidural steroids.27-29 However, they can provide temporary
relief of symptoms. Nerve root blocks are useful in treating radicular pain due to lateral recess stenosis.30
Surgical treatment. Surgery is indicated when conservative
measures fail and if moderate to severe leg symptoms interfere
with the patient's lifestyle. While these indications remain relative, progressive neurological deficit or cauda equina syndrome
represent absolute indications for surgery.
The greater the degree of compression, the better the outcome of surgery. While the primary objective of surgery is to
relieve the patient's leg symptoms, it is important to consider the
mechanical back pain and/or instability before deciding on the
type of surgical procedure.
The surgical options include:
• Decompressive laminotomy and partial facetectomy
• Decompressive laminectomy and partial facetectomy
• Micro-decompression
• Decompression and non-instrumented fusion
• Decompression and instrumented fusion
• Decompression and flexible stabilisation
• Inter-spinous spacer devices.
Decompressive Laminotomy and Laminectomy. The aim of
decompression is to remove the pressure on the cauda equina
and the individual nerve roots. The standard wide midline
decompressive laminectomy involves the removal of the spinous
processes, laminae, ligamentum flavum, medial part of the facet
joints and the facet capsule at all involved vertebral levels. However, the potential for segmental instability has led to more conservative operations.
The popular technique of multiple laminotomies may preserve segmental spinal stability, but Postacchini et al found that
patients who had laminotomies had less back pain but a slightly
higher incidence of nerve damage.31 Laminectomy was found to
be better for tight stenosis, as it allowed safer neural decompres-
sion. Multiple laminotomies are recommended in developmental stenosis since the patients are younger, the stenosis is rarely
severe and additional disc excision is often necessary.16
The results of surgical decompression for lumbar spinal stenosis vary from 57% to 81% excellent and good.32 The results for
open31,33 or microsurgical laminotomy34,35 are similar. No difference between clinical outcome and spondylolisthesis progression
was found when comparing laminectomy with laminotomy.36
While the initial results of decompressive laminectomy are
favourable, they can deteriorate in the longer term. Jonsson et al
reported on a prospective study of 108 patients who had laminectomy without fusion; 67% had excellent results at two years, but
deteriorated to 50% at five years; 18% required re-operation.37
It has been suggested16,37 that the ideal surgical patient
would have:
• Severe osteoligamentous compression of the neural structures
• Severe leg symptoms
• Moderate or no neurological deficit
• Little or no back pain
• Symptoms for less than four years
• No associated condition to impair mobility
Old age does not compromise the results of decompressive
surgery.38
Microdecompression. “Microdecompression” minimises operative trauma by approaching and entering the canal from one side
only. After decompressing the ipsilateral open side, the dissection crosses the midline beneath the overhanging spinous processes and contralateral laminae, allowing trimming of the facet
joints and other compressive structures on the contralateral
side from within the canal39 (Fig. 6). Mayer et al. reported success in 275 patients at a mean of two years, with an improvement in back pain in 48% of patients and of leg pain in 51%.40
In another study, with a longer follow-up of 100 patients, sciatica improved in 90% and back pain in 84%. For 82% of the
patients their results were graded as good or excellent according
to the Macnab criteria.39
Decompression and fusion. Fusion is generally recommended
in addition to decompression in the following circumstances:
• Degenerative spondylolisthesis
• Degenerative scoliosis
• Concomitant moderate to severe back pain
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UNDERSTANDING AND TREATING SPINAL STENOSIS
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Fig. 6
Post-operative axial CT scan showing the spinal canal to be opened up after microdecompression.
• Necessity for wide decompression with facet joint removal
• Recurrent spinal stenosis
Herkowitz and Kurz prospectively compared decompression
alone with decompression and fusion in 50 patients with spinal
stenosis and degenerative spondylolisthesis with a follow-up of
three years.41 The results were satisfactory (excellent or good) in
44% of the unfused and 96% in the fused group. Fischgrund et al
prospectively randomised 76 patients and compared intertransverse non-instrumented fusion with pedicle screw fusion.42
Excellent or good results were obtained in 82% of the intertransverse group (45% fusion rate) and 76% of the pedicle screw
group (82% fusion rate). The authors concluded that the use of
instrumentation leads to a higher rate of fusion but there was no
statistically significant clinical difference.
Kornblum et al later showed that the patients with a solid
fusion had improved long-term clinical results after five to
14 years.43
We can thus conclude that an instrumented fusion should be
performed in addition to decompression in the management of
degenerative spondylolisthesis.
Decompression and flexible stabilisation. In patients with spinal
stenosis who have segmental instability or degenerative spondylolisthesis, spinal decompression and stabilisation with a flexible or dynamic stabilisation system (e.g. Dynesys (Zimmer Ltd,
Swindon, Wilts)), is a controversial option, but Schnake,
Schaeren and Jeanneret found clinical results similar to decompression and fusion with pedicle screws.44
Interspinous spacer devices. Interspinous spacer devices are
inserted between the spinous processes to prevent extension of
Fig. 7
Sagittal, coronal and axial T2-weighted MRI Scans in an 89-year-old patient showing degenerative scoliosis and multilevel spinal stenosis
the symptomatic levels, but allow flexion, axial rotation and lateral bending.
Biomechanical studies have shown that in extension the
implants increase the dimensions of the spinal canal.45 There are
some favourable reports of outcome with interspinous devices;46-48
however, others report high failure rates for these implants and the
need for further surgery.49 The evidence is thus still inconclusive.
Interspinous spacer devices may have a place in elderly patients
who are unfit for anaesthesia and more major surgery.
Degenerative scoliosis
Spinal stenosis associated with degenerative scoliosis is a complex problem and its treatment is controversial. These patients
have multilevel disease with varying combinations of central, lateral recess or foraminal stenosis. They have a mixed pattern of
symptoms, which include stenotic, radicular and arthritic pain
(Fig. 7). Nerve root compression is present more often on the
concave side of the curve.50 True foraminal compression can
occur due to lateral disc herniation, collapse of the disc and scoliosis. The incidence of complications is high after surgery51 as
these are patients of advanced age who may have multiple medical comorbidities. Two types of deformity have been
described.52 Type I is a lumbar scoliosis with no or minimal rota-
6
T. S. RAJAGOPAL, R. W. MARSHALL
Fig. 8a
Fig. 8b
Anteroposterior and lateral radiographs of a 79-year-old patient with degenerative scoliosis, loss of lumbar lordosis and rotational deformity. The patient had persistent
back pain after a single-level fusion that had been performed many years earlier. a) pre-operative views, b) post-operative views showing correction of the degenerative
scoliosis and restoration of sagittal alignment.
tional deformity. Type II curves have degeneration superimposed
on a pre-existing scoliosis with greater rotational deformity and
loss of lordosis. Shorter segmental instrumentation is usually
possible for type I deformities while longer instrumentation with
sagittal plane reconstitution is necessary for type II curves
(Fig. 8).52 The choice of surgical technique remains controversial
but most would agree that decompression and instrumented
fusion is necessary for a successful outcome.13
Trichy S Rajagopal FRCS, Robert W Marshall FRCS
13. Hansraj KK, O'Leary PF, Cammisa FP, Jr., Hall JC, Fras CI, Cohen MS, et al.
Decompression, fusion, and instrumentation surgery for complex lumbar spinal stenosis. Clin Orthop 2001;384:18-25.
14. Hansraj KK, Cammisa FP, Jr., O'Leary PF, Crockett HC, Fras CI, Cohen MS, et
al. Decompressive surgery for typical lumbar spinal stenosis. Clin Orthop
2001;384:10-17.
15. Kirkaldy-Willis WH, Paine KW, Cauchoix J, McIvor G. Lumbar spinal stenosis.
Clin Orthop 1974;99:30-50.
16. Postacchini F. Management of lumbar spinal stenosis. J Bone Joint Surg [Br]
1996;78-B:154-64.
17. Johnsson KE, Rosen I, Uden A. The natural course of lumbar spinal stenosis. Clin
Orthop 1992;279:82-6.
Department of Orthopaedic Surgery, Royal Berkshire Hospital, Reading
RG1 5AN, UK.
18. Amundsen T, Weber H, Nordal HJ, Magnaes B, Abdelnoor M, Lilleas F. Lumbar
spinal stenosis: conservative or surgical management?: A prospective 10-year study.
Spine (Phila Pa 1976) 2000;25:1424-35; discussion 35-6.
Corresponding author: R. W. Marshall,
e-mail: [email protected]
19. Katz JN, Wright EA, Guadagnoli E, Liang MH, Karlson EW, Cleary PD. Differences between men and women undergoing major orthopedic surgery for degenerative arthritis. Arthritis Rheum 1994;37:687-94.
References
20. Spratt KF, Keller TS, Szpalski M, Vandeputte K, Gunzburg R. A predictive model
for outcome after conservative decompression surgery for lumbar spinal stenosis. Eur
Spine J 2004;13:14-21.
1. Portal A (ed.) Cours d'anatomie medicale au elements de l'anatomiede l'homme.
Paris: Badoin, 1802.
2. Sachs B FV. Progressive and Kyphotic rigidity of the spine. J Nerv Ment Dis
1900;27(1).
3. Putti V. New Conception in the treatment of sciatic pain. Lancet 1927;2:53-60.
4. Hirsch C. On lumbar facetectomies. Acta Orthop Scand 1948;17:240-52.
5. Harris RI, Macnab I. Structural changes in the lumbar intervertebral discs; their
relationship to low back pain and sciatica. J Bone Joint Surg [Br] 1954;36-B:304-22.
6. Macnab I. Negative disc exploration: an analysis of the causes of nerve-root involvement in sixty-eight patients. J Bone Joint Surg [Am] 1971;53-A:891-903.
7. Verbiest H. Fallacies of the present definition, nomenclature and classification of the
stenoses of the vertebral canal. Spine 1976;1:217-25.
8. Porter RW. Variations in shape and size of the lumbar spinal canal. Paleopathol
Newsl 1980;32:9-11.
9. Eisenstein S. Measurements of the lumbar spinal canal in 2 racial groups. Clin
Orthop 1976;115:42-6.
10. Papp T, Porter RW, Aspden RM. Trefoil configuration and developmental stenosis
of the lumbar vertebral canal. J Bone Joint Surg [Br] 1995;77(3):469-72.
11. Arnoldi CC, Brodsky AE, Cauchoix J, Crock HV, Dommisse GF, Edgar MA, et
al. Lumbar spinal stenosis and nerve root entrapment syndromes. Definition and classification. Clin Orthop 1976;115:4-5.
12. Postacchini F. Lumbar spinal stenosis and pseudostenosis. Definition and classification of pathology. Ital J Orthop Traumatol 1983;9:339-50.
21. Epstein BS, Epstein JA, Jones MD. Anatomicoradiological correlations in cervical
spine discal disease and stenosis. Clin Neurosurg 1978;25:148-73.
22. Wong DA, Transfeldt, E. Macnab's Backache. Fourth ed. Philadelphia: Lippincott
Williams & Wilkins, 2007.
23. Verbiest H. The significance and principles of computerized axial tomography in idiopathic developmental stenosis of the bony lumbar vertebral canal. Spine (Phila Pa
1976) 1979;4:369-78.
24. Rajagopal TS, Marshall, R.W., McKenzie, J., Archibald, C. Improved diagnosis
of spinal stenosis with coronal MRI, 2010 - Research in Progress.
25. Porter RW, Hibbert C. Calcitonin treatment for neurogenic claudication. Spine (Phila
Pa 1976) 1983;8:585-92.
26. Podichetty VK, Segal AM, Lieber M, Mazanec DJ. Effectiveness of salmon calcitonin nasal spray in the treatment of lumbar canal stenosis: a double-blind, randomized, placebo-controlled, parallel group trial. Spine (Phila Pa 1976) 2004;29:2343-9.
27. Kraemer J, Ludwig J, Bickert U, Owczarek V, Traupe M. Lumbar epidural
perineural injection: a new technique. Eur Spine J 1997;6:357-61.
28. Chou R, Atlas SJ, Stanos SP, Rosenquist RW. Nonsurgical interventional therapies for low back pain: a review of the evidence for an American Pain Society clinical
practice guideline. Spine (Phila Pa 1976) 2009;34:1078-93.
29. Cuckler JM, Bernini PA, Wiesel SW, Booth RE, Jr., Rothman RH, Pickens GT.
The use of epidural steroids in the treatment of lumbar radicular pain. A prospective,
randomized, double-blind study. J Bone Joint Surg [Am] 1985;67-A:63-6.
THE JOURNAL OF BONE AND JOINT SURGERY
UNDERSTANDING AND TREATING SPINAL STENOSIS
30. Datta S, Everett CR, Trescot AM, Schultz DM, Adlaka R, Abdi S, et al. An
updated systematic review of the diagnostic utility of selective nerve root blocks. Pain
Physician 2007;10:113-28.
31. Postacchini F, Cinotti G, Perugia D, Gumina S. The surgical treatment of central
lumbar stenosis. Multiple laminotomy compared with total laminectomy. J Bone Joint
Surg [Br] 1993;75:386-92.
32. Zingg PO, Boos N. Lumbar Spinal Stenosis. In: Boos N, Abei, M (eds). Spinal Disorders. Berlin Heidelberg: Springer-Verlag, 2008:513-37.
33. Aryanpur J, Ducker T. Multilevel lumbar laminotomies: an alternative to laminectomy
in the treatment of lumbar stenosis. Neurosurgery 1990;26:429-32; discussion 33.
34. Khoo LT, Fessler RG. Microendoscopic decompressive laminotomy for the treatment
of lumbar stenosis. Neurosurgery 2002;51(5 Suppl):S146-54.
35. Tsai RY, Yang RS, Bray RS, Jr. Microscopic laminotomies for degenerative lumbar
spinal stenosis. J Spinal Disord 1998;11:389-94.
36. Thomas NW, Rea GL, Pikul BK, Mervis LJ, Irsik R, McGregor JM. Quantitative
outcome and radiographic comparisons between laminectomy and laminotomy in the
treatment of acquired lumbar stenosis. Neurosurgery 1997;41:567-74; discussion 74-5.
37. Jonsson B, Annertz M, Sjoberg C, Stromqvist B. A prospective and consecutive
study of surgically treated lumbar spinal stenosis. Part I: Clinical features related to
radiographic findings. Spine (Phila Pa 1976) 1997;22:2932-7.
38. Sanderson PL, Wood PL. Surgery for lumbar spinal stenosis in old people. J Bone
Joint Surg [Br] 1993;75-B:393-7.
39. Orpen NM, Corner, JA, Shetty R, Marshall RW. Micro-decompression for lumbar
spinal stenosis: the early outcome using a modified surgical technique. J Bone Joint
Surg [Br] 2010;92-B:550-4.
40. Mayer HM, List J, Korge A, Wiechert K. Microsurgery of acquired degenerative
lumbar spinal stenosis. Bilateral over-the-top decompression through unilateral
approach. Orthopade 2003;32:889-95.
41. Herkowitz HN, Kurz LT. Degenerative lumbar spondylolisthesis with spinal stenosis. A prospective study comparing decompression with decompression and intertransverse process arthrodesis. J Bone Joint Surg [Am] 1991;73-A:802-8.
42. Fischgrund JS, Mackay M, Herkowitz HN, Brower R, Montgomery DM, Kurz
LT. 1997 Volvo Award winner in clinical studies. Degenerative lumbar spondylolisthe-
7
sis with spinal stenosis: a prospective, randomized study comparing decompressive
laminectomy and arthrodesis with and without spinal instrumentation. Spine (Phila Pa
1976) 1997;22:2807-12.
43. Kornblum MB, Fischgrund JS, Herkowitz HN, Abraham DA, Berkower DL,
Ditkoff JS. Degenerative lumbar spondylolisthesis with spinal stenosis: a prospective long-term study comparing fusion and pseudarthrosis. Spine (Phila Pa 1976)
2004;29:726-33; discussion 33-4.
44. Schnake KJ, Schaeren S, Jeanneret B. Dynamic stabilization in addition to
decompression for lumbar spinal stenosis with degenerative spondylolisthesis. Spine
(Phila Pa 1976) 2006;31:442-9.
45. Siddiqui M, Karadimas E, Nicol M, Smith FW, Wardlaw D. Influence of X Stop
on neural foramina and spinal canal area in spinal stenosis. Spine (Phila Pa 1976)
2006;31:2958-62.
46. Kuchta J, Sobottke R, Eysel P, Simons P. Two-year results of interspinous spacer
(X-Stop) implantation in 175 patients with neurologic intermittent claudication due to
lumbar spinal stenosis. Eur Spine J 2009;18:823-9.
47. Kondrashov DG, Hannibal M, Hsu KY, Zucherman JF. Interspinous process
decompression with the X-STOP device for lumbar spinal stenosis: a 4-year follow-up
study. J Spinal Disord Tech 2006;19(5):323-7.
48. Zucherman JF, Hsu KY, Hartjen CA, Mehalic TF, Implicito DA, Martin MJ, et
al. A multicenter, prospective, randomized trial evaluating the X STOP interspinous
process decompression system for the treatment of neurogenic intermittent claudication: two-year follow-up results. Spine (Phila Pa 1976) 2005;30:1351-8.
49. Verhoof OJ, Bron JL, Wapstra FH, van Royen BJ. High failure rate of the interspinous distraction device (X-Stop) for the treatment of lumbar spinal stenosis caused
by degenerative spondylolisthesis. Eur Spine J 2008;17:188-92.
50. Epstein JA, Epstein BS, Jones MD. Symptomatic lumbar scoliosis with degenerative changes in the elderly. Spine (Phila Pa 1976) 1979;4:542-7.
51. Cho KJ, Suk SI, Park SR, Kim JH, Kim SS, Choi WK, et al. Complications in posterior fusion and instrumentation for degenerative lumbar scoliosis. Spine (Phila Pa
1976) 2007;32:2232-7.
52. Simmons ED. Surgical treatment of patients with lumbar spinal stenosis with associated scoliosis. Clin Orthop 2001:45-53.